Deep vein thrombosis is an important cause of complications and sudden unexpected death, with an annual incidence of up to 1 in 1,000 in developed countries, and according to incomplete statistics, sudden death due to pulmonary embolism caused by dislodged venous thromboemboli is up to 500,000 in the United States each year, becoming the third leading cause of life-threatening death. Warfarin is a bicoumarin derivative that produces an anticoagulant effect by interfering with the conversion cycle between vitamin K and 2,3 epoxide vitamin K. Oral warfarin therapy is effective in preventing recurrent venous thrombosis, reducing its risk by more than 90%. The annual incidence of major bleeding during oral anticoagulation therapy is approximately 3%, with an annual mortality rate of 0.6%. The annual recurrence rate of venous thrombosis is 12%, and the mortality rate is approximately 5-7%. The recurrence of thrombosis after termination of anticoagulation therapy depends mainly on the removal of the factors that formed the thrombosis. 1, the appropriate anticoagulation intensity: Warfarin in different individuals dose-effect relationship varies greatly. The anticoagulant strength is directly related to its efficacy and side effects, so its monitoring is the key to the treatment process. Warfarin affects the activity of coagulation factors IIa, VIIa, IXa and Xa, which are related to the exogenous coagulation system, so the dose is adjusted by monitoring its effect on the exogenous coagulation system (PT) after oral administration of warfarin. A standardized PT, the international normalized ratio (INR), is used clinically to avoid the effects of different test reagents. Moderate-intensity anticoagulation (INR 2.0-3.0) is as effective as high-intensity anticoagulation (INR 3.0-4.5), but the incidence of bleeding is lower with moderate-intensity, so for the average thrombotic patient, we recommend moderate-intensity anticoagulation, i.e., maintaining an INR of about 2.5. Oral anticoagulation therapy should be ≥ 3 months, while for those with unknown causes or due to irreversible factors, and for patients with recurrent venous thromboembolism the course should be ≥ 6 months, and now there is a trend to further prolong anticoagulation therapy for treatment of unexplained venous blood. 2. Time period for testing warfarin: The ACC and AHA guidelines recommend an initial warfarin dose of 5-10 mg, which generally results in an INR of 2.0 after 5-7 days. the INR should be monitored daily until it reaches and is maintained in the therapeutic range (between 2 and 3) for two consecutive days, and then monitored 2-3 times a week for 1-2 weeks. If the INR value remains stable, it can be reduced to once every 4 weeks. Factors such as the patient’s diet, combination of medications, treatment compliance and alcohol abuse during anticoagulation therapy may cause changes in INR and should be monitored at all times depending on the situation. 3.How to adjust the dose of warfarin If the INR is mildly changed and beyond the therapeutic range, the dose can be increased or decreased by 5%-20%; when the INR changes significantly, we should actively look for possible influencing factors. 1) If the INR is outside the therapeutic range but less than 5, and the patient does not have bleeding from a vital site or the need to perform surgery, the dose may be reduced or suspended once and applied in a reduced dose when the INR returns to the therapeutic range. 2) If the INR reaches 5.0-9.0 and the patient has no bleeding or risk factors for bleeding, warfarin may be discontinued for 1-2 days and applied in reduced doses after the INR returns to the target value. 3) If the patient has other risk factors for bleeding, discontinue warfarin once while giving oral vitamin K1 1 to 2.5 mg; 4) If emergency surgery or tooth extraction is required, give oral vitamin K1 2 to 4 mg so that the INR decreases significantly within 24-48 h. Monitor closely and repeat oral vitamin K1 if necessary. 5) If the INR is greater than 9.0 and there is no clinical bleeding A high dose of oral vitamin K1 3-5mg should be given to bring down the INR significantly within 24-48h and repeated if necessary. 6) If there is severe bleeding or an INR greater than 20, then vitamin K1 10 mg should be given intravenously, supplemented with fresh plasma or prothrombin concentrate, and can be repeated every 12 hours with vitamin K1 sedation. (7) In life-threatening bleeding or severe warfarin overdose, prothrombin complex replacement therapy is necessary, with intravenous vitamin K1 as a supplement. Certain drugs can affect the pharmacokinetics of warfarin by inhibiting the synthesis of VK-dependent coagulation factors, increasing metabolic clearance, and interfering with other hemostatic pathways. These drugs are: (i) broad-spectrum antibiotics: inhibit intestinal flora, reduce the body’s vitamin K content, and enhance the efficacy of oral anticoagulant drugs; (ii) antiplatelet drugs such as aspirin: can have synergistic effects with oral anticoagulant drugs, with increased bleeding side effects; (iii) chloral hydrate, hydroxyprogesterone, methylsulfonylurea, quinidine, etc. can increase the concentration of plasma warfarin due to replacement of plasma proteins, with enhanced effects (d) salicylates, promethazine, metronidazole, cimetidine, etc. may increase the role of oral anticoagulants by inhibiting hepatic drug enzymes and reducing the hepatic metabolism of warfarin; (e) barbiturates, phenytoin sodium, carbamazepine, rifampin, etc. may decrease the role of warfarin by inducing hepatic drug enzymes and increasing the metabolism of warfarin; (f) oral contraceptives may increase coagulation activity and decrease the role of warfarin. Fluctuations in the intake and absorption of VK in food affect the efficacy of warfarin. Hepatic insufficiency impairs the synthesis of VK-dependent coagulation factors and enhances the response to warfarin. Hypermetabolic states, such as hyperthyroidism, increase the metabolism of clotting factors and enhance the efficacy of warfarin. Vitamin K is able to antagonize the anticoagulant effect of warfarin, thereby reducing the anticoagulant effect. In order to maintain the stable anticoagulant strength of warfarin, it is necessary for the patient to maintain a relatively balanced diet, especially a relatively balanced intake of VK-rich green vegetables. Examples of drug effects on warfarin are as follows: clearance of the racemic isomer R is slightly lower in the elderly than in the young, while clearance of the isomer S is not affected by age. The anticoagulant response to warfarin in older adults than 60 years of age is stronger than that shown by PT/INR, and appropriate dose reduction produces the same anticoagulant effect.