Neurological Complications Occurring After Liver Transplantation: Role of Risk Factors, Hepatic Encephalopathy, and Acute (on Chronic) Brain Injury

Abstract

Orthotopic liver transplantation (LT) remains the only way to definitively cure patients with the most severe liver diseases.Because the survival rate is now fairly high, important questions about neurological sequelae or quality of life after LT have emerged. Indeed, LT represents a peculiar situation because up to 30% of patients present with neurological symptoms after LT compared with only 4% after cardiac transplant and 0.5% after renal transplant. These postoperative neurological symptoms have long been interpreted as sequelae of hepatic encephalopathy (HE). However, postoperative decompensation of an unknown cerebral condition due to the pathophysiology of cirrhosis or undiagnosed neurodegenerative disorders or aging constitute other possibilities that are underrecognized. Some patients who undergo LT for acute liver failure and patients with cirrhosis without episodes of HE and without any previous cerebral alteration also display post-LT neurological symptoms. This latter situation speaks in favor of a direct adverse effect of either general anesthesia, the surgical procedure, or factors related to the postoperative intensive care unit (ICU) environment. The role of inflammation, which has been described in the ICU setting, could also be a crucial determinant. In this review, we will discuss the neurological complications associated with LT, the neurocognitive complications after LT, and how to assess the LT-related neurological or neurocognitive complications. Furthermore, we will review the various hypotheses surrounding post-LT neurocognitive impairment and will conclude with recommendations for future directions.

Changes in NSE and S-100β during the perioperative period and effects on brain injury in infants with biliary atresia undergoing parent liver transplantation

“…Currently, it is generally believed that multiple factors are involved in perioperative brain injury during liver transplantation. The pathogenesis is that intraoperative liver ischemia/reperfusion leads to impaired autoregulation mechanism of cerebral blood flow, and intraoperative hemorrhage, infusion, and inferior vena cava blockage cause significant hemodynamic changes, resulting in drastic fluctuation of cerebral blood perfusion and oxygenation, especially in the neohepatic phase [28,29].…”

“…Furthermore, the release of inflammatory factors results in large amounts of oxygen free radicals, leading to cerebral edema, delayed neuronal death, and other serious injuries [28,29]. [15].…”

“…Ultimately, S-100β and NSE levels increase and peak after liver transplantation and reperfusion. Cardiac output does not recover rapidly in the early neohepatic phase; instead, it is decreased further, and numerous acidic metabolites, endotoxins, vasoactive substances, and inflammatory factors can cause damage to the nervous system in the early stage [28,29]. If liver transplantation is successful, the new liver can gradually recover those imbalances, and there is a gradual reduction trend after surgery.…”

Magnetic resonance spectroscopy: A surrogate marker of hepatic encephalopathy?

“…So far, MRS parameters have been shown to be influenced by changes in patient's neurological status 7 and therapeutic strategies, like transhepatic intrajugular portosystemic shunt placement or liver transplantation, for example. 8,9 Currently, MRS is not used as a diagnostic tool for HE in clinical practice, whereas it could be helpful, especially in minimal HE (MHE) where no gold-standard for diagnosis is available. 10 We report here our real-life experience of MRS in our outpatient clinics, where cirrhotic patients are explored when HE is suspected.…”

“…The etiology of cirrhosis was alcohol 35%, metabolic syndrome 13%, viral 26%, mixed 23%, other 3%. The median model for end-stage liver disease score was 10 [7][8][9][10][11][12]. Seven patients were excluded because consensus for diagnosis was not reached.…”