Management of ascites in children

Abstract

Ascites is the pathologic accumulation of fluid within the peritoneal cavity. There are many causes of fetal, neonatal and pediatric ascites; however, chronic liver disease and subsequent cirrhosis remain the most common. The medical and surgical management of ascites in children is dependent on targeting the underlying etiology. Broad categories of management strategies include: sodium restriction, diuresis, paracentesis, intravenous albumin, prevention and treatment of infection, surgical and endovascular shunts and liver transplantation. This review updates and expands the discussion of the unique considerations regarding the management of cirrhotic and non-cirrhotic ascites in the pediatric patient.

Keywords:

• ascites
• cirrhosis
• diuresis
• hypoalbuminemia
• paracentesis
• pediatrics
• renin–angiotensin–aldosterone system
• transjugular intrahepatic portosystemic shunt

Financial & competing interests disclosure

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending or royalties.

No writing assistance was utilized in the production of this manuscript.

Key issues

• Disruption of the balance in hydrostatic and oncotic forces regulating splanchnic, portal and hepatic blood, and lymphatic flow, results in the accumulation of ascites.

• Restriction of sodium intake to 1–2 mEq sodium/kg body weight is critical to the medical management of ascites.

• Combination treatment with spironolactone and furosemide results in more rapid mobilization of ascites, and is usually needed in cases of ascites from significant portal hypertension.

• Development of hepatorenal syndrome in children is often marked by progressive oliguria and a rise in serum creatinine. Caution must be exercised when using diuretics in the setting of cirrhotic ascites and renal dysfunction due to the risk of pre-renal azotemia and renal failure with excessive intravascular volume depletion.

• Fluid restriction is recommended only in setting of hyponatremia with serum sodium values of <125 mEq/l.

• Albumin is integral in maintaining intravascular oncotic pressure. Supplemental albumin (0.5–1 g/kg of dry weight of 5 or 25% albumin intravenously) may be utilized to support intravascular volume when serum concentrations fall below 2.5 g/dl.

• Diagnostic paracentesis should be utilized when ascites accumulates quickly, and in the setting of clinical deterioration suggesting infection, as evidenced by the development of encephalopathy, fever or increasing abdominal pain.

• The difference in simultaneously measured concentrations of albumin in the serum and ascitic fluid, or the serum-ascites albumin gradient (SAAG), aids in the differentiation of cirrhotic from non-cirrhotic ascites. A SAAG ratio of >1.1 g/dl is diagnostic of ascites secondary to portal hypertension, where as a SAAG <1.1 g/dl is seen in the absence of portal hypertension.

• In adults, transjugular intrahepatic portosystemic shunting for the treatment of refractory ascites has been found to be superior to paracentesis and prolongs transplant-free survival, however, does not result in a long-term survival benefit.

Notes