Portal hypertension is a series of pathophysiological changes brought about by increased pressure in the portal venous system due to various causes of cirrhosis. The most serious complication of portal hypertension is ruptured bleeding from the varices of the esophagogastric fundus. The most serious complication of portal hypertension is the rupture of the esophagogastric fundic varices. At present, there are controversies on the indications for surgery, the timing of surgery and the selection of the procedure for gastrointestinal bleeding caused by portal hypertension in clinical practice []. A. Dissection should be the mainstream surgical treatment for portal hypertension The surgical treatment for portal hypertension is broadly divided into bypass surgery and dissection. The theoretical basis of the two treatments are different, and the efficacy reports are different, and there is controversy over which is better or worse. Portal shunts reduce portal vein pressure and are the most effective way to prevent rebleeding in patients with portal hypertension []. However, the diversion of portal blood containing hormones that promote hepatocyte growth, nutrients, and toxins absorbed through the intestine directly into the body circulation results in a decrease in portal to hepatic blood flow, leading to the development of postoperative hepatic encephalopathy and increased liver function impairment. The incidence of hepatic encephalopathy in patients after portal shunt is about 18-45% [], and some patients are in subclinical hepatic encephalopathy after surgery [], TIPSS, as a special form of minimally invasive shunt, has the same complications and cannot correct the problem of decreased red blood cells and platelets due to hypersplenism [], although re-rupture and bleeding of esophageal varices are prevented, but survival and quality of survival was not improved. Theoretically, bypass surgery can reduce thrombosis in the portal venous system, but in practice, it cannot be completely eliminated, and the effect of bypass will diminish and disappear as the chances of thrombosis and occlusion of the anastomosis increase greatly with time. In recent years, there have been cases of small liver syndrome after parental liver transplantation treated with small-bore portosystemic shunts, mainly for the reason of reducing hepatic sinusoidal pressure and facilitating recovery of liver function. Cases of partial portal shunts and relatively stable liver function and longer survival in TIPSS patients also suggest that a certain degree of reduction in pressure and flow of portal venous inflow to the liver is also feasible. toru Ikegami [] has reported the treatment of small liver syndrome with splenectomy or splenic artery ligation. However, we believe that the maintenance of liver function in these approaches is more largely due to the fact that splenic artery ligation increases the inflow of blood into the liver from the hepatic artery, which increases the supply of nutrients and oxygen to the liver, thus facilitating the recovery and compensation of liver function. At the same time, these measures also show precisely the other side of the coin that splenectomy + peripancreatic vessel dissection, while causing a slight decrease in portal vein pressure and blood flow, leads to a significant increase in hepatic artery blood flow, thus facilitating the maintenance of liver function. This is indeed in line with the clinical observation that splenectomy + peripancreatic vascular dissection is not only reliable and durable in the treatment of upper gastrointestinal bleeding due to portal hypertension, but also facilitates the improvement of liver function [,,]. The ideal surgical aim is to prevent and treat gastrointestinal bleeding in a timely and effective manner for a long time, but also to ensure perfusion of portal venous blood to the liver and maintain liver function, as well as to have a relatively simple operation with minimal trauma and fewer complications. Therefore, compared with bypass surgery, flow dissection has greater advantages. Second, the classical dissection procedure is more time-tested. From the initial classical cardia vascular dissection (Hassab procedure), many improved procedures have been derived, including transverse esophagogastric fundoplication, selective dissection, etc., and some advocate routine pyloroplasty after dissection, etc. Theoretically, some people advocate that the main trunk of the gastric coronary vein and the traffic branch between it and the upper middle esophagus can be selectively preserved during dissection surgery, but no definite clinical data are provided as a basis. On the contrary, clinical data of complete dissection of the gastric coronary vein, whether by interventional or surgical dissection, abound, and the efficacy is quite durable and reliable without serious complications. In order to confirm the clinical significance of preserving this traffic branch in the postoperative period, we selected patients with this traffic branch present in portal venous angiography for interventional treatment (TIPSS), catheter was placed into the splenic vein, and the gastric coronary vein was visualized by conventional contrast and high-pressure syringe with pressure pushing contrast agent, and this traffic branch was not visualized, which fully illustrates that under the physiological conditions of portal hypertension cases, although this traffic branch is theoretically In the physiological conditions of portal hypertension cases, although this traffic branch exists theoretically, it does not play an effective role in shunting the flow of gastric coronary vein and portal vein or lowering the pressure in actual clinical practice. Similarly, the presence of other branches at other sites does not in fact provide an effective shunt or reduce portal vein pressure to prevent postoperative gastrointestinal rebleeding, and CT or nuclear magnetic 3D revascularization of the portal vein can predict both preoperative portal vein collateral circulation and postoperative residual varices and their course []. Our experience is that the main purpose of dissection of the gastric lesser curvature laterally according to the highly selective vagotomy method is to protect the main trunk and branches of the vagus nerve as much as possible, without necessarily preserving the main trunk of the gastric coronary vein. For complete dissection, the vagus nerve and coronary vein should be sacrificed. Theoretically, the effect of esophagogastric fundoplication is more complete, but clinically, although the esophageal varices above the anastomosis disappear, the portal hypertensive gastric disease of the fundus below the anastomosis is aggravated, and the transverse esophageal surgery is traumatic, with many postoperative complications and a greater impact on the patient’s general and liver function. Complications of GI leak and stricture have been reported with this procedure, and the consequences are serious and outweigh the losses if they occur. Our experience is that it is feasible to perform transverse esophagogastric fundoplication in selected cases with good hepatic function, especially for those who are skilled in gastrointestinal anastomosis or anastomosis, but it should not be promoted as a routine procedure. There are reports of routine pyloroplasty after dissection to prevent the occurrence of gastroparesis, but this is not necessary in practice. Our experience is that severing the vagus nerve trunk also does not increase the occurrence of gastric storage. For cases with large gastric volume, edema of the gastric wall and poor gastric motility, repeated encapsulation of the greater curvature of the stomach through the plasma muscle layer can reduce gastric volume, accelerate postoperative gastric motility recovery, prevent postoperative gastric retention and gastric leakage, and have no effect on long-term postoperative gastric feeding, and also reduce postoperative portal hypertensive gastropathy in the short term. While peripancreatic vascular dissection although varices still exist in the middle and upper esophagus, generally these varices do not cause bleeding and most of the portal hypertensive gastropathy is attenuated. Our experience is that as long as the standardized dissection of the peri-esophagogastric fundus vessels, including the high esophageal branches, is achieved, the standard is that the lower esophagus and fundus at the diaphragm are all free from the surrounding vessels, and most of the varices in the lower esophagus and fundus are reduced or disappeared after surgery. Even if the varices still exist, often the pressure is reduced, the red sign is reduced or disappeared, and the chance of bleeding is greatly reduced, and the probability of postoperative rebleeding is 7-13% [], and good long-term results can be obtained with additional endoscopic treatment if necessary. Third, prophylactic dissection surgery cannot be dismissed in its entirety The literature reports that varices exist in about 50% of patients with cirrhosis, and about 8% of those who do not yet have varices develop varices each year, and the annual rate of bleeding from varices is 5%-15%, and the mortality rate within 6 weeks due to bleeding under modern treatment conditions is about 20%, and more than 60% of the subsequent 1-2 years after the first bleeding will re Bleeding []. In fact, patients with severe varices are at a greatly increased risk of spontaneous bleeding. The first bleeding in patients with esophageal varices places a great physical, psychological, and hepatic functional as well as financial burden on the patient, even to the point of being life-threatening. The risk of prophylactic surgery itself is much less than the risk of spontaneous bleeding, and the reliability and durability of prophylactic surgery has been proven in long-term clinical practice to be more reliable and complete than drug therapy and endoscopic treatment. Gastroscopic ligature treatment, which is the most commonly used prophylactic treatment, has the disadvantages of restricted conditions, repeated procedures and high recurrent bleeding rate after treatment. Recurrent gastrointestinal bleeding can lead to ischemia, necrosis, atrophy and functional deterioration of the liver and loss of opportunity for further treatment. Flow disconnection surgery is theoretically positive for protecting liver function by targeting the first ruptured bleeding from a severely varicose vein without shunting the portal blood flow to the liver. Thus, prophylactic dissection has been shown to have a positive and reliable preventive effect on bleeding in some patients. However, more opinion, especially in Western countries, is that patients with portal hypertension in the presence of varices should be treated prophylactically with drugs or endoscopic ligation. Our experience is that in China today, medical conditions are extremely unbalanced, especially in remote areas, and the conditions and techniques for endoscopic ligation to stop bleeding are not available or immature. For patients who have not bled but have moderate to severe varices in the esophagus with red signs (++++ – ++++) and are at greater risk of upper gastrointestinal bleeding, prophylactic surgery should be actively considered, especially for Child B patients, otherwise Once the first bleeding then the liver function deteriorates losing the opportunity for surgery. Patients with cirrhosis C who are too hypersplenic to be treated with interferon antiviral therapy need splenectomy to correct the hypersplenism and should undergo prophylactic dissection of the co-existing varices at the same time. Our experience is that aggressive prophylactic splenectomy for peripancreatic vascular dissection can yield good long-term preventive results. Cases with serious complications such as liver failure or death due to the procedure and cases with a high risk of postoperative rebleeding are not defects of the surgical approach itself, but the result of inappropriate selection of surgical indications, inadequate dissection, or hospital conditions []. IV. Splenectomy is an essential and important part of flow weaning surgery In recent years, there have been many reports in the literature about the immune function of the spleen, and there have also been reports in the literature that the loss of the immune barrier effect of the spleen after splenectomy can lead to the occurrence of fulminant infections, so some scholars have suggested that flow weaning surgery should preserve the spleen and thus the immune function of the spleen. In fact, in our clinical practice, we rarely see outbreaks of infection after splenectomy, but those who preserve the spleen often see high rates of postoperative rebleeding, unresolved hypersplenism, and no improvement in liver function.Imura S [] et al. reported that patients with Child-Pugh class B/C liver function who underwent splenectomy along with hepatectomy or radiofrequency therapy were treated with hepatocellular carcinoma after one month. Morinaga A [] even suggested laparoscopic splenectomy in patients with cirrhosis, where increased protein synthesis and liver volume after splenectomy could be used as a transition before awaiting liver transplantation. K. Ikezawa [] followed up splenectomy for patients with hepatitis C cirrhosis as beneficial and did not affect the efficacy of interferon antiviral therapy, and no other serious complications occurred.Ali Cadili [] summarized The incidence of fulminant infection after splenectomy is about 0.5% per year, and when it occurs, the mortality rate is about 50%. The incidence of bleeding and death from portal hypertension is much higher. Therefore, the greatest threat of splenectomy is not the occurrence of fulminant infections; in fact, fulminant infections after splenectomy occur mostly in pediatric patients and rarely in adults.Mbaga S [] performed a comparative analysis of immunological indices such as CD3, CD4, CD8, CD10, complement C3, complement C4, preparedin, and NK cells in splenic artery ligation, splenectomy, and control groups, and the immunity of the treated group did There was no change in immunity in the treated group. It is evident that the damage of splenectomy on the systemic immune system is not supported by convincing clinical facts. The main purpose of surgery for portal hypertension is to prevent and treat bleeding from ruptured varices in the esophagogastric fundus. If the spleen is preserved, the portal venous pressure cannot be reduced, and even the thoroughness of dissection at the short gastric vessels is affected, which discounts the effectiveness in preventing and treating upper gastrointestinal bleeding, which obviously defeats the original purpose of the surgery. Normal splenic venous blood accounts for about 20% of portal blood flow, which can account for more than 60%-70% in cirrhosis. Splenectomy alone reduces portal vein pressure and blood flow, while dissection surgery will disconnect some of the collateral circulation of the portal vein, which will cause a slight increase in portal vein pressure; the total effect of both is that portal vein pressure remains balanced or decreases slightly, which in turn plays an important role in maintaining portal vein blood flow to the liver. The most obvious complication of splenectomy is postoperative portal venous system thrombosis, but those causing symptoms are extremely rare and include intestinal necrosis. With prolonged follow-up, venous system thrombosis is again reduced or disappears. Careful intraoperative manipulation to reduce tissue damage, ligation of the splenic vein at the confluence of the splenic vein and superior mesenteric vein to eliminate the blind end of the splenic vein after splenectomy, no use of any hemostatic drugs during the perioperative period, early postoperative anticoagulation, and oral hydroxyurea to kill platelets in cases of abnormally high platelets, and other comprehensive treatments can effectively reduce the occurrence and severity of postoperative portal venous system thrombosis []. Once severe portal vein system thrombosis occurs after surgery, timely thrombolysis of the portal vein system via the TIPSS route or percutaneous hepatic puncture to retrieve the thrombus can effectively eliminate or reduce the formed portal vein system thrombus in a timely manner. In the past 14 years, our hospital has completed more than 2300 cases of splenectomy peripancreatic vascular dissection, and there was no case of serious thrombosis leading to intestinal necrosis during the perioperative period. Only one case of serious thrombosis with increased abdominal distension and ascites was successfully thrombolysed and embolized, and one case of portal vein thrombolysis and embolization was actively performed to avoid future liver transplantation. The quality of patient survival was obviously much better compared to patients who did not undergo dissection of the spleen. In conclusion: our experience is that splenectomy with peripancreatic vascular dissection for upper gastrointestinal bleeding due to portal hypertension is simple, effective, reliable, and has been tested in long-term clinical practice with few serious complications, and is a recommended procedure to be promoted. When upper gastrointestinal bleeding from portal hypertension is combined with giant spleen or severe hypersplenism, “spleen excision first, spleen preservation second”. The traumatic spleen should be preserved as much as possible, but the principle is “preservation of life first, preservation of spleen second”. V. Minimally invasive laparoscopic treatment is worth advocating If you have a hospital and a skilled laparoscopist, you can use laparoscopy or hand-assisted laparoscopy to achieve the same effect as open surgery, while the risk can be reduced to the same risk as open surgery, or even lower risk than open surgery, because laparoscopic surgery is more careful to stop bleeding and operation. Based on the proficiency of open surgery, our department has actively carried out laparoscopic resection of peripancreatic vessels around the cardia in more than 100 cases, only one case was converted to open surgery, and none of the 100 cases of laparoscopic spleen surgery had serious complications. However, it should be reminded that doctors who are not skilled in open surgery should not rashly perform laparoscopic splenectomy, especially for huge spleens in portal hypertension, because patients with portal hypertension have abundant vessels in the abdominal cavity with collateral circulation and are prone to bleeding during and after surgery, or even hemorrhage that is too late to be rescued. The only way to avoid this is good perioperative management, careful intraoperative manipulation to stop bleeding, and practice makes perfect.