Mechanism of sodium retention and ascites formation in cirrhosis

Abstract

Renal sodium and water retention and ascites associated with cirrhosis develop in the setting of severe sinusoidal portal hypertension, hyperdynamic circulation (characterized by arterial hypotension, hypervolaemia, high cardiac output and low peripheral vascular resistance), homeostatic activation of the renin-angiotensin-aldosterone system, sympathetic nervous system and antidiuretic hormone production (i.e. mechanisms designed to maintain arterial pressure within normal limits) and marked increase in hepatic and splanchnic lymph production that overcomes the transport capacity of the lymphatic vessels to the general circulation, leading to leakage of fluid within the peritoneal cavity. Splanchnic arteriolar vasodilation and the increased splanchnic blood flow that characterize portal hypertensive states could be a major factor in the pathogenesis of cirrhotic ascites because it may account for the hyperdynamic circulation, the activation of endogenous neurohormonal systems that cause sodium and water retention and, also, by altering of splanchnic capillary haemodynamics and permeability, the excessive production of lymph in this vascular territory.