Pathophysiology-ascites

(Hepatology 2021;74:1014) Pathogenesis of ascites and related complications of cirrhosis

• Portal HTN → ↑ NO & prostaglandins → splanchnic vasodilatation→ ↓ effective arterial volume → ↑ RAAS & ADH → renal Na & H2O retention → volume overload and ascites

Portal hypertension leads to increased nitric oxide and prostaglandins, resulting in splanchnic vasodilation and decreased effective arterial volume. This activates the renin-angiotensin-aldosterone system and antidiuretic hormone, leading to renal sodium and water retention, resulting in volume overload and ascites.

• In malignant or inflammatory ascites, leaking of proteinaceous material occurs from tumor or from inflamed/infected/ruptured intraabdominal structures

In cases of malignant or inflammatory ascites, proteinaceous material leaks out from tumors or damaged intraabdominal structures due to inflammation, infection, or rupture.