PRIMARY NONFUNCTION OF HEPATIC ALLOGRAFTS WITH PREEXISTING FATTY INFILTRATION1

One of the unresolved problems in liver transplantation is how to determine accurately the cause of the primary nonfunction that is seen in about 10% of hepatic grafts (1, 2). It is often assumed that ischemic injury has occurred when the new liver does not function. Acute immunologic injury comparable to the humorally mediated hyperacute rejection of kidneys probably occurs rarely, if at all (3), but an indolent version of hyperacute hepatic rejection that is not clearly associated with demonstrable preformed antibodies can cause hemorrhagic necrosis within 1 or 2 days (4). The other most common etiology of primary nonfunction probably is intraoperative injury of the transplant when a flawed operation is performed by the recipient team (1). Preexisting acute or chronic hepatic disease in the recipient will undoubtedly aggravate any of the foregoing factors, or may itself preclude success. Although hepatic injury may occur as part of the trauma that has led to brain death or may be an iatrogenic complication of the care that is provided, this may be difficult to prove even with biopsies of the homograft. Makowka et al. (5) have reported a surprising lack of correlation between so-called good- and bad-risk donor parameters and the clinical outcome of the recipient. We report here 2 examples of acute fatty infiltration of livers that had been procured from seemingly good donors who had been in good health until 1 and 2 ½ days previously. The grafts that were full of fat never functioned and were replaced immediately in 1 case and 3 days later in the other. This report suggests how to identify and avoid this lethal situation.