Thrombus shed by lower extremity deep vein thrombosis (DVT) is the most important source of emboli for pulmonary embolism (PE). Between 100,000 and 180,000 people die from venous thromboembolism each year in the U.S. The sequelae of DVT, such as post-deep vein thrombosis syndrome (PTS) and chronic thromboembolic pulmonary hypertension, can leave patients in a morbid state, reducing their quality of life and incapacitating them for work. In China, the incidence of DVT is also high. risk factors for DVT are generally divided into two categories: acquired and hereditary. Acquired risk factors are mostly temporary and can be prevented, while hereditary factors cannot be prevented. 1.Acquired risk factors of DVT are clinically more important in the following categories. 1.1 Surgery The pathogenic risk of surgery can be subdivided according to the age, type of surgery and the presence or absence of malignant tumor of the patient undergoing surgery. DVT after surgery is mostly seen in patients over 65 years old. High-risk surgeries include neurosurgery, major orthopedic surgery on the lower extremities, thoracic surgery, malignant tumor surgery on the abdomen or pelvis, kidney transplantation and heart surgery. 1.2 Malignancy 20% of patients presenting with DVT outside the hospital have a combined malignancy. Patients with high-risk malignancies include pancreatic cancer, lymphoma, malignant brain tumors, liver cancer, leukemia, and digestive system cancers such as colorectal cancer. Patients with malignancies receiving immunosuppressive or cytotoxic drugs, L-mentholamide, response arrest and tamoxifen are at higher risk of DVT. 1.3 Trauma Foreign studies have indicated that DVT can be detected by venography in 50% of injured patients after severe trauma. Clinically common highly pathogenic traumas include spinal cord injury (62%), pelvic fracture (61%) and leg bone fracture (80%). In contrast, only 19% of people with lower limb cast immobilization develop DVT. patients after severe trauma mostly have altered blood composition and have to be bed-bound and braked, all of which contribute to blood clotting and thrombosis. 1.4 Venous placement or injury In the United States, central venous placement or pacemaker lead retention resulted in 9% of community-acquired DVTs Earlier there was superficial venous thrombosis that was an independent risk factor for subsequent DVT or PE. 1.5 Pregnancy and oral contraceptives In the United States, the incidence of inpatient VTE is 1.78/1000 and the mortality rate is 1.1/100,000, while the risk is 38% higher in women >35 years of age and 64% higher in black women, with thrombosis as the primary etiology. During pregnancy, the risk of thrombosis is present at the beginning of pregnancy. The risk of developing venous thrombosis is highest after delivery. Blood in a hypercoagulable state during pregnancy is needed at the time of evolution to prevent postpartum hemorrhage. Most birth control pills contain both progestin and estrogen. At least 10 million women in the U.S. and at least 100 million worldwide take combination formulations of oral contraceptives. The risk is higher with birth control pills that contain three to four different ingredients. Birth control pills with formulations containing dexprogesterone or progesterone have a double risk. In addition, according to the Heart and Estrogen/Progestin Replacement Therapy Study and a meta-analysis, postmenopausal estrogen replacement therapy can increase the risk of DVT. the highest risk of DVT and PE occurs in the first year of treatment. 1.6 Braking Prolonged bed braking slows venous blood flow in the lower extremities, which facilitates thrombosis. Surgical procedures and severe trauma can cause patients to be bedridden for a long time. In recent years, the economy class syndrome has gradually attracted attention. In fact, the incidence of this disease is very low. In addition, age, obesity, medical disease, and antiphospholipid antibody syndrome are also common risk factors for DVT pathogenesis . Body mass index, smoking history, chronic obstructive pulmonary disease and renal insufficiency are not independent pathogenic risk factors for DVT. 2.Hereditary risk factors for DVT Several specific variants of the coagulation system increase the risk of deep vein thrombosis. These genetic variants are widely available and can be found in 50% of patients with initial DVT without obvious cause. The presence of more than one risk factor in many patients greatly increases the risk of disease if these variants are included. Patients with a propensity for thrombosis are further at risk for DVT when combined with temporary risk factors such as surgery or trauma. Common genetic variants (defects) are as follows. 2.1 Coagulation factor V Leiden variant This variant is formed by a point mutation on the coagulation factor V gene, which can diminish the degradation of coagulation factor V by activated protein C. Heterozygotes for the factor V Leiden variant account for 5-8% of Caucasians. The Leiden variant has been reported to be found in 12-30% of patients with DVT of no apparent etiology, with a 7-fold increased risk of thrombosis in those heterozygous for the Leiden variant and an 8-fold increase in those purely heterozygous. This variant is not a risk factor for recurrence of DVT. 2.2 Coagulation factor II G20210A This variant is the conversion of nucleotides at position 20210 of the 3・non-replicating region of the coagulin gene to adenine nucleotides, and the mechanism by which it increases the risk of thrombosis is unclear. Carriers of this variant have higher prothrombin concentrations than non-carriers. The detection rate of this variant has been reported to be 7-18% in patients with DVT of no apparent etiology, with a 2.8-fold increased risk of DVT in heterozygous carriers. Heterozygous carriers have a modest increased risk of DVT recurrence. 2.3 Natural inhibitor deficiency risk Antithrombin is a potent inhibitor of several thrombin enzymes. The incidence of antithrombin deficiency in the general population is low (1/250-500), and its detection rate in unscreened DVT patients is less than 1%. People with antithrombin deficiency have an 8-fold increased risk of developing DVT over their lifetime and an increased risk in the presence of transient DVT risk factors. Protein C is a vitamin K-dependent glycoprotein that exists in the body as a proteasome and is activated by thrombomodulin to inhibit coagulation factors V and VIII. The incidence of protein C deficiency in the general population is 1 in 200-500, and the detection rate in unscreened VTE patients is 3.2%. Its heterozygous carriers have a 7-fold increased risk of DVT. Protein S, a vitamin K-dependent glycoprotein, is a cofactor for protein C. Carriers have a more than 8-fold increased lifetime risk of thrombosis. 2.4 Increased coagulation factors Increased coagulation factors, including factor VIII >150 IU/dL, factor IX >129 IU/dL, and factor D >121 IU/dL, are independent risk factors for patients with primary DVT, with adjusted risk increases of 4.8, 2.8, and 2.2-fold, respectively. The mechanism of increased coagulation factors is unknown, and whether it is genetic is unclear. Factor VIII >234 IU/dL is a high risk factor for thrombotic recurrence. Increased factor IX and factor D is a moderate risk factor for thrombotic recurrence. 2.5 Moderate homocysteinosis Homocysteinosis is caused by a number of genetic defects, most typically in the pure form of the methylene reductase heat-resistant mutant. The etiology of the disease also includes vitamin cofactor deficiency and drugs. Moderate homocysteine increase can be found in 25% of patients with DVT. It increases the risk of thrombosis two to three times and is also a risk factor for recurrence of thrombosis