I. Etiology of portal hypertension in liver cirrhosis
In normal people, the portal vein pressure is 13-24cmH2O, but due to various reasons, the portal venous system is obstructed, the blood flow is stagnant and the pressure is increased in a pathological state, which 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 reasons, it mostly becomes cirrhotic portal hypertension.
1, intrahepatic type: due to various causes of hepatocyte damage, fibrous connective tissue proliferation and hepatocyte regeneration, liver pseudobullet formation, intrahepatic pressure increases, portal vein to liver blood flow is blocked and causes 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 the secondary cause of portal hypertension, in addition, biliary hepatic steatosis and malnutrition hepatic steatosis are also the causes of portal hypertension.
2, prehepatic type: spongy degeneration of portal vein caused by various reasons, such as abnormal development of portal vein, thrombosis, etc., can lead to obstruction of portal blood return, resulting in portal hypertension. In addition, the left-sided portal hypertension caused by the compression of splenic vein, which is a branch of portal vein, also belongs to this type.
3.Post-hepatic type: that is, Bu-plus syndrome.
Second, the main comorbidities of portal hypertension in cirrhosis
The two main syndromes of cirrhosis are hepatic hypofunction and portal hypertension. The former manifests as loss of appetite, nausea and abdominal distension, jaundice and emaciation, etc. The latter mainly includes rupture and bleeding of esophagogastric fundic varices, 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.
Third, the 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 surgery of “symptoms”. Although there are various surgical methods, the following 3 aspects should be considered at the same time.
1, disconnecting the peripheral blood vessels in the lower esophagus and gastric fundus bleeding risk area, blocking the abnormal blood flow between the portal oddities, and directly stopping the variceal vein from rupture and bleeding, i.e. “blocking”.
2.Establish artificial channel to expand the downward inter-portal shunt in the “gastro-splenic area”, and divert the stagnant high-pressure blood flow in the portal system, so as to effectively alleviate the hyperdynamic circulation in the portal vein and prevent the formation of new side branches in the esophagogastric fundus and improve the portal hypertensive gastropathy, thus eliminating the risk factors triggering upper gastrointestinal bleeding, i.e. “sparing”.
3, maintain a certain portal vein pressure and blood flow 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
1. Advantages
①Maintain a certain portal vein pressure and increase the amount of 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 in the lower esophagus and cardia area of the fundus that cause variceal rupture and bleeding, and the hemostatic effect is exact, and the operation is simple and easy to carry out in primary hospitals.
③Effective control of hypersplenism, suitable for patients with embolism in the portal venous system and unsuitable for bypass surgery.
2.Defects.
①Can cause or aggravate portal hypertensive gastropathy.
(ii) The lateral branch vessels are prone to regeneration after surgery leading to a high rate of postoperative rebleeding.
③It can cause splenic-portal vein thrombosis, which adds extrahepatic obstruction to intrahepatic obstruction, making the portal vein pressure even higher and ascites not easy to subside after surgery. (ii) It has been reported that the incidence of thrombosis in the splenic vein after dissection is over 90% due to the presence of blind end, and part of it spreads to the main trunk of portal vein.
(iv) Peripancreatic vascular dissection can 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, dissection has limitations in the management of portal hypertensive gastrointestinal disease, ascites, and bleeding from ruptured varices, while the spread of splenic vein thrombosis may lead to thrombosis of the main trunk and major branches of the portal vein.