Lymph imbalance in the genesis and perpetuation of the ascites syndrome in hepatic cirrhosis.

Despite extensive study, the pathogenesis of cirrhotic ascites and its relationship to salt and water retention and the hepatorenal syndrome remain unclear. This article reexamines the underlying disturbance in microcirculatory exchange of fluid and protein in the liver and digestive tract and specifically stresses that, in keeping with current interpretation of the Starling hypothesis, ascites appears when the driving force of elevated portal pressure overwhelms the "safety factors" of widened transmural colloid asmotic pressure gradient and accelerated regional lymph flow. In light of recent findings that enhancement of ascitic fluid returned to the bloodstream produces a natriuresis, diuresis, and amelioration of ascites, a "lymph imbalance" theory distinct from the "classic" and "overflow" theories is advanced. This theory proposes that a circulatory imbalance between the rate of fluid leaving and returning to the bloodstream (i.e., the relative rates of lymph formation and lymph absorption) is responsible for a maldistribution of extracellular fluid, which, in turn, stimulates renal salt and water retention, progression of ascites, and finally, the hepatorenal syndrome. Should compensatory factors suffice to prevent or reverse this lymph imbalance, the full cycle is not activated or, if already operating, is deactivated. Thus, portacaval shunt (by reducing the rate of lymph formation) or peritoneovenous shunt (by acting as a megalymphatic collateral to accelerate resorption as well as prevent sequestration of peritoneal fluid), both tend to restore the lymph balance and thereby suppress salt and water retention, correct functional oliguria, and ameliorate ascites.