As a surgeon associated with liver disease, there is no way to avoid facing and solving the problem of portal hypertension. Two problems caused by patients with portal hypertension require clinician attention: ruptured esophagogastric fundic varices and hypersplenism. Bleeding from ruptured esophagogastric fundic varices is often the primary and most serious cause of emergency room visits in patients with cirrhosis, with clinical manifestations such as vomiting of blood and black stools. Patients who have had the experience of ruptured esophagogastric fundic varices and bleeding will generally remember it for the rest of their lives, and it is scary to think about it. Their willingness to seek treatment is eager and strong, and they attach a high degree of importance to it, so the proportion of timely consultations is also relatively high. The problem of hypersplenism due to portal hypertension seems to be less important to patients. In the early stage of hypersplenism, there is often no specific clinical manifestation, which is only reflected in routine blood tests, lowered white blood cells and platelets, and an abdominal ultrasound report showing an enlarged spleen. Patients are often unaware of this subjectively. As the disease progresses, the spleen is significantly enlarged in the later stages, and some patients show symptoms of abdominal pressure. White blood cells and platelets are significantly reduced, and patients show reduced immune defenses and easy bleeding manifestations, such as: patients are prone to aggravated infections, bleeding gums, and easy petechiae and petechiae on the peripheral skin …… At this time some severe patients may show poor liver function and poor coagulation function. If the patient also occurs liver tumor, esophagogastric fundic varices rupture bleeding and other conditions, because of the splenomegaly hypersplenism caused by low platelets, poor coagulation function and other problems, so that, for example, surgery, endoscopic treatment, interventional therapy and other means of diagnosis and treatment are relatively contraindicated, some patients will have no effective treatment means to delay treatment, aggravating the disease … … …At this time to deal with hypersplenism, it is often helpless, or half-hearted …… hypersplenism does not seem to be a problem in the early stages, but left to develop, the problems it causes in the later stages are often so fatal that you can not deal with other problems, which is a very serious problem in itself. This is a serious problem in itself. This is a serious problem in itself. It’s a bit of a mouthful, but the reasoning is not hard to understand. It is like boiling a frog in warm water, if you are not vigilant in the early stages, it will become frog soup in the later stages. In the clinical treatment will see a certain percentage of patients, found portal hypertension for many years, did not take targeted treatment, let its development, until the late liver function is very poor, coagulation is very bad, platelets are very low, bleeding, tumor growth to go to the doctor, the result is the treatment is tricky, the treatment effect is poor, the patient and spend money and suffer, but also may not be able to save lives. There are excellent surgical treatments for ruptured esophagogastric fundic varices and hypersplenism caused by portal hypertension that can reduce the near and long-term risk of ruptured esophagogastric fundic varices and hypersplenism, while also addressing splenomegaly and maintaining a durable outcome. For example, partial splenectomy dissection, a procedure that eliminates the problem of reduced white blood cells and platelets due to hypersplenism by removing most of the spleen and preserving a small lobe of the spleen, allowing for normalization of white blood cells and platelets while preserving some of the function of the spleen. The peripancreatic vascular dissection disconnects the shunt channel from the portal venous system to the vena cava system through the varices of the esophagogastric fundus, allowing the relief or disappearance of the varices of the esophagogastric fundus and greatly reducing the risk of bleeding from ruptured varices of the esophagogastric fundus. Unlike the embolization of shunted vessels, the surgical approach is a complete disconnection of the shunted channel from the portal vein to the vena cava, with immediate and long-lasting results. The following pictures show the preoperative and postoperative comparison of a patient with portal hypertension combined with esophagogastric fundic varices and hypersplenism treated with partial splenectomy. The huge spleen before surgery became a tiny one-lobed spleen. The severe esophagogastric fundic varices formed by the thick coronary veins before surgery completely disappeared after surgery. White blood cells and platelets, which were significantly lower before surgery, returned to normal after surgery. The coagulation function, which was poor before surgery, was basically normalized after surgery. This is the efficacy of surgical procedure with clear target and immediate problem solving. Most of our portal hypertension is caused by cirrhosis. Portal hypertension is only a manifestation, and its essential cause is in cirrhosis. The surgical approach to treating portal hypertension is only to treat the problems caused by portal hypertension, and it has no therapeutic effect on cirrhosis. At this stage, there is no good treatment for cirrhosis, the existing treatment means are to control and slow down the progress of cirrhosis, and we have not seen any way to reverse cirrhosis. Although surgical treatment cannot cure cirrhosis, in the absence of effective treatment for cirrhosis, surgical approach improves the patient’s quality of life and prolongs the patient’s survival by reducing the risk of bleeding from ruptured esophagogastric fundic varices and resolving hypersplenism, while creating the conditions for other treatments for liver disease, which is the significance of surgical treatment for portal hypertension.