- IDCS symptoms
- IDCS reasons
- Treatment of the IDCS
IDCS - the most widespread type of pathology of a hemostasis. Its basis is a generalized blood coagulation in vessels of a microcirculator bed with formation of a large number of microblood clots and units of blood cells. At the same time there is a blocking of normal blood circulation in most bodies and systems leading to development in them profound dystrophic changes. After an intensive blood coagulation develop hypocoagulation (decline in the ability of blood to coagulation), thrombocytopenia (decrease in quantity of thrombocytes in blood unit of volume) and hemorrhages (bleeding). The syndrome arises at the most various diseases, always leading to loss of liquid properties of blood and disturbance of its circulation in capillaries that is incompatible with normal life activity of an organism. At the same time weight, prevalence and speed of development of the IDCS are very different - from fulminant deadly forms to latent (hidden) and long, from a generalized blood coagulation to regional and organ trombogemorragiya.
The IDCS can be acute, becoming aggravated, long and hidden. At all these options, especially at acute, repeated transitions from trombotichesky complications to hemorrhagic and vice versa are possible.
The I stage - hypercoagulation and aggregation of thrombocytes.
The II stage - transitional. In this stage the accruing coagulopathy with thrombocytopenia, multidirectional shifts in the general coagulability tests is noted.
The III stage - a stage of deep hypocoagulation. In this stage ability of blood to coagulation can be lost completely.
The IV stage - recovery. In case of an adverse current of the IDCS in this stage various complications form, leading in most cases to a lethal outcome.
It is almost more convenient to use the following major indicators:
1) a condition of system of a hemostasis which is defined:
a) according to the general coagulative tests;
b) on the content of soluble fibrin and decomposition products of fibrinogen in
c) on the content in blood of thrombocytes and their units with approximate assessment
functions of cells;
d) on antithrombin III level;
e) on a reserve of plasminogen and its activators;
e) on detection of inferiority of coagulation at record of a tromboelastogramma (anomaly of structure, fixing and mechanical properties of a clot);
g) on ability of plasma of the patient to accelerate or slow down coagulation and formation of a clot in a tromboelastogramma of normal blood or plasma;
2) existence, expressiveness and localization:
3) expressiveness and duration of hemodynamic disturbances (decrease in arterial and central venous pressure, volume of the circulating blood and another) taking into account the leading mechanisms of their origin:
a) the causative factor which caused the IDCS (an injury, intoxication,
4) existence and expressiveness of respiratory insufficiency and a hypoxia with the indication of their form and stage;
5) existence and weight of damage of other target organs suffering most at the IDCS:
a) kidneys (acute renal failure);
e) adrenal glands and hypophysis;
e) a stomach and intestines (acute ulcers, bleedings at a hyperpermeability of a vascular wall);
6) expressiveness of anemia;
7) disturbances of balance of electrolytes of blood (sodium, potassium, chlorine, calcium) and acid-base balance.
The clinic of the IDCS consists of symptoms of the basic disease which served as its reason, signs of the developed shock (at acute forms), deep disturbances of all links of system of a hemostasis, thromboses and bleedings, a hypovolemia (decrease in filling of a vascular bed) and anemia, dysfunction and dystrophic changes in bodies, metabolism disturbances.
The more sharply the IDCS, especially the hypercoagulation phase (the increased blood coagulation) is short-term and the phase of the expressed hypocoagulation (a reduced blood coagulation) and bleeding is heavier. Such acute forms are characteristic generally for infectious and septic, obstetric, posttraumatic (a krash-syndrome, burns, fractures of bones), surgical (at traumatic operations), toxic (stings of snakes) and all types shockogenic (including cardiogenic shock) the IDCS. Weight of the IDCS in similar cases depends not only on expressiveness of the main pathology and the general initial condition of an organism of the patient, but also on timeliness and sufficiency of first aid, completeness of anesthesia and further anesthesiology providing, timeliness and the maximum atravmatichnost of operative measures, control of system of a hemostasis and completeness of the prevention and elimination of its disturbances, maintenance of rheological properties of blood, fight against disorders of microcirculation and the general hemodynamics.
Emergence and progressing of the IDCS are promoted by insufficiently bystry and full removal of the patient from shock and hypotonia (the lowered tone), the increased injury of operative measures (allocation of bodies from commissures in the stupid way with their puddling and anguishes, intensive massage of a uterus after the delivery), insufficient correction of a hypovolemia and not shown transfusions of the stored blood containing a huge number of microclots and aggravating the IDCS instead of plasma, albumine, a reopoliglyukin and other solutions.
The acute IDCS is observed also at destructive processes in bodies, at destructions of lungs of staphylococcal and other origin, acute dystrophy of a liver of a toxic or virus origin (a gepatorenalny syndrome), acute necrotic or hemorrhagic pancreatitis. The specified pathology forms very often are combined with a septicaemia (appearance of the pathological agent in blood) and various forms of the superinfection which is difficult giving in to treatment. At all these types of pathology also the wavy current of the IDCS is possible – the periods of heavy disturbance of a hemostasis temporarily are replaced by quite satisfactory condition of patients then again there occur catastrophic deteriorations.
Except symptoms of a basic disease, the clinical picture of an acute IDCS consists of the following main components.
Hemocoagulative shock. It results from disturbance of blood circulation in microvessels of various bodies, a hypoxia of fabrics, with education in blood and receipt in it from the outside of the toxic products including which are formed in the course of a blood coagulation (hemocoagulation) and a fibrinolysis (fusion of the formed blood clots). It is quite difficult to track transformation of the shock which was the reason of the IDCS in hemocoagulative as they merge in the general acute failure of a hemodynamics with catastrophic falling of arterial and central venous pressure, disturbances of microcirculation in bodies with development of their acute functional insufficiency. As a result acute renal or gepatorenalny (hepatonephric) failure, a shock lung and other complications can develop. The IDCS beginning with shock always proceeds katastrofichny, than besshokovy forms, and the are heavier and more long shock, the forecast for the patient's life is worse.
When developing bleedings hemocoagulative shock is transformed in hemorrhagic at once or after temporary improvement.
Disturbances of a hemostasis take place different phases - from hypercoagulation to more or less deep hypocoagulation up to total loss by blood of ability to coagulation. Identification of hypercoagulation does not demand special efforts - it is found already at extraction of blood from a vein: blood immediately turns in a needle or in a test tube. In such cases from laboratory the answer arrives that it is impossible to investigate coagulant system of blood as the sent blood turned. If at capture of blood there was no technical mistake, then such answer in itself has diagnostic value, confirming the expressed hypercoagulation.
In the second phase one coagulative tests reveal hypercoagulation, and others - hypocoagulation. The divergence of these shifts confusing doctors at koagulogramma assessment, also typical laboratory sign of the IDCS. There is moderate thrombocytopenia (decrease in quantity of thrombocytes), aggregation function of thrombocytes is significantly reduced.
In a hypocoagulative phase thrombin time is sharply increased and other parameters of a koagulogramma - sg-stki small are in a varying degree broken, friable or are not formed at all. The effect of "transfer" plasma of the patient is observed or accelerates coagulation of normal plasma, or slows down it. In the third phase thrombocytopenia goes deep, function of thrombocytes is sharply broken. At coagulation by poison of an efa a large amount of the blocked (soluble) fibrin is found. A part of soluble fibrin is curtailed also the strong thrombin (causing coagulation of normal plasma for 3-4 c).
The true afibrinogenemiya (lack of fibrin in a blood plasma) at the IDCS almost never happens, and are available more or less expressed hypofibrinogenemia (decrease in amount of fibrin in a blood plasma) and linkng of a considerable part of fibrinogen with soluble fibrin. Test with poison of an efa reveals both this blocked fibrinogen/fibrin, and ability of blood to coagulation against the background of a geparinoterapiya (therapy by fibrin). Only in a terminal phase of the IDCS coagulation and in the test with efa poison is sharply extended that is a bad predictive sign.
Decrease in level of fibrinogen in plasma in comparison with initial is observed at an acute IDCS always, and at long and chronic forms happens seldom. However at the acute forms which developed against the background of an initial fibrinosis (the increased amount of fibrin), this decrease leads only to the fact that concentration of fibrinogen in plasma reaches normal level. Such forms happen often as the fibrinosis is observed at all septic and acute inflammatory diseases, a myocardial infarction and other bodies, pregnancy, especially with toxicosis, immune diseases. In total about 50% of cases of an acute IDCS are the share of all these forms.
Early and steadily at the IDCS antithrombin III level in plasma, being a physiological antiagregant decreases. It is spent for an inactivation of all blood-coagulation factors. Assessment of this disturbance has great clinical value as the antithrombin III depression to 75% and reflects weight of the IDCS below.
Rather early in plasma the content of plasminogen and some of its activators decreases that comes to light rapid tests. Level of endothelial activators of fusion of blood clots in most cases is considerably increased. Naturally also the content in plasma of patients of a factor of Villebrand increases that speaks about deep damage of an internal cover of blood vessels.
Hemorrhagic syndrome - frequent and dangerous, but not obligatory manifestation of the disseminated intravascular coagulation. In most cases it arises at an acute IDCS, a thicket in a hypocoagulative phase though quite often multiple and plentiful bleedings are registered also in the second phase against the background of the normal or slightly reduced content of fibrinogen in plasma. The heaviest bleedings are observed, naturally, at full or almost full incoagulability of blood. From the clinical point of view it is important to differentiate accurately the bleedings of local type connected with damage or destructive changes in bodies and the widespread hemorrhagic syndrome caused by cumulative changes in system of a hemostasis.
Bleedings at injuries and operative measures belong to bleedings of local type, puerperal and postabortion uterine bleedings, bleedings from sharply created stomach ulcers or a duodenum, a hamaturia (emergence of blood in urine) owing to a kidney heart attack. These bleedings are connected not only with the general disturbances of a hemostasis, but also with local (organ) pathology which has to be revealed, correctly estimated by the doctor in time and is considered when performing complex therapy. So, for example, the frequent combination of the IDCS to an atony of a uterus demands, in addition to haemo static therapy, a complex of the influences recovering a normal tone of this body at bleedings from acute stomach ulcers - a local stop of bleeding (through фиброгастроскоп) and changes of the general tactics of treatment.
The general bleeding is characterized by emergence of bruises, bruises and hematomas in skin, hypodermic and retroperitoneal cellulose, nasal, gastrointestinal, pulmonary and renal bleedings, hemorrhages in various bodies (a brain and its covers, heart, adrenal glands, lungs, a uterus), diffusion transuding of blood in pleural and belly cavities, sometimes - in a pericardiac bag. At each patient prevail one, other forms of bleedings.
Bleeding leads to acute posthemorrhagic anemia, in hard cases - to hemorrhagic shock. Decrease in a hematocrit is lower than 15-17% and impossibility to raise it by replacement therapy by eritrotsitny weight predictively are adverse and tell about the proceeding blood loss though it not always easily comes to light.
Disturbance of microcirculation in bodies with their dysfunction and dystrophy - other group of the major disturbances defining a clinical picture, weight, an outcome and complications of the IDCS. At different patients and at different pathogenetic forms of this syndrome suffer one, other bodies designated in literature as target organs.
Extremely often such body are lungs in which vessels from venous system the huge number of microclots of fibrin, units of blood cells and products of proteolysis is brought. As a result acute pulmonary and circulator insufficiency - short wind, cyanosis, decrease in saturation of blood oxygen, and then increase in carbon dioxide in an arterial blood develops; there are intersticial hypostasis, heart attacks of a lung and other signs of "a shock lung", is frequent with development respiratory a distress syndrome. The intensive transfusion care applied at the IDCS quite often aggravates these disturbances, increasing accumulation of water, sodium and albumine in lung tissue.
The special p-vstvitelnost to vn-trivenny administration of liquid and massive hemotransfusions sometimes often is found in patients excess 200300 ml of liquid sharply strengthen a hypoxia and provoke a fluid lungs. At pulmonary option of defeat with special care it is necessary to compare amount of the entered liquid with a diuresis and blood loss, to timely add diuretics, lasixum to complex therapy. It is also necessary to transfer timely the patient to artificial ventilation of the lungs with creation of positive pressure on an exhalation.
Acute renal failure - organ defeat, the second for frequency, at the IDCS. It is shown in the form of decrease in amount of the emitted urine up to a full anury (lack of a mocheotdeleniye), allocation with urine of protein, erythrocytes. At the same time the water and electrolytic balance, and also acid-base balance in an organism is broken, in blood serum increase of level of creatinine, and afterwards - residual nitrogen and urea is noted. In general this syndrome does not differ from other types of an acute renal failure.
Heavier the combined forms - "a shock lung" with an acute renal failure or a gepatorenalny syndrome (hepatonephric insufficiency) proceed. In these cases metabolic disturbances are heavier and various that creates additional difficulties at treatment of patients.
The gemolitiko-uraemic syndrome of Gasser, all types of an acute intravascular hemolysis can be considered as typical renal forms of the IDCS, but hemolysis is frequent also at many other forms of the IDCS.
There is a damage of a liver with development of parenchymatous jaundice less often, and sometimes and acute pains in right hypochondrium. The return phenomenon - development of the IDCS against the background of acute or crushing chronic damage of a liver (acute toxic and viral hepatitises, a terminal phase of cirrhosis) is more often observed.
The stomach and intestines belong to target organs. These defeats are followed by deep focal dystrophy of a mucous membrane of a duodenum and stomach, formation of microblood clots and stazy in their vessels, emergence of the multiple bleedings turning in hard cases into continuous hemorrhagic treatment of bodies, formation of acute erosive and ulcer defects, being a source of the repeating bleedings giving a high lethality. High doses of glucocorticosteroids (for the purpose of removal of the patient from shock), speed up the drugs causing erosion of a mucous membrane of a stomach (acetylsalicylic acid), and also adrenostimulyator (adrenaline, noradrenaline) and aggravate these terrible manifestations of the IDCS.
At the IDCS also other part of intestines which can become a source not only heavy bleedings, but also additional intoxication owing to paresis, rejection of fibers and a massive autolysis hard is surprised.
Disturbances of cerebral circulation, fibrinferment and bleeding in this area give the most various symptomatology - from a headache, dizziness, confusion of consciousness and unconscious states to typical trombotichesky or hemorrhagic strokes, the meningism phenomena.
The damages of adrenal glands and hypophysis leading to a typical picture of acute adrenal insufficiency (a long collapse, a diarrhea, electrolytic disturbances, dehydration) and not sugar mocheiznureniye are observed generally at the IDCS of a septic and shockogenic origin. They are connected or with thrombosis of the vessels feeding these glands or with hemorrhages in them.
IDCS frequency at different types of pathology is heterogeneous. At one diseases and influences it arises surely and becomes an integral part of pathological process, at others meets less often.
More often the IDCS is caused by the following pathological processes and influences.
Generalized infections and septic states (bacteremia, a virusemia - existence of viruses in blood), including at abortions, in labor, at long catheterization of vessels. At septic shock the acute IDCS happens always. The majority of cases of the IDCS at newborns is connected with infections.
All types of shock, such, as hemorrhagic, traumatic, burn, anaphylactic (arising at an allergy), septic and cardiogenic. The IDCS is the obligatory satellite of shock of any origin. At the same time severity of the considered syndrome is in directly proportional dependence on expressiveness and duration of a depressed case.
The operative measures which are especially traumatic for the patient (especially at malignant new growths, operations on parenchymatous bodies, use of agrarian and industrial complex and intravascular interventions). Bleedings, a collapse massive hemotransfusions speed up the IDCS.
Any terminal states are followed by an IDCS.
The IDCS always develops if the patient has an acute intravascular hemolysis (destruction of cells in blood vessels), including at incompatible transfusions (hemotransfusions, not suitable this patient on group accessory).
Obstetric pathology, in particular placental presentation, premature placental detachment or its manual department, obstruction of vessels of a uterus amniotic waters, pre-natal death of a fruit. At all listed states the heavy IDCS is registered in 20-35% of cases.
Treatment of the IDCS:
Treatment of the IDCS presents great difficulties and not always happens successful. The lethality at acute forms makes 30%. Inconsistency and insufficient reliability of data on a lethality are connected, on the one hand, with the fact that statistical reports join patients with background diseases, different in weight, and with different expressiveness of the IDCS.
First of all at treatment of a syndrome of the disseminated intravascular coagulation intensive fight against the pathological processes causing and aggravating the IDCS is conducted. Such therapy has to be directed to elimination is purulent - the septic processes which are often the cornerstone of the IDCS. The earliest is in this situation necessary, the antimicrobic therapy based on clinical indications, but not on the late bacteriological researches.
The basis for the above-stated therapy are data on communication of the IDCS with an infection, abortion, an early bursting of waters (especially muddy), fervescence, signs of destructive and inflammatory process in lungs, an abdominal cavity, urinary tract, genitalias, signs of intestinal toxicoinfection, meningeal signs.
Prompt fervescence, and also changes of laboratory indicators of blood tests, such as a leukocytosis, a deviation to the left, are an additional reason for purpose of antibacterial therapy. As a rule, this therapy is carried out by antibiotics of a broad spectrum of activity, often include in therapy at - globulins.
At staphylococcal and other bacterial destructions in bodies therapy often happens effective only at addition to antibiotics of high doses of anti-proteases (for example, Contrykal on 100 000-300 000 PIECES/days and more). These drugs join in therapy to tear off disintegration of fabrics, and also intoxication and receipt in a blood stream of fabric thromboplastin owing to destruction of fabrics.
Also leading moment in therapy of the IDCS is stopping of the developing depressed case which bystry elimination can tear off the begun IDCS or it is enough soften of it. As such therapy intravenous injections of saline solutions, jet and drop transfusions of plasma, реополиглюкин (to 500 ml/days), glucocorticosteroids are applied (Prednisolonum intravenously on 80 mg). At use of plasma at intravenous injections it is necessary to add 5000 PIECES of heparin.
At the very first stages of development of a syndrome of the disseminated intravascular coagulation rather good effect is given and - adrenoblockers. Their action is based on improvement of microcirculation in bodies, preventing to thrombosing of vessels, decrease in aggregation of thrombocytes. Majeptil, phentolamine which are applied in 1% solution on 5 mg intravenously have such properties триопроперазин, дибенамин.
Also high performance and - adrenoblockers is noted at the IDCS in case of their early use. It should be noted that adrenaline and noradrenaline very noticeably aggravate the IDCS, strengthening both fibrillation, and aggregation of thrombocytes, and also increasing adjournment of fibrin in capillaries of kidneys, easy and other bodies.
Microcirculation and preservation in a blood-groove of active thrombocytes are favorably influenced by complex use of trental and curantyl on 100–200 mg intravenously repeatedly. The above-stated drugs have to be used both in an early stage of process, and at development of acute renal and respiratory failure, and also when carrying out a hemodialysis, plasma exchange and in other situations when blood contacts to an alien surface.
It should be noted that heparin can strengthen a decrease of functionally active thrombocytes from a blood channel and deepen thrombocytopenia, creating this way, and not just anticoagulating action threat of bleedings.
Dynamic control of the maintenance of thrombocytes in blood gets at the IDCS including in the course of its treatment by heparin, extremely important value.
Heparin is often inefficient because of its late appointment when formation of fibrin and aggregation of thrombocytes with their adjournment in a microcirculator bed generally already came to the end, and also owing to major deficit of antithrombin III and high content in blood of the proteins of an acute phase blocking heparin or because of formation of abnormal forms of thrombin.
At a geparinoterapiya it is necessary to follow the following basic rules. It is necessary to apply heparin perhaps earlier – in a hypercoagulation phase in doses of 20 000-40 000 PIECES/days, and in the second (transitional) phase - in the doses which are not exceeding 20 000 PIECES/days.
During these periods heparin is used for "cover" of basic therapy by freshly frozen plasma.
In a stage of hypocoagulation and bleedings heparin is used only in small doses for "cover" of transfusion therapy (on 2500 PIECES before hemotransfusions and plasmas). In a little high doses it can be applied in combination with Contrykal and other anti-proteases.
If the IDCS is caused by severe bleedings, include antienzymes (Contrykal, Gordoxum) in treatment.
At bleeding it is not necessary to apply for the purpose of blood substitution реополиглюкин as it in addition breaks a hemostasis.
At development of the third stage of a syndrome of the disseminated intravascular coagulation, at accession to this morbid condition of plentiful bleedings, an incoagulability of the blood expressed to hypocoagulation and also if the clinical picture is complicated by bleedings from digestive tract ulcers (a hematemesis, a tar-like chair), severe uterine bleedings, heparin is categorically contraindicated.
Also it should be noted that blood loss is found not always in time therefore as indications to cancellation of heparin serve symptoms of quickly progressing hemorrhagic collapse and an anemization (a lowering of arterial pressure and tachycardia at simultaneous falling of a hematocrit, lack of their correction at transfusions of eritrotsitny weight, albumine, plasma).
As other contraindication serves quickly progressing thrombocytopenia as heparin can sharply strengthen this disturbance.
In a phase of deep hypocoagulation, bleedings and thrombocytopenia the most urgent is administration not of heparin, and high doses of inhibitors of proteases (Contrykal on 50 000-100 000 PIECES intravenously kapelno). When resuming bleeding this dose can be repeated several times a day.
At the syndrome of the disseminated intravascular coagulation which developed against the background of bleedings or connected with destructive processes in bodies, such as staphylococcal destruction of lungs high doses of Contrykal have to join in therapy from the very beginning. This therapy not only stops the IDCS, but also suppresses disintegration of fabrics, eliminates intoxication and intake of thromboplastin from fabrics in blood.
Anti-proteases also suppress products of fabric thromboplastin and activation of coagulation by the proteases associated with cancer cells and blasts. The possibility of stopping is explained by Contrykal and other anti-proteases of the IDCS this effect at an acute promiyelotsitarny leukosis. In some cases the disseminated intravascular coagulation the good therapeutic effect gives complex use of Contrykal and heparin.
Transfusion therapy makes a basis of treatment of a syndrome of the disseminated intravascular coagulation that provides correction of disturbances of a hemostasis; compensation of volume of liquid in circulation and recovery of the central venous pressure, broken owing to shock and (or) blood losses; substitution of blood cells - erythrocytes and thrombocytes.
Some of the above-stated purposes are reached by massive plasma transfusions, the system of a blood coagulation and other plasma fermental systems containing all components and the possessing anti-protease activity including a large amount of antithrombin III.
Treatment by freshly frozen plasma should be begun perhaps earlier at a stage of hypercoagulation and to continue before elimination of all manifestations of a syndrome of the disseminated intravascular coagulation. It is proved that plasma promotes stopping not only the IDCS, but also destructive processes in bodies, intoxication, immunity disturbances.
In the absence of freshly frozen plasma treatment can be carried out by means of anti-hemophilic or native plasma though these drugs are less effective.
Also in infusional therapy, except plasma, saline solutions, Polyglucinum, albumine solution are applied. Use of a reopoliglyukin is possible, it is used generally in a hypercoagulation phase of no more than 400 ml/days. In this phase реополиглюкин functions not only as a blood substitute, but also as the agent inhibiting aggregation of thrombocytes and erythrocytes, improving microcirculation in bodies.
In the period of hypocoagulation and bleedings, and also the expressed thrombocytopenia should not appoint it as, by experience of many authors, in such situation реополиглюкин can strengthen bleedings and weaken therapeutic effect of other drugs.
Anemization, decrease in a hematocrit, plentiful bleedings serve as the indication to substitution of erythrocytes. For achievement of this purpose appoint transfusions of eritrotsitny weight, an eritrotsitny suspension.
Summing up the result, it should be noted that at transfusion therapy of a syndrome of the disseminated intravascular coagulation the doctor needs to aim at achievement of the following main objectives.
Bystry recovery of volume of the circulating blood and hemodynamics (cryoplasma, albumine, saline solutions, Polyglucinum and reopoliglyukiny) and maintenance of mass of erythrocytes in blood above a critical level (on a hematocrit - it is higher than 22%, on erythrocytes - it is higher than 2,5 P 1012/l).
If the specified level does not manage to be reached, it is necessary to pay attention to all perhaps proceeding bleedings visible or invisible.
Quite often combined use of freshly frozen plasma and concentrates of thrombocytes (on 4-8 doses) possible to stop many such bleedings.
Even at the latest stages of a syndrome of the disseminated intravascular coagulation the effective stop of bleedings, especially uterine, occurs thanks to simultaneous intravenous administrations of high doses of Contrykal (on 50 000-100 000 PIECES and more; a daily dose - to 500 000 PIECES and more).
It is necessary to use as well local influences, such as irrigations of the bleeding sites, erosion, wounds Adroxonum, 6% solution of aminocapronic acid, drawing on these sites of biological glue.
Use plasma - and a cytapheresis in therapy of the IDCS
Successful influence of use of a plasma exchange in therapy of the IDCS is also proved, especially at its long and recurrent forms. Delete 600-800 ml of plasma, replacing it with freshly frozen plasma. At such procedure which as required can be repeated from blood of the patient cell-bound and proteinaceous immune complexes, the activated coagulation factors are removed, and at a partial cytapheresis (removal of a leukocytic layer) - the activated monocytes and units of thrombocytes.
The most urgent is use of a medical plasma exchange at the long forms of the IDCS connected with a renal and liver failure, with is purulent - destructive processes, and also with a chronic hemodialysis.
At chronic IDCS the bystry therapeutic effect gives эритротромбоцитаферез in a combination to the following drugs: trental, Dipiridamolum, тиклопидин, and - adrenoblockers.
Acetylsalicylic acid at an acute IDCS is dangerous: aggravating a trombotsitopatiya and creating acute erosion in a stomach, it creates premises for heavy massive bleedings.
Thus, the main components of complex therapy of the IDCS are:
1) the treatment directed to elimination of a causative factor; antishock therapy and maintenance of necessary volume of the circulating blood: transfusion of freshly frozen plasma with heparin; administration of inhibitors of proteases and antibradikininovy drugs (especially at destructive processes and in the period of bleedings);
2) perhaps earlier use of the adrenoblockers and drugs improving microcirculation and reducing a decrease from a blood-groove of thrombocytes (trental, curantyl, тиклодипин);
3) substitution of a decrease of erythrocytes and maintenance of a hematocrit is higher than 22%; at heavy hypocoagulation and bleedings - transfusion of concentrates of thrombocytes, administration of Contrykal in high doses;
4) use according to indications of a plazmatsitaferez.
The following in therapeutic influence is the direction on elimination of "a shock lung" and an acute renal failure using such drugs as lasixum, osmotic diuretics, heparin, with carrying out the managed artificial ventilation, impact on an acid-base state and electrolytic balance.
At a syndrome of the disseminated intravascular coagulation it is necessary to avoid use of fibrinogen which easily turns in a blood-groove, strengthening microcirculation blockade.
In most cases the IDCS both fibrinolysis inhibitors like aminocapronic acid, and activators of this system (Streptokinasa, an urokinase) are contraindicated. Their use is fraught with dangerous complications.
At gastroduodenal bleedings use whenever possible local influences through гастрофиброскоп - a covering of the bleeding erosion haemo static drugs of local action.
Patients with a syndrome of the disseminated intravascular coagulation need intensive round-the-clock observation and treatment with monitor tracking efficiency of breath and blood circulation, frequent repetition of laboratory researches. Proceeding from all above-mentioned such patients have to be in intensive care units or in chambers of an intensive care.