[Liver failure after hepatic resection]

Pathophysiology of hepatic resection in 89 cases was investigated from the point of endotoxemia and phagocytic function in order to clarify the mechanism of postoperative liver failure. In the control group (n = 44) and the bile stasis group (n = 9) plasma endotoxin increased to 22 to 160pg/ml early after operation and decreased thereafter: but in the liver failure group (n = 10) it increased higher corresponding to high risk operation and the massive bleeding or anastomosis leakage. In control and bile stasis groups phagocytic K value, serum CH50, plasma fibronectin decreased to half of the preoperative level on the first postoperative day, and later improved. In liver failure group these levels decreased but never improved. Liver failure group was characterized by an irreversible platelets count decrease corresponding to the increase of serum bilirubin level. It was concluded that endotoxemia in the presence of a self defence system dysfunction is thought to be a trigger for organ failure.