Patients with portal hypertension do not always have hemorrhage; bleeding from ruptured esophagogastric fundic varices is the most serious and difficult complication of portal hypertension to manage. Esophagogastric fundic varices are present in approximately 40-60% of patients with cirrhosis. Studies have found that ruptured variceal bleeding may occur in only 50-60% of patients. This means that ruptured variceal bleeding occurs in approximately 30% of patients with cirrhosis who have no previous history of bleeding. However, once a variceal vein ruptures and bleeds, the patient’s morbidity and mortality rate is very high and can reach 30-50%. Clearly, it is important to predict the risk of bleeding in patients with portal hypertension. Risk factors for bleeding include: 1. Liver function: When liver function deteriorates in patients with cirrhotic portal hypertension, the risk of bleeding is greatly increased, and the Child-Pugh classification is often used to evaluate the status of liver function; the higher the score the worse the liver function, and the more likely it is to have issued blood. 2, Size, color and tone of varices: Under gastroscopy, severe varices are red worm-like and may have red spots on them, which is more dangerous than white or light red mild varices, and the risk of bleeding is greater. The level of variceal tension is also considered to be a key factor in venous rupture and bleeding. 3. Patient hepatic venous pressure gradient: The patient’s hepatic venous pressure gradient (HVPG) is an independent risk factor for variceal bleeding and is recognized by physicians worldwide as the gold standard for determining bleeding risk. When the hepatic venous pressure gradient is greater than 16 mm Hg, the patient is at high risk of bleeding. If the hepatic venous pressure gradient is less than 12 mm Hg, ruptured variceal bleeding is rare, and even patients do not experience major bleeding throughout their lives.