Percutaneous portal venoplasty and stenting for anastomotic stenosis after liver transplantation.

Aim: To review percutaneous transhepatic portal venoplasty and stenting (PTPVS) for portal vein anastomotic stenosis (PVAS) after liver transplantation (LT).

Methods: From April 2004 to June 2008, 16 of 18 consecutive patients (11 male and 5 female; aged 17-66 years, mean age 40.4 years) underwent PTPVS for PVAS. PVAS occurred 2-10 mo after LT (mean 5.0 mo). Three asymptomatic patients were detected on routine screening color Doppler ultrasonography (CDUS). Fifteen patients who also had typical clinical signs of portal hypertension (PHT) were identified by contrast-enhanced computerized tomography (CT) or magnetic resonance imaging. All procedures were performed under local anesthesia. If there was a PVAS < 75%, the portal pressure was measured. Portal venoplasty was performed with an undersized balloon and slowly inflated. All stents were deployed immediately following the predilation. Follow-ups, including clinical course, stenosis recurrence and stent patency which were evaluated by CDUS and CT, were performed.

Results: Technical success was achieved in all patients. No procedure-related complications occurred. Liver function was normalized gradually and the symptoms of PHT also improved following PTPVS. In 2 of 3 asymptomatic patients, portal venoplasty and stenting were not performed because of pressure gradients < 5 mmHg. They were observed with periodic CDUS or CT. PTPVS was performed in 16 patients. In 2 patients, the mean pressure gradients decreased from 15.5 mmHg to 3.0 mmHg. In the remaining 14 patients, a pressure gradient was not obtained because of > 75% stenosis and typical clinical signs of PHT. In a 51-year-old woman, who suffered from massive ascites and severe bilateral lower limb edema after secondary LT, PVAS complicated hepatic vein stenosis and inferior vena cava (IVC) stenosis. Before PTPVS, a self-expandable and a balloon-expandable metallic stent were deployed in the IVC and right hepatic vein respectively. The ascites and edema resolved gradually after treatment. The portosystemic collateral vessels resulting from PHT were visualized in 14 patients. Gastroesophageal varices became invisible on poststenting portography in 9 patients. In a 28-year-old man with hepatic encephalopathy, a pre-existing meso-caval shunt was detected due to visualization of IVC on portography. After stenting, contrast agents flowed mainly into IVC via the shunt and little flowed into the portal vein. A covered stent was deployed into the superior mesenteric vein to occlude the shunt. Portal hepatopetal flow was restored and the IVC became invisible. The patient recovered from hepatic encephalopathy. A balloon-expandable Palmaz stent was deployed into hepatic artery for anastomotic stenosis before PTPVS. Percutaneous transhepatic internal-external biliary drainage was performed in 2 patients with obstructive jaundice. Portal venous patency was maintained for 3.3-56.6 mo (mean 33.0 mo) and all patients remained asymptomatic.

Conclusion: With technical refinements, early detection and prompt treatment of complications, and advances in immunotherapy, excellent results can be achieved in LT.