[Organ failure during the perioperative period: pathophysiology and strategy]

After the establishment of the theoretical and clinical background of SIRS, the mechanism of organ failure induction during the perioperative period was gradually clarified. The deterioration of the mutual regulation of cytokines after surgical stress is considered to be a major cause of organ failure. Hypercytokinemia is one of the pathophysiological features after surgical stress, and thus a new therapeutic approach ameliorating the impaired cytokine network has been applied instead of direct targeting therapy for impaired organs. Organ failure can be anticipated based on a precise assessment of the severity of SIRS or CARS. For example, to prevent postsurgical hepatic failure it is important to minimize surgical stress by assessing the preoperative liver reserve capacity. Excessive surgical stress coupled with underestimation of liver function may result in primary multiple organ failure (MOF) after hepatic surgery. Secondary MOF after postsurgical infection may implicate the bacterial translocation mechanism. At present, only CHDF is considered to be a promising therapy for hypercytokinemia. Therefore the prophylactic approach cannot be neglected. The monitoring of cytokines such as IL-6 during the perioperative period provides valuable information for the prediction of organ failure.