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- Accumulation of fluid in the peritoneal cavity; may occur in conditions that cause generalized edema
- Men generally have no fluid in peritoneal cavity; women may have up to 20 mL depending on menstrual phase.
- Children: nephrotic syndrome and malignancy most common
- Adults: cirrhosis (81%), cancer (10%), heart failure (3%), other (6%)
~50–60% of patients with cirrhosis develop ascites within 10 years (1).
10% of patients with cirrhosis have ascites.
Etiology and Pathophysiology
- Portal hypertensive versus nonportal hypertensive causes
- Cannot reliably establish/confirm etiology without paracentesis
- Serum-ascites albumin gradient (SAAG): (serum albumin level: ascites albumin level) helps to differentiate causes
- High portal pressure (SAAG ≥1.1)
- Hepatitis (alcoholic, viral, autoimmune, medications)
- Acute liver failure
- Liver malignancy (primary or metastatic)
- Elevated right-sided filling pressures from heart failure or constrictive pericarditis
- Hepatic venous thrombosis (Budd-Chiari syndrome)
- Portal vein thrombosis
- Normal portal pressure (SAAG <1.1)
- Peritoneal carcinomatosis
- Severe hypoalbuminemia (nephrotic syndrome; severe enteropathy with protein loss)
- Meigs syndrome (ovarian cancer)
- Lymphatic leak (chylous ascites)
- Inflammatory (vasculitis, lupus serositis, sarcoidosis)
- Other infections (parasitic, fungal)
- Hemoperitoneum (trauma or ectopic pregnancy)
- Pathophysiology is best described for portal hypertensive (typically cirrhotic) ascites.
- Reduced renal and carotid perfusion activates systemic vasoconstrictors and antinatriuretic mechanisms. This stimulates the sympathetic nervous system and renin-angiotensin-aldosterone system to retain sodium and water.
- Most ascites is due to portal hypertension, with preferentially dilated splanchnic vasculature causing systemic hypotension.