Relief and joy after a planned operation carried out by the best specialists at the highest level can turn into misfortune in an instant. The patient, who was on the mend and made the most daring plans for the future, suddenly died. To the grief-stricken relatives, the doctors, using the unfamiliar word "TELA", intelligibly explained that a blood clot had come off and closed the pulmonary artery.

The condition after surgery is not the only cause of pulmonary embolism.

Thrombi formed in the bloodstream and for the time being attached to the walls of blood vessels can break off at any time and create obstacles to blood flow in the pulmonary trunk and branches of the pulmonary artery, as well as other venous and arterial vessels of the body, holding the risk of developing a situation that we called thromboembolism.

The main thing about a terrible complication

Pulmonary embolism or PE is a sudden complication of acute venous thrombosis of deep and superficial veins that collect blood from various organs of the human body. More often, the pathological process that creates conditions for increased thrombus formation concerns. However, in most cases, the embolism will declare itself before the symptoms of thrombosis appear, it is always sudden onset.

Blockage of the pulmonary trunk (or LA branches) is predisposed not only by long-term chronic processes, but also by temporary difficulties experienced by the circulatory system at different periods of life (trauma, surgery, pregnancy and childbirth ...).

Some people perceive pulmonary embolism as always deadly disease. This is a really life-threatening condition, however, it does not always proceed in the same way, having three variants of the course:

• Fulminant (hyperacute) thromboembolism - does not give thought, the patient can go to another world in 10 minutes;
• Acute form - releases for urgent thrombolytic treatment up to a day;
• Subacute (recurrent) PE - characterized by a weak severity of clinical manifestations and a gradual development of the process ().

In addition, the main symptoms of PE (severe shortness of breath, sudden onset, blue skin, chest pain, tachycardia, drop in blood pressure) are not always pronounced. Often, patients simply note pain in the right hypochondrium due to venous congestion and stretching of the liver capsule, cerebral disorders caused by a drop in blood pressure and the development of hypoxia, renal syndrome, and cough and hemoptysis, characteristic of PE, may linger and appear only after a few days (subacute course ). But an increase in body temperature can be observed from the first hours of the disease.

Considering the variability of clinical manifestations, various variants of the course and forms of severity, as well as the particular tendency of this disease to disguise itself as another pathology, PE requires more detailed consideration (symptoms and syndromes characteristic of it). However, before embarking on the study of this dangerous disease, every person who does not have a medical education, but who has witnessed the development of a pulmonary embolism, should know and remember that the very first and urgent help to the patient is to call a team of doctors.

Video: medical animation of PE mechanisms

When should you be afraid of an embolism?

A serious vascular lesion, which often (50%) causes the death of a patient - pulmonary embolism, occupies a third of all thromboses and embolisms. The disease threatens the female population of the planet 2 times more often (pregnancy, taking hormonal contraceptives) than men, weight and age of a person, lifestyle, as well as habits and food addictions are of no small importance.

Pulmonary thromboembolism always requires emergency care (medical!) and urgent hospitalization in a hospital- there can be no hope for "maybe" in the case of pulmonary embolization. The blood that has stopped at some part of the lung creates a “dead zone”, leaving the respiratory system without blood supply, and, therefore, without nutrition, which quickly begins to experience suffering - the lungs collapse, the bronchi narrow.

The main embolic material and the culprit of PE is a thrombotic mass that has detached from the place of formation and started to "walk" in the bloodstream. The cause of PE and all other thromboembolism is considered to be conditions that create conditions for increased formation of blood clots, and the embolism itself is their complication. In this regard, the causes of excessive formation of blood clots and the development of thrombosis should be sought, first of all, in the pathology that occurs with damage to the vascular walls, with a slowdown in blood flow through the bloodstream (congestive insufficiency), with impaired blood clotting (hypercoagulation):

1. Diseases of the vessels of the legs (,) - which is very conducive to the formation of blood clots, more often than others (up to 80%) contributes to the development of thromboembolism;
2. (you can expect anything from this disease);
3. Heart disease (, endocarditis,);
4. (polycythemia, multiple myeloma, sickle cell anemia);
5. Oncological pathology;
6. Compression of the vascular bundle by the tumor;
7. Huge cavernous hemangiomas (blood stasis in them);
8. Violations in the hemostasis system (increased concentration of fibrinogen during pregnancy and after childbirth, hypercoagulability as a protective reaction in fractures, dislocations, soft tissue bruises, burns, etc.);
9. Surgical operations (especially vascular and gynecological);
10. Bed rest after surgery or other conditions that require prolonged rest (forced horizontal position slows down blood flow and predisposes to the formation of blood clots);
11. Toxic substances produced in the body (- LDL fraction, microbial toxins, immune complexes), or coming from outside (including components of tobacco smoke);
12. infections;
13. Ionizing radiation;

The lion's share among the suppliers of blood clots in the pulmonary artery is the venous vessels of the legs. Stagnation in the veins of the lower extremities, violation of the structural structure of the vascular walls, thickening of the blood provokes the accumulation of red blood cells in certain places (future red blood clot) and turns the vessels of the legs into a factory that produces unnecessary and very dangerous clots for the body, which create the risk of detachment and blockage of the pulmonary artery. Meanwhile, these processes are not always caused by some kind of severe pathology: lifestyle, professional activity, bad habits (smoking!), pregnancy, the use of oral contraceptives - these factors play an important role in the development of a dangerous pathology.

The older the person, the more "prospects" he has for getting PE. This is due to an increase in the frequency of pathological conditions with aging of the body (the circulatory system suffers first of all), in people who have crossed the 50-60-year mark. For example, a fracture of the femoral neck, which very often follows old age, ends with a massive thromboembolism for a tenth of the victims. In people over 50, all kinds of injuries, conditions after surgery are always fraught with complications in the form of thromboembolism (according to statistics, more than 20% of victims have such a risk).

Where does the thrombus come from?

Most often, PE is considered as the result of embolism with thrombotic masses that came from other places. First of all, the source massive LA thromboembolism, which in most cases causes death, is seen in the development of the thrombotic process:

Therefore, it is clear that the presence in the patient's "arsenal" of embologenic venous thrombosis of the legs, thrombophlebitis and other pathology, accompanied, creates a risk of developing such a formidable complication as thromboembolism and becomes its cause when the clot breaks away from the attachment site and begins to migrate, that is, it becomes potential "stopper for the vessel" (embolus).

In other (rather rare) cases, the pulmonary artery itself can become a site for the formation of blood clots - then they talk about the development primary thrombosis. It originates directly in the branches of the pulmonary artery, but is not limited to a small area, but tends to capture the main trunk, forming the symptoms of cor pulmonale. Changes in the vascular walls of an inflammatory, atherosclerotic, dystrophic nature occurring in this zone can lead to local LA thrombosis.

Will it go away on its own?

Thrombotic masses, blocking the movement of blood in the pulmonary vessel, can provoke active formation of blood clots around the embolus. How quickly this object takes shape and what its behavior will be depends on the ratio of coagulation factors and the fibrinolytic system, that is, The process can go one of two ways:

1. With the predominance of the activity of coagulation factors, the embolus will tend to firmly "grow" to the endothelium. Meanwhile, it cannot be said that this process is always irreversible. In other cases, resorption (a decrease in the volume of a blood clot) and restoration of blood flow (recanalization) is possible. If such an event occurs, then it can be expected in 2-3 weeks from the onset of the disease.
2. The high activity of fibrinolysis, on the contrary, will contribute to the fastest dissolution of the thrombus and the complete release of the lumen of the vessel for the passage of blood.

Of course, the severity of the pathological process and its outcome will also depend on the size of the emboli and how many of them arrived in the pulmonary artery. A small embolizing particle stuck somewhere in a small branch of the LA may not give any special symptoms and not significantly change the patient's condition. Another thing is a large dense formation that has closed a large vessel and turned off a significant part of the arterial bed from the blood circulation, most likely will cause the development of a violent clinical picture and may cause the death of the patient. These factors formed the basis for the classification of pulmonary embolism according to clinical manifestations, where distinguish:

• Non-massive (or small) thromboembolism- no more than 30% of the volume of the arterial bed fails, symptoms may be absent, although when 25% is turned off, hemodynamic disturbances are already noted (moderate hypertension in the LA);
• More pronounced (submassive) blockage with a shutdown of 25 to 50% of the volume - then the symptoms of right ventricular failure are already clearly visible;
• Massive TELA- more than half (50 - 75%) of the lumen does not participate in the blood circulation, followed by a sharp decrease in cardiac output, systemic arterial hypotension and the development of shock.

From 10 to 70% (according to different authors) of pulmonary embolism is accompanied by pulmonary infarction. This occurs in cases where the share and segmental branches suffer. The development of a heart attack, most likely, will go on for about 3 days, and the final design of this process will take place in about a week.

What can be expected from a lung infarction is difficult to say in advance:

1. With small heart attacks, lysis and regression are possible;
2. The accession of infection threatens the development of pneumonia (heart attack-pneumonia);
3. If the embolus itself turns out to be infected, then inflammation may occur in the blockage zone and an abscess may develop, which sooner or later will break into the pleura;
4. Extensive pulmonary infarction can create conditions for the formation of cavities;
5. In rare cases, a pulmonary infarction is followed by a complication such as pneumothorax.

Some patients who have had a pulmonary infarction develop a specific immunological reaction, similar to that that often complicates myocardial infarction. In such cases, frequent recurrent pneumonia is very frightening for patients, as it is mistakenly perceived by them as a recurrence of pulmonary embolism.

Hiding behind a mask

A variety of symptoms can be tried to line up, but this does not mean that all of them will be equally present in one patient:

• Tachycardia (pulse rate depends on the form and course of the disease - from 100 beats / min to severe tachycardia);
• Pain syndrome. The intensity of pain, as well as its prevalence and duration, varies greatly: from unpleasant sensations to tearing unbearable pain behind the sternum, indicating an embolism in the trunk, or dagger pain that spreads through the chest and resembles a myocardial infarction. In other cases, when only small branches of the pulmonary artery are closed, pain sensations can be veiled, for example, by an upset of the gastrointestinal tract, or completely absent. The duration of the pain syndrome ranges from minutes to hours;
• Respiratory failure (from lack of air to shortness of breath), moist rales;
• Cough, hemoptysis (later symptoms, characteristic of the stage of pulmonary infarction);
• Body temperature rises immediately (in the first hours) after occlusion and accompanies the disease from 2 days to 2 weeks;
• Cyanosis is a symptom often accompanying massive and submassive forms. The color of the skin can be pale, have an ashy hue, or reach a cast-iron color (face, neck);
• A decrease in blood pressure, the development of collapse is possible, and the lower the blood pressure, the more massive the lesion can be suspected;
• Fainting, possible development of convulsions and coma;
• Sharp filling with blood and bulging of the veins of the neck, positive venous pulse - symptoms characteristic of the syndrome of "acute pulmonary heart" are detected in severe PE.

Symptoms of PE, depending on the depth of hemodynamic disturbances and suffering from blood flow, may have varying degrees of severity and develop into syndromes that may be present in a patient alone or in a crowd.

The most commonly observed syndrome of acute respiratory failure (ARF), as a rule, begins without warning with respiratory distress of varying severity. Depending on the form of PE, respiratory failure may be not so much shortness of breath, but simply a lack of air. With embolism of small branches of the pulmonary artery, an episode of unmotivated shortness of breath can end in a few minutes.

Not typical for PE and noisy breathing, "quiet shortness of breath" is more often noted. In other cases, rare, intermittent breathing is observed, which may indicate the onset of cerebrovascular disorders.

cardiovascular syndromes, which are characterized by the presence of symptoms of various insufficiencies: systemic vascular or "acute cor pulmonale". This group includes: acute vascular insufficiency syndrome(drop in blood pressure, collapse), circulatory shock, which usually develops with a massive variant of PE and is manifested by severe arterial hypoxia.

Abdominal syndrome very strongly resembles an acute disease of the upper gastrointestinal tract:

1. A sharp increase in the liver;
2. Intense pain "somewhere in the liver" (under the right rib);
3. Belching, hiccups, vomiting;
4. Bloating.

cerebral syndrome occurs against the background of acute circulatory failure in the vessels of the brain. Difficulty in blood flow (and in severe form - cerebral edema) determines the formation of focal transient or cerebral disorders. In elderly patients, PE can debut with fainting, which misleads the doctor and puts the question before him: what is the primary syndrome?

Listing all the signs of PE, involuntarily one can come to the conclusion that all of them are not specific, therefore, the main ones should be distinguished from them: suddenness, shortness of breath, tachycardia, chest pain.

How much to whom is measured ...

Clinical manifestations that occur during the pathological process determine the severity of the patient's condition, which, in turn, forms the basis of the clinical classification of PE. Thus, there are three forms of severity of the patient's condition with pulmonary embolism:

1. Severe form characterized by maximum severity and mass of clinical manifestations. As a rule, a severe form has a hyperacute course, therefore, very quickly (in 10 minutes) it can lead a person to a state of clinical death from loss of consciousness and convulsions;
2. Moderate form coincides with the acute course of the process and is not as dramatic as the fulminant form, but, at the same time, requires maximum composure when providing emergency care. A number of symptoms can lead to the fact that a person has a catastrophe: a combination of shortness of breath with tachypnea, rapid pulse, non-critical (yet) decrease in blood pressure, severe pain in the chest and right hypochondrium, cyanosis (cyanosis) of the lips and wings of the nose against the background of general pallor faces.
3. Light form pulmonary thromboembolism with a recurrent course is not so rapid development of events. An embolism affecting small branches manifests itself sluggishly, creates a resemblance to another chronic pathology, so the recurrent variant can be mistaken for anything (exacerbation of bronchopulmonary diseases, chronic heart failure). However, one should not forget that mild PE can be a prelude to a severe form with a fulminant course, so treatment should be timely and adequate.

Diagram: proportions of thromboembolism, undiagnosed cases, asymptomatic forms and deaths

Often, from patients who have undergone PE, one can hear that they "found chronic thromboembolism." Most likely, patients have in mind a mild form of the disease with a relapsing course, which is characterized by the appearance of intermittent attacks of shortness of breath with dizziness, short-term pain in the chest and moderate tachycardia (usually up to 100 beats / min). In rare cases, a short-term loss of consciousness is possible. As a rule, patients with this form of PE received recommendations even at its debut: until the end of their lives they should be under the supervision of a doctor and constantly take thrombolytic treatment. In addition, various bad things can be expected from the recurrent form itself: the lung tissue is replaced by connective tissue (pneumosclerosis), pressure in the pulmonary circle increases (), pulmonary emphysema develops and.

First of all, an emergency call

The main task of relatives or other people who, by chance, found themselves next to the patient is to be able to quickly and sensibly explain the essence of the call, so that the dispatcher at the other end of the wire understands that time does not endure. The patient just needs to be laid down, slightly raising the head end, but do not try to change his clothes or bring him to life by methods far from medicine.

What happened - the doctor of the ambulance team who arrived at the urgent call will try to figure it out, after conducting a primary diagnosis, which includes:

• Anamnesis: suddenness of clinical manifestations and the presence of risk factors (age, chronic cardiovascular and bronchopulmonary pathology, malignant neoplasms, injuries, condition after surgery, prolonged bed rest, etc.);
• Examination: the color of the skin (pale with a grayish tint), the nature of breathing (shortness of breath), the measurement of the pulse (rapid) and blood pressure (low);
• Auscultation - accent and bifurcation of the II tone over the pulmonary artery, some patients have III tone (right ventricular pathological), pleural friction rub;
• ECG - acute overload of the right heart, blockade of the right leg of the bundle of His.

Emergency care is provided by a medical team. Of course, it is better if it turns out to be specialized, otherwise (a lightning-fast and sharp version of TELA), the linear brigade will have to call for more equipped "help". The algorithm of its actions depends on the form of the disease and the patient's condition, but clearly - no one, except for qualified health workers, should (and is not entitled to):

1. To stop the pain syndrome with the use of narcotic and other potent drugs (and with PE this is necessary);
2. Introduce hormonal and antiarrhythmic drugs.

In addition, with pulmonary thromboembolism, the likelihood of clinical death is not excluded, so resuscitation should be not only timely, but also effective.

After the necessary measures have been taken (pain relief, recovery from a state of shock, relief of an attack of acute respiratory failure), the patient is taken to the hospital. And only on a stretcher, even if there has been significant progress in his condition. Having informed using the means of communication available (walkie-talkie, telephone) that a patient with suspected PE is on the way, the ambulance doctors will no longer waste time registering him in the emergency room - the patient, laid on a stretcher, will proceed directly to the ward , where doctors will be waiting for him, ready to immediately start saving lives.

Blood tests, x-rays and more ...

The conditions of the hospital, of course, allow for more extensive diagnostic measures. The patient is quickly taken tests (general blood test, coagulogram). It is very good if the laboratory service of a medical institution has the ability to determine the level - a fairly informative laboratory test prescribed for the diagnosis of thrombosis and thromboembolism.

Instrumental diagnosis of PE includes:

Of course, only well-equipped specialized clinics can afford to choose the most optimal research methods, the rest use those that they have (ECG, R-graphy), but this does not give reason to think that the patient will be left without help. If necessary, he will be urgently transferred to a specialized hospital.

Treatment without delay

The doctor, in addition to saving the life of a person who has suffered from PE, sets himself another important task - to restore the vascular bed as much as possible. Of course, it is very difficult to do “as it was”, but the Aesculapius do not lose hope.

The treatment of pulmonary embolism in the hospital is started immediately, but deliberately, striving to improve the patient's condition as soon as possible, because further prospects depend on this.

The first place in the number of therapeutic measures belongs to- the patient is prescribed fibrinolytic agents: streptokinase, tissue plasminogen activator, urokinase, streptase, as well as direct anticoagulants (heparin, fraxiparin) and indirect action (phenylin, warfarin). In addition to the main treatment, supportive and symptomatic therapy is carried out (cardiac glycosides, antiarrhythmic drugs, antispasmodics, vitamins).

If the cause of embalogenic thrombosis is varicose veins of the lower extremities, then, as a prevention of repeated episodes, it is advisable to perform percutaneous implantation of an umbrella filter into the inferior vena cava.

As for the surgical treatment - thrombectomy, known as the Trendelenburg operation and performed with massive blockages of the pulmonary trunk and the main branches of the LA, it is associated with certain difficulties. Firstly, from the onset of the disease to the moment of the operation, a little time should pass, secondly, the intervention is carried out under conditions of artificial circulation, and, thirdly, it is clear that such methods of treatment require not only the skill of physicians, but also good equipment of the clinic.

Meanwhile, hoping for treatment, patients and their relatives should know that grades 1 and 2 give good chances for life, but a massive embolism with a severe course, unfortunately, often causes death if timely (!) is not carried out thrombolytic and surgical treatment.

Patients who survived PE receive recommendations upon discharge from the hospital. It - lifelong thrombolytic treatment, selected on an individual basis. Surgical prophylaxis consists in the installation of clips, filters, the imposition of U-shaped sutures on the inferior vena cava, etc.

Patients who are already at risk (diseases of the vessels of the legs, other vascular pathology, heart disease, disorders of the hemostasis system), as a rule, are already aware of the possible complications of major diseases, so they undergo the necessary examination and preventive treatment.

Currently answering questions: A. Olesya Valerievna, candidate of medical sciences, lecturer at a medical university

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Treatment of PE is challenging. The disease occurs unexpectedly, progresses rapidly, as a result of which the doctor has at his disposal a minimum of time to determine the tactics and method of treating the patient. First, there can be no standard treatment regimens for PE. The choice of method is determined by the localization of the embolus, the degree of impaired pulmonary perfusion, the nature and severity of hemodynamic disorders in the systemic and pulmonary circulation. Secondly, the treatment of PE cannot be limited to the elimination of an embolus in the pulmonary artery. The source of embolization should not be overlooked.

Urgent care

Emergency care measures for PE can be divided into three groups:

1) maintaining the life of the patient in the first minutes of PE;

2) elimination of deadly reflex reactions;

3) elimination of the embolus.

Life support in cases of clinical death of patients is carried out primarily by resuscitation. Priority measures include the fight against collapse with the help of pressor amines, correction of the acid-base state, and effective oxygen barotherapy. At the same time, it is necessary to start thrombolytic therapy with native streptokinase preparations (streptodecase, streptase, avelizin, celease, etc.).

The embolus located in the artery causes reflex reactions, due to which severe hemodynamic disorders often occur with non-massive pulmonary embolism. To eliminate the pain syndrome, 4-5 ml of a 50% solution of analgin and 2 ml of droperidol or seduxen are administered intravenously. Drugs are used when necessary. With severe pain syndrome, analgesia begins with the introduction of drugs in combination with droperidol or seduxen. In addition to the analgesic effect, the feeling of fear of death is suppressed, catecholaminemia, myocardial oxygen demand and electrical instability of the heart are reduced, the rheological properties of blood and microcirculation are improved. In order to reduce arteriolospasm and bronchospasm, eufillin, papaverine, no-shpa, prednisolone are used in normal doses. The elimination of the embolus (the basis of pathogenetic treatment) is achieved by thrombolytic therapy, started immediately after the diagnosis of PE. Relative contraindications to thrombolytic therapy, which are present in many patients, are not an obstacle to its use. The high likelihood of death justifies the risk of treatment.

In the absence of thrombolytic drugs, continuous intravenous administration of heparin at a dose of 1000 units per hour is indicated. The daily dose will be 24,000 IU. With this method of administration, relapses of pulmonary embolism occur much less frequently, rethrombosis is more reliably prevented.

When clarifying the diagnosis of pulmonary embolism, the degree of occlusion of the pulmonary blood flow, the localization of the embolus, a conservative or surgical method of treatment is chosen.

Conservative treatment

The conservative treatment of pulmonary embolism is currently the main one and includes the following measures:

1. Ensuring thrombolysis and stopping further thrombosis.

2. Reducing pulmonary arterial hypertension.

3. Compensation for pulmonary and right heart failure.

4. Elimination of arterial hypotension and removal of the patient from the collapse.

5. Treatment of pulmonary infarction and its complications.

The scheme of conservative treatment of pulmonary embolism in the most typical form can be represented as follows:

1. Complete rest of the patient, lying position of the patient with a raised head end in the absence of collapse.

2. With pain in the chest and a strong cough, the introduction of analgesics and antispasmodics.

3. Oxygen inhalations.

4. In case of collapse, the whole complex of therapeutic measures for acute vascular insufficiency is carried out.

5. With cardiac weakness, glycosides (strophanthin, corglicon) are prescribed.

6. Antihistamines: diphenhydramine, pipolfen, suprastin, etc.

7. Thrombolytic and anticoagulant therapy. The active principle of thrombolytic drugs (streptase, avelizin, streptodecase) is a metabolic product of hemolytic streptococcus - streptokinase, which, by activating plasminogen, forms a complex with it that promotes the appearance of plasmin, which dissolves fibrin directly in the thrombus. The introduction of thrombolytic drugs, as a rule, is made in one of the peripheral veins of the upper extremities or in the subclavian vein. But with massive and submassive thromboembolism, the most optimal is their introduction directly into the area of ​​the thrombus that occludes the pulmonary artery, which is achieved by probing the pulmonary artery and bringing the catheter under the control of the X-ray machine to the thrombus. The introduction of thrombolytic drugs directly into the pulmonary artery quickly creates their optimal concentration in the area of ​​thromboembolism. In addition, during probing, an attempt is simultaneously made to fragment or tunnel thromboembolism in order to restore pulmonary blood flow as quickly as possible. Before the introduction of streptase, the following blood parameters are determined as initial data: fibrinogen, plasminogen, prothrombin, thrombin time, blood clotting time, bleeding duration. The sequence of drug administration:

1. 5000 IU of heparin and 120 mg of prednisolone are injected intravenously.

2. 250,000 units of streptase (trial dose) diluted in 150 ml of physiological saline are injected intravenously for 30 minutes, after which the above blood parameters are examined again.

3. In the absence of an allergic reaction, which indicates a good tolerability of the drug, and a moderate change in control parameters, the administration of a therapeutic dose of streptase begins at the rate of 75,000-100,000 U/h, heparin 1000 U/h, nitroglycerin 30 mcg/min. The approximate composition of the solution for infusion:

The solution is administered intravenously at a rate of 20 ml/h.

4. During the administration of streptase, 120 mg of prednisolone is injected intravenously every 6 hours. The duration of the administration of streptase (24-96 hours) is determined individually.

Monitoring of the listed blood parameters is carried out every four hours. During treatment, it is not allowed to reduce fibrinogen below 0.5 g / l, prothrombin index below 35-4-0%, changes in thrombin time above a six-fold increase compared to the original, changes in clotting time and bleeding duration above a three-fold increase compared to the original data . Complete blood count is performed daily or according to indications, platelets are determined every 48 hours and within five days after the start of thrombolytic therapy, urinalysis - daily, ECG - daily, lung perfusion scintigraphy - according to indications. The therapeutic dose of streptase ranges from 125,000-3,000,000 units or more.

Treatment with streptodecase involves the simultaneous administration of a therapeutic dose of the drug, which is 300,000 IU of the drug. The same indicators of the coagulation system are controlled as in the treatment with streptase.

At the end of treatment with thrombolytics, the patient is transferred to treatment with maintenance doses of heparin at 25,000-45,000 IU per day intravenously or subcutaneously for 3-5 days under the control of clotting time and bleeding duration.

On the last day of heparin administration, indirect anticoagulants (pelentan, warfarin) are prescribed, the daily dose of which is selected so that the prothrombin index is kept within (40-60%), the international normalized ratio (MHO) is 2.5. Treatment with indirect anticoagulants can, if necessary, continue for a long time (up to three to six months or more).

Absolute contraindications to thrombolytic therapy:

1. Disturbed consciousness.

2. Intracranial and spinal formations, arteriovenous aneurysms.

3. Severe forms of arterial hypertension with symptoms of cerebrovascular accident.

4. Bleeding of any localization, excluding hemoptysis due to pulmonary infarction.

5. Pregnancy.

6. The presence of potential sources of bleeding (ulcer of the stomach or intestines, surgical interventions within 5 to 7 days, condition after aortography).

7. Recent streptococcal infections (acute rheumatism, acute glomerulonephritis, sepsis, prolonged endocarditis).

8. Recent traumatic brain injury.

9. Previous hemorrhagic stroke.

10. Known disorders of the blood coagulation system.

11. Unexplained headache or blurred vision in the last 6 weeks.

12. Craniocerebral or spinal operations within the last two months.

13. Acute pancreatitis.

14. Active tuberculosis.

15. Suspicion of a dissecting aortic aneurysm.

16. Acute infectious diseases at the time of admission.

Relative contraindications to thrombolytic therapy:

1. Exacerbation of peptic ulcer of the stomach and duodenum.

2. History of ischemic or embolic strokes.

3. Reception of indirect anticoagulants at the time of admission.

4. Serious injuries or surgical interventions more than two weeks ago, but not more than two months;

5. Chronic uncontrolled arterial hypertension (diastolic blood pressure over 100 mm Hg).

6. Severe renal or hepatic insufficiency.

7. Catheterization of the subclavian or internal jugular vein.

8. Intracardiac thrombi or valvular vegetations.

In vital indications, one must choose between the risk of disease and the risk of therapy.

The most common complications in the use of thrombolytic and anticoagulant drugs are bleeding and allergic reactions. Their prevention is reduced to the careful implementation of the rules for the use of these drugs. If there are signs of bleeding associated with the use of thrombolytics, the following are administered intravenously:

• epsilon-aminocaproic acid - 150-200 ml of a 50% solution;
• fibrinogen - 1-2 g per 200 ml of saline;
• calcium chloride - 10 ml of a 10% solution;
• fresh frozen plasma. Intramuscularly administered:
• hemophobin - 5-10 ml;
• vikasol - 2-4 ml of a 1% solution.

If necessary, a transfusion of freshly citrated blood is indicated. In case of an allergic reaction, prednisolone, promedol, dimedrol are administered. The antidote of heparin is protamine sulfate, which is administered in an amount of 5-10 ml of a 10% solution.

Among the drugs of the latest generation, it is necessary to note a group of tissue plasminogen activators (alteplase, actilyse, retavase), which are activated by binding to fibrin and promote the transition of plasminogen to plasmin. When using these drugs, fibrinolysis increases only in the thrombus. Alteplase is administered at a dose of 100 mg according to the scheme: bolus administration of 10 mg over 1-2 minutes, then during the first hour - 50 mg, in the next two hours - the remaining 40 mg. Retavase, which has been used in clinical practice since the late 1990s, has an even more pronounced lytic effect. The maximum lytic effect with its use is achieved within the first 30 minutes after administration (10 IU + 10 IU intravenously). The frequency of bleeding when using tissue plasminogen activators is significantly less than when using thrombolytics.

Conducting conservative treatment is possible only when the patient retains the ability to provide relatively stable blood circulation for several hours or days (submassive embolism or embolism of small branches). With embolism of the trunk and large branches of the pulmonary artery, the effectiveness of conservative treatment is only 20-25%. In these cases, the method of choice is surgical treatment - embolothrombectomy from the pulmonary artery.

Surgery

The first successful operation for pulmonary embolism was performed by F. Trendelenburg's student M. Kirchner in 1924. Many surgeons attempted pulmonary embolism, but the number of patients who died during the operation was significantly higher than those who underwent it. In 1959, K. Vossschulte and N. Stiller proposed to perform this operation under conditions of temporary occlusion of the vena cava by transsternal access. The technique provided a wide free access, a quick approach to the heart and the elimination of dangerous dilatation of the right ventricle. The search for safer methods of embolectomy led to the use of general hypothermia (P. Allison et al., 1960), and then artificial circulation (E. Sharp, 1961; D. Cooley et al., 1961). General hypothermia has not gained popularity due to lack of time, but the use of cardiopulmonary bypass has opened up new horizons in the treatment of this disease.

In our country, the technique of embolectomy under conditions of vena cava occlusion was developed and successfully applied by B.C. Saveliev et al. (1979). The authors believe that pulmonary embolectomy is indicated for those who are at risk of death from acute cardiopulmonary failure or the development of severe post-embolic hypertension of the pulmonary circulation.

Currently, the optimal methods of embolectomy for massive pulmonary embolism are:

1 Operation under conditions of temporary occlusion of the vena cava.

2. Embolectomy through the main branch of the pulmonary artery.

3. Surgical intervention under cardiopulmonary bypass.

The use of the first technique is indicated for massive embolism of the trunk or both branches of the pulmonary artery. In the case of a predominant unilateral lesion, embolectomy through the corresponding branch of the pulmonary artery is more justified. The main indication for surgery under cardiopulmonary bypass for massive pulmonary embolism is widespread distal occlusion of the vascular bed of the lungs.

B.C. Saveliev et al. (1979 and 1990) allocate absolute and relative indications for embolothrombectomy. The absolute indications are:

• thromboembolism of the trunk and main branches of the pulmonary artery;
• thromboembolism of the main branches of the pulmonary artery with persistent hypotension (with pressure in the pulmonary artery below 50 mm Hg. Art.)

Relative indications are thromboembolism of the main branches of the pulmonary artery with stable hemodynamics and severe hypertension in the pulmonary artery and right heart.

They consider contraindications to embolectomy:

• severe comorbidities with a poor prognosis, such as cancer;
• diseases of the cardiovascular system, in which the success of the operation is doubtful, and its risk is not justified.

A retrospective analysis of the possibilities of embolectomy in patients who died from massive embolism showed that success can be expected only in 10-11% of cases, and even with a successful embolectomy, the possibility of repeated embolism is not ruled out. Therefore, the main direction in solving the problem should be prevention. PE is not a fatal condition. Modern methods for diagnosing venous thrombosis make it possible to predict the risk of thromboembolism and to carry out its prevention.

The method of endovascular rotary pulmonary artery obstruction (ERDA) proposed by T. Schmitz-Rode, U. Janssens, N.N. Schild et al. (1998) and used in a fairly large number of patients by B.Yu. Bobrov (2004). Endovascular rotary deobstruction of the main and lobar branches of the pulmonary artery is indicated for patients with massive thromboembolism, especially in its occlusive form. ERDLA is performed during angiopulmonography using a special device developed by T. Schmitz-Rode (1998). The principle of the method lies in the mechanical destruction of massive thromboembolism in the pulmonary arteries. It can be an independent method of treatment for contraindications or ineffectiveness of thrombolytic therapy or precede thrombolysis, which significantly increases its effectiveness, reduces its duration, reduces the dosage of thrombolytic drugs and reduces the number of complications. ERDLA is contraindicated in the presence of a rider embolus in the pulmonary trunk due to the risk of occlusion of the main branches of the pulmonary artery due to the migration of fragments, as well as in patients with non-occlusive and peripheral form of embolism of the branches of the pulmonary artery.

Prevention of pulmonary embolism

Prevention of pulmonary embolism should be carried out in two directions:

1) prevention of the occurrence of peripheral venous thrombosis in the postoperative period;

2) with already formed venous thrombosis, it is necessary to carry out treatment to prevent the separation of thrombotic masses and their throwing into the pulmonary artery.

To prevent postoperative thrombosis of the veins of the lower extremities and pelvis, two types of preventive measures are used: nonspecific and specific prevention. Nonspecific prevention includes combating physical inactivity in bed and improving venous circulation in the system of the inferior vena cava. Specific prevention of peripheral venous thrombosis involves the use of antiplatelet agents and anticoagulants. Specific prophylaxis is indicated for thromboprone patients, nonspecific - for all without exception. The prevention of venous thrombosis and thromboembolic complications is described in detail in the next lecture.

With already formed venous thrombosis, surgical methods of antiembolic prophylaxis are used: thrombectomy from the iliocaval segment, plication of the inferior vena cava, ligation of the main veins, and implantation of a cava filter. The most effective preventive measure, which has been widely used in clinical practice over the past three decades, is the implantation of a cava filter. The most widespread is the umbrella filter proposed by K. Mobin-Uddin in 1967. Throughout the years of filter use, various modifications of the latter have been proposed: the hourglass, the Simon nitinol filter, the bird's nest, and the Greenfield steel filter. Each of the filters has its advantages and disadvantages, but none of them fully meets all the requirements for them, which determines the need for further searches. The advantage of the hourglass filter, which has been used in clinical practice since 1994, is its high embolic activity and low ability to perforate the inferior vena cava. The main indications for the implantation of a cava filter:

• embolic (floating) thrombi in the inferior vena cava, iliac and femoral veins, complicated or uncomplicated pulmonary embolism;
• massive thromboembolism of the pulmonary artery;
• repeated PE, the source of which is not established.

In many cases, the implantation of cava filters is more preferable than surgical interventions on the veins:

• in elderly and senile patients with severe concomitant diseases and a high risk of surgery;
• in patients who have recently undergone surgery on the organs of the abdominal cavity, small pelvis and retroperitoneal space;
• with recurrence of thrombosis after thrombectomy from the iliocaval and iliac-femoral segments;
• in patients with purulent processes in the abdominal cavity and in the retroperitoneal space;
• with pronounced obesity;
• during pregnancy for more than 3 months;
• with old non-occlusive thrombosis of the iliocaval and iliac-femoral segments, complicated by PE;
• in the presence of complications from the previously installed cava filter (weak fixation, the threat of migration, wrong size selection).

The most serious complication of the installation of cava filters is thrombosis of the inferior vena cava with the development of chronic venous insufficiency of the lower extremities, which is observed, according to different authors, in 10-15% of cases. However, this is a small price to pay for the risk of possible PE. The cava filter itself can cause thrombosis of the inferior vena cava (IVC) in violation of blood clotting properties. The occurrence of thrombosis late after filter implantation (3 months later) may be due to both the capture of emboli and the thrombogenic effect of the filter on the vascular wall and flowing blood. Therefore, at present, in a number of cases, it is envisaged to install a temporary cava filter. Implantation of a permanent vena cava filter is advisable in detecting disorders of the blood coagulation system that create a risk of recurrence of PE during the patient's life. In other cases, it is possible to install a temporary cava filter for up to 3 months.

The implantation of a cava filter does not completely solve the process of thrombosis and thromboembolic complications, therefore, constant drug prophylaxis should be carried out throughout the patient's life.

A serious consequence of the transferred pulmonary embolism, despite the ongoing treatment, is chronic occlusion or stenosis of the main trunk or main branches of the pulmonary artery with the development of severe hypertension of the pulmonary circulation. This condition is called chronic post-embolic pulmonary hypertension (CPEPH). The incidence of this condition after thromboembolism of large arteries is 17%. The leading symptom of CPEPH is shortness of breath, which can occur even at rest. Patients are often worried about dry cough, hemoptysis, pain in the heart. As a result of hemodynamic insufficiency of the right parts of the heart, an increase in the liver, expansion and pulsation of the jugular veins, ascites, and jaundice are observed. According to most clinicians, the prognosis for CPEPH is extremely unfavorable. The life expectancy of such patients, as a rule, does not exceed three to four years. With a pronounced clinical picture of post-embolic lesions of the pulmonary arteries, surgery is indicated - intima thrombectomy. The outcome of the intervention is determined by the duration of the disease (the period of occlusion is not more than 3 years), the level of hypertension in the small circle (systolic pressure up to 100 mm Hg) and the state of the distal pulmonary arterial bed. Adequate surgical intervention can achieve regression of severe CPEPH.

Pulmonary embolism is one of the most important problems in medical science and practical public health. Currently, there are all opportunities to reduce mortality from this disease. It is impossible to put up with the opinion that PE is something fatal and unavoidable. Past experience suggests otherwise. Modern diagnostic methods make it possible to predict the outcome, and timely and adequate treatment gives successful results.

It is necessary to improve the methods of diagnosis and treatment of phlebothrombosis as the main source of embolism, to increase the level of active prevention and treatment of patients with chronic venous insufficiency, to identify patients with risk factors and sanitize them in a timely manner.

Selected lectures on angiology. E.P. Kokhan, I.K. Zavarina

Pulmonary embolism- symptoms and treatment

What is pulmonary embolism? We will analyze the causes of occurrence, diagnosis and treatment methods in the article by Dr. Grinberg M.V., a cardiologist with an experience of 30 years.

Definition of disease. Causes of the disease

Pulmonary embolism(TELA) - blockage of the arteries of the pulmonary circulation by blood clots formed in the veins of the systemic circulation and the right parts of the heart, brought with the blood stream. As a result, the blood supply to the lung tissue stops, necrosis (tissue death) develops, heart attack-pneumonia, and respiratory failure occur. The load on the right parts of the heart increases, right ventricular circulatory failure develops: cyanosis (blue skin), edema in the lower extremities, ascites (accumulation of fluid in the abdominal cavity). The disease can develop acutely or gradually, over several hours or days. In severe cases, the development of PE occurs rapidly and can lead to a sharp deterioration in the condition and death of the patient.

Every year, 0.1% of the world's population dies from PE. In terms of the frequency of deaths, the disease is second only to coronary artery disease (IHD) and stroke. More PE patients die than AIDS patients and road traffic injuries combined. The majority of patients (90%) who died from PE were not diagnosed in time, and the necessary treatment was not carried out. PE often occurs where it is not expected - in patients with non-cardiological diseases (trauma, childbirth), complicating their course. Mortality in PE reaches 30%. With timely optimal treatment, mortality can be reduced to 2-8%.

The manifestation of the disease depends on the size of blood clots, the suddenness or gradual onset of symptoms, the duration of the disease. The course can be very different - from asymptomatic to rapidly progressive, up to sudden death.

PE is a ghost disease that wears the masks of other diseases of the heart or lungs. The clinic can be heart attack-like, reminiscent of acute pneumonia. Sometimes the first manifestation of the disease is right ventricular circulatory failure. The main difference is the sudden onset in the absence of other visible causes of the increase in shortness of breath.

PE develops, as a rule, as a result of deep vein thrombosis, which usually precedes 3-5 days before the onset of the disease, especially in the absence of anticoagulant therapy.

Risk factors for pulmonary embolism

When diagnosing, the presence of risk factors for thromboembolism is taken into account. The most significant of them: fracture of the neck of the femur or limb, prosthetic hip or knee joint, major surgery, trauma or brain damage.

Dangerous (but not so strong) factors include: arthroscopy of the knee joint, central venous catheter, chemotherapy, chronic, hormone replacement therapy, malignant tumors, oral contraceptives, stroke, pregnancy, childbirth, postpartum period, thrombophilia. In malignant neoplasms, the frequency of venous thromboembolism is 15% and is the second leading cause of death in this group of patients. Chemotherapy increases the risk of venous thromboembolism by 47%. Unprovoked venous thromboembolism may be an early manifestation of a malignant neoplasm, which is diagnosed within a year in 10% of patients with an episode of PE.

The safest, but still risky, factors include all conditions associated with prolonged immobilization (immobility) - prolonged (more than three days) bed rest, air travel, old age, varicose veins, laparoscopic interventions.

Some risk factors are common with arterial thrombosis. These are the same risk factors for complications and hypertension: smoking, obesity, sedentary lifestyle, as well as diabetes mellitus, hypercholesterolemia, psychological stress, low consumption of vegetables, fruits, fish, low physical activity.

The older the patient, the more likely the development of the disease.

Finally, the existence of a genetic predisposition to PE has been proven today. The heterozygous form of factor V polymorphism increases the risk of initial venous thromboembolism by three times, and the homozygous form - by 15-20 times.

The most significant risk factors contributing to the development of aggressive thrombophilia include antiphospholipid syndrome with an increase in anticardiolipin antibodies and deficiency of natural anticoagulants: protein C, protein S and antithrombin III.

If you experience similar symptoms, consult your doctor. Do not self-medicate - it is dangerous for your health!

Symptoms of pulmonary embolism

The symptoms of the disease are varied. There is not a single symptom in the presence of which it was possible to say for sure that the patient had PE.

With pulmonary embolism, retrosternal heart attack-like pain, shortness of breath, cough, hemoptysis, arterial hypotension, cyanosis, syncope (fainting) can occur, which can also occur with other various diseases.

Often the diagnosis is made after exclusion of acute myocardial infarction. A characteristic feature of dyspnea in PE is its occurrence without connection with external causes. For example, the patient notes that he cannot climb to the second floor, although he did it without effort the day before. With the defeat of small branches of the pulmonary artery, the symptoms at the very beginning may be erased, non-specific. Only on the 3rd-5th day do signs of pulmonary infarction appear: pain in the chest; cough; hemoptysis; the appearance of pleural effusion (accumulation of fluid in the internal cavity of the body). Feverish syndrome is observed in the period from 2 to 12 days.

The full complex of symptoms occurs only in every seventh patient, however, 1-2 signs occur in all patients. With the defeat of small branches of the pulmonary artery, the diagnosis, as a rule, is made only at the stage of formation of a pulmonary infarction, that is, after 3-5 days. Sometimes patients with chronic PE are observed for a long time by a pulmonologist, while timely diagnosis and treatment can reduce shortness of breath, improve quality of life and prognosis.

Therefore, in order to minimize the cost of diagnosis, scales have been developed to determine the likelihood of a disease. These scales are considered almost equivalent, but the Geneva model turned out to be more acceptable for outpatients, and the P.S.Wells scale for inpatients. They are very easy to use, include both underlying causes (deep vein thrombosis, history of neoplasms) and clinical symptoms.

In parallel with the diagnosis of PE, the doctor must determine the source of thrombosis, and this is a rather difficult task, since the formation of blood clots in the veins of the lower extremities is often asymptomatic.

The pathogenesis of pulmonary embolism

The pathogenesis is based on the mechanism of venous thrombosis. Thrombi in the veins are formed due to a decrease in the speed of venous blood flow due to the shutdown of the passive contraction of the venous wall in the absence of muscle contractions, varicose veins, compression of their volumetric formations. To date, doctors cannot diagnose pelvic veins (in 40% of patients). Venous thrombosis can develop when:

• violation of the blood coagulation system - pathological or iatrogenic (obtained as a result of treatment, namely when taking GPRT);
• damage to the vascular wall due to injuries, surgical interventions, damage to it by viruses, free radicals during hypoxia, poisons.

Thrombi can be detected using ultrasound. Dangerous are those that are attached to the wall of the vessel and move in the lumen. They can break off and travel with the bloodstream to the pulmonary artery.

The hemodynamic consequences of thrombosis are manifested when more than 30-50% of the volume of the pulmonary bed is affected. Embolization of pulmonary vessels leads to an increase in resistance in the vessels of the pulmonary circulation, an increase in the load on the right ventricle, and the formation of acute right ventricular failure. However, the severity of damage to the vascular bed is determined not only and not so much by the volume of arterial thrombosis, but by hyperactivation of neurohumoral systems, increased release of serotonin, thromboxane, histamine, which leads to vasoconstriction (narrowing of the lumen of blood vessels) and a sharp increase in pressure in the pulmonary artery. Oxygen transport suffers, hypercapnia appears (the level of carbon dioxide in the blood increases). The right ventricle dilates (expands), there is tricuspid insufficiency, a violation of coronary blood flow. Cardiac output decreases, which leads to a decrease in the filling of the left ventricle with the development of its diastolic dysfunction. The resulting systemic hypotension (lowering blood pressure) may be accompanied by fainting, collapse, cardiogenic shock, up to clinical death.

Possible temporary stabilization of blood pressure creates the illusion of hemodynamic stability of the patient. However, after 24-48 hours, a second wave of blood pressure drop develops, which is caused by repeated thromboembolism, ongoing thrombosis due to insufficient anticoagulant therapy. Systemic hypoxia and insufficiency of coronary perfusion (blood flow) cause a vicious circle leading to the progression of right ventricular circulatory failure.

Small emboli do not worsen the general condition, they can manifest as hemoptysis, limited infarction pneumonia.

Classification and stages of development of pulmonary embolism

There are several classifications of PE: according to the severity of the process, according to the volume of the affected bed, and according to the rate of development, but all of them are difficult for clinical use.

According to the volume of the affected vascular bed There are the following types of PE:

1. Massive - the embolus is localized in the main trunk or main branches of the pulmonary artery; 50-75% of the channel is affected. The patient's condition is extremely serious, there is tachycardia and a decrease in blood pressure. There is a development of cardiogenic shock, acute right ventricular failure, characterized by high mortality.
2. Embolism of the lobar or segmental branches of the pulmonary artery - 25-50% of the affected channel. There are all the symptoms of the disease, but blood pressure is not reduced.
3. Embolism of small branches of the pulmonary artery - up to 25% of the affected bed. In most cases, it is bilateral and, most often, asymptomatic, as well as repeated or recurrent.

Clinical course of PE it can be acute (“lightning-fast”), acute, subacute (prolonged) and chronic recurrent. As a rule, the rate of the course of the disease is associated with the volume of thrombosis of the branches of the pulmonary arteries.

By severity they distinguish severe (registered in 16-35%), moderate (in 45-57%) and mild form (in 15-27%) of the development of the disease.

Of greater importance for determining the prognosis of patients with PE is risk stratification according to modern scales (PESI, sPESI), which includes 11 clinical indicators. Based on this index, the patient is assigned to one of five classes (I-V), in which the 30-day mortality ranges from 1 to 25%.

Complications of pulmonary embolism

Acute PE can cause cardiac arrest and sudden death. With gradual development, chronic thromboembolic pulmonary hypertension, progressive right ventricular circulatory failure occurs.

Chronic thromboembolic pulmonary hypertension (CTEPH) is a form of the disease in which thrombotic obstruction of small and medium-sized branches of the pulmonary artery occurs, resulting in increased pressure in the pulmonary artery and an increased load on the right heart (atrium and ventricle).

CTEPH is a unique form of the disease because it can potentially be cured with surgical and therapeutic methods. The diagnosis is established on the basis of data from pulmonary artery catheterization: an increase in pressure in the pulmonary artery above 25 mm Hg. Art., increase in pulmonary vascular resistance above 2 Wood's units, detection of emboli in the pulmonary arteries against the background of prolonged anticoagulant therapy for more than 3-5 months.

A severe complication of CTEPH is progressive right ventricular circulatory failure. Characteristic is weakness, palpitations, decreased exercise tolerance, the appearance of edema in the lower extremities, accumulation of fluid in the abdominal cavity (ascites), chest (hydrothorax), heart sac (hydropericardium). At the same time, there is no shortness of breath in a horizontal position, there is no stagnation of blood in the lungs. Often it is with these symptoms that the patient first comes to the cardiologist. There are no data on other causes of the disease. Prolonged decompensation of blood circulation causes dystrophy of internal organs, protein starvation, and weight loss. The prognosis is most often unfavorable, temporary stabilization of the condition against the background of drug therapy is possible, but the reserves of the heart are quickly exhausted, edema progresses, life expectancy rarely exceeds 2 years.

Diagnosis of pulmonary embolism

Diagnostic methods applied to specific patients depend primarily on determining the likelihood of PE, the severity of the patient's condition and the capabilities of medical institutions.

The diagnostic algorithm is presented in the 2014 PIOPED II (the Prospective Investigation of Pulmonary Embolism Diagnosis) study.

In the first place in terms of its diagnostic significance is electrocardiography which should be performed in all patients. Pathological changes on the ECG - an acute overload of the right atrium and ventricle, complex rhythm disturbances, signs of coronary blood flow insufficiency - make it possible to suspect the disease and choose the right tactics, determining the severity of the prognosis.

Assessment of the size and function of the right ventricle, the degree of tricuspid insufficiency according to ECHOCG allows you to get important information about the state of blood flow, pressure in the pulmonary artery, excludes other causes of the patient's serious condition, such as pericardial tamponade, dissection (dissection) of the aorta, and others. However, this is not always feasible due to the narrow ultrasound window, the patient's obesity, the impossibility of organizing a round-the-clock ultrasound service, often with the absence of a transesophageal probe.

Method for determination of D-dimer proved its high significance in suspected PE. However, the test is not absolutely specific, since increased results are also found in the absence of thrombosis, for example, in pregnant women, the elderly, with atrial fibrillation, malignant neoplasms. Therefore, this study is not indicated for patients with a high probability of the disease. However, with a low probability, the test is informative enough to exclude thrombus formation in the vascular bed.

To determine deep vein thrombosis, high sensitivity and specificity has Ultrasound of the veins of the lower extremities, which for screening can be carried out at four points: inguinal and popliteal areas on both sides. An increase in the study area increases the diagnostic value of the method.

Computed tomography of the chest with vascular contrast- a highly evidence-based method for diagnosing pulmonary embolism. Allows visualization of both large and small branches of the pulmonary artery.

If it is impossible to perform a CT scan of the chest (pregnancy, intolerance to iodine-containing contrast agents, etc.), it is possible to perform planar ventilation-perfusion(V/Q) lung scintigraphy. This method can be recommended to many categories of patients, but today it remains inaccessible.

Probing of the right heart and angiopulmonography is the most informative method at present. With its help, you can accurately determine both the fact of embolism and the extent of the lesion.

Unfortunately, not all clinics are equipped with isotope and angiographic laboratories. But the implementation of screening methods during the initial visit of the patient - ECG, plain chest X-ray, ultrasound of the heart, ultrasound of the veins of the lower extremities - allows you to refer the patient to MSCT (multi-slice spiral computed tomography) and further examination.

Treatment of pulmonary embolism

The main goal of treatment for pulmonary embolism is to save the patient's life and prevent the formation of chronic pulmonary hypertension. First of all, for this it is necessary to stop the process of thrombosis in the pulmonary artery, which, as mentioned above, does not occur at once, but over several hours or days.

With massive thrombosis, restoration of the patency of clogged arteries is shown - thrombectomy, as this leads to the normalization of hemodynamics.

To determine the treatment strategy, the scales for determining the risk of death in the early period PESI, sPESI are used. They make it possible to identify groups of patients who are indicated for outpatient care or who require hospitalization with MSCT, emergency thrombotic therapy, surgical thrombectomy, or percutaneous intravascular intervention.

Options	Original PESI	Simplified sPESI
Age, years	Age in years	1 (if > 80 years old)
Male gender	+10	-
Malignant neoplasms	+30	1
Chronic heart failure	+10	1
Chronic lung diseases	+10	-
Heart rate ≥ 110 per minute	+20	1
Systolic BP	+30	1
Respiratory rate > 30 per minute	+20	-
Temperature	+20	-
Disturbance of consciousness	+60	-
oxygen saturation	+20	1
Risk levels for 30-day mortality
	Class I (≤ 65 points) Very low 0-1.6%	0 points - 1% risk (confidential interval 0-2.1%)
	Class II (66-85 points) Low risk 1.7-3.5%
	Class III (86-105 points) Moderate risk 3.2-7.1%	≥ 1 point - risk 10.9% (confidential interval 8.5-13.2%)
	Class IV (106-125 points) High risk 4.0-11.4%
	Class V (> 126 points) Very high risk 10,0-24,5%
Note: HR - heart rate, BP - blood pressure.

To improve the pumping function of the right ventricle, dobutamine (dopmin), peripheral vasodilators that reduce the load on the heart, are prescribed. They are best administered by inhalation.

Thrombolytic therapy has its effect in 92% of patients, which is manifested by an improvement in the main hemodynamic parameters. Since it radically improves the prognosis of the disease, there are fewer contraindications to it than in acute myocardial infarction. However, it is advisable to carry out thrombolysis within two days after the onset of thrombosis, in the future its effectiveness decreases, and hemorrhagic complications remain at the same level. Thrombolysis is not indicated in low-risk patients.

Produced in cases of impossibility of prescribing anticoagulants, as well as the ineffectiveness of the usual doses of these drugs. Implantation of a filter that captures blood clots from peripheral veins is performed in the inferior vena cava at the level of the confluence of the renal veins into it, in some cases - above.

In patients with contraindications to systemic fibrinolysis, the technique of transcatheter thrombus fragmentation with subsequent aspiration (ventilation) of the contents can be applied. In patients with central pulmonary thrombi, surgical embolectomy is recommended in the event of refractory cardiogenic shock to ongoing therapy, in the presence of contraindications to fibrinolytic therapy or its ineffectiveness.

The cava filter freely passes blood, but traps blood clots in the pulmonary artery.

The duration of anticoagulant therapy in patients with acute venous thrombosis is at least three months. Treatment should begin with intravenous unfractionated heparin until the activated partial thromboplastin time is increased by 1.5-2 times compared with baseline values. When the condition stabilizes, it is possible to switch to subcutaneous injections of low molecular weight heparin with the simultaneous administration of warfarin until the target INR (international normalized ratio) of 2.0-3.0 is reached. Currently, new oral anticoagulants (pradaxa, xarelto, eliquis) are used more often, among which xarelto (rivaroxaban) is the most preferred due to its convenient single dose, proven efficacy in the most severe groups of patients, and the absence of the need to control INR. The initial dose of rivaroxaban is 15 mg 2 times a day for 21 days with a transition to a maintenance dose of 20 mg.

In some cases, anticoagulant therapy is carried out for more than three months, sometimes indefinitely. Such cases include patients with repeated episodes of thromboembolism, proximal vein thrombosis, right ventricular dysfunction, antiphospholipid syndrome, lupus anticoagulant. At the same time, new oral anticoagulants are more effective and safer than vitamin K antagonists.

Pregnancy

The frequency of PE in pregnant women varies from 0.3 to 1 case per 1000 births. Diagnosis is difficult, since complaints of shortness of breath may be associated with physiological changes in the woman's body. Ionizing radiation is contraindicated due to its negative effect on the fetus, and the level of D-dimer can be elevated in 50% of healthy pregnant women. The normal level of D-dimer makes it possible to exclude pulmonary embolism, with an increase - to send for additional studies: ultrasound of the veins of the lower extremities. Positive results of the study allow prescribing anticoagulants without chest x-ray, with negative results, chest CT or perfusion lung scintigraphy is indicated.

Low molecular weight heparins are used to treat PE in pregnant women. They do not cross the placenta, do not cause fetal developmental disorders. They are prescribed for a long course (up to three months), up to childbirth. Vitamin K antagonists cross the placenta, causing malformations when given in the first trimester and fetal bleeding in the third trimester of pregnancy. Perhaps cautious use in the second trimester of pregnancy (similar to the management of women with mechanical prosthetic heart valves). New oral anticoagulants are contraindicated for pregnant women.

Anticoagulant therapy should be continued for three months postpartum. Warfarin can be used here, as it does not pass into breast milk.

Forecast. Prevention

PE can be prevented by eliminating or minimizing the risk of thrombus formation. To do this, use all possible methods:

• the maximum reduction in the duration of bed rest while in the hospital for any diseases;
• elastic compression of the lower extremities with special bandages, stockings in the presence of varicose veins.

In addition, people at risk are routinely prescribed anticoagulants to prevent blood clots. This risk group includes:

• people over 40;
• patients suffering from malignant tumors;
• bedridden patients;
• people who have previously experienced episodes of thrombosis in the postoperative period after surgery on the knee, hip joint, etc.

On long flights, it is necessary to ensure a drinking regimen, get up and walk every 1.5 hours, take 1 aspirin tablet before the flight, even if the patient does not take aspirin as a preventive measure all the time.

With already existing venous thrombosis, surgical prophylaxis can also be carried out by methods:

• filter implantation in the inferior vena cava;
• endovascular catheter thrombectomy (removal of a blood clot from a vein using a catheter inserted into it);
• ligation of the great saphenous or femoral veins - the main sources of blood clots.

Thromboembolism of the pulmonary artery (PE) is a sudden blockage of the branches or trunk of the pulmonary artery by a thrombus (embolus) formed in the right ventricle or atrium of the heart, the venous bed of the systemic circulation and brought with the blood stream. As a result of PE, the blood supply to the lung tissue is cut off. The development of PE is often rapid and can lead to the death of the patient.

PE kills 0.1% of the world's population every year. About 90% of patients who died from pulmonary embolism did not establish the correct diagnosis at the time and the necessary treatment was not carried out.

Among the causes of death of the population from cardiovascular diseases, PE is in third place after coronary artery disease and stroke. PE can lead to death in non-cardiac pathology, occurring after surgery, injuries, childbirth. With timely optimal treatment of PE, there is a high rate of mortality reduction to 2-8%.

Reasons for the development of PE

The most common causes of PE are:

- deep vein thrombosis (DVT) of the lower leg (in 70 - 90% of cases), often accompanied by thrombophlebitis. Thrombosis of both deep and superficial veins of the lower leg may occur

- thrombosis of the inferior vena cava and its tributaries

- cardiovascular diseases predisposing to the appearance of thrombi and embolism in the pulmonary artery (CHD, active phase of rheumatism with the presence of mitral stenosis and atrial fibrillation, hypertension, infective endocarditis, cardiomyopathy and non-rheumatic myocarditis)

- septic generalized process

- oncological diseases (more often cancer of the pancreas, stomach, lungs)

- thrombophilia (increased intravascular thrombosis in violation of the system of regulation of hemostasis)

- antiphospholipid syndrome - the formation of antibodies to phospholipids of platelets, endothelial cells and nervous tissue (autoimmune reactions); manifested by an increased tendency to thrombosis of various localizations.

Risk factors for venous thrombosis and PE are:

- a prolonged state of immobility (bed rest, frequent and prolonged air travel, trips, paresis of the limbs), chronic cardiovascular and respiratory failure, accompanied by a slowdown in blood flow and venous congestion.

- taking a large number of diuretics (massive loss of water leads to dehydration, increased hematocrit and blood viscosity);

- malignant neoplasms - some types of hemoblastosis, polycythemia vera (a high content of erythrocytes and platelets in the blood leads to their hyperaggregation and the formation of blood clots);

- long-term use of certain drugs (oral contraceptives, hormone replacement therapy) increases blood clotting;

- varicose veins (with varicose veins of the lower extremities, conditions are created for stagnation of venous blood and the formation of blood clots);

- metabolic disorders, hemostasis (hyperlipid proteinemia, obesity, diabetes mellitus, thrombophilia);

- surgery and intravascular invasive procedures (for example, a central catheter in a large vein);

- arterial hypertension, congestive heart failure, strokes, heart attacks;

- spinal cord injuries, fractures of large bones;

- chemotherapy;

- pregnancy, childbirth, postpartum period;

smoking, old age, etc.

TELA classification

Depending on the localization of the thromboembolic process, the following variants of PE are distinguished:

Massive (thrombus is localized in the main trunk or main branches of the pulmonary artery)

- embolism of segmental or lobar branches of the pulmonary artery

- embolism of small branches of the pulmonary artery (usually bilateral)

Depending on the volume of arterial blood flow cut off in PE, the following forms are distinguished:

- small (less than 25% of the pulmonary vessels are affected) - accompanied by shortness of breath, the right ventricle is functioning normally

- submassive (submaximal - the volume of the affected vessels of the lungs is from 30 to 50%), in which the patient has shortness of breath, normal blood pressure, right ventricular failure is not very pronounced

- massive (the volume of the disconnected pulmonary blood flow is more than 50%) - there is a loss of consciousness, hypotension, tachycardia, cardiogenic shock, pulmonary hypertension, acute right ventricular failure

- fatal (the volume of blood flow cut off in the lungs is more than 75%).

PE can be severe, moderate, or mild.

The clinical course of PE can be:

- the most acute (fulminant), when there is an immediate and complete blockage by a thrombus of the main trunk or both main branches of the pulmonary artery. Acute respiratory failure, respiratory arrest, collapse, ventricular fibrillation develop. The lethal outcome occurs in a few minutes, the pulmonary infarction does not have time to develop.

- acute, in which there is a rapidly increasing obturation of the main branches of the pulmonary artery and part of the lobar or segmental ones. It starts suddenly, rapidly progresses, symptoms of respiratory, cardiac and cerebral insufficiency develop. It lasts a maximum of 3-5 days, is complicated by the development of pulmonary infarction.

- subacute (protracted) with thrombosis of large and medium branches of the pulmonary artery and the development of multiple pulmonary infarcts. It lasts for several weeks, slowly progresses, accompanied by an increase in respiratory and right ventricular failure. Recurrent thromboembolism may occur with exacerbation of symptoms, which is often fatal.

- chronic (recurrent), accompanied by recurrent thrombosis of the lobar, segmental branches of the pulmonary artery. It is manifested by repeated pulmonary infarctions or repeated pleurisy (usually bilateral), as well as gradually increasing hypertension of the pulmonary circulation and the development of right ventricular failure. It often develops in the postoperative period, against the background of already existing oncological diseases, cardiovascular pathologies.

Symptoms of PE

The symptomatology of PE depends on the number and size of thrombosed pulmonary arteries, the rate of development of thromboembolism, the degree of disturbances in the blood supply to the lung tissue, and the initial state of the patient. PE has a wide range of clinical conditions, from virtually asymptomatic to sudden death.

Clinical manifestations of PE are nonspecific, they can be observed in other pulmonary and cardiovascular diseases, their main difference is a sharp, sudden onset in the absence of other visible causes of this condition (cardiovascular insufficiency, myocardial infarction, pneumonia, etc.). For PE in the classical version, a number of syndromes are characteristic:

1. Cardiovascular:

- acute vascular insufficiency. There is a drop in blood pressure (collapse, circulatory shock), tachycardia. The heart rate can reach more than 100 beats. per minute.

- acute coronary insufficiency (in 15-25% of patients). It is manifested by sudden severe pain behind the sternum of a different nature, lasting from several minutes to several hours, atrial fibrillation, extrasystole.

- Acute cor pulmonale. Due to massive or submassive PE; manifested by tachycardia, swelling (pulsation) of the cervical veins, positive venous pulse. Edema in acute cor pulmonale does not develop.

- acute cerebrovascular insufficiency. There are cerebral or focal disorders, cerebral hypoxia, in severe form - cerebral edema, cerebral hemorrhage. It is manifested by dizziness, tinnitus, deep syncope with convulsions, vomiting, bradycardia or coma. Psychomotor agitation, hemiparesis, polyneuritis, meningeal symptoms may be observed.

1. Pulmonary-pleural:

- acute respiratory failure is manifested by shortness of breath (from a feeling of lack of air to very pronounced manifestations). The number of breaths is more than 30-40 per minute, cyanosis is noted, the skin is ash-gray, pale.

- moderate bronchospastic syndrome is accompanied by dry wheezing.

lung infarction, infarct pneumonia develops 1-3 days after PE. There are complaints of shortness of breath, cough, pain in the chest from the side of the lesion, aggravated by breathing; hemoptysis, fever. Become audible small bubbling wet rales, pleural friction rub. Significant pleural effusions are observed in patients with severe heart failure.

1. Feverish syndrome - subfebrile, febrile body temperature. Associated with inflammatory processes in the lungs and pleura. The duration of the fever is from 2 to 12 days.
2. Abdominal syndrome is caused by acute, painful swelling of the liver (combined with intestinal paresis, peritoneal irritation, hiccups). Manifested by acute pain in the right hypochondrium, belching, vomiting.
3. The immunological syndrome (pulmonitis, recurrent pleurisy, urticaria-like rash on the skin, eosinophilia, the appearance of circulating immune complexes in the blood) develops at 2-3 weeks of the disease.

Complications of PE

Acute PE can cause cardiac arrest and sudden death. When compensatory mechanisms are triggered, the patient does not die immediately, but in the absence of treatment, secondary hemodynamic disorders progress very quickly. The patient's cardiovascular diseases significantly reduce the compensatory capacity of the cardiovascular system and worsen the prognosis.

Diagnosis of PE

In the diagnosis of PE, the main task is to establish the location of blood clots in the pulmonary vessels, assess the degree of damage and the severity of hemodynamic disorders, and identify the source of thromboembolism to prevent relapses.

The complexity of diagnosing PE dictates the need to find such patients in specially equipped vascular departments, which have the widest possible opportunities for special studies and treatment. All patients with suspected PE undergo the following examinations:

- careful history taking, assessment of risk factors for DVT / PE and clinical symptoms

general and biochemical blood and urine tests, blood gas analysis, coagulogram and D-dimer analysis in blood plasma (method for diagnosing venous thrombi)

- ECG in dynamics (to exclude myocardial infarction, pericarditis, heart failure)

chest x-ray (to rule out pneumothorax, primary pneumonia, tumors, rib fractures, pleurisy)

- echocardiography (to detect increased pressure in the pulmonary artery, overload of the right heart, blood clots in the heart cavities)

- lung scintigraphy (impaired blood perfusion through the lung tissue indicates a decrease or absence of blood flow due to PE)

– angiopulmonography (to accurately determine the location and size of a blood clot)

— Ultrasound of peripheral veins, contrast phlebography (to identify the source of thromboembolism)

Treatment of PE

Patients with PE are placed in the intensive care unit.

In an emergency, the patient undergoes full resuscitation.

Further treatment of PE is aimed at normalizing pulmonary circulation and preventing chronic pulmonary hypertension.

In order to prevent recurrence of PE, strict bed rest is necessary. To maintain oxygenation, a constant inhalation of oxygen is carried out.

Massive infusion therapy is carried out to reduce blood viscosity and maintain blood pressure.

In the early period, the appointment of thrombolytic therapy is indicated in order to dissolve the thrombus as quickly as possible and restore blood flow in the pulmonary artery. In the future, to prevent recurrence of PE, heparin therapy is performed.

With the phenomena of heart attack-pneumonia, antibiotic therapy is prescribed.

In cases of massive PE and ineffectiveness of thrombolysis, surgical thromboembolectomy (removal of a blood clot) is performed. As an alternative to embolectomy, catheter fragmentation of the thromboembolus is used. For recurrent PE

Prognosis and prevention of pulmonary embolism is practiced by placing a special filter in the branch of the pulmonary artery, the inferior vena cava.

With early provision of full assistance to patients, the prognosis for life is favorable. With severe cardiovascular and respiratory disorders against the background of extensive pulmonary embolism, mortality exceeds 30%.

Half of the recurrences of PE occur in patients who have not received anticoagulants. Timely, correctly performed anticoagulant therapy reduces the risk of recurrence of PE by half.

To prevent thromboembolism, early diagnosis and treatment of thrombophlebitis, the appointment of indirect anticoagulants in patients at risk are necessary.

Pulmonary embolism occurs when a clot clogs the artery that carries venous blood from the heart to the lungs for oxygen enrichment.

Embolism is different (for example, gas - when the vessel is clogged with an air bubble, bacterial - closing the lumen of the vessel with a clot of microorganisms). Usually, the lumen of the pulmonary artery is blocked by a thrombus that has formed in the veins of the legs, arms, pelvis, or in the heart. With the blood flow, this clot (embolus) is transferred to the pulmonary circulation and blocks the pulmonary artery or one of its branches. This disrupts blood flow to part of the lung, causing the exchange of oxygen to carbon dioxide to suffer.

If pulmonary embolism is severe, then the human body receives little oxygen, which causes the clinical symptoms of the disease. With a critical lack of oxygen, there is an immediate danger to human life.

The problem of PE is dealt with by doctors of various specialties, including cardiologists, cardiac surgeons, and anesthesiologists.

Causes of PE

Pathology develops due to deep vein thrombosis (DVT) in the legs. A thrombus in these veins can break off, travel to the pulmonary artery, and block it. The reasons for the formation of thrombosis in the vessels are described by the Virchow triad, to which they belong:

1. Violation of blood flow.
2. Damage to the vascular wall.
3. Increased blood clotting.

1. Violation of blood flow

The main cause of violations of blood flow in the veins of the legs is a person's inactivity, which leads to stagnation of blood in these vessels. Usually this is not a problem: as soon as a person begins to move, blood flow increases and blood clots do not form. However, prolonged immobilization leads to a significant deterioration in blood circulation and the development of deep vein thrombosis. Such situations occur:

• after a stroke;
• after surgery or injury;
• with other serious diseases that cause a person to lie down;
• during long flights in an airplane, traveling in a car or train.

2. Damage to the vascular wall

If the vessel wall is damaged, its lumen may be narrowed or blocked, which leads to the formation of a thrombus. Blood vessels can be damaged during injuries - when bones are broken, during operations. Inflammation (vasculitis) and certain medications (such as chemotherapy drugs for cancer) can damage the artery wall.

3. Increased blood clotting

Pulmonary embolism very often develops in people with diseases in which the blood clots more easily than normal. These diseases include:

• Malignant neoplasms, the use of chemotherapeutic drugs, radiation therapy.
• Heart failure.
• Thrombophilia is a hereditary disease in which a person's blood has an increased tendency to form blood clots.
• Antiphospholipid syndrome is an immune system disease that causes an increase in blood density, which makes it easier for blood clots to form.

Other factors that increase the risk of PE

There are other factors that increase the risk of developing PE. They belong to:

1. Age over 60 years.
2. Previous deep vein thrombosis.
3. Having a relative who has had deep vein thrombosis in the past.
4. Overweight or obesity.
5. Pregnancy: The risk of PE is increased up to 6 weeks postpartum.
6. Smoking.
7. Taking birth control pills or hormone therapy.

Characteristic symptoms

Symptoms of pulmonary embolism include:

• Chest pain, which is usually sharp and aggravated by deep breathing.
• Cough with bloody sputum (hemoptysis).
• Shortness of breath - a person may have difficulty breathing even at rest, and shortness of breath worsens with exertion.
• Increase in body temperature.

Depending on the size of the blocked artery and the amount of lung tissue in which blood flow is impaired, vital signs (blood pressure, heart rate, oxygen saturation, and respiratory rate) may be normal or abnormal.

The classic signs of PE include:

• tachycardia - increased heart rate;
• tachypnea - increased respiratory rate;
• a decrease in blood oxygen saturation, which leads to cyanosis (a change in the color of the skin and mucous membranes to blue);
• hypotension is a drop in blood pressure.

Further development of the disease:

1. The body tries to compensate for the lack of oxygen by increasing the heart rate and breathing rate.
2. This can cause weakness and dizziness, as the organs, especially the brain, do not have enough oxygen to function properly.
3. A large clot can completely block the blood flow in the pulmonary artery, which leads to the immediate death of a person.

Since most cases of pulmonary embolism are caused by thrombosis of blood vessels in the legs, doctors must pay special attention to the symptoms of this disease, which include:

• Pain, swelling and tenderness in one of the lower extremities.
• Hot skin and redness over the site of thrombosis.

Diagnostics

The diagnosis of thromboembolism is established on the basis of the patient's complaints, medical examination and with the help of additional examination methods. Sometimes pulmonary embolism is very difficult to diagnose, as its clinical picture can be very diverse and similar to other diseases.

To clarify the diagnosis is carried out:

1. Electrocardiography.
2. A blood test for D-dimer is a substance whose level increases in the presence of thrombosis in the body. With a normal level of D-dimer, pulmonary embolism is absent.
3. Determination of the level of oxygen and carbon dioxide in the blood.
4. X-ray of the chest organs.
5. Ventilation-perfusion scanning - used to study gas exchange and blood flow in the lungs.
6. Angiography of the pulmonary artery - X-ray examination of the vessels of the lungs using contrast. With this examination, emboli in the pulmonary artery can be detected.
7. Angiography of the pulmonary artery using computed or magnetic resonance imaging.
8. Ultrasound examination of the veins of the lower extremities.
9. Echocardioscopy is an ultrasound examination of the heart.

Treatment Methods

The choice of tactics for the treatment of pulmonary embolism is carried out by the doctor based on the presence or absence of an immediate danger to the patient's life.

PE is treated primarily with anticoagulants, drugs that reduce blood clotting. They prevent an increase in the size of a blood clot, so that the body slowly dissolves them. Anticoagulants also reduce the risk of further blood clots.

In severe cases, treatment is needed to eliminate the clot. This can be done with thrombolytics (drugs that break up blood clots) or surgery.

Anticoagulants

Anticoagulants are often called blood-thinning drugs, but they do not actually have the ability to thin the blood. They affect blood clotting factors, thereby preventing the easy formation of blood clots.

The main anticoagulants used for pulmonary embolism are heparin and warfarin.

Heparin is administered into the body by intravenous or subcutaneous injection. This drug is used mainly in the initial stages of the treatment of PE, since its action develops very quickly. Heparin can cause the following side effects:

• increase in body temperature;
• headache;
• bleeding.

Most patients with pulmonary thromboembolism require heparin treatment for at least 5 days. They are then given oral warfarin tablets. The action of this drug develops more slowly, it is prescribed for long-term use after stopping the introduction of heparin. This drug is recommended to take at least 3 months, although some patients need longer treatment.

Since warfarin acts on blood clotting, patients should be carefully monitored for its effects with regular coagulation tests (blood clotting tests). These tests are performed on an outpatient basis.

Tests may be needed 2 to 3 times a week at the start of warfarin treatment to help determine the appropriate dose. After that, the frequency of determining the coagulogram is approximately 1 time per month.

Various factors affect the action of warfarin, including diet, other medications, and liver function.

Currently, newer and safer oral anticoagulants have been introduced into clinical practice - rivaroxaban, dabigatran, apixaban. These drugs are safer than warfarin, so patients who take them do not need to carefully monitor blood clotting. Their disadvantage is the very high cost.

Treatment to remove a blood clot from a pulmonary artery

Severe pulmonary embolism carries an immediate danger to the patient's life. Therefore, in such cases, treatment is aimed at eliminating the thrombus that blocks the lumen of the vessel. For this, thrombolysis or surgery can be used.

thrombolysis

Thrombolysis is the breaking down of blood clots with the help of certain medications. The most commonly used are alteplase, streptokinase, or urokinase. However, when using thrombolytics, there is a rather high risk of dangerous bleeding, including cerebral hemorrhage.

Operation

Sometimes it is possible to remove a blood clot from the pulmonary artery surgically. This operation is called an embolectomy. This is a major surgical intervention performed in the chest cavity, near the heart. It is performed by cardiac or thoracic surgeons only in specialized medical institutions. Embolectomy is considered the last resort for patients with critical pulmonary embolism.

New treatments for PE

• Catheter-directed thrombolysis - the introduction of a drug that dissolves blood clots directly into the blocked pulmonary artery.
• Catheter embolectomy is the removal of a blood clot or its fragmentation using a small catheter inserted into the pulmonary artery through the blood vessels.

Some patients undergo implantation of cava filters - special filters that are placed in the inferior vena cava to stop new blood clots from entering the pulmonary artery from the legs.

Prevention

If a person has an increased risk of blood clots, you can reduce it in the following ways:

1. The use of anticoagulants.
2. Wearing compression stockings that improve blood flow in the legs.
3. Increased mobility and physical activity.
4. To give up smoking.
5. Healthy food.
6. Maintaining normal weight.

Prognosis for PE

Pulmonary embolism is a life-threatening disease. The prognosis in patients depends on several factors - the presence of concomitant diseases, timely diagnosis and correct treatment.

Approximately 10% of patients with PE die within an hour of the onset of the disease, 30% die later from repeated pulmonary embolism.

Mortality rates also depend on the type of PE. With a life-threatening pulmonary embolism, which is characterized by a drop in blood pressure, mortality reaches 30-60%.

I have pulmonary embolism, I have been drinking Prodax 150 ml for half a year now. Headaches have now begun, I have lost 20 kg over these six months. I gave all the good tests, what is happening to me, I don’t know the Sergachsky doctors shrug, I don’t know what to do and where to go. group, but in Sergach, Nizhny Novgorod region, they did not put them to work, they sent them. That's it.

Elena, the doctors had to establish the cause of thromboembolism, and in order for the treatment to be effective, complex treatment is needed. To do this, you need to consult various highly specialized specialists, such as cardiac surgeons and cardiologists. It is also important to eliminate factors that increase the risk of PE (overweight, smoking, taking hormones, etc.), and on the contrary, try to increase physical activity a little. The development of recurrent PE is facilitated by the presence of chronic diseases of the cardiovascular and respiratory systems, as well as oncological pathologies, so consultation of specialists should be frequent, if possible.

If an episode of PE has been transferred, or there are risk factors, the alertness in relation to this pathology should be maximum.

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Treatment and prevention of pulmonary embolism

One of the main causes of sudden death is an acute violation of blood flow in the lungs. Pulmonary embolism refers to conditions that in the vast majority of cases lead to an unexpected cessation of the body's vital functions. Pulmonary thrombosis is extremely difficult to cure, so it is optimal to prevent a deadly situation.

Sudden occlusion of arterial trunks in the lungs

The lungs perform an important task of saturating venous blood with oxygen: the main main vessel, which brings blood to the small branches of the arterial network of the lungs, departs from the right heart. Thrombosis of the pulmonary artery becomes the cause of the cessation of the normal functioning of the pulmonary circulation, the outcome of which will be the absence of oxygenated blood in the left cardiac chambers and the rapidly growing symptoms of acute heart failure.

See how a blood clot forms and leads to pulmonary embolism

The chances of saving life are higher if a pulmonary thrombus breaks off and leads to blockage of a small-caliber arterial branch. It is much worse if a thrombus breaks off in the lungs and provokes cardiac occlusion with sudden death syndrome. The main provoking factor is any surgical intervention, therefore, it is necessary to strictly follow the doctor's preoperative prescriptions.

Age is of great prognostic value (in people under 40 years of age, pulmonary thromboembolism during surgery is extremely rare, but for an older person the risk is very high - up to 75% of all cases of fatal blockage in the pulmonary artery occur in elderly patients).

An unpleasant feature of the disease is the delay in diagnosis - in 50-70% of all cases of sudden death, the presence of pulmonary thromboembolism was detected only at a post-mortem autopsy.

Acute obstruction of the pulmonary trunk: what is the cause

The appearance of blood clots or fat emboli in the lung is explained by blood flow: most often, the primary focus of the formation of thrombotic masses is the pathology of the heart or the venous system of the legs. The main causes of occlusive lesions of the main vessels of the pulmonary system:

• any type of surgical intervention;
• severe lung disease;
• congenital and acquired heart defects with various types of valvular defects;
• anomalies in the structure of the pulmonary vessels;
• acute and chronic ischemia of the heart;
• inflammatory pathology inside the cardiac chambers (endocarditis);
• severe forms of arrhythmia;
• complicated variants of varicose veins (vein thrombophlebitis);
• bone injury;
• gestation and childbirth.

Predisposing factors are of great importance for the occurrence of a dangerous situation, when a blood clot forms and breaks off in the lungs:

• genetically predetermined blood clotting disorders;
• blood diseases that contribute to the deterioration of fluidity;
• metabolic syndrome with obesity and endocrine disorders;
• age over 40;
• malignant neoplasms;
• prolonged immobility due to injury;
• any variant of hormone therapy with constant and long-term use of drugs;
• smoking.

Pulmonary artery thrombosis occurs when a blood clot enters the venous system (in 90% of cases, blood clots in the lungs appear from the vasculature of the inferior vena cava), so any form of atherosclerotic disease does not affect the risk of blockage of the main trunk, leaving the right ventricle.

Types of life-threatening occlusion: classification

A venous clot can disrupt circulation anywhere in the pulmonary circulation. Depending on the location of the thrombus in the lungs, the following forms are distinguished:

• blockage of the main arterial trunk, in which sudden and inevitable death occurs in most cases (60-75%);
• occlusion of large branches that provide blood flow in the pulmonary lobes (probability of death 6-10%);
• thromboembolism of small branches of the pulmonary artery (minimal risk of a sad outcome).

The volume of the lesion is prognostically important, which is divided into 3 options:

1. Massive (almost complete cessation of blood flow);
2. Submassive (problems with blood circulation and gas exchange occur in 45% or more of the entire vascular system of the lung tissue);
3. Partial thromboembolism of the branches of the pulmonary artery (shutdown from gas exchange is less than 45% of the vascular bed).

Depending on the severity of symptoms, 4 types of pathological blockage are distinguished:

1. Fulminant (all symptoms and signs of pulmonary embolism unfold in 10 minutes);
2. Acute (manifestations of occlusion are growing rapidly, limiting the life of a sick person to the first day after the first symptoms);
3. Subacute (slowly progressing cardiopulmonary disorders);
4. Chronic (typical signs of heart failure, in which the risk of a sudden cessation of the pumping function of the heart is minimal).

Fulminant thromboembolism is a massive occlusion of the pulmonary artery, in which death occurs within minutes.

It is very difficult to guess how long a person can live with an acute form of the disease, when all the necessary emergency medical and diagnostic procedures must be completed within 24 hours and a fatal outcome must be prevented.

The best survival rate is in subacute and chronic types, when most of the patients treated in the hospital can avoid a sad outcome.

Symptoms of dangerous occlusion: what are the manifestations

Pulmonary embolism, the symptoms of which are most often associated with venous diseases of the lower extremities, can occur in the form of 3 clinical variants:

1. The initial presence of complicated varicose veins in the area of ​​the venous network of the legs;
2. The first manifestations of thrombophlebitis or phlebothrombosis occur during an acute disturbance of blood flow in the lungs;
3. There are no external changes and symptoms indicating venous pathology in the legs.

A large number of various symptoms of pulmonary embolism are divided into 5 main symptom complexes:

The most dangerous situations are when a pulmonary thrombus breaks off and completely blocks the lumen of a vessel that supplies the vital organs of the human body. In this case, the probability of survival is minimal, even if medical care is provided in a timely manner in a hospital setting.

Symptoms of brain disorders

The main manifestations of cerebral disorders in case of an occlusive lesion of the main trunk extending from the right ventricle are the following symptoms:

• severe headache;
• dizziness with fainting and loss of consciousness;
• convulsive syndrome;
• partial paresis or paralysis on one side of the body.

Often there are psycho-emotional problems in the form of fear of death, panic, restless behavior with inappropriate actions.

Cardiac symptoms

The sudden and dangerous symptoms of pulmonary embolism include the following signs of heart failure:

• severe chest pain;
• frequent heartbeat;
• a sharp drop in blood pressure;
• swollen neck veins;
• pre-fainting state.

Often, severe pain in the left side of the chest is due to myocardial infarction, which has become the main cause of pulmonary thromboembolism.

Respiratory disorders

Pulmonary disorders in a thromboembolic state are manifested by the following symptoms:

• increasing shortness of breath;
• feeling of suffocation with the appearance of fear and panic;
• severe pain in the chest at the time of inspiration;
• cough with hemoptysis;
• cyanotic changes in the skin.

The essence of all manifestations in thromboembolism of small branches of the pulmonary artery is a partial pulmonary infarction, in which the respiratory function is necessarily impaired.

With abdominal and renal syndrome, disorders associated with internal organs come to the fore. Typical complaints will be the following manifestations:

• intense pain in the abdomen;
• predominant localization of pain in the right hypochondrium;
• disruption of the intestines (paresis) in the form of constipation and cessation of gas discharge;
• detection of signs typical of peritonitis;
• temporary cessation of urination (anuria).

Regardless of the severity and compatibility of symptoms of pulmonary embolism, it is necessary to start therapy as soon as possible and quickly using resuscitation techniques.

Diagnosis: is it possible to detect early

Often, pulmonary thromboembolism occurs after surgery or surgical manipulation, so the doctor will pay attention to the following manifestations that are atypical for the normal postoperative period:

• repeated episodes of pneumonia or lack of effect from standard treatment for pneumonia;
• unexplained fainting;
• angina attacks against the background of cardiac therapy;
• high fever of unknown origin;
• sudden onset of symptoms of cor pulmonale.

Diagnosis of an acute condition associated with blockage of the main trunk extending from the right ventricle of the heart includes the following studies:

• general clinical tests
• assessment of the blood coagulation system (coagulogram);
• electrocardiography;
• plain x-ray of the chest;
• duplex echography;
• lung scintigraphy;
• angiography of the vessels of the chest;
• phlebography of venous vessels of the lower extremities;
• tomography with contrast.

None of the examination methods is able to make an accurate diagnosis, therefore, only the complex use of techniques will help to identify signs of pulmonary embolism.

Emergency medical measures

Emergency care at the stage of the ambulance team involves the following tasks:

1. Prevention of death from acute cardiopulmonary failure;
2. Correction of blood flow in the pulmonary circulation;
3. Preventive measures to prevent repeated episodes of pulmonary vascular occlusion.

The doctor will use all medications that will help eliminate the mortal risk, and will try to get to the hospital as quickly as possible. Only in a hospital setting can you try to save the life of a person with pulmonary thromboembolism.

The basis of successful therapy is the following treatment methods in the first hours after the onset of dangerous symptoms:

• the introduction of thrombolytic drugs;
• use in the treatment of anticoagulants;
• improvement of blood circulation in the vessels of the lungs;
• support of respiratory function;
• symptomatic therapy.

Surgical treatment is indicated in the following cases:

• blockage of the main pulmonary trunk;
• a sharp deterioration in the patient's condition with a drop in blood pressure;
• lack of effect from drug therapy.

The main method of surgical treatment is thrombectomy. 2 variants of surgical intervention are used - with the use of a heart-lung machine and with temporary closure of blood flow through the vessels of the inferior vena cava. In the first case, the doctor will remove the obstruction in the vessel using a special technique. In the second, a specialist will block the blood flow in the lower body during the operation and perform a thrombectomy as quickly as possible (the time for the operation is limited to 3 minutes).

Regardless of the chosen therapy tactics, it is impossible to give a full guarantee of recovery: up to 80% of all patients with occlusion of the main pulmonary trunk die during or after surgery.

Prevention: how to prevent death

In the case of thromboembolic complications, the optimal therapy option is the use of non-specific and specific preventive measures at all stages of examination and treatment. Of the non-specific measures, the best effect will be when using the following recommendations:

• the use of compression stockings (stockings, tights) for any medical procedures;
• early activation after any diagnostic and therapeutic manipulations and operations (you can’t lie down for a long time or take a forced posture for a long time in the postoperative period);
• constant monitoring by a cardiologist with courses of therapy for heart pathology;
• complete cessation of smoking;
• timely treatment of complications of varicose veins;
• weight loss in obesity;
• correction of endocrine problems;

Measures of specific prevention are:

• constant intake of medicines prescribed by a doctor that reduce the risk of thrombosis;
• the use of a cava filter at a high risk of thromboembolic complications;
• the use of special physiotherapeutic techniques (intermittent pneumocompression, electrical muscle stimulation).

The basis for successful prevention is the careful and strict implementation of the doctor's recommendations at the preoperative stage: often ignoring elementary methods (refusal of compression stockings) causes the formation and separation of a blood clot with the development of a deadly complication.

Prediction: what are the chances of life

Negative outcomes in case of blockage of the pulmonary trunk are due to the fulminant form of the complication: in this case, the prognosis for life is the worst. In other variants of the pathology, there are chances of survival, especially if the diagnosis is made on time and treatment is started as quickly as possible. However, even with a favorable outcome after acute pulmonary vascular occlusion, unpleasant consequences can form in the form of chronic pulmonary hypertension with severe shortness of breath and heart failure.

Complete or partial occlusion of the main artery from the right ventricle is one of the main causes of sudden death after any medical intervention. It is better to prevent a sad outcome, using the advice of a specialist at the stage of preparation for diagnostic and treatment procedures.

Thromboembolism of the pulmonary artery and its branches. Treatment

Treatment of PE is challenging. The disease occurs unexpectedly, progresses rapidly, as a result of which the doctor has at his disposal a minimum of time to determine the tactics and method of treating the patient. First, there can be no standard treatment regimens for PE. The choice of method is determined by the localization of the embolus, the degree of impaired pulmonary perfusion, the nature and severity of hemodynamic disorders in the systemic and pulmonary circulation. Secondly, the treatment of PE cannot be limited to the elimination of an embolus in the pulmonary artery. The source of embolization should not be overlooked.

Urgent care

Emergency care measures for PE can be divided into three groups:

1) maintaining the life of the patient in the first minutes of PE;

2) elimination of deadly reflex reactions;

3) elimination of the embolus.

Life support in cases of clinical death of patients is carried out primarily by resuscitation. Priority measures include the fight against collapse with the help of pressor amines, correction of the acid-base state, and effective oxygen barotherapy. At the same time, it is necessary to start thrombolytic therapy with native streptokinase preparations (streptodecase, streptase, avelizin, celease, etc.).

The embolus located in the artery causes reflex reactions, due to which severe hemodynamic disorders often occur with non-massive pulmonary embolism. To eliminate the pain syndrome, 4-5 ml of a 50% solution of analgin and 2 ml of droperidol or seduxen are administered intravenously. Drugs are used when necessary. With severe pain syndrome, analgesia begins with the introduction of drugs in combination with droperidol or seduxen. In addition to the analgesic effect, the feeling of fear of death is suppressed, catecholaminemia, myocardial oxygen demand and electrical instability of the heart are reduced, the rheological properties of blood and microcirculation are improved. In order to reduce arteriolospasm and bronchospasm, eufillin, papaverine, no-shpa, prednisolone are used in normal doses. The elimination of the embolus (the basis of pathogenetic treatment) is achieved by thrombolytic therapy, started immediately after the diagnosis of PE. Relative contraindications to thrombolytic therapy, which are present in many patients, are not an obstacle to its use. The high likelihood of death justifies the risk of treatment.

In the absence of thrombolytic drugs, continuous intravenous administration of heparin at a dose of 1000 units per hour is indicated. The daily dose will be ED. With this method of administration, relapses of pulmonary embolism occur much less frequently, rethrombosis is more reliably prevented.

When clarifying the diagnosis of pulmonary embolism, the degree of occlusion of the pulmonary blood flow, the localization of the embolus, a conservative or surgical method of treatment is chosen.

Conservative treatment

The conservative treatment of pulmonary embolism is currently the main one and includes the following measures:

1. Ensuring thrombolysis and stopping further thrombosis.

2. Reducing pulmonary arterial hypertension.

3. Compensation for pulmonary and right heart failure.

4. Elimination of arterial hypotension and removal of the patient from the collapse.

5. Treatment of pulmonary infarction and its complications.

The scheme of conservative treatment of pulmonary embolism in the most typical form can be represented as follows:

1. Complete rest of the patient, lying position of the patient with a raised head end in the absence of collapse.

2. With pain in the chest and a strong cough, the introduction of analgesics and antispasmodics.

3. Oxygen inhalations.

4. In case of collapse, the whole complex of therapeutic measures for acute vascular insufficiency is carried out.

5. With cardiac weakness, glycosides (strophanthin, corglicon) are prescribed.

6. Antihistamines: diphenhydramine, pipolfen, suprastin, etc.

7. Thrombolytic and anticoagulant therapy. The active principle of thrombolytic drugs (streptase, avelizin, streptodecase) is a metabolic product of hemolytic streptococcus - streptokinase, which, by activating plasminogen, forms a complex with it that promotes the appearance of plasmin, which dissolves fibrin directly in the thrombus. The introduction of thrombolytic drugs, as a rule, is made in one of the peripheral veins of the upper extremities or in the subclavian vein. But with massive and submassive thromboembolism, the most optimal is their introduction directly into the area of ​​the thrombus that occludes the pulmonary artery, which is achieved by probing the pulmonary artery and bringing the catheter under the control of the X-ray machine to the thrombus. The introduction of thrombolytic drugs directly into the pulmonary artery quickly creates their optimal concentration in the area of ​​thromboembolism. In addition, during probing, an attempt is simultaneously made to fragment or tunnel thromboembolism in order to restore pulmonary blood flow as quickly as possible. Before the introduction of streptase, the following blood parameters are determined as initial data: fibrinogen, plasminogen, prothrombin, thrombin time, blood clotting time, bleeding duration. The sequence of drug administration:

1. 5000 IU of heparin and 120 mg of prednisolone are injected intravenously.

2. Intravenous drip for 30 minutes, a unit of streptase (trial dose) diluted in 150 ml of saline is injected, after which the above blood parameters are examined again.

3. In the absence of an allergic reaction, which indicates a good tolerability of the drug, and a moderate change in control parameters, the administration of a therapeutic dose of streptase at the rate of 0,000 U/h, heparin 1000 U/h, nitroglycerin 30 mcg/min. The approximate composition of the solution for infusion:

I% solution of nitroglycerin

0.9% sodium chloride solution

The solution is administered intravenously at a rate of 20 ml/h.

4. During the administration of streptase, 120 mg of prednisolone is injected intravenously every 6 hours. The duration of the administration of streptase (24-96 hours) is determined individually.

Monitoring of the listed blood parameters is carried out every four hours. During treatment, it is not allowed to decrease fibrinogen below 0.5 g/l, prothrombin index below %, changes in thrombin time above a six-fold increase compared to the original, changes in clotting time and bleeding duration above a three-fold increase compared to the original data. Complete blood count is performed daily or according to indications, platelets are determined every 48 hours and within five days after the start of thrombolytic therapy, urinalysis - daily, ECG - daily, lung perfusion scintigraphy - according to indications. Therapeutic dose of streptase ranges from ED or more.

Treatment with streptodecase involves the simultaneous administration of a therapeutic dose of the drug, which is ED of the drug. The same indicators of the coagulation system are controlled as in the treatment with streptase.

At the end of treatment with thrombolytics, the patient is transferred to treatment with maintenance doses of heparin, 000 IU per day intravenously or subcutaneously for 3-5 days, under the control of clotting time and bleeding duration.

On the last day of heparin administration, indirect anticoagulants (pelentan, warfarin) are prescribed, the daily dose of which is selected so that the prothrombin index is kept within (40-60%), the international normalized ratio (MHO) is 2.5. Treatment with indirect anticoagulants can, if necessary, continue for a long time (up to three to six months or more).

Absolute contraindications to thrombolytic therapy:

1. Disturbed consciousness.

2. Intracranial and spinal formations, arteriovenous aneurysms.

3. Severe forms of arterial hypertension with symptoms of cerebrovascular accident.

4. Bleeding of any localization, excluding hemoptysis due to pulmonary infarction.

6. The presence of potential sources of bleeding (ulcer of the stomach or intestines, surgical interventions within 5 to 7 days, condition after aortography).

7. Recent streptococcal infections (acute rheumatism, acute glomerulonephritis, sepsis, prolonged endocarditis).

8. Recent traumatic brain injury.

9. Previous hemorrhagic stroke.

10. Known disorders of the blood coagulation system.

11. Unexplained headache or blurred vision in the last 6 weeks.

12. Craniocerebral or spinal operations within the last two months.

13. Acute pancreatitis.

14. Active tuberculosis.

15. Suspicion of a dissecting aortic aneurysm.

16. Acute infectious diseases at the time of admission.

Relative contraindications to thrombolytic therapy:

1. Exacerbation of peptic ulcer of the stomach and duodenum.

2. History of ischemic or embolic strokes.

3. Reception of indirect anticoagulants at the time of admission.

4. Serious injuries or surgical interventions more than two weeks ago, but not more than two months;

5. Chronic uncontrolled arterial hypertension (diastolic blood pressure over 100 mm Hg).

6. Severe renal or hepatic insufficiency.

7. Catheterization of the subclavian or internal jugular vein.

8. Intracardiac thrombi or valvular vegetations.

In vital indications, one must choose between the risk of disease and the risk of therapy.

The most common complications in the use of thrombolytic and anticoagulant drugs are bleeding and allergic reactions. Their prevention is reduced to the careful implementation of the rules for the use of these drugs. If there are signs of bleeding associated with the use of thrombolytics, the following are administered intravenously:

• epsilon-aminocaproic acid ml of 50% solution;
• fibrinogen per 200 ml of saline;
• calcium chloride - 10 ml of a 10% solution;
• fresh frozen plasma. Intramuscularly administered:
• hemophobinml;
• vikasolml 1% solution.

If necessary, a transfusion of freshly citrated blood is indicated. In case of an allergic reaction, prednisolone, promedol, dimedrol are administered. The antidote of heparin is protamine sulfate, which is administered in an amount of 5-10 ml of a 10% solution.

Among the drugs of the latest generation, it is necessary to note a group of tissue plasminogen activators (alteplase, actilyse, retavase), which are activated by binding to fibrin and promote the transition of plasminogen to plasmin. When using these drugs, fibrinolysis increases only in the thrombus. Alteplase is administered at a dose of 100 mg according to the scheme: bolus administration of 10 mg over 1-2 minutes, then during the first hour - 50 mg, in the next two hours - the remaining 40 mg. Retavase, which has been used in clinical practice since the late 1990s, has an even more pronounced lytic effect. The maximum lytic effect with its use is achieved within the first 30 minutes after administration (10 IU + 10 IU intravenously). The frequency of bleeding when using tissue plasminogen activators is significantly less than when using thrombolytics.

Conducting conservative treatment is possible only when the patient retains the ability to provide relatively stable blood circulation for several hours or days (submassive embolism or embolism of small branches). With embolism of the trunk and large branches of the pulmonary artery, the effectiveness of conservative treatment is only 20-25%. In these cases, the method of choice is surgical treatment - embolothrombectomy from the pulmonary artery.

Surgery

The first successful operation for pulmonary embolism was performed by F. Trendelenburg's student M. Kirchner in 1924. Many surgeons attempted pulmonary embolism, but the number of patients who died during the operation was significantly higher than those who underwent it. In 1959, K. Vossschulte and N. Stiller proposed to perform this operation under conditions of temporary occlusion of the vena cava by transsternal access. The technique provided a wide free access, a quick approach to the heart and the elimination of dangerous dilatation of the right ventricle. The search for safer methods of embolectomy led to the use of general hypothermia (P. Allison et al., 1960), and then artificial circulation (E. Sharp, 1961; D. Cooley et al., 1961). General hypothermia has not gained popularity due to lack of time, but the use of cardiopulmonary bypass has opened up new horizons in the treatment of this disease.

In our country, the technique of embolectomy under conditions of vena cava occlusion was developed and successfully applied by B.C. Saveliev et al. (1979). The authors believe that pulmonary embolectomy is indicated for those who are at risk of death from acute cardiopulmonary failure or the development of severe post-embolic hypertension of the pulmonary circulation.

Currently, the optimal methods of embolectomy for massive pulmonary embolism are:

1 Operation under conditions of temporary occlusion of the vena cava.

2. Embolectomy through the main branch of the pulmonary artery.

3. Surgical intervention under cardiopulmonary bypass.

The use of the first technique is indicated for massive embolism of the trunk or both branches of the pulmonary artery. In the case of a predominant unilateral lesion, embolectomy through the corresponding branch of the pulmonary artery is more justified. The main indication for surgery under cardiopulmonary bypass for massive pulmonary embolism is widespread distal occlusion of the vascular bed of the lungs.

B.C. Saveliev et al. (1979 and 1990) allocate absolute and relative indications for embolothrombectomy. The absolute indications are:

• thromboembolism of the trunk and main branches of the pulmonary artery;
• thromboembolism of the main branches of the pulmonary artery with persistent hypotension (with pressure in the pulmonary artery below 50 mm Hg. Art.)

Relative indications are thromboembolism of the main branches of the pulmonary artery with stable hemodynamics and severe hypertension in the pulmonary artery and right heart.

They consider contraindications to embolectomy:

• severe comorbidities with a poor prognosis, such as cancer;
• diseases of the cardiovascular system, in which the success of the operation is doubtful, and its risk is not justified.

A retrospective analysis of the possibilities of embolectomy in patients who died from massive embolism showed that success can be expected only in 10-11% of cases, and even with a successful embolectomy, the possibility of repeated embolism is not ruled out. Therefore, the main direction in solving the problem should be prevention. PE is not a fatal condition. Modern methods for diagnosing venous thrombosis make it possible to predict the risk of thromboembolism and to carry out its prevention.

The method of endovascular rotary pulmonary artery obstruction (ERDA) proposed by T. Schmitz-Rode, U. Janssens, N.N. Schild et al. (1998) and used in a fairly large number of patients by B.Yu. Bobrov (2004). Endovascular rotary deobstruction of the main and lobar branches of the pulmonary artery is indicated for patients with massive thromboembolism, especially in its occlusive form. ERDLA is performed during angiopulmonography using a special device developed by T. Schmitz-Rode (1998). The principle of the method lies in the mechanical destruction of massive thromboembolism in the pulmonary arteries. It can be an independent method of treatment for contraindications or ineffectiveness of thrombolytic therapy or precede thrombolysis, which significantly increases its effectiveness, reduces its duration, reduces the dosage of thrombolytic drugs and reduces the number of complications. ERDLA is contraindicated in the presence of a rider embolus in the pulmonary trunk due to the risk of occlusion of the main branches of the pulmonary artery due to the migration of fragments, as well as in patients with non-occlusive and peripheral form of embolism of the branches of the pulmonary artery.

Prevention of pulmonary embolism

Prevention of pulmonary embolism should be carried out in two directions:

1) prevention of the occurrence of peripheral venous thrombosis in the postoperative period;

2) with already formed venous thrombosis, it is necessary to carry out treatment to prevent the separation of thrombotic masses and their throwing into the pulmonary artery.

To prevent postoperative thrombosis of the veins of the lower extremities and pelvis, two types of preventive measures are used: nonspecific and specific prevention. Nonspecific prevention includes combating physical inactivity in bed and improving venous circulation in the system of the inferior vena cava. Specific prevention of peripheral venous thrombosis involves the use of antiplatelet agents and anticoagulants. Specific prophylaxis is indicated for thromboprone patients, nonspecific - for all without exception. The prevention of venous thrombosis and thromboembolic complications is described in detail in the next lecture.

With already formed venous thrombosis, surgical methods of antiembolic prophylaxis are used: thrombectomy from the iliocaval segment, plication of the inferior vena cava, ligation of the main veins, and implantation of a cava filter. The most effective preventive measure, which has been widely used in clinical practice over the past three decades, is the implantation of a cava filter. The most widespread is the umbrella filter proposed by K. Mobin-Uddin in 1967. Throughout the years of filter use, various modifications of the latter have been proposed: the hourglass, the Simon nitinol filter, the bird's nest, and the Greenfield steel filter. Each of the filters has its advantages and disadvantages, but none of them fully meets all the requirements for them, which determines the need for further searches. The advantage of the hourglass filter, which has been used in clinical practice since 1994, is its high embolic activity and low ability to perforate the inferior vena cava. The main indications for the implantation of a cava filter:

• embolic (floating) thrombi in the inferior vena cava, iliac and femoral veins, complicated or uncomplicated pulmonary embolism;
• massive thromboembolism of the pulmonary artery;
• repeated PE, the source of which is not established.

In many cases, the implantation of cava filters is more preferable than surgical interventions on the veins:

• in elderly and senile patients with severe concomitant diseases and a high risk of surgery;
• in patients who have recently undergone surgery on the organs of the abdominal cavity, small pelvis and retroperitoneal space;
• with recurrence of thrombosis after thrombectomy from the iliocaval and iliac-femoral segments;
• in patients with purulent processes in the abdominal cavity and in the retroperitoneal space;
• with pronounced obesity;
• during pregnancy for more than 3 months;
• with old non-occlusive thrombosis of the iliocaval and iliac-femoral segments, complicated by PE;
• in the presence of complications from the previously installed cava filter (weak fixation, the threat of migration, wrong size selection).

The most serious complication of the installation of cava filters is thrombosis of the inferior vena cava with the development of chronic venous insufficiency of the lower extremities, which is observed, according to different authors, in 10-15% of cases. However, this is a small price to pay for the risk of possible PE. The cava filter itself can cause thrombosis of the inferior vena cava (IVC) in violation of blood clotting properties. The occurrence of thrombosis late after filter implantation (3 months later) may be due to both the capture of emboli and the thrombogenic effect of the filter on the vascular wall and flowing blood. Therefore, at present, in a number of cases, it is envisaged to install a temporary cava filter. Implantation of a permanent vena cava filter is advisable in detecting disorders of the blood coagulation system that create a risk of recurrence of PE during the patient's life. In other cases, it is possible to install a temporary cava filter for up to 3 months.

The implantation of a cava filter does not completely solve the process of thrombosis and thromboembolic complications, therefore, constant drug prophylaxis should be carried out throughout the patient's life.

A serious consequence of the transferred pulmonary embolism, despite the ongoing treatment, is chronic occlusion or stenosis of the main trunk or main branches of the pulmonary artery with the development of severe hypertension of the pulmonary circulation. This condition is called chronic post-embolic pulmonary hypertension (CPEPH). The incidence of this condition after thromboembolism of large arteries is 17%. The leading symptom of CPEPH is shortness of breath, which can occur even at rest. Patients are often worried about dry cough, hemoptysis, pain in the heart. As a result of hemodynamic insufficiency of the right parts of the heart, an increase in the liver, expansion and pulsation of the jugular veins, ascites, and jaundice are observed. According to most clinicians, the prognosis for CPEPH is extremely unfavorable. The life expectancy of such patients, as a rule, does not exceed three to four years. With a pronounced clinical picture of post-embolic lesions of the pulmonary arteries, surgery is indicated - intima thrombectomy. The outcome of the intervention is determined by the duration of the disease (the period of occlusion is not more than 3 years), the level of hypertension in the small circle (systolic pressure up to 100 mm Hg) and the state of the distal pulmonary arterial bed. Adequate surgical intervention can achieve regression of severe CPEPH.

Pulmonary embolism is one of the most important problems in medical science and practical public health. Currently, there are all opportunities to reduce mortality from this disease. It is impossible to put up with the opinion that PE is something fatal and unavoidable. Past experience suggests otherwise. Modern diagnostic methods make it possible to predict the outcome, and timely and adequate treatment gives successful results.

It is necessary to improve the methods of diagnosis and treatment of phlebothrombosis as the main source of embolism, to increase the level of active prevention and treatment of patients with chronic venous insufficiency, to identify patients with risk factors and sanitize them in a timely manner.

Selected lectures on angiology. E.P. Kokhan, I.K. Zavarina

It is advisable to consider the clinic of deep vein thrombosis of the limb by segments of the lesion, since in each case there are specific features of venous hemodynamic disturbances that determine the clinical picture of the disease.

The vascular suture is the basis of vascular surgery. N.N. Burdenko wrote: "If we evaluate all our surgical operations from a physiological point of view, then the operation of the vascular suture belongs, by right, one of the first places." The seam superimposed on the wall of the vessel is called vascular. He may be c.

The use of modern instrumental methods has significantly expanded the diagnostic capabilities of the doctor, allowing a deeper analysis and evaluation of the nature and course of the pathological process, and most importantly, to identify vascular disorders at an early stage of the disease, when clinical symptoms are not expressed.

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