and ALT values are not useful in the assessment of PI. Eighty liver allografts were studied to determine the (HEPATOLOGY 1997;25:184-189
.) predictive value of intraoperative biopsies and postoperative liver function tests for the development of preservation injury (PI). Peak transaminase (aspartate transaminase [AST] and alanine transaminase [ALT])Graft viability is of the utmost importance for successful and prothrombin time (PT) values achieved by each pa-orthotopic liver transplantation. Virtually all liver allografts tient during postoperative days (POD) 1 through 7 were are injured during transplantation, either as a result of determined. PI in day 0 preperfusion biopsies (0Pre) (ob-events leading to donor death, donor life support, or during tained immediately before implantation) and postperfu-the process of allograft extraction, cold preservation, implansion biopsies (0Post) (obtained immediately after revas-tation, hypoxic rewarming, and reperfusion. Allograft injury cularization) was categorized by histological criteria as resulting from the transplantation process is commonly represent or absent. PI in biopsies taken during POD 2 ferred to as preservation injury (PI). Preservation injury is through 14 was histologically graded as either moderate-a major contributor to primary allograft dysfunction, a term to-severe, mild, or absent. Of the 80 allografts, 8 were encompassing both primary nonfunction, defined as complete omitted because of primary nonfunction or postopera-allograft failure in the absence of apparent technical or imtive complications. 0Pre and 0Post biopsies were avail-munologic complications, and initial poor function (IPF), deable on 25 of 72 (35%) and 69 of 72 (96%) allografts, respec-fined as borderline graft function immediately after transtively. Only 2 (8%) of the 0Pre biopsies showed plantation.
histological PI compared with 48 (70%) of the 0Post biop-Several studies have attempted to identify donor, intraopsies. Fifty-nine patients were biopsied between POD 2 erative, and recipient factors predictive of primary allograft through 14. Of these, 15, 28, and 16 patients developed dysfunction. Primary dysfunction has been consistently assomoderate-to-severe, mild, or no evidence of PI, respec-ciated with prolonged cold and warm ischemia, severe macrotively. The presence of PI in the 0Post biopsy strongly vesicular steatosis, ABO blood group incompatibility, and docorrelated with the development of PI during POD 2 nor age over 50 years. [1][2][3][4][5][6][7][8][9][10][11][12] Additional risk factors include through 14 (P õ .0005). Peak AST and ALT values in retransplantation, markedly elevated donor transaminase patients with moderate-to-severe PI on POD 2 through levels, the use of pressors in the donor, and the use of re-14 were significantly elevated compared with those pa-duced-size liver grafts. 1-12 Despite efforts to avoid using donor tients with either mild (P Å .01 and .03) or no PI (P Å .02 organs with these and other potentially adverse variables, and .006). Because of ext...