Refractory ascites is defined as ascites that does not recede or that recurs shortly after therapeutic paracentesis, despite sodium restriction and diuretic treatment.
For the correct diagnosis of true refractory ascites, the patient’s condition should fulfill the following criteria.
Failure of mobilization or the early recurrence of ascites which cannot be prevented because of a lack of response to sodium restriction and diuretic treatment is called diuretic-resistant ascites.
Failure of mobilization or the early recurrence of ascites which cannot be prevented because of the development of diuretic-induced complications that prevent the use of an effective diuretic dosage is called diuretic-intractable ascites.
Patients must be on intensive diuretic therapy (spironolactone 400 mg/d and furosemide 160 mg/d) for at least 1 wk and on a salt-restricted diet of less than 90 mmol/d.
Lack of response
Mean weight loss of less than 0.8 kg over 4 d and urinary sodium output less than the sodium intake.
Early ascites recurrence
There is an reappearance of grade 2 or 3 ascites (clinically detectable) within 4 wk of initial mobilization. However, it is important to notice that in patients with severe peripheral edema, reaccumulation of ascites within 2-3 d of paracentesis must not be considered as early ascites recurrence because it represents a shift of interstitial fluid to the intraperitoneal space.
Diuretic-induced hepatic encephalopathy is the development of encephalopathy in the absence of any other precipitating factor. Diuretic-induced renal impairment is indicated by an increase of serum creatinine by > 100% to a value of > 2 mg/dL in patients with ascites otherwise responding to treatment.
Diuretic-induced hyponatremia is defined as a decrease of serum sodium by > 10 mEq/L to a serum sodium of < 125 mEq/L. Diuretic-induced hypo- or hyperkalemia is defined as a change in serum potassium to < 3 mEq/L or > 6 mEq/L despite appropriate measures.
In addition to this, we should exclude dietary non-compliance (patient taking excess sodium in diet) and exclude the use of nonsteroidal antiinflammatory drugs (NSAIDs), which can induce renal vasoconstriction and diminish diuretic responsiveness
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- Senousy BE, Draganov PV. Evaluation and management of patients with refractory ascites. World J Gastroenterol. 2009 Jan 7;15(1):67-80. [Medline]
- Moore KP, Wong F, Gines P, Bernardi M, Ochs A, Salerno F, Angeli P, Porayko M, Moreau R, Garcia-Tsao G, Jimenez W, Planas R, Arroyo V. The management of ascites in cirrhosis: report on the consensus conference of the International Ascites Club. Hepatology. 2003 Jul;38(1):258-66. [Medline]
Created: Aug 27, 2009