In a group of 276 consecutive liver transplants 8 primary graft nonfun
ctions were identified (2.9%). Recipients showed a progressive elevati
on of transferases (mean maximum value ALT: 5000+/-1892 U/l) and bilir
ubin (mean maximum value: 20+/-11,8 mg/dl) and a decrease in the perce
nt prothrombin time (mean minimum value 26+/-13 min.) in the post-impl
antation survival time of the 8 grafts (range 1-5 days). No statistica
lly significant differences were observed between mean cold and warm-i
schemia times for these 8 donor organs and those of a control group of
92 consecutive grafts. All organs except one were ABO isogroup and al
l except another one displayed negative lymphocytotoxic crossmatch. Pr
edominantly small-droplet hepatocytic vacuolization with no nuclear di
splacement was observed in plastic-embedded semithin sections of all p
ost-primary nonfunction liver tissues (severe in 4 grafts, centri-medi
ozonal in 2, and centrolobular in 2). In 3 cases where fresh liver tis
sue was available the lipidic nature of the vacuoles was confirmed wit
h electron microscopy and with frozen sections stained with Sudan III.
Other microscopic lesions were also observed: spotty monocellular coa
gulative necroses, variable extension of zonal coagulative necroses an
d hemorrhages, cholestasis and minor mixed inflammatory infiltrate. Co
mparative microscopic study of these tissues with the protocol biopsy
specimens obtained 2-4 hours after reperfusion demonstrated previous l
iver cell-vacuolization in only 3 cases. In conclusion, an acute progr
essive microvacuolar steatosis developed in this primary nonfunction s
eries. No specific etiopathogenic factors were identified.