Intractable ascites in cirrhosis is a sign of severe decompensated liver dysfunction in liver cirrhosis. As defined by the International Ascites Society, intractable ascites is the unsatisfactory regression of ascites after drug therapy and/or the failure to prevent early recurrence of ascites after treatment with discharge ascites. The mechanism of its occurrence is mostly thought to be related to abnormalities in the production and inactivation of humoral substances such as diminished hepatic inactivation, significantly reduced effective circulating blood volume, inadequate renal perfusion, increased antidiuretic hormone (ADH) and estrogen, and reduced vasodilator kinin system and prostaglandins and cardiac natriuretic hormones. Because patients with cirrhotic intractable ascites often have a large amount of abdominal water, symptoms are often accompanied by dilutional hyponatremia, renal insufficiency, and insensitivity to a variety of diuretics, therefore, posing many difficulties in clinical treatment. In recent years, with the continuous research on cirrhotic ascites, many new methods and approaches have been proposed for the treatment of intractable ascites, and the current status of its treatment is reviewed as follows. 1. sodium restriction and water restriction Regarding sodium restriction, Sherlock et al. believe that 0.75 g of urinary sodium excretion (1 g of sodium is equivalent to 2.5 g of sodium chloride) in patients with cirrhotic ascites will result in the formation of ascites, so sodium intake must be strictly controlled within 22 mmol/d. In contrast, Runyon concluded that in patients without fever and diarrhea extrarenal sodium excretion1, 24 h renal excretion of sodium can be >78 mmol/d, so sodium restriction of 88 mmol/d (equivalent to 2 g sodium and 5 g NaCl) is more appropriate, and it is believed that stricter sodium restriction is beneficial to ascites excretion, but compliance is poor. Some domestic studies have also concluded that overly strict sodium restriction may reduce urinary sodium excretion, weaken the effect of diuretics, and prolong the time of ascites remission. At present, the standard of sodium restriction is mostly advocated to balance sodium intake and urinary sodium excretion. Patients with cirrhosis are often associated with water retention, i.e. impaired clearance of free water by the kidneys, also known as water intolerance. In patients with intractable ascites, ADH increases, glomerular filtration rate (GFR) decreases, and sodium-water reabsorption increases greatly when blood sodium is 500 ml/d and abdominal circumference is reduced by more than 3 cm, effective in 14 cases. The mechanism is that mannitol, taken orally, can make the intestine in a hypertonic state, reducing water absorption and increasing water discharge from the gastrointestinal tract, thus playing an indirect role in eliminating ascites. 2, combined Chinese and Western medicine treatment Huang Baishou reported 12 cases of intractable ascites treated with combined Chinese and Western medicine. After 2 courses~5 courses of treatment, all 12 patients showed small amount or trace amount of ascites by ultrasound test, and all of them were effective. METHODS: All patients were treated with the following formula on the basis of the conventional treatment: Extra-strength treatment with the addition and subtraction of the formula of “Expelling Blood Stasis and Facilitating Water” (composed of turtle nail, angelica, white peony, Yin Chen, poria, large abdominal bark, psyllium, mu tong, aromatic herb, Chen Pi, astragalus, yam and atractylodes). At the same time, the “wheel method” was used, that is, 2,000 ml~3,000 ml of ascites was released on day 1, followed by aminophylline 0.25 added to 500 ml of 10% glucose injection intravenously, albumin 10 g intravenously on day 2, and 10% glucose 200 ml + dopamine 20 mg + tachyphylaxis on day 3. 60 mg~80 mg intravenously, and on the 4th day, 10% glucose injection 500 ml + compound salvia injection 16 ml intravenously. Stop 3 d for 4 d of weekly treatment, and 1 week is 1 course of treatment until the patient’s ascites disappears. 3.Surgical treatment For patients with intractable cirrhotic ascites who are still ineffective after 8~12 weeks of active treatment such as sodium restriction, diuresis and ascites transfusion, and for those who are not contraindicated by infection, hepatic coma, gastrointestinal bleeding and abnormal coagulation mechanism, abdominal jugular vein shunt, portal vein shunt, catheter shunt, internal and external drainage of ascites can be considered. In conclusion, since persistent ascites is an advanced manifestation of liver cirrhosis, although there are many methods, the treatment effect mainly depends on the liver reserve and the speed of complications. Therefore, we must pay attention to the rational use of drugs and take comprehensive measures to minimize the occurrence of various complications and adverse reactions after treatment in order to achieve better results.