To understand why patients with cirrhosis develop portal hypertension and splenomegaly, let’s first understand the blood supply system of the liver. The blood supply of the liver is dually supplied by the hepatic artery and portal vein. The hepatic artery is rich in oxygen, which is needed for the liver’s own metabolism and is the nutritive vessel of the liver; the portal vein is a larger vein at the population of the liver, which is formed by the confluence of the superior mesenteric vein and the splenic vein, and is divided into two branches at the hepatic portal into the liver. The liver gets 75% of its blood from the portal vein and 25% from the hepatic artery. The portal vein is mainly responsible for collecting the venous return blood from the esophagus, stomach, intestines, pancreas, gallbladder and spleen and transporting it to the liver parenchyma, acting as a bridge for the liver’s external “feed processing”. The blood entering the liver from the portal vein reaches about 1 liter per minute, passes through the numerous hepatic portal capillary networks into the sinusoidal gap of the hepatic lobules, and then converges step by step into three large hepatic veins, which are injected directly into the inferior vena cava back to the right heart. In cirrhosis, due to fibrosis of liver lobules and stiffening of liver parenchyma, the resistance within the hepatic sinusoids increases, and the main and terminal branches of the intrahepatic vascular system (hepatic artery, hepatic vein, portal vein and lymphatic vessels) become thin, twisted and stiff, and the resistance of blood flow in the lumen increases. Among them, the portal vein collects the venous blood from the stomach and intestines, then the return flow is blocked and stagnates in the portal system, causing portal hypertension. When the pressure in the portal vein rises to a certain level, it finds another way to return blood to the right heart. These tributaries, which are normally rarely opened, gradually open to relieve pressure under portal hypertension and large amounts of blood, resulting in the opening of the collateral circulation between the portal vein and the vena cava, commonly the esophageal and fundic veins. The esophageal veins are thin and superficial, and the influx of stagnant blood from the portal vein causes them to twist and open angrily, resembling earthworms, forming varices at the lower end of the esophagus. There are also varices of the abdominal wall and dilated hemorrhoidal veins. When the varices of esophagus and fundus reach a certain degree, they can rupture under the action of external factors and cause upper gastrointestinal hemorrhage. This is manifested as massive vomiting of blood or tarry stools; when it leads to rectal vein rupture and bleeding, there is massive blood in the stool (some of them are misdiagnosed as hemorrhoids). Another cause of portal hypertension formation is splenomegaly, which in turn is caused by cirrhosis. In cirrhosis, the resistance within the liver parenchyma increases and the perfusion of blood from the hepatic artery is obstructed, and over time, the hepatic artery and its branches become thin and sparse. The common hepatic artery and the splenic artery are a pair of arteries that originate from the abdominal trunk artery and go in opposite directions. Due to the principle of hydrodynamics, when the perfusion resistance of the hepatic artery increases, the blood flow from the celiac trunk artery into the spleen increases significantly, and the loose spleen tissue gradually enlarges to several or even a dozen times its original size under the impact of the strong blood flow and the large increase of nutrients. At the same time, the splenomegaly is accompanied by hypersplenism, which leads to a decrease in blood components such as white blood cells, platelets and red blood cells, resulting in anemia and a decrease in complete blood picture, low immune function, and a decrease in the body’s resistance. The increase in portal vein pressure creates further difficulties for blood carrying nutrients and oxygen from the hepatic artery to enter the hepatic sinusoids. The reduced blood supply to the liver itself, the lack of nutrients and the inadequate perfusion of blood in the terminal arteries of the hepatic artery are, in turn, one of the main causes of cirrhotic ascites. The presence of ascites often predisposes to insufficient effective circulating blood volume, decreased blood pressure, electrolyte disturbances, and involves the function of various organs such as heart, brain, and kidney. How to effectively reduce portal vein pressure while simultaneously improving the state of low liver function is a top priority in the treatment of cirrhosis combined with portal hypertension. According to the view that splenomegaly is the main cause of portal hypertension, traditional surgical splenectomy with peripancreatic vascular dissection is one of the effective means to cure cirrhotic portal hypertension, and most of them have received good results. The specific performance is as follows: 1. The pressure of portal vein is effectively reduced, which can maximize the prevention and control of ruptured esophagogastric fundic vein bleeding, so that the possibility of upper gastrointestinal bleeding or rebleeding of patients is significantly reduced. 2. Removal of the hyperfunctioning spleen has increased the number of platelets and white blood cells in peripheral blood to normal levels, improved the immunity of the body, and effectively prevented the occurrence of primary peritonitis 3.