Acidaemia is less severe following reperfusion via the hepatic artery compared with the portal vein during liver transplantation

Abstract

Reperfusion of the liver during transplantation can cause cardiovascular changes such as systemic vasodilatation, pulmonary hypertension and cardiac dysfunction. We have previously demonstrated a slower increase in oxygen consumption when the hepatic artery was used for reperfusion rather than the portal vein, and had the clinical impression that overall patient stability was greater with the former technique.1 We therefore compared the acid–base changes which occur following reperfusion with each of these techniques. Twenty patients undergoing liver transplantation were studied. In all cases the piggyback technique was used, and anaesthetic management was similar. In 10 patients liver reperfusion was first via the portal vein followed by the hepatic artery; in the other 10 patients the hepatic artery was anastomosed first followed by the portal vein. Ventilation remained constant during the study period. Arterial blood was drawn for acid–base and whole blood lactate measurement at three time points: (1) immediately prior to reperfusion, (2) 30 min after reperfusion, (3) 60 min after reperfusion. Changes in variables were compared between the groups by Mann–Whitney U test corrected for multiple tests using the Bonferroni method. Data are shown in Table 18. All acid–base variables were similar between the groups prior to reperfusion. Following reperfusion acidaemia (H+ concentration) was more marked in the portal vein group and was accompanied by a larger increase inPaCO2. Changes in blood lactate and acidosis (Standard Bicarbonate Concentration) were similar between the groups. Our data indicate that a smaller acid load is released into the systemic circulation immediately after reperfusion when the hepatic artery is anastomosed first rather than the portal vein, as is conventional. This may be because the release of ischaemic metabolites from the splanchnic circulation is delayed, or because the rate of flushing of acid from the donor liver is slower via the hepatic artery which has a lower overall flow and is a higher resistance circulation. Less marked acidosis and hypercapnia are potentially beneficial particularly in high risk patients, such as those with fulminant hepatic failure who are at risk of intracranial hypertension following reperfusion.