title: Hepatic and splanchnic oxygenation during liver transplantation.
abstract: OBJECTIVE
  To evaluate hepatic and splanchnic oxygenation during liver transplantation.
  
  
  METHODS
  Prospective study.
  
  
  METHODS
  University hospital.
  
  
  METHODS
  Ten adult patients undergoing liver transplantation.
  
  
  METHODS
  Standardized surgery and anesthesia without venovenous bypass.
  
  
  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 P(CO2) 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.
authors.affiliation: Department of Anesthesia, Helsinki University Central Hospital, Finland.
authors.forename: M
authors.initials: M
authors.lastname: Tallgren
authors.forename: H
authors.initials: H
authors.lastname: Mäkisalo
authors.forename: K
authors.initials: K
authors.lastname: Höckerstedt
authors.forename: L
authors.initials: L
authors.lastname: Lindgren
mesh_terms: D000328:Adult; D001784:Blood Gas Analysis; D005260:Female; D005753:Gastric Mucosa / Q000378:metabolism; D006454:Hemoglobins / Q000378:metabolism; D006503:Hepatic Veins; D006785:Hospitals, University; D006801:Humans; D006863:Hydrogen-Ion Concentration; D019344:Lactic Acid / Q000097:blood; D008099:Liver / Q000098:blood supply / Q000378:metabolism*; D008102:Liver Circulation; D016031:Liver Transplantation / Q000502:physiology; D008875:Middle Aged; D010100:Oxygen / Q000097:blood*; D010101:Oxygen Consumption; D011169:Portal Vein; D011312:Pressure; D011446:Prospective Studies; D013152:Splanchnic Circulation; D013154:Spleen / Q000098:blood supply / Q000378:metabolism*; D013270:Stomach / Q000502:physiology
chemical_list: D006454:Hemoglobins; D019344:Lactic Acid; D010100:Oxygen