Placement of a LeVeen shunt for ascites: anesthetic considerations.

Ascites is a frequent sequela of severe hepatic disease. Recently, surgical intervention in the form of a peritoneovenous (P-V) LeVeen shunt has been introduced in the treatment of ascites. Anesthetic management of the patient with ascites undergoing placement of a LeVeen Shunt requires an understanding of: (1) the physiology of hepatic circulation; (2) the systemic consequences of ascites; (3) surgical technique; and (4) anesthetic considerations. The liver receives approximately 25% of the cardiac output via the hepatic artery and 75% from the portal vein. The portal vein is at the junction of the superior mesenteric vein and the splenic vein; it supplies the liver with blood from capillaries in the gastrointestinal (GI) tract. Blood from the heart is transported to the liver from the hepatic artery. It flows through the sinusoids of the liver from the hepatic arterioles and portal venules. The sinusoids are the vessels of exchange for the liver and function through active transport, diffusion and pinocytosis. The sinusoids empty into an intralobular vein which drains into a hepatic vein and, finally, into the inferior vena cava.1 Ascites formation Normal pressure in the portal vein is approximately 10 mmHg and in the hepatic vein, is 0 mmHg.2 Portal hypertension is a persistent increase in portal vein pressure. The exact etiology is not fully understood but may be generated by a primary increase in vascular resistance in the portal system.1 Degeneration of the parenchymal cells of the liver leads to impairment of circulation through the liver, which interferes with the low-pressure portal vein system. The resulting portal hypertension favors the exudation and accumulation of fluid in the abdomen, both from the capillaries within the liver and also from the capillaries in the intestine. Portal hypertension is not the only factor involved in ascites formation and collection. Impaired liver function results in hypoalbuminemia, lowered colloid osmotic pressure, and an effective outward gradient for filtration of fluid. There may also be an increased level of antidiuretic hormone (ADH) in the urine, probably due to failure of the liver to inactivate this hormone. Aldosterone activity may also be enhanced, thus favoring salt and water retention. ' 4