Pathogenesis and Treatment of Ascites in Hepatic Cirrhosis

Abstract

In cirrhosis of the liver structural distortion of the sinusoidal vessels is the major factor responsible for the increase in portal venous pressure and the development of abdominal ascites. The mechanisms by which advanced cirrhosis of the liver leads to widespread changes in the systemic circulation including vasodilatation, increased cardiac output and expanded plasma volume, together with activation of a range of antina-triuretic and natriuretic factors, are unclear. Several hypotheses have been proposed to explain these pathophysiological consequences, including underfilling of the systemic arterial system, overflow and peripheral vasodilatation, with a decrease in effective arterial blood volume. The evidence for and against these hypotheses is critically examined. In patients with hepatic cirrhosis complicated by ascites, increased intra-renal release of vasodilating prostaglandins may assist in sustaining renal blood flow and glomerular filtration rate by counteracting the vasoconstrictor effects of noradrenaline and angiotensin II. In advanced stages of the syndrome, cirrhotic ascites may become refractory to medical treatment. In this situation renal function becomes progressively impaired and eventually acute renal failure, so-called hepatorenal syndrome, supervenes due to intense renal vasoconstriction and opening of intrarenal arteriovenous shunts. The progressive renal vasoconstriction may also be accentuated by the reduced synthesis of renal vasodilating prostaglandins. The medical treatment of ascites is based on bed-rest, a low-sodium diet and administration of aldosterone antagonists and loop diuretics. Patients who are refractory to such therapy may be further treated by paracentesis or by the LeVeen shunt, though the long-term results of these physical therapies are unsatisfactory.

Determination of Physical and Chemical Properties of Blood Plasma and Ascetic Fluid in Patients With Liver Cirrhosis

“…Viral hepatitis play an important part in increasing the incidence of LC, as it was shown that in patients with viral hepatitis B and C the chronic pathological process in the liver during the first year can be registered in 15-22.7% of cases [2]. As the course of viral hepatitis B goes on for about 3-5 years -the chronic process is observed in 40.9% of patients and in 74.4% of patients with hepatitis C. It is shown that on average 20-30% of these patients develop liver cirrhosis, and about 20% of the disease is transformed into cancer [2,3,9]. Therefore, adverse environmental conditions, consistently high level of alcoholism, drug addiction growth, reinforced by economic difficulties, promote the growth of the liver disease as well as the diseases in general organs of the gastro-duodenohepatobiliary system, as it is the leader in the maintenance and regulation of homeostasis .…”