The establishment and opening of portal collateral circulation is a unique manifestation of portal hypertension, which is not only an important basis for the diagnosis of portal hypertension, but also has important clinical significance. Portal hypertension is a group of syndromes caused by a persistent increase in portal venous pressure. It is caused by cirrhosis in the majority of patients, but in a minority of patients it is secondary to obstruction of the main portal vein or hepatic veins and some unexplained factors. Increased portal pressure is caused when portal blood does not flow smoothly back through the liver into the inferior vena cava. This is manifested by the opening of the portal-body venous communication branch, and a large amount of portal blood enters the body circulation directly through the communication branch before entering the liver, resulting in dilatation of the abdominal wall and esophageal veins; splenomegaly and hypersplenism; hepatic dysfunction and ascites. Portal venous gas (PVG) is an imaging sign of abnormal accumulation of gas in the portal vein and its intrahepatic branches due to various causes and is usually diagnosed by abdominal radiographs. It is commonly seen in neonates with necrotizing small bowel colitis. Neonatal necrotizing small bowel colitis is a serious disease with abdominal distention, vomiting and blood in the stool as the main clinical manifestations and cystic gas accumulation in the intestinal wall as the radiographic features. Portal vein thrombosis (PVT) is the main cause of extrahepatic portal hypertension. Portal vein thrombotic obstruction is usually secondary to chronic liver disease and tumor disorders. Simple extrahepatic portal vein obstruction is more common in adolescents and children. The most prominent and common symptom is bleeding from varices in the esophagogastric fundus. Acute onset is associated with abdominal pain, vomiting, and distention, but rarely results in liver infarction.