Cirrhotic Ascites: Pathophysiological Changes and Clinical Implications

Abstract

Liver cirrhosis is associated with a wide range of systemic and pulmonary vascular abnormalities. Cardiac dysfunction also occurs in patients with advanced liver disease (cirrhotic cardiomyopathy). The circulation in cirrhosis is hyperdynamic, which is typically characterized by hypotension resulting from the associated vasodilatation and reflex tachycardia. The circulatory dysfunction in cirrhosis is the proposed pathophysiological mechanism leading to sodium and water retention in patients with liver cirrhosis. Hyperdynamic circulation is triggered by increased intrahepatic resistance due to cirrhosis, leading to a progressive increase in portal venous pressure. As portal hypertension worsens, local production of vasodilators increases due to endothelial activation, leading to splanchnic and systemic arterial vasodilation. Nitric oxide (NO) is considered one of the most important vasodilator molecules in the splanchnic and systemic circulation. The reduction in the effective arterial blood volume results in diminished renal arterial blood flow and subsequently triggers the rennin-angiotensin-aldosterone system (RAAS), antidiuretic hormones (ADHs) and sympathetic nervous system (SNS), leading to renal artery vasoconstriction. All these changes lead to sodium retention and volume expansion, manifested as ascites and peripheral edema. Furthermore, disease progression is associated with various degrees of renal dysfunction.

Serum Homocysteine as an Early Diagnostic Marker of Spontaneous Bacterial Peritonitis in Patients with Hepatic Cirrhosis

“…Large amounts of circulating endotoxin were found in the ascitic patients that may persist even without obvious clinical manifestations of infection. These endotoxins are assumed to induce, indirectly or directly, an increase in NO synthesis and production, which increases the methionine-synthase inactivation, giving rise to Hcy accumulation in the extracellular space and cells (19) .…”