ABSTRACT
The clinical course of patients with decompensated Laennec's cirrhosis is complicated frequently by derangements of renal function varying from progressive impairment of renal sodium and water handling to the hepatorenal syndrome. Traditionally, ascites formation in cirrhotic patients is considered to begin when a critical imbalance of Starling forces develops in the hepatic sinusoids and splanchnic capillaries. The cause of the peripheral vasodilation of liver disease has not been established and is undoubtedly complex. It may be due, at least in part, to vasodilatory hormones secreted by the intestines, such as glucagon, vasoactive intestinal peptide, substance P, or some other undefined vasodilator. The promulgation of the overflow theory of ascites formation has engendered much controversy. The demonstration that plasma volume is increased in cirrhosis with ascites, and that a spontaneous diuresis and natriuresis have been found to occur, independent of measurable changes in the volume of the nonsplanchnic vascular compartment, has been cited as evidence in support of the overflow hypothesis.
