Pulmonary embolism (PE) is an occlusion of one or more pulmonary arteries by blood clots that form elsewhere, usually in large veins in the lower extremities or pelvis.
Risk factors are conditions that impair venous flow and cause damage or dysfunction of the endothelium, especially in patients with hypercoagulable conditions. Symptoms of pulmonary embolism (PE) include shortness of breath, pleuritic chest pain, cough, and, in severe cases, fainting or cardiac and respiratory arrest. The changes detected are uncertain and may include tachypnea, tachycardia, hypotension, and increased pulmonary component of the second heart sound. Diagnosis is based on ventilation perfusion scan, CT with angiography, or pulmonary arteriography. Pulmonary embolism (PE) is treated with anticoagulants, thrombolytics, and sometimes surgery to remove the clot.
Pulmonary embolism (PE) occurs in approximately 650,000 people and causes up to 200,000 deaths per year, accounting for approximately 15% of all hospital deaths per year. The prevalence of pulmonary embolism (PE) in children is approximately 5 per 10,000 admissions.
ICD-10 code
I26 Pulmonary embolism
I26.0 Pulmonary embolism with mention of acute cor pulmonale
I26.9 Pulmonary embolism without mention of acute cor pulmonale
Causes of pulmonary embolism
Almost all pulmonary embolism results from thrombosis in the lower extremities or pelvic veins (deep venous thrombosis [DVT]). Blood clots in any system can be dumb. Thromboemboli can also occur in the veins upper limbs or in the right heart. Risk factors for deep venous thrombosis and pulmonary embolism (PE) are similar in children and adults and include conditions that impair venous flow or cause endothelial damage or dysfunction, especially in patients with an underlying hypercoagulable state. Bed rest and restriction of walking, even for several hours, are characteristic provoking factors.
As soon as deep venous thrombosis develops, the thrombus can break off and move along the venous system to the right side of the heart, then linger in the pulmonary arteries, where one or more vessels can be partially or completely closed. The consequences depend on the size and number of emboli, the response of the lungs and the ability of the internal thrombolytic system of a person to dissolve a thrombus.
Small emboli may not have any acute physiological effects; many begin to lyse immediately and dissolve within hours or days. Large emboli can cause a reflexive increase in ventilation (tachypnea); hypoxemia due to ventilation-perfusion (V / P) mismatch and shunting; atelectasis due to alveolar hypocapnia and surfactant disturbances and an increase in pulmonary vascular resistance caused by mechanical obstruction and vasoconstriction. Endogenous lysis reduces most emboli, even of a fairly large size, without treatment, and physiological responses subside within hours or days. Some emboli are resistant to lysis and can organize and persist. Occasionally, chronic residual obstruction leads to pulmonary hypertension (chronic thromboembolic pulmonary hypertension), which can develop over the years and lead to chronic right ventricular failure. When large emboli block large arteries, or when many small emboli occlude more than 50% of the distal arteries in the system, pressure in the right ventricle increases, causing acute right ventricular failure, failure with shock (massive pulmonary embolism (PE)), or sudden death in severe cases. The risk of death depends on the degree and frequency of the increase in right heart pressure and on the patient's previous cardiopulmonary status; higher blood pressure is more common in patients with preexisting heart disease. Healthy patients may experience a pulmonary embolism that obstructs more than 50% of the pulmonary vascular bed.
Risk factors for deep venous thrombosis and pulmonary embolism (PE)
- Age> 60 years
- Atrial fibrillation
- Smoking cigarettes (including secondhand smoke)
- Estrogen receptor modulators (raloxifene, tamoxifen)
- Limb injuries
- Heart failure
- Hypercoagulable states
- Antiphospholipid syndrome
- Antithrombin III deficiency
- Factor V Leiden mutation (activated protein C resistance)
- Heparin-induced thrombocytopenia and thrombosis
- Hereditary fibrinolysis defects
- Hyperhomocysteinemia
- Increased factor VIII
- Increase in factor XI
- Increased von Willebrand factor
- Paroxysmal nocturnal hemoglobinuria
- Protein C deficiency
- Protein S deficiency
- Prothrombin G-A gene defects
- Tissue factor pathway inhibitor
- Immobilization
- Venous catheter delivery
- Malignant neoplasms
- Myeloproliferative Disorders (High Viscosity)
- Nephrotic syndrome
- Obesity
- Oral contraceptives / estrogen replacement therapy
- Pregnancy and the postpartum period
- Preceding venous thromboembolism
- Sickle cell anemia
- Surgery in the previous 3 months
Pulmonary infarction occurs in less than 10% of patients diagnosed with pulmonary embolism (PE). This low percentage is attributed to the double blood supply to the lungs (i.e., bronchial and pulmonary). A heart attack is typically characterized by radiographically detectable infiltration, chest pain, fever, and sometimes hemoptysis.
Non-thrombotic pulmonary embolism (PE)
Pulmonary embolism (PE) arising from a variety of non-thrombotic sources causes clinical syndromes that differ from pulmonary thromboembolism (PE).
Air embolism occurs when a large number air into the systemic veins or into the right heart, which then moves into the pulmonary arterial system. Causes include surgery, blunt or barotrauma (eg, with mechanical ventilation), use of defective or uncovered venous catheters, and rapid decompression after diving. The formation of microbubbles in the pulmonary circulation can cause endothelial damage, hypoxemia and diffuse infiltration. With large air embolism, obstruction of the outflow tract can occur, which can lead to rapid death.
Fat embolism is caused by the ingress of fat or particles bone marrow into the systemic venous circulation and then into the pulmonary arteries. Causes include long bone fractures, orthopedic procedures, capillary occlusion or bone marrow necrosis in patients with sickle cell crisis and, rarely, toxic modification of native or parenteral serum lipids. Fat embolism causes a pulmonary syndrome similar to acute respiratory distress syndrome, with severe, rapid-onset hypoxemia, often accompanied by neurologic changes and petechial rash.
Amniotic fluid embolism is a rare syndrome caused by amniotic fluid entering the maternal venous bed and then into the pulmonary arterial system during or after childbirth. The syndrome can sometimes occur with prenatal uterine manipulation. Patients may have cardiac shock and respiratory distress due to anaphylaxis, vasoconstriction causing acute severe pulmonary hypertension, and direct damage to the pulmonary capillaries.
Septic embolism occurs when infected material enters the lungs. Causes include drug use, right valve infective endocarditis, and septic thrombophlebitis. Septic embolism causes symptoms and manifestations of pneumonia or sepsis and is initially diagnosed when focal infiltrates are detected on chest x-ray, which may increase to the periphery and abscess.
Foreign body embolism is caused by particles entering the pulmonary arterial system, usually due to the intravenous administration of inorganic substances, such as talcum powder by heroin addicts or mercury by patients with mental disorders.
Tumor embolism is a rare complication of malignant neoplasms (usually adenocarcinoma), in which tumor cells from the tumor enter the venous and pulmonary arterial system, where they are retained, multiply and obstruct blood flow. Patients usually have symptoms of shortness of breath and pleuritic chest pain, as well as signs of cor pulmonale, which develop over weeks to months. The diagnosis, which is suspected in the presence of small-node or diffuse pulmonary infiltration, can be confirmed by biopsy or sometimes cytological examination of aspirated fluid and histological examination of pulmonary capillary blood.
Systemic gas embolism is a rare syndrome that occurs with barotrauma during mechanical ventilation with high airway pressure, causing air to burst from the lung parenchyma into the pulmonary veins and then into the systemic arterial vessels. Gas emboli cause CNS damage (including stroke), heart damage, and livedo reticularis to the shoulders or anterior chest wall. The diagnosis is based on the exclusion of other vascular processes in the presence of established barotrauma.
Pulmonary embolism symptoms
Most pulmonary embolisms are small, physiologically insignificant, and asymptomatic. Even when present, the symptoms of pulmonary embolism (PE) are nonspecific and vary in frequency and intensity depending on the prevalence of pulmonary vascular occlusion and preexisting cardiopulmonary function.
Large emboli cause acute shortness of breath and pleuritic chest pain and, less commonly, coughing and / or hemoptysis. Massive pulmonary embolism (PE) causes hypotension, tachycardia, syncope, or cardiac arrest.
The most common symptoms of pulmonary embolism (PE) are tachycardia and tachypnea. Less commonly, patients have hypotension, a loud second heart sound (S2) due to increased pulmonary component (P), and / or crackling and wheezing. In the presence of right ventricular failure, there may be a clearly visible swelling of the internal jugular veins and bulging of the right ventricle, the gallop rhythm of the right ventricle may be heard (third and fourth heart sounds ) and by the severity of the development of the pathological process (acute, subacute and chronic recurrent [show] )
| The volume of lesions of the pulmonary vessels | Typical clinical features |
| Massive PE- obstruction of more than 50% of the volume of the vascular bed of the lungs | Symptoms of shock and / or systemic hypotension (a decrease in systolic blood pressure (BP) below 90 mm Hg or a drop in blood pressure ≥ 40 mm Hg for at least 15 minutes, unrelated to arrhythmia, hypovolemia, or sepsis) ... In addition, shortness of breath, diffuse cyanosis are characteristic, fainting is possible. |
| Submassive PE- obstruction of less than 50% of the volume of the vascular bed of the lungs | Symptoms of right ventricular failure (hypokinesia of the right ventricle) confirmed by echocardiography. No arterial hypotension |
| Non-massive PE- obstruction of small, mainly distal branches | Hemodynamics are stable, there are no signs of right ventricular failure, symptoms indicate a pulmonary infarction. |
PE variants according to the severity of the pathological process
In the new 2008 guidance, the terms “massive”, “submassive” and “non-massive PE” are considered “misleading” and incorrect. The authors of the document propose to use the stratification of patients into high and low risk groups, and among the latter to distinguish subgroups of moderate and low risk. To determine the risk, ESC recommends focusing on three groups of markers - clinical markers, markers of RV dysfunction, and markers of myocardial damage (Table 1).
| Risk groups for early PE-dependent death (death in hospital or within 30 days after PE) | Risk markers | Management tactics | |||
| Clinical | Right ventricular dysfunction | Myocardial injury | |||
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|
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| High - exceeding 15% | + | + | + | Thrombolysis / Thrombectomy | |
| In the presence of high-risk clinical markers (shock, hypotension), confirmation of belonging to a high-risk group due to markers of RV dysfunction and myocardial damage is not required. | |||||
| Not high< 15% | Moderate up to 15% | - | + | + | Hospitalization |
| + | - | ||||
| - | + | ||||
| Short< 1 % | - | - | - | Discharge from hospital and outpatient treatment | |
Thus, already with a quick examination at the patient's bedside, it is possible to determine whether the patient is at high risk of early death or not. With further examination of those who do not have clinical signs high risk (shock, hypotension), the risk can be assessed more accurately. This approach allows you to maximize early dates determine the tactics of managing patients and timely prescribe the necessary treatment for high-risk patients.
Sudden accelerated and rapid breathing, dizziness, pallor of the skin, chest discomfort can speak not only of angina pectoris, hypertension, osteochondrosis, but also of blockage of the pulmonary artery by a blood clot moving in it. This condition of the impossibility of blood flow in the vessel is called pulmonary embolism (PE) code according to μB 10.
The causes of pulmonary embolism can be an air bubble, the ingress of objects from the outside, or amniotic fluid in severe labor. But the risk of blockage of the vessel with a thrombus is much higher in all of the above methods. Moreover, a person may not even notice that a thrombus embolism is developing in some area of the body. After all, a clot that has come off and stopped in some place can be of different sizes or in different quantities. The severity of the disease depends on this. With a very dense and sharp blockage of the pulmonary artery, the patient may suddenly die.
As a rule, a healthy person cannot develop PE. Violations in cordially- vascular system and blood clotting can lead to a strong thickening, as a result, thrombus formation. Its greatest likelihood of occurrence is noted in the vessels of the extremities, right heart, pelvis and abdomen.
The main reasons for the formation of blood clots in the veins and blood vessels are distinguished:
- anomalies of the structure of the heart, existing from birth or acquired, characterized by changes in the valves and chambers of the heart.
- problems of the genitourinary system;
- benign and malignant tumors in different organs;
- inflammation of the venous walls with the formation of blood clots in it and blockage of blood vessels, which impedes blood flow in the legs.
However, there are exceptions. A person who does not suffer from cardiovascular diseases may experience PE (mkb 10). A sedentary lifestyle can lead to this. So, for example, with frequent and long-term air travel, constant stay in an airplane seat, circulatory disorders develop in the form of stagnation. Thereby, forming a blood clot.
In pregnant women after childbirth, with varicose veins, obesity, or, if the childbirth is not the first, as well as with an insufficient amount of fluid in the body, the risk of developing the disease increases.
The syndrome can take a person by surprise at any age, even a newborn.
Depending on the number of blood clots affected by blood vessels, pulmonary embolism is classified:
- Massive- if more than 50% of the vascular system is affected;
- Submassive- from one third to half;
- Small- less than one third of the vessels with pathology.
Symptoms
The main symptoms of PE, which can be used to determine that the patient has a pulmonary embolism:
- Rapid and labored breathing;
- Accelerated work of the heart muscle;
- Painful manifestations in the chest area;
- When coughing up blood appears;
- Increased temperature;
- Moist hoarse breathing sounds;
- Blue lip color;
- Violent cough;
- Friction noise of the membrane covering the lungs and the wall of the chest cavity;
- A sharp and rapid drop in blood pressure.
Depending on the number of blood clots affected by blood vessels, the signs of the manifestation of the disease also differ. So, for example, with massive thromboembolism, blood pressure drops, which leads to sudden cardiovascular failure, even with loss of consciousness, severe pain in the chest area. If not provide emergency care there is a threat of death. Outwardly, this can be seen by the strongly protruding veins.
With small and submassive, shortness of breath, cough, and chest pains develop.
In the elderly, it is often accompanied by convulsions, paralysis. In addition, a combination of symptoms can be combined.
Pulmonary embolism is very difficult to diagnose. Since, its manifestations are typical for other diseases, for example, myocardial infarction or pneumonia.
Therefore, in order to understand the direction of treatment, the most effective methods such as: CT, perfusion scintigraphy, selective angiography.
Computed tomography can accurately identify thromboembolism. The second method (perfusion scintigraphy), quite cheap, but 90% contributes to the calculation of this disease. And finally, angiography. Thanks to this method, the diagnosis, the place of thrombosis, is determined, the movement of blood is monitored.
To others, less effective ways diagnosis of pulmonary embolism, include:
- Electrocardiography... For most patients, this diagnostic method does not bring the desired results. Symptoms of PE may be absent. Here, attention is paid to signs of overload of the atria, ventricles, that is, it can be an increase or change in their shape, in addition to this, the tilt of the cardiac axis changes. But such a change in the heart can be present in other diseases.
- X-ray organs of the chest. Symptoms of the disease are changes in the shape of the lung system: an abnormally elevated unpaired muscle that separates the pectoral and abdominal cavity organism, expansion of parts of the lungs, pulmonary artery and some others.
- Echocardiography. Here they look at the changes in the right ventricle of the heart, its expansion or displacement of the septum closer to the left. What can we say about the presence of a blood clot in the heart?
- Spiral CT. The movement of blood in the branches of the pulmonary artery is monitored. To carry out this diagnostic method, it is necessary to inject a special drug into the patient, which will be visible to the sensor. On the computer, with the help of the latter, a picture is created on which you can see the delays in the movement of blood and their causes.
- Ultrasonography deep veins of the lower limb. The presence of a thrombus in the peripheral arteries is determined in two ways. Compression and Doppler study. In the first case, first, a picture of the patient's large vessels is obtained, then the skin is translucent with ultrasound. Where the lumen does not occur, there is a thrombosed area. In the second case, the blood flow velocity is determined by changing the frequency and wavelength of the radiation received by the transmitter. Thus, it becomes visible where the blockage has occurred. The methods are combined - ultrasonography.
Also, the disease can be determined using the laboratory method. Blood is taken for the content of d-dimer in it. The presence of this element indicates that not so long ago, a blood clot formed in the vessel. But an increase in the content of an element may also indicate other diseases.
As mentioned above, in order to accurately assess the patient's condition, it is necessary to know the degree of vascular pathogenicity, this helps to derive a contrast radiological index of severity and the level of blood deficiency - perfusion deficiency (product of the defect area by the degree of decrease in fixation of the radiopharmaceutical of the studied area).
The severity index is calculated by points:
- 16 points and below, perfusion deficit in 29% - minor embolism;
- 17-21 points, a deficit of 30-44%, the blood supply to the lungs is slightly impaired;
- 22-26 points and perfusion deficit in 45-59% - indicators of massive embolism;
- 27 points and 60% deficit, a sign of the extreme severity of the patient's condition.
Treatment
The patient's condition can fade away very quickly, so you need to hurry up with the treatment of pulmonary embolism. As soon as the specialist understands that he is dealing with the formation of a blood clot in the pulmonary artery, a drug that prevents blood clotting is injected. Then, treatment is carried out in one of two ways: operative and conservative.
In the first case, the blood clot is removed surgically through the chambers of the heart and blood vessels. In the second, thrombus is liquefied with the help of special preparations. Due to this, the thrombus is absorbed, and the blood moves freely further along the vessel.
There are two groups of such drugs for blood clots:
- Fibrinolytics- act directly on the blood clot itself, diluting it.
- Anticoagulants- do not allow the blood to thicken, as a result, the risk of an incident is reduced.
All drugs that can improve the patient's condition, relieve symptoms are administered intravenously or with a nasal, pulmonary catheter.
But we must not forget that the easier the stage of PE, the more the treatment has a percentage of success. With massive embolism, the prognosis is worse. If you do not provide first aid at the right time - enter absorbable, thinning drugs or do not operate, the patient will die.