This is a common disease of the elderly, thromboembolic disease is a condition that includes thrombosis and embolism, and can occur anywhere in the blood circulation in the heart chambers, arteries, or veins. If the blood coagulates in one part of the body to form a clot, it is called thrombosis; if the clot breaks away from its original position and blocks other parts of the bloodstream, it is called embolism. I. Symptoms and signs 1. Venous thrombosis is the most common. Commonly found in deep veins, such as: iliac vein, femoral vein, mesenteric vein and portal vein, etc., the elderly especially common lower extremity venous thrombosis, the common causes for surgery, trauma, malignant tumors, vasculitis and so on. The common causes are surgery, trauma, malignant tumor, vasculitis and so on. Thrombus type is mostly erythrocyte thrombus myofibrin thrombus. The main manifestations are: ○1 local swelling and pain due to thrombosis ○2 clinical abnormalities due to impaired blood return at the distal end of the thrombus, such as lower limb edema, swelling and pain, skin color change, ascites, etc. ○3 thrombus dislodgement caused by pulmonary infarction, etc. 2, arterial thrombosis is seen in the coronary arteries of the cerebral artery, mesenteric artery and limb arteries, etc., age is an important factor in coronary atherosclerotic heart disease, coronary artery disease can be elderly people total common heart disease, and a direct threat to their lives. The high prevalence of cerebrovascular disease, high recurrence rate, highly disabling to middle-aged and elderly people bring great pain. The type of thrombus is mostly platelet thrombus in the early stage, followed by fibrin thrombus. Clinical manifestations include: ○1 sudden onset, localized severe pain, such as angina, headache, abdominal pain, severe pain in the limbs, etc. ○2 ischemia in the blood-supplying part of the tissue, functional abnormalities due to hypoxia, such as cardiac failure, cardiogenic shock, cardiac arrhythmia, impaired consciousness and hemiparesis. ○3 Thrombus dislodgement causing cerebral embolism, myocardial infarction, renal embolism, splenic embolism and other related signs and symptoms, ○4 ischemic necrosis of blood-supplying tissues triggered by the clinical manifestations, such as fever, etc. ○3 capillary thrombosis is commonly seen in disseminated intravascular coagulation, snowy mountain thrombocytopenic purpura, and hemolytic uremic syndrome. The performance often lacks specificity, mainly for microcirculation disorders, skin and mucous membrane embolic necrosis, organ dysfunction, bleeding tendency. Second, the etiology of the disease 1, vascular endothelial damage to the integrity of the vascular endothelium, vascular endothelial cells, anti-platelet aggregation and anticoagulant activity is to maintain blood flow is an important condition. When the vascular endothelial cells are damaged due to mechanical, infectious immunity and vascular lesions, thrombosis can be induced by the following mechanisms: ○1 reflex vasoconstriction and other factors slowing down blood flow and stagnation of blood, ○2 exposure of subendothelial tissues, release of vWF, etc. leading to platelet adhesion, aggregation, and release of platelets in the vascular wall, ○3 expression and release of TF and exposure of subendothelial collagen fibers to initiate the coagulation process, ○4 endothelial platelet aggregation, and ○4 platelet aggregation and release of platelets. The platelet activation platelet adhesion and aggregation outside the damaged intima leads to platelet activation and release reaction, which is involved in the formation of snow mountain through the following mechanisms: ○1 platelet aggregation directly forms platelet thrombus, ○2 release of PF-3 is involved in the coagulation process, and ○3 initiates the metabolism of arachidonic acid, TXA, and vWF release, which leads to the formation of arachidonic acid. enoic acid metabolism, TXA2, etc., vasoconstriction and platelet aggregation, ○4 release of SHT and ADP, etc., to accelerate platelet biphasic aggregation, ○5 under certain conditions, the direct activation of F Ⅻ, Ⅺ, to start the coagulation process. 3, coagulation process initiation in the blood coagulability increased under the conditions of the conditions of the blood, due to vascular endothelial damage, platelet activation and other factors to cause the coagulation process initiated to promote the formation of thrombus: ○1 coagulation activation The formation of fibrin thrombus, ○2 thrombin formed during the coagulation process, feedback acceleration of the coagulation process, ○3 thrombin and other activation of fibrinogen, initiating the process of fibrinolysis, ○4 thrombin to guide the irreversible platelet aggregation and release reaction, etc. 4, anticoagulant activity is reduced the human body’s physiological anticoagulant activity is reduced is an important condition for the formation of blood clots, the human body caused by the common cause of anticoagulant activity is reduced are: ○1 AT The common causes of reduced anticoagulant activity are: ○1 AT-III reduction or deficiency ○2 PC and PS deficiency ○3 Anti-protein c phenomenon (APC-R) caused by structural abnormalities of FV, etc. ○4 Heparin cofactor II (HC-II) deficiency, etc. 5. Reduced fibrinolytic activity is commonly seen in the clinic. Abnormalities, such as abnormal fibrinogenemia, ○2 fibrinogen activator (PA) release disorders, ○3 fibrinogen activator inhibitor (PAI) is too much, these factors lead to a decrease in the body’s ability to clear fibrin, which is conducive to the formation and expansion of thrombus. 6, blood flow abnormalities caused by a variety of causes of systemic or local blood stagnation, slow blood flow is an important factor in the formation of thrombosis, such as hyperfibrinogenemia, Hyperlipidemia, dehydration, hyperviscosity syndrome due to erythrocytosis and circulatory disorders, etc. It can promote thrombosis through the following mechanisms: ○1 erythrocyte aggregation into clusters, the formation of red thrombus ○2 promotion of platelet adhesion with endothelium and aggregation, release reaction ○3 damage to the vascular endothelium, initiating the coagulation process. Third, pathophysiology 1, vascular endothelial damage to the integrity of the vascular endothelium, vascular endothelial cells, anti-platelet aggregation and anti-coagulant activity is an important condition to maintain the smooth flow of blood. When the vascular endothelial cells are damaged due to mechanical, infectious immunity and vascular lesions, thrombosis can be induced by the following mechanisms: ○1 reflex vasoconstriction and other factors slowing down blood flow and stagnation of blood, ○2 exposure of subendothelial tissues, release of vWF, etc. leading to platelet adhesion, aggregation, and release of platelets in the vascular wall, ○3 expression and release of TF and exposure of subendothelial collagen fibers to initiate the coagulation process, ○4 endothelial platelet aggregation, and ○4 platelet aggregation and release of platelets. The platelet activation platelet adhesion and aggregation outside the damaged intima leads to platelet activation and release reaction, which is involved in the formation of snow mountain through the following mechanisms: ○1 platelet aggregation directly forms platelet thrombus, ○2 release of PF-3 is involved in the coagulation process, and ○3 initiates the metabolism of arachidonic acid, TXA, and vWF release, which leads to the formation of arachidonic acid. enoic acid metabolism, TXA2, etc., vasoconstriction and platelet aggregation, ○4 release of SHT and ADP, etc., to accelerate platelet biphasic aggregation, ○5 under certain conditions, the direct activation of F Ⅻ, Ⅺ, to start the coagulation process. 3, coagulation process initiation in the blood coagulability increased under the conditions of the conditions of the blood, due to vascular endothelial damage, platelet activation and other factors to cause the coagulation process initiated to promote the formation of thrombus: ○1 coagulation activation The formation of fibrin thrombus, ○2 thrombin formed during the coagulation process, feedback acceleration of the coagulation process, ○3 thrombin and other activation of fibrinogen, initiating the process of fibrinolysis, ○4 thrombin to guide the irreversible platelet aggregation and release reaction, etc. 4, anticoagulant activity is reduced the human body’s physiological anticoagulant activity is reduced is an important condition for the formation of blood clots, the human body caused by the common cause of anticoagulant activity is reduced are: ○1 AT The common causes of reduced anticoagulant activity are: ○1 AT-III reduction or deficiency ○2 PC and PS deficiency ○3 Anti-protein c phenomenon (APC-R) caused by structural abnormalities of FV, etc. ○4 Heparin cofactor II (HC-II) deficiency, etc. 5. Reduced fibrinolytic activity is commonly seen in the clinic. Abnormalities, such as abnormal fibrinogenemia, ○2 fibrinogen activator (PA) release disorders, ○3 fibrinogen activator inhibitor (PAI) is too much, these factors lead to a decrease in the body’s ability to clear fibrin, which is conducive to the formation and expansion of thrombus. 6, blood flow abnormalities caused by a variety of causes of systemic or local blood stagnation, slow blood flow is an important factor in the formation of thrombosis, such as hyperfibrinogenemia, Hyperlipidemia, dehydration, hyperviscosity syndrome due to erythrocytosis and circulatory disorders, etc. It can promote thrombosis through the following mechanisms: ○1 red blood cells aggregated into clusters, forming a red thrombus ○2 promotion of platelet adhesion and aggregation of platelets and endothelium and release reaction ○3 damage to the vascular endothelium, initiating the coagulation process. Fourth, diagnostic examination of this disease diagnostic points are: 1, in hypercoagulable or non-thrombotic pre-thrombotic state of the underlying disease such as atherosclerosis, diabetes mellitus, renal disease, pregnancy, prone to thrombosis, recent surgery and trauma, long-term use of contraceptives and so on. It should be noted that some elderly people are healthy in appearance but there is a physiological pre-thrombotic state.2. Symptoms and signs of various thrombosis and thromboembolic diseases.3. Imaging tests such as angiography, vascular ultrasound Doppler, CT, MRI, electrical impedance, etc.4. Hematology can be examined according to the above six factors of thrombosis, combined with the patient’s condition, and selected items. If thrombosis is mainly related to hypercoagulability, it is feasible to conduct tests on coagulation image, molecular markers of coagulation activation, AT-III, APC-R, etc. If thrombosis involves vascular lesions, it is feasible to conduct tests on endothelin, vWF, TM, angiography and imaging. The purpose of treatment program is to improve the pre-thrombotic state or hypercoagulable state, to prevent thrombus expansion and new thrombus formation, to dissolve thrombus, to rebuild the blood flow channel, to restore blood supply and function of related tissues and organs.1.Treatment of underlying diseases: such as prevention and treatment of atherosclerosis, control of diabetes mellitus, etc.2.General treatment: bed rest, elevation of the resting limb of venous thrombosis.3.Symptomatic treatment: including pain relief, correction of organ function and failure, etc.4.Thrombosis treatment: including pain relief, correction of organ function and failure, etc..5. Thrombotic drugs: (1) anticoagulant therapy: ○1, heparin and small molecular weight heparin: mainly used in the treatment of thrombotic diseases that occurred recently. Initial dose 10000-20000U/d, titrate once every 8h, later adjust the dose with AFTT as the monitoring index, in order to make AFTT prolonged 1-2 times as appropriate, the total course of treatment should not be more than 10d. In recent years, the introduction of small molecular weight heparin has a stronger role of anti-factor Xa, antithrombin as a weak, less dependent on AT-III, less dependent on AT-III, and more effective. The recent introduction of small molecular weight heparin has the advantages of stronger anti-Factor Xa effect, weaker antithrombin effect, less dependence on AT-III, less thrombocytopenia, high bioavailability (80%) and half-life (24h) of subcutaneous injection, etc., and has been widely used in the clinic. Dose 30000U/d, subcutaneous injection, 1-2/d. ○2, AT-III: mainly used for people with low AT-III level, can enhance the anticoagulant effect of heparin and reduce the bleeding complications of heparin, commonly used dose of 1500U/d, intravenous drip, 3-5d1 course of treatment. The usual dose is 1500U/d, intravenous drip, 3-5d1 course of treatment. 3.Coumarins：Block the biosynthesis of vitamin K-dependent priming by competing with vitamin K. Mainly used for thrombosis prevention and maintenance therapy after heparin anticoagulation. Commonly used for warfarin, the first dose of 10-15 mg / d, divided oral, followed by 5-10 mg / d, PT as a monitoring indicator to regulate the dosage, so that PT prolongation of 1.5-2.0 times or INR = 2.0-3.0 for the optimal therapeutic Dosage. (2) Antiplatelet drug therapy: ○1. Aspirin: It plays the role of antiplatelet aggregation by inhibiting cyclooxygenase, blocking the metabolism of arachidonic acid, and reducing the claim of TXA2. It is mainly used for prevention of thrombosis and maintenance therapy after heparin application. The common dose is 150-300mg/d in divided doses. ○2. Dipyridamole: It can inhibit platelet aggregation by inhibiting phosphodiesterase or increasing adenylyl cyclase activity and increasing cAMP level in platelets, and it has the effect of increasing the claim of pre-vascular cyclin (PGI2) and inhibiting the generation of platelet TXA2. Dosage: 200-600mg/d, intravenous drip, for 3-5d. It is generally believed that small oral doses have no therapeutic effect. ○3, Ticlopidine: specific antiplatelet aggregation agent. The mechanism of action is: blocking platelet fibrinogen receptor (GPIb) and fibrinogen binding, enhance the activity of adenylyl cyclase, increase the level of cAMP in platelets, stabilize the platelet membrane to reduce TXA2 synthesis. This drug can be used in the prevention and treatment of thrombotic diseases. Commonly used dose is 250-500mg/d, taken at once or in divided oral doses, and can be used for 5-7d and longer. (3) Thrombolytic therapy is mainly used in the treatment of newly formed thrombus or thromboembolism: arterial thrombosis should be carried out preferably within 3h of the onset of the disease and not later than 6h, and venous thrombosis should also be carried out within 24 hours of the onset of the disease and not later than 5d.