Deep vein thrombosis of the lower extremities, also known as lower extremity deep vein thrombosis, is a common condition that involves the clotting of venous blood in the deep vein vessels of the lower extremities. This disease can leave behind lower extremity edema, secondary varicose veins, dermatitis, hyperpigmentation, and stagnant ulcers. In severe cases, it is life-threatening and forms fatal pulmonary embolism. 1, venous blood stagnation There are many reasons for blood stagnation, such as prolonged braking, lying in bed due to illness, sedentary, varicose veins and so on. Spinal anesthesia or general anesthesia during surgery leads to expansion of peripheral veins and slowing down of venous flow; the lower limbs are completely paralyzed due to anesthesia during surgery and lose their contraction function; and the muscles of the lower limbs are in a state of relaxation due to pain of the incision and other reasons of bed-rest after the surgery, which results in stagnation of blood flow and triggers the formation of deep vein thrombosis in the lower limbs. 2, the damage of the vein wall (1) chemical damage intraventricular injection of various irritating solutions and hypertonic solutions, such as antibiotics, organic iodine solution, hypertonic glucose solution, etc. can be stimulated to varying degrees of venous lining, resulting in phlebitis and venous thrombosis. (2) Mechanical injury of vein local contusion, laceration or fracture fragment trauma can cause venous thrombosis. Femoral neck fracture can damage the common femoral vein, and pelvic fracture can often damage the common iliac vein or its branches, which can be complicated by iliofemoral vein thrombosis. (3) Infectious injury septic thrombophlebitis is caused by infection foci around the vein, which is rare, such as infectious endometritis, which can cause septic thrombophlebitis of uterine vein. 3.Hypercoagulable state of blood This is one of the basic factors causing venous thrombosis. The causes of congenital hypercoagulability are lack of thrombosis inhibitor, abnormal blood fibrinogen, abnormal fibrinolysis, etc. The causes of acquired hypercoagulability are trauma, shock, surgery, tumor, long-term use of estrogen, pregnancy, etc. The platelet adhesion after various major surgeries can cause thrombophlebitis and thrombophlebitis. Platelet adhesion is enhanced after various major surgeries; postoperative serum levels of inhibitors of both pro-fibrinolytic activator and fibrinolytic enzyme are elevated, resulting in decreased fibrinolysis. Blood coagulability can be increased after splenectomy due to a sudden increase in platelets, and blood concentration by burns or severe dehydration can also increase blood coagulability. Advanced cancer such as lung cancer, pancreatic cancer, others such as ovarian, prostate, stomach or colon cancer, when cancer cells destroy tissues at the same time, they often release many substances, such as mucin thromboplastin, etc., and the activity of certain enzymes is increased, which reduces the level of antithrombin III, thus increasing the coagulability of blood. The application of hemostatic drugs in large doses can also make the blood in a hypercoagulable state. The two main causes of venous thrombosis are stagnant venous blood flow and hypercoagulability. A single factor can not yet cause the disease independently, often the combined effect of two or three factors cause deep vein thrombosis. For example, the high incidence of postpartum DVT is due to a combination of factors. Placental abruption in the uterus after delivery can quickly stop bleeding in a short period of time without causing postpartum hemorrhage, and the hypercoagulable state of the blood is closely related. During pregnancy, the placenta produces a large amount of estrogen, which reaches its peak at term, and the amount of estriol can be increased to 1,000 times that of non-pregnancy. Estrogen promotes the production of various clotting factors by the liver, and at the same time, the fibrinogen in the body also increases a lot at the end of pregnancy, resulting in hypercoagulable state of the blood, and then bed rest after delivery, so that the blood flow of the lower limbs is stagnant, which has a tendency to occur deep vein thrombosis. Stagnant blood flow alone is not enough to produce this disease, but sometimes it is accompanied by damage to the vessel wall, such as direct injury, chronic disease, or injury to distant tissues, which produces leukocyte chemotactic factors that cause leukocytes to move to the vessel wall. Similarly, fissures in the endothelial cell layer and the exposure of subendothelial collagen in the basement membrane can cause platelets to migrate to the intima, leading to the agglutination process. 1, Symptoms The most common main clinical manifestation is the sudden swelling of one side of the limb. Patients suffering from deep vein thrombosis of the lower limbs have localized pain, which is aggravated when walking. In mild cases, the localized pain is only heavy, and the symptoms are aggravated when standing. Physical examination has the following characteristics: ① the degree of development of swelling of the affected limb must be based on the daily measurement with tape measure and the healthy side of the lower limb against the thickness of the reliable, purely relying on the naked eye observation is unreliable. This sign is of high value in confirming the diagnosis of deep vein thrombosis, calf swelling is severe, often resulting in increased tissue tension; ② pressure pain venous thrombosis sites often have pressure pain. Therefore, the lower limbs should be examined calf muscles, N fossa, adductor tuberosus and femoral vein below the groin; ③Homans sign can cause deep pain in the calf muscles when the foot is bent sharply to the dorsal side. The Homans sign is often positive in the case of deep calf vein thrombosis. This is due to the gastrocnemius muscle and flounder muscle passive elongation, stimulation of the calf blood full vein and caused; ④ superficial varicose veins deep vein obstruction can cause superficial venous pressure, the onset of 1, 2 weeks after the superficial varicose veins can be seen. Treatment: Acute lower extremity deep vein thrombosis advocates the placement of the umbrella of life protection (inferior vena cava and the purchase of filters) can basically reduce the possibility of fatal pulmonary embolism to the limit. 1, bed rest and elevation of the affected limb 2, anticoagulant therapy This is one of the most important modern treatments for deep vein thrombosis. The correct use of anticoagulants reduces the complication rate of pulmonary embolism and the sequelae of deep vein thrombosis. Their role is to prevent the continued growth of formed thrombi and the formation of new thrombi elsewhere, and to induce a more rapid recanalization of the thrombosed vein. Heparin or low molecular heparin is usually used in the acute phase, transitioning to oral anticoagulants such as warfarin, which needs to be monitored due to its complex drug- or food-related effects, wide variation in individual dosage, and risk of bleeding, and, in recent years, the development of a number of new oral anticoagulants such as rivaroxaban. Rivaroxaban is rarely affected by drugs or food, generally no need to test, easy to use. Thrombolytic therapy includes systemic thrombolysis and catheter contact thrombolysis, and the drugs used are mostly urokinase. Systemic thrombolysis through the vein systemic thrombolysis: through the superficial vein for systemic drug administration, so that the drug with the blood circulation in the body uniform distribution, to achieve the purpose of thrombolysis. Interventional thrombolysis mostly refers to the retention of catheter contact thrombolysis: also known as CDT. through the proximal deep vein catheterization retrograde insertion of the distal deep vein of the limb, the first use of guidewire and catheter to the lumen of the blood vessel to physically open part of the relief of outflow tract obstruction, and then through the placement of thrombolytic catheter so that the drug and the thrombus direct contact with the thrombus, will be sparse and fresh thrombus in the acute stage of the dissolution of the trunk vein in a timely manner to restore the smoothness of the main vein. Some scholars believe that catheter thrombolysis for iliofemoral vein thrombosis can improve the quality of life more than simple anticoagulation. 4.Long term treatment of DVT The duration of anticoagulation for DVT is still controversial. Long term anticoagulation helps to reduce recurrence of DVT as well as post-thrombotic syndrome. For simple factors such as surgical or sedation-induced DVT, anticoagulation should be continued for 3 months, and for idiopathic DVT, anticoagulation is recommended for 6 to 12 months. For patients with malignant tumors, low molecular heparin is administered for 3 to 6 months due to warfarin. For a first episode of DVT with anticoagulant antibodies or two or more risk factors for thrombosis, anticoagulation is recommended for at least 12 months, and for patients with a history of two episodes of DVT, lifelong anticoagulation is indicated.