Cirrhosis from all causes is the main cause of portal hypertension formation, accounting for approximately 85% of cases. Almost all patients with cirrhosis inevitably develop portal hypertension as a complication. The natural course of cirrhosis is broadly divided into two phases: the asymptomatic phase, also known as the compensated phase, and the subsequent progression to the decompensated phase, which is characterized by the complications of portal hypertension and/or liver malfunction. Combining two previous large-scale studies on the natural history of cirrhosis (a total of 1649 patients were included), cirrhosis can be further divided into four stages, each with significantly different clinical characteristics and prognosis (see Table 14-3-1), with stages 1 and 2 falling within the compensated stage and stages 3 and 4 within the decompensated stage [1,2]. Stage 1: neither esophageal varices nor ascites This stage has a mortality rate of less than 1% per year, with a cumulative annual incidence of 11.4% for further progression beyond this stage Stage 2: presence of esophageal varices but no ascites or bleeding 3.4% per year, with 6.6% per year progression to ascites from this stage and 4.4% per year bleeding from varices at or before ascites formation Stage 3: ascites with or without esophageal varices but never bleeding Veins, but never bleeding 20% per year, significantly higher than the first two stages, 7.6% per year progressing from this stage to bleeding Stage 4: Gastrointestinal bleeding with or without ascites 57% mortality within 1 year (about half of these deaths occur within 6 weeks of the first bleeding) In patients with compensated cirrhosis, portal vein pressure may be normal or below the threshold level for the formation of varices or ascites ( threshold). As the disease progresses, portal pressure increases further and liver function decreases further, leading to ascites, portal hypertensive gastrointestinal bleeding, hepatic encephalopathy, and jaundice. Thus, portal hypertension plays a crucial role in the development of cirrhosis, and portal hypertension and its related complications are the main cause of death in patients with cirrhosis and an indication for liver transplantation in patients with end-stage cirrhosis. For the vast majority of patients with cirrhosis, varices eventually develop, with the incidence of esophageal varices being relatively highest and reported to be present in approximately 40% of patients with initially diagnosed cirrhosis in the compensated phase and up to 60% of patients with ascites [1,3]. At subsequent follow-up, varices newly appear in approximately 5% of patients each year [1]. Once formed, varicose veins change from small to large, with an overall incidence of 10-15% and a general incidence of 12% (95% CI: 5.6-18.4%) progression to large varicose veins within 1 year, 25% (16.0-34.0%) within 2 years, and 31% (21.1-40.8%) within 3 years [4]. Progression of liver failure is an important factor in promoting or accelerating variceal changes. Conversely, improvement in liver function and abstinence from alcohol can cause varicose veins to change from large to small or even disappear [5]. Once formed, varicose veins change from small to large, and large varicose veins eventually rupture and bleed, which occurs in 8-35% of untreated patients within 2 years. It is exceptionally important to find risk indicators to predict variceal bleeding, and the most important predictors that have been identified are: the size of the variceal vein, the red sign of the variceal vein, and the degree of hepatic impairment (using Child-Pugh classification). These indicators are usually evaluated in combination, however, they are not yet satisfactory. According to a recent study, varicose vein size is the best predictor of variceal rupture bleeding, with the incidence of rupture bleeding in patients with small varicose veins (<5 mm< span="">) being approximately 7% over 2 years, increasing to 30% in patients with large varicose veins [1]. Variceal size and redness sign as predictors of variceal rupture may be because of the association with enhanced variceal wall tension. In addition, hepatic venous pressure gradient (HVPG), which reflects the transmural pressure of varicose veins, may also be used as a risk factor to predict variceal rupture. When HVPG is <12 mmhg< span="">, bleeding from ruptured varices is almost never observed. It has been previously reported that approximately 30-50% of patients with cirrhosis combined with acute variceal rupture bleeding die within 6 weeks, a figure that may overestimate the actual mortality of variceal bleeding at this time. A more accurate mortality rate within the first 6 weeks is 20%, with an early mortality rate of 5-8% due to uncontrolled bleeding [1]. The presence of endoscopically visualized acute bleeding, bacterial infection and HVPG >20 mmHg on admission predicts that bleeding will be difficult to control. It is important to emphasize that 40-50% of patients with variceal bleeding can stop bleeding on their own. The possible reason for this is that the hypovolemic state after bleeding leads to reflex contraction of the splenic veins, which results in a decrease in portal venous blood flow associated with a decrease in pressure. The incidence of short-term rebleeding (defined as rebleeding within 6 weeks from the time of bleeding) after the first bleeding is 30-40%. The risk of rebleeding is highest in the first 5 days after the first bleeding with an incidence of 40%, especially in the first 48h to 72h, with a gradual decrease in the incidence of rebleeding in the following 6 weeks. According to the literature, risk factors associated with rebleeding in the short term include fundic variceal bleeding, active bleeding visualized by emergency endoscopy, low plasma albumin, renal failure, and HVPG >20 mm Hg. Short-term rebleeding and renal failure are the most critical predictors of mortality in patients within 6 weeks; therefore, during the treatment of acute variceal rupture bleeding, short-term rebleeding and the possibility of renal failure. In those who survive the initial bleeding, the rate of late rebleeding (meaning after the 6th week from the onset of bleeding) and mortality remain relatively high, with the incidence of late rebleeding ranging from 32 to 84%, with a mean of 59%. Long-term mortality rates ranged from 4 to 78% (mean 46%). It is because of this high risk that measures must be taken to prevent rebleeding from occurring. Risk factors predicting rebleeding and death include: variceal vein size, Child-Pugh classification, continued alcohol consumption, and hepatocellular liver cancer .