Impairment of hepatocellular excretory function, sepsis and liver insufficiency after liver resection

We appreciated the article by Gonnert and colleagues on hyperbilirubinemia from septic hepatocellular excretory dysfunction [1], a still improperly characterized issue in clinical settings. We address postoperative liver resection patients with prominently conjugated (~50 to 70 % conjugated) hyperbilirubinemia. Less relevant causes include transient insufficiency of remnant liver and prolonged intraoperative ischemia [2]; a threatening cause is occult sepsis. The pattern may be similar: prominently conjugated hyperbilirubinemia, with normal/moderately altered aspartate aminotransferase and alanine aminotransferase, alkaline phosphatase and gamma-glutamyltransferase. In occult sepsis this involves the risk of dismissing hyperbilirubinemia as transient liver insufficiency expected to spontaneously recover, with dreadful consequences, also because sepsis and liver insufficiency might coexist [3]. In post-hepatectomy patients, interpretation of hyperbilirubinemia is challenged by unreliability of landmarks based on hepatobiliary enzymes. Aspartate aminotransferase and alanine aminotransferase increase due to par-