Tela code for mkb 10 in adults. Thromboembolism of the branches of the pulmonary artery in pregnant women

There are a number of diseases that develop in a patient suddenly, may appear for no apparent reason. These include pulmonary embolism.

Today we will talk about what pulmonary embolism is, whether it can cause death, what are its symptoms, treatment, methods of preventing the disease.

Features:

Pulmonary embolism (PE) is a blockage of the branches or trunk of an artery due to a blood clot that forms in the right ventricle or atrium, as well as in the venous bed.

Pulmonary embolism according to ICD-10 corresponds to codes I26.0, I26.9.

It is noteworthy that about 0.1% of the world's population dies from this pathology every year, while 90% of PE is diagnosed posthumously. The disease is characterized by severe pain, hemoptysis and shortness of breath, however, it is difficult to diagnose due to the lack of specific signs.

The following video will tell you more about the features of pulmonary embolism:

Kinds

Clinical classification

The clinical classification divides PE into such types as:

• Massive. More than 50% of the vascular bed is affected. The disease is manifested by shock, systemic hypotension may appear.
• Submassive. The vascular bed is affected within 30-50% of the volume. Symptoms correspond to those of the right ventricular.
• Non-massive. Less than 30% of the volume of the vascular bed is affected, while the disease may be asymptomatic.

Classification along the pathology

There is also a classification along the pathology course, which distinguishes forms such as:

• The sharpest. Death occurs a few minutes after development.
• Acute pulmonary embolism. It is characterized by sudden onset, chest pain, shortness of breath, and similar symptoms.
• Subacute. It is characterized by hemoptysis, signs of infarction pneumonia, respiratory and right ventricular failure.
• Recurrent. Differs in repeated episodes of shortness of breath, fainting, as well as symptoms of pneumonia.

Forms

Also, PE can be divided into forms, depending on the reasons, into primary, secondary and idiopathic. The secondary form differs from the primary one in that the patient has one or more risk factors that lead to the development of pathology.

If, during the examination, no causes or risk factors are found for PE, they speak of an idiopathic form. The causes of pulmonary embolism will be discussed below.

Causes of occurrence

The most common cause of PE is a deep vein in the legs or pelvis.The risk factors for PE include conditions like:

• Genetic predisposition to this pathology.
• Blood clotting disorders.
• Surgical interventions, especially open ones.
• Injury to the bones of the pelvis and thighs.
• Pregnancy and postpartum period.
• Diseases of the cardiovascular system.
• Obesity.
• Taking contraceptives with estrogen.

Also, people who are cured can lead to PE.

Read on for signs of pulmonary embolism.

Symptoms

In some cases, PE may be asymptomatic until a certain stage of development. The most characteristic symptoms for pathology are:

• Signs of impaired cerebral circulation.
• Shortness of breath with sudden onset. Usually, it is quiet and manifests itself regardless of the position of the patient.
• Hypotension. With low blood pressure, the pressure in the veins rises.
• ... The severity of this symptom depends on the percentage of artery involvement.
• Weakness.
• Cough, the severity of which depends on the degree of the lesion. This is usually a cough with phlegm.
• Hemoptysis. A characteristic feature that occurs in about 30% of patients. Most often, hemoptysis is profuse, the blood is in the form of streaks or clots.
• Multiple organ failure, which most often occurs in elderly patients.

The most common symptom of PE is pain. In young people, pain is more often localized in the chest, the elderly poorly determine the localization of pain, but all patients note its intensity.

about the diagnosis and treatment of pulmonary embolism in the clinic, read on.

Diagnostics

Diagnosing the disease is difficult due to the absence of pronounced symptoms and imperfection of diagnostic tests. Diagnosis begins with standard procedures such as life history, family history, and symptom history, physical examination, and auscultation to suggest PE and the cause / risk factors of the condition.

To confirm the primary diagnosis are used:

• Elucidation of the level of D-dimers, fibrin breakdown products. An increase in this level indicates a recent thrombus formation. Normally, the level of d-dimers is within 500 μg / L.
• Analyzes of urine and blood. They are necessary to clarify the general well-being of the patient and detect possible causes of pathology.
• ECG. Despite the fact that signs of pulmonary embolism on the ECG are often absent, the patient may have sinus tachycardia.
• X-ray of the chest. Allows you to identify concomitant diseases, detect signs.
• EchoCG. Reveals violations in the work of the right ventricle, pulmonary hypertension, etc. Transesophageal echocardiography often finds a blood clot in the heart. The study is necessary to exclude other pathologies.
• CT angiopulmonography, which detects a blood clot in the pulmonary artery.
• Ultrasound of the veins of the lower extremities, which reveals a blood clot in this area. Most often, it is he who is the cause of thromboembolism.
• Ventilation perfusion scintigraphy. The study reveals areas of the lung that are ventilated, but the blood reaches them poorly. With a normal test result, PE can be excluded with 90% probability.
• Lung angiography. The most accurate test, however, is invasive. Allows you to identify an open branch of an artery, a thrombus, a narrowing of a branch of the pulmonary artery.

Other tests may be used depending on the indication and equipment available, such as CT and MRI. It is also recommended to visit other specialists for accuracy, in particular a therapist.

In more detail about the diagnosis and treatment of pulmonary embolism, specialists tell in the video below:

Treatment

The basis of treatment is drug therapy, which is carried out in combination with a therapeutic technique. If the patient's condition does not improve, surgery may be used. Treatment with folk remedies is strictly prohibited, since this can smooth out the symptoms, deceiving the patient, and leading to death.

Let's first of all talk about emergency first aid for pulmonary embolism.

Urgent care

If you suspect pulmonary embolism, you must urgently call an ambulance. Before the patient is hospitalized, it is necessary:

• Provide the patient with rest by laying him on a flat surface and freeing him from tight clothes.
• Inject 10-15k units at a time into a vein, then inject 15 ml of 2.4% diluted in 400 ml of rheopolyglucin into a vein, maintaining a rate of 60 drops / min.
• If observed, it is necessary to inject rheopolyglucin into the vein (20-25 ml / min).
• If there are pronounced phenomena of ARF, it is necessary to carry out therapy for respiratory failure.

In case of cardiac arrest in a patient, it is necessary to urgently carry out resuscitation measures.

Therapeutic methods

When treating PE, it is necessary to observe strict bed rest. Exercise can provoke a recurrence of thromboembolism.

• To maintain oxygenation, patients inhale oxygen.
• Massive infusion therapy is performed to reduce blood viscosity and maintain blood pressure in a normal state.

Medication methods

Thrombolytic and anticoagulant therapy forms the basis of drug treatment. The following drugs may be prescribed:

• Morphine with isotonic sodium chloride solution to eliminate severe pain syndrome.
• Non-narcotic analgesics for developing infarction pneumonia.
• Heparin, which reduces spasm of the bronchi and areoles.
• Therapy with pressor amines for right ventricular failure, hypotension or shock.
• Norepinephrine if pressor amines cannot be used.

Other medications may also be prescribed depending on the symptoms.

Operation

If the patient does not respond to drug therapy, he may be prescribed thrombectomy, that is, surgical removal of a blood clot. If there is an increased risk of recurrent PE, the patient may be fitted with a cava filter, which is a mesh filter.

Prevention of the disease

It is advisable to carry out preventive measures in patients with risk factors. They consist in:

1. Ultrasound of leg veins;
2. the need to bandage your legs tightly;
3. wearing cuffs that compress the veins on the lower leg;
4. taking heparin subcutaneously;
5. implantation of cava filters appropriate for the situation of modification;

In the latter case, it is important to correctly insert the cava filter, as incorrect installation increases the risk of blood clot formation.

Complications of pulmonary embolism

The disease, even with timely diagnosis, can be complicated by dangerous conditions, for example:

• lung infarction;
• pleurisy;
• pneumonia;
• abscess;
• empyema;
• pneumothorax;
• acute renal failure;

Pulmonary embolism itself often leads to disability of the patient.

Finally, read about the prognosis and consequences of pulmonary embolism.

Forecast

If the patient receives first aid and competent treatment of PE on time, then the prognosis for recovery is favorable. High mortality (up to 30%) is observed with severe cardiovascular disorders and with an extensive form.

When PE is examined, frequent recurrence is noted. However, statistics show that half of the relapses occur in patients who did not take anticoagulants.

Even more useful information about TELA contains a video with Elena Malysheva:

PE classification

Given the many options for the course, manifestations, severity of symptoms of PE, the classification of this pathology is carried out based on various factors:

1. According to the severity of the development of the pathological process
   • Acute - sudden onset, chest pain, shortness of breath, decreased blood pressure, signs of acute pulmonary heart disease, obstructive shock may develop;
   • Subacute - progression of respiratory and right ventricular failure, signs of thrombin-infarction pneumonia;
   • Chronic, relapsing - repeated episodes of shortness of breath, signs of thrombin-infarction pneumonia, the onset and progression of chronic heart failure with periods of exacerbations, the appearance and progression of signs of chronic pulmonary heart disease.
2. Depending on the localization of the thrombus (the site of the vessel blockage)
   • Embolism at the level of segmental arteries.
   • Embolism at the level of the lobar and intermediate arteries.
   • Embolism at the level of the main pulmonary arteries and pulmonary trunk.

   In a simplified form, the division of PE according to the level of localization is classified as blockage of small or large branches of the pulmonary artery (by the volume of vascular lesions)

   • massive (accompanied by shock / hypotension);
   • submassive (accompanied by right ventricular dysfunction without hypotension);
   • non-massive (no hemodynamic disturbances or signs of right ventricular failure).
3. Depending on the localization of the thrombus (side of the lesion)
   • right;
   • left;
   • bilateral
4. Depending on the degree of impairment of lung perfusion
5. Depending on the nature of hemodynamic disorders

   Hemodynamic disorders	Pressure, mmHg Art.					SI, l / (min m 2)
   	in the aorta	in the right ventricle
   		systolic	end-diastolic	the average	in the pulmonary trunk
   Moderate or not	Above 100	Below 40	Below 10	Below 19	Below 25	Equal to and above 2.5
   Expressed	Also	40–59	10–14	19–24	25–34	Also
   Pronounced	Below 100	Equal to and above 60	Equal to and above 15	Equal to and above 25	Equal to and above 35	Below 2.5

6. By clinical symptoms (presence of complications)
   • With the development of a pulmonary infarction (I26) - "Infarction pneumonia" (corresponds to thromboembolism of small branches of the pulmonary artery) - manifests itself as acute shortness of breath, aggravated by the patient's transition to an upright position, hemoptysis, tachycardia, peripheral chest pain (the site of lung injury) as a result involvement in the pathological process of the pleura.
   • With the development of pulmonary heart (I26.0) - "Acute cor pulmonale" (corresponds to thromboembolism of large branches of the pulmonary artery) - sudden dyspnea, cardiogenic shock or hypotension, chest pain.
   • "Unmotivated dyspnea" (corresponds to recurrent pulmonary embolism of small branches) - episodes of sudden, rapidly passing dyspnea, which after some time can manifest itself as a chronic pulmonary heart disease. Patients with such a course of the disease in history usually do not have chronic cardiopulmonary diseases, and the development of chronic pulmonary heart disease is a consequence of the cumulation of previous episodes of PE.
7. By etiology:
   • associated with deep venous thrombosis;
   • amniotic associated:
     • with abortion (O03-O07);
     • ectopic or molar pregnancy (O00-O07, O08.2);
     • pregnancy and childbirth (O88);
   • idiopathic (no known cause).

In the 2000 guidelines of the European Society of Cardiology, it was proposed to classify PE by the volume of pulmonary vascular lesions (massive, submassive and non-massive [show] ) and by the severity of the development of the pathological process (acute, subacute and chronic recurrent [show] )

Pulmonary vascular lesion volume	Typical clinical features
Massive PE - obstruction of more than 50% of the volume of the vascular bed of the lungs	Symptoms of shock and / or systemic hypotension (a decrease in systolic blood pressure (BP) below 90 mm Hg or a drop in blood pressure ≥ 40 mm Hg for at least 15 minutes, unrelated to arrhythmia, hypovolemia, or sepsis) ... In addition, shortness of breath, diffuse cyanosis are characteristic, fainting is possible
Submassive PE - obstruction of less than 50% of the volume of the vascular bed of the lungs	Symptoms of right ventricular failure (hypokinesia of the right ventricle) confirmed by echocardiography. No arterial hypotension
Non-massive PE - obstruction of small, mainly distal branches	Hemodynamics are stable, there are no signs of right ventricular failure, symptoms indicate a pulmonary infarction.

PE options for the severity of the pathological process

In the new 2008 guidance, the terms "massive", "submassive" and "non-massive PE" are considered "misleading" and incorrect. The authors of the document propose to use the stratification of patients into high and low risk groups, and among the latter to distinguish subgroups of moderate and low risk. To determine the risk, ESC recommends focusing on three groups of markers - clinical markers, markers of RV dysfunction, and markers of myocardial damage (Table 1).

Risk groups for early PE-dependent death (death in hospital or within 30 days after PE)		Risk markers			Management tactics
		Clinical	Right ventricular dysfunction	Myocardial damage
		hypotension - a decrease in systolic blood pressure below 90 mm Hg. Art. or a drop in blood pressure ≥ 40 mm Hg. Art. for at least 15 minutes, without regard to arrhythmia, hypovolemia or sepsis;	EchoCG - signs of dilatation, hypokinesia, or RV overload RV dilation according to the results of spiral CT Increased blood levels of BNP or NT-Pro-BNP Increased pressure in the right heart according to the results of cardiac catheterization	Positive troponin T or I test
High - exceeding 15%		+	+	+	Thrombolysis / Thrombectomy
			In the presence of high-risk clinical markers (shock, hypotension), confirmation of belonging to a high-risk group due to markers of RV dysfunction and myocardial damage is not required.
Not high< 15%	Moderate up to 15%	-	+	+	Hospitalization
			+	-
			-	+
	Low< 1 %	-	-	-	Discharge from hospital and outpatient treatment

Thus, already with a quick examination at the patient's bedside, it is possible to determine whether the patient belongs to a high risk of early death or not. With further examination of those who do not have clinical signs of high risk (shock, hypotension), it is possible to assess the risk more accurately. This approach makes it possible to determine the tactics of managing patients as soon as possible and to prescribe the necessary treatment for high-risk patients in a timely manner.

PE (or in decoding - pulmonary embolism) is accompanied by the formation of a blood clot in the vessels of the lungs. Depending on the affected artery, the blood supply to a specific area of \u200b\u200bthe soft tissue stops. As a result, soft tissue ischemia develops.

A person begins to suffocate, a sufficient amount of oxygen ceases to enter the body. There is a risk of death, therefore it is important to know the first aid technique.

Pulmonary embolism is the closure of the lumen of the branches of the pulmonary artery with a piece of blood clot, which is formed by platelets glued to each other. In this case, the main thrombus can be located outside the respiratory system.

As a result of the formation of a clot, the blood supply to a small area of \u200b\u200bsoft tissues is interrupted. Because of this part of the lungs stops transporting oxygen to the blood... Thromboembolism develops - a condition characterized by suffocation due to the spread of small blood clots in the vessels of the lungs.

The pathological process often occurs during the operation, which increases the risk of death by 30%. Without medical care, 20% of patients die within 2 hours after the onset of PE.

ICD-10 code

Pulmonary embolism - I26. Includes heart attack, thromboembolism, pulmonary artery and vein thrombosis. Complicated abortions (O03-O07), ectopic or molar pregnancy (O00-O07, O08.2), pregnancy, childbirth and the puerperium (O88.-) are excluded.

Pulmonary embolism with mention of acute cor pulmonale - I26.0, without mention - I26.9.

Does pulmonary thrombophlebitis happen?

Thrombophlebitis, in contrast to thrombosis, is characterized by inflammation of the venous vessel wall followed by the formation of a thrombus. In theory, the disease can affect any vein in the body. At the same time, in clinical practice, it has been revealed that the disease often affects the superficial, saphenous veins, subject to temperature extremes.

In the pulmonary artery flows blood saturated with carbon dioxide. Therefore, with the development of a severe respiratory tract infection, the development of pulmonary thrombophlebitis is possible. The bacteria can provoke inflammation of the vascular wall, which can lead to PE. This pathology develops in exceptional cases in less than 0.01% of patients..

Most often, pulmonary thromboembolism develops due to thrombophlebitis in the veins of the lower extremities. A blood clot forms in the legs, parts of which break off and enter the vessels of the lungs.

What happens in the body with PE?

To generate energy, constant oxidative reactions take place inside cells, the main reagent of which is oxygen. In the process of breathing, air enters the lungs, where the alveoli are located.

Small tissue bubbles are entangled in a network of capillaries in which gas exchange takes place. The pulmonary artery delivers venous blood to the alveoli to release carbon dioxide and saturate it with oxygen molecules.

With thromboembolism, the blood flow in the affected vessel stops, due to which gas exchange does not occur. Blood entering the lungs stops being saturated with oxygen. Cells throughout the body stop producing the energy needed for organs to function. Under conditions of hypoxia, the death of brain and myocardial cells begins, blood pressure drops, and shock develops.

If untreated, a heart attack and atelectasis (a decrease in the lung lobe) occur.

Epidemiology in adults

TELA develops in 500-2000 people a year. Pathology occurs not only during the operation, but also during childbirth. Mortality in women in childbirth varies from 1.5% to 3% per 10,000 cases. 2.8-9.2% of women die from complications during the rehabilitation period.

Causes and pathogenesis

The following reasons can provoke the development of PE:

• deep vein thrombosis of the lower extremities, in 90% of cases complicated by thrombophlebitis;
• generalized sepsis;
• cardiovascular pathologies with a high risk of thrombosis: ischemic disease, mitral stenosis, hypertension, cardiomyopathy, infective endocarditis;
• thrombophilia;
• thrombus in the inferior vena cava;
• malignant neoplasms in the pancreas, lungs and stomach;
• hemorrhoids;
• artificial heart valve;
• antiphospholipid syndrome.

PE begins with damage to the vascular endothelium... The latter normally produces nitric oxide and endothelin, which prevent vasospasm and platelet adhesion.

When endothelial cells are damaged, blood clotting increases and the blood flow subendothelium is exposed. The latter releases into the blood a substance that stimulates thrombus formation. Platelets activate the transformation of fibrinogen into fibrin, produce thrombin, which sticks platelets together.

Only part of the thrombus is fixed on the vessel wall. 75-80% of the blood clot remains free and may break off... The cleaved platelets through the vessels enter the right ventricle of the heart. Along the way of its advance, the cleaved section of the thrombus can be destroyed into smaller parts.

From the heart, microthrombi enter the pulmonary circulation and begin to circulate through the vessels of the lungs, causing blockage of the branches of the pulmonary artery.

The consequences of PE depend on the size and number of blood clots... Large clots impair the blood supply to entire lobes and segments of the lung, which leads to hypoxia, respiratory and hemodynamic disorders:

• hyperventilation of the lungs;
• shock;
• tachypnea;
• pulmonary heart.

In some cases, metabolic disorders are possible. Smaller blood clots cause pulmonary infarction.

Risk factors

The following factors increase the risk of developing PE:

• prolonged bed rest with post-infarction and post-stroke conditions;
• cardiovascular pathologies: atrial fibrillation, heart failure, arterial hypertension, active phase of rheumatism;
• paralysis of the limbs, fractures or immobility of the body for more than 12 weeks;
• surgical operation on the organs of the abdominal cavity, lower limbs and small pelvis;
• the use of an indwelling catheter in the central vein;
• pregnancy, early delivery;
• purulent-inflammatory diseases;
• long-term use of drugs: hormonal, diuretics, laxatives, contraceptives for oral use;
• diabetes;
• systemic connective tissue damage: lupus erythematosus, vasculitis.

PE classification

There is no single classification for PE. The following criteria are used to determine the type of pathology:

• the degree of damage to the lung tissue;
• the rate of development of the pathological process;
• the severity of thromboembolism;
• clinical manifestations of PE;
• the degree of blood flow disturbance.

Amount of damage: massive, submassive, non-massive

According to the level of lung damage, pulmonary embolism is divided into 3 types:

1. Massive... In such a situation, blood clots stop blood supply in 50% or more of the lungs. The main branch of the pulmonary artery is affected, or a pulmonary embolism begins. As a result, shock and systemic hypotension develop.
2. Submassive... From 30% to 50% of the vessels of the lungs are affected: the pathological process captures the segments and lobes of the organs. Patients have right ventricular failure.
3. Non-massive... Thromboembolism extends to 30% of the volume of the vascular bed of the lower respiratory system. PE is asymptomatic. There may be no consequences.

Clinic and severity

According to the severity, the following forms of PE are distinguished:

1. Heavy... Pathology is characterized by impaired respiratory function and hemodynamic disorder. Tachycardia, severe shortness of breath and shock develop rapidly. Due to hypoxia, the skin becomes blue. In some cases, loss of consciousness is observed. In 40-60% of cases, there is a feeling of anxiety and fear, chest pain appears.
2. Moderate... Heart rate reaches 100-120 beats / min, blood pressure decreases, and tachypnea develops. The patient has a pain syndrome in the pleural cavity, cough, sputum with blood leaves. The person feels fear, periodically loses consciousness.
3. Easy... The pulse reaches 100 beats / min. There is no hyperventilation of the lungs, short-term dyspnea develops. In rare cases, a dry cough appears, patients cough up blood.

The degree of impaired blood supply to the lungs

3 forms of violations are classified:

1. Partial... It is asymptomatic. Small clots clog the capillaries, without harming the main gas exchange. The function of the affected vessels is taken over by the adjacent branches of the artery.
2. Average... Multiple thromboembolism of branches leading to one of the lung segments. Pathology extends to 30% of tissues.
3. Full... It is characterized by the formation of a blood clot in the central branch of the pulmonary artery with congestion or severe slowing of blood flow. The result is severe respiratory failure.

Clinical classification

According to the distinctive features of the clinical picture, the following types of PE are distinguished:

1. Heart attack pneumonia: PE develops in small arteries. The progressive disease is characterized by acute shortness of breath, coughing up blood, and tachycardia. Respiratory failure develops when moving to an upright position. In the place of organ damage in the chest area, pain syndrome develops due to the spread of pathology along the pleural tissue.
2. Unmotivated shortness of breath: PE spreads through the small vessels of the lungs. The patient periodically suffers from sudden shortness of breath. Symptoms of pulmonary heart disease appear, despite the absence of cardiopulmonary pathologies.
3. Acute cor pulmonale: thromboembolism of large arteries occurs. The patient has sudden shortness of breath and blood pressure drops. The development of cardiogenic shock and angina pectoris pain is observed.

Dynamics

The classification of embolism along the pathological process is also important. There are the following types of pulmonary artery thrombosis:

• lightning dynamics - death occurs within 5-30 minutes;
• acute course diseases in which symptoms appear suddenly in sequence: chest pain, shortness of breath, hypotension, acute cor pulmonale;
• subacute - characterized by heart and respiratory failure, symptoms of infarction pneumonia and expectoration of blood clots;
• recurrent pathology: repeated attacks of shortness of breath, symptoms of pneumonia, loss of consciousness.

Clinical picture

With the development of PE, shortness of breath immediately develops. When small arteries are damaged, the patient does not have enough air, he begins to panic. When the central branches of a large caliber are blocked, severe suffocation is observed, accompanied by cyanosis.

In 85% of cases, shortness of breath is quiet, not accompanied by noisy inhalation and exhalation... Patients are comfortable in a supine position. Respiratory failure leads to a number of other signs of impairment.

Symptoms of brain disorders

In a state of acute hypoxia, with damage to the branches of the pulmonary artery of a large caliber, a violation of cerebral circulation is observed. Neurons in the brain do not receive the required amount of oxygen, which provokes the development of the following symptoms:

• violation of consciousness;
• fainting;
• impaired coordination of movements;
• an increase in body temperature up to + 38 ° C;
• darkening in the eyes;
• decreased cognitive function;
• dizziness and headache.

Signs in cardiology

The second most common symptom of PE is chest pain that is felt from a few moments to 12 hours depending on the degree of damage to the respiratory system.

In pulmonary embolism of small branches of the pulmonary artery, the pain syndrome is practically not felt, the symptoms are erased. Thrombosis of large vessels leads to prolonged aching-stitching pains. If the pathology extends to the pleura, there are stabbing pains during coughing, movement and deep sighing.

In rare cases, small-caliber artery involvement results in pain that is similar to a heart attack.

In most cases, abdominal syndrome developsarising from a disruption of the right ventricle or due to irritation of the phrenic nerve. In such a situation, the pain is felt in the right hypochondrium. With right ventricular failure, the appearance of a gag reflex, abdominal distension is possible.

With PE, tachycardia and a decrease in blood pressure also appear.

Respiratory disorders

In addition to acute shortness of breath after 2-3 days after the onset of the disease cough develops as a symptom of infarction pneumonia... At the same time, hemoptysis is observed in 30% of cases. Gas exchange disturbances lead to the development of oxygen starvation of the cells, therefore, during a physical examination of the patient, cyanosis is noted - blue skin.

How to determine the likelihood before the survey?

At the prehospital stage, the onset of pulmonary embolism cannot be determined. It is almost impossible to prevent the development of the pathological process during surgery and delivery. To relieve an acute condition, resuscitation measures are carried out, the patient is transferred to the intensive care unit.

First aid emergency care: algorithm of actions

If pulmonary embolism is suspected it is necessary to call a team of paramedics. After that, you need to help the victim sit down or take a horizontal position with his head raised. It will be necessary to remove dentures from the patient, free the chest from clothes, and provide fresh air to the room.

When a patient has panic, it is necessary to calm him down in order to prevent rapid breathing and heart rate during stress. You can not give the sick person food and drink. With the development of pain, you need to give the victim narcotic painkillers. These drugs can help to further reduce shortness of breath. Giving neuroleptanalgesia is prohibited when blood pressure is lowered.

Pain during breathing or movement indicates the development of heart attack pneumonia. Doctors should be informed of this upon arrival.

Until the ambulance arrives, the pulse should be counted and the patient's pressure measured... The indicators need to be reported to the paramedics. In case of cardiac arrest and respiration, it is necessary to start resuscitation measures: 2 breaths from mouth to mouth, pinching the patient's nose, alternate with 30 presses in the area of \u200b\u200bthe heart.

To thin the blood clot, it is necessary to start anticoagulant therapy. In a critical situation, 15,000 U of heparin will need to be administered intravenously. It is forbidden to administer the drug if bleeding and hemophilia develop. During hypotension, a rheopolyglucin drip should be given instead of heparin.

Diagnostics

If pulmonary embolism is suspected the main goal of diagnostics is to find out the exact localization of the thrombus... After that, the tasks are: to assess the degree of lung damage and the severity of the pathological process, determine hemodynamic disturbances, and establish the source of pulmonary embolism. The latter is necessary to eliminate the main thrombus, from which a small clot has broken off, and to prevent relapses.

During the diagnosis, anamnesis is collected, the symptoms manifested are recorded, instrumental examinations are carried out, and laboratory tests are prescribed.

Laboratory methods

The following laboratory tests are performed to diagnose PE:

• general and biochemical blood test;
• lipid profile;
• study of the gas composition of blood;
• urine analysis as part of differential diagnosis;
• coagulogram;
• determination of the level of D-dimers.

D-dimers are products of fibrinolysis. The norm should be 500 mcg of the compound. An increased concentration of a substance indicates a recent thrombus formation. In the diagnosis of PE in 90% of cases, the level of D-dimers is measured as the most sensitive method.

Instrumental methods

• Electrocardiography (ECG): With PE, right ventricular failure and sinus tachycardia develop, these changes can be recorded using a cardiogram. At the same time, some patients have no signs of pulmonary embolism on the ECG. In 20% of patients, using a cardiogram, an acute cor pulmonale can be detected due to the load on the right ventricle.
• Chest x-ray: in the picture, you can fix the high standing of the diaphragmatic dome from the side of the development of pathology. X-ray signs - expansion of the right ventricle and right descending pulmonary artery, enlargement of the roots of the lung.

  

  Chest X-rays in patients with confirmed PE on the left - discoid atelectasis against the background of fluid in the chest cavity and expansion of the lung root, on the left - pulmonary infarction due to PE

  

  Right lung infarction on x-rays in a patient with confirmed PE

  

  

• Echocardiography: the procedure reveals a violation of the right ventricle, displacement of the interventricular septum to the left. During the diagnosis, hypertension is observed in the pulmonary circulation. In rare cases, blood clots are recorded in the region of the heart.
• Spiral computed tomography: during the diagnosis, the localization of blood clots can be detected. The patient is injected with a contrast agent, with which a volumetric image of the lungs can be obtained. During the procedure, the patient must hold his breath for a few seconds. The research method is safer for the patient compared to angiography.

  Embolism of the upper lobe pulmonary artery on the left, revealed by CT scan of the chest with contrast, an embolus in the lumen of the artery is clearly visualized (marked with arrows and a circle)

  

  Massive pulmonary embolism revealed in a patient with computed tomography in both pulmonary arteries, hypodense (against the background of contrasting blood) thrombi are visualized in their lobar branches

  

  An example of polysegmental infarction pneumonia detected in a patient with PE of small branches of both pulmonary arteries by computed tomography

  

  

• Ultrasound of deep veins of the lower limb: The procedure allows you to determine the presence of blood clots in the veins of the legs, which can be the cause of pulmonary embolism.
• Ventilation perfusion scintigraphy: During the procedure, it is possible to identify areas of the lung without blood supply, into which air enters. Scintigraphy allows the diagnosis of PE with an accuracy of 90%.
• Angiography - the most accurate method for diagnosing pulmonary embolism. Despite the accuracy, the procedure is invasive and not safe for the patient's health. In pulmonary embolism, the pulmonary artery is sharply narrowed with slow removal of the contrast agent.

Treatment: first aid standards

Treatment is focused on saving the patient's life and restoring the natural blood supply to the lungs. For treatment the patient is transferred to intensive care, where he will stay until the blood clot is removed... In the intensive care unit, the work of the respiratory and circulatory systems is supported with the help of mechanical ventilation.

In the presence of pain, the patient is administered pain relievers. To eliminate thrombosis, treatment with anticoagulants is performed. In some cases, due to drug therapy, the thrombus is destroyed on its own, but if this does not happen, an operation is prescribed.

Treatment of patients with acute pulmonary embolism. Gilyarov M.Yu .:

Correction of hemodynamics and hypoxia

In case of cardiac arrest, resuscitation is performed. Oxygen therapy is used to prevent hypoxia: Oxygen is supplied through masks or nasal catheters. Mechanical ventilation is used for the defeat of large branches of the artery.

To stabilize the pressure in the vessels and prevent venous congestion, saline, adrenaline, or dopamine are injected intravenously. To restore blood circulation in a small circle, anticoagulants are administered.

Anticoagulant therapy

Anticoagulant therapy helps prevent death. In the intensive care unit with a high risk of PE, sodium heparin is given intravenously. The dosage of the drug is affected by the patient's body weight, thromboplastin time (APTT) indicators. After 6 hours of droppers, a blood test is taken from the patient every 3 hours to monitor the APTT indicator.

Heparin therapy for PE is not prescribed for renal failure, hemophilia... In addition to heparin, on the first day of hospitalization, the patient is prescribed warfarin, which must be taken at least 3 months after discharge. The daily dosage is set by the attending physician, depending on the individual characteristics of the patient and the severity of the pathology.

Reperfusion therapy

To remove the thrombus and restore natural blood flow, reperfusion therapy is performed. Thrombolysis is used at high risk of developing complications of PE. The following drugs are used to dissolve a blood clot:

• streptokinase;
• alteplase;
• urokinase.

There is a high risk of bleeding during thrombolytic therapy... In 2% of patients, cerebral hemorrhage occurs, in 13% of cases, severe internal bleeding.

Hospital surgery

Thrombus removal is performed by thrombectomy. In such a situation, the surgeon makes an incision at the site of the vessel lesion and removes the blood clot using instruments. After removing the thrombus, the incision is sutured. As a result, normal blood circulation is restored.

Despite the high efficiency, surgical intervention is associated with a high risk to the patient's life... A cava filter is used as a safer treatment for PE.

Installing a cava filter

The kava filter is installed in patients with a high probability of developing a recurrent pulmonary embolism. The indication for the procedure is also the presence of contraindications to the use of anticoagulants.

The product is a mesh filter that catches the broken parts of a blood clot and prevents them from entering the vessels of the lungs... Kava-fil is placed through a small incision in the skin, passing the product through the femoral or jugular vein. The instrument is fixed below the veins of the kidneys.

Recurrent PE

In 10-30% of cases, patients who have undergone pulmonary embolism may face a relapse of the disease. Pathology can be repeated many times. The high incidence of episodes is associated with blockage of the small branches of the pulmonary artery. The causes of relapse are:

• malignant neoplasms;
• cardiovascular pathology;
• deep vein thrombosis, accompanied by the gradual destruction of a large thrombus;
• cardiovascular and respiratory diseases;
• carrying out the operation.

The repeated development of pathology does not have pronounced symptoms., therefore it is practically impossible to diagnose. In most cases, the symptoms that appear are confused with other diseases.

An accurate diagnosis can be made only if you know about the previous PE and take into account the risk factors. Therefore, the main diagnostic method is a detailed history of the patient. After the survey, X-ray, ECG, ultrasound of the lower extremities are performed.

Recurrent pulmonary embolism can lead to the following consequences:

• hypertension in the pulmonary circulation;
• restructuring of blood vessels in the lower respiratory system with the formation of cor pulmonale;
• blockage of the central branch of the pulmonary artery.

Lung thrombosis prognosis

Acute pathology can lead to cardiac and respiratory arrest. In the absence of resuscitation measures, a lethal outcome occurs. If the compensatory mechanisms of the body are triggered or small-caliber arteries are affected, the patient does not die. But in the absence of anticoagulant therapy, secondary hemodynamic disorders develop.

With timely treatment, the prognosis is favorable - after removing the blood clot, the patient recovers quickly.

With prolonged hypoxia, there is a risk of brain damage, which leads to the irreversible loss of certain vital functions or human abilities.

Primary and secondary prevention

With the primary prevention of PE, it is necessary to treat varicose veins on time, undergo anticoagulant therapy and wear compression stockings with high blood clotting. After the birth of a child or in the postoperative period, it is necessary to strictly follow medical recommendations. Blood tests should be done twice a year for people at high risk of PE.

As a secondary preventive measure, you need to adhere to a healthy lifestyle:

• treat infectious diseases;
• avoid injury;
• eat properly;
• prevent obesity;
• avoid stress;
• do sport;
• drink plenty of fluids;
• to refuse from bad habits.

PE is a dangerous disease that requires immediate hospitalization. In most cases, it develops in women during childbirth or during surgery. To eliminate the thrombus, treatment with anticoagulants, thrombectomy, and installation of a cava filter are performed. With timely treatment, the patient fully recovers. Otherwise, hypoxia develops, disrupting the work of the brain, heart and respiratory failure. To reduce the risk of developing PE, cardiovascular pathologies should be diagnosed and treated in time.

Video "Living Healthy"

Pulmonary embolism. Live healthy! Fragment of the release from 11/28/2016:

Now you know everything about PE: what it is in medicine, what are the causes, how to treat lung disease - modern principles and approaches to treatment, as well as the consequences of the disease.

Pulmonary embolism (PE) is usually a complication of another serious condition, a secondary pathology. PE is considered one of the most dangerous and formidable consequences of primary diseases, which in most cases leads to sudden death.

Thromboembolism is an abrupt and sudden blockage of a pulmonary artery by a detached blood clot. As a result, blood stops flowing to the area of \u200b\u200bthe lung. This condition requires immediate medical attention.

It is a life-threatening condition with a high percentage of deaths. The essence of the disease is that a blood vessel or artery is clogged with a blood clot. Blood cannot flow to the lung, resulting in decreased respiratory function. With prolonged cessation of blood circulation, part of the lung tissue begins to die off, causing various complications.

As you know, thromboembolism of the pulmonary artery (ICD code 10) is provoked by a thrombus. It is sometimes called an embolus. However, an embolus can also be fat, a foreign body, gas, part of a tumor, etc. This is the main cause of PE. However, in a healthy person, this condition does not occur. The disease can be triggered by various factors:

1. ... Existing thrombosis (deep veins, inferior vena cava) very often leads to thromboembolism. In this disease, increased blood clotting is found, which leads to the appearance of blood clots. Blood clots grow over time and break off, which leads to pulmonary embolism and death of the patient.
2. Oncological diseases. The formation of tumors in the body leads to many pathological processes. Cancer can provoke increased thrombus formation, or a fragment of a malignant tumor will serve as an embolus.
3. Sedentary lifestyle. Especially susceptible to increased thrombosis are people who are prescribed bed rest after or, operations, injuries, frail elderly people, people with obesity.
4. Genetic predisposition. Hereditary blood diseases, which are accompanied by increased blood clotting, often lead to PE. In this case, prevention is very important.
5. Sepsis. Inflammation of the blood disrupts the functioning of all systems and organs in the body. Blood clots are not uncommon in this case. Blood clots appear especially easily in damaged areas of blood vessels.

Also, provoking factors include smoking, old age, abuse of diuretics, an indwelling catheter in a vein, excess weight, multiple injuries that interfere with a person's mobility.

Symptoms and diagnostics

The severity of symptoms depends on the degree of lung damage. A weak degree of damage canaccompanied by mild symptoms.

Symptoms are often nonspecific. It can cover cardiac and pulmonary manifestations.

The most common signs of pulmonary embolism are:

• ... Since part of the lung tissue is affected, severe shortness of breath, a feeling of lack of air, shallow breathing occurs. Severe shortness of breath often causes a person to panic, which only exacerbates the situation.
• Painful sensations in the chest. When a pulmonary artery is blocked, chest pain often occurs, which increases with breathing. The pain can be of varying intensity.
• Weakness. Due to the deterioration of the blood supply to the lung, the patient may feel severe weakness, dizziness, and lethargy. Fainting is also common.
• Cyanosis. Cyanosis is the blue discoloration of the skin around the mouth. This indicates a strong violation of blood circulation and gas exchange in the lungs. Cyanosis is a sign of severe and extensive thromboembolism.
• Cough. With PE, the patient develops a reflex dry cough. After a while, sputum begins to separate. A severe cough damages blood vessels, so blood can be found in the sputum.
• ... In patients with PE, there is a rapid heartbeat: more than 90 beats per minute.
• Also, in people with pulmonary embolism, a sharp decrease is observed, which also worsens well-being and leads to dizziness.

It is not easy to diagnose pulmonary embolism because the disease has no specific symptoms. The doctor will take a history, but it is impossible to make an accurate diagnosis based on the symptoms.

To determine PE, you need to pass a number of tests: urine analysis, expanded coagulogram.

In addition to tests, several other diagnostic procedures will be required.

Radiography and ultrasound will help determine the extent of the lesion and the consequences of PE on the body. To find the source of the blood clots, an ultrasound scan of the veins of the extremities is prescribed.

Classification of pulmonary embolism

TELA has several classifications and varieties. They are based on the features of the course of the disease and the extent of damage to the lung tissue. If we talk about the localization of thromboembolism, we distinguish between massive, segmental and small branch embolism.

Massive embolism is characterized by the fact that a large thrombus covers the entire artery trunk. As a result, blood flow stops completely. The symptoms in this case are very pronounced, accompanied by severe shortness of breath and loss of consciousness.

Segmental thromboembolism is accompanied by symptoms of moderate severity. There are chest pains, shortness of breath, tachycardia. This condition can last for several days. Thromboembolism of small branches of the pulmonary artery may not be recognized at all. Symptoms are mild. The patient may experience mild chest pain and shortness of breath.

The clinical course of PE can be of 4 types:

1. Lightning fast. In this case, there is a complete and sharp blockage of the artery with a large thrombus, which completely blocks its lumen. The disease develops very quickly. There is severe shortness of breath, respiratory arrest, collapse. Usually, with lightning-fast pulmonary embolism, the patient dies within a few minutes.
2. Sharp. Pathology occurs suddenly and develops rapidly. Symptoms of respiratory and heart failure appear, which can last up to 5 days. This is followed by a pulmonary infarction. In the absence of medical care, there is a high risk of death.
3. Subacute. This condition can last for several weeks with a constant increase in symptoms. There are signs of respiratory and heart failure, multiple lung infarctions, which are repeated during this period and often lead to the death of the patient.
4. Chronic. This condition is accompanied by recurrent lung infarctions and pleurisy, which occur against their background. This condition develops slowly and lasts a long time. It often arises as a complication against the background of previous operations or cancer.

There is also a classification based on the volume of cut off blood flow. It is fatal to shut off more than 75% of the artery's blood flow.

Treatment and prognosis

Treatment usually begins with the patient being admitted to the intensive care unit. Pulmonary embolism is a dangerous condition that requires emergency medical attention.

First of all, treatment is aimed at restoring blood flow and normalizing respiratory function. After stabilization of the patient's condition, a thorough diagnosis is carried out, the causes of the embolism are identified and treatment is prescribed to eliminate these causes.

Treatment usually includes the following elements:

• Oxygen therapy. With PE, the patient experiences severe oxygen deprivation. To replenish the body's need for oxygen, a procedure is prescribed, which consists in inhaling an oxygen-enriched mixture.
• ... These are drugs that reduce and prevent new blood clots from forming. Drugs containing heparin are commonly used. In a serious condition of the patient, they are administered intravenously. A blood test is carried out in parallel. Overdose of anticoagulants can lead to internal bleeding.
• Embolectomy. This operation is prescribed only for critically ill patients who have extensive thromboembolism with occlusion of the artery trunk. It is carried out urgently in a condition that threatens the patient's life. There are several methods of performing the operation, but the essence is the same - the surgeon removes the clot in the lumen of the artery. Modern technology allows the operation to be carried out closed, using an X-ray machine. Less commonly, an open operation is performed.
• Installing a kava filter. If the disease constantly recurs, a special filter is installed in the inferior vena cava. It traps blood clots and prevents them from entering the pulmonary artery.
• Antibiotics Lung infarction often leads to an inflammatory process, pneumonia. To eliminate inflammation and prevent complications, antibiotic therapy is prescribed.

If the lung lesion is non-mass and assistance was provided in the early stages, the prognosis is quite favorable. With extensive PE, the mortality rate reaches 30%. When taking anticoagulants, the likelihood of relapse is significantly reduced.

Complications and prevention

Pulmonary embolism can lead to various complications, the worst of which is death.

With serious lung damage, sudden death occurs even before the ambulance arrives. In this case, it is almost impossible to save the patient.

Other consequences of thromboembolism include:

1. Lung infarction. With the cessation of blood circulation, part of the lung tissue dies off. In this place, a focus of inflammation develops, which leads to infarction pneumonia. This process may not be fatal if the affected area is small. However, multiple heart attacks can be life-threatening.
2. Pleurisy. Each lung is surrounded by a membrane called the pleura. Pleurisy is an inflammation of the pleura, which is accompanied by the accumulation of fluid in the pleural cavity. The symptoms are similar to PE: shortness of breath, chest pain, cough, weakness.
3. ... This is a pathology in which the respiratory system cannot provide the body with the required amount of oxygen. Respiratory dysfunction leads to a number of other complications, provokes the development of severe diseases of internal organs.
4. Relapses. If the doctor's recommendations are not followed and if there are other severe chronic diseases (especially of the cardiovascular system), relapses are possible. Pulmonary embolism repetitions can be more severe and lead to patient death.

Pulmonary embolism usually occurs unexpectedly, without any precursors. To avoid this life-threatening pathology, you need to adhere to the rules of prevention.

More information about pathology can be found in the video:

Especially it is necessary to pay attention to prevention for those who have a genetic predisposition to this disease. Prevention measures include proper nutrition, rejection of bad habits, physical activity, and regular preventive examinations. It is recommended to wear compression garments for people who are prone to varicose veins and increased blood clots.

Summary

In recent decades, despite the appearance in the clinic of modern drugs for the prevention of PE, the number of patients with this pathology is growing. The presented material describes in detail the pathogenesis, clinic and treatment of this suffering. The modern recommendations for the management of patients with various forms of PE are presented.

Keywords

pulmonary embolism, diagnosis, treatment.

Pulmonary embolism (PE) is an acute blockage of the branches of the pulmonary artery by emboli separated from blood clots that form in the veins of the systemic circulation.

Most cases of PE are due to deep venous thrombosis (DVT). PE and HBT are two clinical manifestations of venous thromboembolism (VTE). Fifty percent of patients with proximal HBT (above the knee) develop PE, which is often asymptomatic and detected on lung scans. On the other hand, HWT of the lower extremities is found in 70% of patients with PE.

In the United States, the prevalence of PE in hospitalized patients is 0.4%. From 600 thousand to 2 million cases of PE are registered in the USA annually. In general, according to American and European observations, the number of cases of lifetime diagnosis of PE ranges from 6 to 53 cases per 100,000 population per year. At the same time, repeated episodes of PE are observed 3 times more often after initial PE than after HT (60% and 20%, respectively). Acute cases of PE are fatal in 7-11% of patients. However, the true prevalence of PE can be judged by the data of pathological studies. Thus, according to M. Nodstrom and B. Lindblant (1998, Sweden), VTE was detected in 25% of autopsies, including PE - in 18%, in 13.1% of cases PE was the cause of death. At the same time, pulmonary embolism diagnosed during life was only 2%. In Ukraine, PE is the cause of 10% of deaths in surgical and orthopedic hospitals.

In 80% of cases, PE occurs when predisposing factors (secondary pulmonary embolism). However, according to the International Cooperative Pulmonary Embolism Registry (1999), unprovoked idiopathic PE is observed in 20% of cases. The appearance of PE and VTE is generally determined by the interaction dependent (from the patient) and independent situational risk factors (Tables 1, 2), but this division is rather arbitrary. The average age of patients with PE is 62 years. Surgical interventions remain the most significant cause of PE, but a recent analysis (ENDORSE, 2008) of 358 hospitals in 32 countries showed that only 39.5% of patients at risk of VTE were adequately prevented. Heredity also plays a role in the development of VTE, although specific genes have not yet been identified. At the same time, the presence of VTE in relatives allows us to consider this as a predisposing factor.

Among the diseases encountered in the practice of the therapist, the increased risk of PE are: heart failure and myocardial infarction, stroke, nephrotic syndrome, polycythemia, systemic lupus erythematosus.

The greatest risk of development PE is observed after surgery for 2 weeks, but persists for 2-3 months. Most patients with symptoms of HBT have proximal thrombi, complicating in 40-50% of cases of PE, often asymptomatic. PE, as a rule, occurs 3-7 days after HBT, and the appearance of the "clinic" leads to death within the first hour in 10% of cases. The clinical presentation of PE in 5-10% of patients is hypotension; in half of the cases, shock with signs of right ventricular failure develops. Without anticoagulants, 50% of patients develop recurrent thrombosis within 3 months.

Pathophysiology TELA includes the following effects:

1. Increased pulmonary vascular resistance due to vascular obstruction or platelet secretion of neurohumoral factors, including serotonin.

2. Disruption of gas exchange due to increased alveolar dead space due to vascular obstruction, hypoxemia due to alveolar hypoventilation relative to perfusion in the intact lung, right-to-left shunting of blood, and impaired carbon monoxide transport due to a decrease in the respiratory surface.

3. Alveolar hyperventilation due to reflex stimulation of irritative receptors.

4. Increased airway resistance due to constriction of the airways distal to the main bronchi.

5. Decreased lung mobility due to pulmonary edema, pulmonary hemorrhage and loss of surfactant.

PE is stratified by the risk of early death (in-hospital or 30-day mortality) based on risk markersdetermined clinically (using echocardiography (EchoCG), computed tomography (CT)) or laboratory:

1. Clinical markers - shock, hypotension (systolic blood pressure< 90 мм рт.ст. или падение ≥ 40 мм рт.ст. за 15 мин, если не возникли аритмия, гиповолемия или сепсис).

2. Right ventricular dysfunction:
- dilatation, hypokinesia or pressure overload on echocardiography and / or CT;
- increased levels of BNP (brain natriuretic peptide; brain natriuretic peptide) or NT-proBNP;
- increased pressure in the right ventricle (RV) during catheterization.

3. Myocardial damage - increased levels of cardiac troponins T and I.

Risk markers are used for its stratification in order to select the appropriate diagnostic and treatment tactics (Table 3).

In 90% of cases, the assumption about PE is based on clinical symptoms (Table 4). Shortness of breath usually appears suddenly, may be isolated, but it happens that it progresses over a week or more. Syncope (fainting, loss of consciousness) is not a frequent, but an important initial sign of PE, indicating a critical decrease in hemodynamic reserve. Pleural chest pain with or without shortness of breath is the most common clinical manifestation of PE. Pain is more often associated with distal emboli and pleural reaction to pulmonary infarction, sometimes associated with hemoptysis. The development of cyanosis of the upper part of the body, the appearance of an accent of the II tone on the pulmonary artery and rales of various sizes in the lungs during auscultation are possible.

Isolated, acute dyspnea in combination with acute hemodynamic disturbances is characteristic of central PE. However, with central pulmonary embolism, chest pain resembling myocardial infarction is also possible; it can also be a consequence of pancreatic ischemia. Analysis of predisposing factors helps in making a diagnosis.

Laboratory and instrumental research include:

1. Radiography - pathological, but, as a rule, nonspecific:
- high and inactive standing of the dome of the diaphragm;
- disc-like atelectasis;
- expansion of the shadow of the superior vena cava;
- bulging of the second arch along the left contour of the heart shadow;
- infiltrates of lung tissue (zones of lung infarction).

X-rays can often rule out other causes of shortness of breath or chest pain.

2. Determination of the partial pressure of gases in the blood - PE in 80% of cases is associated with blood hypooxygenation (decrease in PaO2).

3. ECG - signs of RV overload are determined: inversion "T" in V 1 -V 4, QR in V 1, classic - deepening SI, Q III, T III, as well as incomplete or complete blockade of the right bundle branch, especially valuable for diagnosis as for the first time arisen. Sinus tachycardia is characteristic, first-onset atrial fibrillation is possible, often an angle α\u003e 90 °.

4.D-dimer - a product of fibrin degradation. It increases in plasma in the presence of an acute thrombus due to stimulation of coagulation and fibrinolysis.

Normal D-dimer levels make the diagnosis of PE or HBT unlikely, and in combination with clinical data (Wells scale, Table 5), it completely excludes VTE. However, elevated D-dimer levels do not confirm PE, since fibrin is produced in a variety of conditions (cancer, inflammation, infections, necrosis, etc.). The specificity of the test decreases in the elderly and\u003e 3 days after thrombosis. In general, the specificity of the test for PE is 40-50%. The norm (upper limit) when determined by the enzyme-linked immunosorbent assay (ELISA) is 500 ng / ml, however, it may differ for different manufacturers of kits (250, 300 ng / ml). When determined by the calorimetric method / latex test -\u003e 0.5 mg / l (500 μg / l).

5. Compression ultrasonography and CT venography... In 90% of cases, PE is caused by HBT of the lower extremities. Compression ultrasonographic venography determines HBT in 70% of PE patients. It can be used as an additional procedure or in case of contraindications to the use of contrast. CT venography detects HBT in up to 90% of PE patients. Moreover, both methods have a specificity of ≈ 95%.

6. Ventilation perfusion scintigraphy. Used in / in the introduction of radioactive technetium Tc-99. Currently, the application is limited.

7. Spiral CT angiography of the pulmonary artery in combination with intravenous administration of contrast (usually 100 ml into the cubital vein - 3-4 ml / s).

The diagnostic value depends largely on the technique used. With a single-detector tomograph - 53% and specificity - 73%, and with a multi-detector technique (with contrast), the sensitivity and specificity increase to 100%. Allows you to see blood clots in the PA at the subsegmental level.

8. Magnetic resonance imaging (with contrast enhancement), it is inferior in diagnostic value to multidetector CT and is comparable to monodetector CT. It can be used in cases of intolerance to iodine-containing contrasts (gadolin is used), renal failure, as well as in pregnant women as not having a "radiation load".

9. Pulmonary angiography. Used since 1960. Direct pulmonary angiography detects blood clots 1–2 mm in size in subsegmental arteries. It also reveals indirect signs of PE, such as slowing of the contrast current, regional hypoperfusion, cessation of venous flow, etc. Intravenous injection of contrast poses some danger, while mortality is 0.2%. Previously considered the gold standard for diagnosing pulmonary embolism, recently it is beginning to recede before multi-CT, which provides the same information, but does not lead to complications. It is reliable but invasive, expensive and sometimes difficult to interpret, and can be used when CT results are questionable.

10. EchoCG.RV dilatation is established in more than 25% of patients with PE; the appearance of this sign is used for risk stratification. The echo criteria used to diagnose PE are tricuspid insufficiency, ejection rate, and RV size. Sensitivity - 60-92%, specificity - 78-92%. A negative test does not exclude pulmonary embolism, since echo criteria can also be found in other diseases of the heart and lungs. In patients with suspected PE, they help manage critically ill patients.

In patients with shock or hypotension, the absence of echocardiographic signs of RV overload or dysfunction precludes PE.

Basic Echo-Doppler criteria:

A. RV overload criteria:

1. Right-sided cardiac thrombosis.

2. RV change in diastole (parasternal view)\u003e 30 mm or RV / LV\u003e 1.

3. Systolic fluttering of the interventricular septum.

4. Acceleration time< 90 мс или трикуспидальная недостаточность с градиентом давления ≤ 60 мм рт.ст. при отсутствии ПЖ-гипертрофии.

B. Sign "60/60": acceleration of RV ejection time< 60 мс при наличии трикуспидальной недостаточности и градиента давления ≤ 60 мм рт.ст.

C. Sign McConnel: normokinesia and / or hypokinesia of the apical segment of the free wall of the pancreas, despite hypokinesia and / or akinesia of the rest of the free wall of the pancreas.

Concomitant echocardiographic signs of pressure overload require exclusion of a false diagnosis of acute PE in patients with hypokinesia and / or akinesia of the free wall of the pancreas corresponding to pancreatic infarction.

Today, multi-detector CT is the standard for the diagnosis of PE.

Clinical classification of PE (ICD-10 - I26)

A. According to the severity of the development of the pathological process:
- sharp;
- subacute;
- chronic (recurrent).

B. By the volume of vascular lesions:
- massive (accompanied by shock / hypotension);
- submassive (accompanied by right ventricular dysfunction without hypotension);
- non-massive (no hemodynamic disturbances or signs of right ventricular failure).

B. By the presence of complications:
- with the development of lung infarction (I26);
- with the development of pulmonary heart (I26.0);
- without mention of acute pulmonary heart (I26.9).

G. By etiology:
- associated with deep venous thrombosis;
- amniotic, associated:
- with abortion (O03-O07);
- ectopic or molar pregnancy (O00-O07, O08.2);
pregnancy and childbirth (O88);
- idiopathic (without an established cause).

Modern diagnostic strategy is based on dividing patients into two categories depending on the risk of early death in PE: patients with high and low risk (Table 3).

The diagnosis of PE in the presence of high-probability signs, especially in combination with shock or hypotension, is based on the use of multi-detector CT. It should be noted that, despite the clinical need for an urgent CT scan, this is not always possible due to the severity of the patient's condition (inability to transport). In such cases, an immediate echocardiography is necessary at the patient's bedside. If signs of RV overload and the impossibility of CT scan are detected, the patient should be treated like a patient with diagnosed PE. If the CT scan is negative, the doctor should look for other causes of the shock.

When a low risk is established, the clinical likelihood of PE is assessed using the analysis of symptoms and predisposing factors. There are several different tables for this, the most common are the Geneva score and the Wells score (Table 5).

When establishing a low risk, ESC (2008) proposes a diagnostic algorithm that takes into account two-level and three-level clinical probability. With a low risk, but high clinical probability, the diagnostic strategy is based on CT. If CT is negative, compression ultrasonographic venography is performed to determine HWT. At a low or intermediate clinical probability, the most appropriate is to determine the level of D-dimer, and at its increased damage - CT. If D-dimer levels are normal and CT results are negative, no treatment is given.

Treatment

With suspected or established PE with shock or hypotension, hemodynamic and respiratory support is required. Acute pancreatic insufficiency with low systemic output leads to death of patients.

Patients with massive and submassive PE should be admitted to the intensive care unit (ward).

Hemodynamic and respiratory support

In patients with PE and reduced cardiac output, arterial hypotension or shock, non-glycoside drugs with a positive inotropic effect, vasopressors (dobutamine, dopamine, norepinephrine, etc.) and the introduction of plasma substitutes are mainly used.

1. Use of blood substitutes is a prerequisite for shock or hypotension. A fairly rapid (≈ 20 ml / min) intravenous administration, as a rule, ≤ 500 ml of plasma substitute (rheopolyglucin, isotonic sodium chloride solution, etc.) can increase the cardiac index from 1.6 to 2.0 l / min / m 2, mainly in patients with normal blood pressure. However, aggressive volume loading in PE can impair RV function by increasing preload and exacerbate hemodynamic disturbances. Therefore, the introduction of fluid to patients with PE should be carried out under the control of the cardiac index.

2. Inotropic support also needed for severe PE. At the same time, the ESC recommendations (2008) consider it possible to use the following drugs:

— Dobutamine and Dopamine - the main drugs used for inotropic support in PE. Increase cardiac output and improve O 2 transport and tissue oxygenation with stable arterial PaO 2. Indicated for PE with low cardiac output and moderate hypotension. They can be used both independently and in combination 1: 1 intravenously.

Dobutamine / dopamine use can be discussed in low CI and normal BP. However, an increase in SI above the physiological norm can increase ventilation-perfusion mismatches with further redistribution of blood flow for obstructed (partially) and non-obstructed vessels.

Dobutamine - IV infusion 5-20 mcg / kg / min.

Dopamine - IV infusion 5-30 mcg / kg / min.

— Norepinephrine used to a limited extent in hypotensive patients. Improves RV function through a direct positive inotropic effect, improves coronary perfusion of the RV through stimulation of peripheral vascular a-adrenergic receptors and an increase in systemic blood pressure. The introduction of norepinephrine (2-30 mcg / min, intravenous drip) is indicated only for massive PE with a significant decrease in blood pressure (systolic blood pressure< 70 мм рт.ст.).

— Adrenalin combines the positive properties of norepinephrine and dobutamine in the absence of systemic vasodilation. In patients with PE, it can be beneficial.

— Isoproterenol, besides inotropic action, induces pulmonary vasodilation, but this positive effect is often leveled by peripheral vasodilation.

3. Vasodilators reduce pressure in the PA and pulmonary vascular resistance. However with the development of acute right ventricular failure the use of vasodilators (nitrates, sodium nitroprusside, etc.) and diuretics contraindicatedbecause they, by decreasing preload and cardiac output, can lead to severe systemic hypotension.

This limitation can be overcome by inhalation administration. There is some evidence of the effectiveness of aerosol administration prostacyclin in the treatment of pulmonary hypertension secondary to pulmonary embolism. Inhalation nitric oxide improves hemodynamics and gas exchange in patients with PE.

Preliminary Usage Data Appeared levosimendan - a drug from the group of non-glycoside cardiotonic drugs, restoring the interaction between the pancreas and PA in acute PE as a result of a combination of pulmonary vasodilation and increased pancreatic contractility. Levosimendan leads to a dose-dependent increase in cardiac output and stroke volume, a dose-dependent decrease in pulmonary capillary pressure, mean blood pressure and total peripheral vascular resistance.

Levosimendan (sindax) - intravenous infusion 0.05-0.2 mcg / kg / min, 24 hours.

There is an increasing interest in the use of endothelin antagonists and phosphodiesterase-5 inhibitors in PE, which weaken the severity of pulmonary hypertension in PE. Using sildenafil reduces the pressure rise in the aircraft. However, to date, only the oral form of the drug is registered in Ukraine, which has proven itself in chronic pulmonary hypertension, but does not allow effective use of the drug in shock.

Sildenafil citrate (revazio) - 0.02 3 r / day.

4. Correction of hypoxemia and hypocapnia often required in patients with PE, although in most cases these changes are of moderate severity. Hypoxemia usually eliminated by nasal oxygen administration and rarely mechanical ventilation. Oxygen consumption should be minimized by measures that reduce fever and agitation, and mechanical ventilation with increased RR. When carrying out mechanical ventilation, it is necessary to limit its side hemodynamic effect. In particular, mechanical ventilation-induced positive intrathoracic pressure may decrease venous return and worsen RV failure in patients with massive PE. Therefore, positive expiratory pressure (end-expiratory) can be applied. A low tidal volume (≈ 6 ml / kg body weight) can be used to achieve an end-inspiratory pressure plateau below 30 cm H2O.

5. Anesthesia - adequate analgesic therapy (using fentanyl, morphine, promedol) eliminates / prevents the development of reflex pain shock, reduces fear and excitement, improves the patient's adaptation to hypoxia.

6. Thrombolytic therapy promotes rapid resorption of thrombolytic obstruction and has a positive effect on hemodynamic parameters. In 80% of cases, the cardiac index increases and in 40% the pressure in the PA decreases 72 hours after treatment with streptokinase.

100 mg of recombinant tissue plasminogen activator (rtAP) at the end of the 2-hour infusion period causes a 30% decrease in PA pressure and a 15% increase in CI, a decrease in vascular obstruction, a decrease in the end-diastolic volume of the pancreas, while the introduction of heparin does not give any changes. Urokinase and streptokinase give similar results at the end of the infusion period\u003e 12-24 hours. 100 mg rtAP administered\u003e 2 hours give faster angiographic and hemodynamic results than urokinase 4400 U / kg / h, but by 24 hours the differences disappear.

Direct administration of rtAP into LA does not provide advantages over systemic administration. Rapid (15 min) administration of rtAP has advantages over two-hour administration.

Heparin is not a competitor to thrombolytic therapy, but it certainly complements it.

Overall, 92% of PE patients are classified as requiring thrombolysis in the first 36 hours. A significant effect is observed up to 48 hours, then the effectiveness progressively worsens, but thrombolysis can be performed in patients with PE within 6-14 days. Thrombolysis one week after the episode results in improvement, but the differences in efficacy with heparin are not significant.

There is a risk of bleeding during thrombolysis, especially in persons with intercurrent diseases (13%). In 1.8% of patients after thrombolysis, intracerebral hemorrhage occurs. Therefore, contraindications must be taken into account.

Contraindications to fibrinolytic therapy

1. Absolute:

- Hemorrhagic (or unknown origin) stroke in history.

- Ischemic stroke in the previous 6 months.

- Recent major trauma / surgery / head injury (3 weeks).

- Gastrointestinal bleeding within 1 month.

- Other known bleeding.

2. Relative:

- Transient ischemic attack within 6 months.

- Oral anticoagulant therapy.

- Pregnancy and 1 week. after childbirth.

- Uncovered wounds.

- Traumatic resuscitation.

- Refractory hypertension (SBP\u003e 180 mm Hg).

- Severe liver disease.

- Infective endocarditis.

- Active peptic ulcer.

Thrombolytic therapy is the first line of treatment for patients at high risk of PE, starting with cardiogenic shock and / or arterial hypotension, with a very small number of absolute contraindications.

At intermediate risk, thrombolysis is discussed in light of research findings and relative contraindications.

Thrombolysis is not indicated at low risk.

7. Surgical pulmonary embolectomy useful in patients with absolute contraindications to thrombolysis or in case of its ineffectiveness. Despite the high efficiency of thrombolytic therapy, it is important to note that 30-40% of patients with PE have relative contraindications, and 20% develop various bleeding, and 3% of patients have intracerebral bleeding.

8. Percutaneous catheter embolectomy and fragmentation performed in the presence of proximal LA thrombi as an alternative to surgical treatment. The operation is performed only on large vessels (main and lobar) and is not performed on segmental pulmonary arteries.

9. Relatively compression bandages there is no reliable data on their effectiveness in PE, but with HVT, wearing elastic stockings reduces the number of new cases of PE with significant differences after 2 years. When diagnosed with HBT, wearing elastic stockings for 1 year reduces the number of recurrences of proximal HBT.

10. Initial anticoagulation.

Anticoagulant therapy (ACT) has played a major role in the management of patients with PE since 1960, when D.W. Barrit and S.C. Jordan have proven the use of anticoagulation in the prevention of death and relapse.

Rapid anticoagulation can only be achieved with parenteral drugs: intravenous unfractionated heparin (heparin), subcutaneous low molecular weight heparin (LMWH), or fondaparinux sodium.

The IV heparin regimen is based on the APTT (activated partial thromboplastin time), which should be determined 4-6 hours after the initial bolus and then 3 hours after each dose change or daily after the target dose is reached. As a rule, intravenous administration of heparin begins with a bolus of 80 U / kg, followed by an infusion of 18 U / kg / h, with a change in the mode of administration depending on the APTT (Table 7).

When prescribing unfractionated heparin, it is not the dose that is fixed, but the clotting indices!

LMWH are often used in pulmonary embolism and are much more convenient to use. They should not be used in critically ill patients with a "high risk of death", hemodynamically unstable, renal failure with GFR< 30 мл/мин (гепарин не выводится почками). Это же относится к синтетическому ингибитору Ха-фактора — фондапаринуксу.

As of today, not all LMWH have been tested at PE, in addition, not all of them are registered in Ukraine (Table 8).

Other LMWHs can be used with success for HBT.

Parenteral ACT is prescribed for 5-7 days, and with HBT and / or the appointment of heparin - 10-14 days. The target level of anticoagulation is to achieve a level of international normalization ratio (INR) in the range of 2.0-3.0. If this level is maintained for at least 2 days, you can switch to oral anticoagulants (warfarin) in accordance with the recommended ESC (2008) tactics "Long-term anticoagulation and secondary prevention". It is best to start warfarin with a dose of 10 mg in otherwise healthy persons under 60 years of age and with 5 mg in the elderly. Subsequently, the doses of warfarin are adjusted depending on the INR with a target level of 2.5.

A number of new oral anticoagulants, in particular Xa and IIa inhibitors, do not require monitoring; they are currently in the final stage of clinical trials.

ACT should begin immediately in patients with established PE, as well as at high and medium probability, as soon as the examination is started.

Patients with a high risk of bleeding and severe renal failure are prescribed only unfractionated heparin.

Treatment strategy

Patients at high risk of pulmonary embolism. Patients with PE and shock or hypotension (presumed to be massive PE) have a high risk of nosocomial death within the first hours. Once the diagnosis is established, such patients undergo thrombolysis and / or heparin is prescribed. In case of absolute contraindications / ineffectiveness of thrombolysis, surgical embolectomy (catheter thrombofragmentation) is performed.

Low risk of PE. Normotensive patients with a low risk of PE have a favorable short-term prognosis. In most cases (absence of chronic renal failure and high risk of bleeding), LMWH or fondaparinux subcutaneously weight-based, without monitoring, is used.

Intermediate The risk of PE is determined upon admission in hemodynamically stable patients, but with evidence of RV dysfunction and / or myocardial injury. Thrombolysis is indicated, but if heparin treatment was started earlier, then thrombolysis does not make sense.

Low the risk is determined in patients with the absence of fundamental risk factors associated with PE, for whom early discharge from the hospital is planned.

Treatment for high risk of PE

- ACT with heparin should be started without delay.

- Thrombolytic therapy should be used immediately in patients with cardiogenic shock and / or arterial hypotension.

- Systemic hypotension should be corrected to prevent the progression of RV failure and death.

- In hypotensive patients, vasopressor agents are used.

- Oxygen should be prescribed in patients with hypoxemia.

- Dobutamine and dopamine can be used in patients with PE with normal blood pressure and low cardiac output.

- Catheter embolectomy or fragmentation of thrombi in the proximal PA can be performed as an alternative to surgical treatment in patients with absolute contraindications to thrombolysis or if it is ineffective.

Low-risk treatment for PE

- Initial ACT should be carried out for at least 5 days and then replaced with vitamin K antagonists only after reaching the target INR for at least 2 consecutive days.

- In patients with intermediate risk, ACT should begin simultaneously with the beginning of the PE diagnosis and be carried out in parallel with it.

- In patients with a high risk of bleeding and severe renal dysfunction, unfractionated heparin is used with a target APTT of 1.5-2.5 times the norm.

Long-term anticoagulation and secondary prevention

Long-term ACT in patients with PE is intended to prevent fatal and non-fatal recurrent VTE.

Vitamin K antagonists are the most widely used, but LMWH may be an effective and safe alternative in cancer patients. The target dose of vitamin K antagonists is determined by an INR ≈ 2.5 (2.0-3.0). A statistically significant decrease in the number of PE relapses is noted after 4-6 weeks of treatment. Therefore, the duration of treatment cannot be less than 4-9 weeks. Discontinuation of treatment leads to a return of the risk of PE. Negative determination of D-dimer after 1 month. after the termination of treatment with warfarin indicates the preservation and positive effect of treatment.

Sodium warfarinate (warfarin) - t. 1; 2.5; 3; 5 mg orally 1 r / day.

It should be remembered that the action of warfarin is enhanced in combination with other drugs, and in particular with non-steroidal anti-inflammatory, antibacterial, ethyl alcohol, etc. The inconvenience for patients is the regular determination of INR.

With long-term ACT, the risk of bleeding increases.

Currently, research is underway on promising anticoagulants, oral factor Xa inhibitors (rivaroxaban and apixaban).

Venous filters. Installing a filter in the inferior vena cava as a method of preventing PE was first proposed by Trousseau in 1868. But venous filters became available only after 1960, when percutaneous insertion techniques became possible. Filters are usually located in the infrarenal part of the inferior vena cava (cava filters).

Kava filters are classified into temporary (set for the period of childbirth, surgery, course of thrombolytics) and permanent (installed in venous thrombosis with the danger of blood clots rupture). In this case, the detached thrombus does not enter the heart, but is retained by the filter. In Ukraine, the most commonly used cava filters "Osot".

Venous filters are especially recommended:
- with absolute contraindications to prolonged ACT and a high risk of repeated VTE;
- established proximal HVT;
- planned surgery with a high risk of bleeding;
- repeated VTE, despite ongoing anticoagulation.

Permanent filters contribute to lifelong prevention of PE, but they are associated with complications including recurrent HBT and post-thrombotic syndrome.

Complications are possible:
- early - intercalary thrombosis (10% of patients);
- late - recurrent HBT (20% of patients), post-thrombotic syndrome (40%).

In general, occlusion of the inferior vena cava (complete or partial) develops in 22% of patients within 5 years, in 33% within 9 years, depending on the use and duration of ACT.

Routine installation of filters in patients with PE is not recommended.

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