INTRODUCTION

Ascites due to cirrhosis can be mobilized in approximately 90 percent of patients with a treatment regimen consisting of dietary sodium restriction (usually 88 meq [2000 mg/day]) and oral diuretics (usually consisting of spironolactone and furosemide) [1]. (See "Initial therapy of ascites in patients with cirrhosis".)

This topic review will discuss the approach to the 10 percent of patients who appear to be diuretic-resistant. This topic is also addressed in a guideline (updated for 2009) issued by the American Association for the Study of Liver Diseases (AASLD) (table 1) [2]. The AASLD guideline for the management of adult patients with ascites due to cirrhosis, as well as other AASLD guidelines, can be accessed through the AASLD web site at www.aasld.org/practiceguidelines/Pages/default.aspx.

DEFINITION

Diuretic-resistant ascites in patients with cirrhosis is considered to be present when one or both of the following two criteria is present in the absence of therapy with a nonsteroidal anti-inflammatory drug (NSAID), which can induce renal vasoconstriction and diminish diuretic responsiveness [3]:

• An inability to mobilize ascites despite compliance with dietary sodium restriction (as confirmed by a 24-hour urine collection containing less than 78 meq of sodium or urine sodium less than the urine potassium on a random sample) and the administration of maximum tolerable doses of oral diuretics (400 mg per day of spironolactone and 160 mg per day of furosemide) [4]. The 78 meq of sodium represents the recommended 88 meq intake minus 10 meq in nonurinary losses. Patients who gain weight despite excreting more than 78 meq of sodium per day (or urine sodium > urine potassium on a random sample) are not compliant with the diet. (See "Patient information: Collection of a 24-hour urine specimen (Beyond the Basics)".)
• The development of prohibitive diuretic-related complications, such as progressive azotemia, hepatic encephalopathy, or progressive electrolyte imbalance.

Differential diagnosis — Resistant ascites in patients with cirrhosis must be differentiated from malignant ascites due to peritoneal carcinomatosis, Budd-Chiari syndrome (hepatic vein thrombosis), or from chylous malignant ascites. These disorders are typically refractory to diuretic therapy because of an inability to mobilize the ascitic fluid [5]. In contrast, massive hepatic metastasis, another cause of malignant ascites, is due to intrahepatic portal hypertension and can be treated in a similar fashion to patients with cirrhosis [5].