Initial Poor Graft Dysfunction and Primary Graft Non-Function After Orthotopic Liver Transplantation

Orthotopic liver transplantation (OLT) has become the effective treatment for end-stage liver diseases. Since the 1980s, the successful rate of liver transplantation has increased with the improvement of operative methods and the use of University of Wisconsin (UW) solution. Nevertheless, liver procurement and implantation are inevitably associated with allograft damage. Lack of donor liver hinders OLT and leads to an increase in the number of deaths on the waiting list and as a consequence the transplant community has greatly expanded the use of non-ideal donors to improve the rate of transplant (Delmonico et al., 2005). Donor pool expansion strategies such as the use of living donors, cadaveric split livers, and “extended criteria donors” (ECD)/marginal donors are being pursued. These may predispose recipients to graft dysfunction and increase long-term risk and survival in recipients. Primary graft non-function (PGNF) is the most severe type of graft damage after OLT, followed by initial poor graft function (IPGF) (Chui et al., 2000). Emergency hepatic retransplantation is necessary because of the extreme high mortality of PGNF. Evaluation of IPGF is determined by a high level of alanine aminotransferase (ALT) and/or aspartate aminotransferase (AST). IPGF directly influences the survival in the hepatic graft. Ultimately, some grafts recover completely while others need to be retransplanted (Pokorny et al., 2000). IPGF and PGNF are associated with many factors, such as status of donor, quality of hepatic graft, long-term warm ischemia, cold ischemia, primary liver disease, status of liver function of recipients and operative techniques (Brokelman et al., 1999). For evaluation of the donor hepatic allograft with regard to pre-existing diseases, in particular macrovesicular steatosis and post-transplant evaluation of hepatic graft function, liver biopsy is the most challenging and valuable clinical practice. Recently, some progress has been made in the prevention and treatment of early hepatic graft dysfunction. The present review provides broad discussion in the relevant sections.