Pulmonary embolism in pregnancy

Introduction to pregnancy with pulmonary embolism Pulmonary embolism (PE) is the most serious complication of obstetric venous thrombosis. More than 50% of patients with massive pulmonary thrombosis die within 30 minutes. Most of them are less than rescued. Only from early recognition, prevent pulmonary embolism to reduce death. . basic knowledge The proportion of sickness: 0.01% Susceptible population: pregnant women Mode of infection: non-infectious Complications: sepsis diffuse intravascular coagulation

Pregnancy with pulmonary embolism

(1) Causes of the disease

Thrombosis (35%):

The most common pulmonary embolism is thrombosis. Pulmonary embolism (PE) caused by thrombosis is also called pulmonary thromboembolism (PTE). 70% to 95% is due to deep venous thrombosis (DVT). Blood circulation into the pulmonary artery and its branches, the primary site of the lower extremity deep veins, the literature reported that 90% to 95%, such as sputum, femoral, deep femoral and external iliac vein, chest, abdomen and hip surgery, suffering from The incidence of DVT in patients with cerebrovascular accident and acute myocardial infarction is very high. During the operation or within 24 to 48 hours after surgery, thrombus can form in the calf vein of the calf, but most of the activity can disappear after the activity, 5% to 20%. The thrombus can extend to the deep deep vein, and 3% to 10% cause PTE within 4 to 20 days after surgery. Under the armpit, the subclavian vein often has thrombosis, but only 1% of the thrombus is from the pelvic cavity. Venous thrombosis is an important source of PTE in women. It occurs in gynecological surgery, pelvic diseases, etc. Very few thrombi are from the right ventricle or right atrium. In addition, it should be noted that although lower extremity superficial phlebitis cannot directly produce PTE, 20% of them are related to DVT. Have a close relationship.

Other emboli: If there are fat plugs, air plugs, amniotic fluid, bone marrow, parasites, placental trophoblasts, metastatic cancer, bacterial plugs, heart sputum, etc. can cause PE.

Stasis of blood flow (15%):

As the most important condition, the activated coagulation factor is not easily inhibited by circulating anticoagulant substances, which is conducive to fibrin formation and promotes thrombosis. It is common in old age, chronic illness in bed, lower extremity varicose veins, obesity, shock, and congestion. Patients with sexual heart failure or pregnant women, according to the case of Peking Union Medical College Hospital, 40% of PE has various types of heart disease, of which rheumatic heart disease is the most common.

Venous wall injury: such as surgery, tumor, burn, diabetes, etc., due to tissue damage, endogenous and exogenous active thromboplastin is easily produced.

Hypercoagulable state (15%):

Seen in tumors, true erythrocytosis, severe hemolytic anemia, platelet lysis after splenectomy, homocystinuria, oral contraceptives, etc. Foreign literature reports that pancreatic cancer has the highest incidence of DVT, so DVT may be a precursor to malignant tumors. Laboratory tests have reported abnormalities in coagulation mechanisms in patients with recurrent DVT, such as increased platelet adhesion and decreased lifespan, increased levels of factor V and VII, and antithrombin factor III (antithrombinIII). Lack of abnormality of coagulation factor I, decreased plasminogen activator in endothelial cells of the vein wall, increased inhibitor of plasminogen and plasmin.

All diseases and pathological conditions that produce the above conditions are the danger of thrombosis and become the birthplace of thromboembolism.

(two) pathogenesis

1. Pathophysiological changes

(1) Physiological changes during pregnancy:

1 During pregnancy, the blood agglutination factor increases, the fibrinolytic activity decreases, and the pregnant woman is in a hypercoagulable state, which is prone to thrombosis.

2 venous reflux disorder during pregnancy: increased uterus compression of the iliac vein and inferior vena cava, venous return disorder, blood flow siltation, causing damage to vascular endothelial cells, changes in the blood vessel wall, easy to form a thrombus.

3 The role of progesterone: can relax the venous smooth muscle, slow blood flow, congestion in the inferior vena cava, increasing the possibility of deep vein thrombosis.

(2) Pathological changes after PE: PTE is often multiple and bilateral, the lower lung is more than the upper lung, especially in the right lower lobe lung is about 85%, which is undoubtedly related to blood flow and gravity, autopsy Only 5% to 10% of patients with PTE have found pulmonary infarction, mainly because the oxygen supply from the lung tissue comes from three aspects: the pulmonary artery, the bronchial artery and the airway of the local lung field. Only when the above two sources are seriously affected Infarction, but when suffering from chronic lung disease, left heart failure, even small embolism is prone to pulmonary infarction, usually determined by the degree and speed of vascular embolism.

The size of the embolus can be divided into:

1 riding straddle type embolization: the embolus completely blocks the pulmonary artery and its main branches.

2 huge embolism: more than 40% of the pulmonary artery is embolized, equivalent to two or more pulmonary artery.

3 large embolizations: less than two lobular arteries were blocked.

4 medium embolism: the main lung segment and sub-segmental artery embolization.

5 microembolism: fibrin clots, aggregated platelets, etc. enter the deep lung tissue.

When the main branch of the pulmonary artery is blocked, the trunk of the pulmonary artery is dilated, the right ventricle is rapidly enlarged, and the venous return is blocked, resulting in pathological manifestations of right heart failure. If the pulmonary artery occlusion is removed in time, it can still return to normal, if not properly treated, and repeated PTE occurs, pulmonary vascular occlusion is blocked, resulting in the formation of pulmonary hypertension, followed by chronic pulmonary heart disease.

In the case of pulmonary infarction, there is coagulative necrosis of the alveolar wall under the microscope. The alveolar cavity is filled with red blood cells and a slight inflammatory reaction. Generally, the chest X-ray film can show the infiltrating infarct shadow after 1 week, and the incomplete infarction, alveolar There are exuded red blood cells in the cavity, so there is no alveolar wall necrosis. Therefore, the infiltration shadow displayed on the chest radiograph disappears within 2 to 4 days without scarring. About 30% of patients in the pulmonary infarction can produce bloody pleural effusion.

2. Pathophysiological PTE occurs, the pulmonary blood vessels are blocked, and the resulting nerve reflex, the action of neurohumoral fluid can cause significant changes in respiratory physiology and hemodynamics.

(1) Pathophysiology of the respiratory system:

1 Increased alveolar void: no blood perfusion occurs in the embolized area, causing ventilatory-perfusion abnormalities, unable to perform effective gas exchange, so the alveolar void is enlarged.

2 Ventilation is limited: serotonin released by emboli, histamine, bradykinin, etc., can cause bronchospasm, ventilation is reduced, the diameter of the central airway is reduced, airway resistance is significantly increased.

3 Alveolar surfactant loss: surface active substances are mainly to maintain the stability of alveolar, when the pulmonary capillary blood flow is interrupted for 2 ~ 3h, the surface active substance is reduced; 12 ~ 15h, the damage has been very serious; blood flow is completely interrupted 24 ~ 48h, alveoli can be deformed and collapsed, congestive atelectasis, clinical manifestations of hemoptysis.

4 hypoxemia: due to the above reasons, hypoxemia is common, when the pulmonary artery pressure is significantly increased, the original normal hypoventilation zone increased blood flow, ventilation - perfusion is obviously abnormal, severe shunt can occur, heart failure Because of the low blood oxygen partial pressure of mixed venous blood, hypoxia can be aggravated.

5 hypocapnia: In order to compensate for the ineffective ventilation caused by ventilation-perfusion abnormalities, hyperventilation occurs, and the arterial blood PaCO2 is decreased.

(2) Hemodynamic changes: after PTE occurs, it causes a decrease in pulmonary vascular bed, an increase in pulmonary capillary resistance, an increase in pulmonary arterial pressure, acute right ventricular failure, an increase in heart rate, a sudden decrease in cardiac output, a decrease in blood pressure, etc. The average pulmonary artery pressure was higher than 2.67 kPa (20 mmHg) in 70% of patients, generally 3.33 to 4.0 kPa (25 to 30 mmHg). The degree of hemodynamic changes was mainly determined by the following conditions.

1 degree of vascular occlusion: the reserve capacity of the pulmonary capillary bed is very large. Only when more than 50% of the vascular bed is blocked, pulmonary hypertension occurs. In fact, when the pulmonary vascular occlusion is 20% to 30%, pulmonary hypertension occurs. It is due to the involvement of neurohumoral factors.

2 nerve, body fluid factors: In addition to causing pulmonary artery contraction, it also causes coronary artery, systemic vasoconstriction and life-threatening, to respiratory arrest.

3 pre-embolization cardiopulmonary disease status: can affect the results of PTE, such as pulmonary artery pressure can be higher than 5.33kPa (40mmHg).

(3) Changes in neurohumoral medium: The fresh thrombus is covered with a large amount of platelets and thrombin, and the inner layer has a fibrin network. The net has plasminogen, which causes platelets when the embolus moves in the pulmonary vascular network. Degranulation, release of various vasoactive substances such as adenine, adrenaline, nucleotides, histamine, serotonin, catecholamines, thromboxane A2 (TXA2), bradykinin, prostaglandins and fibrinogen degradation products ( Fibrinogen degradation products (FDP), etc., which stimulate various nerves of the lungs, including J receptors on the alveolar wall and stimulating receptors of the airways, causing dyspnea, increased heart rate, cough, bronchial and vasospasm, and vascular permeability. Increased sex, but also damage the non-respiratory metabolic function of the lungs.

Pregnancy with pulmonary embolism prevention

1. Generally, through careful clinical examination, early detection of deep vein thrombosis of the lower extremities, 80% of patients can prevent the occurrence of pulmonary embolism, to prevent venous thrombosis can take the following measures:

(1) Caesarean section or dystocia surgery should be gentle and meticulous, reduce tissue damage, especially to avoid damage to blood vessels and induce thrombosis. In the process of childbirth, the dehydration should be corrected in time to maintain water and electrolyte balance and prevent blood coagulation. increase.

(2) After childbirth, encourage patients to turn over and flex their lower extremities as much as possible after surgery to guide patients to get out of bed early, promote blood return and enhance blood circulation.

(3) Apply prophylactic anticoagulant therapy if necessary.

2. Anticoagulation of drugs to prevent thrombosis

(1) Low-dose heparin has a positive effect on the prevention of postoperative DVT, especially in patients over 40 years old, obese, with tumors and varicose veins, before pelvic cavity, hip surgery, etc., partial thromboplastin time (APTT) and Platelet, if normal, subcutaneous injection of heparin 5000U 2 hours before surgery, and once every 12 hours, until the patient can get up, usually 5 to 7 days, because the dose of heparin is low, it is not easy to have complications, no need to do coagulation mechanism monitor.

(2) Oral anticoagulants: such as acenocoumarol (sinfrom), warfarin (warfarin, warfarin) is commonly used in patients with DVT history, severe varicose veins Preventive anticoagulation.

(3) anti-platelet preparation: dipyridamole, 100mg orally per day, can inhibit platelet aggregation and adhesion, non-steroidal anti-inflammatory agents, such as low-dose aspirin (orally 0.3-1.2g per day), induced by indomethacin can inhibit Thrombin A2 reduces venous thrombosis.

Pregnancy with pulmonary embolism complications Complications, sepsis, diffuse intravascular coagulation

Due to pulmonary embolism, the blood supply to the alveoli can be interrupted, which can cause difficulty in breathing. In this disease, amniotic fluid usually enters the blood circulation, which can directly cause serious infectious diseases such as sepsis. It is also possible to activate endogenous and exogenous coagulation pathways to induce diseases such as disseminated intravascular coagulation.

Pregnancy with pulmonary embolism symptoms common symptoms pulmonary embolism cardiopulmonary embolism dyspnea anxiety abdominal pain nausea cerebral hypoxia diastolic galloping cold sweat coma

The size of the embolus and its degree of obstruction of the pulmonary artery make its clinical manifestation a priority.

1. Symptoms have no specific clinical manifestations, mostly with a sudden onset of symptoms, a series of cerebral hypoxia. According to Goldhaber (1999), the clinical manifestations of pulmonary embolism in 2500 non-pregnant women are:

(1) Sudden onset, sudden onset of unexplained cardiovascular collapse, pale, cold sweat, weak, sudden breathing difficulties accounted for 82%, chest pain accounted for 49%, cough accounted for 20%, syncope 14%, hemoptysis 7% .

(2) Cerebral hypoxia symptoms: The patient is extremely anxious, fearful, indifferent, burnout, nausea, convulsions and coma.

(3) Acute pain: chest pain, shoulder pain, neck pain, precordial area and upper abdominal pain.

2. Large arterial embolism can cause symptoms of acute right heart failure, and even sudden death.

(1) The main signs of the cardiovascular system are tachycardia, and even diastolic galloping, pulmonary artery second hyperthyroidism, aortic valve and pulmonary valve have second division, shock, cyanosis, central venous pressure, Jugular vein engorgement, large liver.

(2) The main signs of the lungs are rapid breathing, wet snoring, pleural friction, wheezing and signs of lung consolidation.

(3) Electrocardiogram has right axis deviation, T wave inversion and right beam branch block.

(4) Blood gas analysis showed low performance of both PaO2 and PaCO2.

(5) X-ray chest radiograph showed congestive atelectasis or pulmonary infarction, which occurred within 12 to 36 hours.

Pregnancy with pulmonary embolism

1. Blood routine and biochemical enzymes Lactate dehydrogenase, aspartate aminotransferase (AST), phosphocreatine kinase (CPK) is meaningless for the diagnosis of PTE, when there is pulmonary infarction, white blood cells and erythrocyte sedimentation rate can be increased .

2. Soluble fibrin complex (SFC), fibrinolytic substance (FDP) and D-dimer SFC suggest that thrombin is produced recently, and FDP indicates plasmin activity. The positive rate in PTE is 55%-75. %, when both are positive, it is beneficial to the diagnosis of PTE.

3. Arterial blood gas analysis and lung function

(1) When inhaling air, approximately 85% of PTE patients showed PaO2 below 10.7 kPa (80 mmHg), which may indicate the degree of embolization.

(2) The determination of the alveolar oxygen partial pressure and the arterial oxygen partial pressure difference (PA-aDO2) is more meaningful than PaO2. After embolization, the patient often has hyperventilation, so the PaCO2 decreases and the oxygen partial pressure of the alveolar gas ( PaO2) increased, PA-aDO2 should be significantly increased.

(3) Ineffective lumen/tidal volume ratio (VD/VT) increases during embolization. When the patient has no restrictive or obstructive ventilatory disorder, a ratio of >40% suggests PTE may be, <40% without clinical embolism. Exclude PTE.

4. Electrocardiogram examination: mainly manifested as acute right ventricular dilatation and pulmonary hypertension, showing a significant right deviation of the ECG axis, extreme clockwise transposition, right bundle branch block, and a typical SI Q III T III wave pattern ( I lead S wave depth, III lead Q wave significant and T wave inversion), sometimes pulmonary P wave, or pulmonary-crown reflex myocardial ischemia, such as ST segment elevation or depression abnormal, above Changes often occur within 5 to 24 hours after onset, and most recover within a few days or 2 to 3 weeks. Only 26% of patients have the above ECG changes. Most patients have normal ECG, or only non-specific changes, so ECG Normal, the disease cannot be ruled out, and ECG is also used as a means of distinguishing from acute myocardial infarction.

5. Chest X-ray performance: Because of the pathological changes of pulmonary embolism, X-ray findings are also diverse, patients with suspected pulmonary embolism should be continuously chest X-ray examination, more than 90% of patients have some abnormal changes, such as normal Pulmonary embolism cannot be excluded.

6. Pulmonary perfusion imaging and pulmonary ventilation/perfusion imaging: a relatively popular PE diagnosis method. The typical findings of pulmonary perfusion scan in PE patients are perfusion defects in the distribution of lung segments. Radioactive gases are distributed throughout the lungs with air. Recently, the United States randomized a multicenter study in a population of suspected acute PE to estimate the sensitivity and specificity of PE diagnosis. A prospective study of PE diagnosis (PIOPED) ), compared with pulmonary angiography (CPA), the sensitivity of the diagnosis was found to be 92%, specificity was 87%, but the normal diagnosis still has 4% to 5% of subclinical PE, so it can be used for suspicious PE. Standard screening tests, but pulmonary angiography is still required for patients who are highly suspicious and cannot be determined.

7. Spiral CT: Spiral CT is a new type of PE diagnostic method. Its direct signs are half-moon shape, annular filling defect, complete obstruction and orbital sign, indirect signs are main pulmonary artery and left and right pulmonary artery expansion, etc. The positive rate of PE diagnosis above and above the level is 96%, but the diagnosis of PE below the segment is prone to false positive.

8. Pulmonary angiography (CPA): Selective pulmonary angiography is the most accurate method for diagnosing PE. The positive rate is 85%-90%. It can determine the location and extent of obstruction. If supplemented with partial enlargement and oblique imaging, It can even display emboli in blood vessels with a diameter of 0.5mm. Within 72h of embolization, CPA diagnoses PE with high sensitivity and specificity. It is generally not easy to miss diagnosis, false positives are rare, error rate is 6%, sometimes due to embolism. Too small to detect, so it can produce positive perfusion imaging, and pulmonary angiography is negative, as a basis for diagnosis of pulmonary embolism, X-ray signs of pulmonary angiography: there must be filling defects or vascular interruption in the pulmonary lumen, other suggestive meaning Signs such as localized lobes, reduced vascular texture in the lungs or slow blood flow and decreased blood volume.

Pulmonary angiography can also be used to obtain some other diagnostic data, such as pulmonary wedge pressure can indicate the presence of left heart failure; the distance between the catheter and the heart shadow can determine whether there is pericarditis; the pulmonary artery pressure is correctly measured, but the pulmonary artery 4% to 10% of angiography complications, such as cardiac perforation, pyrogen reaction, arrhythmia (more common atrial and ventricular premature contractions), bronchospasm, allergic reactions, hematoma, etc., occasional death, mortality 0.4 %, therefore, selective pulmonary angiography must be combined with clinical, chest X-ray and lung imaging, the main indications are: 1 lung imaging can not be diagnosed, but can not rule out PE patients, especially the original congestive heart failure and chronic obstructive pulmonary disease 2 patients before the preparation of pulmonary embolectomy or inferior vena cava surgery, in order to avoid the risk of pulmonary angiography, pulmonary artery pressure should be measured first, if the pulmonary artery pressure is too high, it is easy to produce cardiac arrest in the angiography, so in Contrast was performed under right heart bypass.

9. Digital subtraction angiography (DSA): This method can significantly reduce contrast agent concentration, dosage and side effects, basically no complications and death, and the coincidence rate with imaging is 83.5%. This method is applicable to suspicious height imaging. Or to estimate that the embolism is located in the main branch of the pulmonary artery, especially those with chronic obstructive pulmonary disease and those who cannot receive pulmonary angiography, and its X-ray signs are similar to angiography.

10. Magnetic Resonance Angiography (MRA): In 1997, Meaney and colleagues used a new noninvasive method of sputum-enhanced pulmonary MRA to diagnose PE and compared it with traditional CPA and found that its sensitivity was 75%. 95%, although lower than the traditional CPA, MRA avoids ionizing radiation, avoids iodine contrast agents that may cause nephrotoxicity, and is safer to operate, so it is a PE diagnosis method worthy of further study, but the price is too expensive.

11. Echocardiography: including conventional transthoracic ultrasound (TTE) and transesophageal ultrasound (TEE), in recent years, the role of PE in the diagnosis of PE has been paid more and more attention, TTE can show the pulmonary artery trunk and its branch embolism, indirect signs have right ventricle Expansion, abnormal wall motion, tricuspid regurgitation, pulmonary hypertension, etc., Rudoni et al. performed a retrospective case-control study of 71 patients with PE confirmed by CPA, and found that 13 of the 24 CPA-confirmed PEs had TTE The above positive findings, the sensitivity was 0.54; 13 cases of TTE positive in 13 cases of CPA confirmed the presence of PE, the positive predictive value of 0.90, TTE is considered a promising PE detection method, recently TEE also began to be used for the diagnosis of PE, The performance of the right ventricle is enlarged, the ventricular septum is shifted to the left, the left ventricle becomes smaller in D shape, the right ventricle is weakened, and the pulmonary artery is widened. Pruszozky et al. performed TEE on 40 patients with CPA or lung confirmed PE. Central type PE (embolism in the main pulmonary artery and leaf pulmonary artery) was 32 (80%), but the rate of detection of distal PE (segment and below) was low (46%). These data suggest that TEE has more central type PE. Can clearly diagnose, but far in the arteries of the segment and below PE should take caution.

12. D-dimer: D-dimer mass concentration increases when thrombus is formed, is a promising test method, D-dimer >500g / L as a diagnostic criteria Its sensitivity is only 35.2%, so this method can not be used to diagnose thrombotic diseases, except for such diseases.

When suspected pulmonary embolism, chest X-ray, ECG, blood gas analysis, etc., should be performed, but the diagnosis depends on lung perfusion scan or pulmonary angiography.

Diagnosis and differential diagnosis of pregnancy complicated with pulmonary embolism

Diagnostic criteria

According to the history and clinical manifestations, it is extremely important to identify superficial vein thrombosis and deep vein thrombosis. Because of pulmonary embolism from the lower extremities, 95% are formed by deep vein thrombosis. It is easier to diagnose superficial thrombosis, but the symptoms of deep thrombosis are not. Obviously, it is difficult to make a clear diagnosis. Therefore, it is extremely important to master certain clinical manifestations of thrombosis. In addition to the above clinical symptoms, such as local gastrocnemius muscle and thigh muscle group, there is no effect on position change, lower limb pain during cough, and gastrocnemius during walking. Partial tear pain, the skin temperature of the disease side is higher than the healthy side, indicating the occurrence of deep thrombosis.

If deep venous thrombosis is known, it is not difficult to diagnose pulmonary embolism, but local signs are often lacking. Moreover, the embolus can also come from a hidden part of the pelvic cavity. The risk of pulmonary embolism is generally no thrombosis. The period of abnormal intravascular blood vessels is most dangerous on the 9th day after delivery or on the 11th day after cesarean section, which can cause sudden fatal consequences.

Differential diagnosis

Differential diagnosis should consider any disease that can cause respiratory circulatory symptoms in pregnant women, mainly amniotic fluid embolism, the latter occurs mostly in the time of birth, often using uterine contractions to strengthen the history of contractions, in addition to severe respiratory and circulatory failure, There are mainly diffuse intravascular coagulation, and generally no chest pain is the key point for identification.

Identification of acute pulmonary embolism and myocardial infarction.

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