A Review of the Risk Factors and Approaches to Prevention of Post-Reperfusion Syndrome During Liver Transplantation

Abstract

Post-reperfusion syndrome (PRS) is a severe and highly lethal syndrome that occurs after declamping the portal vein forceps during liver transplantation. It is marked by severe hemodynamic disturbances manifested by decreased mean arterial pressure, increased heart rate and elevated pulmonary artery pressure. The complex pathogenesis of PRS remains understudied. It is generally believed to be related to the large amount of acidic, cold blood that enters the circulation after release of the portal clamp. This blood is rich in oxygen-free radicals and metabolic toxins, which not only aggravate the ischemia-reperfusion injury of the liver but also further attack the systemic organs indiscriminately. Considering the range of possible adverse prognoses including acute kidney injury, delirium and graft nonfunction, it is imperative that clinicians increase their awareness and prevention of PRS. The aim of this article is to review the current risk factors, pathophysiological mechanisms and prevention strategies for PRS.

Keywords: Ischemia; liver transplantation; reperfusion injury; review; risk factors.

Figure 1.

The model of liver transplantation progress. (a) Acquire liver graft from donation after cardiac death or donation after brain death then repair it. (b) Remove the deceased liver from recipient. (c) Implant the liver graft into recipient. (d) Declamping the portal vein forceps into new hepatic phase.

Figure 2.

The production of ROS during IRI. (a) With the massive consumption of ATP, XDH changes into XOD. Accumulating large amounts of xanthine. (b) BH4 is heavily consumed, prompting the uncoupling of the NOS. (c) Activated Kupffer cells also promote ROS production.