Liver and intestinal lactate metabolism in patients with acute hepatic failure undergoing liver transplantation

Objective: To determine the relative contribution of the gastrointestinal t ract and the liver in lactate metabolism in patients with acute liver failu re (ALF) and the effect of liver transplantation on this. We hypothesized t hat the liver and gut are net producers of lactate in ALF and that this is reversed after liver transplantation. Setting. A university-affiliated specialist liver transplant operating thea ter. Subjects. Eleven patients with ALF undergoing liver transplantation. Measurements and Interventions: After ethical approval, 11 patients with AL F listed for orthotopic hepatic transplantation were studied. Whole blood w as analyzed for lactate concentration from radial artery (RA) catheter, por tal vein (PV), and hepatic vein (HV) during the dissection phase and was re peated postreperfusion of the liver graft. Gradients across the gut and the liver were calculated to see if there was net production or consumption. Results, HV lactate was significantly higher than arterial (p = .028) in pa tients with ALF before liver transplantation, suggesting splanchnic product ion of lactate. Total splanchnic lactate gradient (HV-RA) is positive in AL F. Both the gut (PV-RA) and the liver (HV-PV) were net producers of lactate . After liver transplantation, hepatic venous lactate falls below arterial levels but not significantly. The gradient across the gut (PV-RA) remained positive, but the transhepatic gradient (HV-PV) became significantly negati ve, showing consumption by the graft (p = .021). The magnitude of lactate c onsumption after transplantation correlated positively with portal venous l actate concentration (p = .029) and inversely with graft cold ischemic time (p = .007). Conclusion: The liver is a net producer of lactate in patients with ALF and an elevated whole blood lactate. After liver transplantation, the graft be comes a consumer of lactate as shown by the negative lactate gradient. The degree of consumption is dependent on portal venous lactate concentration a nd cold ischemic time.