Portal hypertension is a group of syndromes caused by a persistent increase in portal venous pressure due to different etiologies. According to the site of obstruction of blood flow, it can be divided into intrahepatic (85%-95%) and extrahepatic portal hypertension (5%-15%), while extrahepatic portal hypertension is mainly caused by portal vein embolism and malformation, and intrahepatic type is caused by diffuse lesions of the liver, mainly post necrotizing hepatic sclerosis in China. When the portal pressure rises from 10 to 24 cmH2O at normal to 40 cmH2O, the portal interventricular traffic branch opens, forming the anterior abdominal wall, retroperitoneum, upper and lower rectal veins and the esophageal traffic branch of the gastric fundus, the latter of which will have fatal complications once it ruptures and bleeds. The development of portal hypertension is followed by splenomegaly, hypersplenism, open and dilated portal-interbody venous communication branches and ascites. Diagnosis (a) The patient has a history of hepatitis or schistosomiasis, or a history of chronic alcohol consumption. Some patients may have a history of black stools or vomiting of blood. (b) Splenomegaly with hypersplenism, hematocrit and thrombocytopenia. (c) Barium esophagogram or fiberoptic endoscopy reveals images of varices in the esophagus or gastric fundus. (d) Ultrasonography reveals echogenicity in the liver parenchyma, splenomegaly, portal vein dilatation, opening of the portal venous system in the abdominal cavity, and abnormal portal hemodynamics. Differential diagnosis When ruptured esophagogastric fundic varices bleed, it must be differentiated from gastroduodenal ulcer bleeding, gastric cancer bleeding, biliary bleeding, etc. Detailed medical history, comprehensive physical examination and necessary auxiliary examinations can help the differential diagnosis. In patients with hepatosplenomegaly and hepatosclerosis, the spleen may shrink further after bleeding, and even cannot be retrieved, which may lead to misdiagnosis. If necessary, an emergency endoscopy or a triple-lumen double-bladder compression method can be used to differentiate. Treatment The treatment of bleeding from variceal arrangement of esophagogastric fundus in portal hypertension is preferred to conservative treatment such as sclerosing agent injection or endoscopic ligation and internal medicine. Transjugular vein intrahepatic portal shunt can be considered if available. (1) Steps for treatment of acute hemorrhage (1) Replenish blood volume, transfusion to correct hemorrhagic shock, and timely use of three-lumen tube compression to stop bleeding. First inflate the gastric balloon (200 ml), traction the three-lumen tube to compress the cardia, and then inflate the esophageal balloon (150 ml) and fix it (see “Application of three-lumen double-bladder tube”). (2) Intravenous infusion of pituitary pressin at an initial dose of 20 u/200 ml of solution over 30 minutes or continuously at 0.4 u per minute. Somatostatin may also be applied intravenously at 150-200 μg per dose, and may be repeated every 6-8 hours. (4) Give pro-coagulant drugs such as vitamin K1, prothrombinogen mixture, and fibrinogen. After 24 hours of triple-lumen tube placement, the balloon can be emptied for observation if there is no bleeding from gastric lumen suction. After 2-3 days of hemostasis, different treatment plans can be developed according to the patient’s liver function status. (B) Introduction of non-surgical treatment methods Fibroendoscopic sclerotherapy The advantage is to preserve portal perfusion and not to aggravate liver function damage. It is suitable for high-risk patients with poor general condition. Sclerotherapy can be started within 2 to 3 days after hemostasis, and the application of 1% Aethekysklerol solution injected directly into the varicose vein can achieve immediate hemostasis, and perivenous injection to promote fibrosis is used for selective planned treatment. The injection site starts from the lower part of the esophagus 5.0 cm above the cardia, and 2 to 3 circumferential layers of sclerotherapy are injected in the direction of the cardia. The treatment can achieve a good near-term outcome. Drug treatment: Non-selective beta blocker (Takuan) can reduce the cardiac output and make the portal pressure drop, but its dose must reach to make the heart rate drop by 25%. Oral administration of this drug for a short period of time after hemorrhage can help prevent rebleeding in the near future. However, it should not be used as a first-line treatment in the long term because it affects blood flow to the liver and may have a negative effect on existing chronic liver damage. Transjugular intrahepatic portosystemic shunt (TIPS): This technique involves placing a stent between the hepatic vein and the portal vein via the jugular vein to reduce portal pressure. (iii) Surgery is an option after the above conservative treatment has failed, and there are many surgical options, with simple and reliable peripancreatic vascular dissection being the first choice.