THROMBO EMBOLISM
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.
ETIOLOGY OF SHARP
ARTERIAL IMPASSABILITY.
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.
ETIOLOGY OF SHARP
ARTERIAL THROMBOSES.
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.
PATHOGENESIS OF THE
SYNDROME OF THE SHARP ISCHEMIA
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.
CLINIC AND DIAGNOSTICS OF
THROMBOSES AND EMBOLISMES.
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.
TREATMENT.
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:
Easy;
Medium-weight;
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.
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.
THROMBOEMBOLISM OF PULMONARY ARTERY (TEPA)
On a level of defeat:
Т. pulmonary
trunk
Т. Share
and segmentary trunks
Т. Fine
branches
Etiology:
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
SOURCES:
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)
CLINIC
I. PULMONARY SYNDROME
1. THE SHORT WIND
2. ASHY CYANOSIS
3. HEMOPTYSIS
4. The PAIN IN the THORAX
(such as a stenocardia)
If there will not come death
in the first weeks after the beginning:
Pleurisy
-infarction-pneimonia (3-5 day)
II. THE SYNDROME SHARP
PULMONARY HEART
Pulsation of cervical veins
Increase CVP
Tachycardia
Rhythm of gallop
Accent of II tone on PА
III. THE ABDOMINAL SYNDROME
Nausea, vomitting
Sharp pain in the right
hypochondrium (a stretching of Glisson capsule
because of a hypostasis of a liver)
-leukocytosis
IV.HEMODYNAMIC SYNDROME
(decrease of AP)
-oliguria (hematuria,
proteinuria)
Coronary insufficiency
(changes on an electrocardiogram)
V. THE CEREBRAL SYNDROME
- Loss of consciousness
- Spasmes
- A hypostasis of a brain
CURRENT
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
Pleurisies
Pneumonias
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
|
Degree
|
Angiographic
index, points
|
Perfusion
deficiency,
%
|
|
I (easy)
|
Up to 16
|
Up to 29
|
|
II (average)
|
17-21
|
30-44
|
|
III (heavy)
|
22-26
|
45-59
|
|
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
Diagnostics
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.
TREATMENT
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.
|
|
|
|
SHARP
THROMBOSIS OF THE SUBCLAVIAN VEIN (SYNDROME OF PEGET- SCHRETTER-CRISTELLI)
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.
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.
