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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