Regional portal hypertension after severe pancreatitis is not uncommon in clinical practice, and in our country, the number of such patients is even less. Unfortunately, this clinical condition has not received enough attention so far. So, 2 years after recovery from severe pancreatitis, why does it still cause upper gastrointestinal hemorrhage? The mechanism is like this: In severe pancreatitis, the pancreas undergoes heavy bleeding and necrosis, and a large amount of pancreatic enzymes and other strong corrosive fluids leak out and accumulate around the pancreas, causing serious damage to the tissues around the pancreas. We know that the splenic vein travels along the upper edge of the dorsal surface of the pancreas, and pancreatitis is eroded by pancreatic enzymes in the pancreatic juice, and pathological changes such as phlebitis can occur. Although severe pancreatitis is cured, the inflammatory changes in the splenic vein will persist and easily cause thrombosis and venous occlusion. Although the splenic artery is accompanied by the splenic vein, it is not prone to arteritis due to the thicker arterial wall and fast blood flow, and it is even rarer to cause embolism or even occlusion. When the splenic vein is narrowed or even occluded, the blood entering the spleen from the splenic artery has no clear outlet, and the pressure of the blood vessels in the spleen will rise significantly, causing congestive enlargement of the spleen, and furthermore, the blood that has no outlet must find a way out, and the blood vessels between the spleen and the stomach become the inevitable choice. Under normal circumstances, the blood vessels between the spleen and the stomach are very thin and only a small amount of blood passes through them. When the reflux of the splenic vein becomes obstructed, the blood in the spleen will inevitably flow back into the liver around these potential vascular channels, thus causing the blood vessels around the stomach to thicken significantly and the pressure to rise significantly, leading to varicose veins in the submucosa of the stomach and causing rupture and bleeding in severe cases. The portal hypertension that occurs after severe pancreatitis is significantly different from the portal hypertension that we commonly see due to cirrhosis of the liver. The first is the difference in etiology, the former is due to pancreatitis complicated by splenic vein embolism or occlusion, while the latter is due to cirrhosis caused by liver lesions. The second point is that the characteristics of the disease are very different, post-pancreatitis portal hypertension often does not have underlying liver lesions, the blood return to the liver and gastrointestinal tract is normal, varicose veins are mainly gastric fundic varices, esophageal varices are often not obvious; while post-cirrhosis portal hypertension due to the obstruction of blood return to the liver, the blood from the spleen and gastrointestinal needs to “bypass “The esophageal varices are often more serious. The third point is that the danger is different. After pancreatitis portal hypertension patients’ disease is hidden, the development of the disease is often ignored, only when the varices are serious, rupture, only to be treated, only to mend the sheep; while after cirrhosis portal hypertension has obvious abnormalities of liver function, the patient is the hospital “regular”, esophageal varices can often be detected at an early stage. Prevent the problem before it happens. In conclusion, patients with severe pancreatitis should also be examined regularly after recovery for early diagnosis and treatment of possible complications of regional portal hypertension.