Diagnosis and treatment of pulmonary artery embolism
Wu Da-Wei, Department of Respiratory Medicine, Qilu Hospital, Shandong University
Pulmonary embolism is a general term for the clinical syndrome of various emboli obstructing the pulmonary arterial system, including pulmonary thromboembolism, amniotic fluid embolism, air embolism and fat embolism syndrome. Pulmonary thromboembolism (PTE) is a clinical and pathological syndrome of obstruction of pulmonary circulation caused by thrombus emboli entering the pulmonary circulation and blocking the pulmonary artery or its branches, and is the most common type of pulmonary embolism. Wu Dawei, ICU Department, Qilu Hospital, Shandong University
After embolism of pulmonary artery, if necrosis occurs in the lung tissues in its innervated area due to obstruction or interruption of blood flow, it is called pulmonary infarction. Due to the multiple blood supply mechanisms of lung tissues, pulmonary infarction occurs in only about less than 15% of pulmonary embolism.
The thrombus that causes pulmonary embolism is mainly from deep vein thrombosis . Deep vein thrombosis and pulmonary artery embolism together are called venous thromboembolism (VTE).
Epidemiology
The annual incidence of VTE in Western countries is estimated to be 1‰-5‰, and can be as high as 1% in the elderly population. In the United States, there are at least 200,000 new cases of VTE each year, and the number of deaths due to pulmonary embolism reaches more than 50,000 each year, and the mortality rate is the third cause of death, after tumor and myocardial infarction. Considering the high underdiagnosis rate of pulmonary embolism, the actual incidence may be even higher. Pulmonary embolism The underdiagnosis rate is up to 80% or more, and the mortality rate is 20%-30% without treatment; the mortality rate can be reduced to 2%-8% for those who are diagnosed clearly and treated actively.
There is no accurate epidemiological data in China, and in the past, due to insufficient attention to pulmonary embolism and insufficient diagnostic techniques, there were more missed diagnoses of pulmonary embolism. In recent years, with the improvement of diagnostic awareness and examination technology, the number of diagnosed cases has increased significantly.
Risk factors and pathogenesis
Most of the thrombi that cause pulmonary embolism come from the deep veins of the lower limbs (including femoral vein, N vein and gastrocnemius deep vein), and the thrombi of pulmonary embolism in women often come from the pelvic vein, mostly after pelvic disorders and gynecological surgery. About 1% of thrombi originate from the axillary and subclavian veins, and rarely from the right ventricle or right atrium. In situ thrombosis in the pulmonary artery is rare. After the formation of deep vein thrombosis, the tail of the thrombus often floats in the blood flow, which can cause partial or complete dislodgement of the thrombus once the blood flow suddenly increases (e.g., sudden activity after prolonged bed rest, straining to defecate), and then enters the pulmonary circulatory system with the blood flow. Therefore, the etiology of pulmonary artery embolism is closely related to deep vein thrombosis, and both can be considered as the manifestation of a disease in different stages and locations, and it can also be considered that deep vein thrombosis is the primary cause of pulmonary artery embolism, and pulmonary artery embolism is a complication of deep vein thrombosis. They can be divided into two categories, primary and secondary.
Primary risk factors are caused by genetic variants and often have recurrent venous thrombosis and embolism as the main clinical manifestation. If a patient under 40 years of age has no obvious cause or recurrent deep vein thrombosis and pulmonary embolism, or has a family genetic predisposition, attention should be paid to the examination of relevant primary risk factors. Secondary risk factors refer to a variety of pathological and pathophysiological changes acquired later in life that predispose to deep vein thrombosis and pulmonary artery embolism. These include fractures, trauma, surgery, malignancy, and oral contraceptive use. The above risk factors can be present alone or in concert and act synergistically. Age can be an independent risk factor, and the incidence of deep vein thrombosis and pulmonary artery embolism gradually increases with increasing age.
The severity of symptoms and signs of pulmonary artery embolism depends on the degree of mechanical embolization of the embolus (size and number of thrombus, embolic range), the speed of attack (the amount and speed of vasoactive substance release) and the original cardiopulmonary function status, and the clinical manifestations can vary greatly, from asymptomatic to sudden death.
I. Symptoms ① unexplained dyspnea and shortness of breath are the most important clinical manifestations; ② chest pain, often manifested as pleuritic chest pain, but also angina-like pain; ③ cough, mostly dry or a little white sputum; ④ hemoptysis, mostly a small amount of bright red blood, suggesting pulmonary infarction or congestive atelectasis; ⑤ syncope, suggesting large pulmonary embolism; ⑥ huge pulmonary embolism can cause shock or even sudden death.
Signs ① Fever: mostly around 38.C, can last for more than a week, those who continue to be higher than 38.C should pay attention to whether there is secondary infection. ②Respiratory system, shortness of breath, cyanosis, auscultation can be heard fine wet monk snail woven N even targeting the targeting of Σ烈艋虺鱿中厍换禾 escape from the sole Noah indistinct congestion matte first and woven (15 units) to stop the food displays live crab feed K feed “chalk waste low often border < ne cut mu Tong9惴悍嗡 Noah taste gingival clone ridge vortex mou] squid quality stupid piggyback on the man palpitating Tonga umbrella (4) mythical crannies jan locus right woven bombs intimidation warship navigation amine to choose the month of the month by their scalping The black hospital stole off the ditch to take "carambola mackerel !We are silly far from the spring swallowed escape from the sole drought (19) stole milk escape from the nightmare trick enough to fold (8) Ben spring oval stains stop 50% of patients lack of clinical manifestations and this is not the specific symptom of deep vein thrombosis.
Laboratory and special tests
Arterial blood gas analysis often shows hypoxemia, hypocarbia, and increased alveolar-arterial partial pressure of oxygen [P(A-a)O2], but in some patients the blood gas results can be normal.
II. ECG Most cases present with nonspecific ECG abnormalities. When there is elevated pulmonary artery and right heart pressure, SIQIIITIII sign (i.e. deepening of S wave in lead I, Q/q wave and T wave inversion in lead II), complete or incomplete right bundle branch conduction block, pulmonary P wave, rightward deviation of electrical axis and cis-clockwise transposition may appear. ECG changes are more diagnostic if there are dynamic changes.
X-ray chest film Large pulmonary embolism can show regional pulmonary texture thinning or disappearance and pulmonary hypertension. In case of pulmonary infarction, a wedge-shaped shadow with the tip pointing to the pulmonary hilum can be seen. In most patients, the abnormalities of X-ray chest film are not obvious, but it is important to help identify other chest diseases.
Echocardiography In cases of massive pulmonary embolism, reduced local motion of the right ventricular wall is seen (as a basis for classifying submassive pulmonary embolism); enlargement of the right ventricle and/or right atrium; leftward shift of the septum and abnormal motion; dilatation of the proximal pulmonary artery; and increased velocity of tricuspid regurgitation.
V. Plasma D-dimer (D-dimer) Elevated in acute pulmonary embolism. If its level is less than 500 μg/L, acute pulmonary embolism can be largely excluded.
VI. Radionuclide lung ventilation/perfusion scan The typical sign is a lung perfusion defect that is distributed in lung segments and does not match the ventilation picture. Localized perfusion defects in at least 2 or more lung segments are diagnostic only if the area is well ventilated or if there is no abnormality on the chest radiograph.
VII. Spiral CT and electron beam CT With CT pulmonary angiography (CT-PA), it is possible to detect above-segment pulmonary artery thrombosis, which is manifested as a low-density filling defect in the pulmonary artery. It is one of the most commonly used means to confirm the diagnosis of pulmonary embolism. This method is reliable, non-invasive, rapid and easy to master, and has largely replaced the traditional invasive pulmonary arteriography.
Magnetic resonance imaging (MRI) MRI pulmonary arteriography (MRPA) has a high sensitivity and specificity for the diagnosis of thrombosis in the pulmonary arteries above the segment. It can also be used for patients who are allergic to iodine contrast agents.
Pulmonary arteriography is the classic method to confirm the diagnosis of pulmonary embolism. Direct signs include contrast filling defects in the pulmonary arteries. Indirect signs include slow flow of pulmonary artery contrast, local hypoperfusion, and delayed venous return. It is an invasive examination technique and has the possibility of fatal or serious complications, so its indications should be strictly controlled.
X. About the examination of deep vein thrombosis The examination of deep vein thrombosis should be performed in patients with suspected pulmonary artery embolism, and the examination of lower limb venous ultrasound, radionuclide or X-ray venography, CT venography (CTV), MRI venography (MRV), limb impedance volumetry (IPG), etc. can be selected according to the specific situation to help clarify whether there is deep vein thrombosis and the emboli source.
【Diagnosis】 The clinical manifestations of pulmonary embolism are diverse and lack specificity. The key to diagnosis is to raise awareness of the diagnosis. Patients with unexplained dyspnea, shortness of breath, syncope and other symptoms, especially those with risk factors, should consider the possibility of PET. If the patient also has unilateral or bilateral asymmetric lower limb swelling, the possibility of PET is extremely high, and the corresponding examination should be performed promptly. Confirmatory methods include radionuclide lung ventilation/perfusion scan, CT-PA , MRPA and pulmonary arteriography. Plasma D-dimer is only of diagnostic relevance for exclusion. All patients with PET should be examined for deep vein thrombosis to clarify the source of the thrombus.
Differential diagnosis】Because of the lack of specificity of the clinical manifestations of pulmonary embolism, it is easy to be confused with other diseases, so the rate of clinical omission and misdiagnosis is very high. It is important to make a good differential diagnosis of pulmonary embolism to detect and diagnose pulmonary embolism in time.
About 19% of patients with pulmonary embolism have angina pectoris, and some of them have myocardial ischemia-like changes in ECG, which are easily misdiagnosed as angina pectoris or myocardial infarction caused by coronary artery disease. Evidence of coronary artery obstruction is seen on coronary angiography in patients with coronary artery disease, and there are corresponding characteristic dynamic changes in the electrocardiogram and myocardial enzyme levels in myocardial infarction.
Second, pneumonia When patients with pulmonary artery embolism have fever, hemoptysis, pleurisy-like chest pain and X-ray chest shadow, they are often misdiagnosed as pneumonia. However, patients with pneumonia mostly have chills and pus sputum, and the effect of antibacterial drug treatment is obvious.
The differentiation of CTEPH from primary pulmonary hypertension is sometimes difficult. CTEPH shows evidence of hypodense filling defects in the pulmonary arteries by CT-PA, and radionuclide pulmonary perfusion scans show pulmonary perfusion defects distributed in lung segments, whereas primary pulmonary hypertension has no filling defects in the lumen of the pulmonary arteries , and radionuclide pulmonary perfusion scans are normal or generally radiologically sparse.
PET should also be differentiated from other causes of pleural effusion, syncope, and shock.
The goals of pulmonary embolism treatment are to eliminate pulmonary vascular embolism, relieve clinical symptoms caused by embolism, maintain or restore adequate circulating blood volume, prevent secondary chronic pulmonary hypertension, and prevent recurrence of pulmonary embolism.
II. Thrombolytic therapy is mainly applied to cases of massive pulmonary embolism. Thrombolysis is not recommended for cases with normal blood pressure and right ventricular motor function. The time window for thrombolysis is generally set at 14 days or less. Thrombolytic therapy must be performed under the guidance of an experienced physician.
Anticoagulation therapy is the basic treatment for pulmonary thromboembolism, which can effectively prevent the re-formation and recurrence of thrombus, and at the same time use the body’s own fibrinolytic mechanism to dissolve the formed thrombus. For patients with obvious clinical symptoms and high suspicion of pulmonary thromboembolism, effective anticoagulation therapy with heparin or low molecular heparin can be arranged without waiting for the test results. The main anticoagulant drugs are heparin, low molecular heparin and warfarin. Antiplatelet agents do not meet the anticoagulation requirements for pulmonary embolism or deep vein thrombosis.
Hemorrhagic disease or active bleeding is a relative contraindication to anticoagulant therapy.
(i) Heparin and low-molecular-weight heparin (LMWH) Continuous drip is the preferred method of heparin administration: 2,000-5,000 IU or 80 IU/kg intravenously, followed by 18 IU/kg-1/h – 1 continuous intravenous drip. The APTT should be measured every 4-6 hours during the first 24 hours after the start of treatment, and the dose should be adjusted according to the APTT to achieve and maintain the APTT at 1.5-2.5 times the normal value as soon as possible. Heparin intermittent subcutaneous injection method: 3,000-5,000 IU should be injected sedatively first, and then 250 IU/kg q12h should be injected subcutaneously. Heparin intermittent intravenous infusion method: 5000 IU q4h, or 7500 IU q6h intravenous. Heparin can affect the function and number of platelets, and the platelet count should be checked regularly.
The anticoagulant efficacy of LMWH is similar to that of heparin, and the former has relatively less effect on platelets and fewer bleeding complications. However, for patients with severe renal failure, intravenous heparin is better than LMWH. The recommended therapeutic doses vary according to the anti-Xa:IIa ratios of various LMWH, so please refer to the product instructions for use.
(B) Coumarins oral anticoagulants are antagonists of vitamin K. Warfarin is commonly used clinically. It is recommended to start coadministration of warfarin on day 1 of common heparin or LMWH therapy, and the starting dose of warfarin is 3.0~5.0 mg/d. Since warfarin needs 3-5 days to exert its full effect, it should be overlapped with heparin or LMWH for at least 4-5 days, and the INR should be stabilized at 2.0-3.0 before stopping heparin or LMWH and continuing warfarin, and the INR should be measured and the warfarin dose adjusted periodically.
The length of anticoagulation therapy depends on whether the patient’s risk factors can be eliminated, whether the first episode or recurrence, and co-morbidities. Patients who have a first episode with clear risk factors that can be eliminated (surgery, fracture, pregnancy, etc.) can be treated for 3 months.
Patients with a first episode of idiopathic pulmonary embolism-deep vein thrombosis without clear risk factors should be treated with anticoagulation for at least 6 to 12 months or indefinitely, with periodic risk-benefit assessments to decide whether to continue treatment.
For patients with two or more pulmonary embolisms, those with non-eliminable risk factors, and those with combined pulmonary heart disease, the course of therapy needs to be extended, or even lifelong anticoagulation.
Warfarin overdose is prone to bleeding. Vitamin K antagonism can be given via parenteral route, and fresh whole blood or fresh frozen plasma can be transfused for severe bleeding.
Surgical and interventional treatment Pulmonary artery thrombectomy and pulmonary artery catheter fragmentation aspiration are only indicated for massive pulmonary embolism with fatal blockage of the main trunk or major branches of the pulmonary artery where aggressive medical therapy has failed, or where thrombolysis is absolutely contraindicated. A vena cava filter should be placed in patients with contraindications or complications to anticoagulation, or recurrent thromboembolism despite adequate anticoagulation therapy. In most patients with pulmonary embolism, a vena cava filter should not be placed blindly.
V. Treatment of chronic thromboembolic pulmonary hypertension If the embolism site is in the central pulmonary artery, endothelial stripping of pulmonary artery thrombosis can be considered. For patients with CTEPH who have undergone pulmonary artery thromboendarterectomy and who are not eligible for surgery, they should be treated with warfarin anticoagulation for life to maintain INR in the range of 2.0~3.0. A vena cava filter can be placed in patients with CTEPH.