Description

• 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.

Epidemiology

• Children: most commonly associated with nephrotic syndrome and malignancy
• Adults: cirrhosis (81%), cancer (10%), heart failure (3%), other (6%)

Incidence
~50–60% of cirrhotic patients develop ascites within 10 years (1).

Prevalence
10% of patients with cirrhosis have ascites.

Etiology and Pathophysiology

• Portal hypertension versus nonportal hypertension 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)
  • Cirrhosis
  • 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
  • Tuberculosis
  • Severe hypoalbuminemia (nephrotic syndrome; severe enteropathy with protein loss)
  • Meigs syndrome (ovarian cancer)
  • Lymphatic leak (chylous ascites)
  • Pancreatitis
  • 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.