A retrospective review is presented of neurologic complications in our first 143 consecutive adult patients (208 liver transplants in 143 adults and 18 children) undergoing liver transplantation. Nineteen (13.2%) of the 143 patients developed neurologic complications in the postoperative period. Immunosuppression was initiated intraoperatively with steroids with the addition of azathioprine on Day 1 and cyclosporine, adjusted by RIA to a level of 400‐600 ng/ml, on Day 2 post‐transplantation. Azathioprine is discontinued in the third month. Fourteen of the 19 patients (73.6%) presented with CNS complications characterized by: diffuse multifactorial encephalopathy (5 patients); leukoencephalopathy (2 patients) which required temporary (1 case) or permanent (1 case) discontinuation of cyclosporine A; hemorrhage (in 2 cases due to arterial hypertension and coagulopathy and another due to unknown causes); ischemic/anoxic injury secondary to cardiorespiratory arrest (2 patients) or arteriothrombosis (1 patient); and myelopathy (1 patient) due to vertebral compression (T10‐T11) secondary to osteoporosis. The diagnostic studies most often employed were computed tomographic (CT) (85.7%) and electroencephalography (EEG) (42.8%). Five of 19 patients (26.3%) suffered peripheral nervous system (PNS) complications: 1 patient with reversible Claude‐Bernard‐Horner Syndrome caused by central venous catheterization during anesthesia: 2 patients with peroneal nerve palsy due to compression below the knees by operating room table supports; 1 patient with an irreversible lesion of the right recurrent laryngeal nerve secondary to prolonged intubation and central venous catheterization; and 1 patient with a reversible lesion of the left brachial plexus secondary to inadvertant hyperextension of the upper extremity on the O.R. table due to the need for dialysis and catheterization of the axillary vein for veno‐venous bypass. Nine of fourteen (9/14, 64.2%) of patients with CNS lesion died. In five of the nine patients (55.5%) who died with CNS lesion, the neurologic lesions (CNS hemorrhage and anoxic‐isquemic injury) were directly or indirectly responsable for death. Strict control of patient positioning in the operating room, arterial hypertension and coagulation disturbance in the immediate postoperative period and serum cyclosporine A levels would eliminate the majority of neurologic complications in patients undergoing liver transplantation.
Fulminant hepatic failure without liver transplantation is associated with a high mortality rate (80-100 per cent). Some 254 liver transplantations were performed on 202 patients between April 1986 and February 1992. Of these, 26 patients had fulminant hepatic failure. The median age was 31.5 (range 3-60) years. Reduced-size grafts were used in seven patients. The preoperative mortality rate was six of 26 patients, and five patients died during follow-up. Ten patients underwent retransplantation and two a second retransplant. The overall mortality rate was 16 of 26 and actuarial survival rate was 62.7 per cent at 12 months and 48.7 per cent at 36 months. The preoperative mortality rate is relatively high but liver transplantation is currently recommended as a last-resort treatment for patients with fulminant hepatic failure in the absence of response to medical treatment.
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