Enhancing ex vivo perfusion of the liver by restoring positive pressure in the inferior caval vein


I.J. Schurink, F.H.C. de Goeij, J.N.M. IJzermans, L.J.W. van der Laan, J.J. de Jonge

Thursday 5 march 2020

14:30 - 14:40h at Theaterzaal

Parallel session: Parallel sessie XII – Klinische en Basale abstracts


Background: In the field of liver transplantation, organ shortage pushes physicians to use more marginal organs. Machine perfusion provides the opportunity to test or even improve the quality of these grafts. For ex-vivo organ therapy, e.g. with stem cells or drug components, the perfusion time needs to be extended. However, ill-perfused macroscopic spots appear in the liver parenchyma during long-term perfusion. Ex vivo perfusion controls the pressure in the portal vein and hepatic artery, however, the pressure in the inferior caval vein is not monitored or controlled. Therefore, we aim to investigate if inducing positive pressure in the inferior caval vein (IVC) – like positive end-expiratory pressure in the lung -can enhance ex vivo perfusion.

Methods: Normothermic machine perfusion (NMP), with an erythrocyte based perfusate, was performed in 2 human livers and 5 pig livers. The pressure in the hepatic artery and portal vein was set on 70 and 11 mmHg. The IVC was cannulated and the pressure was monitored. The pressure in the IVC was adjusted by clamping the IVC cannula. Flow was monitored within an IVC pressure range of 0-10 mmHg. Furthermore, we monitored the blood flow in the liver parenchyma with laser speckle technique in 3 conditions: no pressure intervention, pressure increase to 2 mmHg and 5 mmHg in the IVC.

Results: Without any intervention, the pressure in the IVC was between -6 and 0 mmHg. After inducing the pressure in the IVC, the flow in the portal vein remained stable until a pressure of 6 mmHg, above 6 mmHg the portal flow decreased. The flow in the hepatic artery was not altered by the pressure in the IVC.

Laser speckle imaging at the start of the perfusion showed a heterogeneously perfused liver, with almost no detectable blood flow in several places of the liver while there was increased flow in other spots in the liver. After increasing the IVC pressure to 2 mmHg, the parenchyma parts of the livers became 50 % (40 - 70%) more perfused, and after adjusting the pressure to 5 mmHg the flow was increased by 34 % ( 8 – 58%) in the parenchyma, compared to no pressure intervention.

Conclusions: In conclusion, adjusting the IVC pressure to a positive pressure of 2 mmHg induces optimal perfusion of the liver parenchyma and this strategy may be incorporated in ex-vivo organ perfusion.