The annual incidence of venous thromboembolism is about 0.1%, and the incidence increases gradually with age, up to 1% in elderly people over 60 years of age. More than half of thromboembolic events are associated with deep vein thrombosis, and it is important to treat patients promptly in order to reduce the chances of fatal pulmonary embolism. According to Virchow, there are three major factors that contribute to the formation of venous thrombosis, namely venous wall injury, venous stasis and hypercoagulable blood. Most DVTs originate in the muscular plexus of the lower leg, and approximately 25% of untreated DVTs in the lower leg extend to the proximal veins, while most fatal embolisms originate from proximal vein thrombosis. Deep vein thrombosis (DVT) may be asymptomatic or may involve pressure, pain, edema, increased temperature, skin discoloration, and superficial venous bulging over the affected area. DVT affects the femoral and iliac veins, and hard streaks may be palpable over the affected veins in the femoral triangle of the groin, mid-thigh, or fossa. In iliofemoral vein thrombosis, dilated superficial collateral veins are seen in the calf, thigh, hip, and lower abdomen. Because there are at least three major veins that collect blood flow in the lower leg and one vein thrombosis does not affect venous return, edema, skin cyanosis, and superficial venous dilatation do not occur. The patient complains of soreness or pain when standing or walking, which is usually relieved by rest and elevation of the lower extremity. In 50% of cases, acute deep vein thrombosis cannot be diagnosed clinically alone, and Homan’s sign cannot be used as a basis for diagnosis. It is not often used in clinical practice. Non-invasive color Doppler ultrasound is the diagnostic method of choice for DVT when deep vein thrombosis is suspected, and it has been reported that the sensitivity of venous ultrasound for symptomatic, central DVT diagnosis is 95% and specificity is 96%; for peripheral DVT diagnosis the sensitivity and specificity are 60% and 70%, respectively. Studies have shown that the detection of plasma D-dimer levels is also an effective means of DVT screening. It was found that elevated plasma D-dimer levels in patients with DVT confirmed by venography had a sensitivity and specificity of 95% and 77%, respectively, and a negative predictive value of 92% if D-dimer >50ng/ml was used as a positive test. Therefore, normal D-dimer results in patients with suspected DVT can help to exclude the diagnosis of DVT. Deep venography is still the “gold standard” for DVT diagnosis, and venography should be performed if the diagnosis is suspicious, and pulmonary embolism can be detected by lung scan or pulmonary arteriography. If DVT is missed, it can lead to pulmonary embolism and death. However, if anticoagulation is applied without ultrasonography, venography or lung scan, there is a risk of serious bleeding. 2.Treatment Once DVT is diagnosed, the aim of acute treatment is to relieve symptoms and prevent pulmonary embolism and chronic venous insufficiency. In recent years, the acute treatment of DVT is mainly non-surgical: thrombolysis, anticoagulation, filter placement and other interventions, and occasionally surgery. 2.1 General treatment
Bed rest and elevation of the affected limb 30° above the level of the heart are required for acute DVT, which requires bed rest for 1 to 2 weeks to make the thrombus adhere tightly to the intima, reduce local pain, and promote the inflammatory response to subside. 2.2 Anticoagulation therapy is currently the most basic means of treatment for DVT, and commonly used drugs include heparin, low molecular weight heparin and warfarin. 2.2.1 Conventional normal heparin (UFH)
Usually a loading dose is given followed by continuous intravenous infusion, for example, a loading dose of 80 IU/kg is first pushed intravenously, followed by a maintenance dose of 18 IU/(kg・h); APTT is rechecked at 6h, and the dosage is adjusted according to APTT so that APTT is within 1.5-2.5 times of normal control; long-term use of heparin (>1 month) can lead to osteoporosis and heparin-induced Thrombocytopenia, patients with a history of heparin-induced thrombocytopenia need to use other anticoagulants, such as: danaparoid,lepirudin,argatroban. 2.2.2 Low molecular heparin (LMWH)
Analysis of some data shows that LMWH is as effective as conventional heparin in preventing recurrence of venous thromboembolism, but LMWH causes less bleeding. Low molecular heparin is usually administered subcutaneously, once or twice a day, with dose adjustment according to body weight, and monitoring is generally not required. Although low-molecular heparin causes less thrombocytopenia than conventional heparin, low-molecular heparin often cross-reacts with antibodies, which can lead to thrombocytopenia, and therefore low-molecular heparin should be contraindicated in patients with a history of this condition. LMWH also causes less osteoporosis than conventional heparin. lMWH does not cross the placental barrier and is safer for use in pregnant women. the anticoagulant effect of LMWH is assessed with anti-Xa levels so that it is between 0.5 and 1.5 U/ml.