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continue to rise beyond 12 to 24 hours following transplantation, a more complete evaluation including assessment of mental status, coagulation profile, renal function, and hemodynamic stability should be carried out (Table 9.18).

A diagnosis of severe dysfunction or primary nonfunction must be differentiated from that of technical vascular complications including hepatic artery thrombosis, portal vein thrombosis, and hepatic congestion secondary to venous outflow obstruction. Preservation injury is generally associated with improving mental status and stable or improving prothrombin time which is easily correctable. In contrast, primary nonfunction is manifested by a patient who does not awaken and has progressive deterioration of mental status, a worsening coagulation profile which is not correctable, renal dysfunction, and hemodynamic instability. The treatment of severe hepatic dysfunction is primarily supportive. Intravenous prostaglandin E1 has been shown to be beneficial.23 Bioartificial liver support has been also used as a "bridge" until the liver either recovers or a suitable donor liver is located for urgent retransplantation. In cases of less severe dysfunction, the transaminases normalize over time as do the coagulation parameters. These patients, however, become severely cholestatic in the recovery period, likely as a result of impaired bile transport mechanisms and liver biopsy in these patients may reveal extensive bile plugging with ballooning hepatocyte degeneration consistent with severe cholestasis.

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