Comprehensive introduction of the pathogenesis of ascites

        The formation of ascites is the result of the loss of fluid production and absorption in the abdominal cavity. The formation mechanism of ascites in each disease is caused by several factors combined or alone.

        1 systemic factors

        (1) decrease in plasma colloid osmotic pressure: the plasma colloid osmotic pressure is mainly maintained by albumin. Plasma albumin is lower than 25g/L or at the same time accompanied by portal hypertension, liquid leakage from the capillary into the tissue gap and abdominal cavity, if the water leakage into the abdominal cavity is the formation of ascites. This is seen in severe liver failure, cirrhosis (reduced protein synthesis), lack of nutrition (protein intake), nephrotic syndrome and protein loss of gastrointestinal disease, and so on.

        (2) sodium, water retention: common in the heart, renal insufficiency and the middle and late stage of cirrhosis with secondary aldosterone. In liver cirrhosis and right heart failure, the activity of sodium and sodium decreased, and the absorption of sodium in the proximal tubule of the kidney increased. In recent years that the proximal tubule sodium reabsorption mechanism in aldosterone distal tubule is more important; heart failure and end-stage liver cirrhosis caused by massive ascites to reduce effective blood volume, and glomerular volume receptor stimulation device; sympathetic nerve activity increased, activation of the renin angiotensin aldosterone system; antidiuretic hormone release the increase in renal blood flow decreased, decreased glomerular filtration rate and renal tubular reabsorption of sodium and water retention increased, prompting the persistent ascites, therefore, renal sodium and water retention is constant factor of ascites.

        (3) endocrine disorders: liver function impairment in patients with liver cirrhosis or liver dysfunction. On the one hand, antidiuretic hormone and aldosterone induced inactivation of sodium and water retention function is reduced; on the other hand, blood circulation in expanding blood vessels of vasoactive substances concentration, these substances caused by peripheral and splanchnic arteriolar resistance decreased, cardiac output increased in the splanchnic hyperdynamic circulatory state. The visceral vascular bed expansion, visceral congestion, caused by the relative lack of effective circulating blood volume and blood pressure, compensatory release of angiotensin II and norepinephrine to maintain blood pressure. Due to the stimulation of the sympathetic nervous system reflex release of vasoconstrictor substances, the renal blood flow decreased, glomerular filtration rate decreased, and the release of ADH, cause renal tubular sodium and water absorption increased, leading to retention of sodium and water and the formation of ascites.

        2 local factors

        (1): the increase in hydrostatic pressure due to liver cirrhosis and portal vein thrombosis or foreign oppression itself lead to increased portal venous pressure and blood capillary, thereby causing ascites.

        (2) lymph flow increased, cirrhosis due to obstruction of portal vein and hepatic subcapsular sinus pressure increased significantly, such as lymphatic dendritic tree, the absorption area reduced, lymph growth increased over the ability of lymph circulation reabsorption, causing lymph deposition. The lymphatic leakage through the visceral peritoneum or liver surface into the abdominal cavity, increase the accumulation of ascites, tumor, retroperitoneal tumor of mediastinum and filariasis caused by thoracic duct or chylocyst obstruction, and traumatic rupture, chyle leak into the abdominal cavity formation of chylous ascites.

        (3) increased peritoneal vascular permeability: peritoneal inflammation, tumor invasion or organ perforation caused by gastric juice, pancreatic juice, bile, blood stimulation can promote vascular permeability increase induced by peritoneal ascites.

        (4) abdominal visceral rupture: the rupture and perforation of the parenchyma or cavity can cause pancreatic ascites, bile ascites, bloody ascites and blood.