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.
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