Mobile turbidity is the result of a loss of dynamic balance in the production and absorption of fluid in the abdominal cavity, and the mechanism of ascites formation in each disease is the result of several factors acting in combination or individually. Decreased plasma colloid osmotic pressure: plasma colloid osmotic pressure depends mainly on albumin to maintain plasma albumin below 25 g/L or with concomitant portal hypertension, fluid tends to leak from capillaries into the tissue interstitium and abdominal cavity, and ascites forms if water leaks into the abdominal cavity. This condition is seen in severe hepatic insufficiency, moderate to advanced cirrhosis (reduced protein synthesis), nutritional deficiency (insufficient protein intake) nephrotic syndrome and protein-losing enteropathy. Sodium and water retention: common in cardiac and renal insufficiency and moderately advanced cirrhosis with secondary aldosteronism. In cirrhosis and right heart failure, decreased natriuretic factor activity increases sodium reabsorption from the proximal tubule. In recent years, it is believed that the mechanism of sodium reabsorption in the proximal tubule is more important than the action of aldosterone in the distal tubule. Endocrine disorders: In cirrhosis or hepatic insufficiency, hepatic degradation is diminished. On the one hand, the inactivation of antidiuretic hormone and aldosterone decreases, resulting in sodium and water retention. Due to the dilatation of visceral blood vessels and visceral stasis, the effective circulating blood volume is relatively insufficient and hypotensive, and the body compensates by releasing angiotensin II and norepinephrine to maintain blood pressure. This is due to reflex excitation of the sympathetic nervous system to release some vasoconstrictive substances, resulting in reduced renal blood flow and decreased glomerular filtration rate.