Cirrhotic ascites is commonly known as hepatic ascites. Under normal circumstances, there is about 50ml of fluid in the abdominal cavity, which plays a lubricating role for intestinal peristalsis. If the amount of fluid in the abdominal cavity exceeds 200ml, it is called ascites. Generally, ascites does not appear in patients with hepatitis, but only in heavy hepatitis and cirrhosis. When ascites appears, the first thing you feel is abdominal distension and a decrease in urine output. Cirrhosis is the main cause of the formation of liver ascites, cirrhosis ascites development of the four stages 1, cirrhosis ascites pre-cirrhotic patients at this time, no ascites, there is no dilatation of the body circulation arteries and underfilling, but excessive intake of sodium will cause water sodium storage, that is, at this time the kidneys have been impaired in the processing of sodium. This is due to hepatic insufficiency and increased portal pressure directly affecting the renal processing of sodium through neural reflexes, but this water-sodium retention is self-limiting. 2, reactive cirrhosis ascites stage this period of renal sodium and water retention significantly increased and the total blood volume expansion, followed by peripheral artery dilation to reduce vascular resistance. The dilatation of peripheral arteries is due to the release of a large amount of various diastatic substances from visceral tissues, which causes the sequential expansion of visceral circulation and body circulation. Subsequently, ascites is formed according to the peripheral artery hypothesis. 3, intractable cirrhotic ascites stage This stage of patients with severe liver disease, obvious sodium and water retention, insensitive to diuretic therapy, and hemodynamic instability. The plasma renin-angiotensin-aldosterone system and sympathetic nervous system are hyperactive, and the peripheral vasculature is less responsive to vasoactive substances. However, the renal vasculature is very sensitive to vasoconstrictors and there is a further increase in sodium reabsorption and decreased excretion by the kidneys, resisting the action of diuretics and natriuretic factors. 4, hepatorenal syndrome phase This phase occurs mostly in patients with decompensated cirrhosis who have intractable ascites. As a result of further peripheral arterial dilatation and hypotension, the mechanism to maintain the effective circulating volume, resulting in increased synthesis of vasoconstrictor substances, especially the increase in plasma endothelin levels. Due to the high sensitivity of the renal vasculature to constricting substances at this time, this leads to selective renal hypoperfusion, severe sodium retention and renal failure. There are many treatments for cirrhotic ascites, and the hepatology department of the Third Hospital has formed its own treatment characteristics over a long period of time and is adept at dealing with all kinds of refractory and intractable ascites, and we wish this patient a successful recovery!