Pulmonary embolism is a pathological process in which dislodged blood clots or other substances obstruct the pulmonary arteries or their branches, and is often a comorbid condition. The occurrence of necrosis of lung tissue after vascular obstruction is called pulmonary infarction. Clinical symptoms include dyspnea, severe chest pain, hemoptysis, and fever.
Overview
Acute pulmonary embolism is a clinical and pathophysiological syndrome caused by endogenous or exogenous emboli blocking the main trunk or branches of the pulmonary artery causing pulmonary circulatory disorders, which is second only to coronary heart disease and hypertension in human lung morbidity, and has the third highest mortality rate after tumor and myocardial infarction. The combination of factors such as blood flow stagnation, venous injury and blood hypercoagulation can easily cause thrombosis, and the dislodgement of thrombus can lead to pulmonary embolism.
Etiology
Most of the patients with APE have causes, such as thrombosis of the lower limbs or pelvic veins, long-term bed rest or inactivity, slow-acute pulmonary embolism X-ray cardiopulmonary disease, surgery, trauma, malignant tumor, pregnancy and oral contraceptive pills, etc. Special attention should be paid when taking medical history. Symptoms and signs include dyspnea, severe chest pain, hemoptysis, and fever.
Classification of pulmonary embolism
The pulmonary vascular bed has a large reserve capacity, and one of the roles of pulmonary function has the filtration function of blood to prevent small thrombus from flowing into the body circulation. The lung tissue of acute pulmonary embolism specimen has a strong autolysis effect on thrombus and has a lysis effect on small thrombus. Therefore, in some patients clinically, when small thrombi block the pulmonary vascular bed, the clinical symptoms do not appear continuously due to the self-lysis of lung tissue, which is also called clinically non-manifest pulmonary embolism, so it is difficult to make clinical diagnosis.
(1) Clinically occult pulmonary embolism: clinically undiagnosed.
(2) Pulmonary embolism with some clinical symptoms of transient nature: clinically difficult to diagnose.
(3) Clinically manifest pulmonary embolism: clinically diagnosable, including.
(1) Acute extensive pulmonary embolism: refers to thrombus blocking more than two pulmonary lobar arteries or equivalent pulmonary vascular bed range.
②Acute subextensive pulmonary embolism: refers to thrombus blocking more than one pulmonary segment or two or less lobar arteries or the same range of pulmonary vascular beds.
③Chronic pulmonary embolism with pulmonary hypertension.
(1) Pulmonary embolism due to large thrombus: the thrombus blocked the artery above the regional pulmonary artery branch.
(2) Pulmonary embolism due to microthrombus: A disease in which myenteric arteries (small arteries with outer diameter of 100μm to 1000μm or less) are diffusely embolized.
1) Acute pulmonary embolism: refers to those with a short onset time, usually within 14 days, and fresh thrombus blocking the pulmonary artery. If the onset time is more than 14 days, within 3 months, it is subacute pulmonary embolism.
(2) Chronic pulmonary embolism: Those with onset time longer than 3 months and pulmonary artery thrombus has been mechanized.
(1) Pulmonary infarction type: acute pulmonary embolism combined with necrosis of lung tissue is called pulmonary infarction, and the pathology is called hemorrhagic necrosis. When the thrombus blocks the end of the pulmonary artery, it is easy to cause pulmonary infarction.
(2) Non-infarct type: Pulmonary infarction is less likely to occur after blockage of the pulmonary artery trunk with a coarse diameter.
The severity of acute pulmonary infarction is determined by the extent of blockage of the pulmonary artery; the greater the extent of blockage of the vascular bed, the more severe the disease. The chance of pulmonary infarction is low, and it is thought that patients with pulmonary embolism combined with pulmonary infarction account for about 10% to 15% of the total number of patients with pulmonary embolism.
That is, the critical stage of multiple diseases is combined with pulmonary embolism, and the clinical symptoms and degree appearing in different diseases are different, which may be related to the easy combination of pulmonary embolism in the end stage of certain diseases, so the possibility of pulmonary embolism appearing in clinical critical diseases should not be ignored.
Diagnosis
The diagnostic criteria proposed by Japanese scholars are widely used in clinical practice. It is easier to judge according to the score. Acute pulmonary embolism radiograph pulmonary embolism determination score table
Item Score Item Score
Primary disease and factors ①WBC>80001
①Malignant tumor1 ② Platelets1
②Thrombophlebitis1 ③Bilirubin>1.2mg/dl1
③Heart disease1 ④GOT>40u1
④Surgery1 ⑤GPT>35u1
⑤Pregnancy, obstetrical and gynecological diseases1 ⑥Lactate dehydrogenase>450u1
⑥Quiet bed rest1 ⑦CO diffusion <80%1< p="">
①Respiratory distress2 ⑨Fibrinogen <150mg/dl2
②chest pain2⑩fibrinogen>350mg/dl2
③blood sputum211 fibrin degradation products>5ng/ml3
④cough212 antithrombin II<28mg/dl1
⑤Fever2(5)ECG
⑥Palpitations1①Right ventricular hypertrophy3
⑦swelling1②lung-type P wave3
⑧ sweating1 ③electrical axis right deviation3
⑨Loss of consciousness1 ④SIQIIITIII2
①Temperature>37.8℃1(6)Chest X-ray
②Breathing>16 times2①Infiltrative shadow2
③pulse rate>100 times2②pleural effusion1
④Blood pressure <100 mmhg1 ③Granular, reticular shadows3< p="">
⑤ lung2④pulmonary hypertrophy in the hilar region2
(6) Large liver2 ⑤ Diaphragm elevation2
(4) Examination findings
(7)Pulmonary ventilation-perfusion scan imaging
(1) The pulmonary perfusion scan showed a regional blood flow defect;
②Lung ventilation scan was normal;
③Both of the above were examined.
(6) Large liver2 (5) Elevated diaphragm2
(4)Examination results
(7)Pulmonary ventilation-perfusion scan imaging
①lung perfusion scan showed regional blood flow deficit;
②Lung ventilation scan was normal;
(3) Both of the above were examined.
(8)Pulmonary arteriogram
①Vascular obstruction sign;
②Vessels showing filling defects.
Judgment
①The diagnosis can be confirmed by 22 points or more;
②20 points or more are highly suspicious;
③17～19 points are suspicious;
④ (7) and (8) tests must be performed at 15 to 16 points.
Laboratory tests
Although some of the laboratory tests are non-specific, they can be of great value to primary care hospitals if they are used appropriately. The pathophysiological basis for microscopic observation of electrocardiographic changes in APE is acute right ventricular dilatation, whose electrocardiographic changes are often transient and variable and need to be observed dynamically, Patients with pulmonary embolism may have normal chest X-rays, but they may show regional reduced pulmonary blood flow or uneven pulmonary blood distribution, elevation of the affected diaphragm, peripheral wedge-shaped dense shadow above the diaphragm (hump sign), pulmonary shadow or pleural effusion, widening of the right lower pulmonary artery, arterial blood Arterial blood gas analysis: if PaCO2 decreases, PH value increases, and PaO2 decreases with or without PaCO2, it is favorable to the possibility of APE.
1.Blood picture, blood lactate dehydrogenase, blood gas analysis, coagulation function test.
2.Electrocardiogram has heart rate arrhythmias, such as atrial fibrillation, right bundle branch block, etc.; electrocardiogram can be seen in the right side of the electrical axis, obvious cis-clockwise transposition; S ⅠQ Ⅲ T wave inversion, pulmonary P wave.
3, chest X-ray may have multiple infiltrates, pleural effusion, diaphragm elevation.
4, pulmonary ventilation ~ perfusion scan with radioactive elements 133Xe inhalation scan and lung perfusion scan at the same time, the former is normal while the latter shows defects, most of them are pulmonary embolism.
5.Pulmonary angiography can confirm the diagnosis. Selective pulmonary angiography has the best effect, such as adding magnification technique (geometric magnification and oblique technique) can distinguish the obstruction of small arteries of 0, 5 mm in diameter. If possible, digital subtraction angiography can be performed for better image clarity. Pulmonary artery pressure >10,6kPa (80mmHg) is contraindicated.
Clinical types
①Sudden death type;
②Acute pulmonary heart disease type;
(iii) Unexplained dyspnea;
④Pulmonary infarction type;
⑤ chronic embolic pulmonary hypertension.
Clinical experience shows that the combination of pulmonary embolism should be considered in cases of sudden aggravation of the symptoms of existing cardiopulmonary disease or sudden dyspnea, and the effect is not obvious after corresponding cardiotonic, diuretic and vasodilator treatments, especially in those who are bedridden for a long time, accompanied by atrial fibrillation or severe cardiac insufficiency, using a large amount of diuretics, with obvious signs of dehydration or lower limb swelling.
Differential diagnosis
Extensive pulmonary embolism is a clinical emergency, serious and critical disease, and the treatment method is different from that of coronary heart disease and acute myocardial infarction, so the diagnosis of acute pulmonary embolism should be made early. The chest pain caused by pulmonary embolism is related to the invasion of the pleura, and compared with coronary heart disease and myocardial infarction, the chest pain is dull and characterized by dyspnea. If chest pain occurs, electrocardiogram should be done first, and electrocardiogram is one of the indicators for early differential diagnosis. After the onset of myocardial infarction, the ST segment of II, III and aVF rises, and the ST segment of V1 to V5 falls, showing the pattern of inferior wall myocardial infarction, and ST segment elevation is more obvious after 3h, and pathological Q waves appear in II, III and aVF after 24h; while the P wave of pulmonary embolism II, III and aVF rises (pulmonary P wave), and the ST segment of I, II, aVF and V1 to V5 decreases, and then gradual recovery. Right ventricular hypertrophy, pulmonary P waves, and right bundle branch conduction block are more common in chronic pulmonary embolism with persistent pulmonary hypertension and less common in acute pulmonary embolism.
Chest pain is present in all diseases, but pneumonia is clinically evident with fever, cough, rust-colored sputum, significantly elevated blood leukocytes, and inflammatory infiltrative shadows in the lungs seen on chest X-ray. In pleurisy, there are night sweats, low fever, pleural effusion, pleural adhesions and positive tuberculin test. The X-ray of pneumothorax may show special signs of the chest such as compressed shadow of the lung and diminished breath sounds on the affected side.
In thoracic aortic coarctation aneurysm, there can be chest pain or sudden onset, but the patient often has a history of hypertension. x-ray can see the widening of the upper mediastinal shadow, the aorta becomes wide and prolonged, often due to hypertension and the electrocardiogram shows the left ventricular surface high voltage and left ventricular strain, occasionally see secondary ST-T changes, thus can be distinguished.
The treatment of acute pulmonary embolism is to save lives and stabilize the disease, to recanalize pulmonary blood flow, and to prevent progression to chronic pulmonary embolism. In the acute phase, anticoagulation and thrombolytic therapy are used to correct right heart insufficiency and hypotension as the mainstay, as well as to correct hypoxemia, analgesia, and antiarrhythmias. Interventional or surgical treatment is chosen when medical treatment is unsuccessful.
Treatment options
The treatment of acute pulmonary embolism is aimed at saving lives and stabilizing the disease, recanalizing pulmonary blood flow, and preventing progression to chronic pulmonary embolism. In the acute phase, anticoagulation and thrombolytic therapy are used to correct right heart insufficiency and hypotension as the mainstay, as well as to correct hypoxemia, analgesia and antiarrhythmias. Interventional or surgical treatment is chosen when medical treatment is unsuccessful. Acute pulmonary embolism (I) Emergency treatment
1.General treatment
Pulmonary embolism is most dangerous within 1~3 days after the onset of pulmonary embolism. Patients should be admitted to the monitoring ward, and blood pressure, heart rate, respiration, electrocardiogram and arterial blood gas should be monitored continuously.
2.Symptomatic treatment
(1) Sedation and pain relief: keep the patient quiet, keep warm, administer oxygen, and give morphine, dulcolax, codeine, etc. if necessary for pain relief.
(2) Treatment of acute right heart insufficiency: digitalis is less effective and easy to poison, if necessary, rapid digitalis preparations (such as cetiran) can be used with caution, now generally use dobutamine or dobutamine 20-40mg, dissolved in 5% glucose 250m1 slowly intravenous drip to increase the amount of heart beat.
(3) Anti-shock treatment: first of all, replenish fluids, but pay attention to avoid the occurrence of pulmonary edema; if rehydration does not work, intravenous dobutamine, alamine, etc. can be infused. Maintain the body circulation systolic blood pressure above 90 mmHg.
(4) Improve respiration: if combined with bronchospasm, apply bronchodilators and mucolytic agents such as aminophylline and gastrin.
(II) Anticoagulation therapy
The objectives are to.
(1) Prevent thrombus extension around the pulmonary artery thrombus.
(2) Inhibit the secretion of neurological and humoral factors caused by thrombus.
(3) To stop the progression of venous thrombosis.
Heparin is used at the beginning of anticoagulation therapy and later maintained with Warfarin (Warhdn). Heparin has a rapid action with the above three effects, while Warhdn has a relatively long onset of action and lacks the inhibitory effect on the secretion of neurohumoral factors. Heparin has an important role in the treatment of pulmonary embolism, with a survival rate of 92% in the heparin group compared to 42% in the non-heparin group, with a significant difference between the two groups. The rate of pulmonary re-embolization also varied by whether or not heparin was used, with 16% in the heparin group compared to 55% in the non-heparin group. The results demonstrate the value of heparin use, but heparin use is limited in the case of some diseases.
Absolute contraindications: cerebral hemorrhage, acute phase of gastrointestinal bleeding, malignancy, arteriovenous malformations.
Relative contraindications: previous bleeding disorders, untreated severe hypertension, postpartum, major surgery within 2 weeks, biopsy. Heparin is metabolized in the liver, excreted in the urine, and the dosage should be reduced in combination with severe liver and kidney disease.
During the stage of suspected acute pulmonary embolism, heparin is first administered intravenously with 5000 units, and after the diagnosis is established, heparin is continuously ordered silently 500-1000 units per hour to prolong the APTT by 1.5-2.0 times compared to the control value. To prevent new thrombosis and thrombus extension, heparin was administered for 7 to 10 days. The biggest side effect of heparin is bleeding, the incidence of bleeding by intermittent intravenous injection is 10%-12%, the incidence of bleeding by continuous intravenous drip is 1%-5%, the chance of bleeding appears with long-term alcohol consumption, women and combined with anti-platelet drugs to reduce platelets, etc. The cumulative effect often appears on the third day after the drug is administered.
Low-molecular-weight heparin is widely used in clinical practice because of its long half-life and low bleeding tendency compared with regular heparin. The side effects of low-molecular-weight heparin are basically the same as those of ordinary heparin, except for less thrombocytopenia than ordinary heparin, and the dose is usually in the range of 4000-8000 units/12h subcutaneous injection for acute pulmonary embolism shot.
The purpose of adding Warfarin after heparin treatment is to prevent recurrent pulmonary embolism and to prevent the extension of venous thrombosis. The recurrence rate of venous thrombosis was 2% in the Warfarin group and 17% in the non-use group; after 1 year, the recurrence rate was 4% in the Warfarin group and 32% in the non-Warfarin group, showing a significant difference. The onset of action of warfarin is 2 to 3 days, so the dose of warfarin started 3 to 4 days before heparin discontinuation, and the dose of warfarin prolonged the PT value 1.5 to 2.5 times compared to the control value, with the international standardized ratio to between 2.0 and 2.5. A side effect of Warfarin is also bleeding, with bleeding rates up to 2.4-10%. Factors that increase the risk of bleeding are: over 60 years of age, diastolic hypertension, peptic ulcers, liver and kidney disease, and the combination of drugs that affect the metabolism and increase the efficacy of Warfarin. Warfarin affects the development of the fetus in the first trimester through the placenta, so it is better to use heparin instead of warfarin during pregnancy.
(C) Thrombolytic therapy
The ultimate goal of treatment for acute pulmonary embolism is to remove the thrombus, and thrombolytic therapy has been safe and effective in recent years. 16 hospitals in the United States conducted studies on thrombolytic therapy from 1967 to 1973, and the thrombolytic effects of urokinase and streptokinase were evaluated by pulmonary arteriography, hemodynamics and pulmonary perfusion imaging. The rate of flow defects on pulmonary angiography results improved by 53% in the urokinase group compared to 9% in the heparin alone group, showing a definite thrombolytic effect. Thrombolytic therapy improved deep venous valve function, improved pulmonary capillary diffusion capacity, and increased pulmonary capillary volume, thus establishing the treatment of acute pulmonary embolism.
Thrombolytic drugs and regimens approved by the U.S. Drug and Food Administration (FDA).
(1) Streptokinase: a loading dose of 250,000 units administered intravenously for 30 min, followed by 100,000 units/h for 24 h, approved in 1977.
(2) Urokinase: loading dose of 4400 units/kg, 10min intravenous injection, then 4400 units/kg/h, continuous 12-24h intravenous administration, approved in 1978.
(3) t-PA: 100mg, continuous intravenous injection in 2h, approved in 1990. Domestic commonly used thrombolytic regimens.
(1)UK: 20,000 IU/kg, 2h intravenous drip;
(2) rt-PA: 50-100mg, 2h intravenous drip;
(3) SK: 500,000 IU loading dose, followed by 10,000 IU/h, continuous intravenous drip.
The results of the study showed that the three thrombolytic agents have the same efficacy and safety. rt-PA 2-hour infusion can rapidly dissolve the blood clot than UK and SK 12-24-hour infusion, which can improve the hemodynamic instability more quickly.
The use of UPET (urokinasePulmonaryembolismtrial) is to first administer UK4400 units/kg intravenously within 10 min, and then the same dose every hour for 12 h. In 1997, a national clinical observation study on acute pulmonary embolism hosted by Fu Wai Cardiovascular Hospital in China recommended the use of 1 million to 1.5 million units (20,000 units/kg). In 1997, a national clinical observation study on acute pulmonary embolism hosted by Fu Wai Cardiovascular Hospital in China recommended the use of 1 million to 1.5 million units (20,000 units/kg) for 2h intravenous drip, followed by low molecular weight heparin anticoagulation for one week.
Indications for thrombolytic therapy.
(1) Widespread acute pulmonary embolism.
(2) Non-extensive acute pulmonary embolism combined with severe cardiopulmonary disease, where anticoagulation therapy is ineffective.
(3) Deep vein thrombosis.
Contraindications
(1)Gastrointestinal ulcer with bleeding.
(2)Recent cerebrovascular disease or post-operative cerebrospinal surgery.
(3)Intracranial tumor, etc.
The main complication of thrombolytic therapy is bleeding, and the incidence of bleeding is reported to be 5%-7% in the United States. To reduce its bleeding, a small dose (250,000 to 500,000 units) of urokinase can be injected directly into the pulmonary artery thrombus via catheter for better thrombolytic effect. In patients with recurrent acute pulmonary embolism, a large dose (1.5 million units) of urokinase can be applied intravenously once (within 2 h), and then a small to medium dose (250,000 to 500,000 units) can be continuously injected intravenously every day (used for 3 days), while heparin is used for anticoagulation, and the total amount of urokinase reaches 2.5 to 4 million units, which can also receive the expected therapeutic effect. Among the thrombolytic therapy, it should be different according to the degree of disease and the clinical type of pulmonary embolism, and the individualization of treatment should be emphasized.
Preventive measures
Taking appropriate measures for prevention can reduce the incidence and mortality of pulmonary embolism.
(i) Drug approach: It should be aimed at preventing deep vein thrombosis.
(ii) Surgical methods: mainly the method of inferior vena cava block is used to prevent the occurrence of lethal massive pulmonary embolism or recurrent non-lethal pulmonary embolism. It is mainly applied to the following cases :
①There are contraindications to anticoagulation: such as large deep vein thrombosis that occurs rapidly after major surgery and severe trauma, heparin allergy or bleeding quality.
②Recurrence of pulmonary embolism during anticoagulation therapy.
③Recurrent deep vein thrombosis and pulmonary embolism due to congenital abnormalities of coagulation mechanism.
④Recurrent pulmonary embolism in patients with severe cardiopulmonary disease.
⑤ Need to perform major surgical procedures, but the patient has acute iliac and femoral vein thrombosis.
1.Inferior vena cava ligation
The disadvantages of this procedure are large, such as the risk of surgery, the reduction of venous return after vena cava blockade, which affects the cardiac output and postoperative complications such as swelling, bruising and skin ulcers in the lower limbs. Therefore, this method is rarely used nowadays.
2.Inferior vena cava placement or placement of special umbrella filter
This is a widely used method. Its indications are.
①Proximal thrombosis of the veins of the lower extremities, where anticoagulation therapy is contraindicated or has complications.
②Pulmonary embolism with recurrent episodes of adequate anticoagulation.
③Large pulmonary embolism with hemodynamic changes. The advantage of placing a venous filter is that it prevents lethal pulmonary embolism due to dislodgement of larger emboli without significantly affecting venous return and with fewer complications. Inferior vena cava mesh placement is performed under anesthesia and carries a greater risk. Inferior vena cava placement with an umbrella filter through a catheter is relatively easy. If properly placed, more than 98% of patients can maintain long-term inferior vena cava blood flow and have a lower incidence of recurrent pulmonary embolism. The disadvantage is that lower extremity venous stasis may still be present, as well as the risk of filter dislodgement, migration, and venous perforation.