Circulating endotoxins and postreperfusion syndrome during orthotopic liver transplantation

Improvements in surgical technique and pretransplant evaluation, the intraoperative use of venous bypass, and the introduction of CsA immunosuppressive therapy have all contributed to confirm orthotopic liver transplantation as a therapeutic option in end-stage liver diseases. Since 1967, when the first extended survival of such a patient was reported, this procedure has unquestionably remained the most challenging encountered by anesthesiologists, especially in the hepatic reperfusion period. Liver revascularization during transplantation has been associated with complex and unpredictable changes in cardiovascular homeostasis, including decreased mean arterial pressure (MAP*) with sudden and significant increased cardiac index (CI) due to increased venous return and decreased systemic vascular resistances. The CI remains, however, lower than its preclamping value, and this is suggestive of ventricular dysfunction in terms of an abnormal response to volume loading during vena cava unclamping. This cardiovascular depression after the initial perfusion of the new grafted liver remains unexplained and shares some analogies with septic shock, in which the role of circulating endotoxins is now well established. A few authors have found relationships between perioperative endotoxemia levels at the end of the anhepatic period and postoperative complications and outcome, but none of them had ever related endotoxemia and postreperfusion syndrome (PRS). We have prospectively evaluated the evolution of circulating endotoxins during OLT, and have researched any relationship with the severity of PRS, in 15 consecutive adult patients without preoperative documented infection who underwent liver transplantation.