Ascites may occur in patients with cirrhosis and alcoholic hepatitis, and portal hypertension is an essential factor in the development of ascites. Ascites is the most prominent clinical manifestation of cirrhosis. The increased portal venous pressure increases the filtration pressure in the capillary bed of the portal system, while the hypoproteinemia, decreased plasma colloid osmotic pressure and excessive lymphatic fluid production caused by cirrhosis contribute to the leakage of fluid from the liver surface and intestinal plasma membrane surface into the abdominal cavity and the formation of ascites. Although intravenous blood flow increases in portal hypertension, central blood flow is reduced, thus stimulating excessive renal aldosterone secretion, leading to water and sodium retention and exacerbating ascites formation. Prior to the appearance of ascites, patients often have intestinal distention, such as a feeling of increasing abdominal circumference and weight gain. When there is a large amount of ascites, the abdomen is distended and the abdominal wall is taut and shiny, causing the patient to have difficulty moving around. The increased abdominal pressure compresses the intra-abdominal organs and can cause an umbilical hernia, which can also cause dyspnea and palpitations due to the elevation of the diaphragm. In cases with more than moderate ascites, mobile turbid sounds can be heard by percussion, and in cases with a small amount of ascites, mobile turbid sounds are not obvious, and the diagnosis can be confirmed with the help of abdominal ultrasound.