The portal vein is a crucial structure in the body, transporting approximately 75% of the blood to the liver from the gastrointestinal tract and spleen1. In patients with advanced liver diseases, portal vein thrombosis may develop, consisting of the formation of clots within the vein, obstructing the blood flow2. Portal vein thrombosis (PVT) is a complex complication that poses a significant challenge during liver transplantation3. To ensure optimal graft and patient survival, it is essential to maintain good portal inflow1,3.
Portal Vein Thrombosis can be classified as acute or chronic and categorized based on the extent of vein involvement4. Among the numerous PVT categorizations, the Yerdel Classification is often used to guide surgical approaches in liver transplantation (Table 1)4. It consists of four categories: restricted to the main portal vein trunk and affecting less than 50% of its lumen; Grade 1 with more than 50% of occluded lumen, including complete obstruction of the main portal vein trunk; complete obstruction of the portal vein and proximal portion of the superior mesenteric vein; entire venous splanchnic system thrombosis with development of large or small collaterals3,4.
Intraoperatively, Yerdel Grade I/II or early PVT can be managed with a simple thrombectomy (cutting of the vein and the thrombus together with eversion of the vein wall and removal of the thrombus with the aid of a needle holder), or even a thromboendovenectomy (resection of the affected part of the vein with the thrombus)1,5. However, complications with these two techniques (traditional thrombectomy and thromboendovenectomy) include thrombus fragmentation, incomplete removal, or vein injury in anatomically challenging positions, such as the retro-pancreatic portion of the portal vein5.
Yerdel Grade III PVT may require other techniques such as a jump graft from the superior mesenteric vein or splenic vein2. It is important to remember that varices often have thin walls, making them difficult to handle during anastomosis2,6. For a jump graft from the superior mesenteric vein, first we must pass the venous graft obtained from the cadaver donor through the transverse mesocolon and place it anatomically straight in the direction of the portal vein to avoid compression or kinking6. After that, the superior mesenteric vein is isolated for better vascular control. After clamping the vein, an end-to-side anastomosis of the superior mesenteric vein and venous graft is performed5. The surgery is then completed with an end-to-end anastomosis of the venous graft and portal vein of the liver graft6.
Grade IV presents a significant challenge, depending on the presence of portosystemic shunts, enlarged left gastric vein, or pericholedochal varices3,6. The best options include a reno-portal anastomosis if a large splenorenal shunt is present or a direct anastomosis between the graft and an enlarged collateral vein4. In cases where an adequate portal inflow cannot be obtained with these measures, a multivisceral transplant may be the best option6.
This new technique ensures less risk for thrombus fragmentation, incomplete removal, or vein injury5. Delicately performing this technique can guarantee an integral removal of the thrombus in selected cases, so we developed this new type of thrombectomy6.
Two cases of Grade II portal vein thrombosis are presented in which a new technique for thrombectomy was utilized.
Case 1: A 64-year-old man presented with a diagnosis of cirrhosis of the liver with hepatocellular carcinoma. As a complication of the liver disease, he presented with liver encephalopathy and ascites. The patient had a history of heavy drinking that led to cirrhosis. Laboratory examinations revealed a MELD-Na (Model of End-Stage Liver Disease-Sodium) Score of 17 and CHILD-PUGH Class C11. Triphasic dynamic contrast-enhanced abdominal computed tomography (CT) scan showed hematic thrombosis of the main trunk and of the right and left branches of the portal vein (Figure 1).
Case 2: A 37-year-old man presented with primary sclerosing cholangitis that led to cirrhosis. As a complication of the liver disease, he presented with acute-on-chronic liver failure, triggered by spontaneous bacterial peritonitis, leading to liver encephalopathy, ascites, and hepatorenal syndrome. Laboratory exams revealed a MELD-Na Score of 36 and CHILD-PUGH Class C11. Triphasic dynamic contrast-enhanced abdominal CT scan revealed chronic hematic thrombosis in the main trunk of the portal vein, extending to its intrahepatic branches, which were partially recanalized (Figure 2).