Cerebral hemodynamic and metabolic changes in patients with fulminant hepatic failure during liver transplantation

Cerebral autoregulation and metabolism may be seriously compromised in patients with fulminant hepatic failure (FHF). The mechanism responsible for the alteration in cerebral blood flow (CBF) has not been yet clearly defined; however, it is known that it does correlate with liver function. Orthotopic liver transplant (OLT) rapidly restores normal liver function, but little is known about the restoration of cerebral metabolism and hemodynamics. To investigate the relationship between liver function and CBF, we evaluated autoregulation and metabolic changes during OLT in six patients comatose due to FHF.

We evaluated autoregulation based on a linear regression analysis between mean arterial blood pressure and parallel CBF velocity (CBFV) changes using transcranial Doppler ultrasound. Cerebral metabolism rate was estimated by the arterial-jugular venous oxygen content difference (a-jDO2), while the percentile variation in cerebral metabolic rate for oxygen (CMRO2) was estimated using CBFV percentile variation rather than CBF percentile variation (eCMRO2).

Prior to transplant autoregulation was impaired in all patients. However it markedly improved at the end of surgery (P <.05). The eCMRO2 improved as well, particularly among subjects who displayed prompt neurological recovery. In all patients the a-jDO2 was low before transplantation increasing to normal values at the end of surgery.

A hallmark of FHF seems to be failure of autoregulation, which is linked to uncoupling between CBF and CMRO2 as attested by an a-jDO2 lower than normal in all patients (luxury perfusion). The recovery of liver function rapidly improves cerebral hemodynamics and metabolic stability. The study of autoregulation and eCMRO2 recovery using Doppler monitoring proffers the possibility to predict early graft function after liver reperfusion. In our patients eCMRO2 seemed to be associated with improved neurological outcomes.