The Effects of Intravenous Injection of Concentrated Human Serum Albumin upon Blood Plasma, Ascites and Renal Functions in Three Patients with Cirrhosis of the Liver.

The mechanism of ascites formation has been a subject of interest for many years and remains a challenge to the investigator. In previous reports (1, 2) on 61 patients with cirrhosis of the liver, it was pointed out that those with ascites have lower values for serum albumin than do those without ascites and that the tendency to diuresis (and the loss of ascites) was correlated with a rise of the serum albumin level. The "critical" point of diuresis was found to be about 3.1 grams per cent. However, the slowness of diuresis, frequently taking place over a period of several months, did not provide a sharp endpoint for establishing a critical level. Although other factors, such as an increased portal capillary pressure, were considered to be contributory, it seemed likely that the colloid osmotic pressure of the plasma was the chief determinant for the presence or absence of ascites. There are several objections to this concept: the rise of serum albumin did not regularly precede a diuresis although it appeared to accompany the phenomenon; wider experience in a series of 115 cases with ascites revealed 7 cases in which diuresis failed to take place even though the serum albumin rose above 3.5 grams per cent; and, conversely, there were 3 cases in which diuresis took place when values of serum albumin were less than 3.0 grams per cent. Ralli and her associates (3) have cited instances in which diuresis with loss of ascites took place at low values for serum albumin in patients receiving intravenous liver extract. Furthermore, they presented