Background/aims: Patients at high risk of liver failure sometimes suffer such failure with hyperbilirubinemia after hepatectomy. This report clarifies the clinicohistological findings in liver failure cases after excessive hepatectomy, and discusses the mechanisms of liver failure.
Methodology: Of 16 patients who suffered liver failure after hepatectomy between May 1992 and December 1999, 7 patients who underwent liver biopsy or autopsy were studied. The biopsy findings showed that, in each case, the percentages of hepatocytes that were apoptotic or binucleated were calculated. The number of bile plugs per 1000 micron 2 was counted and the thickness of collagen fibers in Disse's space was measured at 10 sites. The total bilirubin level was monitored over time, and the triggers, other than excessive hepatectomy, of increases in the bilirubin level were investigated.
Results: From the histological findings, liver failure cases were classified into cholestatic and nonregenerative types. Regeneration of hepatocytes and fibrosis in Disse's space were characteristic of the cholestatic type, while apoptosis of hepatocytes was characteristic of the nonregenerative type. Other than excessive hepatectomy, postoperative infection was the only trigger of liver failure in the cholestatic type, and ischemic changes of the liver resulted in liver failure in the nonregenerative type. The total bilirubin level changed more slowly in the cholestatic type than in the nonregenerative type after postoperative complications occurred.
Conclusions: Liver failure after excessive hepatectomy is of two types: cholestatic, mainly induced by postoperative infection, and nonregenerative, mainly induced by severe ischemia reperfusion injury.