Pulmonary thromboembolism (PTE) is a type of pulmonary embolism.
Pulmonary embolism (PE) is a general term for a group of diseases or clinical syndromes in which various emboli obstruct the pulmonary arterial system as their pathogenesis, including PTE, fat embolism syndrome, amniotic fluid embolism, and air embolism. There are four main adverse clinical outcomes, namely recurrent non-lethal venous thromboembolism, lethal PTE, post-embolism syndrome and chronic embolic pulmonary hypertension. Identifying which patients are susceptible to these outcomes is important in determining treatment options.
PTE is the most common type of PE and accounts for the majority of PE, which is commonly referred to as PTE.
When acute PTE causes extensive obstruction of the pulmonary artery, it can cause pulmonary hypertension to a certain extent, resulting in right heart failure, right heart enlargement, and acute pulmonary heart disease. Common venous thrombosis includes skeletal femoral vein thrombosis in the lower limbs, saphenous vein thrombosis, axillary vein and subclavian vein thrombosis in the upper limbs. In addition, there are abundant venous networks and plexuses in some parts of the body, which are important pathways for collateral circulation and have a role in increasing the venous bed, and these networks or plexuses may also form thrombi. Fresh thrombi do not adhere tightly to the vein walls and are easily dislodged. When these thrombi are dislodged from the wall, they follow the venous blood flow through the right heart and obstruct the pulmonary artery, which is known as PTE. when the pulmonary artery is embolized, necrosis occurs in the lung tissue in its innominate zone due to obstruction or interruption of blood flow, which is known as pulmonaryinfarction (PI). PI occurs in less than 15% of PTEs due to the multiple blood and oxygen supply mechanisms of the lung tissue.
Intravascular coagulation may occur when the slow flow of blood in the lumen of a large volume is further slowed under certain conditions such as obstruction of blood flow, damage to the intima (e.g., inflammation, trauma), or when the blood becomes hypercoagulated, which is known as venous thrombosis. DVT and PTE are essentially the manifestations of a disease process at different sites and stages, and together they are called venousthromboembolism (VTE). DVT is the result of a combination of three factors: blood stasis, increased viscosity, and venous wall damage, and DVT thrombi most often originate in the gastrocnemius plexus.
Deep venous thrombosis (DVT)
Major DVT types.
1.Primary acute iliac vein thrombosis: it is more common in the left lower extremity, 2~3 times more common than the right, because the iliac vein is the main conduit for venous blood return in the lower extremity, so once the thrombosis is formed, the onset is often more acute, with obvious clinical manifestations of DVT, and its actual onset period often coincides with the symptomatic period, which often occurs easily after medullary surgery or trauma especially bone injury.
2, acute calf deep vein thrombosis: because of the calf deep vein thrombosis less, more venous branches, rich blood flow, after the local deep vein thrombosis, there is still enough blood flow can be returned to the heart through other veins, the clinical manifestation of DVT is often lighter or missing, the systemic symptoms are not obvious, the actual disease period is longer than the symptomatic period. The actual period of disease is longer than the symptomatic period. The disease mostly occurs in the second week after surgery, in patients who are bedridden or less active for a long time.
3.Secondary skeletal vein thrombosis: It is secondary to the expansion of thrombus from the deep veins of the lower leg to the iliac and femoral vein system, and is the most common clinical type of DVT. The onset of the disease is relatively insidious, and most patients are found only when the iliac and femoral veins are involved with typical symptoms, so the actual duration of the disease is longer than the symptomatic time. There are nutritional changes in the foot and boot area, including desquamation, itching, hyperpigmentation, eczema, ulceration, etc. Because the traffic veins are involved at the onset, the regression is more severe than primary iliac and femoral vein thrombosis.
4. Upper extremity, subclavian or axillary vein thrombosis: Because they are important channels for venous reflux in the upper extremity, once thrombosis is formed, it often starts acutely, with arm swelling, issuing and pain, and bundles can be felt, and the actual disease period and symptomatic period often match. If the thrombus extends to the superior vena cava, it can cause edema of the face and neck and even dilatation of the superficial veins of the chest and arms. It is commonly seen in indwelling catheters, intravenous chemotherapy, parenteral nutrition, trauma due to scapular or crutch use, and breast surgery.
5. Renal vein thrombosis: It is common in patients with nephrotic syndrome, with membranous glomerulonephritis being the most common, and is associated with loss of antithrombin in the urine and a hypercoagulable blood state. Renal vein thrombosis can be asymptomatic or have mild abdominal pain and back pain, or more severe abdominal pain or pressure pain, and pulmonary embolism is a relatively common complication of renal vein thrombosis.
(A) The evolution of deep vein thrombosis
1, thrombus dissolution, contraction and blood flow recanalization: thrombus can be dissolved, partially dissolved and contracted due to its own fibrinolytic system, and fissures or new vascular lumen can be formed between thrombus and vessel wall and inside thrombus, and also open side branch circulation, or new capillaries from vessel, the lumen is highly expanded and connected to each other, communicating the original vascular lumen at both ends, so that deep vein blood flow can be recanalized.
2, thrombus extension: as the starting point of new thrombosis, the thrombus enlarges and can extend in the direction of blood flow until the inferior vena cava or reverse the direction of blood flow and involve the whole inferior vena cava system, so that the vascular cavity is blocked, the local blood flow stops, the blood rapidly coagulates and new thrombus is formed. The larger thrombus as well as fresh thrombus or unstable thrombus tail in the deep human vascular cavity can be dislodged and displaced by the impact of blood flow or by the compression of lower limb activities and the squeezing of calf muscles during walking, and PTE occurs.
3, thrombus mechanization: deep vein thrombus that is not completely dissolved can be gradually replaced by new granulation tissue within days or weeks, resulting in deep vein stenosis or occlusion, and the mechanized thrombus is neither extended nor easily dislodged from the vessel causing PTE.
(B) Prognosis and regression of deep vein tether formation: Prognosis.
(l) Most DVT confined to the calf muscle has small thrombus and can be autolyzed, so the symptoms and signs are not obvious and easily missed, and it rarely causes long-term disability and clinically significant PTE, but about 20% of asymptomatic and 20%-30% of symptomatic patients have venous thrombus that can extend upward to the rouge vein, and 40%-50% of them may dislodge the thrombus and complicate PTE. while the proximal lower limb Most clinically significant and fatal PTE emboli come from DVT in the rouge, femoral and skeletal veins of the lower extremities (and are the cause of recurrent PTE in the future). causes). Superficial phlebitis of the lower extremities is rarely associated with PTE because of the inflammatory thickening of the venous wall, and the thrombus is not easily dislodged from the wall (but in nearly 15% of cases, the thrombus can extend upward and DVT may be present at the same time). 10% of chronic PTE will eventually occur if not treated adequately and 10% of them are fatal.
(2) DVT recurrence: 47% and 20% of untreated or inadequately treated proximal lower extremity DVT and symptomatic lower leg DVT have recurrent DVT after three months, respectively. the risk of DVT recurrence is increased in those with a prior history of DVT, especially when other DVT risk factors are present. The risk of recurrence of DVT is higher for those who had DVT of unknown cause for the first time and then in the presence of DVT risk factors, such as prolonged bed rest or malignant neoplastic disease.
(3) Post-thromboembolic syndrome (PTS) is characterized by pain, chronic venous insufficiency, leg swelling, and in some patients, venous ulcers. In general, the thicker and more completely obstructed the thrombosed vein is, the more difficult it is to recanalize; while the smaller and less obstructed the involved vein is, the greater the chance of recanalization by canalization and endothelialization. The risk of PTS is significantly higher in those with recurrent DVT in the same limb. Regression: The incidence of PTE can be significantly reduced in DVT treated with adequate anticoagulation, but PTS can still occur in 10-30% of patients. for symptomatic DVT of the lower leg, the likelihood of recurrent DVT is less than 2% after heparin treatment is given early to achieve adequate anticoagulation, if oral anticoagulant or subcutaneous injection of appropriate amount of heparin is continued for 3 months after that, the recurrence rate of DVT is The possibility of recurrent DVT after one year is only 5% to 10%, and PTE rarely occurs.
Venous thromboembolism (VTE)
The first case of hereditary antithrombin-III (AT-III) deficiency with venous thrombosis was reported by Egeberg in 1965, followed by the discovery of hereditary protein C (PC) deficiency, protein S (PS) deficiency, activated protein C resistance (APCR) phenomenon, and the discovery of the VTE mutation. In 1996, Poort et al. discovered the mutation 20210G-A at the 3′ end of the prothrombin gene in the Netherlands. Since then, a large number of genetic epidemiological studies on VTE have been conducted in Europe and the United States, and more susceptibility genes associated with VTE have been discovered. The role of FVL and prothrombinogen G20210-A in venous thrombosis in white race has been confirmed, while preliminary studies in Hong Kong, Taiwan, Beijing and Japan have shown that FVL is rare and prothrombinogen G20210A is rare, and the factors affecting VTE in Asian race remain to be elucidated.
Secondary VTE refers to VTE triggered by acquired risk factors. common acquired risk factors include: braking, underlying cardiopulmonary pathology, malignancy, major general surgery, orthopedic surgery of the medullary knee, urological surgery, gynecological surgery, neurosurgery, severe trauma, spinal cord injury, etc. Most critically ill patients in the ICU ward have risk factors for VTE, so for Each patient in the ICU should be carefully analyzed for the possibility of VTE.
Epidemiological and molecular epidemiological studies to investigate the acquired and genetic risk factors for VTE can not only provide a basis for guiding the prevention of VTE, but also play a very important role in improving clinical diagnosis awareness, selecting appropriate treatment plans, deciding the duration of treatment, and implementing individualized treatment.