Abstract
Although the factors involved in cirrhotic ascites have been studied for a century, a number of observations are not understood, including the action of diuretics in the treatment of ascites and the ability of the plasma-ascitic albumin gradient to diagnose portal hypertension. This communication presents an explanation of ascites based solely on pathophysiological alterations within the peritoneal cavity. A quantitative model is described based on experimental vascular and intraperitoneal pressures, lymph flow, and peritoneal space compliance. The model's predictions accurately mimic clinical observations in ascites, including the magnitude and time course of changes observed following paracentesis or diuretic therapy.
Highlights
Ascites commonly is regarded as a clinical condition that can be understood in terms of classic physiological principals
Summary As discussed in the Introduction, in recent years ascites research largely has focused on the systemic changes observed in cirrhosis with particular emphasis on the “hyperdynamic circulation” syndrome
We theorize that ascites formation is dependent on just three factors: 1) the rate of protein leak from the liver, which is a function of the difference between the liver tissue pressure and the peritoneal pressure (PL PA); 2) the colloid osmotic fluid movement between the intestinal tissue and the peritoneal space; and 3) the rate of lymph drainage of the peritoneal space, which is a function of the peritoneal pressure (PA) and the central venous pressure (PRA)
Summary
Ascites commonly is regarded as a clinical condition that can be understood in terms of classic physiological principals. In an attempt to better understand the physiology of ascites, we present what appears to be the first quantitative model of the formation and removal of ascitic fluid In this model, ascites accumulation is explained solely by pathophysiological alterations within the peritoneal cavity; systemic abnormalities are considered relevant only to the extent that they alter intraperitoneal physiology. This discussion includes mechanistic explanations for several clinically important, but poorly understood phenomena. This model accurately predicts the magnitude and time course of the changes in ascites volume that are observed clinically with diuretic treatment or paracentesis. The attached Additional file 1 (Section A), provides a more detailed discussion of the evidence supporting (or contradicting) the model’s assumptions
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