Since Richter’s description in the literature in 1989 of the first procedure on human patients, transjugular intrahepatic portosystemic shunt (TIPS) has been worldwide considered as a noninvasive technique to manage portal hypertension complications. TIPS succeeds in lowering the hepatic sinusoidal pressure and in increasing the circulatory flow, thus reducing sodium retention, ascites recurrence, and variceal bleeding. Required several revisions of the shunt TIPS can be performed in case of different conditions such as hepatorenal syndrome, hepatichydrothorax, portal vein thrombosis, and Budd-Chiari syndrome. Most of the previous studies on TIPS procedure were based on the use of bare stents and most patients chose TIPS 2-3 years after traditional treatment, thus making TIPS appear to be not superior to endoscopy in survival rates. Bare stents were associated with higher incidence of shunt failure and consequently patients required several revisions during the follow-up. With the introduction of a dedicated e-PTFE covered stent-graft, these problems were completely solved, No more reinterventions are required with a tremendous improvement of patient’s quality of life. One of the main drawbacks of the use of e-PTFE covered stent-graft is higher incidence of hepatic encephalopathy. In those cases refractory to the conventional medical therapy, a shunt reduction must be performed. 1. Introduction Portal hypertension is the result of pressure increase within the portal vein when the blood flowing through the liver is blocked. Increase of pressure usually leads to the development not only of varices in the esophagus and stomach but also of ascites [1]. The most common cause of portal hypertension is cirrhosis or liver scarring [2]. Cirrhosis results from the healing of a liver injury provoked by hepatitis, by alcohol abuse, or by any serious liver damage. In cirrhosis, blood flowing through the liver is obstructed by the scarred tissue that slows down its forward movement [3, 4]. Thrombosis and clotting in the portal vein are equally responsible for portal hypertension. Portal hypertension can also be related to a prehepatic disease, such as inflammation of the umbilical vein in early infancy, resulting in portal vein thrombosis and cavernomatous transformation. A block in the portal flow located before the sinusoids of the liver does not create an increased portal hypertension and usually causes neither a disturbance in the function of hepatocytes nor ascites [2, 3]. There also exists a form of portal hypertension caused by blockage of effluent blood from
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