Diagnostic Criteria for Refractory Ascites

For the correct diagnosis of true refractory ascites, the patient’s condition should fulfill the following criteria.

Diuretic-resistant ascites
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.

Diuretic-intractable 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.

Treatment duration
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 complications
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

References:

1. Hou W, Sanyal AJ. Ascites: diagnosis and management. Med Clin North Am. 2009 Jul;93(4):801-17. [Medline]
2. Senousy BE, Draganov PV. Evaluation and management of patients with refractory ascites. World J Gastroenterol. 2009 Jan 7;15(1):67-80. [Medline]
3. 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]