Mechanisms of ascites formation

Abstract

Dr. Frederick K. Heath: The development of ascites in patients with cirrhosis of the liver has long been correlated with portal hypertension and hypoalbuminemia. The manner in which these and other factors may contribute to this process is considered in this clinic. In the otherwise normal animal obstruction to the hepatic outflow (hepatic veins or vena cava) produces ascites but occlusion of the portal system results in the development of collateral circulation and hypersplenism. Portal hypertension alone, then, may furnish a larger vascular bed for diffusion and because of stasis may also tend to render this area more permeable. While both conditions are favorable to ascites formation, they do not of themselves produce it. The role of the lymphatics has not been determined. On this background osmotic forces operate. The net hydrostatic pressure (capillary blood pressure minus ascitic hydrostatic pressure) tending toward the formation of ascites is opposed by the net colloid pressure (plasma colloid osmotic pressure minus ascitic colloid osmotic pressure). Dr. Mankin showed that in the presence of ascites, irrespective of whether it was increasing or decreasing, the difference between the capillary and ascitic colloid osmotic pressures remains fairly constant. This state of dynamic equilibrium between opposing forces need be only slightly altered to influence the direction of fluid flow before equilibrium is regained. Thus mercurial diuresis, presumably by hemoconcentration, tends to decrease ascites. In the same fashion intravenous albumin may or may not decrease ascites depending upon how rapidly it diffuses from plasma to the ascitic compartment. Of great interest is the finding that patients with ascites do not excrete sodium in the urine proportionally to their intake. The magnitude of this deficiency would appear to correlate with the degree of ascites and the deficiency in serum sodium levels. Ingested sodium is almost entirely diverted to the ascitic fluid which tends to increase when the daily intake of sodium chloride exceeds 1 gm. However, if salt be restricted to about 1 gm. daily, water excretion rises, serum protein values slowly increase, serum sodium concentration remains constant and no further ascitic fluid is formed. In this fashion progression of this phase of the disease may be interrupted. About one-half of Dr. Kunkel's patients maintained on low-sodium diets over a period of six months regained their ability to excrete sodium normally and concomitantly showed improvement in their ascites. Dangerous depletion of sodium has been observed on this regimen in the presence of renal damage or following the use of mercurial diuretics. Similar to the depression in the urinary excretion of sodium, Dr. Ralli described a marked reduction in water output in cirrhotic patients with ascites. She has proposed that the renal abnormality may be due to greater tubular reabsorption of water dependent upon an increase in the posterior pituitary antidiuretic hormone and has reported finding unusual amounts of antidiuretic substances in the urine of ascitic patients. According to this evidence, the disappearance of ascites without change in hypoalbuminemia becomes understandable. While the relative importance of these mechanisms undoubtedly varies from patient to patient and cannot be determined in advance so as to indicate a single line of therapy, they nevertheless suggest several special therapeutic approaches such as are indicated in the clinic.