Primary lower extremity venous insufficiency (PDVI) is a new disease concept that emerged in the early 1980s and is a venous reflux disease of the lower extremities. The incidence is high, accounting for about 40% to 50% of venous diseases of the lower extremities. According to its clinical manifestations, this disease should be classified as “tendon tumor” in Chinese medicine, and if there is ulcer formation, it is “polyposis”. There are two major theories that are accepted by the public, namely the venous valve theory and the tubular wall theory, both of which can exist separately or in combination. Pathology 1, the valve theory: (1) congenital venous valve dysplasia or orthopedic, it has been found that some patients with deep venous valve insufficiency have similar clinical manifestations and a certain family history of hereditary disease. Patients are seen to have smooth deep venous walls, lack of valve sinuses, and significant venous blood reflux in the lower extremities on both paralleling and retrograde lower extremity venograms. In 1986, the Plare study demonstrated that congenital venous valve dysplasia or agenesis is an autosomal dominant disorder. However, the incidence of the disease is low, accounting for only 1-5% of cases, and cannot yet satisfactorily explain most cases of PDVI. (2) Theory of degenerative degeneration of valves: Some scholars believe that with age, venous valves undergo tissue degeneration and their number decreases, pending further study. (3) Theory of valve injury: Primary deep venous valve insufficiency occurs in people with heavy work and long standing. Deep vein valves in the lower limbs are subjected to the gravitational force of the blood column for a long time, and their free edges become loose and prolapsed, so that there is a funnel-shaped gap when the valves are closed, and they lose the function of blocking the backflow of blood, and when the backflow of blood passes through the femoral vein without valves or poorly tolerated, the blood column with elevated pressure acts on the saphenous vein, superficial femoral vein and deep femoral vein valves at the same time. The saphenous vein is the most vulnerable due to its highest position, superficiality, and lack of muscle protection. The superficial femoral vein, which is a direct continuation of the femoral vein, bears the greatest gravity of the blood column and is often damaged. In this way, the deep vein trunk and the traffic vein of the lower leg are gradually damaged, so in this “domino” effect, the valves of the deep and superficial veins of the lower limbs are destroyed, causing the backflow of venous blood. 2, the wall theory: because the lesion of the venous wall elasticity is obviously decreased, the strength is reduced, so in the long-term blood column under the action of gravity, the expansion occurs, the diameter of the valve ring increases and the relative valve closure insufficiency, too long, the valve disuse atrophy or even disappear. Completely lose the role of preventing blood backflow. Due to the weakness or absence of venous valves, the poor elasticity of the wall, coupled with long-term standing, weight-bearing and long-distance travel, or chronic abdominal pressure increasing disease chronic cough, habitual constipation and other reasons. It can lead to the increase of venous pressure in the lower limbs, resulting in incomplete valve closure and backflow of blood, causing this disease. The pathophysiology of primary lower limb deep vein valve insufficiency is characterized by damage to the venous valves, increased intravenous pressure, blood stagnation and hemodynamic changes under the action of pathogenic factors, leading to gradual aggravation of the disease and causing a series of clinical manifestations, when the gravity of the venous blood column acts on the femoral vein valve, the iliofemoral vein valve is firstly destroyed and its free prolapse; then the gravity of the blood column acts on the saphenous vein, which can occur alone. The superficial femoral vein valve is also more likely to be involved; while the deep femoral vein is less affected by the gravity of the blood column because of the anatomical relationship. Second, the clinical performance of primary lower extremity deep vein valve insufficiency is slow to develop, mostly with varicose veins of lower extremity as the main manifestation, and gradually aggravated with age. Its clinical symptoms and signs are caused by venous backflow, venous system high pressure and blood stagnation, mainly manifested as superficial venous tortuosity, dilatation, calf heaviness, fatigue, swelling and distension, aggravated by long standing and long distance travel, reduced after lying down and resting, and occasionally painful calf muscle spasms and twitches at night. With the prolongation of the disease, the incompetence of the valves of the deep and superficial venous traffic branches may lead to swelling of the calf boot area, skin pigmentation, eczema-like dermatitis, and in severe cases, bruised ulcers and oozing, which are difficult to heal or recurrent. It can also be complicated by dermatitis, soft tissue infection, thrombotic superficial phlebitis, or deep vein thrombosis. The time and degree of clinical manifestations depend on the site of venous valve lesions and the functional status of the valves, as well as the functional status of the traffic branches of the deep and superficial veins, and most patients develop the disease after the age of 20. Auxiliary examination 1.Limb ultrasound detection. 2.Limb venography. (1)Parallel venography. (2) Retrograde angiography.