Treatment of the body of small branches of the pulmonary artery. Thromboembolism of the branches of the pulmonary artery: pathophysiology, clinical picture, diagnosis, treatment Tel of segmental branches of both pulmonary arteries

Pulmonary embolism, or PE - acute blockage (occlusion) by a thrombus or embolus of any part of the pulmonary artery. This is a serious disease that in many cases threatens human life. It is the most common cause of sudden death in hospitalized patients. Unfortunately, it is more widespread than is commonly believed - according to the data of pathological studies, about 60% of PE remain unrecognized during the life of patients and are diagnosed only posthumously.

You will learn about why pulmonary embolism occurs, what symptoms it accompanies, as well as the principles of diagnosis and treatment of this disease, you will learn from our article.

Sources of blood clots or emboli in PE

One of the leading risk factors for PE is diseases of the veins of the lower extremities.

Most often, PE develops against the background or inferior vena cava - a thrombus breaks off from the vessel wall and enters the pulmonary artery with blood flow, clogging one or more of its branches.

In 3-4% of cases, the source is thrombosis in the right atrium or veins of the upper extremities.

In every 10th patient, the source of thromboembolism cannot be detected.

Regardless of localization, the most dangerous are the so-called floating blood clots - they are only one edge attached to the wall of the vessel, and the second edge is freely located in its lumen, as if it oscillates, floats in it.

Predisposing factors

80% of cases of PE is a secondary pathology that occurs when a patient has one or (more often) several predisposing factors at once. All these factors are divided by specialists into independent of the patient and dependent, that is, those that he can control in order to reduce the risk of developing this formidable pathology in himself.

Independent factors

These are:

or other tubular bones;
hip or knee replacement surgery;
large abdominal operations;
any laparoscopic surgery;
severe, massive injuries;
spinal cord injury;
hereditary deficiency of antithrombin 3, proteins C or S;
deficiency of fibrinogen in the blood;
the presence of a central venous catheter;
chemotherapy;
prolonged bed rest (3 days or more) or motionless position of the body (travel by bus or plane);
age 60 and over.

Human-dependent factors

The list includes:

(CHF);
chronic respiratory failure (DN);
accompanied by paralysis;
malignant neoplasms;
taking oral (hormonal) contraceptives;
thrombophilia;
erythremia;
paroxysmal renal hemoglobinuria;
period of pregnancy, childbirth;
previously transferred vascular thromboembolism;
excess weight;
or others;
smoking.

Classification

Depending on which part of the pulmonary artery the thrombus is located in, the following variants of PE are distinguished:

massive (a thrombus clogs the lumen of the main trunk or the main branches of the vessel);
occlusion of lobar or segmental branches;
occlusion of small branches of the pulmonary artery.

Depending on how much volume of the pulmonary vessels is excluded from the bloodstream system, 4 forms of the disease are distinguished:

if less than ¼ of the pulmonary vessels are affected, this is a small form of PE (manifested only by shortness of breath or proceeds without symptoms at all);
if 30-50% of the pulmonary vessels are affected, this is a submassive or submaximal form of PE (the patient is worried about shortness of breath, some signs of right ventricular failure are found);
if more than half of the vessels are disconnected from the blood flow, pulmonary embolism is massive (the patient loses consciousness, his pulse quickens, develops, cardiogenic shock, acute right ventricular failure);
if more than 75% of the pulmonary artery is affected, the patient dies instantly - this is a fatal form of PE.

Depending on the severity of the course, there are 3 degrees of thromboembolism - mild, moderate and severe.

Symptoms, clinical picture

The vast majority of pulmonary embolism occurs due to deep vein thrombosis of the lower extremities.
The average age of people suffering from this disease is 62 years.
After operations, the maximum risk of thrombosis remains for 2 weeks, then it decreases slightly, but thrombosis is expected for another 2-3 months.
Thromboembolism usually develops 3-7 days after deep vein thrombosis.
PE is often asymptomatic in persons with deep venous thrombosis.
PE, accompanied by symptoms, in 1 out of 10 cases ends with the death of the patient within the first hour.
Half of those who have had PE but are not taking anticoagulants will develop a second episode of thromboembolism within 90 days.

The main symptoms of pulmonary embolism are presented below:

shortness of breath (this is the leading symptom that occurs in 80% of patients);
chest pain, aggravated by coughing, sneezing, when moving (indicates involvement in the pathological process of the pleura) or by the type of angina pectoris (retrosternal);
cough;
fainting or light-headedness.

Objectively, this reveals an increase in heart rate (more than 100 beats per minute), (more than 20 respiratory movements per minute), a decrease in blood pressure, less often - blue skin (cyanosis), an increase in body temperature to febrile values (more than 38.5 ° C), signs deep vein thrombosis of the lower extremities or other localization.

Diagnostic principles

The ECG of PE will show signs of right ventricular overload.

Diagnosis of pulmonary embolism is based on the patient's complaints, anamnesis of his life and disease (the presence of predisposing factors), objective examination data (tachypnea, tachycardia, hypotension and other signs), laboratory and instrumental research methods.

The patient can be assigned:

analysis of the gas composition of blood (decrease in the partial pressure of oxygen);
a blood test for the level of D-dimer (this is a product of the destruction of fibrin; its level in the blood increases if there is an acute thrombus in the bloodstream; a normal concentration of this substance refutes the diagnosis of PE, but an increased concentration does not confirm it, but only makes it probable, since fibrin and active processes of its degradation also take place in other diseases, in particular, in infections, non-infectious inflammatory processes, malignant neoplasms);
(pathological changes in the images are determined, but they are nonspecific; atelectasis (collapse of a part of the lung), effusion in the pleural cavity and other changes can be detected; the study does not confirm PE, but allows to exclude other causes of the patient's symptoms);
electrocardiography, or (signs of right ventricular overload are found - inversion of the T wave in 1-4 chest leads, high R wave in 1 chest lead, blockade of the right bundle of His bundle - complete or incomplete);
(signs of violation of the structure and functions of the right ventricle are found);
compression ultrasonography (70% allows to diagnose a deep vein thrombus);
CT venography (detects a venous thrombus in 9 out of 10 cases);
ventilation-perfusion scintigraphy (implies the introduction of radioactive technetium into the bloodstream and subsequent X-ray examination; a reliable method to exclude thromboembolism);
multidetector CT (diagnostic standard);
spiral CT angiography of the pulmonary artery (allows you to verify even small blood clots in the pulmonary artery);
(allows you to detect 1-2 mm blood clots and reveal indirect signs of PE - slowing down the flow of contrast agent along the branches of the pulmonary artery, reducing blood flow in a separate area of the lung, and others); the introduction of a radiopaque substance intravenously in some patients can be fatal due to a possible allergic reaction to the drug; the method is highly informative, but it is used strictly according to indications in order to confirm the diagnosis.

Severity of thromboembolism

Pulmonary embolism is dangerous because it can cause sudden death of the patient. The risk of this is greatest during the first 30 days and when the patient has a number of risk factors. These include:

shock, systolic blood pressure below 90 mm Hg. Art. or decrease it by more than 40 mm Hg. Art. in 15 minutes;
Echo-KG or CT-signs of dysfunction of the right ventricle of the heart;
detection of cardiac troponins T and I in the blood (a sign of damage to the heart muscle).

Treatment principles

If pulmonary embolism is suspected, treatment should be started immediately in the intensive care unit. The patient is prescribed:

strict bed rest;
in severe cases - mechanical ventilation;
oxygen therapy (oxygen inhalation);
infusion therapy (infusion of saline and other blood substitutes to reduce blood viscosity and increase blood pressure);
thrombolysis (drugs urokinase, streptokinase, alteplase, tenecteplase; affect blood clots, causing their destruction; thrombolysis is most effective in the first hours and days of PE, the further, the lower its effectiveness);
anti-shock drugs (dobutamine, dopamine, norepinephrine, adrenaline and others; increase blood pressure);
(heparin, fraxiparin, warfarin; can reduce the risk of re-clotting);
drugs that dilate blood vessels (prostacyclin, levosimendan, sildenafil; reduce pulmonary artery pressure);
painkillers, or analgesics (fentanyl, promedol, morphine; prevent the development of painful shock or relieve it);
antibiotics (with the development of a heart attack pneumonia).

In case of massive thromboembolism, as well as in cases of insufficient efficiency of thrombolysis, the patient is surgically removed from the thrombus or its catheter fragmentation is performed. If pulmonary embolism recurs, the person needs a kava filter.

Forecast and prevention

With non-massive thromboembolism and timely provision of adequate medical care to the patient, the prognosis for life is favorable. Severe concomitant pathology, late medical intervention significantly worsens the prognosis.

If after the first thromboembolism the patient does not receive anticoagulant therapy, there is a high risk of relapse within the first 3 months. Accordingly, correctly administered anticoagulant therapy reduces the likelihood of recurrent thromboembolism by more than 2 times.

To prevent the occurrence of PE, it is necessary to promptly eliminate the provoking factors that are determined in a particular patient: varicose veins, and others (read above).

Another method for the prevention of PE is the installation of a filter, a cava filter, into the inferior vena cava. They are temporary (installed for the period of surgery, childbirth, or in other situations that contribute to thrombus formation) and permanent (they are installed with an already diagnosed deep vein thrombosis, accompanied by the danger of a thrombus rupture). Once in the filter, the thrombus is crushed and then easily dissolved by the anticoagulants taken by the patient.

One of the possible formidable complications of sympathectomy is thrombosis of large vessels.

Pulmonary embolism is one of the most common causes of sudden death caused by pathologies of the cardiovascular system. It occurs with a frequency of 1 case per 100,000 population and is diagnosed in vivo in only 30% of cases.

Pulmonary embolism (or PE) is a condition accompanied by complete or partial clogging of the main trunk or branches of the pulmonary artery by a thrombus and a sharp decrease in blood volume in the vascular bed of the lungs.

With thromboembolism, a venous thrombus that appears in deep veins (more often in the veins of the lower extremities) clogs the lumen of the pulmonary artery and less blood flows to a specific area of the lung (or to the entire lung). The heart stops contracting, and the affected part of the lung does not participate in gas exchange, and the patient develops hypoxia. This condition results in decreased coronary blood flow, left ventricular failure, decreased blood pressure, or pulmonary atelectasis. PE often leads to the development of cardiogenic shock.

The following factors can cause thromboembolism:

damage to the walls of a venous vessel with phlebitis and injuries;
increased blood clotting in hereditary diseases of the blood system, taking medications (hormonal contraceptives, etc.), chronic inflammatory diseases;
local slowing down of blood flow velocity with prolonged compression of tissues, prolonged bed rest, long flights and trips.

The risk group may include the following categories of persons:

Symptoms

The clinical picture of pulmonary embolism depends on the scale of thrombosis:

non-massive pulmonary embolism: if 30% of the pulmonary arteries are affected by blood clots, there are no signs of lesion in the patient for some time, then shortness of breath, cough with blood in the sputum, pain in the chest and fever, X-ray reveals a "triangular shadow" - a site of death (heart attack) lung;
submassive PE: if 30-50% of the pulmonary arteries are affected, the patient develops pallor, shortness of breath, rapid breathing, cyanosis of the ears, nose, lips and fingertips, anxiety, heart palpitations, blood pressure may not decrease, appear, which become more pronounced when trying lie down;
massive PE: if more than 50% of the pulmonary arteries are affected, the patient's blood pressure sharply decreases, shortness of breath increases and fainting occurs, and rapid death may occur.

The most common signs of PE are rapid breathing. As a rule, they appear suddenly and the patient's condition worsens when trying to lie down. Pulmonary artery thrombosis can be accompanied by pain or discomfort in the chest area and hemoptysis. With massive and submassive PE, cyanosis of the lips, ears, nose can reach a cast-iron shade.

Diagnostics

The diagnosis of PE can only be carried out in a hospital setting. The patient can be assigned the following research methods:

analysis of D-dimers of blood;
chest x-ray;
lung scintigraphy;
Echo-KG;
Ultrasound of the veins of the lower extremities;
CT with a contrast agent;
angiopulmonography.

Treatment

PE treatment includes the following activities:

saving the patient's life;
restoration of blood circulation;
prevention of repeated pulmonary embolism.

In case of signs of pulmonary embolism, the patient must be provided with complete rest and call the team of the cardiological "Ambulance" for emergency hospitalization in the intensive care unit.

The complex of emergency care may include the following activities:

Emergency catheterization of the central vein and infusion of Rheopolyglucin or glucose-novocaine mixture.
Intravenous administration of Heparin, Dalteparin or Enoxaparin.
Pain relief with narcotic analgesics (Morin, Promedol, Fentanyl, Droperidol, Lexir).
Oxygen therapy.
Administration of thrombolytics (tissue plasmogen activator, streptokinase, urokinase).
With signs of arrhythmia, antiarrhythmic drugs are administered (Digoxin, Magnesium sulfate, ATP, Nifidipin, Panangin, Lisinopril, Ramipril, etc.).
In case of shock reactions, the patient is injected with Girocortisone or Prednisolone and antispasmodics (Papaverine, Eufillin, No-shpa).

If it is impossible to eliminate PE in a conservative way, the patient undergoes pulmonary embolectomy or intravascular emboectomy through a special catheter, which is inserted into the chambers of the heart and the pulmonary artery.

After providing emergency care, the patient is prescribed drugs for the prevention of secondary blood clots:

low molecular weight heparins: Nadroparin, Dalteparin, Enoxaparin;
indirect anticoagulants: Warfarin, Fenindion, Sinkumar;
thrombolytics: Streptokinase, Urokinase, Alteplase.

The duration of drug therapy depends on the likelihood of recurrent PE and is determined individually. While taking these anticoagulant drugs, the patient should regularly take blood tests for a possible dose adjustment of the drug.

In some cases, a significant improvement in the patient's condition occurs within a few hours after the start of drug therapy, and after 1-2 days, complete lysis (dissolution) of blood clots occurs. The prognosis of treatment success is determined by the number of blocked pulmonary vessels, the size of the embolus, the presence of adequate treatment, and severe concomitant diseases of the lungs and heart that can complicate the course of PE. With a complete blockage of the pulmonary artery trunk, the patient's death occurs instantly.

A short educational video on how PE arises:

Channel One, the program "Living Healthy" with Elena Malysheva on the topic "Pulmonary embolism"

With pulmonary embolism, a thrombus closes the artery carrying venous blood from the heart to the lungs for oxygenation.

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

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, anesthesiologists.

PE reasons

The pathology develops due to deep vein thrombosis (DVT) in the legs. A blood clot 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 Virchow's triad, to which they belong:

Violation of blood flow.
Damage to the vascular wall.
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. This is usually not a problem: as soon as a person starts 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;
on long flights by plane, traveling by car or train.

2. Damage to the vascular wall

If the vessel wall is damaged, its lumen can be narrowed or blocked, which leads to the formation of a blood clot. Blood vessels can be damaged by trauma - bone fracture, during surgery. Inflammation (vasculitis) and certain medications (such as cancer chemotherapy drugs) can damage the vascular wall.

3. Increased blood clotting

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

Malignant neoplasms, the use of chemotherapy 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 a disease of the immune system that causes an increase in the thickness of the blood, which makes blood clots easier to form.

Other factors that increase the risk of PE

There are other factors that increase your risk of developing PE. These include:

Age over 60.
Previous deep vein thrombosis.
Having a relative who has had deep vein thrombosis in the past.
Being overweight or obese.
Pregnancy: The risk of PE is increased up to 6 weeks postpartum.
Smoking.
Taking birth control pills or hormone therapy.

Typical symptoms

In pulmonary embolism, the symptoms are as follows:

Chest pain, usually acute and worse with deep breathing.
Cough with bloody expectoration (hemoptysis).
Shortness of breath - A person may have difficulty breathing even at rest, and with exertion the shortness of breath worsens.
Increased 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 - a drop in blood pressure.

Further development of the disease:

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

Since most cases of pulmonary embolism are caused by vascular thrombosis 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 patient complaints, medical examination and using 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, carry out:

Electrocardiography.
A blood test for D-dimer is a substance whose level increases in the presence of thrombosis in the body. At a normal level of D-dimer, pulmonary thromboembolism is absent.
Determination of the level of oxygen and carbon dioxide in the blood.
Chest x-ray.
Ventilation perfusion scan - used to study gas exchange and blood flow in the lungs.
Pulmonary angiography - X-ray examination of the vessels of the lungs using contrast. With this examination, you can identify emboli in the pulmonary artery.
Pulmonary angiography using computed tomography or magnetic resonance imaging.
Ultrasound examination of the veins of the lower extremities.
Echocardioscopy is an ultrasound examination of the heart.

Treatment methods

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

In pulmonary embolism, treatment is mainly carried out with anticoagulants - drugs that weaken blood clotting. They prevent the clot from increasing in size, so that the body slowly absorbs them. Anticoagulants also reduce the risk of further blood clots.

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

Anticoagulants

Anticoagulants are often called blood thinning drugs, but they don't really have the ability to thin the blood. They affect blood clotting factors, thereby preventing easy blood clots.

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

Heparin is injected into the body using intravenous or subcutaneous injections. This drug is used mainly in the initial stages of PE treatment, as its action develops very quickly. Heparin can cause the following side effects:

increased body temperature;
headache;
bleeding.

Most patients with pulmonary thromboembolism need 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 administration after the termination of heparin administration. It is recommended to take this drug for at least 3 months, although some patients need longer treatment.

Since warfarin affects blood clotting, patients need to carefully monitor its effect by regularly measuring a coagulogram (blood clotting test). These tests are performed on an outpatient basis.

At the beginning of the course of treatment with warfarin, you may need to be tested 2-3 times a week, this helps to determine the appropriate dose of the drug. After that, the frequency of determining the coagulogram is approximately 1 time per month.

Various factors affect how warfarin works, including diet, other medications, and liver function.

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

Treatment that removes a blood clot from the pulmonary artery

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

Thrombolysis

Thrombolysis is the breakdown of blood clots with the help of certain medications. The most commonly used are alteplase, streptokinase or urokinase. However, with the use of thrombolytics, there is a fairly high risk of developing dangerous bleeding, including cerebral hemorrhage.

Operation

Sometimes it is possible to surgically remove a blood clot from the pulmonary artery. This operation is called embolectomy. This is a serious surgical procedure performed in the chest cavity, near the heart. It is performed by cardiac surgeons 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 is the administration of a drug that dissolves blood clots directly into a blocked pulmonary artery.
Catheter embolectomy is the removal or fragmentation of a blood clot with 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.

Prophylaxis

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

The use of anticoagulants.
Wearing compression hosiery that improves blood flow in the legs.
Increased mobility and physical activity.
To give up smoking.
Healthy eating.
Maintaining a healthy weight.

Forecast for pulmonary embolism

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

Approximately 10% of patients with pulmonary embolism 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 life-threatening pulmonary embolism, which is characterized by a drop in blood pressure, the mortality rate reaches 30-60%.

I have thromboembolism of the pulmonary artery, I've just been drinking 150 ml of product for half a year. Now headaches started, I lost 20 kg. For these six months. I did all the good tests, what was happening to me, I don’t know the Sergachskys doctors shrug their shoulders, what to do and where to go don’t know. I was in the hospital in Nizhny Novgorod. Semashko was told by the doctors that they would put on group, and in Sergach, Nizhny Novgorod region, they did not put them to work.

Elena, the doctors had to establish the cause of the thromboembolism, and in order for the treatment to be effective, complex treatment is needed. To do this, you need to go through a consultation with various narrow-profile specialists, for example, cardiac surgeons and cardiologists. It is also important to eliminate factors that increase the risk of PE (overweight, smoking, hormone intake, 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, therefore, specialist consultation should be frequent, if possible.

If an episode of pulmonary embolism has been transferred, or there are risk factors, alertness to this pathology should be maximized.

Treatment and prevention of pulmonary embolism

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

Sudden occlusion of the arterial trunks in the lungs

The lungs perform an important task of saturating the venous blood with oxygen: the main great vessel, which brings blood to the small branches of the arterial network of the lungs, departs from the right heart. Pulmonary artery thrombosis becomes the reason for 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 thromboembolism

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

Age has great predictive 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 - with 50-70% of all cases of sudden death, the presence of pulmonary thromboembolism was detected only on a postmortem examination.

Acute blockage of the pulmonary trunk: what is the reason

The appearance of blood clots or fatty emboli in the lung is explained by the 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 great vessels of the pulmonary system:

any types of surgical interventions;
severe lung disease;
congenital and acquired heart defects with different types of defects of the valve apparatus;
anomalies in the structure of the pulmonary vessels;
acute and chronic ischemia of the heart;
inflammatory pathology inside the cardiac chambers (endocarditis);
severe arrhythmias;
complicated variants of varicose veins (thrombophlebitis of the veins);
bone injuries;
gestation and childbirth.

Of great importance for the occurrence of a dangerous situation, when a blood clot has formed and torn off in the lungs, are predisposing factors:

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 against the background of injury;
any variant of hormone therapy with constant and long-term administration of drugs;
tobacco 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), therefore, any form of atherosclerotic disease does not in any way affect the risk of blockage of the trunk extending from 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:

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

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

Lightning fast (all symptoms and signs of pulmonary embolism unfold in 10 minutes);
Acute (manifestations of occlusion are rapidly increasing, limiting the life of a sick person to the first days from the moment of the first symptoms);
Subacute (slowly progressive cardiopulmonary disorders);
Chronic (signs of heart failure are typical, 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 imagine how long a person can live with an acute form of the disease, when all the necessary emergency medical and diagnostic procedures must be performed in 24 hours and a lethal outcome must be prevented.

The best survival rate is in subacute and chronic types, when the majority of patients undergoing treatment 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 proceed in the form of 3 clinical variants:

The initial presence of complicated varicose veins in the area of the venous network of the legs;
The first manifestations of thrombophlebitis or phlebothrombosis occur during an acute disturbance of blood flow in the lungs;
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 has come off and completely blocked the lumen of the vessel that provides the vital organs of the human body. In this case, the likelihood of survival is minimal, even with timely medical care in a hospital.

Symptoms of brain disorders

The main manifestations of cerebral disorders in occlusive lesions 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.

Psycho-emotional problems often arise 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;
fast heartbeat;
a sharp drop in blood pressure;
swollen neck veins;
light-headedness.

Often, severe pain in the left side of the chest is caused by 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;
a feeling of suffocation with the appearance of fear and panic;
severe chest pain at the time of inhalation;
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 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:

intense pain in the abdomen;
preferential 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 the symptoms of pulmonary embolism, it is necessary to start therapy with the use of resuscitation techniques as early as possible and quickly.

Diagnosis: is it possible to identify 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 no response to standard treatment for pneumonia;
unreasonable fainting conditions;
attacks of angina pectoris against the background of cardiac therapy;
high fever of unknown origin;
sudden onset of cor pulmonale symptoms.

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

general clinical analyzes
assessment of the blood coagulation system (coagulogram);
electrocardiography;
an overview x-ray of the chest;
duplex echography;
lung scintigraphy;
angiography of the vessels of the chest;
phlebography of the venous vessels of the lower extremities;
tomographic examination using contrast.

None of the examination methods is capable of making an accurate diagnosis, therefore, only the complex application of techniques will help to identify signs of pulmonary embolism.

Emergency treatment

Emergency assistance at the stage of the ambulance team involves the solution of the following tasks:

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

The doctor will use all medications that will help eliminate the fatal 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 implementation of 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;
respiratory support;
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. Two types of surgical intervention are used - with the use of a heart-lung machine and with a temporary closure of blood flow through the vessels of the inferior vena cava. In the first case, the doctor will remove the obstacle in the vessel using a special technique. In the second, the specialist will cut off the blood flow in the lower body during the operation and perform thrombectomy as quickly as possible (the time for the operation is limited to 3 minutes).

Regardless of the chosen therapy tactics, a complete guarantee of recovery cannot be given: 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 treatment option is the use of non-specific and specific preventive measures at all stages of examination and treatment. Of non-specific activities, the best effect will be when using the following recommendations:

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

Specific prevention measures are:

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

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

Forecast: what are the chances of life

Negative outcomes with blockage of the pulmonary trunk are due to a fulminant form of complication: in this case, the prognosis for life is the worst. With other variants of 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 occlusion of the vessels of the lungs, 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 great 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 medical and diagnostic procedures.

Thromboembolism of the pulmonary artery and its branches. Treatment

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

Urgent care

Emergency measures for pulmonary embolism can be roughly divided into three groups:

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

2) elimination of fatal reflex reactions;

3) elimination of the embolus.

Life support in cases of clinical death of patients is carried out primarily by resuscitation. The primary measures include combating collapse with 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, avelisin, celease, etc.).

The embolus located in the artery causes reflex reactions, due to which severe hemodynamic disorders often occur with non-massive PE. To eliminate the pain syndrome, 4-5 ml of a 50% solution of analgin and 2 ml of droperidol or seduxen are injected intravenously. Drugs are used as needed. With severe pain syndrome, analgesia begins with the introduction of drugs in combination with droperidol or seduxen. In addition to the analgesic effect, this suppresses the feeling of fear of death, decreases catecholaminemia, myocardial oxygen demand and electrical instability of the heart, improves the rheological properties of blood and microcirculation. In order to reduce arteriolospasm and bronchospasm, aminophylline, papaverine, no-shpa, prednisolone are used in usual 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, available in many patients, are not an obstacle to its use. The high probability of death justifies the risk of treatment.

In the absence of thrombolytic drugs, constant intravenous administration of heparin at a dose of 1000 U per hour is indicated. The daily dose is ED. With this method of administration, relapses of PE occur much less often, and re-thrombosis is more reliably prevented.

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

Conservative treatment

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

1. Providing thrombolysis and stopping further thrombus formation.

2. Reducing pulmonary arterial hypertension.

3. Compensation of pulmonary and right heart failure.

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

5. Treatment of lung infarction and its complications.

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

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

2. For chest pains and severe coughs, the administration of analgesics and antispasmodics.

3. Oxygen inhalation.

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

5. In case of cardiac weakness, glycosides are prescribed (strophanthin, korglikon).

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

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

1. Intravenous stream injected 5000 IU of heparin and 120 mg of prednisolone.

2. An ED of streptase (test dose) diluted in 150 ml of physiological solution is injected intravenously for 30 minutes, after which the blood parameters listed above are re-examined.

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 0,000 U / h, heparin 1000 U / h, nitroglycerin 30 μg / min. The approximate composition of the solution for infusion:

1% solution of nitroglycerin

0.9% sodium chloride solution

The solution is injected 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 streptase administration (24-96 hours) is determined individually.

Monitoring of the listed blood parameters is carried out every four hours. In the course of treatment, a decrease in fibrinogen below 0.5 g / l, prothrombin index below%, changes in thrombin time above a six-fold increase in comparison with the baseline, changes in clotting time and bleeding duration above a three-fold increase in comparison with the initial data are not allowed. A general blood test is performed daily or according to indications, platelets are determined every 48 hours and within five days after the start of thrombolytic therapy, a general urinalysis - daily, an ECG - daily, perfusion lung scintigraphy - according to indications. The therapeutic dose of streptase ranges from ED and more.

Treatment with streptodecase involves the simultaneous administration of a therapeutic dose of the drug, which is the ED of the drug. The same parameters of the coagulation system are monitored 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 U 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 for 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 (stomach or intestinal ulcer, surgery within 5 to 7 days, condition after aortography).

7. Recently transferred streptococcal infections (acute rheumatism, acute glomerulonephritis, sepsis, protracted 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 past 6 weeks.

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

13. Acute pancreatitis.

14. Active tuberculosis.

15. Suspicion of aortic dissecting aneurysm.

16. Acute infectious diseases at the time of admission.

Relative contraindications to thrombolytic therapy:

1. Exacerbation of gastric ulcer and 12 duodenal ulcer.

2. History of ischemic or embolic strokes.

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

4. Serious injury or surgery more than two weeks ago, but not more than two months;

5. Chronic uncontrolled arterial hypertension (diastolic blood pressure more than 100 mm Hg. Art.).

6. Severe renal or hepatic impairment.

7. Catheterization of the subclavian or internal jugular vein.

8. Intracardiac thrombi or valvular vegetation.

For vital indications, a choice must be made between the risk of disease and the risk of therapy.

The most common complications with 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, intravenous drip is administered:

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

If necessary, transfusion of fresh citrated blood is indicated. In case of an allergic reaction, prednisolone, promedol, diphenhydramine are administered. The antidote to 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 contribute to 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 for 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 during its application 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.

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 - pulmonary embolothrombectomy.

Surgery

The first successful operation for pulmonary embolism was performed by F. Trendelenburg's student M. Kirchner in 1924. Many surgeons attempted embolothrombectomy from the pulmonary artery, but the number of patients who died during the operation was much greater than those who had undergone it. In 1959 K. Vossschulte and N. Stiller proposed to perform this operation in conditions of temporary occlusion of the hollow veins by transsternal access. The technique provided wide free access, fast approach to the heart and 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 become widespread due to the lack of time, but the use of artificial circulation 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 used 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 postembolic hypertension of the pulmonary circulation.

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

1 Operation under conditions of temporary vena cava occlusion.

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

3. Surgical intervention in the conditions of artificial circulation.

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 an operation under artificial circulation in case of massive pulmonary embolism is a widespread distal occlusion of the vascular bed of the lungs.

B.C. Saveliev et al. (1979 and 1990) distinguish absolute and relative indications for embolothrombectomy. They refer to absolute indications:

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

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 concomitant diseases 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 only be expected in 10-11% of cases, and even with a successfully performed embolectomy, the possibility of re-embolism is not excluded. Therefore, prevention should be the main focus in solving the problem. TELA is not a fatal condition. Modern methods of diagnosing venous thrombosis make it possible to predict the risk of thromboembolism and to carry out its prevention.

The method of endovascular rotary disobstruction of the pulmonary artery (ERDLA), 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 is the mechanical destruction of massive thromboemboli in the pulmonary arteries. It can be an independent method of treatment in case of contraindications or ineffectiveness of thrombolytic therapy or precede thrombolysis, which significantly increases its effectiveness, shortens its duration, reduces the dosage of thrombolytic drugs and helps to reduce 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 prophylaxis. Non-specific prophylaxis includes combating hypodynamia in bed and improving venous circulation in the inferior vena cava system. Specific prevention of peripheral venous thrombosis involves the use of antiplatelet agents and anticoagulants. Specific prophylaxis is indicated for thrombotic patients, nonspecific - for all without exception. 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 ileocaval segment, plication of the inferior vena cava, ligation of the great 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 was the umbrella filter proposed by K. Mobin-Uddin in 1967. Throughout the years of use of the filter, various modifications of the latter have been proposed: "hourglass", Simon's nitinol filter, "bird's nest", 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 a high embolism trapping activity and a low ability to perforate the inferior vena cava. The main indications for the implantation of a cava filter:

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

In many cases, cava filter implantation is preferable to vein surgery:

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

The most serious complication of installing 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 kava filter itself can cause thrombosis of the inferior vena cava (IVC) when the blood clotting properties are impaired. The occurrence of thrombosis late after the filter implantation (after 3 months) may be due to 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 cava filter is advisable when detecting disorders of the blood coagulation system that create a risk of PE recurrence during the patient's life. In other cases, it is possible to install a temporary cava filter for up to 3 months.

Implantation of a cava filter does not completely solve the process of thrombus formation and thromboembolic complications, therefore, constant drug prevention should be carried out throughout the patient's life.

A serious consequence of the postponed 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 postembolic 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, heart pain. As a result of hemodynamic insufficiency of the right heart, enlargement of the liver, expansion and pulsation of the jugular veins, ascites, and jaundice are observed. According to most clinicians, the prognosis for CPEPH is extremely poor. The life expectancy of such patients, as a rule, does not exceed three to four years. With a pronounced clinical picture of postembolic lesions of the pulmonary arteries, surgery is indicated - intimothrombectomy. 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. Regression of severe CPEPH can be achieved with adequate surgical intervention.

Pulmonary embolism is one of the most important problems in medical science and practical health care. Currently, there are all possibilities to reduce mortality from this disease. One cannot put up with the opinion that TELA is something fatal and inevitable. The accumulated experience suggests the opposite. 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 to sanitize them in a timely manner.

Selected Lectures on Angiology. E.P. Kohan, I.K. Zavarina

It is advisable to consider the clinic of deep vein thrombosis of the extremity by segments of the lesion, since each case has its own peculiarities of venous hemodynamic disorders that determine the clinical picture of the disease.

The vascular suture is the mainstay 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 suture applied to the vessel wall is called vascular. It can be c.

The use of modern instrumental methods has significantly expanded the diagnostic capabilities of the doctor, allowing a deeper analysis and assessment 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.

Video about sanatorium Egle, Druskininkai, Lithuania

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PULMONARY EMBOLISM

Pulmonary embolism(PE) is one of the most severe and catastrophic acute vascular diseases, accompanied by high mortality.
PE - blockage of the arterial bed of the lung by a thrombus formed in the venous system of the systemic circulation, in the right atrium or in the right ventricle of the heart.

Epidemiology. There are no domestic statistics on PE. In the United States, it is diagnosed annually in 630,000 patients, of whom 200,000 die; it ranks third among the causes of mortality.
Even massive embolic lesions of the pulmonary arteries are not diagnosed in vivo in 40-70% of patients.

Etiology. The cause of PE is the separation of a venous thrombus and blockage of part or all of the pulmonary artery bed by it.
In most cases, the source of embolism is located in the inferior vena cava or in the veins of the lower extremities and pelvis, less often in the right chambers of the heart and veins of the upper extremities.
Sometimes thromboembolism can lead to right atrial thrombosis, which develops against the background of atrial fibrillation and dilated cardiomyopathy.
Embolization of the pulmonary vascular bed is also possible with tricuspid endocarditis and endocardial pacing, complicated by right heart thrombosis.

Pathogenesis. Conditions conducive to the occurrence of phlebothrombosis occur with heart failure, injuries (including operating ones), oncological, purulent-septic, neurological and other diseases, especially in bed rest.
Usually PE occurs with floating (floating) thrombi, which are freely located in the lumen of the vessel and have a single fixation point in their distal part.
With the flow of blood, such a thrombus can easily be washed away and brought into the pulmonary circulation.
An occlusive thrombotic lesion, in which the blood clots are tightly adhered to the vein wall for a considerable length, are not complicated by embolism. In principle, thrombosis of any localization can cause thromboembolism, meanwhile, the source of massive PE, which is understood as embolic damage to the pulmonary trunk and / or main pulmonary arteries, is thrombosis of the ileocaval segment in 65% of cases, thrombosis of the popliteal-femoral segment in 35%.
Changes in the lung parenchyma in the affected area can manifest as simple transient ischemia with rapid restoration of blood flow.
With more massive or prolonged occlusion, hemorrhagic pulmonary infarction may develop, followed by an aseptic inflammatory reaction (infarction-pneumonia).

A pleural response to PE can be fibrinous pleurisy, hemorrhagic pleurisy, or transudative pleural effusion.
Pulmonary arterial occlusion partially or completely blocks the blood flow in the small circle, causes generalized vasospasm of the small circle and bronchospasm. As a result, acute PAH, overload of the right heart, arrhythmias develop.
A sharp deterioration in ventilation and lung perfusion leads to a right-to-left shunting of insufficiently oxygenated blood.
A sharp drop in CO and hypoxemia in combination with vasospastic reactions lead to ischemia of the myocardium, brain, kidneys and other organs. The cause of death in massive acute PE may be VF, which develops as a result of acute overload of the right ventricle and myocardial ischemia.

Clinical manifestations varied, can be represented by various combinations of symptoms from the following five syndromes: pulmonary-pleural, cardiac, abdominal, cerebral and renal.

Pulmonary pleural syndrome is manifested by bronchospasm, shortness of breath, cough, hemoptysis, pleural friction, symptoms of pleural effusion, changes on the chest x-ray.

Cardiac syndrome includes chest pain, tachycardia, hypotension, increased CVP, swelling of the cervical veins, cyanosis, accent II tone and murmurs (systolic and diastolic) over the pulmonary artery, pericardial friction noise, ECG changes.
Orthopnea is uncommon and patients usually remain in a horizontal position.

Abdominal syndrome (pain in the right upper quadrant of the abdomen) is caused by irritation of the right dome of the diaphragm with reactive pleurisy and (or) stretching of the liver capsule that develops in acute right ventricular failure.

Cerebral (loss of consciousness, convulsions, paresis) and renal (anuria) syndromes are a manifestation of organ ischemia and hypoxia.

In order of decreasing frequency of occurrence, the main symptoms of PE are located in the following sequence:
1) tachycardia;
2) chest pain;
3) shortness of breath;
4) hemoptysis;
5) increased body temperature;
6) wet wheezing;
7) cyanosis;
8) cough;
9) pleural friction noise;
10) collapse.

Diagnostics. When examining a patient with suspected pulmonary embolism, the doctor must solve the following tasks:
1) confirm the presence of pulmonary embolism, since the methods of treating this disease are quite aggressive and should not be used without strict objective grounds;
2) to assess the volume of embolic lesions of the pulmonary vascular bed and the severity of hemodynamic disorders in the pulmonary and systemic circulation;
3) determine the localization of thromboemboli, especially when it comes to possible surgical intervention;
4) to establish the source of embolization, which is extremely important for choosing a method to prevent the recurrence of embolism.

Laboratory diagnostic methods allow detecting the presence of siderophages in sputum, in the blood - moderate hypercoagulation.

On the ECG with massive PE, you can see signs of acute LS: Me Ginn-White syndrome (S1 Q3 T3), displacement of the transition zone (deep S in V5-6 in combination with negative T in V5-6), due to an increase in pressure in the small circle circulation over 50 mm Hg. Art. Difficulties in interpreting ECG changes arise in elderly patients with organic lesions of the coronary arteries.
At the same time, the absence of ECG manifestations does not exclude the presence of PE.

Radiographs of the chest organs may show enlargement of the root of the lung,
signs of diffuse or local oligemia and high standing of the dome of the diaphragm on the side of the lesion, as well as pulmonary infarction, pleural effusion, basal atelectasis, expansion of the shadow of the heart.

Plain chest X-ray allows you to exclude other than embolism, lung pathology, similar to it in symptomatology. Dilation of the right heart with widening of the venous inflow pathways, high position of the diaphragm on the side of occlusion and depletion of the pulmonary vascular pattern indicate the massive nature of the embolic lesion.
A third of patients have no radiographic signs of embolism at all.

The classic triangular shadow of pulmonary infarction is detected extremely rarely (less than 2%), much more often it has a large polymorphism.
Ultrasonic and radionuclide research methods are more informative.

Echocardiography allows you to detect the occurrence of acute drugs, to exclude the pathology of the valve apparatus and left ventricular myocardium.
With its help, it is possible to determine the severity of hypertension of the pulmonary circulation, assess the structural and functional state of the right ventricle, detect thromboemboli in the cardiac cavities and the main pulmonary arteries, visualize the open oval window, which can affect the severity of hemodynamic disorders and cause paradoxical embolism.

However, a negative echocardiogram does not in any way preclude the diagnosis of pulmonary embolism. Ultrasound angioscanning of the veins of the lower extremities makes it possible to detect the source of embolization.
At the same time, it is possible to obtain comprehensive information about the localization, length and nature of thrombotic occlusion, the presence or absence of the threat of re-embolism.
Difficulties arise in visualizing the ileocaval segment, which can be obstructed by intestinal gas.

Perfusion lung scanning performed after intravenous administration of 997C-labeled albumin macrospheres is recognized as the most adequate method for screening PE.

With a stable condition of the patient, this method should be ahead of other instrumental studies.

The absence of impaired pulmonary blood flow on scintigrams performed in at least two projections (anterior and posterior) completely excludes the diagnosis of thromboembolism.
The presence of perfusion defects is interpreted ambiguously.
A highly probable criterion for embolism is a segmental absence of blood flow in the lungs, not accompanied by changes on the plain chest x-ray.
If there is no strict segmentation and multiplicity of perfusion defects on scintigrams, the diagnosis of PE is unlikely (violations may be caused by bacterial pneumonia, atelectasis, tumor, tuberculosis, and other reasons), but it is possible that angiographic verification is required.

A comprehensive radiopaque study, including probing of the right heart, angiogulmonography and retrograde ileocavagraphy, remains the "gold standard" and allows to unambiguously solve all diagnostic problems in case of suspected pulmonary embolism.

Angiography is absolutely indicated in all cases when a massive embolic lesion of the lung vessels is not excluded (including with questionable scan data) and the choice of a treatment method is being decided. It is better to perform an X-ray contrast study, if the patient's condition allows, at the final stage of diagnosis, after a thorough analysis of the information obtained using non-invasive methods. If the doctor's actions are limited in time by a worsening clinical and hemodynamic situation, one should immediately resort to the most reliable angiographic diagnosis.

Unfortunately, so far, emergency angiography is only possible in specialized vascular surgery centers.

Flow acute, with a sudden onset of symptoms, and always, even with their rapid disappearance in case of a favorable outcome, threatening fatal thromboembolism.
Recurrent course is common.
Forecast always serious.

Treatment. The main thing is to prevent the death of the patient in the acute stage of the disease and the development of chronic cor pulmonale in the long term.
The tasks of treatment include:
1) normalization of hemodynamics;
2) restoration of the patency of the pulmonary arteries;
3) prevention of recurrence of the disease.

Treatment of acute pulmonary embolism can be conditionally divided into three stages.
Stage 1. At the first suspicion of pulmonary embolism, it is necessary to immediately inject 10-15 thousand units of heparin into / in and only after that proceed to a more detailed examination. The only exception to this rule can be cases when there is or is suspected external or internal bleeding.
According to the indications, sedatives, oxygen, analgesics are prescribed, after which they proceed to a more detailed examination and treatment.
It is advisable to widely use low-molecular-weight heparins (dalteparin sodium, nadroparin sodium, enoxyparin sodium), which are easier to dose compared to conventional unfractionated heparin, less likely to cause hemorrhagic complications, and have less effect on platelet function.
They have a longer action and high bioavailability when injected subcutaneously, therefore, low molecular weight heparins for therapeutic purposes are injected 2 times a day under the skin of the abdomen.
Their use does not require frequent laboratory monitoring of the state of the hemostasis system. The duration of heparin therapy is 5-10 days.
Before reducing the dose of heparin, indirect anticoagulants are prescribed, which, after selecting an adequate dose, the patient should take at least 6 months to prevent recurrence of phlebothrombosis and PE.

Stage 2. When the diagnosis is confirmed, fibrinolytic agents are prescribed (intravenous drip of streptokinase or its derivatives at 100,000 U / h), vasoactive drugs (verapamil - 2-4ml 0.25% solution intravenous drip to reduce pressure in the pulmonary artery), anti -acidotic therapy (100-200 ml of 3-5% sodium bicarbonate solution intravenously), with the development of asthmatic syndrome - 10 ml of 2.4% aminophylline solution and 3-4 ml of 3% prednisolone solution intravenously. Continue the introduction of heparin 5-10 thousand units 4 times a day, under the control of the time of blood coagulation.

The use of thrombolytics in peripheral localization of embolic occlusion in most cases is not justified in terms of the risk / benefit ratio.
The magnitude of their pulmonary blood pressure does not approach a dangerous level, a favorable outcome is usually not in doubt.
At the same time, the risk of hemorrhagic and allergic complications is extremely high, and the cost of thrombolytic drugs is quite high.

With massive PE, thrombolytic therapy is indicated in most clinical situations.
It is absolutely necessary for patients with severe pulmonary perfusion disorders accompanied by significant hypertension in the pulmonary circulation system (more than 50 mm Hg).
Thrombolytic therapy is also justified in cases where the volume of the lesion is relatively small, but pulmonary hypertension is pronounced. This discrepancy may be due to previous cardiopulmonary pathology and age-related characteristics, which leads to a limitation of the body's adaptive capabilities.

In clinical practice, streptokinase preparations are most often used despite the frequent occurrence of severe allergic reactions.
It is prescribed at a dose of 100,000 units per hour.
The duration of therapeutic thrombolysis is usually 2-3 days. Under the influence of streptokinase, there is a significant acceleration of the process of restoration of pulmonary blood flow, which reduces the time of dangerous hemodynamic overload of the right ventricle.

At the same time, there is currently no rigorous evidence of a decrease in mortality in patients with massive PE during thrombolytic therapy, although a number of our observations indicate the life-saving effect of activators of endogenous fibrinolysis.

Urokinase lacks antigenic properties, but is rarely used due to its high cost. Clinicians pinned great hopes on the use of tissue plasminogen activator obtained using genetic engineering methods (alteplase).
It was believed that these drugs will be able to lyse thromboemboli even with organization phenomena without the risk of hemorrhagic complications, which are quite frequent during streptokinase therapy.
Unfortunately, expectations were not fully justified.
These drugs are characterized by a rather narrow "therapeutic window".
The recommended doses are often not effective enough, but their increase is fraught with a significant increase in the number of hemorrhagic complications.

Stage 3. In the absence of the effect of stages I and II, the question of embolectomy (no later than 2 hours from the onset of the disease) is raised - with acute PE, ligation of the main vein or the installation of an "umbrella" filter in the inferior vena cava - with its recurrent form.

The progressive deterioration of the condition of patients with massive PE may also require urgent surgical intervention. Embolectomy is indicated for patients with thromboembolism of the pulmonary trunk or both of its main branches with an extremely severe degree of impairment of pulmonary perfusion, accompanied by pronounced hemodynamic disorders.
These include persistent systemic hypotension, refractory to the introduction of vasopressors, or the level of systolic pressure in the right ventricle above 60 mm Hg. Art.
with high numbers of end diastolic pressure. In such conditions, the patient has very little chance of surviving even with thrombolytic therapy.
The risk of surgery is justified primarily in young people.

Three different pulmonary embolectomy techniques are currently used.
Embolectomy under conditions of temporary vena cava occlusion does not require complex technical support, and in case of emergency it can be successfully performed by an experienced general surgeon.

One of the most dangerous stages of such an intervention is induction anesthesia, when bradycardia, hypotension and asystole can occur. Aggravation of hemodynamic disorders is due to the fact that the sharply dilated right heart is extremely sensitive to significant fluctuations in intrapleural pressure that occur during mechanical ventilation.

All manipulations to remove emboli after clamping the vena cava should last no more than 3 minutes, since this interval is critical for patients who are operated under conditions of severe initial hypoxia.
Unfortunately, such an operation is accompanied by a very high mortality rate (up to 90%).

It is optimal to perform embolectomy under cardiopulmonary bypass with the use of trans-sternal access.
Ancillary venoarterial perfusion should be started at the first stage of surgery (before induction of anesthesia!) By cannulating the femoral vessels.

Cardiopulmonary bypass allows to a large extent to secure embolectomy in patients with severe hemodynamic disorders.
Nevertheless, mortality after such interventions reaches 50%.
If we remember that every second of the hopeless patients manages to save their lives, this result cannot be called unsatisfactory.
According to relative indications, with unilateral lesion, it is possible to perform surgical deobstruction of the vascular bed from the lateral thoracotomy access, in conditions of clamping the corresponding pulmonary artery. Now a few words about the use of warfarin in pulmonary embolism therapy.

Patients who are to undergo surgery should start treatment with warfarin 2-3 days before surgery.
In the case of acute thrombosis, treatment with warfarin should be supplemented with the appointment of heparin until the effect of oral anticoagulant therapy is fully manifested (not earlier than 3-5 days of treatment). Initial doses of warfarin are 2.5-5 mg per day. The daily dose of warfarin should be taken once a day and at the same time.
The drug is taken orally.
If necessary, the tablet or part of it can be chewed and washed down with water.
Further dosing regimen is set individually, depending on the determination of prothrombin time or international normalized ratio (MHO).
The prothrombin time should be increased 2-4 times from the initial, and the INR should reach 2.2-4.4, depending on the disease, the risk of thrombosis, the risk of bleeding and the individual characteristics of the patient.

Preventive treatment of venous thrombosis and pulmonary embolism requires an INR of 2-3.
Before starting therapy, the INR indicator is determined (corresponding to the prothrombin time, taking into account the thromboplastin sensitivity coefficient).
In the future, regular, every 4-8 weeks, laboratory control is carried out.
The duration of treatment depends on the clinical condition of the patient. Treatment can be canceled immediately.

Prevention. Primary prevention of PE is a set of measures to prevent venous thrombosis in the inferior vena cava system. Non-specific (physical) measures are applicable to all inpatients without exception.
They consist in elastic compression of the lower extremities, reduction of the duration of bed rest, and the earliest possible activation of patients.
In persons forced to stay in bed for a long time, it is advisable to use the simplest simulators that simulate walking, therapeutic exercises, as well as intermittent pneumocompression of the lower extremities.
Doctors of all specialties should be involved in such prevention.
Prophylactic use of enoxaparin sodium at a dose of 40 mg 1 time per day in patients with a high risk of postoperative venous thrombosis is 2 times more effective than unfractionated heparin.
You can also use polyglucin or rheopolyglucin 400 ml IV infusion 1 time per day.
Antiplatelet agents and anticoagulants (dipyridamole, ticlopedin 0.25 2 times a day, fluke 0.075 g once a day, acetylsalicylic acid 0.025 g 1-2 times a day) and drugs stimulating fibrinolysis (nicotinic acid according to 0.05-OD g 3 times a day and its derivatives).

Secondary prevention of PE is carried out with developed phlebothrombosis or pulmonary embolism.
It is an integral component of the treatment of PE, as patients often die from a relapse of the disease.
For this purpose, direct anticoagulants are prescribed in therapeutic doses.
However, they only prevent the spread of thrombosis and are unable to prevent the separation of an already formed floating thrombus.

In such cases, it is necessary to resort to surgical methods for the prevention of pulmonary embolism.
The optimal method is indirect transvenous implantation of cavafilters of various designs directly below the orifices of the renal veins.
Depending on the clinical situation, for the same purpose, it is possible to perform the application of the inferior vena cava with a mechanical suture, thrombectomy, and ligation of the great veins.
Such operations, subject to adequate diagnosis, are feasible in general surgical hospitals.

TELA is an abbreviation for a medical term. This is the name of pulmonary embolism. This is a blockage in the pulmonary artery of its trunk and branches by an embolus (thrombus), which occurs suddenly. A thrombus forms in the ventricle on the right side or in the atrium. It can also form in the veins of a large circle of blood flow. The blood clot is brought in with the blood stream. As a result of the blockage, blood stops flowing to the lung tissue. Pulmonary embolism, clinical picture, diagnosis, treatment, prevention of which are described below is a very serious disease. As a result of a rapidly developing disease, death can occur.

TELA: causes of

The most common causes of the development of the disease can be:

thrombosis of the tributaries and the inferior vena cava;
a generalized process that is septic in nature;
cardiovascular diseases, which lead to the formation of embolism and blood clots in the vessels, including the pulmonary artery, for example, ischemic heart disease, rheumatism in its active phase with mitral stenosis, atrial fibrillation, endocarditis of infectious etiology, cardiomyopathy, non-rheumatic myocarditis);
oncological diseases (for example, cancer of the lungs, stomach, pancreas);
DVT (deep vein thrombosis) located in the lower leg, often accompanied by thrombophlebitis; often develops venous thrombosis (superficial and deep);
thrombophilia, that is, intravascular thrombosis, which occurs when there are disorders in the hemostasis system);
antiphospholipid syndrome, when antibodies to phospholipids of platelets, nervous tissue and endothelial cells are formed.

: clinic

The disease happens:

Lightning fast (sharpest). In this case, the thrombus instantly and completely clogs the main trunk of the artery and both of its branches. Breathing immediately stops, collapse and ventricular fibrillation occurs. Death can occur in minutes.
Sharp. In this case, the obstruction of the branches of the artery rapidly increases. The attack comes on unexpectedly, the symptoms progress rapidly. Heart, respiratory and cerebral insufficiency develops. The process can last up to 5 days, there may be complications in the form of a pulmonary infarction.
Prolonged (subacute). In this case, thrombosis is formed in the medium and large branches of the pulmonary artery and multiple pulmonary infarction occurs. The process takes up to several weeks. It progresses rather slowly and is accompanied by right ventricular and respiratory failure. Secondary thromboembolism often occurs, and the symptoms in this case are more aggravated. Often the attack ends in death.
Recurrent (chronic). In this case, recurrent thrombosis of the lobar branches of the artery is manifested. Repeated pulmonary infarctions and pleurisy, which are often bilateral, may develop. Gradually, hypertension of the small circle of blood flow increases and right ventricular failure develops. This happens, as a rule, after operations in the presence of oncological diseases and pathologies of the heart and blood vessels.

Thromboembolism: diagnostics

When making a diagnosis, the main thing is to determine the location of blood clots in the vessels of the lungs and assess the degree of their damage. At the same time, in order to prevent relapses, it is still necessary to identify the main cause of the development of thromboembolism.

It is very difficult to diagnose pulmonary embolism, therefore, patients must be in the hospital under the supervision of a doctor. Those who are suspected of developing PE are examined as follows:

Anamnesis is collected, the degree of development of PE or DVT, clinical symptoms are assessed,
Do biochemical and general analyzes of urine and blood, examine the gas composition of blood, D-dimer in plasma (diagnosis of venous thrombi), coagulogram,
In order to exclude myocardial infarction, heart failure and pericarditis, an ECG is performed (in dynamics),
In order to exclude pneumothorax, primary pneumonia, tumors, pleurisy and rib fractures, an x-ray of the chest area is performed,
To detect increased blood pressure in the pulmonary artery, the presence of thrombosis in the cardiac cavities and overloads in the right parts of the heart muscle, echocardiography is done,
If blood perfusion through the lung tissue is impaired, this means that due to PE, blood flow is reduced or not at all, therefore, lung scintigraphy is performed,
To determine the size of the thrombus and its location, angiopulmonography is done, and to identify the cause of the development of thromboembolism, contrast phlebography and ultrasonography of the veins (peripheral) are done.

Pulmonary embolism: treatment

Those who are suspected of developing pulmonary embolism are admitted to a hospital in intensive care.

If the patient's condition is urgent, then all measures of the resuscitation plan are carried out.

Subsequent treatment of the disease aims to normalize pulmonary circulation in order to prevent the development of chronic hypertension in the lungs.

Strict bed rest must be observed. In order to reduce blood viscosity and maintain blood pressure, massive infusion therapy is performed.

At the initial stage, thrombolytic therapy is prescribed in order to dissolve the thrombus as soon as possible and restore blood flow. Then, to prevent recurrence of pulmonary embolism, heparin therapy is performed. If infarction pneumonia occurs, antibiotic therapy is prescribed.

With the development of massive PE, and if thrombolysis is ineffective, surgical thromboembolectomy is performed, that is, the thrombus is removed. As an alternative to embolectomy, thromboembolic catheter fragmentation is performed.

TELA: relapses

To prevent PE, a special filter is placed in the inferior vena cava.

If the patient is assisted on time and all the necessary therapeutic measures are taken, then the prognosis is favorable. If cardiovascular and respiratory disorders are expressed against the background of pulmonary embolism, then in these cases the mortality rate is above thirty percent.

More than half of the relapses of the disease occur in those who have not received anticoagulants. If anticoagulant therapy was carried out correctly and on time, the risk of relapse is halved. To prevent the development of thromboembolism, it is necessary to diagnose and begin treatment of thrombophlebitis on time.

TELA: prevention

It consists in promptly expanding bed rest after surgery, diagnosing and treating developing thrombophlebitis of the legs. Those who suffer from heart failure, obesity, those who have found malignant tumors and have had surgery on organs in the small pelvis and retroperitoneal space, as well as those who are immobilized, should undergo the introduction of low molecular weight heparin in order to prevent it. If thromboembolism has the properties of relapsing, it is necessary to put a filter in the vein.