In active cirrhosis, ascites is often present. The mechanism of ascites formation is a very complex process, because it is the result of multiple pathological factors, multiple organs and multiple links interacting with each other. In summary, there are several aspects: 1. portal hypertension: the portal vein of the liver and the inferior vena cava, also known as the portal vein, which is the link between the liver and other parts of the blood circulation. It is also the necessary route for the hepatic artery and hepatic vein to enter and exit. Under normal conditions the volume of their arteriovenous beds is basically equal, and the amount of incoming and outgoing blood flow is in equilibrium. In cirrhosis, due to the degeneration, necrosis and proliferation of fibrous tissue of hepatocytes, the vascular bed in the liver is compressed, distorted, deformed and narrowed, blocking the blood vessels, causing the hepatic sinusoids to stagnate, and the blood flow is greatly reduced, and the input volume is obviously larger than the output volume, causing the portal vein pressure to rise. At the same time, capillary venous pressure is also elevated, and over time, blood reflux in the gastrointestinal tract, mesentery and peritoneum is obstructed, vascular permeability is elevated, and plasma components in the blood leak out, forming ascites. 2, hypoproteinemia: It is due to the inability of the liver to synthesize the nutrients digested and absorbed by the stomach and intestines into albumin. Due to the decrease of serum albumin, the intravascular colloid osmotic pressure decreases and the plasma components extravasate and form ascites. 3, endocrine disorders: In active cirrhosis, the inactivation of antidiuretic hormone by the liver is greatly reduced, and its content is elevated, while urination is reduced, which can also cause swelling and ascites. 4, lymphatic reflux disorder: the human lymphatic circulation, also known as the third circulation, refers to a circulatory system located outside the arteries, veins and capillaries. There is no lymphatic circulation anywhere in normal people, especially between the liver sinusoids and liver cells, which have abundant lymphatic fluid. Due to the lesion, the liver not only makes the portal vein pressure rise, but also makes the lymph from the pressure rise, the lumen dilates, and the lymphatic reflux is impaired, which makes the lymphatic fluid overflow and forms ascites.