In Asia, including China, the vast majority of cirrhotic portal hypertension develops chronically from hepatitis B virus infection. If the disease develops after hepatitis B virus infection, the patient’s condition may be in the following seven states: ① hepatitis B carrier ② hepatitis B marker positive abnormal liver function (hepatitis B) ③ cirrhotic liver function compensated portal hypertension splenomegaly and hypersplenism (mild) WBC>4.0×108/L Plt>50×109/L ④ cirrhotic liver function loss compensated portal hypertension splenomegaly and hypersplenism (WBC<3.0×109/L) Plt<50×109/L (Child A, B) ⑤ cirrhotic decompensated portal hypertension with splenomegaly and hypersplenism with upper gastrointestinal bleeding (Child A, B) ⑥ cirrhotic decompensated portal hypertension with splenomegaly and hypersplenism (Child C) ⑦ cirrhotic decompensated portal hypertension with splenomegaly and hypersplenism with upper gastrointestinal bleeding (Child C). In any of the above states, a few patients can also develop hepatocellular carcinoma, complicating the condition. The complex pathophysiological changes of cirrhosis, cirrhosis and complex hepatic hemodynamic (including portal system, hepatic arterial system and its regulation) changes make the condition of cirrhotic portal hypertension complex. Cirrhosis results in decreased liver function, impaired liver reserve function and reduced liver size (reduced number of functioning hepatocytes). Poorer liver function and liver reserve function and smaller liver size mean that patients have a limited survival period. Patients in states ①, ② and ③ above need only outpatient follow-up or medical treatment. Patients in status 6 and 7 above need to be considered for liver transplantation if liver function does not return to Child B or Child A after regular medical treatment. Liver transplantation has been rapidly developed in China and is the only radical treatment for portal hypertension in hepatic sclerosis, and it has become a routine procedure for the treatment of end-stage liver disease in our department. The indications for liver transplantation in cirrhotic portal hypertension are: (1) liver function loss with intractable ascites, which cannot be controlled by medical treatment; (2) esophagogastric fundic varices with liver function loss, ruptured bleeding or recurrent bleeding; (3) recurrent hepatic encephalopathy, in which the patient's quality of life is significantly reduced; (4) hepatorenal syndrome with progressive oliguria; (5) progressive hepatopulmonary syndrome. After the appearance of these conditions, it means that the patient's survival period is only 6-12 months. In patients in the above-mentioned ④ and ⑤ states, conventional splenectomy with flow dissection and/or shunt remains one of the preferred treatment measures. The 5-year survival rate after surgery is up to 90%. It is also a routine procedure in our department. Transjugular intrahepatic portosystemic shunt (TIPS) is also a common clinical treatment for ruptured variceal bleeding in patients with acute ruptured variceal bleeding who have failed medical therapy, patients with intractable hepatic ascites, and bleeding in patients awaiting liver transplantation.