Endotoxemia and Bacteremia During Hemorrhagic Shock The Link Between Trauma and Sepsis?

TLDR

Hemorrhagic shock in rats frequently leads to gut‑derived bacteremia. The study quantified bacteremia and endotoxemia during acute shock and compared the results with human trauma patients across shock severities. In rats, 50 % developed bacteremia and 87 % endotoxemia within 2 h of severe shock, while 56 % of trauma patients with systolic blood pressure ≤80 mmHg had bacteremia and two had endotoxemia, indicating that shock permits gut bacteria and endotoxin to enter the bloodstream and likely initiates sepsis.

Abstract

Previous investigations of a treated model of hemorrhagic shock in the rat indicated the frequent occurrence of bacteremia that appeared to derive from the gut. This paper determines the incidence of bacteremia and endotoxemia during the acute shock period and compares this with similar observations in humans in varying degrees of shock. Studies in 26 rats indicated that bacteremia and endotoxemia was present in 50% and 87%, respectively, by the end of 2 hours at a mean arterial pressure of 30 mmHg. Observations in 50 patients admitted to the trauma unit showed that positive bacterial blood cultures were present in 56% when the admission systolic blood pressure was 80 mmHg or less (p < 0.01 compared with either of the other groups). Endotoxemia was noticed in two such patients. Direct access of bacteria and endotoxin to the blood stream may occur during hemorrhagic or traumatic shock and is the probable cause of subsequent sepsis in traumatized patients when no other source is apparent.