A thrombus is a semi-solid formed when blood components coalesce in the circulation. It can occur anywhere in the circulation, including the atria and microcirculation, and often adheres to the surface of the atria or blood vessels, and can be dislodged to cause embolism. Thrombosis (thrombosis) is the process of forming a hemostatic blood clot when blood vessels of human tissues are damaged. Depending on the anatomical location of the thrombus in the body, the size of the thrombus and its components, it can be classified as venous thrombosis, arterial thrombosis and mixed thrombosis. Embolism is a process in which a blood clot formed locally in a blood vessel is embedded in other parts of the blood vessel along the blood flow, resulting in ischemia, necrosis or serious physiological disorders in the corresponding tissues or organs. Under normal circumstances, thrombosis is an important protective mechanism in the human body, which prevents life-threatening overflow of blood from the circulatory system in the event of an accident or man-made trauma to a living individual. Accordingly, the human body is simultaneously inhibiting thrombosis (anticoagulation) and preventing unrestricted expansion of blood clots and abnormal thrombosis. After the thrombus formed with trauma has completed its “mission” to stop bleeding, the body also has a mechanism to remove the thrombus (fibrinolysis). Fibrinolytic activators and fibrinolytic inhibitors mediate the fibrinolytic activity of the body, maintaining a dynamic balance. This “yin-yang balance” ensures that under normal physiological conditions, blood can flow normally in the blood vessels without forming clots or bleeding; in addition, it ensures that the individual can form hemostatic clots locally in trauma and that the clots can be removed in a timely manner when the hemostatic task is completed. Diseases caused by thrombosis are very common in clinical practice. Some of the most common diseases that endanger human life, such as atherosclerosis, coronary heart disease, myocardial infarction, ischemic cerebral infarction, etc., are closely related to arterial thrombosis. Thrombotic diseases belong to “blood stasis evidence”, “purpura”, “stroke”, “chest paralysis”, “heart pain”, etc. in Chinese medicine. The thrombotic disorders belong to “blood stasis”, “purpura”, “stroke”, “chest paralysis”, “heart pain” and so on. The triggering factors and pathogenesis of thrombosis in Western medicine are complex, and only some of them are known so far. It is generally believed that the formation of thrombus includes a variety of composite factors, such as blood vessel wall, platelets, coagulation and fibrinolysis, blood flow and blood viscosity. The factors contributing to thrombosis still follow the model proposed by the German pathologist Virchow as early as 1845, that is, thrombosis is associated with an imbalance between coagulation factors, altered blood flow and the vascular endothelial triangle. Thus abnormal endothelial function, altered blood flow, and abnormal blood composition, independently or in combination, can all promote thrombosis. Abnormalities in blood composition usually include abnormal platelet volume and function (abnormal initial hemostasis), abnormal coagulation (second stage hemostasis), and abnormal fibrinolytic function. In the past decade, with the in-depth research on the pathogenesis of thrombosis, a consensus has been reached on the multi-component, multifactorial and potential pathogenesis of thrombosis, and the role of high-risk genes and abnormal hemostatic regulatory functions in the pathogenesis of thrombosis has received increasing attention. Although there are still many doubts about the underlying pathological mechanisms of arterial and venous thrombosis, advances in both basic and clinical aspects have provided many new tools for mechanistic exploration, detection of thrombotic disease progression, and early diagnosis and treatment. A decade ago, the understanding of thrombophilia was limited by the belief that venous thrombosis was caused by a group of congenital anticoagulant protein deficiencies, such as protein C, protein S, antithrombin III, heparin cofactor II deficiency, and abnormal fibrinogenemia. In fact, these congenital anticoagulant deficiencies account for only 15-20% of venous thrombosis (approximately 2-5% each). In the last decade, important advances have been made in the study of thrombopathogenesis. Starting with venous thrombosis, clinical analyses and new experimental methods of investigating family lines have confirmed that venous thrombosis is often a multifactorial, multigene defective disease, a group of molecular diseases in the blood category, with significant ethnic and geographic differences in the incidence of molecular defects. The pathogenesis of arterial thrombosis is more complex, involving not only imbalance of coagulation and fibrinolytic system, but also intercellular reactions. Research on arterial thrombosis has not yet achieved a breakthrough. So far, the research on the mechanism of thrombosis has not been separated from the above three basic factors, but the specific contents have been greatly enriched and updated. The causes of these three aspects are described as follows: 1. The role of platelets. Due to vascular endothelial injury, the subendothelial collagen tissue is exposed, resulting in local platelet adhesion and aggregation; followed by the release of endogenous adenosine diphosphate (ADP), 5-hydroxytryptophan and other substances to further promote the role of platelet aggregation and vasoconstriction. At the same time, the arachidonic acid of platelet membrane is transformed into thromboxane A2 (TXA2) under the action of enzyme system, which further promotes platelet aggregation and vasoconstriction. Platelet membrane phospholipids are exposed to exert the procoagulant effect of platelet factor 3. Platelet endogenous ADP allows more platelets to aggregate locally and form platelet thrombi. Platelet thrombus is repeatedly washed, destroyed and re-formed by blood flow, and the thrombus keeps increasing in size and narrowing the lumen of the affected vessels, and even vascular occlusion occurs. 2.Vascular wall factors. The intact vascular endothelial cells also contain arachidonic acid, which is synthesized by the action of cyclooxygenase, prostaglandin endoperoxide (PGG2, PGH2), and then synthesized by the action of prostacyclin synthase PGI2. PGI2 has the effect of increasing the concentration of cyclic adenosine (cAMP), inhibiting platelet aggregation and diastolic blood vessels. Arachidonic acid of platelet membrane can synthesize TXA2, which can reduce the content of cAMP in platelets, promote platelet aggregation, and cause vasoconstriction. Under normal conditions, PGI2 and TXA2 are antagonistic to each other and work together to maintain a dynamic balance between platelets and the vessel wall. In the pathological state, this balance is disrupted, and platelet adhesion and aggregation occur at the site of injury, gradually leading to local thrombosis. The normal vascular endothelium can play a balancing and regulating role between platelets and coagulation factors. Therefore, in terms of vascular wall factors that can cause thrombosis, several conditions must be present: ① physical injury; ② inflammation and edema of the vascular wall; ③ endothelial fracture and breakage, as well as bleeding of the intima and interstitium; ④ rupture of necrotic atherosclerotic plaque, etc. 3. Blood flow and blood viscosity. Any changes in the lumen of blood vessels, such as local narrowing or enlargement of the lumen or bifurcation, T- or Y-shaped branching of blood vessels, etc., can result in local changes in blood flow velocity or the formation of vortices. In conditions such as erythrocytosis and hyperglobulinemia, blood viscosity may increase, causing a slowing of blood flow velocity and a decrease in blood flow. All of the above conditions may cause platelets to aggregate in the blood vessels and contribute to thrombosis. The site of arterial thrombosis is often at the exit or bifurcation of blood vessel branches. 4. Hypercoagulable state. There is a clear relationship between thrombosis and increased activity of coagulation factors. Clinically known thrombophilia (congenital antithrombin III deficiency) is a rare disease with a significant lack of anticoagulant activity. Patients are prone to recurrent venous thrombosis and pulmonary embolism due to the inability to antagonize factor Xa and thrombin activity. Other conditions such as hereditary hyperlipoproteinemia, gestational toxicity and oral contraceptives are prone to thrombosis due to increased coagulation factor activity and hypercoagulability of the blood. In addition, disseminated intravascular coagulation is induced by other diseases, and arterial and venous microthrombosis can also occur. The etiology and pathogenesis of blood stasis in Chinese medicine includes four main aspects: 1. According to TCM theory, “qi is the handsome of blood, and blood is the mother of qi.” The normal operation of blood depends on the promotion and maintenance of qi. Once the qi of an entire body is malfunctioned due to the action of pathogenic factors, such as the six lewdnesses or the seven emotions, the promotion and control function of qi will be malfunctioned, resulting in qi stagnation and blood stasis, and thus blood stasis will occur. 2. Qi deficiency and blood stasis. Because of the close relationship between Qi and blood, if Qi is weak and unable to promote the normal operation of blood due to congenital or acquired factors, it will lead to Qi deficiency and blood stasis, which will then become stasis of blood. For example, a person with a weak spleen and stomach is originally weak in the spleen and stomach, which is not enough to transform the qi and move the blood. 3. Cold coagulates the blood vessels. Cold is a Yin evil, and its nature is to attract. Blood running in the veins, need to rely on the Qi to promote warmth, in order to run properly. If the cold invades outside or the Yang deficiency produces internal cold, it will lead to stasis in the veins and veins, and then the evidence of blood stasis will occur. 4.Phlegm and blood stasis are intertwined. Phlegm is the coalescence of fluid, so phlegm is not only a pathological product, but also a pathogenic factor. If the phlegm is blocked in the blood vessels, it will affect the normal operation of blood, and over time, phlegm and blood stasis will form and gradually become the evidence of blood stasis. Blood stasis can occur in any part of the body, and wherever there is blood flow, blood stasis may occur, resulting in evidence of blood stasis. For example, the extremities, the brain and the five organs (especially the heart, followed by the lungs, liver, spleen and kidneys). Clinical manifestations] Blood clots can occur in any part of the body, and even systemic diffuse intravascular coagulation can occur. The common site of thrombosis is artery or vein. Physiological thrombosis occurs mostly outside the blood vessels as a protective mechanism to stop bleeding in response to trauma, while pathological thrombosis occurs mostly inside the blood vessels, causing tissue ischemia or stasis, resulting in vascular events and even vascular death. Thromboembolic diseases mainly include atherothrombosis, venous thromboembolism and peripheral arterial embolism. Arterial thrombosis mainly involves cardiovascular, cerebrovascular and peripheral arterial vasculature, and most thrombosis in these areas is formed on the basis of atherosclerotic plaque rupture, i.e., damage to the inner wall of blood vessels leads to thrombosis, which seriously leads to myocardial infarction, cerebral infarction and acute lower limb ischemia and necrosis. Therefore, atherothrombosis is the process of plaque rupture and thrombosis on the basis of atherosclerosis, leading to vascular events and even vascular death. Usually, atherosclerosis is a decades-long process, while plaque rupture is an instantaneous event and thrombus formation is only 10 seconds or so, leading to a fatal and disabling vascular event. Without thrombosis, there is no event. Atherothrombosis is divided into two categories: occlusive and nonocclusive: occlusive (oclusive) leads to myocardial infarction, cerebral infarction, and acute lower extremity ischemia, necrosis, or gangrene. Non-occlusive (nonocclusive) is further divided into two categories: stable and unstable. Stable (stable) is the episodic ischemic clinical manifestations caused by unruptured fixed stenotic plaques, including stable angina pectoris, chronic ischemic encephalopathy (such as vascular dementia, standing dizziness, etc.) and intermittent claudication of the lower extremities. Unstable (unstable) is the presence of plaque rupture and thrombosis without interruption of vascular flow and includes acute coronary syndrome with non-ST segment elevation, transient ischemic attack, and intermittent claudication and rest pain in the lower extremities. The most dangerous complication of deep vein thrombosis (DVT) is pulmonary embolism, often referred to as venous thromboembolism (VTE). Deaths due to venous thromboembolism in Europe and America rank third after cardiovascular disease and malignancy. The incidence of DVT in China is also quite high, and the incidence of DVT in major surgical procedures is around 50%. According to TCM theory, the clinical manifestations of thrombotic disease (stasis of blood) appear differently depending on the site where the thrombus (stasis of blood) occurs. For example, the site of thrombosis may have fixed pain (so-called “pain if it does not pass”), headache or pain in other parts of the limbs, and in severe cases, it may cause local edema and bruising of the limbs; if blood stasis blocks the brain, dizziness of the head and eyes, weakness of the limbs or even hemiplegia, slurred or awkward speech, or even aphasia and confusion; if blood stasis blocks the chest, chest tightness may occur. If blood stasis is blocked in the chest, chest tightness, chest pain, palpitation, and pulse knotting. In addition, the general evidence of stasis of blood has a purple tongue or petechiae, and a fine and astringent pulse. Laboratory and other tests] Currently, there is a lack of clinically meaningful specific tests for thrombotic diseases, while for atherothrombotic diseases, long-term follow-up monitoring of relevant indicators can be performed. This is very important to determine the presence or absence of disease and prognosis, such as blood pressure, blood lipids, blood sugar and its control. In high-risk groups, relevant risk factors should be detected early through health checkups for early and effective intervention. Intermediate endpoints, such as carotid plaque and intima-media thickness, ankle-brachial index (ratio of lower and upper extremity blood pressure), elevated C-reactive protein (CRP), elevated brain natriuretic peptide (NT-proBNP) and proteinuria are valuable for the diagnosis of vascular thrombotic disease, understanding its functional status, prognosis and treatment decisions. For example, carotid plaque and intima-media thickness is a marker of vascular lesions and vascular events; CRP itself is an inflammatory substance and a marker of inflammation; there are many factors affecting CRP, and many disease processes are accompanied by elevated CRP, making it difficult to use CRP as a basis for treatment decisions. Even in apparently healthy populations, elevated NT-proBNP has prognostic value. In high-risk populations, NT-proBNP is a very important prognostic indicator. The results of blood rheology tests do not assist in the diagnosis or prediction of cardiovascular thrombotic disease. Hemorheology cannot be used as a basis for treatment decisions or medication, nor can it determine the effectiveness of treatment. The same is true for other hematologic test indicators, such as blood coagulation analysis. The diagnosis of deep vein thrombosis (DVT) relies on vascular ultrasound. The absence of blood flow or incompressibility of the ultrasound vessel is highly suggestive of DVT, and the sensitivity and specificity of vascular ultrasound for the diagnosis of proximal DVT is very high. For venous thromboembolism, although D-dimer cannot establish the diagnosis, a negative D-dimer can basically exclude acute thrombosis or embolism. Diagnosis and differential diagnosis] I. Diagnostic points (a) Western medical diagnosis The diagnosis of thromboembolic disease is mainly based on medical history, such as previous history of hypertension, hyperlipidemia, diabetes mellitus or myeloproliferative disorders (true erythrocytosis, primary thrombocytosis), varicose veins, physical examination and ancillary tests, such as blood analysis, coagulation function, coagulation factors, electrocardiogram, cardiac troponin, cardiac troponin, and cerebral CT examination, vascular ultrasound, cardiac troponin, CT brain examination, vascular ultrasound, angiography, etc. Symptoms and signs: The main symptoms are local pain and malfunction of corresponding organs caused by vascular embolism, such as palpitation, chest tightness, dizziness and headache, mental changes, weakness of hands and feet and even hemiparesis, pain, swelling, fever or chill in the affected limbs caused by arterial and venous thrombosis of lower extremities, local skin color change, dotted or patchy bleeding foci. （The diagnosis of TCM is mainly based on the patient’s past medical history, clinical manifestations and tongue and pulse signs. The clinical manifestations vary according to the location of the stasis of blood. If blood stasis is blocked in the brain, dizziness, limb weakness or even hemiplegia, slurred speech, or even aphasia and confusion may occur; if blood stasis is blocked in the chest, chest tightness, chest pain, palpitations and pulse knotting may occur. The tongue and pulse signs of blood stasis evidence are mainly purple and dark tongue or petechiae and fine and astringent pulse. At the same time, the diagnosis and identification of TCM must be combined with the relevant laboratory and vascular examination means. Clinically, lower extremity arterial and venous thrombotic diseases and DIC, if skin and mucous membrane bleeding occurs, need to be distinguished from thrombocytopenic diseases: (a) Immune thrombocytopenic purpura is a common acquired bleeding disease of unknown cause in the blood system. It is characterized by thrombocytopenia, normal or increased bone marrow megakaryocyte count, and lack of any cause, including exogenous or secondary factors. It is currently believed that the disease is due to the production of anti-platelet antibodies in the body, resulting in excessive platelet destruction and shortened platelet lifespan, while the bone marrow has normal or increased megakaryocytes and degeneration and infantilization of megakaryocytes, and is also known as autoimmune thrombocytopenic purpura because its pathogenesis is related to autoimmunity. The main feature of this disease is a decrease in platelet count. It is not difficult to differentiate by clinical manifestations and blood system examination. (2) Secondary thrombocytopenic purpura Because there are many causes of thrombocytopenia, such as aplastic anemia, acute leukemia, thrombotic thrombocytopenic purpura, autoimmune hemolytic anemia with thrombocytopenia (Evans syndrome), hypersplenism, etc., all need to be carefully analyzed and differentiated by combining clinical manifestations, laboratory tests and changes in bone marrow image. Treatment] I. Chinese medicine treatment Through Chinese medicine diagnosis and treatment, from the method of activating blood circulation, removing blood stasis, moving qi and replenishing qi, etc., can obtain better results. As Wang Qingren said in the “Correction of the Medical Forest”: “The key to treating the disease is to understand qi and blood. Qi has deficiency and blood has deficiency and stasis.” Therefore, it is appropriate to identify the evidence flexibly. （Main symptoms: localized pain in the limbs, or headache and dizziness, limb weakness, slurred speech, blurred mind; or chest tightness, palpitation, shortness of breath; bruised skin spots or plaques; accompanied by purple tongue or petechiae, thin white or thin yellow moss, and stringent pulse. Analysis: Qi stagnation and blood stasis, blood vessels do not run smoothly, and pain occurs when they do not pass, thus localized pain. If stasis blocks the brain, weakness of limbs, slurred speech and blurred mind; if stasis blocks the heart, chest tightness, palpitation and shortness of breath; if stasis blocks the blood vessels of the extremities, purple-red or bruised patches appear on the skin; purple-dark tongue or petechiae and petechiae, stringent and astringent pulse, all are signs of blood stasis. Treatment: Promote Qi and Blood circulation, resolve blood stasis and relieve pain. Radix: Blood Mansions and Blood Stasis Soup (《Medical Forest Correction》). Radix Angelicae Sinensis, Rhizoma Chuanxiong, Rhizoma Peach, Rhizoma Red Flower and Radix Paeoniae Alba are the main herbs for promoting blood circulation and resolving blood stasis, which have the function of promoting blood circulation, resolving blood stasis and relieving pain. Citrus Aurantium, Radix Platycodon and Radix Bupleurum move Qi. Niu Knee induces blood to return to the meridian. Glycyrrhiza glabra harmonizes the herbs. Addition and reduction: If blood stasis is more serious, add Salvia miltiorrhiza, Curcuma longa, Wu Ling Li, Qiang Huang, Pu Huang, Ze Lan, etc. 2.Qi deficiency and blood stasis Main symptoms: numbness of limbs, weakness of hands and feet, or hemiplegia, slurred speech, shortage of breath and lazy speech, pale or purple face, purple skin or petechiae; accompanied by purple tongue or petechiae, thin white fur, thin and astringent pulse. Analysis: Qi deficiency and blood stasis, weak blood flow, lack of blood to moisten and warm the extremities, therefore, numbness and insensitivity of the limbs, weakness of the hands and feet, or hemiplegia. If stagnant blood is stagnant in the brain and veins, there will be hemiplegia and slurred speech. Shortness of breath and lazy speech, pale or purple face are signs of Qi deficiency and blood weakness. Purple skin or petechiae, purple tongue or petechiae, and thin and astringent pulse are all signs of Qi deficiency and blood stasis. Treatment: Benefit Qi and blood circulation, resolve blood stasis and clear the channels. Remedy: Tonic Yang Returning Five Soup (《醫林改错》). In this formula, Huang Qi tonifies Qi, while Angelica sinensis, Chuanxiong, Tao Ren, Hong Hua, Red Peony and Di Long invigorate blood circulation and remove blood stasis. Add and subtract: if Qi deficiency is obvious, add Radix Codonopsis or Ginseng; if blood stasis is obvious, add Danshen, Curcuma longa, Curcuma longa, Puhuang, or worm-like medicine turtle worms, Silkworm, whole worms, and blood exhaust. 3.Cold blood clotting Main symptoms: Pain in the limbs or other parts of the body is obvious, decreases with warmth and increases with cold, the pain is acute and fixed. Cold hands and feet, fear of cold, clear and long urine, loose stools. The tongue is purple or light fat, the coating is white and smooth, and the pulse is sunken and astringent or sunken and tight. Analysis: Cold is a yin evil, its nature is stagnant and astringent, depleting yang qi, leading to blood stasis, then the pain in the limbs or other parts of the body is obvious; it decreases with warmth and intensifies with cold, the pain is acute and immovable, all of which are characteristics of cold condensing blood vessels. Cold evil injures Yang, and the blood vessels are not warmed, so the hands and feet become cold and afraid of cold. Clear and long urine and loose stools are caused by cold evil injuring Yang. The tongue is purple or light fat, the coating is white and smooth, and the pulse is sunken and astringent or sunken and tight, all of which are signs of cold evil injuring Yang and blood stagnation. Treatment: Warming Yang and expelling cold, activating blood circulation and resolving blood stasis. Radix et Rhizoma ginseng and Radix et Rhizoma pseudostellariae (The Good Formula for Women) combined with Tao Hong Si Wu Tang (The Golden Guide to Medicine). In this formula, ginseng, Radix et Rhizoma, ginger and jujube benefit Qi and warm Yang to expel Yin and cold; peach kernel, safflower, angelica, red peony, Chuanxiong and Shu Di Huang invigorate Blood and resolve blood stasis. Addition and subtraction: if the cold is severe, add Cinnamon, Cornu Cervi Pantotrichum, Epimedium, Cuscuta; if the blood stasis is obvious, add Salvia, Curcuma, Yanhuo, etc. 4.Phlegm and stasis intertwine Main symptoms: In addition to localized pain in the limbs, head or chest, the patient is mostly obese, accompanied by chest tightness, abdominal stuffiness, white face, unheated hands and feet, drowsiness and other symptoms. The tongue is dark or fat and tender, the tongue coating is white and smooth or thick and greasy, and the pulse is stringent and slippery. Analysis: Phlegm evil is both a pathological product and a pathogenic factor. If phlegm evil stops in the body and blocks Yang Qi, it can lead to poor Qi and blood flow and stasis of blood. If the phlegm is blocked in the limbs, the limbs will be painful; if it stays in the brain, the headache; if it stops in the chest, the chest will be painful and stuffy in the chest. Generally, fat people have more phlegm and this type of patient is more obese. If phlegm and dampness block the operation of Yang Qi and do not warm the body, the face is white, the hands and feet are not warm, and there is drowsiness. The tongue is dark or fat and tender, the coating is white and smooth or thick and greasy, and the pulse is string and slippery, all due to phlegm-dampness blocking the ligament. Treatment: Warming phlegm-drink and activating blood circulation to remove blood stasis. Remedy: Er Chen Tang (Taiping Huimin Hodong Bureau Formula) combined with Tao Ren Hong Hua Decoction (Suan Medical Case). In this formula, Radix et Rhizoma, Chen Pi, Poria and Radix et Rhizoma are used to resolve phlegm and move Qi; Salviae Miltiorrhizae, Peach kernel, Safflower, Radix Aromaticus, Radix et Rhizoma Yanhuo, Green Peel, Radix Angelicae Sinensis, Rhizoma Chuanxiong and Radix Rehmanniae are used to move Qi and invigorate Blood, nourish Blood and nourish deficiency. Addition and subtraction: for heavy phlegm and dampness, add Gua Bao and Zhu Ru as appropriate; for blood vessels, add Gui Zhi, Allium, Panax notoginseng, Sandalwood, etc. (2) Commonly used Chinese patent medicine 1, compound Danshin Drops is a folk formula processed, mainly composed of Danshin, Chuanxiong, Tao Ren, Safflower and other drugs, with the efficacy of activating blood circulation, removing blood stasis, moving Qi and relieving pain, widely used in the treatment and prevention of various thrombotic vascular diseases. It is well made and easy to carry and take. It has the characteristics of reliable efficacy and little side effects. 2.Hemifu Bangyu Wan is a pill of Hemifu Bangyu Tang, which can be used for the treatment and prevention of various thrombotic vascular diseases and myeloproliferative diseases. Western medical treatment (a) General treatment For thrombotic diseases, it is more important to actively prevent them (tertiary prevention), including good dietary habits, light diet and proper exercise; active treatment to control blood lipids, blood pressure and blood sugar. For those who have family history of thrombotic diseases, timely prevention and treatment are required. If once it occurs, more active interventions should be taken and complications should be prevented and treated. Currently, the prevalent preventive measures worldwide, mainly for high-risk patients, are long-term prophylaxis with enteric aspirin, 50mg-100mg per day, which can greatly reduce the incidence of thrombophilia. It is also necessary to regularly review blood lipids, blood pressure, blood sugar, blood analysis, coagulation function, cardiac and vascular ultrasound, etc. Therapeutic drugs for thrombosis can be used in certain doses to prevent thrombosis. Prophylactic antithrombotic therapy is often used in patients at high risk for thrombosis in specific high-risk settings such as surgery, trauma, and thrombolysis in order to prevent thrombosis or recurrence. For thrombosis in the venous system, emphasis should be placed on avoiding factors that cause slowing of blood flow, such as early removal from bed for surgical patients, regular movement of the lower extremities for prolonged flight travel, and postoperative use of antithrombotic drugs for patients with major surgery or severe trauma. For hospitalized patients, risk assessment should be routinely performed, and prophylactic treatment using pre-prepared prophylaxis protocols should be used according to the risk stratification. Superficial thrombosis often resolves spontaneously and does not require specific treatment. For deep or organ venous or arterial thrombosis, in addition to active treatment of the primary disease, different treatment methods should be used according to the lesion site, the functional damage of the organ or limb caused by arterial or venous thrombosis and its progress rate: medical antithrombotic, thrombolytic treatment or surgical thrombectomy treatment. (2) Drug treatment 1, antithrombotic therapy The preventive measures of venous thromboembolism include two types of drugs and devices. The main drugs are low molecular heparin, common heparin and warfarin. The device approach includes intermittent inflation compression pumps (IPC) and gradient compression stockings (GCS), both of which can be used in combination; see the 2004 American College of Chest Physicians (ACCP) antithrombotic guidelines for specific indications and usage. The goals of deep vein thrombosis (DVT) treatment are to prevent thrombus extension and pulmonary embolism, to prevent recurrence of thrombosis, and to prevent post-thrombotic syndrome, with anticoagulation as the main line of treatment. Thrombolysis should be limited to those patients with massive iliac femoral DVT at risk of gangrene secondary to venous occlusion of the limb. Vena cava filters are indicated in patients with proximal lower extremity venous thrombosis, where anticoagulation is contraindicated or a complication, and in patients with recurrent pulmonary embolism with adequate anticoagulation and pulmonary thrombectomy or pulmonary thromboendarterectomy. Surgical and interventional treatment is limited to cases where venous gangrene may occur, in order to save the limb. Anticoagulation is the basic treatment for venous thromboembolism, and low-molecular heparin and warfarin are started simultaneously with an international normalized ratio (INR) of between 2,0 and 3,0, with discontinuation of low-molecular heparin and continuation of warfarin after two consecutive days. For the treatment of venous thromboembolism, heparin should only be applied intravenously and monitored for APTT. In addition to active treatment, warfarin must be taken for a period of time with monitored blood at regular follow-up after discharge to prevent recurrence of thromboembolism. The duration of secondary prevention, i.e. warfarin use, should be determined according to the patient’s risk stratification and adjusted as appropriate. If the occurrence of venous thromboembolism (VTE) has a clear trigger, such as DVT after trauma and surgery, and no other risk factors, warfarin anticoagulation for 3 months is sufficient; if the trigger for the occurrence is less severe or clear, or if other risk factors exist, such as severe untreated disease, remaining bedridden, or having diabetes, anticoagulation for 6 months is required. Recurrent VTE, VTE of easy or unknown origin, malignancy with VTE should be anticoagulated for a long time or for life. The drugs to dissolve the formed thrombus are intravenous, and there is no internationally recognized oral “clot-busting” drug (thrombolytic drug) so far. Warfarin and heparin (including low-molecular heparin) are anticoagulants that prevent the formation of new blood clots, but they have no direct effect on the dissolution of existing blood clots. The fresher or newly formed thrombus is, the easier it is to dislodge and cause embolism. Inhibiting new thrombus formation also prevents the possibility of deep vein thrombosis or pulmonary embolism or cerebral embolism in patients with atrial fibrillation. With the imminent introduction of the oral direct thrombin inhibitor Ximelagatran and the oral factor Xa inhibitor BAY-59-7939, anticoagulation therapy will undergo a great change, and the anticoagulation clinic alone will gradually decrease or disappear, gradually replaced by a thrombosis clinic or center, and the history of monitored dosing will be gone. The history of monitored drug administration will be gone, and warfarin will be replaced.