Interventional percutaneous trans-splenic approach in the management of portal venous occlusion after living donor liver transplantation

Abstract

A 2-year-old Chinese boy with progressive familial intrahepatic cholestasis type II–related end-stage liver disease underwent living donor liver transplantation (LDLT) using a left lateral segment graft from his mother. Preoperative computed tomography angiography showed that the hepatic artery, inferior vena cava, and portal vein were patent. The left portal vein of the graft was connected to the recipient's right anterior portal vein. The left hepatic vein of the graft was connected to the recipient's hepatic veins with triple venoplasty. The left hepatic artery of the graft was connected to the recipient's right hepatic artery. The left hepatic duct of the graft was connected to the recipient's common hepatic duct with a microsurgical technique. After the operation, the infant underwent reworking of the hepatic artery anastomosis twice because of early hepatic artery thrombosis. He also underwent revision of the biliary reconstruction to Roux-en-Y hepaticojejunostomy because of biliary anastomotic stricture. At 18 months post-transplant, there was poor visualization of the intrahepatic portal vein, but there was hepatofugal flow inside the left portal vein during Doppler ultrasound follow-up studies. Splenomegaly and minimal ascites were also noted by ultrasound. The computed tomography angiography study showed mild intrahepatic bile duct dilatation, marked splenomegaly, and occlusion of the transverse portion of the portal vein with collateral vessels also noted. The patient was subsequently referred for a possible interventional radiological procedure as initial management for the occluded portal vein. The patient underwent vascular catheter intervention under general anesthesia. The percutaneous trans-splenic approach was performed to puncture the splenic vein with a 21-gauge Chiba needle (Cook, Bloomington, IN) under ultrasonographic and fluoroscopic guidance. The needle was changed to a 4-French coaxial dilator and a 7-French sheath (Terumo, Tokyo, Japan) over a 0.035-inch angled hydrophilic guide wire (Terumo) after confirmation that the needle was in the splenic vein. Direct main portal venography and the pressure gradient across the stenosis were then obtained. Portography showed total occlusion of the portal vein at its umbilical portion (Fig. 1). The coronary vein was prominent, and gastroesophageal varices were also noted. The extrahepatic portal pressure was 18 mm Hg, and the intrahepatic portal pressure was 18 mm Hg. Hence, there was no pressure gradient across the area of stenosis. A 0.035-inch guide wire and a 4-French J curve catheter (Terumo) were used to traverse the area of portal vein stenosis (Fig. 2). A wall stent (9.0 mm × 5.0 cm; Boston Scientific, Natick, MA) was placed to bypass the area of stenosis from the umbilical portion up to the visualized segment 3 portal vein. A second similarly sized wall stent was placed from the mid portion of the native main portal vein to the splenic vein. Percutaneous trans-splenic portography showed total occlusion of the portal vein with the formation of multiple collateral vessels. Percutaneous trans-splenic approach: the catheter was manipulated through the occluded portal vein into the intrahepatic portal vein (graft side). Balloon angioplasty (6.0–40 mm, 80 cm; Wanda, Boston, MA) following stent placement was performed with subsequent stent expansion. Portography done after angioplasty via the splenic vein showed patent extrahepatic and intrahepatic portal veins (Fig. 3). The guide wire and angiocatheter were withdrawn, and the percutaneous tract was sealed with 5 hemostatic coils (3 mm × 5 cm; Cook) and N-butyl cyanoacrylate. A Doppler ultrasound study after angioplasty and stenting showed that the wall stent was in place and the portal vein was patent with hepatopetal flow. After angioplasty and stent placement, the diameter of the portal vein was 9 mm. Complete portal venography showed a patent portal vein. After the procedure, the patient was given an intravenous heparin drip for 3 days to obtain an international normalized ratio of 1.5 to 2.0 and an oral antiplatelet (aspirin, 100 mg/day). A shortage of appropriately-sized liver grafts for pediatric patients has led to the use of LDLT with segmental liver grafts.1-3 These grafts have become predominant, being used in 99% of pediatric LDLT procedures at our institution. Many reports have indicated that there is a high incidence of portal vein complications when venous conduits are used to reconstruct the donor and recipient portal veins.4, 5 The reported incidence of early portal vein thrombosis varies between 0% and 30%, depending on the series selected.6-9 Several factors have been implicated, including the portal vein size, type of graft used, and graft positional factors. Late portal and hepatic vein stenoses are commonly present with varied clinical signs and syndromes, including new-onset ascites, variceal bleeding, splenomegaly, increases in liver enzymes, lower extremity edema, and renal insufficiency.4 The diagnosis of portal vein stenosis or thrombosis can be suggested by abdominal ultrasound findings. Confirmation and common therapeutic interventions for all venous stenoses are done by invasive angiography; thus, interventional radiology is essential.10 Balloon angioplasty has been successful in treating patients who developed posttransplant portal vein stenosis or thrombosis. However, recurrent stenosis and thrombotic changes in the cryopreserved vein used for portal conduits always occur, and a metallic stent is needed to support the patency of the portal vein. The conventional procedure is the percutaneous transhepatic approach. In this case, the hepatic artery occlusion and biliary anastomotic stricture, which required multiple reoperations, were the major underlying causes of possible portal vein complications. Hypertrophy change associated with graft regeneration is another factor that may lead to the development of kinking and compression of the portal vein. In LDLT using a left lobe graft, the graft is usually fixed to the diaphragm in the left upper quadrant. In the patient, we noted mild dilatation of the intrahepatic bile ducts, severe engorgement of intrahepatic hepatic arteries with prominent Doppler arterial flow, and total occlusion of the intrahepatic portal vein. These problems are risk factors that may cause major complications during the percutaneous transhepatic puncture of the intrahepatic portal vein. A small portal vein without visualized flow is also difficult to approach. In past experience, percutaneous transhepatic puncture has also been a blind procedure in which the catheter is maneuvered toward the occlusion via multi-angulated pathways to the umbilical and transverse portions of the portal vein. It is necessary because of the hepatopetal direction of the portal blood flow and poor visualization of the portal vein. Total occlusion of the portal vein is almost always accompanied by compensative engorgement of the hepatic artery and cavernous transformation inside the liver graft and anastomotic region. Splenomegaly, in cases of portal occlusion, is accompanied by engorgement of the intrasplenic vein. It can be well demonstrated by computed tomography angiography, magnetic resonance angiography, or Doppler ultrasound. To minimize liver graft injury and complications during the interventional procedure, we used the percutaneous trans-splenic approach for metallic stent placement in treating posttransplant portal vein occlusion in this case. Selection of the venous structure over the inferior part of the spleen can be made easily with ultrasound for the percutaneous trans-splenic approach. The antegrade injection of the contrast medium can provide a map of the portal vein and its collaterals. It identifies the point at which the catheter should be placed as it locates the pathological portal vein. Another technical issue is the shortening of the metallic stent during the deployment procedure. It is easier to adjust the stent into the proper position through the antegrade approach, in which the stent is placed from the graft side to the main portal venous side. Hemoperitoneum and hemothorax are common complications in percutaneous transhepatic portal venous angioplasty and stenting.10 The large profile of the angioplasty and stenting apparatus (6–7 French) means that a puncture tract has to be created inside the liver parenchyma. Hemostasis is difficult, especially with a short puncture tract in the liver graft. A low insertion of the diaphragm and a high position of the liver graft are also potential factors that may cause hemothorax. For hemostasis in the percutaneous trans-splenic approach, the splenic puncture site along the pathway inside the big spleen can be well visualized in the anterior-to-posterior X-ray directions. The spleen parenchyma tract can be closed with metallic coils and N-butyl cyanoacrylate. For safety reasons, because there are a lot of venous-biliary-hepatic artery networks inside the liver graft, it is difficult and dangerous to control the liquid embolizer (N-butyl cyanoacrylate), which may go into normal vascular and biliary structures if the transhepatic route is selected. As far as the trans-splenic approach is concerned, the spleen is a simple solid organ without an internal complex anatomy like that of the liver. Hematoma formation within the liver graft and puncture site is invariably seen in the transhepatic procedure. Although it may also occur in the trans-splenic approach, a hematoma within the spleen is less harmful than a hematoma inside the liver. In summary, in situations in which the percutaneous transhepatic approach to the management of portal vein occlusion after LDLT is judged to be difficult, the percutaneous trans-splenic method is an alternative approach with excellent results for carefully selected patients. LDLT, living donor liver transplantation.