The incidence of thrombosis in the splenic vein and portal vein system has been widely reported, but the results are inconsistent, with the incidence of thrombosis ranging from 13.4% to 35.5%. We found that the incidence of portal vein system thrombosis after splenectomy and flow dissection was as high as 91.06% by magnetic resonance examination after surgery, which was much higher than other reports, and all patients with thrombosis had splenic vein thrombosis, and portal vein trunk thrombosis accounted for 25.89% of them. The causes of portal vein system thrombosis after surgery for portal hypertension are complex and mostly thought to be related to hemodynamic changes in the portal vein system, coagulation status, local vascular pathology of the portal vein system, mechanical damage to local vessels during surgery, formation of blind ends of vessels during surgical ligation, unreasonable use of coagulants and inflammation in the local area. In the past, it was thought that the hypercoagulable state of blood after splenectomy was associated with thrombosis. In fact, the increase in blood fraction and coagulation changes after splenectomy mostly do not exceed normal levels, so we do not consider this to be a major factor in thrombosis formation. After splenectomy, the splenic vein is a blind end, with slow and turbulent blood flow. Intraoperative clamping and compression cause damage to the intima of the splenic vein, exposing collagen fibers and activating the coagulation system to form splenic vein thrombosis, which can spread to the main trunk of the portal vein. Therefore, hemodynamic changes after splenectomy, i.e., slow and turbulent flow, play the most important role in portal vein system thrombosis. In contrast, after splenorenal bypass, blood flow in the splenic vein is faster and less prone to thrombosis, whereas in the presence of anastomotic embolism, the splenic vein is more prone to thrombosis. Another evidence of hemodynamic changes leading to thrombosis is the presence of thrombus in the portal vein in a subset of patients after splenorenal shunt plus dissection. This is because when the splenorenal shunt is open, the blood in the superior mesenteric vein flows into the circulation via the splenic vein, while the upward flow into the liver via the portal vein is significantly reduced. However, the patient’s coagulation status and platelet count, especially the latter, should be closely monitored postoperatively. Platelets rise rapidly in the majority of patients after splenectomy, peaking at about 2 weeks and decreasing gradually thereafter. If the platelet count is greater than 800 × 109/L, anticoagulant therapy, including oral pentoxifylline and aspirin, intravenous low molecular dextran, salvia and subcutaneous small molecule heparin, should be administered to prevent further thrombosis or thrombus enlargement. Splenic vein and portal vein thrombosis is often accompanied by the formation of collateral circulation during the formation process, which causes intestinal necrosis unless acute thrombosis occurs, which is rare.