Ascitis complicates end stage liver disease with portal hypertension. Ascitis in cirrhosis  is produced as the result of  increased portal pressure, low circulating albumin, hyperaldosteronism with sodium retention and decreased free water output.

Ascitic patients are in excess of sodium, even when associated to hyponatremia and this should always be kept in  mind .

There are many false  ideas  about ascitis and many attitudes are more related to "medical folklore" than to evidence base. 

At presentation, urinary sodium is low, often below 10 meq/L, reflecting this pathophysiological situation.  

Sodium intake must be limited.  Diuretics aim to increase urinary sodium output. 

Sodium restriction and diuretics are the corne stone of treatment. Spironolactone is given at an initial dosage of 3 mg/kg/day, adapted to reach the natriuretic effect. Urinary sodium and potassium should therefore be monitored during treatment, to reach higher sodium than potassium urinary excretion.

Albumin infusion is indicated if plasma protein concentration is low (< 2,5 - 3 g/dl)  , keeping in mind that albumin solutions contain 140 meq/L of sodium. Total plasma proteins should stay above 5 and possibly reach 6gr/dl to maintain oncotic pressure. Clinicians should consider that total plasma proteins may not reflect truly albumin levels, in view of the major hypergammaglobulinemia in some patients.


In case of  dilutional hyponatremia, the first step of management is  fluid restriction and discontinuation of diuretics.  Vasopressin V2 receptor antagonsits increase free water excretion at the distal collecting ducts of the kidney, but they are so far not available and have not been  tested in children


Many mistakes are observed int he handling of ascitic patients: 

- Fluid restricition is  not helpfull (except in tense ascitis with hyponatremia, see below) and causes patient's discomfort and insufficient energy intake.

- Spironolactone should be adapted  when ascitis is controlled: if continued in absence of ascitis, spironolactone may  lead to excessive sodium depletion and hyponatremia. Such  iatrogenic hyponatremia, with no more ascites, should lead to stop spironolactone and is  the only indication to give moderate sodium transiently . 

- It is a very  common error to   give  patients  sodium supplementation   while still  under spironolactone, which is a non sense..



Paracentesis is performed if abdomen is tense, child uncomfortable, or if abdominal distension causes respiratory distress. It is also indicated in tense ascitis with hyponatremia. 

Large volume  paracentesis is safe and there is no evidence -  that it will create  volemic of circulation disturbances.  IV spironolactone  can be given to  compensate  subsequent  hyperaldosteronism.  

Fears of sudden intravascular hypovolemia  during paracentesis is again a folkloric  more than an evidence based view.  This can anyway be followed by   central venous pressure  monitoring,  while  albumin infusion (1 to 2 gr/kg over  24hrs) will also help to maintain oncotic pressure and intrvascular volume. Paracentesis does not increase hyponatremia either..

Tense ascitis with hyponatremia is not an indication to administer  sodium, since the patient  is already in excess of sodium, and since it will lead to  respiratory distress  due to additional  fluid overload .  Paracentesis, albumin infusion ( which anyway contains isotonic Na+), and if mandatory, gentel oral sodium supplementation is the treatment. 

Rapid correction of hyponatremia may cause iatrogenic  CNS damage in ascitic cirrhotic patients . Infusion of  hypertonic sodium solutions are contraindicated. 

The inconvenience of repeated paracentesis is the progressive protein depletion of the ascitic fluid, with a parallel increase in the risk of infection. Any fluid aspirated should be cultured in blood culture bottles.