Portal hypertension causes increased pressure in the portal system when the blood flow in the portal vein is blocked and blood is stagnant. Clinical manifestations include splenomegaly and hypersplenism, esophagogastric varices and vomiting of blood and ascites. The disease with these symptoms is called portal hypertension. The normal pressure of portal vein is 1.27-2. 35 kPa (13-24 cmH20), and the average value of Chu Yankui of PLA 302 Hospital General Surgery Clinic is 1. 76 kPa (18 crrlH20), which is o.49-0. 88 kPa (5-9 cmH20) higher than the hepatic vein pressure. In portal hypertension, the pressure mostly increases to 2. 9-4.9 kPa (30-50 cmH20). When the hepatic venous pressure gradient (HVPG) does not exceed 1.6 kPa (16 crriH20), the varices of the esophagogastric fundus rarely rupture and bleed. After the development of portal hypertension, the following pathological changes can occur: 1. splenomegaly and hypersplenism Congestive splenomegaly occurs first after the obstruction of portal venous blood flow. In portal hypertension, splenic sinus dilation, fibrous tissue proliferation in the spleen, proliferation of monocytes and phagocytosis of red blood cells are seen. In addition to splenomegaly, there is also a clinical decrease in peripheral blood cells, most commonly leukocytes and platelets, which is called hypersplenism. 2.Dilated traffic branches Due to the obstruction of the normal intrahepatic portal vein access and the absence of venous valves in the portal vein, the four traffic branches open in large numbers and dilate and twist to form varicose veins. Among the dilated traffic branches, the most clinically significant one is the varices formed in the lower esophagus and gastric fundus. It is the closest to the main portal vein and the vena cava, and has the largest pressure difference, so it is also the earliest and most significantly affected by portal hypertension. Patients with cirrhosis often have gastric acid reflux, which corrodes the mucosa of the lower esophagus and causes reflux esophagitis, or the mechanical injury of hard and rough food, as well as the sudden increase of intra-abdominal pressure due to coughing, vomiting, forceful defecation, heavy load, etc., which can cause the rupture of variceal vein and lead to fatal hemorrhage. 3, ascites portal vein pressure rises, so that the filtration pressure of the capillary bed of the portal system increases, while the hypoproteinemia caused by cirrhosis, plasma colloid osmotic pressure decreases and lymphatic fluid production increases, prompting fluid to leak from the liver surface and intestinal plasma membrane surface into the abdominal cavity and form ascites. Clinical manifestations and diagnosis: mainly splenomegaly, hypersplenism, vomiting blood or black stool, ascites or non-specific systemic symptoms (such as fatigue, drowsiness, anorexia). Once the varices of the esophageal and fundic veins rupture, acute hemorrhage occurs immediately, with vomiting of bright red blood. The bleeding does not stop easily due to coagulation disorders caused by liver impairment and thrombocytopenia caused by hypersplenism. Due to severe hypoxia of liver tissue caused by hemorrhage, it can easily lead to hepatic coma. If the spleen can be palpated on physical examination, it may indicate portal hypertension. Signs such as jaundice, ascites, and varices in the anterior abdominal wall indicate severe portal hypertension. The diagnosis of cirrhosis can be established if a hard textured liver with blunt and irregular edges can be palpated, but sometimes cirrhosis shrinks and is difficult to palpate. Other signs of chronic liver disease such as spider nevus, liver palm, gynecomastia, testicular atrophy, etc. may also be present.