Quantitative Modeling of the Physiology of Ascites in Portal

Although the factors involved in ascites formation in cirrhosis have been studied for over a century, the basic pathophysiology remains uncertain. Recent research primarily has focused on associated systemic changes (e.g., renal sodium retention, increased cardiac output and blood volume) and whether these systemic changes are the cause or effect of ascites. However, the physiological linkage between these systemic changes and the intraperitoneal alterations that cause ascites has received limited attention and a variety of clinical observations are not well understood. In this Debate Article we provide a quantitative explanation of ascites accumulation based solely on pathophysiological alterations within the peritoneal cavity. The systemic abnormalities observed in cirrhosis are linked to ascites via their influence on this intraperitoneal pathophysiology. Discussion A detailed literature review of the factors involved in peritoneal fluid and protein balance in normals and cirrhotics is presented. This review indicated that the high liver sinusoidal pressure produced by increased outflow resistance in cirrhosis leads to rupture of the liver capsule and/or lymphatics, leaking high protein liver tissue fluid into the peritoneal space. This fluid then pull