Overdose of Tacrolimus as the Trigger Causing Progression of Posterior Reversible Encephalopathy Syndrome and Subsequent Hepatic Infarction After Liver Transplant: A Case Report.

Posterior reversible encephalopathy syndrome is a neurotoxic state accompanied by unique brain imaging patterns and neurologic abnormalities, typically associated with several complex clinical conditions such as preeclampsia/eclampsia, solid-organ transplant procedures, autoimmune diseases, and immunosuppressive agents. The detailed mechanism of posterior reversible encephalopathy syndrome is not known, and the current therapy is only supportive care. Here, we present a 33-year-old parturient woman with preeclampsia complicated with hemolysis, elevated liver enzymes, and low platelet syndrome, fulminant hepatitis B, acute fatty liver, and posterior reversible encephalopathy syndrome. The patient developed gross hepatic infarction soon after liver transplant. After several possible causes were excluded, we found that progression of underlying posterior reversible encephalopathy syndrome-induced endothelial damage by overdose of tacrolimus may have been the major cause for deteriorating hypoperfusion of the transplanted liver and fatal graft failure. In liver transplant recipients, severe posttransplant hypoperfusion of the grafted liver may result in loss of the liver allograft and even mortality. Poor control of underlying posterior reversible encephalopathy syndrome-associated endothelial damage because of tacrolimus overdose may lead to severe hypoperfusion of grafted hepatic vessels and subsequent hepatic infarction. This report highlights tacrolimus as a potential trigger of posterior reversible encephalopathy syndrome and may inform clinical decisions regarding tacrolimus administration in liver transplant recipients with preexisting or newly developed posterior reversible encephalopathy syndrome.