I. Definition of thrombosis
Thrombosis is the process of forming a haemostatic clot when the blood vessels of human tissues are damaged, and the process of thrombosis begins with platelet adhesion and aggregation at the site of injury to form a platelet plug, on the basis of which the coagulation system is activated to form a thrombin. Thrombin is activated to form thrombin, which turns fibrin, the raw material for thrombosis, into a hemostatic fibrin clot. Thrombosis is an important protective mechanism in the body to prevent excess blood from spilling out of the blood vessels of an individual in case of trauma. In addition to thrombogenic factors in the body, there are mechanisms that inhibit thrombosis, called anticoagulation, which limits the hemostatic process to the site of injury and inhibits abnormal thrombus formation in the body. The hemostatic thrombus formed by physiological hemostasis must be removed in due course after the complete hemostatic mission, and the process by which the body removes the formed thrombus is called (fibrinolysis). If fibrinolysis is too strong, the thrombus will be dissolved and cleared soon after formation, which is bound to cause bleeding; if fibrinolysis is weakened, the thrombus will not be cleared timely and effectively, and the mechanism to regulate fibrinolysis is antithrombolysis.
Thrombosis and thrombolysis, coagulation and anticoagulation, fibrinolysis and antifibrinolysis are a pair of “yin and yang balance”, on the one hand, to ensure the normal flow of blood in the blood vessels, neither thrombosis nor bleeding; on the other hand, to limit the hemostatic process to the local injury, so as not to cause systemic thrombosis due to local injury; thirdly, to ensure that in The third can ensure that after the complete hemostatic mission of the thrombus, it is removed in a timely and effective manner.
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 tissue or organ.
Embolism can occur in any part of the cardiovascular system, even in diffuse intravascular coagulation (DIC), and it often occurs in the arteries or veins of the body. Physiologic thrombosis occurs outside the blood vessels as a protective mechanism in response to trauma (haemostasis), whereas pathologic thrombosis occurs inside the blood vessels, causing tissue ischemia or stasis, resulting in vascular events and even vascular death. Embolism can occur in systemic arteries or pulmonary arteries, but not in the venous system.
The author believes that thrombotic diseases can be called thrombo-embolic diseases, vaso-thrombotic diseases, or thrombosis-related diseases. diseases, the connotation and extension of the three are different, but the basic meaning is the same. The author is also willing to classify thrombotic diseases into three main categories, namely atherothrombosis, venous thrombo-embolism and arterial embolism.
Atherosclerosis thrombosis
Arterial thrombosis mainly involves cardiovascular, cerebrovascular and peripheral arterial vessels (lower limb arteries, renal arteries, etc.), and most of the thrombosis in these areas is formed on the basis of atherosclerosis (atherosclerosis) plaque rupture, i.e., the damage to the inner wall of blood vessels leads to thrombosis, which seriously leads to myocardial infarction (myocardial infarction) and cerebral infarction (cerebral infarction). cerebral infarction and acute lower limb ischemia and necrosis. Therefore, atherosclerotic thrombosis is the process of plaque rupture and thrombosis on the basis of atherosclerosis, leading to vascular events and even vascular death.
Atherosclerosis is a decades-long process, plaque rupture is only an instantaneous event, and thrombus formation is only 10 seconds, but it leads to mortality and morbidity, no thrombosis, no events. The occurrence of a vascular event in one vascular bed implies that other vascular beds will also occur or are susceptible to similar vascular events. Peripheral arterial disease itself mainly affects quality of life and disability, but such patients have a significantly increased risk of future myocardial infarction, cerebral infarction, or vascular death, and the 5-year survival rate for patients with severe lower extremity arterial disease is almost the same as that for colon cancer.
In terms of their pathophysiological basis, acute myocardial infarction (coronary artery thrombosis) and acute cerebral infarction (cerebral artery thrombosis) are actually the same type of disease and can be collectively referred to as atherosclerotic thrombosis, differing only in the site of occurrence and clinical manifestations, but the principles of treatment should be the same, i.e., opening the occluded blood vessels and maintaining them open. Atherosclerotic thrombosis also includes peripheral obstructive artery disease (POAD).
The author classifies atherosclerotic thrombosis into two major categories: occlusive and non-occlusive.
Occlusive (oclusive) means that the thrombus formed on the basis of ruptured atherosclerotic plaque completely blocks the arterial lumen, leading to ST segment elevation myocardial infarction (STEMI), cerebral infarction, and acute lower limb ischemia (ischemia), necrosis ( necrosis) or gangrene (gangrene).
Non-occlusive (non-occlusive) is further divided into two categories: stable and unstable. Stable is the episodic ischemic clinical manifestations caused by unruptured fixed stenotic plaques, including stable angina, “chronic ischemic encephalopathy” (such as vascular dementia, standing dizziness, etc.) and intermittent claudication of the lower extremities. claudication), etc. Unstable (unstable) is the presence of plaque rupture and thrombosis, but the vessel is not occluded and blood flow is not interrupted, including non-ST segment elevation ACS, transient ischemia attack (TIA) and intermittent claudication based on the lower extremity. resting limb pain.
Risk factors for atherosclerotic thrombotic disease include two major categories, one is untreatable and irreversible risk factors, including genetics, gender and age; the other is treatable and reversible risk factors, mainly including hypertension, dyslipidemia, diabetes, smoking, etc. These acquired risk factors are all lifestyle-related and are often part of the metabolic syndrome. Genetics cannot be changed, gender cannot be chosen, age should be the main risk factor, and lifestyle-related risk factors determine a person’s fate.
IV. Venous thromboembolism
Venous thromboembolism (VTE) includes deep vein thrombosis (DVT) and pulmonary embolism (PE), the main complication or consequence of DVT is the occurrence of lethal (fatal or lethal) pulmonary embolism, according to foreign reports, total hip replacement The incidence of surgical fatal pulmonary embolism is 1-4 per 1000 people, and the incidence of fatal pulmonary embolism in hip fractures reaches 3.6%C12.9% (Table 1).
Death due to venous thromboembolism in the West ranks third after cardiovascular disease and malignancy, and the incidence in China is also quite high. The incidence of DVT in major surgical procedures in China is around 50%, which is very consistent with what is reported abroad. Although the incidence of venous thromboembolism in medical disease is not as concentrated as in major surgical procedures (Table 2), the overall incidence of venous thromboembolism is three times higher in internal medicine than in surgery because of the larger patient base.
Eighty percent of deep vein thrombosis has no clinical manifestations, and even if it does, it is often overlooked; pulmonary embolism often lacks specific clinical manifestations, with the result that the incidence of venous thromboembolism is high and the detection rate is very low; if there is a lack of vigilance or “unexpected”, it is difficult to diagnose venous thromboembolism clinically.
Table 1 Incidence of VTE in major orthopaedic surgery (without anticoagulation)
Surgical method
DVT
PE
Total (%)
Proximal (%)
Total(%)
Lethality(%)
Total hip arthroplasty
45C57
23C36
0.7C30
0.1C0.4
Total knee arthroplasty
40C84
9C20
1.8C7
0.2C0.7
Hip fracture surgery
36C60
17C36
4.3C24
3.6C12.9
Table 2 Incidence of VTE in medical patients (not anticoagulated)
Patient’s clinical condition
Incidence of VTE
General internal medicine patients
10-26%
Stroke
11-75%
Myocardial infarction
17-34%
Congestive heart failure
20-40%
Intensive Care Unit
25-42%
Lower extremity deep vein thrombosis is divided into proximal (proximal) and distal (distal), with proximal referring to the deep veins of the lower extremity above the N vein (popliteal), such as the femoral vein (superficial femoral vein, deep femoral vein) and the N vein, and distal referring to the deep veins of the lower leg below the N vein, including the tibial vein (anterior tibial vein, posterior tibial vein) and the peroneal vein. Proximal DVT is more prone to pulmonary embolism, especially fatal pulmonary embolism, while distal is less prone; proximal may require thrombolytic therapy while distal anticoagulation alone is sufficient; proximal is at greater risk of recurrence and often requires longer oral warfarin for secondary prevention; distal is at less risk of recurrence and may require oral warfarin for a shorter period than proximal DVT.
The risk of venous thromboembolism can be divided into three categories according to the basis of occurrence: first, serious reversible risk factors, such as surgical trauma or major surgery; second, less serious and less easily eliminated risk factors, such as most patients with medical disease and malignancy; third, idiopathic, i.e., risk factors that are not clinically detectable, such as the occurrence of venous thromboembolism in healthy young people. thromboembolism in healthy young people. In addition to injuries that lead to venous thrombosis, venous thrombosis is often associated with slow blood flow and poor drainage, and changes in blood components, such as antithrombin deficiency, abnormal fibrinogenemia, and activated protein C resistance, lead to venous thromboembolism, often referred to as thrombophilia.
The occurrence of venous thromboembolism is related to the presence or absence of risk factors, their number, intensity of exposure and duration, based on which patients can be risk stratified, i.e. risk assessment for venous thromboembolism. For example, young people with minor surgery are at low risk, patients with major general surgery are at intermediate risk, patients with major orthopedic surgery are at high risk, and elderly patients with major orthopedic surgery and medical factors associated with venous thromboembolism are at very high risk.
In addition, thrombus in the venous system can also embolize in the pulmonary artery along the blood flow, leading to more serious consequences, and fatal pulmonary embolism is the most serious complication of deep vein thrombosis. (post-thrombotic syndrome), which affects limb function.
V. Peripheral arterial embolism
According to the source of embolus, arterial embolism is classified as arterial, cardiogenic, and paradoxical embolism. Arterial embolism is an upstream to downstream embolism, in which thrombus emboli or ruptured atheromatous material from a larger vessel in the proximal segment embolizes into a small peripheral vessel, such as a non-ST-segment elevation myocardial infarction in which an attached platelet thrombus detaches and embolizes into a small peripheral artery causing microinfarction. Left cardiac origin is embolization of the left heart into peripheral arteries, such as embolization of intra-atrial appendage thrombi downstream into cerebral or limb arteries in patients with atrial fibrillation, embolization due to dislodgement of thrombotic redundancies in prosthetic valves, and embolization of left ventricular appendage thrombi into peripheral arteries in cardiomyopathy. Paradoxical embolism is the embolization of a thrombus embolus in a deep vein into a peripheral artery via an unclosed foramen ovale or other anomalous channel (atrial defect, ventricular defect, unclosed ductus arteriosus) and is likely to occur in conjunction with pulmonary embolism, when pulmonary hypertension raises right heart pressure and tends to cause a right-to-left shunt.
Arterial embolism is a mechanism for the development of non-ST-segment elevation myocardial infarction, and arterial embolism is also an important pathogenic basis for ischemic stroke, but arterial embolism is often easily overlooked in clinical practice.
VI. Diagnosis of thromboembolic disease
The diagnosis of thromboembolic disease is mainly based on medical history, physical examination and auxiliary examinations, such as electrocardiogram, cardiac troponin, brain CT examination, vascular ultrasound, angiography, etc. For atherosclerotic thrombotic diseases, assessment and detection of risk factors are very important to determine the presence or absence of disease and prognosis, and risk factor assessment is also the basis for treatment decisions. These risk factors include age, gender, family genetic history, family history of early-onset vascular thrombotic disease, blood pressure, lipids, blood glucose and its control, and smoking history. In high-risk groups, relevant risk factors should be detected early through health checkups for early and effective intervention.
For the diagnosis of venous thromboembolism, we should raise the awareness of diagnosis and clinical vigilance to the occurrence of venous thromboembolism in high-risk patients. increased D-dimer cannot diagnose venous thromboembolism, but it can be basically excluded if it is not increased. Ultrasound of the deep veins of the lower extremities is not only sensitive but also very specific for the diagnosis of deep vein thrombosis (especially proximal DVT). The diagnosis of pulmonary embolism is firstly based on the basis of occurrence and clinical manifestations, such as dyspnea or syncope when getting out of bed for the first time after major surgery, pulmonary embolism should be thought of first. The blood gas analysis is not very helpful in the diagnosis of pulmonary embolism, but it is mainly used to monitor the changes of the disease, but if the oxygen saturation decreases, the disease is more serious. CT or magnetic resonance pulmonary arteriography is the main tool for the diagnosis of pulmonary embolism, which can provide direct signs about pulmonary embolism.
The results of blood rheology cannot assist in the diagnosis or prediction of cardiovascular thrombotic disease, i.e., they cannot predict cerebral infarction or myocardial infarction. Blood rheology 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 hematological test indices, such as blood coagulation analysis.
VII. Prevention and treatment of atherosclerotic thrombosis
According to Huang Di Nei Jing, “the upper doctor treats the disease that is not yet sick, the middle doctor treats the disease that will be sick, and the lower doctor treats the disease that is already sick”. The prevention and treatment of atherosclerotic thrombosis should adopt a comprehensive prevention and treatment strategy, that is, comprehensive management (horizontal, sectional) and constant control (vertical, longitudinal). The focus should be on preventing the formation of atherosclerotic lesions, stabilizing atherosclerotic plaques from rupture, and using effective antithrombotic drugs to prevent the formation of thrombi that block blood vessels after plaque rupture and lead to serious consequences.
For atherosclerosis thrombosis disease, the lesion begins in adolescence and the onset begins in middle and old age; the death and disability lies in the event, the first offender is thrombus; to prevent from childhood, benefit life and prolong life.
Through publicity and education, we should advocate a civilized and healthy lifestyle, such as eating less and being more active, controlling and restructuring the total amount of diet, and quitting smoking and drinking. The total amount control can be summarized as “drink soup first and then eat, 80% full without additional meals”; the structure adjustment can be understood as “not too sweet, not too salty, not too greasy”. Start with children to avoid being overweight or obese. Detection of body mass index and waist circumference, abdominal circumference is very important to determine overweight / obesity and metabolic syndrome, but is a very troublesome thing, the author recommends a simple method, is the abdomen flat chest (bone) when standing, supine position flat or below the pubic bone (part), under the bed to reach things without gas. Regular checkups and timely detection of risk factors such as hypertension, dyslipidemia and diabetes, control these risk factors through lifestyle changes and drug interventions to delay or avoid the occurrence and development of atherosclerotic lesions. Even with lesions, plaque rupture can be avoided through behavioral and pharmacological interventions, and antithrombotic therapy prevents the formation of thrombus on the basis of plaque rupture to prevent the emergence of vascular events.
Once a vascular event has occurred due to plaque rupture and thrombosis, all that can be done is to mend the fold after death. In addition to aggressive treatment and loss reduction, the next step is to prevent the recurrence of similar vascular events through active interventions. If not contraindicated, low-dose aspirin should be given for life to patients who have already had a vascular event. Statin lipid-regulating drugs can stabilize plaque and prevent further vascular events, and secondary prevention should also be routinely used.
The main risk of patients with peripheral arterial disease is myocardial infarction, cerebral infarction and vascular death. As a surgeon, you should not only have a clear understanding of this, but also assess the risk of cardiovascular and cerebrovascular events in your specific work, and take strong measures to prevent myocardial infarction and other vascular events. drugs, and not to focus only on blood vessels and surgery itself to avoid serious situations such as vascular death.
In fact, primary prevention is far more important than secondary prevention, and more patients are saved, because the base of this group of patients is large, and whether to take primary prevention measures depends on the presence, number and intensity of risk factors. In addition to lifestyle changes and risk factor control, high-risk patients should take long-term aspirin.
Guidelines published by the British Hypertension Society (BHS) in 1999 and 2004 and by the European Society of Cardiology in 2003 include aspirin antithrombotic and these guidelines recommend aggressive lipid intervention in all patients with hypertension.
Primary prevention: aspirin 75 mg/day if the patient is aged ³ 50 years, has controlled blood pressure below 150/90 mmHg, and has target organ damage (e.g., left ventricular hypertrophy, renal damage, or proteinuria), diabetes mellitus, or one of the 10-year cardiovascular disease risks ³ 20 percent.
Secondary prevention (including patients with type 2 diabetes): patients with pre-existing cardiovascular events (e.g., myocardial infarction, angina pectoris, ischemic cerebrovascular disease, peripheral vascular disease, or atherosclerotic vascular disease), unless contraindicated, use aspirin 75 mg/day antithrombotic in all patients.
Diabetes impairs endothelial cell function and induces or exacerbates atherosclerosis; activation of platelets; increased synthesis or activity of coagulation substances; decreased fibrinolytic activity, and abnormal blood rheology. With active inflammation in diabetic atherosclerotic lesions, plaques are more likely to rupture, leading to thrombosis and vascular events.
The American Diabetes Association (ADA) recommends: treatment with aspirin (75C325 mg/day) in all adults with diabetes and macrovascular disease (Level of Evidence A); consideration of initiation of aspirin primary prevention (75C325 mg/day) in patients aged ³40 years with diabetes and one or more other cardiovascular risk factors.