PULMONARY EMBOLIZATION (PE)Prevalence PE is the third prevalent

PULMONARY EMBOLIZATION (PE)

Prevalence PE is the third prevalent kind of pathology of cardiovascular system after coronary heart desease and cerebral thrombosis. For last 10 years the lethality from PE has not changed. Without treatment it makes 30 %, with early therapy by anticoagulants - less than 10 %.

Causes Most often PE is caused by a deep vein thrombosis of an iliofemoral segment. The following factors participate in originating of a venous clottage: retardation blood circulation, damage of a vascular wall, change of structure of a blood.

Risk factors of a deep vein thrombosis Elderly age Long (more than 6 days) confinement to bed Immobilization or paralysis of extremities Smoking Reception of oral contraceptives Neoplasms Varicose phlebectasia of the inferior extremities Diabetes Myocardial infarction Insult Stagnant heart failure Surgical interventions in orthopedics, oncology, general surgery, gynecology and urology. With a combination of several factors the probability of a deep vein thrombosis grows.

The PE occurs at a deep vein thrombosis. The source of an embolism is in the inferior caval system (90%), in the superior caval system and heart cavities (10%). PE is frequently multiple, in 2/3 cases - bilateral. Right lung is affected more often left one, and inferior lobes-more often than top lobes.

Pathogenesis PE complicates outflow of a blood from a right ventricle. The degree and character of process depend on a degree of an occlusion of pulmonary vessels (pv). The pulmonary hypertension educes at occlusion of 30-50 % of (pv). The clinic depends on a background on which there is an occlusion: in a systemic arterial hypoxia clinical features of PE occur at an occlusion of 15 % of pv.

PE is not static process. PE may give rise to the trombotic process. In these cases there is active process of thrombogenesis around the embolus. The speed of this process is determined by a state of both general, and local factors of a coagulation and fibrinolysis, degree of retardation of a blood flow, a degree of blood coagulability, aggregation of thrombocytes contents of Heparinum in a blood, and the level of a fibrinolysis.

PE invokes activization of a fibrinolysis. Activization of a fibrinolysis may result in dissolution of trombotic masses. The second possible variant of embolus evolution is it’s integration into a vascular wall with the subsequent retraction, recanalization and vascularization. It possible within 10-20-days.

The character of pulmonary changes depends, on what vessel is affected - the basic trunk of a pulmonary artery, its larger or smaller branches. Accordingly is observed in lungs - from ordinary developments of stagnation and dystrophia of a pulmonary parenchyma up to formation of pulmonary infarction.

The causes of complications and death: a severe pulmonary hypertension acute right heart failure. The thrombolysis promotes fast pressure decrease in a pulmonary artery and prevents right heart failure.

The basic syndromes PE - an acute disease with the characteristic severe breathlessness, marked cyanosis, pneumorrhagia, pain in the chest, with quickly coming lethal outcome (20 % of cases). In the other 80 % of cases clinical manifestations of PE may be very diverse.

In affection of a pulmonary trunk or main branches of pulmonary artery PE proceeds immediately, very severely and results in sudden circulatory arrest or shock. In the most of patients PE ends up with instant lethal outcome

The affection of lobar and segmentary arteries is manifested by an acute course of PE of moderate severity with breathlessness, arterial hypotension, clinical and ECG signs of an acute pulmonary heart.

The PE of fine branches of a pulmonary artery shows repeated episodes of a unmotivated shortness of breath, It is tend to recurrenses and is extremely difficult for diagnostics.

Clinically the level of affection can be detected only roughly, therefore the series of symptom-complexes exist.

The pulmonary infarction is manifested by pleural pains, breathlessness, sometimes pneumorrhagia. It is observed almost exclusively in left heart failure (because of low collateral circulation in bronchial arteries).

The acute pulmonary heart reveals itself with a shortness of breath, cyanosis, right HF, arterial hypotension. In severe cases a syncope and circular arrest is observed. It happens in PE of large branches of a pulmonary artery, frequently - on a background of heart and lung affection.

Sudden breathlessness without any visible reasons The chronic pulmonary hypertension is characterized by breathlessness, swelling of cervical veins, hepatomegalia, ascites and swelling of legs. Usually educes in multiple PE or not dissolved thrombus with retrograde increase.

Clinical features Diversity of a clinical picture makes the diagnosis PE in many cases extremely inconvenient. Even now, with the use of modern methods of diagnostics, it is possible to diagnose PE intravitally only in 60 % of cases.

An inspiratory breathlessness. It may be moderate (up to 30 respirations per minute), profound (30-50) or very sharply profound (more than 50 respirations per minute). The breathlessness as a rule, is silent, without audible rales on distance or bubbling, without dry or wet rales in lungs, without participation of auxiliary muscles in breathing. It does not depend on a position of the patient in bed.

Development of an arterial hypotension since the first minutes of PE with rising of the central venous pressure is typical. The pain is a sign which also frequently occurs in PE. Nodal tachycardia, or tachysystolic form of atrial fibrillation.

The discoloration of a skin and mucosas. The acyanotic-ashy cutaneous dropsy in a combination with cyanosis of mucosas and nails is the most typical. Skin cyanosis of the top half of the body frequently educes in patients with heart failure.

Clinical signs of an acute “pulmonary heart” Pulsation in the 2-d left intercostal space Dilating of cardiac dullness to the right, accent and splitting of II tone above PA Systolic murmur above a projection of the three-cuspidate valve and a PA Abrupt rising of the central venous pressure The swelling of cervical veins, augmentation of a liver and icteric scleras and skin

ECG signs of "pulmonary heart" Appearance of Q III along side with a augmentation of voltage of R III and SI (syndrome Q III SI); Turn of heart around the longitudinal axis with right ventricle forward (shift of transitive zone to the left precordial leads); Rise of segment ST with (-) peak Т in leads III, аVF, V1-V3; Appearance of blockage of a right bundle branch; High pointed "pulmonary" Р with a deflection of its electrical axis to the right; Nodal tachycardia or tachysystolic form of an atrial fibrillation.

Pulmonary infarction It includes: pleural pain, tussis, fever, and sometimes – exudative pleuritis on one side and allergic manifestations. Tussis in PE occurs in the first day of disease; at first, it is dry, and then - with a scanty mucous sputum and only on 5-7th day is imbued by blood. The fever quite often begins within the first hours of disease.

First signs of PE are: Sudden breathlessness in combination with arterial hypotension ( especially after a long immobilization or a surgical intervention)

Differential diagnostic Differential diagnostics depends on a degree of manifestation of separate clinical signs of PE. The breathlessness and dyspnea, predominating in PE may suggest an idea about presence of a cardiac or bronchial asthma.

In a severe anginous attack there is the necessity to carry out differential diagnostic of PE with acute myocardial infarction. It is necessary to take into account, that the myocardial infarction (especially with spreading of necrosis on a right ventricle) may become complicated with PE.

When an abdominal pain presents it is necessary to carry out differential diagnostic of PE and acute diseases of a gastrointestinal tract (an acute cholecystitis, an acute pancreatitis). Confirmation of presence of PE is the marked enlargement of liver in a combination with swelling cervical veins, hepatojugular reflux, breathlessness, a pleural rubbing sound and arterial hypotension.

The differential diagnosis of PE should also be carried out with such diseases, as: a myocardial infarction, pericarditis, НF, pneumonia, bronchial asthma, chronic nonspecific pulmonary diseases, lung cancer, pneumothorax, fracture of ribs, muscular pains, sepsis, psychogenic hyperventilation, fever of an unknown origin.

Examenations, confirmed diagnosis Gases of an arterial blood: In 94 % of cases at respiration by atmospheric air oxydzen pressure (pO2) – lower than 90mm Hg. p02 and an alveolar-arterial difference p02 tests are low sensitive and non-specific. The ECG Chest X-Ray - to exclude pneumonia, HF, lung tumors, pneumothorax. Ventilation/perfusion scintigraphy of lungs. The reduction of perfusion in one pulmonary segments is typical in PE. Diagnostic search of a deep venous thrombosis The angiopulmonography. Criteria of diagnosis are the detection of breakage of a branch of a pulmonary artery and contour of a thrombus.

Intensive care 1. In case of arrest of a circulation - cardiopulmonary reanimation. Heparinum is indicated additionally. Well-timed diagnostics and adequate intensive care allow to rescue patients and keep their working capacity in more than 80 % of cases.

2. In case of severe arterial hypotension: Oxygenotherapy,catheterization of a central vein Noradrenalinum 4-8 mg in 400 ml 5-10% of glucose i/v by drops Reopolyglucine 400 ml i/v by drops Heparinum 5000 U i/v Prednisolonum i/v 30 mg Streptokinasa 250 000 U i/v by drops during 30 min., then 1250 000 U by drops Acidum acetylsalicylicum 0,25g p/o If Streptokinasa was not infused, Heparinum should be infused i/v by drops.

3.If the state and blood pressure are stable: an oxygenotherapy Heparinum 5000 U intravenously, then by drops (1000 U per hour); Acidum acetylsalicylicum 0,25g per os in case of bronchospasm - Euphyllinum 240 mg i/v. Monitoring of the vital functions Hospitalizaton after stabilization of a state

The main complications: Electromechanical dissociation; Impossibility to stabilize blood pressure; repeated PE; Increasing respiratory failure; Arterial hypotension, Allergic reactions or hemorrhagic complications durring introduction of Streptokinasa.

Treatment The volume and the contents of an acute management PE are determined by the state of the patient which in many respects depends on a degree of affection of a pulmonary vascular system and course of disease.

Indications to thrombolytic therapy shock; acute pulmonary heart failure; severe pulmonary hypertension; repeated episodes of PE.

If thrombolytic therapy was not carried out: the treatment by Heparinum is started. At first infuse 5000 U Heparinum i/v, and then by drops at the rate approximately 1000 U per hour. The dose of Heparinum in first day should be 30 000-35 000 U. The rate of administering of Heparinum is selected so that to increase activated partial thromboplastin time ( APTT) in 1,5-2,5 times in comparison with initial.

Heparinum has anticoagulant, antiinflammatory and anesthetizing effect. Within the next 6-7 day carry out subcutaneous injections of Heparinum with the purpose of augmentation APTT in 1,5-2,5 times. Treatment by Heparinum is to be carried out during 6-7 days.

5 day prior to cancellation of Heparinum indirect anticoagulants (Syncumarum) are administered for a period of not less than 3 months. The insignificant pneumorrhagia (veins of bloods in a sputum) is not a contraindication to anticoagulant therapy.

Low-molecular Heparinum Low-molecular Heparinum (Fragminum Fraxiparinum and Klexanum), introduced twice a day in the dose of 120 U/KG per day subcutaneously during 10 days is effective, as well as non-fractioned Heparinum. 3 days prior to a cancellation of Fragminum indirect anticoagulants (Acenocumarolum) are introduced.

The laboratory control The minimal examination before thrombolytic therapy and during its realization should include: clinical analysis of blood (in which the most significant is the quantity of erythrocytes and thrombocytes); general analysis of urine; analysis of feces for traces of blood.

At suspicion on a bleeding should be carried out tests for: hematocrit, blood group, content of Fibrinogenum With the introduction of anticoagulants or thrombolitics general coagulation tests are to be carried out.

Treatment by direct anticoagulants With the treatment by direct anticoagulants (non-fractioned or low-molecular Heparinum) the control of activated partial thromboplastin time (or index APTT) and amounts of thrombocytes in a peripheric blood is necessary.

Treatment by indirect anticoagulants With the treatment by indirect anticoagulants (Syncumarum, Phenilinum), it is necessary to control International normalization index (INI) or prohrombine, or prothrombin index. It is enough to achieve an increase of INI within 2-3, that corresponds to increase of prothrombin time in 1,3-1.5 times in comparison with initial.

Surgical treatment In PE, surgical treatment may be considered as the reserve approach in the absence of effect heparinum therapy. Thrombectomy is used seldom nowadays in view of its limited efficacy. Pulmonary embolectomy may be carried out in patients with hemorrhagic diathesis, in case of impossibility to carry out anticoagulation treatment, and also if the state of the patient is critical.

Normal values of some laboratory parameters Erythrocytes: men - 4500000-5700000 mc l, women -3900000-5000000 mc l Thrombocytes - 160000-380000 mc l Hematocrit : men - 40.7-50,3 %, women - 36,1-44,3 % Fibrinogenum - 200-400 mg% APTT - 22-40 s Index APTT - 0,9-1,1 Prothrombin index- 90-110 % Thrombine time - 28-31 s Time of coagulation - 8-12 minutes by Lee-White Duration of bleeding 1-3 minutes by Duke

The laboratory control Infringement of an internal path of plasma hemostasis is assessed by the change of APTT and blood coagulation time. Infringement of an external path of plasma hemostasis is assessed by the change of prothrombin time (index). Infringement of the general mechanism of plasma hemostasis is assessed by the change of Fibrinogenum, thrombin time and blood coagulation time. Infringement of thrombocyte-vascular hemostasis – by the change of quantity of thrombocytes, blood coagulation time and duration of bleeding, positive tests (pinch, tourniquet, cuff).

Tactics of management Blood pressure (BP) is normal, PE of small or middle branches of pulmonary artery: Heparinum, then Varfarin. Heparinum does not dissolve a thrombus, but interferes with increase of a thrombus up to an activation of system of an endogenic fibrinolysis.

PE of large branches of pulmonary artery: Heparinum or trombolitics. Thrombolysis frequently results in fast dissolution of a thrombus that may occur in polysegmentary or lobar PE

Pulmonary infarction with a pneumorrhagia: Heparinum, then Varfarin. Anticoagulants in pneumorrhagia are not conterindicated. Acute pulmonary heart failure: Heparinum or trombolitics. Trombolitics are more preferable.

BP normal, anticoagulants and trombolitics are conterindicated: installation of the filter in inferior caval vein or its ligating. More preferably installation of the caval filter, except for a septic embolism.

Arterial hypotension, cervical veins are not swelled: completion volume of blood, observation. Cervical veins swelled, or arterial hypotension persists despite of completion volume of blood: thrombolysis. Fast improvement of right ventricle function owing to thrombolysis improves a survival rate in PE of large branches of pulmonary artery.

Arterial hypotension: anticoagulants and trombolitics conterindicated, cervical veins are not swelled: completion of blood volume, observation. Cervical veins swelled, or the arterial hypotension persists despite of completion of blood volume: angiopulmonography, an embolectomy. The lethality of an embolectomy - 20-30 %. In the stage of clinical tests: transvenous embolectomy and cleavage of a thrombus with the help of a rotatory catheter.

Repeated PE on a background of therapy by anticoagulants. Variants of treatment: Add to therapy Aspirinum; Achieve augmentation INR up to 3,0-,5; Establish caval filter or ligate inferior caval vein, Continue to give Varfarine. Long therapy by anticoagulants is necessary to prevent clottage of the filter and a repeated deep vein thrombosis.

PROPHYLAXIS Risk of a deep vein thrombosis and PE in absence of prophylaxis: cavitary operations: a deep vein thrombosis-25 %, PE-2-5 %, operations on coxofemoral or knee joint: a deep vein thrombosis -50 %, lethal PE-1-3%,urological operations: a deep vein thrombosis -25% (in open prostatectomy-40%, in transurethral-10%.).

Initial prophylaxis of PE Initial prophylaxis of PTE is not carried out: operations in patients in age less 40 years, duration of operation less than 1 hour, absence of malignant tumours, in anamnesis there is no deep vein thrombosis; early activization in the postoperative term

Medicamental prophylaxis of PE Patients who have some risk factors of PE, require preventive treatment by indirect anticoagulants and antiaggregants. It is believed that with adequate realization of preventive actions it is possible to prevent all cases of PE and up to 2/3 cases of a deep vein thrombosis.

Secondary prophylaxis of PE For secondary prophylaxis of PE in patients with embologenic forms of phlebothromboses is used more and more widely an intravenous installation of filters or extravenous caval clipping