DVT is a disorder of venous return caused by abnormal clotting of blood in deep veins, which mostly occurs in the lower limbs; thrombus dislodgement can cause pulmonary embolism, and the two together are called venous thromboembolism. DVT often leads to PE and post-thrombotic syndrome, which significantly affects the quality of life and even leads to death in severe cases. I. Etiology and risk factors The main causes of DVT are venous wall damage, slow blood flow and blood hypercoagulation. The risk factors include primary and secondary factors (Table 1), and DVT is mostly seen in patients who are bedridden for a long time, after limb braking, major surgery or trauma, advanced tumor or have obvious family history. Clinical manifestations DVT mainly manifests as sudden swelling, pain and increased soft tissue tone of the affected limb; it is aggravated by activity and can be alleviated by elevating the affected limb, and there is often pressure pain at the site of venous thrombosis. After 1-2 weeks of disease onset, superficial veins may appear in the affected limb or dilate. When the thrombus is located in the muscular plexus of the calf, Homans’ sign and Neuhof’s sign are positive (Homans’ sign is positive when the affected limb is straightened and the foot is suddenly dorsiflexed, causing pain in the deep calf muscles; Neuhof’s sign is positive when the posterior calf is compressed, causing local pain). Patients with severe DVT of the lower extremities may develop femoral leukomalacia or even femoral cyanosis. Femoral leukomalacia is marked swelling and severe pain in the whole lower extremity, with pressure pain in the femoral triangle, N fossa, and posterior calf, and pale skin, accompanied by elevated body temperature and increased heart rate. Femoral bruise is the most serious case of DVT in the lower extremity, because the iliofemoral vein and its side branches are all blocked by thrombus, the venous return is severely obstructed, the tissue tension is extremely high, resulting in arterial spasm in the lower extremity and limb ischemia; the clinical manifestations are severe pain in the affected extremity, the skin is shiny and blue-purple, the skin temperature is low with blisters, the dorsalis pedis artery pulsation disappears, the systemic reaction is strong, the body temperature is elevated; if not treated in time, shock and venous gangrene may occur If left untreated, shock and venous gangrene may occur. The main symptoms are lower limb swelling, pain, signs including lower limb edema, hyperpigmentation, eczema, varicose veins, and in severe cases, lipid scleroderma and ulcers in the foot and boot area. the incidence of PTS is 20%-50%. The diagnosis of DVT cannot be made only by clinical manifestations, but also needs to be confirmed by auxiliary examinations. (a) Auxiliary tests 1, plasma D-dimer determination: D-dimer is a specific molecular marker reflecting coagulation activation and secondary fibrinolysis, and has a high sensitivity (>99%) for the diagnosis of acute DVT, and > 500ug/L (ELISA method) has an important reference value. It can be used for screening of acute VTE, diagnosis of DVT in special cases, assessment of efficacy, and assessment of the risk level of VTE recurrence. 2.Doppler ultrasonography: with high sensitivity and accuracy, it is the preferred method for DVT diagnosis and is suitable for screening and monitoring of patients. Before ultrasonography, the clinical likelihood of having DVT can be classified as high, moderate or low according to the clinical characteristics score of DVT diagnosis (Table 2). If two consecutive ultrasound examinations are negative, the diagnosis can be excluded for patients with low degree of possibility, and for patients with high and moderate degree of possibility, imaging examinations such as angiography are recommended. 3.Spiral CT venous imaging: it is more accurate and can check the abdomen, pelvis and deep veins of lower limbs at the same time. 4.MRI venous imaging: It can accurately show iliac, femoral and rouge vein thrombosis, but cannot satisfactorily show calf vein thrombosis. No need to use contrast agent. 5. Venography: High accuracy, not only can effectively determine the presence or absence of thrombus, thrombus site, scope, formation time and collateral circulation, but also is often used to identify the diagnostic value of other methods. Treatment (a) Early treatment 1. Anticoagulation is the basic treatment of DVT, which can inhibit the spread of thrombus, facilitate thrombus autolysis and lumen recanalization, thus reducing symptoms, incidence of PE and death rate. However, anticoagulation alone cannot effectively eliminate thrombus and reduce the incidence of PTS. The drugs include common heparin, low-molecular heparin, vitamin K antibodies, direct factor IIa inhibitors, factor Xa inhibitors, etc. (1) Common heparin: The therapeutic dose varies greatly among individuals, and the coagulation function must be monitored when using it. The initial dose is 80-100 U/kg intravenous push, followed by 10-20 U.g-1.h-1 intravenous pump, and then adjusted every 4-6 hours according to the activated partial thromboplastin time (APTT), so that the international normalized ratio (INR) of APTT is maintained at 1.5-2.5. The platelet count should be rechecked on the 3rd-6th day of use; once the diagnosis of HIT is established, normal heparin should be discontinued. (2) Hypoheparin: less bleeding side effects, lower incidence of HIT than regular heparin, no need to monitor coagulation function in most patients when used. It is administered clinically by body mass, 100U/kg per dose, once every 12 hours, subcutaneously, and with caution in renal insufficiency. (3) Direct factor IIa inhibitors (e.g., argatroban): low relative molecular mass, can enter the inside of the thrombus, and have a stronger inhibitory ability on thrombin in the thrombus than common heparin. HIT and patients at risk of HIT are more suitable for use. (4) Indirect factor Xa inhibitors (e.g., sodium fondaparinux): small individual differences in therapeutic dose, once daily, no need to monitor coagulation. The effect on renal function is less than that of low-molecular heparin. (5) Vitamin K antagonists (e.g. warfarin): the main oral drug for long-term anticoagulation therapy, the evaluation of the effect needs to monitor the INR of coagulation function. the therapeutic dose range is narrow, individual differences are large, and the efficacy is easily affected by a variety of foods and drugs. The first day of treatment is combined with low molecular heparin or normal heparin at a recommended dose of 2.5-6.0 mg/d. The INR is measured after 2-3 d. When the INR stabilizes at 2.0-3.0 and lasts for 24 h, the low molecular heparin or normal heparin is stopped and warfarin therapy is continued. (6) Direct factor Xa inhibitors (such as rivaroxaban): individual differences in treatment dose are small and monitoring of coagulation function is not required. Monotherapy for acute DVT is comparable in efficacy to its standard treatment (low molecular heparin in combination with warfarin). Recommendation: For acute DVT, vitamin K antagonist combined with low molecular heparin or normal heparin is recommended; stop low molecular heparin or normal heparin after INR has been achieved and stabilized for 24h. Direct (or indirect) factor Xa inhibitors may also be used. In patients with high suspicion of DVT, if there is no contraindication to anticoagulation, anticoagulation is feasible while waiting for the test results, and the decision to continue anticoagulation is based on the confirmed results. Patients with severe renal insufficiency are recommended to use common heparin. 2, thrombolytic therapy (1) thrombolytic drugs: Urokinase is the most commonly used, with fast onset of action on acute thrombosis, good thrombolytic effect, and few allergic reactions; common adverse reactions are bleeding; no uniform standard for treatment dose, generally the first dose is 4000U/kg, intravenous push within 30min; maintenance dose is 600-1.2 million U/d for 48-72h, and 5-7d if necessary. recombinant Streptokinase, with better thrombolytic effect, but more allergic reactions and high incidence of bleeding. Recombinant tissue-type fibrinogen activator, good thrombolytic effect, low incidence of bleeding, can be used repeatedly. (2) Thrombolysis methods: including catheter contact thrombolysis and systemic thrombolysis. Catheter contact thrombolysis is to place the thrombolytic catheter into the venous thrombus, and the thrombolytic drug acts directly on the thrombus; systemic thrombolysis is to apply the thrombolytic drug systemically through peripheral veins. Catheter-contact thrombolysis has certain advantages, which can improve the dissolution rate of thrombus, reduce the incidence of venous thrombosis sequelae, short treatment time and fewer complications. Systemic thrombolysis has a lower rate of thrombus dissolution than catheter-contact thrombolysis, but it is effective in early DVT, preserves DVT function in some patients, and reduces the occurrence of PTS. Plasma fibrinogen (FG) and prothrombin time (TT) should be monitored during thrombolytic therapy, FG <1.0g/L should be discontinued, and the INR of TT should be controlled at 2.0-3.0. Recommendation: For acute phase central or mixed DVT, catheter-contact thrombolysis is preferred if the systemic condition is good, the expected survival is ≥1 year, and the risk of bleeding is low. If the conditions of catheter thrombolysis are not available, systemic thrombolysis is feasible. 3.Surgical thrombus retrieval: It is an effective method to eliminate thrombus and can quickly release venous obstruction. Fogarty catheter is often used to remove the iliac vein thrombus through the femoral vein, and the femoral N vein thrombus can be removed by squeezing and driving the thrombus or removing the thrombus in a paralleling manner. Recommendation: In case of femoral cyanosis, the thrombus should be removed surgically immediately. For patients with central or mixed type DVT within 7 d of onset, good general condition and no important organ dysfunction, surgical thrombus removal is also feasible. 4.The treatment of combined iliac vein stenosis or occlusion: iliac vein stenosis or occlusion plays an important role in the development of DVT, and the correction of iliac vein stenosis or occlusion at the same time after catheter thrombolysis or surgical embolization can increase the patency rate, improve the treatment effect and reduce the occurrence of PTS. Recommendation: After successful catheter thrombolysis or incisional thrombectomy, imaging reveals iliac vein stenosis >50%, balloon dilation and/or stent placement is recommended as the first choice, and surgical release of iliac vein obstruction is used if necessary. 5.Indications for inferior vena cava filter placement: Inferior vena cava filter can prevent and reduce the occurrence of PE, but complications such as inferior vena cava obstruction and high recurrence rate of DVT caused by long-term placement are gradually attracting attention. Recommendation: For most patients with DVT, the routine use of inferior vena cava filters is not recommended; for those who have contraindications to anticoagulation or complications, or who develop PE despite adequate anticoagulation, inferior vena cava filters are recommended. V. Inferior vena cava filter can be considered in the following cases: 1. floating thrombus in the iliac, femoral or inferior vena cava; 2. acute DVT with proposed thrombectomy such as catheter thrombolysis or surgical thrombectomy; 3. abdominal, pelvic or lower extremity surgery in patients with high risk factors for PE.