Sunday, 3 November 2013


BY everyone in a life at times happens so, that it would be desirable to turn time back, prior to the beginning of unpleasant event and to not allow its occurrence. In practice of the vascular surgeon frequently it is necessary to face with similar situations. The question is sharp vascular diseases, thromboses and embolismes of arteries - sudden corking of the main vessels. The instant termination of delivery of blood to body starts the whole cascade of the pathological reactions bringing in a result to destruction of body, and at times and an organism.
Formation of a blood clot on the changed wall of an artery with its gradual growth and corking (occlusion) of a gleam of a vessel refers to as an arterial thrombosis. A principal cause of a thrombosis is the obliterating atherosclerosis. Change of a vascular wall conducts to a turbulence of blood, pasting of thrombocytes and to formation of blood clots. Embolism it is carry of a blood clot from other organ (heart or an aorta) in other, not changed vessel with sharp it occlusion and the continued growth of a blood clot. Most frequently embolismes happen at illnesses of heart (a heart attack of a myocardium, fibrillation, infectious defeat of mitral valves) and at pathological expansion of large vessels - aneurysms. Process of embolism reminds a roulette when it is impossible to predict where the blood clot will depart. At its hit in brain vessels the insult, in intestines - it cause a necrosis and if the blood clot gets in a hand or a leg, develops their gangrene .
At a thrombosis or an embolism, normal blood supply in pool of the corked vessel suddenly stops and develops a pathological condition named a sharp ischemia. At an ischemia oxygen famine leads to to the termination of functioning, and in the subsequent, and destruction of fabrics of the struck body. Deenergizing of function begins with a nervous fabric - most  specialized. Thus in the beginning there is its irritation that leads to to a strong pain, then carrying out of a nervous pulse stops - sensitivity disappears, finiteness "stiffens". In a result the languid paralysis of muscles develops - active movements stop.
After destruction of a nervous fabric there comes a turn of a muscular fabric. This process is accompanied by stiffness of separate muscles and their groups with development of stiffness of joints, and in the subsequent and impossibility to bend finiteness in one joint. The similar condition refers to muscular contracture. The most viable appears a skin. Quite often fell at full destruction of muscles whereas the skin externally remained not changed. Full muscular contracture testifies to destruction of finiteness and necessity of its urgent amputation with the purpose of rescue of a life as absorbtion of products of muscular disintegration leads to to an irreversible poisoning of an organism with infringement of function of all vital bodies.
Development of a sharp ischemia fast enough, but at the certain stages convertible. If the body or finiteness have lost the function, but not lost yet restoration of blood circulation gives chance of their full restoration. In late terms restoration can be incomplete, loss of time deprives with any hope. The term which has been let off by a sharp ischemia for existence of finiteness, depends on many factors. At a thrombosis the destruction of finiteness comes not at once and not always as the vessel has been initially narrowed atherosclerotic plaque, and finiteness has got used to lead "half-starved" existence. Roundabout ways of blood supply developed. However change of conditions of blood supply deepens deficiency of oxygen and gradually leads to to dying of body.
As a whole at thromboses there are 2-5 days for rescue of finiteness. At embolismes infringement of blood supply comes instantly, that leads to to the sharp spasm, suddenly empty vessels and to the full termination of blood supply of finiteness. If to accept anesthetizing preparations and spasmolytics the spasm can decrease, and blood circulation in finiteness will improve. However, anyhow, delivery of oxygen sharply decreases, that starts process of a sharp ischemia. At embolismes the best results of treatment at restoration of a blood-groove till 6 o'clock, from the beginning of disease. Till 12 o'clock it is possible to rescue only 60 % of finitenesses, after 24 hours only 20 %.

Because of untimely diagnostics or late delivery of patients in a hospital specialized angiosurgical help this patient appears untimely. The convincing proof of it is high death rate of patients on the literary data from 20 up to 35 % and high frequency of amputations of finitenesses concerning a gangrene of 20 % (V.S.Saveljev) achieving almost.
Therefore an actual problem of today is improvement of preparation of doctors of the general structure: surgeons, therapists, neuropathologists, ambulance surgeons on questions of diagnostics and modern principles of treatment arterial embolismes.
Firm mastering of substantive provisions of diagnostics and medical tactics at these urgent diseases is certainly necessary and in preparation of the future doctor.
As embolismes, and sharp thromboses, it is impossible to count independent diseases. They always are consequence of the basic, so-called, embolo-or thrombogenic diseases. Revealing of these diseases, i.e. an establishment of etiology of sharp arterial occlusion in each concrete case, is the vital necessity.
The basic embologenic diseases.
1. Atherosclerotic cardiopathy: diffuse cardiosclerosis, postinfarction cardiosclerosis, a sharp heart attack of a myocardium, sharp an aneurysm of heart, chronic an aneurysm of heart.
2. Rheumatic mitral defect.
3. Congenital heart diseases.
4. Septic endocarditis.
5. Aneurysms of an aorta and its large branches.
6. A pneumonia.
7. Other: tumours easy, thromboses of veins of the big circle of blood circulation (at presence of defects of partitions of heart), an additional cervical edge.
8. A unstated source of embolism.
It is necessary to note, that at the overwhelming majority of patients with embologenic diseases of heart it is marked fibrillation.
The reasons intravascular thromboformation have been established in 1856. R.Virhovym who has united them in a well-known triad: damage of a vascular wall, change of structure of blood and infringement of a current of blood. Depending on what from factors of this triad is the leader in thromboformation, the reasons of sharp arterial thromboses can be systematized as follows.
Damages of a vascular wall:
I. Obliterating  atherosclerosis of 10 %.
II. Arteritises.
1. System allergic angiitis.
а) Obliterating thrombangiitis,
б) Nonspecific аorthoarteritis,
в) Nodular periarteritis.
2. Infectious arteritises.
III. A trauma.
IV. Iatrogenic damages of vessels.
V. Other (at frostbite, influence of an electric current
, etc.).
Changes of structure of blood.
1. Diseases of blood:
а) Polycythemia vera (illness of Vakez),
б) leukemias.
2. Diseases of internal bodies (an atherosclerosis, hypertonic illness, malignant tumours, etc.).
3. Medical products.
Infringement of a current of blood.
1. Extravasative  compression.
2. An aneurysm.
3. A spasm.
4. Sharp insufficiency of blood circulation, a collapse.
5. Previous operation on an artery.
In result of sharply arisen corking the main artery the spasm of peripheral vessels develops. The mechanism of development of arteriospasm is still found insufficiently out. Pathological arteriospasm complicates inclusion of collateral  blood-groove and in this connection it is considered as a principal cause of development of irreversible changes of fabrics as interferes with duly indemnification of the broken main blood circulation for the account of collateral blood circulations. However in case of a long heavy ischemia of fabrics the spasm of fine vessels apparently is replaced paralytic vasodilation owing to metabolic acidosis. Owing to infringement of hemodynamics (stasis of blood), pathological changes of a vascular wall in result of hypoxia and anoxias and changes of coagulant systems of blood the continued thrombosis in proximal (ascending) and in distal (descending) a direction in relation to a place of initial corking develops.
Borders of the continued thrombosis are usually limited to places of origin of large branches in which rather big speed of a blood-groove is kept. In an initial stage of process the blood clot usually floatable not united with an arterial wall also can be rather easily removed.
In the subsequent the blood clot increases, accustomed to drinking with a wall of a vessel, distributed to its lateral branches muscular arteries. Inflammatory reaction of a vascular wall develops. Owing to metabolic changes in fabrics there are micro-and macrounits of uniform elements of blood,microemboluses , thromboses in muscular and even the main veins (at 5-6 % of patients). Attributes of a venous thrombosis are parameters of that the blood-groove in finiteness is completely broken. Distribution of thrombotic process on microcirculated and a venous channel - extremely adverse prognostic  attribute. In such cases elimination of the reason of occlusion cannot be effective as after restoration of passableness of the main vessels normal blood flow in fabrics it is not observed, there is a secondary thrombosis of the main vessels owing to the high peripheral resistance, the complicated outflow.
Sharp impassability of the main arteries leads to to development sharp apoxia(hypoxia) and to infringement of all kinds of an exchange in fabrics.
The major value has development  metabolic acidosis, the aerobic oxidation caused by transition in anaerobic, to accumulation of superfluous quantity of suboxidated products of an exchange. In ischemic fabrics in a plenty there are active enzymes, for example kinins. An anoxia and metabolic acidosis destructions of muscular cells lead to to infringement of permeability of cellular membranes. As a result of it endocellular potassium and myoglobin collect in an interfabric liquid, get in the general blood-groove and develop hyperkalemia and  myoglobinuric nephrosis.
At heavy and long an ischemia of finiteness arises subfascial   hypostasis of muscles. They compression in dense fascial vaginas are aggravated with infringement of a blood-groove in fabrics. It can lead to necrosis of whole groups of muscles, is especial after operative restoration of a blood-groove in the main arteries as the hypostasis of ischemic muscles sharply increases after operation. Metabolic infringements (acidosis, active enzymes), stasis of blood, presence of macroaggregantes uniform metabolic infringements of elements of blood create conditions for intravascular thromboformation in fine vessels, capillaries, that finally leads to to development of irreversible changes in fabrics of finiteness. Deterioration of the general hemodynamics worsen and without that the broken local blood circulation.
Sensitivity an anoxia of various fabrics is various. In nervous and muscular fabrics in 10-12 hours come irreversible pathological changes, and in a skin - in 24 hours.
Clinical picture of sharp arterial impassability extremely variable. In one cases disease begins sharply, at once, within few minutes, the heavy ischemia of finiteness which leads to to a gangrene develops, in others - frustration of blood circulation arises gradually, clinical displays are minimal. The significant part of diagnostic mistakes at a pre-hospital stage is caused by that ambulance surgeons and polyclinics which it is usual the first observe such patients, expecting bright semiology, do not give value to "small" attributes of an ischemia that leads to to an establishment instead of a sharp thrombosis or embolism such diagnoses, as "radiculitis", "neuralgia", periostitis " etc.
On what it is necessary to base first of all at an establishment of the diagnosis? What symptom or symptom complex is pathognomic? Those, certainly, it is possible to count a syndrome of sharp ischemic finiteness. The given syndrome is observed in everything, without exception, cases of sharp arterial impassability and will consist of the following symptoms:
I. Subjective.
1. A pain in the struck finiteness.
2. Feeling of numbness, cold snaps.
II. Objective.
1. Change of painting of the struck covers.
2. Decrease in skin temperature.
3. Frustration of sensitivity.
4. Infringement of active movements in joints of finiteness.
5. Morbidity at palpation of ischemic muscles.
6. Subfascial hypostasis of muscles of a shin (or forearms).
7. Ischemic muscular contracture.
More correctly to solve questions of tactics of treatment, on term and volume classification of an ischemia of fabrics of finiteness (V.S.Saveljev) has been developed.
In classification " the ischemia of a pressure " is allocated three degrees of an ischemia (each of which in turn shares on subgroups), and also. Attributes of an ischemia are absent in rest and appear at loading.
At ischemia I of a degree there are no infringements of sensitivity and movements in the struck finiteness.
1А degrees it is characterized by presence of feeling of numbness, cold snaps, paresthesias.
1Б degrees appear pains in distal departments of finiteness.
For an ischemia of II degree frustration of sensitivity, and also active movements in joints are characteristic
From paresis (II And a degree)
Up to a paralysis (II a degree).
The ischemia of III degree is characterized beginning of necrobiotic  phenomena that is expressed clinically in
IIIа occurrence of subfascial  hypostasis
IIIБ a degree - partial
III In a degree - total contracture.
Absence of a pulsation of an artery distally of arteries occlusions is the unique clinical attribute, allowing to define localization of embolus or a blood clot.
It is necessary to pay attention to necessity frequently missed from a kind to carry out in parallel with palpation and auscultation of large main arteries. Revealing thus systolic noise allows to suspect a stenosis of proximally  located vessels that can change essentially earlier planned tactics of additional inspection and treatment.
From special methods of research the basic are angiography, ultrasonic dopplerography and radionuclide methods of research.

The basic method of treatment is operative: at embolismes - embolectomy, at thromboses - thrombectomy + X-ray operation.
There are no indications to conservative treatment, there are only contra-indications to surgical. Absolute contra-indications are:
1) agonal  condition of patients,
2) Total ischemic contracture of finitenesses (And III In a stage),
3) The heaviest general condition of patients at easy degrees of an ischemia (ИН-ИIБ a degree).
Relative contra-indications - a sharp heart attack of a myocardium, an insult, inoperable tumours, etc. at an easy ischemia (ИН-И1B degrees) and absence its progressing.
In all other cases, both at embolismes , and at thromboses, emergency operation which can be sometimes compelled is shown is deferred.
Tactics of surgical treatment of sharp arterial impassability.
At embolismes.
ИН - embolectomy - can be deferred at 24 o'clock.
ИIА - - "-
ИIB - - " - - emergency.
ИIIА - - "-
ИIIB - - "-
ИIIIА - embolectomy+fasciotomy - emergency.
ИIIIB - - "-
ИIIIC - primary amputation.
Fasciotomy it is carried out only at operations on the bottom finitenesses.
At a sharp thrombosis.
ИН - thrombectomy+ reconstructive operation can be edged for 7 day
ИIА - - " - - - "-
ИIB - - " - - - " - at 48 o'clock.
ИIIА - - " - - - " - at 24 o'clock.
ИIIB - - " - - emergency.
ИIIIА - - " - fasciotomy- - "-
ИIIIB - - " - - - "-
ИIIIC - primary amputation.
In all cases of a delay of operation and as as preoperative preparation, the complex conservative treatment directed on is carried out:
1. Preventive maintenance of increase and distribution of a blood clot.
а) Anticoagulants - heparin, neodicumarin, phenindione, pelentan;
б) Activators of fibrinolysis - a nicotinic acid
в) antiaggregants - reopolyglucin, penthoxiphyllins, acetylsalicylic acid.
2. Lysis of a blood clot.
а) thrombolysics - streptasa, plasminogen activator, actelisa.
3. Improvement of blood circulation in ischemic finitenesses.
а) diadynamic currents,
b) A magnetotherapy,
c) barotherapy,
d) Methods of gravitational surgery.
4. Improvement of a fabric metabolism in a zone of a sharp ischemia vitamin A, В1, В6, C, Е, prednisolone, hordox.
5. Improvement of function of the vital bodies - the preparations improving function of heart, a liver, kidneys, easy.
6. Preventive maintenance of progressing of an atherosclerosis - preparations of group statins.
The given therapy proceeds in the postoperative period. But it is necessary to emphasize, that at an inefficiency of medicamentous therapy, increase of an ischemia, in no event it is impossible to hesitate with operative intervention as passive tactics in the given situation can result not only in loss of finiteness, but also to destruction of the patient from an increasing ischemic intoxication.
In the conclusion it is necessary to note a number of the organizational moments. In all cases of statement of the diagnosis of a thrombosis and embolism, there should be a consultation of the vascular surgeon.

Thromboses of the main veins

 The most often kind of a thrombosis of veins is the thrombosis of deep veins of shin TDV which achieves to 160 cases on 100000 population in one year. So high desease is caused by change of a way of life of the modern person (hypodynamia, character of a feed, superfluous weight of a body, etc.), increase in a traumatism, more and more often occurrence of the hereditary and got infringements of system of a hemostasis, prevalence of oncological diseases, uncontrollable reception of hormonal preparations, etc.
On localization primary thrombotic affect and ways of its distribution distinguish a thrombosis of system bottom and top caval veins.

Thrombosis of system bottom caval vein:
Thrombosis of veins, draining muscles of a shin;
Ileo-femoral thrombosis;
Cava- ileofemoral  thrombosis;
Thrombosis of underrenal, renal, suprarenal segments bottom caval veins or a thrombosis of all trunk bottom caval veins;
Combined  total thrombosis of all deep venous system bottom caval veins.

By etiological  factor:
After infectious diseases;
After traumas;
After operations;
After sorts;
At varicose expansion of superficial veins;
At an allergy;
At presence of the intravascular congenital or got factors (a partition, a diaphragm, soldering, atresias);
At presence of extravascular  congenital or got factors (compression of veins arteries, tumours, aneurysms).

On clinical current:
Sharp thrombophlebitis;
Subacute  thrombophlebitis;
Postthrombophlebitic  syndrome;
Sharp thrombophlebitis on a background of postthrombophlebitic  syndrome.
On a degree of trophic infringements and frustration of hemodynamics:

Heavy forms
      The sharp thrombosis passes or in subacute, which can end with recovery, or develops a postthrombophlebitic syndrome. Researches of dynamics of a thrombosis have shown, that duration of the first stage makes 7-14 days. Later 14 days from the beginning of disease pass a sharp thrombosis in subacute. On the average in three months the third stage begins, thrombotic process gets chronic current - develops a postthrombophlebitic syndrome.
The sharp thrombosis of deep veins of a shin can arise also as independently, and as a result of distribution of thrombotic process of hypodermic veins through a mouth or system of communicant veins.
The shocking facts
From time to time in press there are shocking messages on terrible complication of " a thrombosis of the traveller " - pulmonary embolism. If the blood clot comes off a wall of a vein of the bottom finiteness, rises above on a current of blood and, permeating through heart, gets in lungs - the outcome can be fatal. The carried out researches have shown, that in the Great Britain more than 2000 air passenges annually die from so-called " a syndrome of long travel ". (the Data from " the Spiegel online " from January, 10 2001).

Discrepancy of diameters of veins of a shin and popliteal vein can lead to to formation  of "floatable"  blood clot and to development of embolic complications Diagnostics of sharp thromboses of deep veins of a shin has special value as in 10 % of cases disease proceeds without any symptoms, and in 2 % of cases leads to to a lethal outcome in result of thromboembolism of pulmonary artery (J.Hirsh, 1992). The establishment of the diagnosis demands careful scanning forward and back tibial, fibular and sural veins.
The heaviest form of a sharp venous thrombosis of deep veins of the bottom finitenesses and basin is dark blue phlegmasia. Pathophysiological  basis of disease is the thrombosis of the main deep veins of the bottom finitenesses, a basin and the basic collateral ways of outflow of venous blood.
Owing to thrombotic block of venous system of the bottom finitenesses and a basin hydrostatic pressure in a capillary venous network raises. Progressing of disease is caused by reduction or disappearance of a gradient of pressure between arterial and venous systems. Owing to infringement of processes of a filtration and reabsorption the liquid collects in fabrics, there is a deposition of blood, reduction of volume of circulating blood that leads to to development of hypovolemic  shock at 20-30 % of patients.
The medical program at TDV includes:
The termination of growth and distribution of a blood clot.
Prevention TEPA.
Restoration of passableness of a gleam of a vein.
The termination of growth and distribution of a blood clot can be achieved thanking an anticoagulant therapy, which means consecutive application direct and indirect (phenindione, acenocumarol, etc.) anticoagulants.
Now for anticoagulant therapy of TDV widely use low-molecular heparins (LMH). Their selective mainly anti-Ха action prolongs antithrombotic effect and reduces frequency of hemorragic complications. It is necessary to emphasize, that at use of  LMH the daily laboratory control over system of a hemostasis is unessential, that creates favorable preconditions for out-patient treatment of embolo-not-dangerous TDV.
For 3 - 4 days up to a prospective cancellation of heparin are necessary to appoint indirect anticoagulants. Them effective daily doze is supervised on a level of an index of prothrombin, which size should be stabilized within the limits of 45 - 60 %.
Alongside with anticoagulants in therapy of TDV it is expedient to use the hemorheologically active preparations (rheopolyglucin, derivatives of penthoxiphylline and a nicotinic acid) and nonspecific anti-inflammatory means (NAIM) parenteral or through rectum (in candles).
As to antibiotics their application at not complicated TDV is senseless the same as and at varicothrombophlebitis.
Exception can be made in case of pustular defeats of a skin or presence of " an entrance gate » for an infection (open crises, operational wounds, etc.), and also for patients with high risk of septic complications (a diabetes, a HIV, etc.).
For preventive maintenance of TEPA, besides anticoagulant therapy which in the certain measure prevents it, interfering with progressing of a thrombosis, at embolo-dangerous (floatable) blood clots apply various surgical methods: thrombectomy, implantation of the kava-filter or reefing of  bottom caval vein a mechanical seam.
Completely to restore passableness of a vein in cases early diagnosed (the prescription 3 - 5 days) segmentary TDV sometimes possible with the help of direct surgical intervention of thrombectomy) or thrombolysis  therapy.
Thrombolysis means - the mechanism of action
To thrombolysis  preparations concern fibrinolysin, streptokinase, urokinase, recombinant  activator of plasminogen of tissue type.
Fibrinolysin is a physiological component natural anticoagulative system of an organism. In a basis of its action ability to dissolve a string of fibrin lays.
Streptokinase, urokinase, streptodekase are indirect activators of plasminogen, which possesses ability to split fibrin and fibrinogen. Thereof develops a hypocoagulation and process of thrombolysis.
Recombinant activator of plasminogen is possess the similar mechanism of action, is rather active in the plan of thrombolysis, but causes a condition of generalized fibrinolysis less often.
The technics of  transcutaneous implantation of kava-filters of various designs (umbellate of Mobin-Uddin, Greenfield, Amplats, " the bird's jack ", " tulip of Gunther ", RAPTEPA,) has "sand-glass" much in common. Implantation of kava-filters is carried out in the X-ray-operative.
For an estimation of condition BCV
and reception of the information about embologenics of  blood clot in the beginning it is made retrograde or antegrade ileokavagraphy. A choice of access (retrograde - jugular, subclavian; antegrade - femoral) depends on prospective localization of a blood clot: carrying out of catheter through thrombosed veins is fraught with a fragmentation of a blood clot with development of TEPA.
The kava-filter implant directly below the ostiums of renal veins. At low position of the kava-filter formed between it and ostiums of renal veins the "dead" space raises risk of thromboformation and TEPA.
After implantation of the kava-filter it is carried out the  control radiography for the control of its site. During 2 days the patient is on a confinement to bed; to 5-6 days appoint antibiotics, carry out the treatment by heparin.
At septic thromboembolism the kava-filter does not interfere with passage fine bacterial emboluses, therefore in these cases resort to bandaging BCV. At a septic thrombophlebitis of a small basin besides tie up left ovarian  vein.

On a level of defeat:
Т. pulmonary trunk
Т. Share and segmentary trunks
Т. Fine branches
1. Intimate insufficiency
-fibrillation, IDH
Heart attack of a myocardium
Defects of mitral and tricuspid valves
Bacterial endocarditis
2. Leukemia
3. Malignant formations
4. Burns
5. Profuse bleedings
6. A pathology connected with dehydration (enteritises, vomitting, uncontrolled reception laxative)
7. Operations on bodies of a belly cavity and a small basin

75-95: From system V.C.INF.
5-25 % from the right auricle
0,5-2 % V.C. SUP.
Avulsion of a  blood clot occurs at more often:
- Cough, straining effort - fluctuations of pressure in a belly cavity and a thorax
- To the physical loading increasing volumetric speed of a blood-groove

PATHOGENESIS: Progressing growth of resistance to a blood-groove in easy (the AP in a pulmonary trunk in 3-4 times is higher than norm) - sharp pulmonary heart> shunting of venous blood in easy> increase CVP> decrease of AP in the big circle and reduction of minute volume> hypoxia> global hypoxia
At adhesion of thrombocytes it is liberated a thromboxane and serotonin (vasopressor action)> an ischemia (hypoxia) - compensatory reactions
Intensification of fibrinolysis ,degranulation of corpulent cells> liberation of heparin and transmitters of inflammation (histamine)> increase in permeability of a vascular wall> a bronchospasm> ventilating hypoxemia, interstitial  hypostasis (at infiltration in a pleural cavity - compression atelectasis, in alveoluses - acting with transsudate cholesterol and oleic acid inactivate a SURFACTANT)> congestive atelectasis
HYPOXIA (leading part of  pathogenesis of cellular infringements)

4. The PAIN IN the THORAX (such as a stenocardia)
If there will not come death in the first weeks after the beginning:
-infarction-pneimonia (3-5 day)
Pulsation of cervical veins
Increase CVP
Rhythm of gallop
Accent of II tone on PА
Nausea, vomitting
Sharp pain in the right hypochondrium (a stretching of Glisson capsule because of a hypostasis of a liver)
-oliguria (hematuria, proteinuria)
Coronary insufficiency (changes on an electrocardiogram)
- Loss of consciousness
- Spasmes
- A hypostasis of a brain
I. Sharp (reduction of a blood-groove more than on 75 % - instant death)
II. Subacute (share or segmentary vessels)
Proof decrease of AP
Right-ventricular insufficiency
Infringement of an intimate rhythm
Formation in the subsequent chronic pulmonary heart

There are some classifications of TEPA. Morphological it is based on an estimation of the size of a vessel and volume of occlusive  vascular channel of a small circle (Savelyev B.C. and co-authors.):
1)    Massive - embolism of a trunk and branches of pulmonary artery;
2)    Submassive -embolism of share and fineer branches;
3)    embolism of branches of pulmonary artery.
On the basis of the data of pulmonary angiography and perfusion scannings the index of volume of defeat in points on Miller (1979) and is offered to a degree of weight. This classification has a wide circulation, is especial in the specialized surgical centers under condition of application in diagnostics of pulmonary angiography and perfusion scannings.

Table 1. A degree of infringement of perfusion of lungs

Angiographic  index, points
Perfusion deficiency, %
I (easy)
Up to 16
Up to 29
II (average)
III (heavy)
IV (heaviest)
27 and more
60 and more

Depending on current of disease allocate following forms of TEPA (with Zlochevskij G.M.; Mazaev T N, Kunitsyn D.V.):
1)    Lightning,
2)    Sharp,
3)    subacute,
4)    recurrent
In connection with polymorphism of clinic TELA, for confirmation of the diagnosis the following methods of research are carried out:
Tool researches
·       Research of gases of arterial blood,
·       Registration of an electrocardiogram,
·       radiography of organs of a thorax,
·       Echocardiography,
·       perfusion/ventilating scintigraphy of lungs,
·       Ultrasonic dopplerography of the main veins of legs); under indications
·       pulmonary angiography,
·       Measurement of pressure in cavities of right heart,
·       phlebography.
Electrocardiography in most cases helps to suspect massive TEPA. Occurrence of attributes sharp pulmonary heart: syndrome Me Ginn-White (S1Q3 T3), displacement of a transitive zone (deep SV5-6 in a combination with negative TV1-4) is caused by increase of a level of pressure in a small circle of blood circulation over 50,0 mm рт. An item.
Survey radiography of a thorax. The most typical symptoms are symptoms sharp pulmonary heart: expansion top caval vein, shadows of heart to the right and bulging of a cone of pulmonary artery.
At the embolism in one of the main branches of pulmonary artery, in share or segmentary branches to be observed pauperization ("enlightenment") of pulmonary figure (symptom of Westermark). High standing of a dome of a diaphragm on the side of defeat.
The echocardiography allows to find out occurrence sharp pulmonary heart, to exclude a pathology of valvate  device and a myocardium left ventricle. With its help it is possible to define expressiveness of a hypertensia of a small circle of blood circulation, to estimate a structural and functional condition right ventricle, to find out thromboemboluses in cavities of heart and in main pulmonary arteries, to visualize an open oval window which can influence expressiveness hemodynamic frustration and be the reason paradoxical embolism.
Perfusion scanning easy, carried out after intravenous introduction of macrospheres of albumin, marked 997с, admits as the most adequate method of screening TEPA. Absence of infringements pulmonary  blood-groove on scintigrams, executed at least in two projections (forward and back) completely excludes the diagnosis of thromboembolism.
Ultrasonic scintiangiography of veins of the bottom finitenesses enables to find out a source of embolization. Thus it is possible to receive the exhaustive information on localization, extent and character of thrombotic occlusion , presence or absence of threat repeated embolism. Difficulties arise at visualization of iliocaval  segment to which can be interfered by intestinal gas.
Complex opaque  research including sounding of the right departments of heart, pulmonary angiography and retrograde iliocavography, allows to solve unequivocally all diagnostic problems at suspicion on TEPA. Angiography it is absolutely shown in all cases when it is not excluded massive embolic defeat of vessels easy, and allows will solve the problem on a choice of a method of treatment.
For confirmation of diagnosis TEPA use the following laboratory researches. At massive TEPA decrease of  PaO2 less than 80 mm can be observed. A hg at normal or reduced PaCO2; increase in activity of LDH and a level of the general bilirubin in blood at normal activity of asparaginic transaminase. Last decade in clinical practice for diagnostics the method of definition of markers of activation of coagulation and fibrinolysis, as diagnostics of fibrinopeptide A and D-dimer is applied. These methods are high-sensitivity at a thrombosis, but insufficiently specific to diagnostics of TDV and TEPA. If in case of negative reaction to presence D-dimer in blood it is possible to speak about absence of a venous thrombosis at positive reaction on D-dimer it is necessary to confirm the diagnosis of a thrombosis other methods confidently.
1. Thrombolysis:
- streptodekase (immobilize on molecules of rheopolyglucin enzyme, streptase, plasminogen activator, celiase)
2. Anticoagulants
3. Disaggregants
4. Symptomatic therapy
Surgical treatment
1. Embolectomy
- Indirect (a probe through a femoral vein)
- A straight line
2. Kavareefing
3. Statement of kavafilter. Are shown at relapses of thromboembolism and as preventive methods at floatable blood clots.

To development of disease promote the topographoanatomical  features  of subclavian vein, - located in a circle of bone and tendo
-muscular formations. At strong pressure of muscles of the humeral zone, combined to movements in a humeral joint, the sizes of subclavian space decrease and the vein appears squeezed between the collar bone and I an edge. Especially favorable conditions for infringement of outflow on subclavian  vein and consequently, and thromboformation arise at high standing I of an edge, hypertrophies of subclavian muscle and tendo-muscular part of a small chest muscle.
Clinic and diagnostics: syndrome of Peget- Schretter - Cristelli
is observed mainly at people in the age of 20-40 years with well advanced muscles, engaged in sports or heavy physical work. The basic clinical attributes of a sharp thrombosis of subclavian vein are the expressed hypostasis, cyanosis, a pressure and expansion of hypodermic veins of the top finiteness and a humeral zone of the corresponding side (is more often on the right), pains. Occurrence of these symptoms is preceded usually with significant physical loading.
The hypostasis is characterized by density and absence of fossas
at pressing. Quite often it grasps not only a hand and a humeral zone, but also passes to the top half of thorax. Expansion and a pressure of hypodermic veins in early terms of disease is appreciable only in area of antecubital fossa. Subsequently localization of the expanded veins corresponds to borders of distribution of a hypostasis. Cyanosis of integuments it is most expressed in the field of a brush and a forearm.
At distribution of a thrombosis on axillary
and humeral veins current of disease becomes heavy. The increasing hypostasis of fabrics in some cases conducts to squeezing arterial trunks owing to what weakens pulse on a beam artery and the temperature of finiteness is reduced. Infringements of arterial blood circulation are sometimes so significant, that there is a danger of development of a gangrene.
After the subsiding of
the sharp phenomena there comes return development of a clinical picture.
However at some patients of full recourse of symptoms of disease does not occur, that allows to allocate a chronic stage of a syndrome.
Diagnostics of a sharp thrombosis of  a subclavian vein in most cases does not represent difficulties. It is based on the mentioned above symptoms and on often connection of disease with physical loading. A valuable method of the research, allowing to judge localization and prevalence of a thrombosis, about a degree of development of collateral vessels, is phlebography
at which contrast substance enter in a cubital vein or in one of superficial veins of a back surface of a brush.
Treatment: basically conservative. Indications to thrombectomy
arise at threat of development of the venous gangrene, expressed regional hemodynamics infringements. To remove a compression of a subclavian vein, simultaneously make interventions on muscles, sinews or bones. In a chronic stage of disease carry out the reconstructive vascular operations directed on creation of additional ways of venous outflow from the top finiteness by anastomosing of an axillary vein or a distal  piece of a subclavian vein with external jugular vein. As shunts use the transplants found from the big hypodermic vein of a hip.

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