From Big Medical Encyclopedia

THROMBOEMBOLISM of PULMONARY ARTERIES (Greek thrombos a piece, a clot + embole an insert, invasion) — acute occlusion of a pulmonary trunk or branches of arterial system of lungs the blood clot formed in veins of a big circle of blood circulation or in the right cardial cavities. T. l. and. is a complication of various diseases; it often would be found during the openings in the general profile. On the level of defeat allocate a thromboembolism of a pulmonary trunk and the main pulmonary arteries (massive T. l. and.), thromboembolism of share and segmented branches, thromboembolism of small branches.

Etiology and pathogeny. T. l. and. the thrombogenesis in veins of a big circle of blood circulation or in the right cardial cavities precedes. The diseases which are complicated by T. l. and., as well as in general a thromboembolism (see), are various since premises to a thrombogenesis arise at any patol. processes and states, and also nek-ry to lay down. the influences leading to delay of a blood-groove, emergence of hypercoagulation and damage of a vascular wall (see Thrombosis). T. l. and. it is often observed at patients with heart failure (see) and arrhythmia of heart (see), in particular at a ciliary arrhythmia (see) at patients with a myocardial infarction (see), defects of mitral and three-leaved valves (see the Heart diseases acquired), at a rheumatic carditis (see Rheumatism), a bacterial endocarditis (see), sepsis (see), leukoses (see) and malignant new growths; at injuries, extensive burns and freezing injuries; after profuse bleeding and hemolysis of various origin; at the expressed dehydration and a pachemia owing to neuk-rotpmy vomiting, a gastroenteritis, uncontrolled reception of laxatives or diuretics; during the use of oral contraceptives. To emergence of phlebothromboses and T. l. and. catheterization of veins, abdominal organs operations and in a small pelvis, and also any long or technically difficult surgeries, especially at elderly people promote and at oncological diseases. Are predisposed to T. l. and. women at pathology of pregnancy and in a puerperal period (owing to a frequent vein thrombosis of a small pelvis in these cases), and also sick, forced it is long to be on a high bed rest.

Source of T. l. and., according to various researchers, in 75 — 95% of cases there are blood clots (see Thrombosis) from system of the lower vena cava (preferential ileokaval-ny segment), in 5 — 25% — blood clots from the right auricle or a ventricle and in 0,5 — 2% — blood clots from system of an upper vena cava. Most often the separation of blood clot from the place of its attachment is promoted by considerable fluctuations of pressure in belly and chest cavities (natuzhiva-ny, cough), the exercise stress increasing rate of volume flow of a blood-groove and disturbance of a cordial rhythm (for endocardiac blood clots). Special «embologenny» threat the streamline blood clots connected to a venous wall the distal end, or so-called free, floating represent, blood clots, rykhlo fixed to a vascular wall.

The major pathogenetic factors creating a wedge, manifestations of T. l. and., disturbances of a local hemodynamics in lungs are, and also hypertensia of a small circle of blood circulation (see), edges can become the reason of development of an acute pulmonary heart (see). Sudden mechanical occlusion of a vessel is followed by the local reflex vasoconstriction extending sometimes to arteries of all small circle of blood circulation. Increase of vascular resistance in lungs is promoted by also nonspecific reactions of an organism to a stressful situation — a giperka-tekholaminemiya and increase in viscosity of blood owing to hypercoagulation. In these conditions damage of an endothelium of vessels at implementation of an embolus causes adhesion and aggregation of thrombocytes on a vascular wall with the subsequent inclusion of all chain reaction of intravascular coagulation (see. Coagulant system of blood), what leads to growth of blood clot distalny places of occlusion. During the falling of rate of volume flow of a pulmonary blood-groove patol. process can be complicated by additional thrombosis of small vascular branches, to-ry is gradually transformed from pristenochny to occlusive and imitates hmiozhestvenny T. l. and.

The progressing growth of resistance to a blood-groove in lungs leading to precapillary hypertensia (at massive or recurrent T. l. and. arterial pressure in a pulmonary trunk is 3 — 4 times higher than normal), inevitably is followed by increase in end diastolic pressure in a right ventricle and dilatation of his cavity (an acute pulmonary heart). The minute volume of blood circulation in these conditions decreases, the ABP in a big circle of blood circulation often decreases, and the central venous pressure — increases; at massive T. l. and. quickly the congestive circulatory unefficiency develops.

Resistance to a blood-groove in lungs decreases in connection with disclosure of an arteriovenous anastomosis a little. However shunting of a venous blood in the left departments of heart and switching off from circulation of considerable sites of pulmonary fabric (especially at a massive thromboembolism, the continued thrombosis and multiple occlusion of small vascular branches) leads to the resistant arterial anoxemia which is not compensated by the accruing asthma as a tachypnea (see), edges becomes frequent an origin of a hypocapny see).

At adhesion and aggregation of thrombocytes the A2 thromboxane and serotonin (see) possessing the expressed vasopressor action are released, and compensatory reaction to local hemodynamic disturbances are increase in fibrinolitic activity of blood and degranulation of mast cells (see) in lungs with release of heparin (see) and mediators of an inflammation (see). Excessive release of a histamine (see) causes a bronchospasm and in combination with action on bronchial walls of serotonin causes sometimes development of generalized bronchial obstruction, edges aggravates the respiratory insufficiency caused narushe-niyamp a blood-groove in lungs.

Under the influence of a histamine and slowly reacting substance of an anaphylaxis (I eat.), and also in connection with a hypoxia permeability of vascular walls increases; from thin-walled vessels plasma begins to filter into interstitial fabric (at the same time intersticial hypostasis forms), into a pleural cavity (at subpleural localization patol. process) and in alveoluses. In the beginning the transudate (see) getting into a cavity of alveoluses only raises a layer of surfactant (see), however coming with transudate to alveoluses cholesterol and olein to - that result in insufficiency of surfactant, and fibrinogen completely inactivates it. At the same time permeability of alveoloreapillyarny membranes is broken and amplifies transuding in alveoluses of a liquid part of blood, and then and uniform elements even more. The inactivation of surfactant and accumulation of extravasated liquid in intersticial space of lungs promote formation of a kongestivny atelectasis (see). Hemorrhage in alveoluses with small desquamation of an alveolar epithelium, but without necrosis (shown clinically a pneumorrhagia) comes to the end with development of a focal apoplexy of a lung — on the substance of an incomplete hemorrhagic heart attack (see). At accumulation in a pleural cavity of a significant amount of seroznogemorragichesky exudate perhaps also formation of compression atelectases, and at full obstruction of bronchial tubes a viscous bloody phlegm — obturatsionny atelectases (see the Atelectasis).

Increase in level of endogenous heparin and allocation of an eosinophilic hemotakeichesky factor at degranulation of mast cells lead to increase of number of eosinophils in blood. It can be considered as the compensatory reaction directed to permission patol. process since arylsulphatase of eosinophils inactivates a histamine and slowly reacting substance of an anaphylaxis, and the phospholipase of D inhibits functional activity of thrombocytes and interferes with their degranulation.

The heart attack of a lung does not develop if in a zone T. l. and. sufficient collateral blood supply remains. It develops or against the background of post-capillary hypertensia, including owing to a left ventricular failure, or in a zone of a sclerosis, is more rare than a vasculitis of the pulmonary vessels caused by the previous diseases of various etiology i.e. in the conditions favoring to regional thrombosis and limiting possibilities of collateral blood supply through system of bronchial arteries. At intact pulmonary vessels the first episode of a thromboembolism of pulmonary arteries proceeds quite often without development of a heart attack of a lung.

Pathological anatomy.

At 60,5% of the dead of T. l. and. during the opening find a combination of massive T. l. ampere-second an embolism of small branches, and, according to V. S. Savelyev et al. (1979), more than in 1/3 of these observations the thromboembolism of small branches preceded massive T. l. and. At a research of corpses of the patients who died presumably of T. l. and., opening of heart and a pulmonary trunk should be made without preliminary extraction of bodies. At the dead from massive T. l. and. reveal swelling of jugular veins, stretching of a pulmonary trunk and dilatation of the right cardial cavities (an acute pulmonary heart), especially right auricle. If death came quickly or immediately, it is found or the multiple embolism of lobular and subsegmented or segmented branches of an arterial bed of lungs with switching off more than 60% of its gleam, or existence of large trombo-emboluses in share or leading branchs of a pulmonary trunk, or a vklineniye in a pulmonary trunk of a big tromboembol, a part of a body to-rogo sometimes is located in a cavity of a right ventricle of heart (tsvetn. tab., Art. 400, fig. 8). Often tromboembol lies in a gleam of a pulmonary trunk in the form of a ball or its ends are implemented in both leading branchs (tromboembol - «equestrian»).

Fresh tromboembol, recently implemented into a gleam of a pulmonary artery, lies freely, it is not connected with its wall and has no the shoots corresponding to its branching. Its surface is slightly rough, sometimes has multiple cross deepenings — Cang's furrows, in some cases on a surface of a trom-boembol prints of valves of veins are visible. Usually tromboembol brittle, on its break of a pla a section bedded structure is defined (an elephant of dark red color alternate grayish layers). At differentiation of a tromboembol with a posthumous parcel of blood (see the Parcel blood) consider that the last is more elastic, stretches, has the brilliant surface and shoots corresponding to branching of a pulmonary artery; the cut surface of a parcel more homogen, is wet, red or grayish-yellow color. In some cases, if investigate small tromboembo-la and tromboembola, to-rykh very fresh blood clots were a source, it is impossible to distinguish tromboembol from a posthumous parcel very difficult or even. If death was preceded by a long agony, then on tromboembol the posthumous parcel of blood practically always accumulates. Microscopically tromboembol does not differ from blood clot. The found alternation of uniform elements with layers of fibrin is not reliable criterion of its difference from a posthumous parcel. Detection in freely lying tromboembol of signs of the organization of blood clot is more reliable sign (see the Organization in pathology).

If death came in several days after T. l. and., around a tromboembol quite often there is a secondary thrombogenesis, the endothelium of a vessel in a zone of a prileganiye of a tromboembol is exposed to dystrophy and a necrosis and in tromboembol granulyatsionny fabric gradually grows. In this case differentiation of T can present essential difficulties. l. and. and local thrombosis. If in a zone of thrombosis there are no signs of the previous defeat of pulmonary fabric and a vessel and there are no expressed disturbances of a pulmonary blood-groove, then, considering a wedge, data, the issue is resolved in favor of T. l. and. Trombotichesky process can accrue in proximal and in the distal direction. Small tromboembola with completion of process of the organization can resemble an atherosclerotic plaque, plurality of such plaques causes growth of resistance to a blood-groove and development subacute or hron. pulmonary heart.

When death from T. l. and. came in several hours, it is macroscopically possible to note hypostasis and a plethora of the zone of lungs which is switched off from blood supply of system of a pulmonary artery. If the patient endures the acute period of T. l. and., depending on localization of a tromboembol and a condition of a blood-groove in a lung the heart attack (see Lungs), as a rule, hemorrhagic can develop. The zone of a heart attack usually has incorrectly pyramidal form, the basis of a pyramid is the surface of a lung, and the stupid top is located in a zone corked tromboembol ohm of a vessel (see tsvetn. the tab. to St. Heart attack, t. 9, Art. 177, fig. 2). At the central arrangement of a heart attack form its uncertain. Tissue of a lung in a zone of a heart attack is condensed, a cut surface wet in the beginning, becomes later than dryish. If there is perifocal hypostasis or infarctive pneumonia develops, then borders of a heart attack accurate in the beginning are erased. A pleura in its zone dim with gentle imposings of fibrin. The zone of a heart attack at first slightly eminates, and for the 2nd day sinks down a little. Histologically in the first two days after a thromboembolism the plethora of capillaries develops and there are hemorrhages in alveoluses. Then the necrosis of alveolar partitions joins, is more often incomplete and more expressed in the center of a zone of a heart attack. Erythrocytes in gleams of alveoluses become pale, haemo siderophages appear. The ultrastructure of parenchymatous cells of a lung changes quickly: the first 20 — 30 min. swelling of mitochondrions, disaggregation and swelling of an endoplasmic reticulum is noted. On the second week the organization of a heart attack begins, edges depending on its sizes can drag on for several months. Process comes to an end with formation of a gentle hem with a thickening of a pleura in a zone of the former heart attack. Tromboembol is exposed to the organization and turns or in continuous fibrous tyazh, or into a pristenochny plaque, or re-is channeled in terms from 1 to 2V2 month. At good inflow of blood from bronchial arteries the «incomplete» heart attack can develop. Process is limited to a sharp plethora of alveolar partitions and hemorrhage in a cavity of alveoluses without development of a necrosis. In this case perhaps complete recovery of structure of pulmonary fabric in a zone of a heart attack. If the zone of a heart attack is infected, including as a result of implementation of a septic tromboembol, then suppuration of a zone of a heart attack with formation of abscess is possible. The «white» ischemic heart attack in a lung arises extremely seldom, only in the conditions of sharply reduced blood circulation in system of bronchial arteries. Morfol. its manifestation is the coagulative necrosis (see).

Detection on opening of T. l. and. demands search of a source of education tromboembola-To some extent about its localization in venous system it is possible to judge by diameter of a tromboembol. With a diameter it more than 8 mm a probable source are ileal veins and the lower vena cava, and pz systems of an upper vena cava — subclavial and jugular. Tromboembola to dia. 5 — 8 mm are characteristic of the blood clots which are localized in large veins of a hip, in axillary veins; tromboembola of a smaller diakhmetr — for veins of shins, a basin, an upper extremity. The place of a separation of blood clot seldom manages to be established since usually proximal end still of an unorganized part of blood clot comes off, and the vascular wall is visually not changed. Therefore about a source of T. l. and. judge by an indirect sign — existence of residual blood clots in the right cardial cavities or in veins. As in most cases source of T. l. and. vessels of system of the lower vena cava are, investigate them first of all. 1\rupnye veins to the level of subnodal open longwise, veins of shins and feet investigate by cross sections through muscular arrays of these departments of extremities. Investigate also cellulose of a basin. Vessels of system of an upper vena cava surely are exposed to a research if during lifetime on these veins medical or diagnostic manipulations were made.

Clinical picture. The acute beginning of T is characteristic. l. and., and quite often the first symptoms arise at the time of a natuzhivaniye (at defecation, rise in weight), at cough, bystry change of position of a body. If there does not come the pierniyenosny death, depending on the level of implementation of an embolus and a condition of the patient by the time of emergence of T. l. and. its manifestations vary from single nonspecific symptoms before development of the most serious condition of the patient with formation of syndromes of an acute pulmonary heart (see), a vascular collapse (see), acute respiratory insufficiency (see), disorders of consciousness (see) etc., each of to-rykh can become dominating in a clinical picture T. l. and.

The thorax pain which sometimes is imitating stenocardia (see), but usually not irradiating, amplifying on a breath happens an early symptom often. Pain proceeds till several o'clock, despite repeated introduction of analgetics; quite often she acts after a transfusion of thrombolytic means. Early developing of short wind as a tachypnea with a respiration rate to 30 — 60 in 1 min. at rest is characteristic, and an asthma does not force patients to accept vertical position (orthopnea), except for the persons which already had heart failure. Quite often there are acute fear of death with psychomotor excitement (occasionally block), a sharp exhausting weakness and perspiration. Sometimes early there is a dry irritating cough. At V3 of patients, is more often on

2 — the 3rd days, the pneumorrhagia (see), in some cases — small pulmonary bleeding is noted (see). Fervescence is possible (from subfebrile to gektichesky) in the first days, is more rare — within several days.

The increasing respiratory insufficiency is shown by an asthma and diffusion, is more often <- ashy» cyanosis at the expressed arterial anoxemia (r03 decreases quite often to 80 — 70 mm of mercury.). An asthma leads usually to a gshterventilyation with a hypocapny (see) and development of a respiratory alkalosis (see). G1o wedge. respiratory frustration can remind manifestations acute diseases of bronchopulmonary system: obstructive bronchitis

(I eat.), a focal or lung fever (see), spontaneous pheumothorax (see), exudative pleurisy (see).

Development of a syndrome of an acute pulmonary heart is characterized by emergence of a Crocq's disease, swelling, sometimes the pulsation of cervical veins, high central venous pressure which is suddenly coming and the progressing tachycardia, emergence of a cantering rhythm (see Gallop a rhythm), systolic noise and sharp accent of the II tone over a pulmonary trunk, sometimes systolic noise at the basis of a xiphoidal shoot (as a result of relative insufficiency of the three-leaved valve)'.

Owing to a bystry decompensation of an acute pulmonary heart to the T dominating in manifestations. l. and. there can be a so-called abdominal syndrome: nausea, vomiting and, the main thing, sharp pain in the right upper quadrant of a stomach in connection with stretching of the glissonovy capsule at acute stagnation and swelling of a liver (is more rare in connection with defeat of a diaphragmal pleura). Dominance of these symptoms in combination with frequent at T. l. and. a leukocytosis imitates a picture of an acute abdomen and serves sometimes as the reason of an unjustified operative measure.

To frequent manifestations of T. l. and. acute arterial hypotension belongs, edges in some cases becomes the leader in a wedge, a picture: it is followed by decrease in a renal blood-groove and glomerular filtering with an oliguria (see) both the subsequent a proteinuria (see) and a hamaturia (see). More rare leading manifestations of T. l. and. there are a syndrome of acute coronary insufficiency (anginous attacks and electrocardiographic symptoms of ischemia of a myocardium), a so-called cerebral syndrome, to Krom carry various symptoms of nervous and mental disturbances (sharp dizziness and sudden muscular weakness, obscuring or a loss of consciousness, sometimes epileptiform spasms, emergence focal nevrol. symptoms, signs of wet brain).

At an extensive apoplexy of a lung in blood the level of an indirect bilirubin increases (I eat.), what is followed by pale icteric coloring of mucous membranes and skin.

Current and possible outcomes. For massive T. l. and. the acute current with bystry increase of symptoms of heavy pulmonary hypertensia is characteristic, as a rule; the embolism of a pulmonary trunk or both of its branches with reduction of a blood-groove for 75% and more leads to almost instant death. The subacute current (duration quite often up to several weeks) is noted more often at an embolism of share or segmented branches with the prolonged thrombosis; in these cases permanent decrease in the ABP, acute disorders of a cordial rhythm, the expressed right ventricular insufficiency and the progressing arterial anoxemia with diffusion cyanosis predictively are adverse. The recurrent current is peculiar generally to a thromboembolism of small branches with repeated emergence of pulmonary apoplexies, heart attacks and pleurisy and gradual development hron. a pulmonary heart (see). Compliance between level T. l. and. and the wedge, currents is observed by option not in all cases. Massive T. l. and. the subacute current, and a thromboembolism of small branches — extremely acute accepts sometimes.

The heart attack of a lung (see Lungs) is complicated sometimes by spontaneous pheumothorax (see) or, more often, exudative pleurisy (usually with the unilateral serous or hemorrhagic exudate which is not collecting after evacuation of pleural contents), to-ry comes to the end in some cases with extensive commissural process, education shvart or even with an obliteration of a pleural cavity (see Pleurisy). Considerable destruction of pulmonary fabric leads to developing of acute abscess (see Lungs), and at subpleural localization of the last creates threat of its break in a pleural cavity with development of an acute empyema of a pleura (see Pleurisy). The organization of a heart attack comes to an end with formation of the pneumosclerous centers, bronchiectasias, petrifikat, in some cases — smooth-bore cavities (see).

Diagnosis. In spite of the fact that T. l. and. meets very often, its diagnosis is not always simple and usually demands an exception patol. processes, to-rye the developed T imitates. l. and. — an acute myocardial infarction (see), the stratifying aortic aneurysm (see the Aneurism stratifying), acute pleurisy and other diseases of the bodies of a chest cavity which are followed by respiratory insufficiency (see), acute diseases of abdominal organs (see. An acute abdomen), an acute disorder of cerebral circulation (see), etc. About the developed T. l. and. signs of an acute pulmonary heart testify (including, according to an ECG and rentgenol. researches); an arterial anoxemia (especially in combination with a gipokagshiya and a respiratory alkalosis); identification of hypercoagulation and oppression of fibrinolitic activity (according to koagulologichesky blood analyses), and also decrease in number of thrombocytes in blood and increase

in their adhesive and aggregation properties; emergence of free DNA in a blood plasma, increase of activity of the general lactate dehydrogenase — LDG (see the Lactate dehydrogenase) and especially LDG3 and LDG4 isoenzymes at normal or slightly a superactivity of an asparaginic aminotraneferaza, increase in concentration of an indirect bilirubin in blood. Reliability of the diagnosis increases in the presence of signs of a phlebothrombosis (see Thrombophlebitis.), to-rye are found, however, only in V3 of patients.

Have crucial diagnostic importance radionuclide (see P adioizotopny diagnosis) and rentgenol. methods of a research (see. X-ray inspection). Poe-lipozitsionnoye perfused scanning (see) easy with assessment on separate zones both perfusion, and ventilation (for an exception of inflammatory processes in easy or new growths) allows to reject the diagnosis of T unconditionally. l. and., if the microcirculator bed of lungs is not changed, or to find the centers of uneven distribution of radioactivity with decrease it at incomplete obstruction of a vessel and absence — at full arterial occlusion. At multiple T. l. and. subsegmented or segmented branches expressiveness of perfused defects is, as a rule, various whereas it at an embolism of a share artery — is identical (within this share). Repeated researches give the chance in dynamics to estimate extent of recovery of a pulmonary blood-groove in the course of treatment.

Non-contrast rentgenol. the research at a thromboembolism of large arterial branches reveals on the party of defeat expansion and deformation of a root of a lung, high standing of a dome of a diaphragm and restriction of its excursion, depletion of the pulmonary drawing and increase in transparency in a zone patol. process (symptom of an oligemiya). At a tomography increase in diameter of a vessel proksimalny occlusions and reduction — distalny it is defined. For a thromboembolism of small branches and multiple T. l. and. (fig., a) chaoticity of the pulmonary drawing, existence of discal atelectases and a pleural exudate are indicative. In process of formation of a heart attack of a lung decrease in a pnevmatization of pulmonary fabric against the background of congestive strengthening of the pulmonary drawing is replaced by emergence of one or several centers of infiltration imitating usually acute pneumonia; also intensive blackout of rounded shape and segmented atelectases are possible. A classical shadow triangular or to a game -

Fig. Data of X-ray inspection at a thromboembolism of pulmonary arteries: and — the roentgenogram of a thorax at a multiple thromboembolism of pulmonary arteries (a direct projection); the vascular drawing in upper shares of both lungs is grown poor, in lower parts — is strengthened; roots of lungs are expanded, left — is generally covered with a shadow of heart; on the right, at the level of the fourth — the fifth mezhreberye — the site of infiltration of pulmonary fabric caused by a heart attack of a lung (it is specified by an arrow); the shadow of heart is expanded in both parties, the waist of heart is maleficiated; — an angiopulmonogramma at a thromboembolism of the left pulmonary artery, generally superlobar branch (I — blood clot, impregnirovanny a contrast agent in the left superlobar artery; 2 — the mouth of the left pulmonary artery which is insufficiently contrasted because of an arrangement

of «tail» of a tromboembol in it).

sovidny form with the top turned to a root of a lung, and the basis — to the periphery, meets rather seldom. In the subsequent a certain diagnostic value gets a symptom of the included vessels — thin vascular shadows, coming from a large artery, dugoobrazno bent towards a heart attack of a lung.

The greatest information on localization and prevalence patol. process the angiopuljmono-grafiya gives (see). To direct (morphological) signs of T. l. and. belong the central or regional defect of filling of an artery of large caliber (fig., b) and a symptom of «amputation» of a vascular branch — a stop of a contrast agent at the place of occlusion. Indirect (functional) signs of T. l. and. consider prolongation of an arterial phase of contrasting with delay or absence venous, uneven contrasting of small vessels, the slowed-down passing of a contrast agent on the party of defeat with rather accelerated blood-groove in an intact lung (asymmetry of contrasting of roots of lungs). This method of a research not always allows to reveal an embolism of small branches; besides, it can burden considerably a condition of the patient, promoting sharp raising of the pulmonary ABP, and also development of acute disorders of a cordial rhythm. In this regard carrying out an angiopulmonogra-fiya is reasonable only at suspicion of a thrombembolia of a pulmonary trunk or its leading branchs for the solution of a question of regional introduction of thrombolytic means or emergency a surgical

telstvo of a vmesh — endovascular removal of blood clot or an embolectomy.

Treatment. Pathogenetic therapy at T. l. and. consists in complex use of three groups of drugs (trombolitik, anticoagulants and antiagregant) for the purpose of a lysis of blood clot, recovery of passability of a vessel and normalization of a hemostasis. From trombolitik apply fibrinolysin (see), Streptokinasa (see Streptoliasum) or an urokinase, and also fibrinolitically active plasma (the drug with the high content of plasmin and the activator of plasmin received from blood of suddenly died people). Content of the plasminogen circulating in blood during the use of its activators falls and according to it efficiency of all decreases to lay down. actions; in such cases the replaceable plasmotherapy by means of transfusions of odnogruppny freshly frozen plasma is necessary. Short-term increase in fibrinolitic activity of blood is caused also nicotinic to - that and its derivatives, in particular nikotinat ksan-thinol, to-rye oppress function of thrombocytes. From anticoagulants in all cases apply heparin (see); did not lose the value and use of medical bloodsuckers (especially at small T. l. and.), emitting antithrombic substance hirudine (see). Ilo pro-procession of the acute period of T. l. and. heparin and bloodsuckers cancel, replacing them with anticoagulants of indirect action. Treatment of a trombolitikama and anticoagulants is combined with use of antiagregant — drugs of the most various pharmakol. the groups possessing nevertheless the general for


them ability to brake or suppress functional activity of thrombocytes, to reduce viscosity of blood and to eliminate disorders of microcirculation. Drugs of a low-molecular dextran (reopoliglyukin), acetilsalicylic to - that, Butadionum, anturan (Sulfinpyrazonum), Dipiridamolum (curantyl, Persantinum), theophylline, etc., and also the digidriro-bathing alkaloids of an ergot (see) possessing and - adrenoceptor blocking and antiserotoninovy action are considered as the most effective antiagregant.

Active treatment of the basic and associated diseases taking into account influence of means of therapy on processes of a thrombogenesis is at the same time carried out. For treatment of infarctive pneumonia appoint antibiotics.

The symptomatic treatment includes oxygen therapy (see) and use of means for stopping of a syndrome, dokhminiruyushchy in a wedge, a picture. At the same time consider that glucocorticoids, barbiturates, cardiac glycosides, diuretics, antibiotics of group of aminoglycosides and oral contraceptives reduce effect of heparin and indirect anticoagulants.

After acute manifestations of T. l. and. carry out only symptomatic therapy in connection with complications of a thromboembolism. Development of a pulmonary heart forms quite often the basis for transfer of patients into disability. A question of the direction of the patients who transferred T. l. and., decides on sanatorium treatment strictly individually depending on weight patol. process and its effects.

The main indication to an embolectomy is the massive T. l. ampere-second the heavy course of pathological process — the progressing decrease in the ABP with an oliguria, a decompensation of an acute pulmonary heart (sharp swelling of cervical veins, increase in a liver, etc.), the accruing arterial anoxemia.

Apply a direct and indirect embolectomy. The direct embolectomy in a crust, time is carried out in the conditions of use of the cardiopulmonary bypass. The indirect embolectomy is carried out by means of the special probe catheter with a razduvny cuff and a bowl (a cup-shaped hook) on the end. Access through one of femoral veins the probe catheter is advanced in a pulmonary artery and make its contrasting, then the bowl is brought to a tromboembol, block a blood stream inflating of a cuff and suck in tromboembol in a bowl (in detail operations of removal of a tromboembol — see the Embolism, surgical treatment).

Forecast of T. l. and. depends on level and extensiveness of embolization of a gleam of an arterial bed and disease severity, against the background of to-rogo the T develops. l. and.

Prevention consists in the prevention and timely treatment of phlebothromboses and thrombophlebitis (see), in fight against venous stagnation, preventive use of antiagregant (in some cases and anticoagulants) at persons, forced is long to be on a high bed rest. In the presence of the floating blood clot of any localization surgical prevention of T is shown. l. and. (thrombectomy, partial occlusion of the main vein or its bandaging).

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