In clinical practice, the term ‘ascites’ refers to the detectable and pathologic collection of fluid in the peritoneal cavity. Usually it is a clinical finding and can be confirmed by a diagnostic paracentesis. Subclinical amount of fluid (i.e., less than 1.5 litre) can be detected using ultrasonography or computed tomography of the abdomen.1 Chronic liver disease with portal hypertension, congestive cardiac failure, tuberculosis and malignancy are important causes of ascites. However, it can occur secondary to a number of pathological conditions. In the case of refractory ascites, median survival does not exceed 6 mo, which is due to the development of severe complications including hyponatremia and progressive renal failure.2 The most unfavorable predictors are hyponatremia, arterial hypotonia, high serum creatinine, low urine sodium level, spontaneous bacterial peritonitis, low total protein concentration in the ascitic fluid (≤ 2 g/dL), and the number of red blood cells in the ascitic fluid of more than 10.000/mm.3 In a large number of patients, cirrhosis of liver is the cause of ascites. Several factors contribute to the development of ascites in chronic liver disease. Kidney plays a central role and is responsible for sodium and water retention, through complex mechanisms.3 The mechanism by which the diseased liver affects renal function is not fully understood. The ‘peripheral arterial vasodilatation hypothesis’ proposed in 1988 is based on the presence of characteristic circulatory abnormalities seen in cirrhotic patients. These patients show manifestations of increased cardiac output, arterial hypotension, decreased peripheral vascular resistance and splanchnic vasodilatation.4 The present study was conducted to determine cases of ascites admitted to medicine ward.