Send to

Choose Destination
See comment in PubMed Commons below
Hepatogastroenterology. 1995 Jul;42(3):212-21.

A clinopathologic review of 8 liver graft primary nonfunctions.

Author information

Departamento de Anatomía Patológica, Hospital Universitario Doce de Octubre, Universidad Complutense, Madrid, Spain.


In a group of 276 consecutive liver transplants 8 primary graft nonfunctions were identified (2.9%). Recipients showed a progressive elevation of transferases (mean maximum value ALT: 5000 +/- 1892 U/l) and bilirubin (mean maximum value: 20 +/- 11.8 mg/dl) and a decrease in the percent prothrombin time (mean minimum value 26 +/- 13 min.) in the post-implantation survival time of the 8 grafts (range 1-5 days). No statistically significant differences were observed between mean cold and warm-ischemia times for these 8 donor organs and those of a control group of 92 consecutive grafts. All organs except one were ABO isogroup and all except another one displayed negative lymphocytotoxic crossmatch. Predominantly small-droplet hepatocytic vacuolization with no nuclear displacement was observed in plastic-embedded semithin sections of all post-primary nonfunction liver tissues (severe in 4 grafts, centri-mediozonal in 2, and centrolobular in 2). In 3 cases where fresh liver tissue was available the lipidic nature of the vacuoles was confirmed with electron microscopy and with frozen sections stained with Sudan III. Other microscopic lesions were also observed: spotty monocellular coagulative necroses, variable extension of zonal coagulative necroses and hemorrhages, cholestasis and minor mixed inflammatory infiltrate. Comparative microscopic study of these tissues with the protocol biopsy specimens obtained 2-4 hours after reperfusion demonstrated previous liver cell-vacuolization in only 3 cases. In conclusion, an acute progressive microvascular steatosis developed in this primary nonfunction series. No specific etiopathogenic factors were identified.

[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Loading ...
    Support Center