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Fatty change in donor livers is a risk factor for poor function after orthotopic liver transplantation. Various prevalences of steatosis have been reported in time 0 biopsies. The aim of this research was to determine, in a longitudinal study, the degree (percent of hepatocytes involved) and type (size of vacuoles) of fatty change shown by various histologic techniques. Four staining methods were used on sections from three liver wedge biopsies—at liver procurement, at the back‐table, and after reperfusion—from 83 consecutive donor livers. Results in Sudan III‐stained (SS) sections showed the greatest sensitivity (87.1%), negative predictive value (91.8%), and agreement rate (κ= 0.77) when compared with results in thin (1 μm) plastic‐embedded toluidine blue‐stained (TBS) sections. High‐grade steatosis (>30% steatotic hepatocytes) was identified in 49.4% of SS sections, 46.9% of TBS sections, 38.5% of frozen hematoxylin‐eosin (H&E)‐stained sections, and 20.7% of deparaffinated H&E‐stained sections. Microscopic observations disclosed two types of steatotic pattern: (1) A predominantly small‐droplet lipid vacuolzation (high‐grade microsteatosis), similar to the steatosis associated with Reye syndrome, was seen in 29% of SS sections and 25% of TBS sections—approximately one‐fourth of grafts; and (2) a combined pattern of large and small fat drops (high‐grade macromicrosteatosis) was seen in 20% of SS sections and 22% of TBS sections. We concluded that moderate to severe steatosis is a frequent finding in donor livers. The difficulty in detecting lipidic microvacuoles in H&E‐stained sections may be the reason for underestimating the grade of fatty change or even for diagnosing as normal some biopsies with high‐grade microsteatosis.

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Fourteen cases are presented of preoperative portal vein thrombosis complicating orthotopic liver transplantation from an experience of 195 transplants carried out between April 1986 and April 1991. In four patients who suffered rethrombosis of the portal vein, the mortality rate was 100 per cent from various causes. Overall there were six deaths; two of those who died had a patent portal vein at death. Three patients underwent retransplantation: one for primary non-function, two for rejection. It is concluded that: (1) portal vein thrombosis should not represent an absolute contraindication to liver transplantation; (2) preoperative screening of prospective transplant recipients for portal thrombosis should be routine; (3) postoperative anticoagulation therapy and periodic Doppler ultrasonographic assessment of portal vein flow are important elements of post-transplant management; and (4) with thrombectomy and portal vein resection an end-to-end portal anastomosis may be performed with good results.