Approximately 75% of patients with ascites are caused by cirrhosis, while the rest of patients with ascites can be caused by malignancy, heart failure, tuberculosis, pancreatic disease, etc. Ascites is the most common of the three major complications of cirrhosis and occurs in about 60% of patients with compensated cirrhosis within 10 years. Ascites formation in cirrhosis indicates a poor prognosis, with a mortality rate of approximately 40% at 1 year and 50% at 2 years. The most reliable predictors of poor prognosis include: hyponatremia, low arterial pressure, high blood creatinine and low urinary sodium. Both the International Club of Ascites and the 2010 EASL guidelines recommend that cirrhotic ascites can be classified into 3 grades: grade 1 ascites (small amount of ascites, detected only by ultrasound); grade 2 ascites (moderate amount of ascites with significant moderate symmetric abdominal distention); and grade 3 ascites (large or severe amount of ascites with significant abdominal distention). Because of the significantly decreased survival of patients with grade 2 or 3 ascites, liver transplantation should be considered as a potential treatment option. The initial evaluation of patients with ascites includes history, physical examination, abdominal ultrasound, liver function, renal function, electrolytes, and ascites analysis, with particular emphasis on the cell count and SAAG (ascites-serum albumin gradient) of ascites, which can be attributed to portal hypertension if the SAAG is ≥ 1.1 g/dl (or 11 g/L), with approximately 97% accuracy. Moderate sodium restriction is an important component of ascites treatment (sodium intake of 80-120 mmol/d, equivalent to 4.6-6.9 g/d of sodium), which is roughly equivalent to a sodium diet that avoids the addition of pre-prepared meals. There is no information to support fluid restriction in patients with ascites with normal blood sodium concentrations. Diuretics are the mainstay of treatment for ascites. Patients with first-episode grade 2 (moderate) ascites should receive an aldosterone antagonist such as spironolactone, starting at 100 mg/day and increasing progressively up to a maximum dose of 400 mg/day, and patients with nonresponding or recurrent ascites should be combined with furosemide, increasing progressively from 40 mg/day up to a maximum dose of 160 mg/day. It should be noted that diuretic therapy is predominantly oral and needs to be given in a single dose. Many patients or physicians often prefer intravenous application of furosemide or split oral doses, which is a big misconception. During diuretic therapy, if the patient has severe edema, the rate of weight loss does not need to be limited, and if the edema disappears, it is recommended that the patient lose no more than 0.5 kg/day. In the course of ascites treatment, attention should be paid to the prevention and treatment of hyponatremia, spontaneous peritonitis, and hepatorenal syndrome. For grade 3 (massive) ascites, treatment with massive laparotomy release (LVP) is preferred. LVP is generally safe, and in cases where less than 5 L of ascites is released at a time, albumin infusion is not necessary after laparotomy, and if more than 5 L of ascites is released at a time, 8 g of albumin can be given for each additional L. TIPS is effective in treating intractable ascites, but the risk of postoperative hepatic encephalopathy is high, and studies have not, compared with LVP convincingly show improved survival. Once ascites is medically refractory, patients have a median survival of approximately 6 months; therefore, liver transplantation should be considered in patients with intractable ascites.