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Hepatic and splanchnic oxygenation during liver transplantation

Tallgren, Minna MD; Mäkisalo, Heikki MD, PhD; Höckerstedt, Krister MD, PhD; Lindgren, Leena MD, PhD

Clinical Investigations
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Objective: To evaluate hepatic and splanchnic oxygenation during liver transplantation.

Design: Prospective study.

Setting: University hospital.

Patients: Ten adult patients undergoing liver transplantation.

Interventions: Standardized surgery and anesthesia without venovenous bypass.

Measurements and Main Results: Hepatic oxygenation was assessed by analyzing oxygen tension, oxygen saturation, and lactate concentration in hepatic venous blood. Splanchnic oxygenation was assessed by analyzing oxygen tension, oxygen saturation, and lactate concentration in portal venous blood and by gastric tonometry. Before reperfusion, the grafts were flushed with 1000 mL of acetated Ringer's solution and 400 mL of portal venous blood. The effluent blood from the graft was wasted and showed a mean pH of 6.86 and a lactate concentration of 9.4 mmol/L. Five minutes after portal reperfusion, most of the grafts produced lactate. Portal-hepatic venous PCO2 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 resolved without pharmacologic interventions. Mean gastric mucosal pH was 7.29 during the anhepatic phase and 7.40 at the end of surgery. One of the patients developed hepatic arterial thrombosis intraoperatively. Her data were analyzed separately. Later, the other patients recovered with good liver function, whereas the patient with hepatic arterial thrombosis was successfully retransplanted.

Conclusions: The liver grafts received well-oxygenated portal venous blood during reperfusion, despite the low values of gastric mucosal pH immediately before reperfusion. Hepatic oxygenation became adequate soon after reperfusion. In the patient with hepatic arterial thrombosis, the recovery of hepatic oxygenation was impaired and lactic acidosis persisted.

From the Department of Anesthesia (Drs. Tallgren and Lindgren) and the Fourth Department of Surgery (Drs. Mäkisalo and Höckerstedt), Helsinki University Central Hospital, Helsinki, Finland.

Supported, in part, by the Sigrid Juselius Foundation, Helsinki, Finland.

Address requests for reprints to: Leena Lindgren, MD, PhD, Department of Anesthesia, Surgical Hospital, Helsinki University Central Hospital, Kasarmikatu 11-13, FIN-00130 Helsinki, Finland.

© 1999 Lippincott Williams & Wilkins, Inc.