Lower limb deep vein thrombosis is a common peripheral vascular disease, if patients do not receive timely and effective treatment, it will lead to lower limb bruising, pigmentation, and in serious cases, it may cause femoral bruising, limb ischemic necrosis, and patients may lose part or all of their labor force. Some patients may develop thrombosis with the development of the disease, causing pulmonary embolism, which is life-threatening in severe cases. In the mid-nineteenth century, Virchow proposed three major factors for the formation of deep vein thrombosis: venous blood flow retardation, venous wall damage and blood hypercoagulation, which are still recognized by scholars in various countries. (a) Stagnant venous flow During surgery, spinal anesthesia or general anesthesia leads to dilatation of peripheral veins and slows down venous flow; during surgery, the lower limbs are completely paralyzed due to anesthesia and lose contractile function, and after surgery, the muscles of the lower limbs are in a relaxed state due to incision pain and other reasons, which leads to stagnant blood flow and induces deep vein thrombosis in the lower limbs. According to Borow, the duration of surgery is related to the occurrence of deep vein thrombosis, 20% of the duration of surgery from 1 to 2 hours, 46.7% from 2 to 3 hours, and 62.5% from 3 hours or more (the incidence rate reported abroad is much higher than that in China), and it was found that 50% occurred on the first postoperative day and 30% on the second postoperative day. Sevitt has clinically demonstrated that thrombosis often originates from venous pockets, venous continuities, and venous sinuses such as those in the flounder muscle. The blood flow in the sinus of the flounder muscle relies on muscle contraction to return to the heart, making it an easy site for thrombosis. Thrombosis can also occur without valves, but is prone to thrombosis, probably due to compression by the anterior right common iliac artery. About 24% of the external iliac veins are valved, and there is a considerable incidence of thrombosis in the proximal part of this valve. (B) Damage to the venous wall 1, chemical injury Intravenous injection of various irritating and hypertonic solutions, such as various antibiotics, organic iodine solution, hypertonic glucose solution, etc. can stimulate the venous lining to varying degrees, leading to phlebitis and venous thrombosis. 2.Mechanical injury Local contusion, laceration or fracture fragment trauma of veins can produce venous thrombosis. Fracture of the femoral neck can damage the common femoral vein, and fracture of the pelvis can often damage the common iliac vein or its branches, which can be complicated by the formation of iliofemoral vein thrombosis. 3, infectious injury septic thrombophlebitis caused by perivenous foci of infection, less common, such as infectious endometritis, can cause septic thrombophlebitis of uterine veins. (C) blood hypercoagulable state This is one of the basic factors causing venous thrombosis. Various major surgeries are caused by the enhanced ability of platelet adhesion in hypercoagulable state; the level of inhibitors of both pre-fibrinolytic activator and fibrinolytic enzyme of serum is increased after surgery, which leads to the reduction of fibrinolysis. Blood coagulability can be increased after splenectomy due to the sudden increase in platelets, and blood concentration due to burns or severe dehydration. Advanced cancer such as lung cancer, pancreatic cancer, others such as ovarian, prostate, gastric or colon cancer, when cancer cells destroy tissues at the same time, they often release many substances, such as mucin coagulant, etc. The increased activity of certain enzymes can also make blood coagulation pregnant drugs, which can reduce the level of antithrombin III, thus increasing blood coagulation. High-dose application of hemostatic drugs can also make the blood in a hypercoagulable state. Combining the above causes of venous thrombosis, the two main causes are stagnant venous blood flow and hypercoagulable blood. A single factor cannot yet cause the disease independently, but often the combination of two or three factors causes deep vein thrombosis. For example, the high incidence of postpartum deep vein thrombosis is due to a combination of factors. The ability of placental abruption in the uterus after delivery to stop bleeding rapidly in a short period of time without causing postpartum hemorrhage is closely related to the hypercoagulable state of the blood. The placenta produces a large amount of estrogen during pregnancy, peaking at term, and the amount of estriol can increase to 1000 times that of non-pregnancy. Estrogen promotes the production of various coagulation factors by the liver, and at the same time, the fibrinogen in the body also increases greatly at the end of pregnancy, resulting in a hypercoagulable state of blood, which, together with bed rest after delivery, causes blood flow to stagnate in the lower extremities and thus has a tendency to develop deep vein thrombosis. The stagnant blood flow alone is not sufficient to produce the disease, but sometimes there is damage to the vessel wall, such as direct injury, chronic disease, or distant tissue damage, which produces leukocyte tropism factors that cause leukocytes to move to the vessel wall. Similarly, the appearance of fissures in the endothelial cell layer and the exposure of subendothelial glue in the basement membrane can cause platelets to move toward the intima, leading to the onset of the coagulation process. Third, the pathophysiology of venous thrombosis can be divided into three types: ① red thrombus or coagulation thrombus, the composition is relatively uniform, platelets and leukocytes are scattered in the gelatinous block of red blood cells and fibrin; ② white thrombus, including fibrin, lamellar platelets and leukocytes, only a very small number of red blood cells; ③ mixed thrombus, the most common, containing white thrombus to form the head, lamellar red thrombus and white thrombus to form the body, red thrombus or lamellar thrombus constitutes the tail. Deep vein thrombosis in the lower extremities originates in some cases in the calf veins and in other cases in the femoral and iliac veins. The pathophysiological changes caused by venous thrombosis are mainly due to the various effects of venous return disorders. The degree of venous blood return obstruction depends on the size and location of the involved vessels, as well as the extent and nature of thrombosis. After the formation of venous thrombosis, a series of pathophysiological changes caused by the increase of venous pressure on the distal side of the thrombus, such as the small veins and even capillary veins are in an obvious depressed state, the osmotic pressure of capillaries increases due to the change of venous pressure, and the permeability increases due to the lack of oxygen in the endothelial cells of blood vessels, so that the intravascular fluid components leak outward and move to the tissue interstices, often causing swelling of the limbs. If there is leakage of red blood cells outside the blood vessels, their metabolites contain iron-containing heme, forming skin pigmentation. In the case of venous thrombosis, it can be accompanied by a certain degree of arterial spasm, which, in the case of weakened arterial pulsation, causes lymphatic depression and impaired lymphatic return, aggravating the swelling of the limb. In addition, during the process of venous thrombosis, the inflammatory reaction of the vein itself and its surrounding tissues, the rapid increase of venous pressure on the distal side of the thrombus, the sudden expansion of the vein, the edema of the lower limb caused by the obstruction of lymphatic return, and the arterial spasm caused by venous thrombosis, which puts the limb in a state of hypoxia, all these series of pathophysiological changes can cause painful symptoms of varying degrees. In the acute phase of venous thrombosis, when blood return to the six trunk veins of the limb is impaired, the high pressure venous blood, distal to the thrombus, will increase its return using all the traffic branches that are usually not important. For example, superficial venous anastomotic branches in the upper thigh and lower abdomen may pass to the contralateral trunk and upward through the abdominal wall to the odd vein and the intrathoracic venous system. In the deeper part, anastomotic branches may reach the contralateral internal iliac vein through the pelvic venous plexus. Adaptive dilatation of these veins promotes cardiac return of venous blood distal to the thrombus. The spread of the thrombus may follow the direction of venous flow and extend proximally, as in the calf where the thrombus may continue to extend into the inferior vena cava. When the thrombus completely obstructs the venous trunk, it can extend retrogradely. Fragments of the thrombus can also be dislodged and follow the blood flow through the right heart and then embolize in the pulmonary artery, which is a complication of pulmonary embolism. On the other hand, the thrombus can be mechanized, re-tubularized and re-endothelialized to restore some degree of patency to the venous lumen. The process of thrombus mechanization starts from the periphery and proceeds gradually to the center. The degree of progression varies. The degenerative changes in the thrombus may occur as a result of the action of fibrinolytic enzymes in the blood. It may also be the result of cellular autolysis and phagocytosis. Another important process of mechanization is the growth of endothelial cells and their penetration into the thrombus, which is an important component of retubulation. In animal experiments, it has been observed that 2 to 5 weeks can lead to venous recanalization, but the valves are already damaged. In clinical observations, it has been found that recanalization is a long course of disease, taking about 8 to 15 years. The final result of the organism will restore some degree of function to the vein. However, the effect of the contraction of the lumen love fibrous tissue and the destruction of the venous valve itself, which disappears or adheres to the wall in a hypertrophic form, leads to secondary deep venous valve insufficiency and produces a post-thrombotic venous syndrome.