Portal Inflow Techniques in Deceased Donor Liver Transplantation

Abstract

The liver is characterized by two inflow systems: a low-resistance–high-flow system through the portal vein (PV), which accounts for about 70–80% of hepatic blood flow, and a high-resistance–low-flow system with a high oxygen content, through the hepatic artery (HA), which carries about 20% of hepatic blood flow. In normal conditions, the PV drains the blood from the splanchnic territory with a low resistance; the gradient between the PV and the inferior vena cava (IVC) is less than 5 mm Hg, and the flow is 100 mL/min per 100 g of liver mass [1–3]. The hepatic parenchyma has no active role in regulating the hepatic inflow but is a passive recipient of variable amounts of blood flow from the splanchnic circulation. In cirrhotic patients, the augmented splanchnic volume increases portal pressure progressively because of the high intrahepatic resistance. Collateral circulation develops, diverting splanchnic blood to the systemic circulation. The initial systemic vasodilatation is followed by a decrease in central volume causing relative hypovolemia, which leads to sodium retention and plasma volume expansion, resulting in increased cardiac output [4]. A high cardiac output and decreased peripheral vascular resistance and arterial pressure are the features of this hyperdynamic circulation, which worsens the initial endothelial stress. The reduced portal flow, together with an imbalance of coagulation, may lead to the occurrence of portal vein thrombosis (PVT), which may compromise the outcome of orthotopic liver transplantation (OLT). The replacement of the cirrhotic liver with a normal liver relieves the mechanical component of portal hypertension, but the splanchnic circulation is not restored to normal parameters immediately [5]. Following graft reperfusion, portal vein flow (PVF) increases to almost twice that of healthy subjects because of the loss of normal vascular tone and the persistence of abnormal splanchnic hemodynamics [6]. A prospective study on hepatic hemodynamics with different type of liver grafts showed that the PVF is significantly increased following reperfusion, whereas the hepatic artery flow (HAF) is decreased compared with the native situation [7]. When partial grafts are used, the hemodynamic stress is significantly enhanced (Fig. 9.1). The intrahepatic hepatic arterial buffer response (HABR) operates to compensate for PVF changes: the increased PVF reduces the hepatic artery flow by means of the HABR. The PVF/HAF ratio increases after reperfusion; in more than half of patients, PVF accounts for 93% of the total liver flow [8–10]. The extreme increase in PVF observed after living donor liver transplantation (LDLT) and the HABR are responsible for the reduced HAF usually encountered in this setting [11]. The PVF in cirrhotic and transplanted livers is quite different, showing a low flow in cirrhotic recipients with portal hypertension and a relatively high post-reperfusion flow after implantation (Fig. 9.2). In the pioneering experience of Starzl et al. [12], the HA and PV were reconstructed after caval anastomosis, but the liver was reperfused first via the HA, contrary to the current practice of initial portal vein reperfusion. In the particular setting of donation after cardiac death (DCD), the HAF can be restored before the PVF in order to reduce the rate of ischemic biliary tract lesions [13, 14]. With the development of the cava-preserving technique, a temporary portocaval shunt (PCS) has been proposed in order to decrease the splanchnic congestion during the anhepatic phase (Fig. 9.3), thus avoiding the need for a veno-venous bypass [15]. This technique has led to a reduction in intraoperative blood loss and postoperative renal failure [16]. The PCS has also been proposed as a way to decrease the portal inflow in partial grafts, thus avoiding overperfusion in small-for-size grafts, which leads to specific problems such as prolonged cholestasis, ascites, and increased vascular thrombosis rates, potentially leading to graft loss [17–19].