Surgical treatment of portal hypertension

  Etiology of portal hypertension in cirrhosis
  In normal people, the portal vein pressure is 13-24cmH2O. A pathological state in which the portal venous system is obstructed by blood flow, stagnant blood flow and increased pressure due to various reasons, becomes portal hypertension. In portal hypertension, the portal venous pressure is usually 25-40 cmH2O, or even above 50 cmH2O. Since 85-95% of portal hypertension is caused by cirrhosis due to various causes, it mostly becomes cirrhotic portal hypertension.
  The main causes of portal hypertension are as follows.
  Intrahepatic type: due to various causes of hepatocellular damage, fibrous connective tissue proliferation and hepatocyte regeneration, liver pseudobullet formation, increased intrahepatic pressure, portal vein to liver blood flow obstruction and cause portal hypertension, which is usually called cirrhotic portal hypertension, characterized by the presence of severe lesions in the liver itself. The main clinical cause is hepatic steatosis due to viral hepatitis, with hepatitis B being the most common, followed by hepatitis C. There are also hepatitis caused by a mixture of hepatitis B and C viruses.
  Alcoholic hepatic steatosis is a secondary cause of portal hypertension, in addition, biliary hepatic steatosis and dystrophic hepatic steatosis are also causes of portal hypertension.
  Prehepatic type: spongy degeneration of portal vein caused by various reasons, such as abnormal development of portal vein and thrombosis, can lead to obstruction of portal blood return and result in portal hypertension. In addition, left-sided portal hypertension caused by compression of the splenic vein, a branch of the portal vein, also belongs to this type.
  Post-hepatic type: i.e. Bu-ga syndrome.
  Major comorbidities of portal hypertension in cirrhosis
  The two main syndromes of cirrhosis are hepatic decompensation and portal hypertension. The former manifests as loss of appetite, nausea and abdominal distension, jaundice, and wasting, while the latter mainly includes ruptured esophagogastric fundic varices and bleeding, splenomegaly and hypersplenism, ascites, portal hypertensive gastropathy (portal hypertensive gastrointestinal disease), and some patients may have thrombosis of the portal venous system, and portal hypertension syndrome, which is the main indication for surgical treatment.
  Goals to be achieved by surgery for portal hypertension.
  At present, except for liver transplantation, which can fundamentally solve cirrhosis itself, all surgical methods can only alleviate the development of portal hypertension, and therefore belong to the “symptoms” of surgery. Although there are many different surgical methods, the following 3 aspects should be considered at the same time.
  1, disconnect the peripheral blood vessels in the lower esophagus and gastric fundus bleeding risk area, block the abnormal blood flow between the portal oddities, and directly stop the variceal vein from rupture and bleeding, i.e. “plugging”;
  2.Establish artificial channel to expand the downstream inter-portal shunt in the “gastro-splenic area”, and divert the stagnant high-pressure blood flow in the portal system, so as to effectively relieve the hyperdynamic circulation in the portal vein and prevent the formation of new side branches in the esophagogastric fundus and improve the portal hypertensive gastric disease, thus eliminating the risk factors triggering upper gastrointestinal bleeding, i.e. “sparing”;
  3, maintain a certain portal vein pressure and blood flow, in order to maintain effective hepatic perfusion from the portal vein to the liver, i.e. “irrigation”. In other words, the surgery itself needs to consider dealing with the “four major” syndromes of portal hypertension as well as maintaining the blood supply to the liver to prevent the occurrence of hepatic decompensation or even failure.
  Application, advantages and disadvantages of flow dissection
  Portal vein dissection is the surgical interruption of the abnormal blood flow between the portal veins to prevent and stop the hemorrhage caused by rupture of the varices of the esophagogastric fundus due to portal hypertension. The rationality of flow dissection is to control bleeding while maintaining portal venous blood flow to the liver perfusion, thus facilitating the regeneration of hepatocytes and the improvement of their function, and can be used in patients with poor liver function and in the acute bleeding phase.
  This procedure directly relieves the hypertension in the gastrosplenic region, thus providing definitive and reliable hemostasis. There are more types of flow dissection, such as early coronary vein ligation and dissection of the stomach, transthoracic esophageal variceal ligation, and transabdominal fundic variceal ligation. Later on, such as lower esophageal transection, fundoplication, lower esophageal fundoplication, anastomotic esophageal cut-off anastomosis, transthoracic combined abdominal dissection.
  Several large hospitals in China reported that the overall hemostasis rate was over 95%, the postoperative rebleeding rate was between 3.8% and 21.09%, and the incidence of encephalopathy was between 2.5% and 5.68%.
  The advantages of flow dissection are mainly in.
  ①Maintain a certain portal vein pressure and increase the amount of blood perfusion to the hepatic portal vein, which plays an important role in maintaining the tissue structure and physiological function of the liver.
  ②The dissection directly targets the collateral vessels of the lower esophagus and cardia region of the fundus that cause variceal rupture and bleeding, and the hemostatic effect is precise, and the operation is simple and easy to carry out in primary hospitals.
  ③It is effective in controlling hypersplenism and is suitable for patients with embolism in the portal venous system who are not suitable for bypass.
  However, flow dissection also has defects.
  ①It can cause or aggravate portal hypertensive gastropathy;
  (ii) The collateral vessels are prone to regenerate after surgery, resulting in a high rate of postoperative rebleeding;
  (3) It can cause splenic-portal vein thrombosis, which adds extrahepatic obstruction to intrahepatic obstruction and increases portal vein pressure, making it difficult for ascites to subside after surgery. It has been reported that the incidence of thrombosis in the splenic vein after dissection is more than 90% due to the presence of blind end, and some of them spread to the main trunk of portal vein;
  ④The peripancreatic vascular dissection may form adhesions in the hilar region and the left lobe of the liver, and may also combine with portal vein system thrombosis, which is not conducive to liver transplantation;
  ⑤ And there is a risk of postoperative complications such as intra-abdominal hemorrhage, gastrointestinal fistula and subdiaphragmatic infection. Therefore, in addition to better maintenance of blood in the liver and removal of the spleen to correct hypersplenism, flow dissection has limitations in the management of portal hypertensive gastrointestinal disease, ascites, and bleeding from ruptured varicose veins, while the spread of splenic vein thrombosis may lead to thrombosis of the main trunk and major branches of the portal vein.
  Application, advantages and disadvantages of bypass surgery
  The basic principle of portal shunt surgery is to shunt blood from the portal vein to the vena cava in order to reduce portal vein pressure and ultimately to stop bleeding from ruptured esophagogastric fundic varices. There are three types of shunts: full portal bypass (unrestricted portal bypass), partial portal bypass (restricted portal bypass) and selective bypass.
  At present, full portosystemic shunts have been largely abandoned due to the substantial reduction of postoperative liver blood supply, which aggravates liver dysfunction and hepatic encephalopathy and seriously affects the quality of life of patients after surgery. Although selective portal shunts, including distal splenorenal or splenic cavity shunts and coronal shunts, have been reported to have better clinical results abroad, they are not widely promoted in China because of the difficulty of the operation itself and the fact that hypersplenism cannot be corrected without removing the spleen, which is not suitable for the reality of post-hepatitis cirrhosis in China, where patients with moderate to severe hypersplenism require removal of the spleen to correct hypersplenism.
  Partial portal shunt is based on lateral portosystemic shunt, and by restricting the anastomotic caliber, it can effectively reduce the portal vein pressure while maintaining a certain amount of portal to hepatic blood flow and a certain amount of mesenteric vein pressure in order to achieve rapid, effective and lasting control of bleeding while minimizing the damage to hepatocyte function and reducing the occurrence of postoperative hepatic encephalopathy.
  Surgical modalities include restrictive portal lateral bypass, intestinal luminal lateral bypass, proximal splenorenal bypass, proximal splenic luminal bypass, and transjugular intrahepatic portosystemic bypass (TIPS). Domestic shunts are less commonly used in China, and the procedures include portal, intestinal and splenorenal shunts.
  The first thing to do is to determine a reasonable bypass caliber. It has been found that when the diameter of the bypass anastomosis >12 mm is a full portal bypass, only 3% of patients maintain portal to hepatic flow; when the diameter of the anastomosis is equal to 10 mm, about 50% of patients maintain hepatic flow, and when the diameter of the anastomosis is 8 mm, 80% of patients maintain hepatic flow, and the corresponding incidence of hepatic encephalopathy is 39%, 19% and 9%, respectively.
  The above study provides a good reference for choosing the appropriate anastomosis for bypass surgery. Restricting the anastomosis can control the size of the bypass flow and affect the blood flow to the liver, while a reasonable anastomosis has a significant impact on the regeneration of hepatocytes and maintenance of liver function as well as reducing the incidence of hepatic encephalopathy.
  Secondly, to prevent the spontaneous enlargement of the anastomosis and the loss of restrictive shunt, as the latter is the main cause of postoperative complications of hepatic encephalopathy, a restrictive portal vein lateral bypass with additional restrictive ring has been proposed, and good results have been reported.
  In conclusion, bypass is the main surgical procedure for the treatment of portal hypertension in Western countries and India, with an overall bleeding control rate between 85% and 100%, and improves gastric mucosal circulation, reduces edema, improves mucosal barrier function, and consequently reduces the rate of bleeding due to portal hypertensive gastropathy. However, the disadvantages of bypass surgery are also obvious.
  1, postoperative portal vein to liver blood flow is reduced, or even the formation of off-hepatic blood flow, resulting in postoperative liver nutrient dysfunction, aggravate liver function decompensation, increase the incidence of hepatic encephalopathy, surgery such as portal lateral bypass and intestinal lumen bypass;
  2, high technical requirements of vascular anastomosis, often need to place artificial blood vessels, so the anastomosis thrombosis rate is high, resulting in the failure of the bypass, such as splenic and renal bypass;
  3.Selective bypass surgery is only applicable to cases with spleen volume below medium size because it cannot correct hypersplenism, which is not compatible with the reality that most of the patients with cirrhotic portal hypertension who need surgery are combined with severe hypersplenism in China, and the operation is difficult, so it is difficult to carry out widely in China. Therefore, bypass surgery has significant advantages over dissection in the management of portal hypertensive gastrointestinal disease, ascites, and ruptured variceal bleeding, but at the same time, the incidence of hepatic encephalopathy is significantly higher due to the impact on the portal blood flow to the liver.