In 1869, Balfour et al. first described portal spongiform degeneration, but the lesions occurred outside the portal vein, which itself was already obstructed, causing increased portal pressure, splenomegaly and opening and dilatation of the collateral veins between the portal vein and the vena cava, as well as the gradual formation of multiple collateral veins around the occluded portal vein, which had a spongy appearance. DeGaetano et al. defined the process of localized collateral circulation formation after portal vein thrombosis as portal vein spongiform degeneration, and it is inappropriate to describe it as a diagnosis. The etiology of this disease may be related to the following factors: congenital malformations, which may occur in combination with other congenital malformations such as cardiovascular, renal, gastrointestinal and ovarian; umbilical infection in the newborn causing umbilical phlebitis, which involves the portal system and leads to portal vein occlusion and formation of portal vein angiomas in the peripheral collateral veins of the portal vein. Portal vein cavernous degeneration is divided into primary and secondary, the latter occurs after acute obstruction of the portal vein, while the former is due to congenital abnormal development of the main trunk of the portal vein and its branches. The lesions of this disease are located in the extrahepatic portal vein, so the liver functions well and the internal treatment is not effective, so it mainly relies on surgical treatment. And the aim of surgical treatment is to reconstruct the blood outflow tract of the portal vein and to resolve hypersplenism and gastrointestinal bleeding. The current treatment methods mainly include sclerotherapy, flow disconnection and bypass surgery. In the case of portal vein obstruction, the high pressure visceral venous blood flows to the low pressure hepatic sinus through a large number of collateral veins, which can lead to thrombosis of multiple visceral veins, so this method is rarely used clinically now. Flow dissection is to act directly on the bleeding site, such as splenectomy, portal vein dissection, submucosal circumferential suturing around the esophageal cardia, etc. This type of surgery is less invasive and can be performed at the site of bleeding. This type of surgery is less invasive, and before the formation of collateral circulation outside the esophagus, portal vein dissection is better to control bleeding. The disadvantages are: the rebleeding rate can be as high as 85% and 90% for splenectomy alone; fatal post-splenectomy sepsis; postoperative recurrent bleeding; and postoperative “communication” again. The incidence of rebleeding and the 5-year survival rate of bypass surgery are 12.5% and 100%, so it is rarely used as the procedure of choice. Warren et al. used distal splenorenal vein anastomosis for prehepatic portal hypertension to reduce visceral venous pressure without destroying the hepatic collateral veins, and the incidence of rebleeding and hepatic encephalopathy was low. However, the reobstruction rate of the anastomosis of splenorenal shunt is high, so the probability of rebleeding after surgery increases. In contrast, portal bypass surgery not only has a high flow rate and a significant decrease in portal pressure, but also is less likely to be reobstructed, so portal bypass is now increasingly accepted. Among them, intestinal lumen bypass should be preferred. We use intestinal cavity end-lateral anastomosis technology, so that the portal pressure decreased by more than 50%, effectively reducing the portal pressure, while the end-lateral anastomosis both appropriate anastomosis, but also to avoid tension anastomosis, so that the anastomosis is not easy to block, not to mention the portal system is originally inaccessible, and the patient’s good liver function and effective liver detoxification, to avoid hepatic encephalopathy. Then combined with the flow dissection surgery, more effectively prevented postoperative bleeding. In our opinion, effective intestinal shunt combined with flow dissection is a good choice for patients with extensive thrombosis of the portal vein system after sclerotherapy, who cannot undergo conventional shunts, and for those who fail Warren’s procedure; it is questionable to define the process of localized collateral circulation formation after portal vein thrombosis as portal vein spongiform degeneration or to describe it as a diagnosis.