Thromboembolism of the pulmonary artery (PE)

Thromboembolism of the pulmonary artery (PE) - the occlusion of one or more pulmonary arteries by thrombi, which are formed elsewhere, usually in large veins of the lower extremities or pelvis.

Risk factors are conditions that worsen the venous influx and cause damage or dysfunction of the endothelium, especially in patients with hypercoagulable conditions. Symptoms of pulmonary embolism (PE) include shortness of breath, pleural pain in the chest, cough and in severe cases of fainting or stopping of the heart and breathing. The changes identified are vague and may include tachypnea, tachycardia, hypotension, and enhancement of the pulmonary component of the second heart tone. The diagnosis is based on data from ventilation-perfusion scanning, CT with angiography or pulmonary arteriography. Treatment of pulmonary embolism (PE) is carried out by anticoagulants, thrombolytic agents and sometimes by surgical methods aimed at removing thrombus.

Thromboembolism of the pulmonary artery (PE) is observed in approximately 650,000 people and causes up to 200,000 deaths per year, representing approximately 15% of all hospital deaths per year. The prevalence of pulmonary embolism (PE) in children is approximately 5 per 10 000 receipts.

Causes of pulmonary embolism

Almost all pulmonary embolisms are the result of thrombosis in the lower extremities or pelvic veins (deep venous thrombosis [GWT]). Thrombus in any system can be dumb. Thromboembolism may also occur in the veins of the upper limbs or in the right heart. Risk factors for deep venous thrombosis and pulmonary embolism (PE) are the same in children and adults, and include conditions that worsen the venous influx or cause damage or endothelial dysfunction, especially in patients with an initially present hypercoagulable state. Bed rest and the restriction of walking, even for several hours, are characteristic provoking factors.

Once a deep venous thrombosis develops, the thrombus can break away and move through the venous system to the right heart, then linger in the pulmonary arteries where one or more vessels are partially or completely closed. The consequences depend on the size and number of emboli, the reaction of the lungs and the ability of the person's internal thrombolytic system to dissolve the thrombus.

Small emboli may not have any acute physiological effects; many begin to lyse immediately and dissolve within hours or days. Large emboli can cause a reflex increase in ventilation (tachypnea); hypoxemia due to ventilation-perfusion (V / P) mismatch and shunting; atelectasis due to alveolar hypocapnia and disturbances of the surfactant and an increase in pulmonary vascular resistance caused by mechanical obstruction and vasoconstriction. Endogenous lysis reduces most emboli, even large enough, without treatment, and physiological responses decrease within hours or days. Some emboli are resistant to lysis and can be organized and preserved. Sometimes chronic residual obstruction leads to pulmonary hypertension (chronic thromboembolic pulmonary hypertension), which can develop over the years and lead to chronic right ventricular failure. When large emboli enclose large arteries or when many small emboli cover more than 50% of the distal arteries of the system, pressure in the right ventricle increases, causing acute right ventricular failure, failure with shock (massive pulmonary embolism (PE)), or sudden death in severe cases. The risk of death depends on the degree and frequency of pressure increase in the right heart and from the previous cardiopulmonary status of the patient; higher blood pressure is more common in patients with pre-existing heart disease. Healthy patients can survive pulmonary embolism, which obturates more than 50% of the pulmonary vascular bed.

[1], [2], [3]

Risk factors for deep venous thrombosis and pulmonary embolism (PE)

• Age> 60 years
• Atrial fibrillation
• Smoking cigarettes (including passive smoking)
• Modulators of estrogen receptors (raloxifene, tamoxifen)
• Injuries to extremities
• Heart failure
• Conditions of hypercoagulation
• Antiphospholipid syndrome
• Deficiency of antithrombin III
• Mutation factor V Leiden (activated protein resistance C)
• Heparin-induced thrombocytopenia and thrombosis
• Hereditary defects of fibrinolysis
• Hyperhomocysteinemia
• Increased factor VIII
• Increase factor XI
• Increase in von Willebrand factor
• Paroxysmal nocturnal hemoglobinuria
• Deficiency of Protein C
• Deficiency of Protein S
• Genetic defects of prothrombin GA
• Fabric Factor Pathway Inhibitor
• Immobilization
• Conduction of venous catheters
• Malignant neoplasms
• Myeloproliferative diseases (high viscosity)
• Nephrotic syndrome
• Obesity
• Oral contraceptives / estrogen replacement therapy
• Pregnancy and the puerperium
• Previous venous thromboembolism
• Sickle-cell anemia
• Surgical intervention in the previous 3 months

Lung infarction occurs in less than 10% of patients with diagnosed pulmonary embolism (PE). This low percentage is attributed to the double blood supply to the lungs (ie bronchial and pulmonary). An infarct is typically characterized by an X-ray-detected infiltrate, chest pain, fever, and, occasionally, hemoptysis.

Non -rombotic thromboembolism of the pulmonary artery (PE)

Thromboembolism of the pulmonary artery (PE), which develops from a variety of non-thrombotic sources, causes clinical syndromes that differ from thrombotic pulmonary embolism (PE).

Air embolism occurs when a large amount of air is injected into the system veins or into the right heart, which then moves into the pulmonary arterial system. Causes include surgery, blunt or barotrauma (for example, with artificial ventilation), the use of defective or uncovered venous catheters and rapid decompression after underwater diving. Formation of microbubbles in a small circle of blood circulation can cause damage to the endothelium, hypoxemia and diffuse infiltration. With air embolism of large volume, obstruction of the pulmonary outflow tract can occur, which can lead to rapid death.

Fat embolism is caused by the ingress of fat or bone marrow particles into the systemic venous blood stream and then into the pulmonary arteries. Causes include fractures of long bones, orthopedic procedures, capillary occlusion or bone marrow necrosis in patients with a crisis in sickle cell anemia and, rarely, toxic modification of native or parenteral serum lipids. Fat embolism causes pulmonary syndrome, similar to acute respiratory distress syndrome, with severe hypoxemia with a rapid onset, often accompanied by neurologic changes and petechial rash.

Embolism with amniotic fluid is a rare syndrome caused by the ingestion of amniotic fluid into the maternal venous pathway and then into the pulmonary arterial system during or after delivery. The syndrome can sometimes occur with prenatal manipulations on the uterus. Patients may have cardiac shock and respiratory distress due to anaphylaxis, vasoconstriction causing acute severe pulmonary hypertension, and direct damage to pulmonary capillaries.

Septic embolism occurs when the infected material enters the lungs. The reasons include the use of narcotic substances, infective endocarditis of the right valves and septic thrombophlebitis. Septic embolism causes symptoms and manifestations of pneumonia or sepsis and is initially diagnosed when focal infiltrates are detected on chest radiographs, which can be enlarged to the periphery and abscessed.

Embolism of foreign bodies is caused by the ingress of particles into the pulmonary arterial system, usually due to intravenous administration of inorganic substances, for example talcum heroin addicts or mercury patients with mental disorders.

Tumor embolism is a rare complication of malignant neoplasms (usually adenocarcinomas), in which tumor cells from the tumor enter the venous and pulmonary arterial system where they linger, multiply and obstruct the blood flow. Patients usually have symptoms of shortness of breath and pleural pain in the chest, as well as signs of pulmonary heart that develop within weeks and months. The diagnosis, which is suspected in the presence of small-node or diffuse pulmonary infiltration, can be confirmed by biopsy or sometimes by cytological examination of the aspirated fluid and by histological examination of pulmonary capillary blood.

Systemic embolism is a rare syndrome that occurs during barotrauma during mechanical ventilation of the lungs with high pressure in the airways, which leads to air rupture from the lung parenchyma into the pulmonary veins and then into the systemic arterial vessels. Gas emboli cause CNS lesions (including stroke), heart damage, and reticular livedo reticularis on the shoulders or on the anterior chest wall. The diagnosis is based on the exclusion of other vascular processes in the presence of an established barotrauma.

Symptoms of thromboembolism of the pulmonary artery

Most pulmonary embolisms are small, physiologically insignificant and asymptomatic. Even if they do occur, the symptoms of pulmonary embolism (PE) are non-specific and vary in frequency and intensity, depending on the prevalence of pulmonary vascular occlusion and the previous cardiopulmonary function.

Large emboli cause acute dyspnoea and pleural pain in the chest and, more rarely, cough and / or hemoptysis. Massive pulmonary embolism (PE) causes hypotension, tachycardia, fainting or cardiac arrest.

The most common symptoms of pulmonary embolism (PE) are tachycardia and tachypnea. Less often, patients have hypotension, a loud second heart tone (S2) due to an increase in the pulmonary component (P) and / or crackling and wheezing. In the presence of right ventricular failure, there may be a well visible swelling of the internal jugular veins and right ventricular bulging, the rhythm of the canter of the right ventricle (third and fourth heart tones [S3 and S4), with or without tricuspid regurgitation, can be heard. A fever is possible; deep venous thrombosis and pulmonary embolism (PE) are often excluded as possible causes of fever.

Chronic thromboembolic pulmonary hypertension causes symptoms and manifestations of right ventricular failure, including shortness of breath during physical exertion, rapid fatigue and peripheral edema that develop within months and years.

Diagnosis of pulmonary embolism

The diagnosis is uncertain, since the symptoms and manifestations are not specific, and diagnostic tests are either imperfect or invasive. The diagnosis begins with the inclusion of pulmonary embolism (PE) in the differential diagnostic list of a large number of conditions with similar symptoms, including cardiac ischemia, heart failure, exacerbation of COPD, pneumothorax, pneumonia, sepsis, acute chest syndrome (in patients with sickle cell anemia ) and acute anxiety with hyperventilation. The initial examination should include pulse oximetry, ECG and chest X-ray. Radiography of the chest is usually nonspecific, but can reveal atelectasis, infiltration foci, high diaphragm dome standing and / or pleural effusion. Classical findings are the focal disappearance of the vascular component (a Westermarck symptom), the peripheral triangular infiltrate (Hampton triangle), or the expansion of the right descending pulmonary artery (Pall's symptom), but they are suspicious but insensitive symptoms.

Pulse oximetry is a method of rapid assessment of oxygenation; one of the signs of pulmonary embolism (PE) is hypoxemia, but other expressed disorders should be investigated.

The ECG most often reveals tachycardia and various changes in the ST-T segment that are not specific for pulmonary embolism (PE). Symptom SQT or newly appeared blockade branch of the right leg of the bundle His can indicate the effect of a sharp increase in pressure in the right ventricle to hold on the right ventricle; they are specific, but insensitive, occurring only in about 5% of patients. The deviation of the electric axis to the right and P pulmonale may be present. Inversion of the T wave in the leads 1 - 4 also occurs.

The clinical probability of pulmonary embolism (PE) can be assessed by comparing ECG data and chest X-ray with anamnesis and objective examination data. Patients with a low clinical probability of pulmonary embolism (PE) may need only a minimal additional study or do not need a follow-up at all. Patients with an intermediate clinical probability need additional study. Patients with high probability may be candidates for immediate treatment pending the results of additional studies.

[4], [5], [6], [7],

Noninvasive diagnosis of pulmonary embolism

Non-invasive studies can usually be performed more quickly and rarely cause complications than invasive studies. The most informative tests for diagnosis and exclusion of pulmonary embolism (PE) are studies of D-dimer, ventilation-perfusion scanning, duplex ultrasonography, spiral CT and echocardiography.

There is no universally accepted algorithm for selecting and sequencing studies, but the general requirements are to perform a screening study of D-dimer and ultrasonography of the lower limbs. If the D-dimer is positive, and there are no thrombi from ultrasound, then further CT or V / P determination is performed. Patients with moderate and high probability of pulmonary embolism (PE) by clinical criteria, but having a low or doubtful probability according to the results of W / P, usually require pulmonary arteriography or spiral CT to confirm or exclude the diagnosis. Positive results of ultrasound examination of the lower extremities establish the need for anticoagulant therapy and eliminate the need for further diagnostic research. Negative results of ultrasound study do not exclude the need for additional studies. Positive D-dimer, ECG, arterial blood gas measurements, chest X-ray and echocardiogram are additional studies that are not specific enough to be considered diagnostic without other data.

D-dimer is a by-product of internal fibrinolysis; thus, elevated levels suggest recent thrombosis. The test is extremely sensitive; More than 90% of patients with GWT / LE have elevated levels. However, a positive result is not specific for a venous thrombus, as the level is elevated in many patients without GVT / LE. In contrast, low D-dimer has a negative predictive value of more than 90%, allowing to exclude deep venous thrombosis and pulmonary embolism, especially when the initial assessment of the probability of the disease is less than 50%. There are reported cases of pulmonary embolism (PE) with negative results of D-dimer study, if old methods of enzyme-linked immunosorbent assay are used, but newer, highly specific and rapid methods make negative D-dimer a sufficiently reliable test to exclude the diagnosis of pulmonary embolism (PE) in normal practice.

The V / P scan allows you to detect areas of the lung that are ventilated, but not blood supply, which occurs with pulmonary embolism (PE); the results are assessed as a low, intermediate or high probability of pulmonary embolism (PE), based on the results of W / R. Completely normal scan results essentially exclude pulmonary embolism with almost 100% accuracy, but results with low probability still retain a 15% probability of pulmonary embolism (PE). Deficiency of perfusion can occur in many other conditions, including pleural effusion, chest tumors, pulmonary hypertension, pneumonia and COPD.

Duplex scanning is a safe, non-traumatic, portable method for detecting thrombi of the lower limbs (primarily the femoral vein). The thrombus can be detected in three ways: visualizing the vein contour, demonstrating the non-squeezing of the vein and revealing the reduced fluxes in the Doppler study. The study has a sensitivity of more than 90% and a specificity of more than 95% for thrombosis. The method does not allow the reliable detection of a thrombus in the veins of the tibia or iliac veins. The absence of blood clots in the femoral veins does not exclude the possibility of thrombosis of other localizations, but patients with negative results of duplex ultrasonography have a more than 95% survival rate without the development of pulmonary embolism (PE), as thrombi from other sources are much less common. Ultrasonography has been included in many diagnostic algorithms, as the results of the study revealing thrombosis of the femoral vein indicate the need for anticoagulant therapy, which may make further studies on pulmonary embolism or other thromboses superfluous.

Spiral CT with contrasting is in many cases an alternative to I / P scans and pulmonary arteriography, because it is a quick, affordable and non-invasive method and gives more information about another lung pathology. However, the patient should be able to hold his breath for a few seconds. The sensitivity of CT is highest for pulmonary embolism (PE) in the lobar and segmental vessels and is lowest for emboli in small subsegmental vessels (approximately 30% of all LE) and is thus generally less sensitive than perfusion scanning (60% c> 99%). It is also less specific than pulmonary arteriograms (90% compared to> 95%), since visual findings may result from incomplete contrast mixing. Positive scan results may be diagnostic for pulmonary embolism (PE), but negative results do not necessarily exclude subsegmental lesions, although the clinical significance of embolism in small subsegmental vessels needs to be clarified. Newer scanners with higher resolution are likely to improve diagnostic accuracy and, thus, will be able to replace perfusion scanning and arteriograms.

The expediency of echocardiography as a diagnostic test for pulmonary embolism (PE) is ambiguous. Its sensitivity is more than 80% for the detection of right ventricular dysfunction (eg, dilatation and hypokinesia, which occur if the pulmonary artery pressure exceeds 40 mm Hg). It is a useful method for determining the severity of hemodynamic disorders in acute pulmonary embolism (PE), but right ventricular dysfunction is present in many conditions, including COPD, heart failure and nighttime apnea syndrome, and is therefore a nonspecific method of investigation. Evaluation of the systolic pressure of the pulmonary artery, using Doppler flow studies, provides additional useful information on the severity of acute pulmonary embolism (PE). The absence of right ventricular dysfunction or pulmonary hypertension makes a diagnosis of a large pulmonary embolism (PE) unlikely, but does not exclude it completely.

The study of cardiospecific markers is considered a useful method of stratifying the risk of mortality in patients with acute pulmonary embolism (PE). Elevated levels of troponin may indicate damage to the right ventricle. Elevated brain natriuretic peptide (BNP) and npo-BNP levels do not represent diagnostic significance, but low levels probably reflect a good prognosis. The clinical significance of these tests should be determined, since they are not specific for either right ventricular dilatation or pulmonary embolism (PE).

Investigation of the gas composition of the arterial blood and PaCO2 exhaled air allows us to evaluate the physiological dead space (ie, the fraction of the ventilating, but not the blood-supplying lung). When the dead space is less than 15% and the D-dimer level is low, the negative predictive value for acute pulmonary embolism (PE) is 98%.

Invasive diagnosis of pulmonary embolism

Pulmonary angiography is prescribed in cases where the probability of pulmonary embolism (PE) according to previous studies is moderate or high, and non-invasive tests do not provide definitive information; when there is an urgent need to confirm or exclude a diagnosis, for example in an acutely ill patient; and when anticoagulant therapy is contraindicated.

Pulmonary arteriography is still the most accurate research method for the diagnosis of pulmonary embolism (PE), but the need for it arises much less often due to the sensitivity of ultrasonography and spiral CT. An arteriogram with intraluminal filling defects or a sharp reduction in flow is positive. Suspicious results of the study, but not diagnostic for pulmonary embolism (PE), include partial occlusion of the pulmonary arterial branches with an increase in the proximal caliber and a decrease in the distal sections, hypovolemic zones and a delay in contrast in the proximal artery during the late (venous) phase of the arteriogram. In segments of the lung with obstructed arteries, the venous filling with contrast medium is delayed or absent.

Treatment of thromboembolism of the pulmonary artery

Initial treatment of pulmonary embolism (PE) includes oxygen therapy for the correction of hypoxemia and intravenous administration of 0.9% saline and vasopressors for the treatment of hypotension. All patients with severe suspected or confirmed pulmonary embolism (PE) should be hospitalized and ideally should be monitored for a long time to identify life-threatening cardiovascular complications in the first 24-48 hours. Follow-up treatment includes anticoagulant therapy and sometimes thrombus removal.

Thrombus removal

Lysis or removal of thrombus should be considered in patients with hypotension. It can also be administered to patients with clinical, ECG and / or echocardiographic signs of right ventricular overload or insufficiency, but data supporting this approach are not absolute. Elimination of a thrombus is achieved with the use of embobectomy or intravenous thrombolytic therapy.

Embolectomy prescribed to patients with pulmonary embolism (PE), which are on the verge of stopping the heart or respiration (constant systolic blood pressure <90 mm Hg. V. After the administration of fluids and O ₂ -therapy, or if required vasopressor therapy). Absorption or fragmentation of the embolus through a catheter in the pulmonary artery minimizes the complicated course of surgical embollectomy, but the benefits of this technique are not proven. Surgical embolectomy probably improves survival in patients with massive pulmonary arterial thromboembolism (PE), but is not widely available and is associated with high mortality. The decision to perform embobectomy and choice of technique depends on local capabilities and experience.

Thrombolytic therapy with tissue plasminogen activator (tPA), streptokinase or urokinase suggests a non-invasive pathway for rapid recovery of pulmonary blood flow, but is controversial, since the remote benefit does not substantially outweigh the risk of bleeding. Thrombolytics accelerate the resolution of radiographic changes and restore hemodynamic functions (heart rate and right ventricular function) and prevent cardiopulmonary decompensation in patients with submaxive pulmonary arterial thromboembolism (PE), but do not improve survival. Some authors recommend thrombolytics for normotensive patients with pulmonary embolism (PE) with echocardiographic signs of proximal pulmonary artery embolism or right ventricular dysfunction due to pulmonary embolism (PE) or pre-existing disease. Others recommend thrombolytic therapy for patients with massive pulmonary embolism (PE) (hypotension, hypoxemia or obstruction of 2 or more lobar arteries). Absolute contraindications to thrombolysis include a previous hemorrhagic stroke; active bleeding from any source; intracranial trauma or surgery within 2 months; recent puncture of the femoral or other major artery; gastrointestinal bleeding, including positive tests for occult blood (<6 months); and cardiopulmonary resuscitation. Relative contraindications include recent surgery (<10 days), hemorrhagic diathesis (eg, with liver failure), pregnancy and severe arterial hypertension (systolic BP> 180 or diastolic blood pressure> 110 mm Hg).

For thrombolysis, streptokinase, urokinase and alteplase (recombinant tPA) can be used. None of these drugs has demonstrated a clear advantage over others. Standard intravenous regimens are streptokinase 250,000 units for more than 30 minutes, then continued infusion of 100,000 units per hour for 24 hours; urokinase 4400 U / kg for more than 10 minutes, continue 4400 U / kg / h for 12 hours; or alteplase 100 mg continued administration for more than 2 hours, followed by an additional administration of 40 mg for another 4 hours (10 mg / h) or tenecteplase (the dose is calculated according to body weight, the maximum dose should not exceed 10,000 units 50 mg. The required dose of the drug is administered by a rapid single intravenous injection for 5-10 s). If the clinical manifestations and recurrent pulmonary angiograms indicate a lack of lysis of the thrombus and the initial dosages do not cause bleeding. Streptokinase is now rarely used, since it often causes allergic and pyrogenic reactions and requires a prolonged administration.

The initial introductory dose of heparin should be administered concomitantly, but the activated TTV should be allowed to drop 1.5-2.5 times the baseline level before the onset of continuous infusion. Direct destruction by thrombotic thromboly when administered via a pulmonary artery catheter is sometimes used in patients with massive pulmonary embolism (PE) or for patients with relative contraindications to systemic thrombolysis, but this approach does not prevent systemic thrombolysis. If bleeding occurs, it can be completely discontinued by cryoprecipitate or freshly frozen plasma and by compression of available vascular sites.

Anticoagulant therapy

Because venous thromboses rarely embolize completely, anticoagulant therapy is prescribed urgently, in order to prevent an increase in residual clot and embolism. Patients who are contra-indicated with anticoagulants or whose thromboembolism occur despite therapeutic anticoagulation should undergo percutaneous filter placement in the inferior vena cava.

Heparin, either unfractionated or low molecular, is the basis for the treatment of acute deep venous thrombosis and pulmonary embolism (PE) and should be administered immediately when diagnosed, or as soon as possible if the clinical suspicion is high; Inadequate anticoagulant therapy in the first 24 hours is associated with an increased risk of recurrent pulmonary embolism within 3 months. Heparin accelerates the effect of antithrombin-III, an inhibitor of coagulation factors; unfractionated heparin also has antithrombin III, whose mediated anti-inflammatory properties can promote thrombus organization and reduce thrombophlebitis. The unfractionated heparin is administered bolus and infusion according to the protocol, reaching an activated TTV 1.5-2.5 times higher than normal control. Subcutaneous administration of low molecular weight heparin (LMWH) is as effective as the administration of unfractionated heparin, and causes less thrombocytopenia. Because of the long half-life, this drug is suitable for outpatient treatment of patients with deep venous thrombosis and contributes to an earlier discharge of patients who did not achieve therapeutic anticoagulation with warfarin.

All heparins can cause bleeding, thrombocytopenia, hives and, rarely, thrombosis or anaphylaxis. Prolonged use of heparin can cause hypokalemia, increased levels of liver enzymes and osteoporosis. Screening of patients for possible bleeding is carried out by repeated studies of a clinical blood test and tests for latent blood in the stool. Bleeding due to excessive heparinization can be stopped by prescribing a maximum of 50 mg protamine per 5000 U of unfractionated heparin (or 1 mg in 20 ml of a conventional saline solution administered for more than 10-20 min for LMWH, although the exact dose is not determined, since protamine only partially neutralizes the inactivation of LMWH factor Xa). Treatment with heparin or LMWH should continue until complete anticoagulation is achieved with oral administration of warfarin. The use of LMWH for prolonged anticoagulant therapy after acute pulmonary embolism (PE) has not been studied, but will probably be limited by the cost and complexity of the application compared with oral administration of warfarin.

Warfarin is the oral drug of choice for long-term anticoagulant therapy in all patients, except for pregnant women and patients with new or progressive venous thromboembolism amidst treatment with warfarin. The drug begins with a dose of 5-10 mg in the form of tablets once a day for the first 48 hours from the onset of effective heparinization or, rarely, in patients with protein C deficiency only after therapeutic hypocoagulation is achieved. The therapeutic goal is usually MHO within 2-3.

Physicians prescribing warfarin should beware of multiple drug interactions, including interaction with over-the-counter medicinal herbs. Patients with transient risk factors for deep venous thrombosis or pulmonary embolism (PE) (for example, fracture or surgery) may stop taking the drug after 3-6 months. Patients with persistent risk factors (eg, hypercoagulability) who do not have identified risk factors or after repeated deep venous thromboses or pulmonary embolisms should take warfarin for at least 6 months or possibly for life, unless complications develop . In low-risk patients, warfarin is prescribed in low-intensity mode (to support MHO within 1.5-2.0) and can be safe and effective for at least 2-4 years, but this regimen requires further safety evidence, before than can be recommended. Bleeding is the most frequent complication of warfarin treatment; patients older than 65 years and having concomitant diseases (especially diabetes mellitus, recent myocardial infarction, hematocrit <30%, creatinine> 1.5 mg / dl) and a history of stroke or gastrointestinal bleeding are likely to be at the highest risk group. Bleeding can be completely stopped by subcutaneous or oral administration of 2.5-10 mg of vitamin K and, in severe cases, freshly frozen plasma. Vitamin K can cause sweating, local pain and, rarely, anaphylaxis.

The filtering of the inferior vena cava (cava filter, CF) is prescribed for patients with contraindications to canticoagulant therapy and thrombolysis, with recurrent embolisms on adequate anticoagulation or after pulmonary embolectomy. There are several types of filters that differ in size and replaceability. The filter is placed by catheterization of internal jugular or femoral veins; optimal location - just below the entrance of the renal veins. Filters reduce acute and subacute thromboembolic complications, but are associated with later complications; for example, venous collaterals can develop and provide a bypass pathway through which pulmonary embolism (PE) can develop around the filter. Patients with recurrent deep venous thrombosis or chronic risks of developing deep venous thrombosis may therefore still require anticoagulation; filters provide some protection as long as contraindications to anticoagulation do not disappear. Despite the wide use of filters, the effectiveness in preventing pulmonary embolism (PE) has not been studied and proven.

[8], [9], [10], [11], [12]

Prevention of thromboembolism of the pulmonary artery

Prevention of thromboembolism of the pulmonary artery (PE) means prevention of deep venous thrombosis; The need depends on the risk the patient has. Patients and patients who have undergone surgical, especially orthopedic, interventions are most needed, and most of these patients should be identified before a blood clot forms. Thromboembolism of the pulmonary artery (PE) is prevented by the appointment of low doses of unfractionated heparin (UFH), LMWH, warfarin, new anticoagulants, compression devices and stockings.

The choice of medication or device depends on the duration of treatment, contraindications, relative costs and ease of use.

NDNPH is administered at a dose of 5000 U.sub.2 subcutaneously 2 hours prior to surgery and every 8-12 hours thereafter for 7-10 days or until the patient becomes completely ambulatory. Immobilized patients who do not undergo surgery should receive 5,000 units of SC subcutaneously every 12 hours indefinitely or until the risk disappears.

The dosage of LMWH depends on the drug: 30 mg of enoxaparin subcutaneously every 12 hours, dalteparin of 2500 units once a day, and tinzaparin at a dose of 3500 units once a day are only three of the many equally effective LMWH that are not inferior to NDHP in terms of preventing deep venous thrombosis and thromboembolism of the pulmonary artery (PE).

Warfarin is usually effective and safe at a dose of 2-5 mg once a day or in a dose adjusted to maintain MHO within 1.5-2.

Newer anticoagulants, including hirudin (subcutaneous direct thrombin inhibitor), ximelagatran (melagatran, oral direct thrombin inhibitor) and danaparoid and fondaparinux, which are selective inhibitors of factor Xa, have shown efficacy in deep venous thrombosis and prevention of pulmonary embolism (PE) but require further investigation to determine their profitability and safety with respect to heparins and warfarin. Aspirin is more effective than placebo, but worse than all other available drugs, to prevent deep venous thrombosis and pulmonary embolism (PE).

Intermittent pneumatic compression (PKI) provides rhythmic external compression of the shins or from the shins to the thighs. It is more effective for the prevention of throat throat than for proximal deep venous thrombosis, and is therefore considered ineffective after surgical intervention on the hip or knee joint. PKI is contraindicated in obese patients and can theoretically cause pulmonary embolism in immobilized patients who have developed mute deep venous thrombosis or who have not received preventive treatment.

Graduated elastic stockings have questionable efficacy, except for low-risk surgical patients. However, combining stockings with other preventive measures can be more effective than either of these measures alone.

For surgical interventions with a high risk of venous thromboembolism, such as orthopedic operations on the hip joint and lower limb, the appointment of NDNPH and aspirin is not adequate; LMWH and a selected dose of warfarin are recommended. In prosthetic knee replacement, the risk reduction provided by LMWH and PKI is comparable, the combination is considered for patients with concomitant clinical risks. When orthopedic surgery, drugs can be started to be administered in the preoperative period, taking medications under this scheme should be continued for at least 7 days after the operation. In some patients with a very high risk of both venous thromboembolism and bleeding, the setting of intravenous CF is a preventive measure.

High frequency of venous thromboembolism is also associated with some types of neurosurgical interventions, acute spinal cord injury and polytrauma. Although physical methods (PKI, elastic stockings) were used in neurosurgical patients due to fear of intracranial hemorrhage, LMWH is probably an acceptable alternative. The combination of PKI and LMWH may be more effective than either of these methods alone in patients at risk. Limited data supports a combination of PKI, elastic stockings and LMWH for spinal cord injuries or polytrauma. For patients of a very high risk, CF formulation can be considered.

The most common non-surgical conditions in which prophylaxis of deep venous thrombosis is indicated are myocardial infarction and ischemic stroke. NIDPH is effective in patients with myocardial infarction. If anticoagulants are contraindicated, PKI, elastic stockings or both can be used. Patients with stroke can use NDHNH or LMWH; useful PKI, elastic stockings or both can be together.

Recommendations for some other non-surgical conditions include NDHNH for patients with heart failure; adjusted doses of warfarin (MHO 1,3-1,9) for patients with metastatic breast cancer and warfarin 1 mg / day for cancer patients with a central venous catheter.

Forecast

Thromboembolism of the pulmonary artery (PE) has a disappointing prognosis. Approximately 10% of patients with pulmonary embolism (PE) die within an hour. Of those who survive the first hour, only about 30% are diagnosed and treated; more than 95% of these patients survive. Thus, most lethal cases of pulmonary embolism (PE) occur in patients who are never diagnosed, and the best prospects for reducing mortality are in the field of improving diagnosis, not treatment. Patients with chronic thromboembolic disease constitute a very small proportion of surviving patients with pulmonary embolism (PE). Therapy with anticoagulant drugs reduces the incidence of recurrence of pulmonary embolism (PE) to approximately 5% in all patients.

[13], [14], [15]