hepatic and biliary disorders
Ascites
Pathophysiology of Ascites
Mechanisms are complex and incompletely understood. Factors include nitric oxide-induced splanchnic vasodilation, altered Starling forces in the portal vessels (low oncotic pressure due to hypoalbuminemia plus increased portal venous pressure), avid renal sodium retention (urinary sodium concentration is typically<5 mEq/L [5 mmol/L]), and possibly increased hepatic lymph formation. Mechanisms that seem to contribute to renal sodium retention include activation of the renin-angiotensin-aldosterone system; increased sympathetic tone; intrarenal shunting of blood away from the cortex; increased formation of nitric oxide; and altered formation or metabolism of antidiuretic hormone, kinins, prostaglandins, and atrial natriuretic factor. Vasodilation in the splanchnic arterial circulation may be a trigger, but the specific roles and interrelationships of these abnormalities remain uncertain. 