Quality Improvement Guidelines for Transjugular Intrahepatic Portosystemic Shunt (TIPS)

Portal hypertension is a syndrome caused by increased resistance in the portohepatic circulation and an increase in the splanchnic vein blood supply. In the normal liver, the difference between pressures in the portal vein and the free hepatic veins or right atrium usually does not exceed 5 mm Hg. Portal hypertension is defined as a gradient larger than 6 mm Hg, but clinical complications seem to occur only when the pressure gradient exceeds 10–12 mm Hg. Wedged hepatic pressure measurement has two components. The portal component is the pressure transmitted from the hepatic sinusoids, and the systemic component is the blood pressure transmitted from the central veins. It is the portal component that causes the development of portal systemic collaterals. The term corrected sinusoidal pressure includes only the portal component and is calculated by subtracting the mean right atrial or inferior vena cava pressure from the wedged hepatic venous pressure. Wedged hepatic pressure is obtained through an end-hole catheter that is advanced into a hepatic vein until it can go no further. Alternatively, pressure can be measured through the wire channel of a double lumen balloon catheter inflated in a more central vein. Transjugular intrahepatic portosystemic shunt (TIPS) is the percutaneous method of creating a portosystemic shunt to decrease or treat portal hypertension. TIPS is a side-to-side shunt of a determined diameter designed to function as a partial shunt that preserves a portion of portal flow to the liver [2]. Flow through the completed shunt is assessed by comparing the degree of preferential filling of the shunt to the that of the portal vein branches and portosystemic collaterals (mainly in the gastric veins). The identification of hepatofugal (reversed) blood flow in portal vein branches (total shunting) is a sign of good flow through the shunt. Technical success is defined as a decrease of the portosystemic pressure gradient to 12 mm Hg or less, or a reduction of at least 20 %. Clinical success is defined as cessation of variceal bleeding, decrease of ascites, and conversion into diuretic-sensitive ascites, as well as improvement of liver function in patients referred for massive thrombosis of hepatic veins. Hepatic encephalopathy is defined as the complex of all cerebral dysfunctions that can occur during the course of serious liver disease. Clinical symptomatology, which as a rule is potentially reversible, ranges from disorientation, somnolence, and lethargy to sopor and coma. Hepatic encephalopathy has three forms: type A, associated with acute liver failure; type B, associated with portosystemic bypass without liver disease; and type C, or chronic, associated with liver cirrhosis.