I. Overview.
Pulmonary embolism (PE) : A clinicopathophysiological syndrome in which endogenous or exogenous emboli block the pulmonary artery and its branches, causing pulmonary circulation disorders, manifested as dyspnea, chest pain, hemoptysis, panic, etc. Large PE can cause acute pulmonary origin heart disease and even sudden death. It is seen in thrombosis, fat, air, and amniotic fluid embolism, most commonly thromboembolism (PTE), where the thrombus originates from deep veins, mainly from the deep veins of the lower extremities. Treatment is mainly thrombolysis and anticoagulation.
II. Definition
A clinical and pathophysiological syndrome in which the pulmonary artery and its branches are blocked by thrombus emboli from the body veins or the right heart, causing obstruction of the pulmonary circulation.
Pulmonary infarction (PE): After the occurrence of PE, if the lung tissue in the area of its innervation is blocked or interrupted by blood flow, pulmonary necrosis occurs.
Third, the mechanism of occurrence and risk factors of PTE
The emboli mainly originate from deep venous thrombosis.
Intravenous thrombosis has.
Local injury in the blood vessel.
Blood stagnation.
Hypercoagulable state.
Genetic factors: Factor V mutations, S-protein defects, C-protein defects, antifibrinase deficiency, antithrombin III deficiency, etc.
Secondary factors: surgery, lack of activity, trauma, tumor, obesity, advanced age, hyperlipidemia, hypertension, nephrotic syndrome, oral contraceptives, pregnancy, postpartum, stroke, spinal cord injury, indwelling central venous catheter, SLE, cardiopulmonary disease, etc.
IV. Clinical type and performance
Clinical types.
Sudden death type
Unexplained respiratory distress.
Acute pulmonary origin heart disease: sudden onset of dyspnea, cyanosis, sense of near death, hypotension, shock, right heart failure. Seen in those with embolization of more than two lobes of the lung.
Pulmonary infarction: sudden shortness of breath, chest pain, hemoptysis and pleural friction sounds or pleural effusion.
Recurrent pulmonary thromboembolism. (chronic pulmonary hypertension)
Clinical symptoms.
Dyspnea: 90% of the time.
Chest pain: 88%.
Hemoptysis: 30%.
Panic: 55%.
Cough: 50%.
Syncope: 13%.
Abdominal pain: associated with diaphragmatic irritation.
Shock, irritability, nausea, vomiting, cold sweats.
Physical signs.
Hyperactive second pulmonary artery heart sound
Systolic jet sounds or systolic jet murmurs can be heard in the pulmonary valve region, and diastolic regurgitant-like murmurs may also be present.
A systolic blowing murmur may be heard in the tricuspid region, and systolic fluctuations may be seen.
Pleural effusion
Signs of right heart failure are present in severe cases.
V. Auxiliary tests
Arterial blood gas analysis: often shows hypoxemia and hypocarbia
ECG: sinus tachycardia, T-wave abnormalities, SⅠ QⅢ TⅢ sign, complete or incomplete right bundle branch block, pulmonary P-wave, right-sided electrical axis and clockwise transposition
X-ray chest film
Pulmonary artery obstruction sign: regional thinning, thinning or loss of pulmonary texture and increased translucency of the lung fields.
Pulmonary hypertension and right heart enlargement signs: widening or truncation of the right lower pulmonary artery trunk, bulging pulmonary artery segments and enlargement of the right ventricle.
Secondary changes in the lung tissue: localized lamellar shadows in the lung field, wedge-shaped shadows with the tip pointing to the hilum, pulmonary atelectasis or incomplete expansion, diaphragmatic elevation on the side with pulmonary atelectasis, sometimes combined with small to moderate pleural effusion
Echocardiography: in severe cases, reduced local motion of the right ventricular wall; enlargement of the right ventricle and/or right atrium; leftward shift of the septum and abnormal motion; dilatation of the proximal pulmonary artery; increased velocity of tricuspid regurgitation.
Ultrasonography may occasionally confirm the diagnosis directly by finding a thrombus in the proximal pulmonary artery. Right ventricular wall hypertrophy is seen if there is prolonged pulmonary hypertension
Plasma D-dimer (D-dimer): elevated in acute PTE.
If its level is below 500 μg/L, acute PTE can be largely excluded.
CT pulmonary arteriogram (CTPA): Pulmonary artery truncation, filling defect.
Pulmonary arteriogram
VI. Diagnosis
Raise the awareness of pulmonary embolism and think comprehensively about the possible clinical manifestations.
Chest radiograph, ECG, arterial blood gas analysis, UCG, D-dimer examination for suspected pulmonary embolism.
CTPA, nuclear V/Q scan, PA angiography should be done for the above tests suggesting PTE. CTPA or pulmonary arteriography is an important evidence to confirm the diagnosis.
VII. Differential diagnosis
Acute myocardial infarction and angina pectoris
Aortic coarctation
Pleurisy, pericarditis, spontaneous pneumothorax
Cardiac insufficiency
Bronchopulmonary disease
VIII. Treatment
Symptomatic treatment
Anticoagulation therapy: anticoagulant drugs mainly include heparin, low molecular heparin and warfarin
Thrombolytic therapy: commonly used thrombolytic drugs: recombinant tissue-type fibrinogen activator (rt- PA), urokinase (UK), streptokinase (SK)
Interventional and surgical treatment