Pathophysiology and Therapy of Ascites

Abstract

The Greek word áskov, which means a bag or sack carrying fluid, is where the word "ascites" originates. Ascites is ultimately brought on by increased “sympathetic nervous system activity, renin-angiotensin-aldosterone system activity, increased sodium and water retention, increased production of vasoconstrictors, and decreased ability of fluid to be contained within the vascular space due to impaired hepatic albumin synthesis”. Restricting sodium has been associated with less need for diuretics, quicker ascites resolution, and shorter hospital stays. Spironolactone works by blocking aldosterone's ability to bind to a particular receptor protein located in the cytoplasm of the cortical and medullary collecting ducts. Furosemide increases the quantity of sodium, chloride, and water supplied to the distal tubule by inhibiting active chloride reabsorption at the ascending limb of the loop of Henle.