Regional Cerebral Oxygen Saturation Is a Sensitive Marker of Cerebral Hypoperfusion During Orthotopic Liver Transplantation

In Brief Neurological complications contribute significantly to morbidity and mortality of patients after orthotopic liver transplantation (OLT). One possible cause of postoperative neurological complications is cerebral ischemia during the surgical procedure. In this study, we investigated the relationship between intraoperative changes in regional cerebral oxygen saturation (rSO2) and postoperative values of neuron-specific enolase (NSE) and S-100, which are specific variables that indicate cerebral disturbances due to hypoxia/ischemia. The rSO2 was monitored continuously by near-infrared spectroscopy in 16 patients undergoing OLT. In addition, NSE and S-100 were determined in arterial blood before surgery and 24 h after reperfusion of the donor liver. Interestingly, clamping of the recipient’s liver led to a significant decline in rSO2 in eight patients, whereas the others tolerated clamping without major changes in rSO2. The decrease in rSO2 after clamping correlated significantly with postoperative increases in NSE (r2 = 0.57) and S-100 (r2 = 0.52). However, there were no significant differences between patients with and without rSO2 decline concerning hemodynamic variables. There were no significant correlations between ΔrSO2 and cardiac output (r2 = 0.20), NSE and cardiac output (r2 = 0.37), or S-100 and cardiac output (r2 = 0.24). Monitoring of rSO2 may be a useful noninvasive tool to estimate disturbances in rSO2 during OLT. IMPLICATIONS: Neurologic complications contribute significantly to morbidity and mortality of patients after orthotopic liver transplantation (OLT). We investigated whether monitoring regional cerebral oxygen saturation (rSO2) by near-infrared spectroscopy correlates with postoperative increases in neuron-specific enolase and S-100, two variables of cerebral tissue injury. The rSO2 sensitively reflected transient cerebral hypoperfusion during OLT.