Hepatic and splanchnic oxygenation during liver transplantation

Objective: To evaluate hepatic and splanchnic oxygenation during liver tran splantation. Design: Prospective study. Setting: University hospital. Patients: Ten adult patients undergoing liver transplantation. Interventions: Standardized surgery and anesthesia without venovenous bypas s. Measurements and Main Results:Hepatic oxygenation was assessed by analyzing oxygen tension, oxygen saturation, and lactate concentration in hepatic ve nous blood. Splanchnic oxygenation was assessed by analyzing oxygen tension , oxygen saturation, and lactate concentration in portal venous blood and b y gastric tonometry, Before reperfusion, the grafts were flushed with 1000 mt of acetated Ringer's solution and 400 mL of portal venous blood. The eff luent blood from the graft was wasted and showed a mean pH of 6.86 and a la ctate concentration of 9.4 mmol/L. Five minutes after portal reperfusion, m ost of the grafts produced lactate. Portal-hepatic venous Pco(2) difference ranged from 3 to 16 torr (0.4-2.1 kPa), By the time of restoration of the infrahepatic caval flow mean 24 mins later, eight of the grafts had stopped producing lactate, Mean hepatic venous oxygen tension was 47 torr (6.3 kPa ), stabilizing to 41 torr (5.5 kPa) at the end of surgery. Acidosis resolve d without pharmacologic interventions. Mean gastric mucosal pH was 7.29 dur ing the anhepatic phase and 7.40 at the end of surgery, One of the patients developed hepatic arterial thrombosis intraoperatively, Her data were anal yzed separately. Later, the other patients recovered with good liver functi on, whereas the patient with hepatic arterial thrombosis was successfully r etransplanted. Conclusions: The liver grafts received well-oxygenated portal venous blood during reperfusion, despite the low values of gastric mucosal pH immediatel y before reperfusion, Hepatic oxygenation became adequate soon after reperf usion, In the patient with hepatic arterial thrombosis, the recovery of hep atic oxygenation was impaired and lactic acidosis persisted.