Portal hypertension

Chronic liver diseases that lead to liver cirrhosis may be associated with the development of portal hypertension. This is an increase in pressure within the portal venous system, the vein that carries blood from the intestines, spleen and stomach to the liver. Other causes of portal hypertension are specific liver conditions characterized by changes in the liver architecture, for example Nodular Regenerative Hyperplasia, and thrombosis of the portal vein or of the veins leaving the liver (Budd-Chiari syndrome). When portal hypertension occurs, blood is detoured into other smaller veins that ultimately allow blood to flow back to the heart, so partially bypassing the liver. However, these smaller veins can enlarge in the oesophagus, stomach or at other places - and form varicose veins or varices, which may give rise to bleeding. Bleeding varices are most commonly observed in the oesophagus and in the stomach, but may also occur at other sites such as the rectum or duodenum.

Another frequent complication of portal hypertension is the development of ascites, i.e. accumulation of fluid in the abdominal cavity. Ascites may cause abdominal swelling; other problems are the development of an infection of this fluid and the development of hernias, such as umbilical, inguinal and scar-related hernias.

Variceal bleeding in the oesophagus or stomach is a serious complication in patients with liver cirrhosis and portal hypertension. Around 20% of patients do not survive a first bleeding, 17% will experience a recurrent bleeding within six weeks, and 70% within two years. Dependent on the severity of the underlying liver disease and of the bleeding, the mortality associated with each bleeding episode ranges from 20-40% (1). Apart from treatment of the acute bleeding episode and of the underlying disease, treatment of patients with variceal bleeding is aimed at preventing recurrences (secondary prophylaxis).

Current therapeutic approach
Several options are available for the prevention of recurrent variceal bleedings: endoscopic therapy, treatment with the non-selective ß-blocker propranolol, and TIPS (Transjugular Intrahepatic Portosystemic Shunt). There is consensus that endoscopic therapy, notably rubber band ligation, and treatment with propranolol are equivalent alternatives (2). From the results of a large number of trials and meta-analyses it is generally assumed that TIPS, in comparison with endoscopic therapy, is significantly more effective in preventing recurrent bleedings, but does not improve survival and increases the risk of hepatic encephalopathy (3, 4). This is why TIPS so far has been applied as a valuable second-line treatment when other therapies fail; but rather not as treatment at an earlier stage (2).

The studies that resulted in the above conclusions concerned TIPS procedures using uncoated metal stents. A major problem in these procedures was loss of shunt function by thrombosis and neo-intima proliferation, leading to recurrent bleeding, need of intensive shunt monitoring, and frequent shunt revisions (5). Recent studies have shown that implantation of polytetrafluoroethylene-coated stents strongly reduces the risk of TIPS obstruction (6-8). In a controlled study the one-year integrity of the shunt with conventional stents was 41% and with coated stents 88% (9). A retrospective study suggested improved survival with the use of coated stents (10). Surprisingly, in these studies the improved integrity of the shunt on the long term appeared not to coincide with a greater likelihood of encephalopathy (7-9). Perhaps this can partly be ascribed to the fact that often stents were used with smaller diameter than the conventional 10 mm stents. There may be other possible explanations, however, such as improved effectiveness with regard to ascites, and its associated lower need of diuretic therapy, as well as the less frequent occurrences of bleeding.