Introduction to pulmonary embolism

Introduction

Pulmonary embolism(pulmonary embolism) refers to the pathological and clinical state of the embedding material entering the pulmonary artery and its branches, blocking the blood supply to the tissue.

Cause

(a) thrombosis Pulmonary embolism is often a complication of venous thrombosis. The embolus is usually derived from the deep veins of the lower extremities and pelvis and causes embolism by circulation to the pulmonary artery. But rarely from the upper limbs, head and neck veins. Stasis of blood flow, increased blood coagulation and venous endothelial injury are contributing factors to thrombosis. Therefore, trauma, long-term bed rest, varicose veins, venous cannula, pelvic and hip surgery, obesity, diabetes, contraceptives or other causes of hypercoagulability, etc., are prone to induce venous thrombosis. Early thrombosis and the role of the fibrinolytic system, the highest risk of pulmonary embolism in the first few days of thrombosis.

(B) heart disease is the most common cause of pulmonary embolism in China, accounting for 40%. Several times, all kinds of heart disease, combined with atrial fibrillation, heart failure and subacute bacterial endocarditis have a higher incidence. Right heart chamber thrombosis is most common, and a few are also derived from the venous system. In addition to subacute bacterial endocarditis, bacterial emboli can also be caused by pacemaker infection. The former infectious emboli is mainly from the tricuspid valve. Occasionally, the mitral palsy of the congenital heart can be diverted from the left heart to the right heart and reach the pulmonary artery.

(3) Tumors are the second cause in China, accounting for 35%, which is much higher than 6% in foreign countries. Lung cancer, digestive system tumors, choriocarcinoma, leukemia, etc. are more common. Only about one-third of malignant tumors complicated with pulmonary embolism are tumor thrombi, and the rest are thrombosis. It is speculated that tumor patients may have thromboplastin (thromoboplastin) and other substances that can activate the coagulation system such as histone, cathepsin and proteolytic enzymes. Therefore, the incidence of pulmonary embolism in tumor patients is high, and may even be its first symptoms.

(D) pregnancy and childbirth pulmonary embolism in pregnant women several times the age of non-pregnant women, the highest incidence of postpartum and caesarean section. Increased intra-abdominal pressure during pregnancy and hormonal relaxation of vascular smooth muscle and pelvic vein pressure can cause slow venous blood flow, alter blood rheology and aggravate venous thrombosis. In addition, with the increase of blood coagulation factors and platelets, the plasma pro-plasmin-plasmin proteolytic system activity is decreased. However, these changes were not significantly different from those without thromboembolism. Amniotic fluid embolism is also a serious complication during childbirth.

(5) Other rare causes are fat embolism caused by long bone fractures, air embolism caused by accidents and decompression sickness, parasites and foreign body embolism. In the absence of significant triggering factors, a reduction in hereditary anticoagulant factors or an increase in plasminogen activator inhibitors should also be considered.

symptom

I. Clinical manifestations

The clinical manifestations of pulmonary embolism are diverse and actually a broader clinical spectrum. What you see is mainly determined by the number of vascular occlusions, the speed of occurrence and the basic state of the heart and lungs, 2 to 3 lung segments, without any symptoms; severe 15 to 16 lung segments, can occur shock or sudden death. But there are basically four clinical syndromes: 1 acute pulmonary heart disease: sudden dyspnea, sudden death, cyanosis, right heart failure, hypotension, wet limbs, seen in patients with sudden embolization above the two lungs; 2 pulmonary infarction: sudden breathing Difficulties, chest pain, hemoptysis and pleural friction or pleural effusion; 3 "unexplained dyspnea": relatively small embolization area, is the only symptom suggesting an increase in invalid cavity; 4 chronic recurrent pulmonary thromboembolism: slow onset, found Later, mainly manifested as severe pulmonary hypertension and right heart dysfunction, is a type of clinical progression. In addition, there are rare contraceptive embolisms and non-thrombotic pulmonary embolisms. The former has multiple strokes with pulmonary embolism. It is opened by the pulmonary foramen ovale and the venous embolus reaches the systemic circulation. The latter may be caused by long bone fracture. Fat embolism syndrome or air embolism associated with a central venous catheter.

1. Common symptoms of pulmonary embolism, whether symptoms or signs are non-specific and insensitive to the diagnosis of acute or chronic pulmonary thromboembolism.

(1) Dyspnea: It is the most common symptom of pulmonary embolism, accounting for 84% to 90%, especially after activity. It is often seen after going to the stairs, and it is relieved when resting. Sometimes the patient's self-reported activity is “depressed” and needs to be distinguished from the labor “angina pectoris”. This is often the starting point for correct diagnosis or misdiagnosis, and should be especially seriously asked. Dyspnea may be related to respiratory and circulatory dysfunction. Difficulty breathing (shortness of breath) sometimes disappears quickly, and can occur repeatedly after several days or months. It is caused by recurrence of pulmonary embolism and should be taken seriously. Difficulty breathing can be light and heavy, especially those with mild breathing difficulties.

(2) Chest pain: about 70%, sudden occurrence, more related to breathing, increased cough, about 66% of patients with pleural pain, usually a small embolism located in the periphery, involving the pleura. The cause of pleural chest pain is still controversial, but it is still believed that the onset of chest pain of this nature, whether or not combined with hemoptysis, suggests that there may be pulmonary infarction. Larger emboli can cause severe crushing pain. It is located behind the sternum and is difficult to tolerate. It radiates to the shoulders and chest, which is similar to the onset of angina pectoris, accounting for about 4%, which may be related to coronary artery spasm and myocardial ischemia. In addition to the identification of coronary heart disease and angina pectoris, chest pain should also be differentiated from dissecting aneurysms.

(3) hemoptysis: It is a symptom of pulmonary infarction, which occurs within 24 hours after infarction. The amount is not much, bright red, and it can become dark red after a few days, the incidence rate is about 30%. The hemoptysis of chronic embolic pulmonary hypertension is mostly from the compensatory dilatation and rupture of the bronchial artery system in the bronchial submucosa.

(4) Panic: The incidence rate is about 55%. The cause is unclear and may be related to chest pain or hypoxemia. Do not easily diagnose snoring or hyperventilation syndrome with anxiety and difficulty breathing.

(5) Cough: about 37%, mostly dry cough, or a small amount of white sputum, may also be accompanied by wheezing, the incidence rate is about 9%.

(6) syncope: about 13%, although small pulmonary embolism can also cause dizziness due to temporary cerebral circulatory disorders, but the main cause of syncope is caused by massive pulmonary embolism (blocking blood vessels above 50%) Cerebral insufficiency. This may also be the only or earliest symptom of chronic embolic pulmonary hypertension, which should be taken seriously, most with hypotension, right heart failure and hypoxemia.

(7) Abdominal pain: Pulmonary embolism sometimes has abdominal pain, which may be related to stimulation of the diaphragm or intestinal ischemia.

Although more than 90% of patients with pulmonary embolism may have difficulty breathing, typical pulmonary infarction with pleural pain, dyspnea and hemoptysis account for only 28%.

2. Physical examination

(1) General examination: There is often low fever, accounting for 43% of pulmonary embolism. It can last for about one week, and high fever can reach more than 38.5 °C. Fever can be caused by pulmonary infarction or pulmonary hemorrhage, atelectasis or additional infection, and may also be caused by thrombophlebitis. Therefore, even if the clinician finds that the lung infiltration shadow is not necessarily lung inflammation, it is necessary to think about the possibility of pulmonary embolism. 70% of patients with pulmonary embolism have a faster respiratory rate, ≥20 times/min, which is diagnostic, up to 40-50 times/min. 44% have sinus tachycardia. 19% of cyanosis occurs, which may be caused by intrapulmonary shunting or by the opening of the foramen ovale. Excessive sweating 11%, although low blood pressure is not very common, but usually prompted for massive pulmonary embolism.

(2) Cardiac vascular system signs: mainly the performance of acute and chronic pulmonary hypertension and right heart dysfunction. In addition to increased heart rate, arrhythmia can also occur, such as pre-systolic contraction, supraventricular tachycardia, atrial flutter and atrial fibrillation. There may be systolic pulsation between the second and third intercostals of the left sternal border, which may cause closed vibration of the pulmonary valve, 53% of the second sound of the pulmonary artery, 23% of the jet sound or systolic jet noise. When there is tricuspid regurgitation, the tricuspid systolic murmur may occur between the fourth and fifth ribs of the left sternal border. As the inspiratory increases, when the right ventricle is enlarged and occupyes the apical region, the murmur can be transmitted to the apical region. Even the midline of the sputum is easily confused with mitral regurgitation in rheumatic heart disease. Right atrial atrial gallbladder (24%) and ventricular galloping (3%) can also be heard, reflecting a decline in right heart compliance (such as right ventricular hypertrophy, dilatation) and right ventricular dysfunction. Jugular vein filling and pulsation enhancement are important signs of pulmonary embolism and an important window for right heart function changes. The second heart sound split disappeared or was fixedly split. Signs of right heart failure such as enlarged liver, hepatic jugular vein reflux and lower extremity edema. Acute to pulmonary embolism or severe pulmonary hypertension may have a small to moderate amount of pericardial effusion. Pericardial effusion and pericardial friction sounds can also occur in "post-myocardial infarction syndrome" after pulmonary embolism.

(3) signs of respiratory system: when one side of the lung lobe or whole lung embolism can occur, the trachea can be moved to the affected side, and the diaphragm is lifted. The lesions were percussed with dullness, and the lungs were audible and wheezing and dry and wet voices (15%). Pulmonary vascular murmurs can also be heard, the intensity is not large, which is characterized by increased murmur during inhalation, some patients have pleural friction sounds, and corresponding signs of pleural effusion. In addition to the cardiopulmonary signs caused by pulmonary embolism itself, the signs of other underlying diseases that induce pulmonary embolism should also be carefully examined.

Some literatures suggest that up to 90% of embolism of pulmonary embolism is derived from deep vein thrombosis, and deep vein thrombosis is considered to be a marker of pulmonary embolism. Therefore, examination of venous thrombosis is very important. Unfortunately, about half of the physical examinations of patients with deep venous thrombosis of the lower extremities are normal. Common abnormalities are seen in the swelling of the affected limb or the asymmetrical swelling of the lower limbs. The difference in the circumference of the limbs between the two limbs is diagnostic. Usually the swelling of the lower leg reflects the blockage of the iliac vein. The swelling of the lower extremity suggests that the external iliac vein or the femoral condyle is blocked. The simple femoral vein thrombosis usually does not show swelling. Accompanying swelling can consciously cause limb pain, tenderness, positive Homan sign, increased stiffness, superficial vein dilatation, acute skin flushing, fever, and hyperpigmentation in chronic cases. Simple venous insufficiency without occlusion only varicose veins, otherwise it is often accompanied by swelling. Limb swelling caused by local venous occlusion does not reflect right heart dysfunction, but sometimes it can be both, and should be carefully identified.

Second, diagnosis

Clinical signs and symptoms are often non-specific and vary widely, making it difficult to distinguish from other cardiovascular diseases. Although the severity of symptoms is related to the size of the embolus and the extent of embolization, it is not necessarily proportional, and is often closely related to the compensatory ability of the original heart and lung diseases.

(A) acute large-area pulmonary embolism: manifested as sudden onset of severe dyspnea, myocardial infarction-like sternal pain, syncope, cyanosis, right heart failure, shock, sweating, cold limbs and convulsions. Even cardiac arrest or ventricular fibrillation and rapid death.

(B) medium-sized pulmonary embolism: often have post-sternal pain and hemoptysis. When the patient's original heart and lung disease compensation function is very poor, it can produce syncope and high blood pressure.

(C) microembolism of the lung: can produce adult respiratory distress syndrome.

(D) pulmonary infarction: often have fever, mild jaundice.

About 20% to 30% of patients die without timely or failure to be diagnosed and treated. If they can be diagnosed and given anticoagulant therapy in time, the mortality rate is expected to drop to 8%, so early diagnosis is very important. Care should be taken to collect medical history. Serum LDH increased, arterial blood PO2 decreased, and PA ~ aO2 broadened. Electrocardiograms have T-wave and ST-segment changes (similar to myocardial infarction patterns), P-wave and QRS waveform changes (similar to acute pulmonary heart disease patterns). X-ray shows patchy infiltration, atelectasis, diaphragmatic elevation, pleural effusion, especially the round dense shadow of the pleural basal convex surface toward the hilum (Hamptom hump) and the dilated pulmonary artery with distal lung pattern sparse ( Westermark et al. are of great value in the diagnosis of pulmonary embolism. Radionuclide ventilation/perfusion scan is the most sensitive non-invasive method for diagnosing pulmonary embolism. Although the specificity is low, there are typical multiple, segmental or wedge-shaped perfusion defects and the ventilation is normal or increased. Combined with clinical diagnosis, the diagnosis can be established. . Pulmonary angiography is the most specific method for diagnosing pulmonary embolism and is suitable for clinical and nuclear scans where suspicious and surgical treatment is required. It is characterized by vascular lumen filling defect, arterial truncation or "pruning sign". Contrast can not show small blood vessels ≤ 2mm in diameter, so multiple small embolizations are often missed.

diagnosis

The clinical types of pulmonary embolism vary, and the disease to be identified is not the same. Pulmonary manifestations are often misdiagnosed as other chest and lung diseases. Patients with pulmonary hypertension and heart disease are easily misdiagnosed as other heart diseases. The most important clinically misdiagnosed diseases are myocardial infarction, coronary insufficiency, pneumonia, congestive heart failure (left heart), cardiomyopathy,Primary pulmonary hypertension, pleurisy, bronchial asthma, pericarditis, dissection aneurysms and rib fractures.

1. Acute pulmonary embolism in acute myocardial infarction may have severe chest pain with electrocardiogram resembling myocardial infarction pattern, which needs to be differentiated from acute myocardial infarction.

2. Coronary artery insufficiency in the elderly patients with acute pulmonary embolism or recurrent pulmonary embolism, ECG can appear ST, T wave changes in II, III, aVF lead, and even V1-4 lead shows "coronal T", Chest pain and shortness of breath are easy to diagnose as coronary insufficiency or subendocardial myocardial infarction. In addition to ST, T changes in the ECG of the pulmonary embolism, the right axis of the ECG axis is obvious or SIQIIITIII type and "Pulmonary P" wave appear. The ECG changes often improve or disappear within 1 to 2 weeks, which is different from those of coronary heart disease. Patients with pulmonary embolism have labor dyspnea, and coronary heart disease is labor angina. Radionuclide myocardial imaging is completely different. Pulmonary embolism lacks typical myocardial perfusion defects or "reperfusion" performance.

3. Pneumonia fever, chest pain, cough, leukocytosis, X-ray chest showed infiltration of shadows and other easily confused with pulmonary embolism, is one of the most misdiagnosed diseases of pulmonary embolism. If you can pay attention to obvious breathing difficulties, jugular vein filling, lower extremity phlebitis, X-ray chest radiograph showing repeated infiltration shadows and regional pulmonary vascular texture reduction and blood gas abnormalities, etc., should be suspected of pulmonary embolism, and then further CT and MRI, etc. Check, more can be identified.

4. About 1/3 of patients with pleural effusion can develop pleural effusion, which is easily misdiagnosed as viral or tuberculous pleurisy, and the latter is given long-term anti-tuberculosis treatment. Patients with pulmonary embolism complicated by pleural effusion lack the symptoms of systemic poisoning of tuberculosis. The pleural fluid is mostly bloody, with less amount and absorption faster (natural absorption within 1 to 2 weeks). Arterial blood gas and lower extremity veins are normal. X-ray chest radiographs can also find that the absorption of faster lung infiltration or infarction is different from tuberculous pleurisy.

5. Atelectasis after atelectasis may be confused with pulmonary embolism, arterial blood gas is usually not normal. Peripheral veins are normal for differentiation, and CT, MRI, or pulmonary angiography can be used for identification when needed.

6. Bronchial bronchospasm secondary to pulmonary embolism sometimes needs to be distinguished from wheezing wheezing. Although the wheezing of patients with pulmonary embolism can occur, but it is rare, when it appears, it is only a new episode, lacking the history of asthma; arterial blood gas in patients with bronchial asthma can also be abnormal, but the CT is more normal, such as clinically suspected pulmonary embolism Pulmonary angiography can be performed further.

7. Primary pulmonary hypertension is similar to pulmonary embolism. Symptoms include fatigue, exertional dyspnea, chest pain, syncope and hemoptysis. Right heart failure can occur in both clinics, and hemodynamics has an increase in right ventricular pressure. The lung hair pressure is normal. The difference is that young patients with primary pulmonary hypertension (20 to 40 years old and older than 50 years old), more women, progressive deterioration, uninterrupted stable period, lung perfusion scan without pulmonary segmental defects, pulmonary artery contraction The pressure is more than 60mmHg, and the pulmonary angiography has no changes such as "pruning" and is different from pulmonary embolism.

8. Patients with acute pulmonary embolism in the aortic dissection have severe chest pain, widening of the superior mediastinum (caused by expansion of the superior vena cava), pleural effusion, and shock with the aortic dissection. The latter has a history of hypertension and pain. Widely, regardless of breathing, cyanosis is not obvious, and echocardiography is helpful for identification.

9. Hyperventilation syndrome (anxiety disorder) is mostly dyspnea, chest tightness, dying, arterial blood gas hypocapnia and respiratory alkalosis, ECG can be associated with T wave low and inverted, etc. Pulmonary embolism is different. Hyperventilation syndrome generally has no changes in organic cardiopulmonary disease, often with mental and psychological disorders, and symptoms can be relieved and disappeared.

The thinking of differential diagnosis is as follows: 1 characteristics of symptoms and signs; 2 accompanying symptoms and signs; 3 tips related to medical history; 4 results related to laboratory tests. Taking dyspnea as an example, dyspnea in pulmonary embolism is sudden, often accompanied by chest pain, hemoptysis, shock or syncope. If the medical history suggests some risk factors such as fractures or long-term brakes, laboratory tests revealed lower extremity venous thrombosis, imaging findings of pulmonary hypertension or right ventricular enlargement or even pulmonary obstruction, which is not difficult to identify with other diseases.

complication

Causes acute pulmonary hypertension and right heart failure, followed by lung ischemia, hypoxia, and decreased left ventricular output, circulatory failure. It can also be combined with hemoptysis, pulmonary infarction, massive pulmonary embolism leading to myocardial ischemia and cardiogenic shock.

treatment

(a) treatment

Although some or all of the thrombus of pulmonary embolism can dissolve and disappear spontaneously, the treated patients with acute pulmonary embolism have a 5 to 6 times lower mortality than those without treatment. Therefore, once the diagnosis is confirmed, the treatment should be actively performed. Unfortunately, Only 30% of patients can get the right treatment. The purpose of treatment for pulmonary embolism is to enable patients to survive critical periods, relieve cardiopulmonary dysfunction caused by embolism and prevent recurrence; restore and maintain adequate circulating blood volume and tissue oxygen supply as much as possible. Treatment of patients with massive pulmonary embolism or acute pulmonary heart disease includes timely oxygen inhalation, pulmonary vasospasm, anti-shock, anti-arrhythmia, thrombolysis, anticoagulation and surgery. For patients with chronic embolic pulmonary hypertension and chronic pulmonary heart disease, treatment mainly includes blocking the source of embolism, preventing re-embolization, performing pulmonary thromboendotheliectomy, reducing pulmonary artery pressure and improving cardiac function.

1. Treatment of acute pulmonary embolism

(1) First-aid measures: The first two days after the onset of pulmonary embolism, the patient should be admitted to the ICU ward to continuously monitor blood pressure, heart rate, respiration, electrocardiogram, central venous pressure and blood gas.

1 general treatment: make the patient quiet, keep warm, oxygen; for sedation, pain relief, if necessary, can give morphine, pethidine, codeine; antibiotics for the prevention of intrapulmonary infection and treatment of phlebitis.

2 relieve pulmonary vasospasm and coronary artery spasm caused by excessive vagal tone, intravenous atropine 0.5 ~ 1.0mg, if not relieved can be repeated every 1 ~ 4 hours, can also give papaverine 30mg subcutaneous, intramuscular or intravenous injection 1, once / / h, the drug also has a calming effect and reduce platelet aggregation.

3 anti-shock: combined with shock dopamine 5 ~ 10μg / (kg · min), dobutamine 3.5 ~ 10μg / (kg · min) or norepinephrine 0.2 ~ 2.0μg (kg · min), quickly corrected Arrhythmias that cause hypotension, such as atrial flutter, atrial fibrillation, etc. Maintain mean arterial blood pressure >80 mmHg, heart index >2.5 L/(min·m2) and urine volume >50 ml/h. At the same time, active thrombolysis, anticoagulant therapy, and strive to ease the disease quickly. It should be pointed out that 80% of patients with acute pulmonary embolism die within 2 hours after the onset of the disease. Therefore, treatment and rescue must be carried out.

4 improve breathing: if there is bronchospasm, bronchodilators and mucolytic agents such as aminophylline and hydroxypropyl theophylline (whetting) can be used. It can also be intravenously infused with phentolamine 10-20 mg dissolved in 5%-10% glucose 100-200 ml, which can relieve bronchospasm and dilate pulmonary vessels. Patients with severe hypoxemia with respiratory failure can be treated with mechanical ventilation for a short time.

(2) thrombolytic therapy: 30 years ago, acute pulmonary embolism thrombolysis was introduced into the medical profession as a complex, heroic, desperate final treatment, requiring enormous human, material and financial support. Although the US Food and Drug Administration approved the use of streptokinase and urokinase for pulmonary embolism in 1977 and 1978, it was rarely used until the mid-1980s. The success of thrombolytic therapy for acute myocardial infarction has led to re-examination of thrombolysis with pulmonary embolism, and subsequent series of clinical trials have made contemporary thrombolysis for pulmonary embolism safer, faster, easier, and more effective.

In the United States, it is estimated that less than 10% of patients with pulmonary embolism have been treated with thrombolytic therapy. The lack of universalization of this therapy may be one of the important reasons for the long-term decline in pulmonary embolism mortality. In the 1990s, China began to develop thrombolysis for acute pulmonary embolism, especially after the study of "acute pulmonary embolism urokinase thrombolysis, suppository anticoagulation multi-center clinical trial" from 1997 to 1999, the thrombolytic method has been trending. Standardization.

Thrombolytic therapy is the direct or indirect conversion of plasma protein plasminogen to plasmin, which rapidly cleaves fibrin and dissolves blood clots. At the same time, it interferes with blood coagulation by reinforcing and inactivating coagulation factors II, V and VIII. Degradation of protein and fibrinogen inhibits the conversion of fibrinogen to fibrin and interferes with the polymerization of fibrin, exerting an anticoagulant effect. Commonly used thrombolytic drugs are:

1 streptokinase (SK): a bacterial protein isolated and purified from group C β-hemolytic streptococci, which binds to plasmin to form an activated complex, which converts other plasminogen into plasmin. Streptokinase is antigenic and can no longer be used for at least 6 months. As a circulating antibody, it can inactivate drugs and cause severe allergic reactions.

2 urokinase (VK): isolated from human urine or cultured human embryonic kidney cells, without antigenicity, directly converts plasminogen into plasmin to act as a thrombolytic effect.

3 Alteplase (recombinant tissue plasminogen activator, rt-PA): is a new thrombolytic agent produced by various cell line recombinant DNA technology, and alteplase (rt-PA) is also non-antigenic. Directly converts plasminogen to plasmin, which is more specific for fibrin than SK or UK (less activates systemic plasminogen).

The US Food and Drug Administration approved a thrombolysis regimen for pulmonary embolism: A. Streptokinase loading 250,000 U/30 min, followed by 100,000 U/h for 24 h instillation; B. Urokinase loading 2000 U/lb (lbs) )/10min (1 lb = 0.4536kg), followed by 2000U / (1b · h), continuous infusion of 12 ~ 24h; C. alteplase (rt-PA) 100mg / 2h, continuous peripheral intravenous infusion. In 1992, Goldhaber et al compared urokinase loading dose of 1 million U / l0min, followed by 3 million U / 2h intravenous infusion protocol and alteplase (rt-PA) 100mg / 2h intravenous drip program, the results of acute pulmonary embolism The efficacy and safety aspects are similar.

The thrombolytic regimen prescribed by the domestic “hyperpine embolism urokinase thrombolysis, suppository anticoagulation multi-center clinical trial” is urokinase 20,000 U / (kg · 2h), peripheral intravenous infusion. The urokinase of the thrombolytic regimen in a hospital is the same as that of the above, and the alteplase (rt-PA) is 50-100mg/2h in weight, and is intravenously infused.

The advantages of thrombolytic therapy are: 1 dissolves faster than heparin clot alone; 2 can quickly restore pulmonary blood flow and right heart function, reduce the mortality rate of complicated massive pulmonary embolism; 3 reduce blood pressure and right heart function normal pulmonary embolism The patient's mortality and recurrence rate; 4 accelerate the dissolution of small peripheral thrombus and improve the hemodynamic response of exercise.

The indications for thrombolysis for acute pulmonary embolism are: 1 large pulmonary embolism (more than two pulmonary vascular vessels); 2 anatomical vessel size regardless of pulmonary embolism with hemodynamic changes; 3 concurrent shock and low arterial infusion [ie, hypotension, lactic acidosis and/or decreased cardiac output]; 4 secondary pulmonary embolism of the original cardiopulmonary disease caused by circulatory failure; 5 symptomatic pulmonary embolism.

Contraindications for thrombolysis of pulmonary embolism: Absolute contraindications include: 1 recent active gastrointestinal bleeding; 2 cerebrovascular accident within 2 months, intracranial or spinal trauma or surgery; 3 active intracranial lesions (arterial Tumor, vascular malformation, tumor). Relative contraindications are: 1 uncontrolled hypertension (systolic blood pressure ≥180mmHg, diastolic blood pressure ≥110mmHg); 2 hemorrhagic diabetes, including patients with severe kidney disease and liver disease; 3 recent (10 days) major surgery, can not be squeezed Hemostasis puncture, organ biopsy or childbirth; 4 recent size trauma, including cardiopulmonary resuscitation; 5 infective endocarditis; 6 pregnancy; 7 hemorrhagic retinopathy; 8 pericarditis; 9 aneurysm; 10 left atrial thrombus; Potential bleeding disorders.

Specific implementation of thrombolysis for pulmonary embolism:

1 diagnosis must be confirmed before thrombolysis, non-invasive methods, such as radionuclide lung perfusion (or plus ventilation) scan and enhanced CT, if necessary, pulmonary angiography to confirm the diagnosis. Sometimes the patient's condition is not allowed to move for further examination or the hospital does not have the necessary equipment to confirm the diagnosis. At this time, the patient mainly relies on clinical evaluation. The most important thing is to ask the symptoms of pulmonary embolism, observe the jugular vein, and do deep vein examination of the lower extremity. Combined with electrocardiogram, X-ray chest and arterial blood gas changes, bedside echocardiography (transthoracic and esophageal) was performed to find the direct and indirect signs of pulmonary embolism, and to judge the disease to be identified.

2 The most suitable thrombolysis time window for acute pulmonary embolism is different from acute myocardial infarction. The main purpose of thrombolysis is to dissolve the thrombus, but not to protect the lung tissue. Because the lung tissue has dual blood supply, and can directly The alveoli take oxygen, so the hypoxic necrosis of the lung tissue generally does not occur, even if it occurs relatively light. Therefore, as long as the thrombus has not been machined, there is a chance of thrombolysis. It should be said that the sooner the thrombolysis effect after the onset or after recurrence, the initial thrombolysis time is limited to 5 days, and later found that the thrombolysis on the 6th to 14th days also has a certain effect, so the thrombolysis time window of the pulmonary embolism is now available. Extended to 14 days.

3 Carefully consider the indications and contraindications for thrombolytic therapy, especially to carefully collect the history of neurological diseases, if there is no episode of right or left hand weakness, difficulty speaking, headache, visual changes, and related treatment history and other contraindications.

4 blood test and blood preparation before thrombolysis, blood clots should be filtered out during blood transfusion.

5 venous puncture with a trocar before thrombolysis, retain this venous access to the second day after the end of thrombolysis, avoiding intravenous, arterial puncture and invasive examination.

6 Any thrombolytic drug can be selected, and domestic application is more urokinase. Alteplase (rt-PA) appears to be slightly better than the other two, but it is more expensive. The drug dose is usually adjusted by body weight. Generally, peripherally administered intravenously, Verstraete et al. compared the results of peripheral vein and pulmonary artery administration of alteplase (rt-PA) in 34 patients with pulmonary embolism. No intrapulmonary administration was superior to peripheral intravenous administration. The rate of thrombolysis, bleeding, and thrombolysis were similar. However, in some special cases, if the patient has a relative contraindication or potential bleeding, the intrapulmonary dose can be achieved to achieve the same effect as the large dose of the whole body, and the risk of bleeding is relatively small, but a cardiac catheterization is required. Increase the bleeding at the puncture site.

7 thrombolytic process to minimize patient movement.

8 Unlike myocardial infarction, pulmonary embolism does not require heparin during thrombolysis, and the amount of thrombolytic agent is fixed. Therefore, it is not necessary to monitor activated partial thromboplastin time (APTT), fibrinogen level or other coagulation parameters. After completion of thrombolysis, APTT should be measured. If it is less than 2.0 times (or <80 seconds) than the control value, heparin should be applied (no load dose), APTT should be maintained at 1.5 to 2.0 times of the control value, and if it is greater than 2.0 times, every 2 to 4 hours. The APTT was measured once, and heparin was used again until the treatment range. If APTT cannot be measured in time, heparin can be administered immediately after the end of thrombolysis, and then the dose is adjusted according to APTT.

The efficacy of thrombolytic therapy has been reported in different literatures. 101 patients with acute pulmonary embolism urokinase thrombolysis, suppository anticoagulation multi-center clinical trial with pulmonary perfusion scan and/or pulmonary angiography review used domestic urokinase. The thrombolytic effect was 86.1%.

The most important complication of thrombolytic therapy is bleeding. The statistics vary from 5% to 7% on average and about 1% in fatal bleeding. The incidence of major bleeding in the three thrombolytic drugs was similar, with alteplase (rt-PA), UK and SK being 13.7%, 10.2% and 8.8%, respectively. The most serious is that intracranial hemorrhage is 1.2%, about half of death, diastolic blood pressure is another risk factor for intracranial hemorrhage. The symptoms of retroperitoneal hemorrhage are not many, more insidious, and more manifested as shock of unknown cause, should be observed. In addition, the more important bleeding is the pulmonary angiography of the femoral vein puncture site, which often forms a hematoma. "After acute pulmonary embolism urokinase thrombolysis, suppository anticoagulation multi-center clinical trial" 101 patients with urokinase thrombolysis occurred in 1 case of massive hemorrhage, 5 cases of puncture site bleeding. Generally, a small amount of bleeding can be left untreated, and the drug can be stopped immediately after severe bleeding, cold sedimentation and/or fresh frozen plasma and p-aminobenzylamine or aminocaproic acid. Intracranial hemorrhage should be urgently consulted by a neurosurgeon. Other side effects of thrombolytic drugs may also have fever, allergic reactions, hypotension, nausea, vomiting, myalgia, headache, and the like. Allergic reactions are more common in patients with streptokinase.

Modern pulmonary embolism thrombolysis has made great progress, safe and effective, and the treatment plan tends to be simple and standardized. It is not necessary to have pulmonary angiography to confirm the treatment. The treatment time window is extended to 14 days. The dose is fixed or administered by weight. Peripheral vein 2h instillation, no blood coagulation indicator monitoring, can be implemented in the general ward. Therefore, thrombolytic therapy should be actively promoted and popularized.

(3) Anticoagulant therapy: Pulmonary embolism anticoagulant therapy is effective and important. According to the statistics of a group of 516 patients with pulmonary embolism, the survival rate of the anticoagulation group was 92%, the recurrence rate was 16%, and the non-anticoagulation group was 42% and 55%, respectively. The difference was very significant. Anticoagulant therapy for 1 to 4 weeks, pulmonary blood clots were completely dissolved in 25%, and 50% after 4 months. Commonly used anticoagulant drugs are heparin and warfarin.

Heparin: The standard unfractionated heparin is a high-sulfate mucopolysaccharide obtained by partial purification of porcine intestinal mucosa or bovine liver. Its molecular weight ranges from 3 to 30 kDa, with an average of 15 kDa. Low molecular weight heparin (LMWHs) is a fragment of unfractionated heparin that binds less than unfractionated heparin to plasma proteins and endothelial cells. Therefore, low molecular weight heparin has greater bioavailability, better predictable dose response and longer half-life. Heparin acts primarily through anti-thrombin III (ATIII), an enzyme that inhibits thrombin (factor IIa), X a, IXa, XIa and XIIa, which in turn promotes ATIII conformational changes and increases its activity by approximately 100 Doubled to 1000 times. Prevent the formation of additional thrombus, so that the endogenous fibrinolytic mechanism dissolves the formed blood clot, but heparin cannot directly dissolve the existing thrombus.

Thirty-five patients with pulmonary embolism were randomized to compare the effects of heparin and placebo. None of the 16 patients treated with heparin relapsed, and 10 of 19 patients who received placebo relapsed with pulmonary embolism, 5 of which died, indicating lung Embolization heparin therapy is effective. However, the effect of heparin is limited because the blood clot that binds to thrombin is not inhibited by heparin-antithrombin III, so heparin resistance may occur due to the binding of unfractionated heparin to plasma proteins. Heparin is the basis for the treatment of acute pulmonary embolism. The risk factors for bleeding should be considered before treatment, such as the history of bleeding with anticoagulant, thrombocytopenia, vitamin K deficiency, aging, underlying disease and combined medication. The most frequently overlooked test is a rectal examination of fecal occult blood positive. It has been reported in the literature that the Raschke dosing regimen can achieve rapid, effective and safe heparinization. The application of heparin for several days is sufficient to achieve adequate anticoagulant effect. Heparin instillation often needs to reach 1500-2000 U/h. Table 3 is a table of calculations based on the weight "Raschke" heparin. The heparin administration method commonly used in a hospital is intravenous drip, and the load is 2000-3000 U/h, followed by 700-1000 U/h or 15-20 U/(kg·h). It has been reported that the heparin half-life of patients with pulmonary embolism is shortened, about 50% of normal people, and the therapeutic dose should be appropriately increased.

Treatment with unfractionated heparin requires monitoring. The activated partial thromboplastin time (APTT) is at least 1.5 times greater than the control value (usually 1.5 to 2.0 times), and the minimum heparin therapeutic dose is administered within the effective anticoagulation range. Plasma heparin levels range from approximately 0.2 to 0.5 U/ml. Determination of plasma heparin levels is particularly useful in two situations: 1 monitoring patients with increased baseline APTT due to lupus anticoagulation or anti-cardiac lipid antibodies; 2 monitoring patients with high-dose heparin daily for deep vein thrombosis and pulmonary embolism.

The duration of medication is subsided in an acute process, the clinical condition is improved, and the thrombus is clearly dissolved, usually 7 to 10 days. In a few patients with heparin treatment, thrombocytopenia can occur. Therefore, the platelet count should be reviewed once every 3 to 4 days. Heparin can still be applied when the platelet count is (70-100)×109/L, and should be less than 50×109/L. Stop taking the medicine.

The most important side effect of heparin is hemorrhage. The risk of bleeding is related to age, underlying disease, liver dysfunction, and concurrent medications, in addition to the underlying platelet count. Most moderate hemorrhage discontinuation of heparin therapy is sufficient, because heparin half-life is only 60-90min, APTT usually returns to normal within 6h. Re-application of heparin or starting or alternating administration in small doses depends primarily on the extent of bleeding, the risk of re-embolization, and the extent of bleeding. Life-threatening events or intracranial hemorrhage, stop the heparin while using protamine sulfate (protamine), which combines with acidic heparin to form a stable complex that reverses anticoagulant activity. The amount of protamine sulfate (protamine), about 100 units of heparin, is required to be 1 mg, and slowly intravenously (for example, 50 mg/10 to 30 min). Protamine sulfate (protamine) can cause allergic reactions, especially in diabetic patients who have been exposed to protamine sulfate (protamine). Heparin-related side effects include thrombocytopenia, osteoporosis, and elevated transaminases.

Warfarin: is an antagonist of vitamin K, which prevents the activation of gamma carboxylates of coagulation factors II, VII, IX and X. On the fifth day of warfarin anticoagulation, even if the prothrombin time is prolonged, its effect may still be insufficient. Prolonged prothrombin time may initially reflect the depletion of factor VII, with a half-life of about 6 h, while coagulation factor II has a half-life of 5 days. When warfarin was started in the active thrombosis process, protein C and S protein decreased, and prothrombin produced potential function. After heparin and warfarin were overlapped for 5 days, the pre-coagulation of non-confrontation warfarin Can be offset. A randomized study found that oral anticoagulant alone compared with oral medication?a href=”http://jb.jb39.com/keshi/pifu/pifubing/490b3.html” target=”_blank” class=blue>痈嗡刂瘟 樯罹 樯罹 鲅ㄐ 鲅ㄐ 傻 傻 傻 傻 傻 捶 捶 捶 捶 捶 捶 捶 捶 捶 捶 捶 捶 捶 捶 捶 捶 捶 捶 捶 捶 捶 捶 捶The warfarin dose is adjusted according to prothrombin time and should be adjusted according to the international normalized ratio (INR), not the prothrombin time ratio or the prothrombin time in seconds. There were fewer patients with bleeding complications monitored by INR monitoring than prothrombin time ratio.

Heparin is usually applied for 5 to 7 days. APTT proves that warfarin has been used on the first day of the effective treatment range. The first dose is usually 3.0 mg. The dose is adjusted according to INR. The long-term INR should be maintained between 2.0 and 3.0. . Patients with generalized disease are often accompanied by vitamin K deficiency, which is prone to anticoagulation. Oral anticoagulants last at least 6 months. The anticoagulant should be gradually reduced to avoid rebound and increase blood coagulation. The contraindications for anticoagulant therapy include active gastrointestinal bleeding, trauma, postoperative, infective endocarditis, uncontrolled severe hypertension, cerebrovascular disease, and potentially bleeding disorders. The main side effect of warfarin is bleeding, with an incidence of about 6%, 2% for major bleeding, and 0.8% for fatal bleeding. Bleeding increases with increasing INR. Risk factors for hemorrhage include liver and kidney disease, alcoholism, drug interactions, trauma, malignant tumors, and previous gastrointestinal bleeding. Age is also an important factor. Life-threatening major bleeding requires urgent treatment with cryoprecipitate or fresh frozen plasma to normalize the INR and stop bleeding immediately. Less severe bleeding can be treated with vitamin K10mg subcutaneous or intramuscular injection to reverse the effect of warfarin within 6 to 12 hours. However, this treatment will make patients relatively resistant to warfarin for up to 12 weeks, making it difficult to re-administer warfarin. Mild hemorrhage with INR prolongation only requires interruption of warfarin treatment, without the need to lose frozen plasma until the INR is restored to a suitable therapeutic range. If the INR is bleeding within the therapeutic range, the possibility of occult malignancy may be suspected and excluded.

(4) surgical treatment

1 pulmonary thrombectomy: for massive pulmonary embolism with shock, systolic blood pressure to 100mmHg, increased central venous pressure, renal failure, medical treatment failure or medical treatment. Surgery under cardiopulmonary bypass has a higher operative mortality rate.

2 catheter broken pulmonary embolism: a special pigtail rotary catheter is usually used to break the large acute pulmonary embolism with shock, or partial thrombolysis can be used at the same time. After fracture, the shock index decreased, and the mean pulmonary artery pressure decreased significantly at 48 hours. The effective rate was 60% and the mortality rate was 20%. Mostly used in patients with thrombolytic and anticoagulant treatment contraindications.

3 installation of the inferior vena cava filter: the inferior vena cava filter is mainly used to confirm that the embolism originates from the lower limb or pelvic cavity to prevent the recurrence of pulmonary embolism. Its main indications are:

A. Confirmed pulmonary embolism and anticoagulant treatment contraindications: active bleeding; fear of major bleeding; complications caused by anticoagulation; plans to strengthen cancer chemotherapy.

B. Those who have been adequately treated and who have failed anticoagulation (such as recurrence of pulmonary embolism).

C. Prevention of high-risk patients: extensive, progressive venous thrombosis; catheterization or surgical thrombectomy; severe pulmonary hypertension or pulmonary heart disease. Most non-drifting DVTs are rarely embolized and can be treated with heparin alone. Because the filter can only prevent the recurrence of pulmonary embolism, and can not treat DVT, anticoagulation is still needed after installing the filter to prevent further thrombosis. Recently, there are filters that can be taken out to prevent recurrence of pulmonary embolism caused by embolization during thrombolysis, with better results and fewer complications.

4 treatment of deep vein thrombosis: about 70% to 90% of acute pulmonary embolism is derived from thrombosis of DVT, especially deep veins of the lower extremities are particularly common, therefore, the treatment of patients with acute pulmonary embolism must not ignore the examination of DVT And treatment to prevent recurrence of pulmonary embolism. The principles of DVT treatment are bed rest, limb elevation, anticoagulation (heparin and warfarin), anti-inflammatory and anti-platelet aggregating agents. Thrombolytic therapy in patients with deep vein thrombosis is not mature enough. Most patients have contraindications to thrombolytic therapy. If the thrombolytic drug is administered from a peripheral vein, the completely blocked venous thrombosis cannot be dissolved. Therefore, the US Food and Drug Administration approved the DVT thrombolytic regimen (streptokinase 250,000 U intravenous drip, followed by 100,000 U / h for 24-72 h), the effect is unsatisfactory, because delayed chain kinase infusion often cause allergies The reaction, as well as the concentration of streptokinase, needs to be 2 to 4 times in order to maintain the state of thrombolysis. Urokinase may work better. Therefore, thrombolytic therapy for DVT should be implemented individually as appropriate.

2. Chronic embolic pulmonary hypertension The incidence of chronic embolic pulmonary hypertension is unclear. It was thought to be a rare disease in the past. It is currently considered to be more than expected, accounting for about 1% to 5% of pulmonary embolism. The incidence in the country may be higher. Chronic embolic pulmonary hypertension can be the result of acute pulmonary embolism, more from repeated pulmonary embolism. The onset is slow or insidious. The clinical manifestations are similar to primary pulmonary hypertension, radionuclide lung ventilation/perfusion scan, enhanced CT, MRI, pulmonary angiography and lower extremity venous examination.

Treatment of chronic embolic pulmonary hypertension includes surgery, anticoagulation (oral anticoagulant), vasodilators, oxygen and cardiac, diuretic and so on.

(1) Pulmonary thrombosis endometrial resection: Pulmonary thromboendarterectomy is feasible in patients with chronic macrovascular thromboembolic pulmonary hypertension. The main criteria for selecting a surgical patient are:

1 Resting pulmonary vascular resistance is at least greater than 300 dyn·s·cm-5 or 4 Wood units.

2 Pulmonary angiography and angioscopy to determine the thrombus that can be achieved by surgery, such as the main lung, lobe and segmental arterial thrombosis. Endarterectomy cannot be performed with a thrombus farther away.

3 no kidney disease, coronary heart disease, blood disease, obvious interstitial lung disease or cerebrovascular disease to reduce perioperative mortality.

Filters should be routinely installed a few days before surgery, unless it is clear that the thrombus is from the lower extremities and the pelvis. Usually, venography of the lower extremities is required, and the filter should be placed from the lateral femoral vein to avoid thrombus detachment. Pulmonary thrombectomy is performed under deep hypothermic anesthesia with extracorporeal circulation. The operative mortality rate has dropped to 10% or less. It is worth noting that chronic embolic pulmonary hypertension is generally not suitable for angioplasty and is not suitable for thrombolytic therapy.

(2) Anticoagulant therapy: promote the venous thrombosis of the lower extremities, prevent recurrence of pulmonary embolism, and may promote partial thrombolysis and recanalization. The commonly used drug is warfarin. The course of treatment is more than 6 months. The longest patient in a hospital has been treated for 4 years. Some of the patients have continued to apply due to the aggravation of symptoms after stopping the drug. Most patients are stable. .

(3) treatment of vasodilators: in addition to mechanical blockage factors, embolism pulmonary hypertension may also participate in some of the effects, with partial reversibility. Clinically, vasodilators such as nifedipine and diltiazem can be tried.

(4) treatment of heart failure: when the right atrial pressure is elevated, there may be obvious treatment of digoxin, diuretics, angiotensin-converting enzyme inhibitors and dopamine. The efficacy of early patients is satisfactory.

(two) prognosis

There is no complete data on the natural course of pulmonary embolism in China. The natural course of disease depends mainly on whether embolization is detected and treated, the original cardiopulmonary disease, the extent of embolism, the degree of hemodynamic changes, age and autolysis activity of vascular endothelial thrombosis. In the United States, pulmonary embolism accounts for about 630,000 to 700,000 cases per year. 11% of them died within 1 hour of onset, and 89% lived for at least 1 hour. They should have the opportunity to get diagnosis and treatment, but most of the patients (71%) were not diagnosed, only 29% were treated, and 92% of the patients were treated. Survived, 8% died. If patients with acute pulmonary embolism do not die within a short period of time, the emboli may dissolve to varying degrees. There are at least two mechanisms for dissolving: 1 hour after the embolus moves to the distal pulmonary artery; 2 dissolves within a few days or weeks, and the shortest 14 days after the thrombus completely disappears. Therefore, patients with acute pulmonary embolism with stable hemodynamics have a good prognosis and a low mortality rate. Recurrent pulmonary embolism accounted for about 8.3%. It was seen before or during the treatment. The factors related to recurrence were: 1 heparin treatment had to be stopped due to bleeding; 2 heparinization was not used before oral anticoagulant; 3 larger lungs Embolism (lung perfusion defect more than 35%); 4 with heart disease; 5 obvious deep vein thrombosis. The overall outcome of pulmonary embolism after treatment was 80% re-dissolution, 10% pulmonary infarction, 5% pulmonary hypertension, and 5% death.

prevention

Although embolism of pulmonary embolism can be derived from any body system and right atrium, the room, but most of it comes from deep veins of the lower extremities. Therefore, the most important prevention of pulmonary embolism is for lower extremity thrombophlebitis and thrombosis. Actively treat foot infections (including ankles) and prevent varicose veins. Once acute thrombophlebitis occurs, rest in bed, lower limbs, and antibiotics and anticoagulants. Surgery and trauma should reduce bedtime and encourage early bed-out activities. If you need to stay in bed for a long time, you should regularly do active and passive activities of the lower limbs to reduce blood stasis. In addition to active treatment of cardiopulmonary diseases, patients with chronic cardiopulmonary disease should also reduce bed rest and preventive anticoagulant therapy when there is evidence of thrombosis or embolism. Long-distance rides and passengers should move their lower limbs in time to prevent thrombosis. Suspected venous thrombosis or thrombophlebitis can be done in the lower limb impedance volume map, vascular ultrasound Doppler, radionuclide or conventional venography, in order to timely diagnosis, early treatment. For "primary" (hereditary) hypercoagulable state or family history of deep vein thrombosis - pulmonary embolism, early detection and detection of defects in the coagulation mechanism, such as ATIII, C protein, S protein and plasminogen deficiency Wait. After the onset, anticoagulation should be used for life, and the inferior vena cava filter should be actively installed.

The incidence of pulmonary embolism abroad is very high. The annual incidence rate in the United States is about 600,000, and one third of them die, accounting for the third cause of death. It has also been reported that in recent years, as adults receive anticoagulant therapy, the incidence rate decreases. There is no exact epidemiological data in China, but in the autopsy data of more than 900 cases of cardiopulmonary vascular disease reported by Fuwai Hospital, 100 cases (11%) of the large thrombus blockage above the lung segment accounted for 29% of the heart disease autopsy. 26% of the disease, 19% of pulmonary heart disease, indicating that cardiopulmonary vascular disease is also often complicated by pulmonary embolism.