Medication Summary
The goals of pharmacotherapy are to reduce morbidity and to prevent complications in patients with ascites.
Diuretics should be initiated in patients whose ascites does not respond to sodium restriction. A useful regimen is to start with spironolactone at 100 mg/d. The addition of loop diuretics may be necessary in some cases to increase the natriuretic effect. If no response occurs after 4-5 days, the dosage may be increased stepwise up to spironolactone at 400 mg/d plus furosemide at 160 mg/d.
V2 receptor antagonists may be considered in the management of patients with cirrhosis, ascites, and dilutional hyponatremia. [15]
Diuretics
Class Summary
Diuretic agents are the mainstay of medical therapy in ascites.
Spironolactone (Aldactone)
For the management of edema resulting from excessive aldosterone excretion. Competes with aldosterone for receptor sites in distal renal tubules, increasing water excretion while retaining potassium and hydrogen ions. The peak effect of Aldactone is approximately 3 d.
Furosemide (Lasix)
Increases the excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule. Dose must be individualized to patient.
Depending on the response, administer at increments of 20-40 mg, no sooner than 6-8 h after the previous dose, until the desired diuresis occurs. When treating infants, titrate in increments of 1 mg/kg/dose until a satisfactory effect is achieved.
Amiloride (Midamor)
A pyrazine-carbonyl-guanidine unrelated chemically to other known antikaliuretic or diuretic agents. Potassium-conserving (antikaliuretic) drug which, compared with thiazide diuretics, possesses weak natriuretic, diuretic, and antihypertensive activity.
Metolazone (Mykrox, Zaroxolyn)
Helps treat edema in congestive heart failure. Increases excretion of sodium, water, potassium, and hydrogen ions by inhibiting reabsorption of sodium in distal tubules. May be more effective in those with impaired renal function.
Mannitol (Osmitrol)
Inhibits tubular reabsorption of electrolytes by increasing the osmotic pressure of glomerular filtrate. Increases urinary output.
Vasopressin-Related
Class Summary
The potential benefits of these drugs include the predictability of their effect, rapid onset of action, and limited urinary electrolyte excretion. Conivaptan and tolvaptan are currently the only vasopressin receptor antagonists that are commercially available in the United States and FDA-approved for the treatment of euvolemic hyponatremia in hospitalized patients. These medications should be initiated in a closely monitored setting to prevent rapid correction of serum Na+, which can result in central pontine myelinolysis (CPM). [27]
Tolvaptan (Jynarque, Samsca)
Tolvaptan is an oral selective vasopressin V2-receptor antagonist. It is indicated for hypervolemic and euvolemic hyponatremia (ie, serum Na level < 125 mEq/L) or less marked hyponatremia that is symptomatic and has resisted correction with fluid restriction. It is used for hyponatremia associated with CHF, liver cirrhosis, and syndrome of inappropriate antidiuretic hormone secretion (SIADH).
Initiate or reinitiate the drug in a hospital environment only since there may be overly rapid correction of the hyponatremia. However, it increases thirst (potentially limiting its effects) and is expensive.
Conivaptan (Vaprisol)
Conivaptan is a parenteral nonselective vasopressin receptor antagonist used for the treatment of euvolemic hyponatremia in hospitalized patients. Conivaptan increases urine output of mostly free water, with little electrolyte loss. It is indicated for hospitalized patients with more severe euvolemic or hypervolemic hyponatremia.
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Ascites. This computed tomography scan demonstrates free intraperitoneal fluid due to urinary ascites.
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Ascites. Transjugular intrahepatic portosystemic shunt (TIPS).
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Ascites. Massive ascites.
