Ascites in patients with cirrhosis is most commonly a sign of hepatic decompensation, but in some patients may be the result of progression of hemodynamic changes leading to an outflow block in an otherwise well-compensated liver.1-4 The high mortality of major surgical operations in either type of patient, with rapidly accumulating or uncontrolled chronic ascites, is well known. Unfortunately, the usual medical treatment, consisting of salt restriction, diuretics, high-protein diet, and, recently, prednisolone5 and aldosterone antagonists,6 usually requires several weeks or months for stabilization or disappearance of ascites. It has been shown that a reduced surgical mortality follows operations in patients whose ascites has been eliminated or controlled prior to operation.7 Failure to accomplish such control is all too commonly followed by extensive edema in the wound and the bowel, poor wound healing, progressive hepatic decompensation, and death.
In the past, the usual method of approaching