Description

• 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.

Pathophysiology

• 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

Etiology

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