Percutaneous hepatic perforation of gastric coronary vein embolization (PTVE) is an effective treatment for esophagogastric fundic variceal bleeding by percutaneous hepatic puncture to the intrahepatic portal vein branches, selective cannulation of the gastric coronary vein, and embolization of the esophagogastric fundic variceal vein with embolic material. Interventional therapy. Clinical studies have confirmed that PTVE has obvious efficacy in treating esophagogastric fundal variceal bleeding and reducing the morbidity and mortality rate. I. Hemostatic effect and influence on varicose veins PTVE first occludes the fundic esophageal varicose vein with liquid embolic agent and then permanently and completely embolizes the main trunk of gastric coronary vein with a steel ring to completely block the abnormal blood flow between portal vein and odd vein to achieve the purpose of rapid and effective hemostasis, and the varicose vein is completely blocked or the blood flow is reduced significantly to reduce the risk of rebleeding. PTVE has good efficacy in emergency hemostasis, prevention of rebleeding, blocking or reducing blood flow in varicose veins. Most scholars believe that after gastric coronary vein embolization, due to the redistribution of portal vein blood flow after embolization of varicose veins, resulting in an increase in the blood flow into the hepatic portal vein and an increase in portal vein pressure. Domestic studies have also confirmed that after PTVE, portal vein pressure increases compared with the preoperative period, but there is no significant change in portal vein diameter and blood flow. The increase in portal venous pressure may continue to cause new varicose veins and increase the risk of rebleeding, but it is beneficial to improve hepatic perfusion. Therefore, such pressure changes should be viewed correctly, and transjugular intrahepatic portosystemic shunt can be performed jointly to overcome this unfavorable factor. Impact on liver function Percutaneous hepatic perforation of gastric coronary vein embolization blocks the blood flow of the varices esophagogastric fundus vein, increases the portal venous pressure and promotes hepatic perfusion, which is theoretically beneficial to regeneration of hepatic cells and effective improvement of liver function. Zhang Xiquan et al. reported that after percutaneous transhepatic puncture portal vein embolization in 37 patients with cirrhosis and portal hypertension with acute upper gastrointestinal hemorrhage, liver function was stabilized or improved in 32 cases, accounting for 86%, and hepatic function was reduced in 5 cases, accounting for 14%, after hepatic and anti-infective treatments. However, most of the reports considered that there was no significant change in liver function before and after the operation. Complications Increased portal vein pressure triggered or aggravated portal hypertensive gastropathy: after the varices of fundic esophageal vein (plexus) were embolized, rebleeding was generally easy to occur in about 2 weeks, which was basically consistent with the domestic reports, probably because after the varices of the main vein were embolized, the portal vein pressure was changed again (increased), and the establishment of the new collateral circulation caused rebleeding of the small veins, but the general bleeding volume was Lesser. Wang Qing et al. reported that in 5 patients with gastrointestinal bleeding, rebleeding occurred in 2 cases 2 weeks after PTVE, but the amount of bleeding was significantly reduced (positive fecal occult blood). Quan Qizhen et al. reported 1 case of upper gastrointestinal bleeding in 29 patients during the follow-up period, accounting for 3.1% (1/29). Gastroscopy showed that the original gastric fundal varices had improved significantly, but with extensive gastric mucosal erosion, and the bleeding was stopped after treatment with acid production and gastric mucosal protective agents, which was considered to be portal hypertensive gastric mucosal lesions. Other adverse reactions include bleeding from the puncture channel, reflux of embolic agent, portal vein thrombosis caused by cannula injury, ectopic embolism (pulmonary embolism, cerebral embolism), etc. Careful blockage of the puncture channel before extubation, slow injection of embolic agent, and careful analysis of the portal circulation can usually be avoided. Other minor complications include fever, ascites leakage, etc., which should be given symptomatic treatment. VI.SUMMARY In conclusion, there are various treatment methods for fundic esophageal varices caused by liver cirrhosis, but all of them have their own disadvantages. Transgastric injection of sclerosing agent is ineffective because it is difficult to occlude all varicose veins, especially fundic varices, especially after sclerosing agent treatment, fundic varices will become more obvious with the increase of portal venous pressure. Fundal vein dissection or portal vein shunt or transjugular intrahepatic portacaval shunt can also reduce portal pressure and hemorrhage, but its clinical application is greatly limited due to the poor liver function of the patient and the induction of hepatic encephalopathy. Percutaneous hepatic perforation of gastric coronary vein embolization is a safe, effective and easy-to-operate method of emergency hemostasis, which belongs to the interventional interruption of flow and has a definite effect on hemostasis. At the same time, the interruption of flow increases the pressure of the portal vein and promotes hepatic perfusion, which is conducive to the regeneration of hepatic cells and the improvement of hepatic function effectively. With the continuous maturation of interventional radiology technology, the success rate of percutaneous portal vein puncture and cannulation is high; the popularization of DSA makes it easier and more objective to observe the hemodynamic study of the portal vein system and side branch vessels.