Neuropsychiatric complications after living donor liver transplantation: a prospective case series in an Egyptian center

Abstract

Introduction and aim Neuropsychiatric complications that develop after living donor liver transplantation (LT) are frequently encountered, though not adequately estimated among Egyptian recipients. We aimed to estimate the frequency of neuropsychiatric manifestations and neurocognitive functional changes after living donor LT. Patients and methods A prospective observational cohort study was conducted to evaluate 30 adult patients with end-stage liver disease preoperatively in a single Egyptian Transplant Center from November 2012 till January 2014. Relevant preoperative, intraoperative, and postoperative data were recorded and recollected and at 3 and 6 months of follow-up. The assessment included neurologic evaluation, Child–Turcotte–Pugh score, model of end-stage liver disease score, clinical hepatic encephalopathy staging scale, West Haven criteria, and International Society for Hepatic Encephalopathy and Nitrogen Metabolism score for semiquantitative assessment of encephalopathy. Results Hepatitis C virus was the main etiology for liver disease in 27 (90%) patients. Overt hepatic encephalopathy was seen in 26.6%, whereas covert hepatic encephalopathy occurred in 43.3%. Postoperatively, 76.7% of the patients demonstrated neuropsychiatric manifestations, with 50% of them showing mainly early major events, namely, encephalopathy. Late minor manifestation rates were 50%. Early cyclosporine administration and cold ischemia time longer than 40 min were significant predictors of occurrence of early neurologic events postoperatively (P=0.031 and 0.025, respectively). Both risk factors were associated with earlier and higher rates of neurologic complications. Conclusion Patients of living donor LT are at increased risk of developing early postoperative major neurologic sequelae, which become of less clinical significance later on. The patients’ cognitive functions improve with time after transplant.

Keywords

• calcineurin inhibitors
• cognitive function
• encephalopathy
• neurologic sequelae