This is a common disease of the elderly, thromboembolic disease includes thrombosis and embolism, and can occur anywhere in the circulation in the heart chambers, arteries or veins. If the blood clots in a certain area and forms a blood clot, it is called thrombosis; if the formed clot breaks away from its original position and blocks other parts of the blood flow, it is called embolism.
I. Symptoms and signs
1.Venous thrombosis
It is the most common. It is common in deep veins, such as iliac vein, femoral vein, terminal mesenteric vein and portal vein, etc. Venous thrombosis of lower limbs is especially common in elderly people, and its common causes are surgery, trauma, malignant tumor and vasculitis. However, most of the causes are unknown. The thrombosis type is mostly red blood cell thrombosis myofibrin thrombosis.
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 edema, swelling and pain in the lower limbs, skin color change, ascites, etc. ○3 Pulmonary infarction caused by dislodged thrombus, etc.
2.Arterial thrombosis
Mostly seen in the cerebral artery of coronary artery, mesenteric artery and limb artery, etc. Age is an important factor in coronary artery atherosclerosis heart disease, coronary heart disease can also be a common heart disease in the elderly and directly threaten their lives. The high prevalence of cerebrovascular disease, high recurrence rate, and high degree of disability bring great pain to the middle-aged and elderly. The type of thrombosis is mostly platelet thrombosis in the early stage, followed by fibrin thrombosis.
Clinical manifestations include: ○1 sudden onset, severe local pain, such as angina pectoris, headache, abdominal pain, severe pain in the limbs, etc. ○2 tissue ischemia at the blood supply site, abnormal function due to hypoxia, such as heart failure, cardiogenic shock, arrhythmia, impaired consciousness and hemiparesis, etc. ○3 Symptoms and signs related to cerebral embolism, myocardial infarction, renal embolism and splenic embolism caused by thrombus dislodgement, ○4 Clinical manifestations caused by ischemic necrosis of blood-supplying tissues, such as fever, etc.
3.Capillary thrombosis
It is commonly seen in diffuse intravascular coagulation, snowy thrombocytopenic purpura and hemolytic uremic syndrome. The manifestations often lack specificity and are mainly microcirculatory disorders, skin mucosal embolic necrosis, organ dysfunction, bleeding tendency, etc.
Second, the disease etiology
1.Vascular endothelial injury
The integrity of the vascular endothelium, the anti-platelet aggregation and anti-coagulant activity of vascular endothelial cells are important conditions for keeping blood flow smooth. When endothelial cells are damaged by mechanical, infectious immune and vascular lesions, thrombosis can be induced by the following mechanisms: ○1 reflex vasoconstriction, etc., which slows blood flow and stagnates blood, ○2 subendothelial tissue exposure, vWF release, etc., which leads to platelet adhesion, aggregation and release in the vessel wall, ○3 TF expression and release, subendothelial basal collagen fiber exposure to initiate coagulation process, ○4 endothelial platelet aggregation (prostacyclin I2, etc.) and anticoagulation (heparan sulfate, etc.) are impaired, accelerating the coagulation process.
2. Platelet activation
Platelet adhesion and aggregation outside the damaged endothelium, leading to platelet activation and release reaction, through the following mechanisms involved in snow mountain formation: ○1 platelet aggregation directly form platelet thrombus, ○2 release PF-3 to participate in the coagulation process ○3 initiate arachidonic acid metabolism, TXA2, etc., constrict blood vessels and platelet agglutination, ○4 release SHT and ADP, etc., accelerate the two-phase aggregation of platelets ○5 under certain conditions, direct activation of F Ⅻ, F Under certain conditions, F Ⅻ and D Ⅺ are directly activated to initiate the coagulation process.
3.Coagulation process initiation
Under the condition of increased blood coagulation, the coagulation process is activated due to vascular endothelial damage, platelet activation and other factors to promote thrombosis: ○1 activation of coagulation, formation of fibrin thrombus, ○2 formation of thrombin in the coagulation process, feedback to accelerate the coagulation process, ○3 activation of fibrinogen by thrombin and other enzymes to initiate the fibrinolytic process, ○4 thrombin to guide irreversible platelet aggregation and release reaction, etc.
4.Decrease in anticoagulant activity
Reduced physiological anticoagulant activity of human body is an important condition for thrombus formation. -II) deficiency, etc.
5.Decreased fibrinolytic activity
Clinically, these include: ○1 abnormal fibrinogen structure and function, such as abnormal fibrinogenemia, ○2 impaired release of fibrinogen activator (PA), and ○3 excessive fibrin activator inhibitor (PAI), which lead to a decrease in the body’s ability to clear fibrin and facilitate thrombus formation and expansion.
6.Abnormal blood flow
Systemic or local blood flow stagnation and slowness caused by various reasons are important factors for thrombosis, such as hyperfibrinogenemia, hyperlipidemia, dehydration, hyperviscosity syndrome due to erythropoiesis and circulatory disorders, etc. It can promote thrombosis through the following mechanisms: ○1 Red blood cells aggregate into clusters and form red thrombi ○2 Promote platelet adhesion to endothelium and aggregation and release reaction ○3 Damage vascular endothelium and initiating the coagulation process.
III. Pathophysiology
1.Vascular endothelial injury
The integrity of the vascular endothelium and the anti-platelet aggregation and anti-coagulant activity of the endothelial cells are important for maintaining blood flow. When endothelial cells are damaged by mechanical, infectious immune and vascular lesions, thrombosis can be induced by the following mechanisms: ○1 reflex vasoconstriction, etc., which slows blood flow and stagnates blood, ○2 subendothelial tissue exposure, vWF release, etc., which leads to platelet adhesion, aggregation and release in the vessel wall, ○3 TF expression and release, subendothelial basal collagen fiber exposure to initiate the coagulation process, ○4 endothelial platelet aggregation (prostacyclin I2, etc.) and anticoagulation (heparan sulfate, etc.) are impaired, accelerating the coagulation process.
2. Platelet activation
Platelet adhesion and aggregation outside the damaged endothelium, leading to platelet activation and release reaction, through the following mechanisms involved in snow mountain formation: ○1 platelet aggregation directly form platelet thrombus, ○2 release PF-3 to participate in the coagulation process ○3 initiate arachidonic acid metabolism, TXA2, etc., constrict blood vessels and platelet agglutination, ○4 release SHT and ADP, etc., accelerate the two-phase aggregation of platelets ○5 under certain conditions, direct activation of F Ⅻ, F Under certain conditions, F Ⅻ and D Ⅺ are directly activated to initiate the coagulation process.
3.Coagulation process initiation
Under the condition of increased blood coagulation, the coagulation process is activated due to vascular endothelial damage, platelet activation and other factors to promote thrombosis: ○1 activation of coagulation, formation of fibrin thrombus, ○2 formation of thrombin in the coagulation process, feedback to accelerate the coagulation process, ○3 activation of fibrinogen by thrombin and other enzymes to initiate the fibrinolytic process, ○4 thrombin to guide irreversible platelet aggregation and release reaction, etc.
4.Decrease in anticoagulant activity
Reduced physiological anticoagulant activity of human body is an important condition for thrombus formation. -II) deficiency, etc.
5.Decreased fibrinolytic activity
Clinically, these include: ○1 abnormal fibrinogen structure and function, such as abnormal fibrinogenemia, ○2 impaired release of fibrinogen activator (PA), and ○3 excessive fibrin activator inhibitor (PAI), which lead to a decrease in the body’s ability to clear fibrin and facilitate thrombus formation and expansion.
6.Abnormal blood flow
Systemic or local blood flow stagnation and slowness caused by various reasons are important factors for thrombosis, such as hyperfibrinogenemia, hyperlipidemia, dehydration, hyperviscosity syndrome due to erythropoiesis and circulatory disorders, etc. It can promote thrombosis through the following mechanisms: ○1 Red blood cells aggregate into clusters and form red thrombi ○2 Promote platelet adhesion to endothelium and aggregation and release reaction ○3 Damage vascular endothelium and initiating the coagulation process.
IV. Diagnostic tests
The main points of diagnosis of this disease are.
1, in hypercoagulable or non-thrombotic pre-state underlying diseases such as atherosclerosis, diabetes, renal disease, pregnancy, easy embolism, recent surgery and trauma, long-term use of contraceptives, etc. It should be noted that some elderly people are healthy in appearance but have a physiological pre-thrombotic state.
2.Signs and symptoms of various thrombosis and thromboembolic diseases.
3.Imaging examination Such as angiography, vascular ultrasound Doppler, CT, MRI, electrical impedance, etc.
4.Hematological examination can be carried out according to the above six factors of thrombosis, combined with the patient’s condition. If coagulation thrombosis is mainly related to hypercoagulable state, coagulation image, coagulation activation molecular markers, AT-III, APC-R and other tests are feasible; if coagulation thrombosis involves vascular lesions, endothelin, vWF, TM, angiography and imaging tests are feasible.
V. Treatment plan
The aim is to improve the pre-thrombotic state or hypercoagulable state, prevent thrombus expansion and new thrombus formation, dissolve thrombus, reconstruct blood flow channels, and restore blood supply and function of related tissues and organs.
1.Treatment of underlying diseases: such as prevention and control of arteriosclerosis, control of diabetes, etc.
2.General treatment: bed rest, elevate the resting limb of venous thrombosis.
3.Symptomatic treatment: including pain relief, correction of organ failure, etc.
4.Thrombotic drugs.
(1) Anticoagulation therapy: ○1. Heparin and small molecular weight heparin: mainly used for the treatment of recently occurred thrombotic diseases. The initial dose of 10,000-20,000U/d, titrated once every 8h, after which the dose is adjusted with AFTT as the monitoring index, so that the AFTT is prolonged by 1-2 times, and the total course of treatment should not exceed 10d. The small molecular weight heparin introduced in recent years has a stronger anti-factor Xa effect, weaker anti-thrombin, and less AT-III-dependent. III dependence, less thrombocytopenia, high bioavailability (80%) and half-life (24h) of subcutaneous injection, etc., which have been widely used in clinical practice. Dose 30000U/d, subcutaneous book society, 1-2/d. ○2, AT-III: mainly used for those with low AT-III level, can enhance the anticoagulant effect of heparin, reduce the bleeding complications of heparin, commonly used dose 1500U/d, intravenous drip, 3 -5d1 course of treatment. ○3, coumarins: by competing with vitamin K, blocking the biosynthesis of vitamin K-dependent priming. Mainly used for the prevention of thrombosis and maintenance therapy after heparin anticoagulation therapy. Commonly used is warfarin, the first dose of 10-15mg/d, divided into oral doses, followed by 5-10mg/d, using PT as a monitoring indicator to adjust the dosage, so that PT prolongation 1.5-2.0 times or INR = 2.0-3.0 is the optimal treatment dose.
(2) Anti-platelet drug therapy: ○1. Aspirin: Anti-platelet aggregation effect is exerted by inhibiting cyclooxygenase, blocking arachidonic acid metabolism and reducing the claim of TXA2. It is mainly used for the prevention of thrombophilia and maintenance treatment after heparin application. The commonly used dose is 150-300mg/d in divided doses. ○2.Dipyridamole: It inhibits platelet aggregation by increasing the level of cAMP in platelets through inhibiting phosphodiesterase or increasing adenylyl cyclase activity, and has the effect of increasing the claim of prevascular cyclin (PGI2) and inhibiting the production of platelet TXA2. Dose: 200-600mg/d intravenously for 3-5 d. It is generally believed that small oral doses have no therapeutic effect. Ticlopidine is a specific anti-platelet aggregation agent. The mechanism of action is: blocking platelet fibrinogen receptor (GPIb) and fibrinogen binding, enhancing adenylyl cyclase activity, increasing the level of cAMP in platelets, stabilizing platelet membrane and reducing TXA2 synthesis. This drug can be used for the prevention and treatment of thrombotic diseases. Commonly used dose is 250-500mg/d, taken orally in a single dose or in divided doses, and can be used for 5-7d and longer.
(3) Thrombolytic therapy is mainly used for the treatment of newly formed thrombosis or thromboembolism: arterial thrombosis should preferably be performed within 3h of onset and no later than 6h, and venous thrombosis should also be performed within 24 hours of onset and no later than 5d.