• Ascites is defined as a pathologic accumulation of intraperitoneal fluid.
  • Peritoneal fluid formation is a dynamic process of production and absorption.
  • In children, ascites is usually the result of liver or renal disease.
  • In adults, ascites is most often due to portal hypertension from cirrhosis.
  • Ascites is the most common of the three major complications of cirrhosis; the other two complications of cirrhosis are hepatic encephalopathy and variceal hemorrhage.


  • Normal circulation
    • Blood enters the liver from the hepatic artery and portal vein, perfuses the hepatic sinusoids, and exits the liver via the hepatic veins.
    • Hepatic lymph, formed by the filtration of sinusoidal plasma into the space of Disse, drains from the liver via the transdiaphragmatic lymphatic vessels to the thoracic duct.
    • Hepatic lymph is isosmotic to plasma, as the sinusoidal endothelium is highly permeable to albumin.
    • In the intestine, the mesenteric capillary membrane is impermeable to albumin. The osmotic gradient favors the return of interstitial fluid/lymph into the capillary.
    • Intestinal lymph from regional lymphatics combines with hepatic lymph in the thoracic duct.
  • Portal hypertension
    • Ascitic fluid production is due to a net transfer of fluid that exceeds the drainage capacity of the lymphatics.
  • Cirrhotic ascites results from three pathophysiologic process:
    • Portal hypertension
    • Vasodilation: mediated predominantly by nitric oxide
    • Hyperaldosteronism: Decreased effective volume sensed by the kidneys stimulates the renin-angiotensin-aldosterone system, leading to increased sympathetic activity and antidiuretic hormone secretion.
  • Noncirrhotic ascites can be the result of the following:
    • Proteinaceous material produced by malignant cells or by inflammation of visceral and/or parietal peritoneum: peritoneal carcinomatosis, tuberculous ascites
    • Obstruction of lymphatic flow by mass, tumor, or external pressure
    • Impaired portal flow: right-sided heart failure, Budd-Chiari syndrome, portal venous malformations
    • Decreased effective arterial blood volume: heart failure
    • Decreased oncotic pressure/hypoalbuminemia: nephrotic syndrome, protein-losing enteropathy, severe malnutrition
    • Primary (congenital) abnormalities of the lymphatics, metabolic disorders (lysosomal storage diseases including sialidosis, Wolman disease, GM1 gangliosidosis, Gaucher disease, and Niemann-Pick type C)
    • Rupture of intra-abdominal viscus or peritoneal/mesenteric cyst, bowel perforation, ureteral rupture


Accumulation of fluid occurs with the following:

  • Inflammatory conditions (e.g., mesenteric adenitis, tuberculosis, pancreatitis, secondary to inflammation of visceral, and/or parietal peritoneum)
  • Portal hypertension or obstruction of portal vein flow and/or lymphatic flow by mass, tumor, or external pressure; tumors of abdominal viscera, retroperitoneum, thorax, or mediastinum (often characterized by chylous ascites)
  • Infectious processes: abscess, tuberculosis, Chlamydia infection, schistosomiasis
  • Gastrointestinal: infarcted bowel/perforation, pancreatitis, ruptured pancreatic duct, parenchymal liver disease
  • Gynecologic: ovarian tumors, torsion, or rupture
  • Renal: nephrotic syndrome, obstructive uropathy, perforated urinary tract, peritoneal dialysis
  • Cardiac: congestive heart failure (CHF), constrictive pericarditis, inferior vena cava web
  • Neoplastic: lymphoma, neuroblastoma
  • Miscellaneous: systemic lupus erythematous, eosinophilic ascites, chylous ascites, hypothyroidism, ventriculoperitoneal shunt

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