DIC syndrome in children emergency care. DIC - Phases, Symptoms, Emergency

Disseminated intravascular coagulation syndrome (DIC syndrome, thrombohemorrhagic syndrome, consumption coagulopathy, defibrination syndrome).

This is a complex general pathological process that develops in many disease states, accompanied by widespread blood clotting in the circulatory bed and the development of microcirculation blockade, tissue hypoxia, and organ dysfunction.

It is a frequent and severe complication of various pathological processes of the perinatal period and the neonatal period. It is observed in 36-50% of all cases of perinatal death. DIC in newborns often occurs in an acute and fulminant form, in its course it also proceeds as in older children. 4 stages of the development of DIC:

I. Stage hypercoagulable;

II. Hypocoagulation stage;

III. Stage-fibrinolytic;

IV. Recovery stage.

DIC in the fetus and newborn more often develops in case of tissue damage and necrosis, leading to the release of tissue thromboplastin into the bloodstream of both the mother and the fetus. Violation of the integrity of tissues appears with detachment of a normally located placenta, with placenta previa, the death of one of the two fetuses. In all these cases, DIC develops in the mother. In general, impaired hemostasis in the mother-fetus system occurs more often with placental abruption, amniotic fluid embolism, eclampsia and preeclampsia, induced abortion, intrauterine fetal death, intrauterine infection, hydatidiform mole, uterine rupture, prolonged labor of various etiologies, transfusion of other group blood, significant placental bleeding, etc.

In healthy full-term newborns, DIC is practically not observed. The main problems of the peri- and neonatal periods are prematurity, hypoxia, CNS damage, respiratory distress syndrome (RDS), sepsis, immunoconflict pregnancy for erythrocyte antigens, etc. With these pathological conditions microcirculation and hemodynamics, the function of proteolytic systems, biogenic amines, mediators, etc., i.e., all systems that provide hemodynamic and coagulation hemostasis, may be disturbed. So, for example, a clear correlation between the degree of prematurity, the severity of hypoxic damage to the central nervous system and deep disturbances of hemostasis has been proven (Chuvakova T.K. 1987).

Newborns have predisposing factors that contribute to the development of DIC: underdevelopment of the reticuloendothelial RES system, which ensures the removal of intermediate coagulation products, inadequate vascularization at the microcirculatory level, insufficient ability of the liver to compensate for the synthesis of blood coagulation factors fibrogenogen, vitamin K-dependent factors, AT-III and plasminogen. So, in premature babies, children with IUGR, and those developing in utero against the background chronic hypoxia, at birth, even lower activity values ​​of both procoagulants and anticoagulants, contact factors are detected, but more active fibrinolysis with a lower level of plasminogen, as well as platelet aggregation activity, greater permeability and fragility vascular wall. These children are prone to both increased bleeding and thrombosis due to the rapid depletion of fibrinolysis and anticoagulants in the first hours and days of life.

Hypoxia, which is usually accompanied by acidosis and decreased peripheral perfusion, leads to the development of DIC by releasing tissue factor from damaged leukocytes and endothelial cells. In this case, this mechanism plays a more important role than the platelet link of hemostasis or the internal pathway of coagulation activation; during hypoxia, a decrease in the synthesis of blood coagulation factors by the liver due to its hypoxic damage is also important. DIC occurs against the background of hemolysis of erythrocytes with the release of thromboplastin, as well as under the influence of the formation of indirect bilirubin, which contributes to the disruption of metabolic and oxidative processes in tissues and impaired vascular permeability. Depending on the shape hemolytic disease, which has an acute course, as well as in decompensated subacute course (edematous form, severe icteric form), a decrease in the content of heparin in the blood was noted. Some authors in the scheme treatment of HDN therefore suggest including anticoagulant therapy.

In newborns from mothers with various forms preeclampsia born in asphyxia, in newborns with polycythemic syndrome, blood hyperviscosity, hypercoagulability, and platelet hyperaggregability are usually formed, which predispose to thrombosis. Consequently, the features of the state of the hemostasis system in newborns very closely depend on the course of the perinatal period, including the pharmacotherapy of the mother.

The treatment of DIC is always a complex clinical problem that requires a complex impact on different parts of its pathogenesis - hemocoagulation, hemodynamic, metabolic and organ manifestations of this process.

It is necessary to adhere to the following principles in the treatment of DIC:

1. Treatment of acute DIC should begin immediately after taking blood for research. Only when chronic course ICE, it is permissible to conduct preliminary all necessary studies.

2. Measures must be taken immediately to eliminate all causal factors the development of DIC, as well as the influences that can support and exacerbate it. In this case, first of all, measures should be taken to quickly eliminate shock and eliminate septic intoxication, the most common causes of acute DIC.

3. When conducting treatment, the clinical situation should always be correctly assessed and the potential danger of “therapeutic” effects, which can cause an increase in DIC and the development of profuse bleeding, should be taken into account.

The main components of the complex therapy of DIC are:

1. Etiotropic and pathogenetic treatment underlying disease.

2. Antishock therapy and maintaining the required volume and composition of circulating blood.

3. Heparin therapy.

4. Jet infusions of FFP.

5. Introduction according to indications of protease inhibitors and anti-bradykinin drugs, especially in bacterial destructive processes and in the period of heavy bleeding.

6. Perhaps earlier use of drugs that improve microcirculation and reduce the loss of platelets from the bloodstream (trental, chimes, dopamine, etc.)

7. Replacing the loss of erythrocytes and maintaining a hematocrit above 22%.

8. In severe hypocoagulation, bleeding and severe thrombocytopenia, transfusion of platelet concentrates and administration of high doses of countercal.

9. Use according to indications of plasmacytopherase.

10. Carrying out local hemostasis, for example, through a fibrogastroscope for gastroduodenal bleeding.

In children with signs of disseminated hypercoagulability and the onset of intake deficiency, heparin, which is considered the most common anticoagulant, is used to stop the formation of thrombin. Heparin inhibits all three phases of blood coagulation, inhibits the conversion of prothrombin to thrombin, prevents platelet agglutination, and inhibits the formation of thromboplastin and fibrin. Heparin is contained in all organs and tissues, especially the liver, muscles, and lungs are rich in it. mast cells secrete and deposit heparin, basophils are also heparinocytes. Heparin therapy is aimed at stopping hypercoagulability, the formation of blood clots, restoring the number of platelets and fibrinogen levels. The main task when prescribing heparin is to get the fastest and most lasting effect.

The anticoagulant effect of heparin appears after 10-20 minutes and lasts 2-6 hours.

There is no generally accepted dose of heparin, it depends on many circumstances, in particular, on the stage of DIC. It is believed that in the initial phase of hypercoagulability, before the onset of hemorrhagic syndrome, heparin doses should be small 5-10 units / kg per hour intravenously for 12-24 hours.

Some authors with severe DIC increase the dose to 25 U / kg per hour. The average dose of heparin, most authors suggest 100-150 IU/kg 4 times a day. The use of heparin is currently very reserved, as a growing body of evidence suggests that it does not significantly affect prognosis. At the same time, there are cases of complications of heparin therapy.

Complications of heparin therapy primarily arise either due to the introduction of high doses, or due to the accumulation of the drug with a long course, as well as with individually hypersensitivity to the drug. In newborns, the main sign of heparin overdose is an increase in hemorrhagic syndrome. It should be borne in mind that in vivo (as opposed to in vitro) heparin at the beginning of its use (on the 2-4th day) can cause thrombocytopenia in 24-31% of patients. This is the so-called first type of heparin thrombocytopenia, it is believed to be associated with the retention of platelets in the places of their deposition in the body. With the introduction of basic solutions (toluidine blue, protamine), this thrombocytopenia can be immediately eliminated.

The second type of thrombocytopenia usually occurs on the 6-12th day of heparin treatment. It is considered as a result of the formation of antiheparin antibodies (IgG, M), leading simultaneously to platelet aggregation (disturbing microcirculation) and to a decrease in the coagulation properties of blood. More often this form of thrombocytopenia occurs from the introduction of porcine heparin preparations than from bovine ones. Since the formation of antibodies in newborns is slow and less active, the second type of thrombocytopenia from the appointment of heparin rarely occurs in them. Nevertheless, with prolonged administration of heparin, it is recommended to cancel it gradually (in 1-2 days) by reducing doses and against the background of inhibitors of platelet aggregation (dipyridamole, ascorbic acid). Older children and adults may develop allergic reactions(fever, skin rashes, rhinitis, conjunctivitis, lacrimation, joint pain, burning sensation in the feet, etc.), impaired renal function (hyperkalemia, etc.), osteoporosis, hypoaldosteronism. We emphasize once again that excessive doses are the main cause of complications of heparin therapy, another is irregular, with large intervals, administration of the drug, as well as insufficient monitoring of the effects of therapy in a particular patient.

Strengthening of the hemorrhagic syndrome against the background of excessive heparin therapy (the occurrence of massive ecchymosis, hematomas, the appearance of massive hematuria) is an indication for the use of heparin antagonists. The main one is protamine sulfate. It is administered intravenously in the form of a 1% solution in an isotonic sodium chloride solution. The dose of the drug is 1 mg per 1 mg (i.e., per 100 IU) of heparin, administered 30-60 minutes ago. If more time has passed after the administration of heparin, then the dose of protamine should be reduced, since a significant proportion of the administered amount of heparin has already been eliminated. Due to the rapid excretion of heparin by the kidneys after the cessation of its infusion, its blood level decreases by 50% in 60 minutes. If necessary, protamine sulfate can be administered repeatedly.

Toluidine blue, administered intravenously in a single dose of 1-2 mg/kg, diluted in isotonic sodium chloride solution, is also a heparin antagonist. Given the frequency of complications of heparin therapy, most researchers recommend limiting its use to cases where there is an actual widespread thrombus formation, for example, with fulminant purpura. When indications for treatment, heparin should be administered at a dose of 100 IU / kg IV every 4-6 hours. However, continuous infusion with low doses of heparin minimizes the risk of bleeding. The effectiveness of heparin therapy is better controlled by increasing fibrinogen, i.e. it slows down the consumption of clotting factors. If the venous blood coagulation time increases to 20-25 minutes. then the dose of heparin should be halved. At the same time, FFP should be transfused as a source of blood clotting factors. The need for heparin therapy disappears with clinical and laboratory relief of DIC. With deep thrombocytopenia and uncontrolled hemorrhagic syndrome, local gastric bleeding, cerebral hemorrhage, the use of heparin should be avoided. In these situations, one should also refrain from prescribing antiplatelet agents and transfusions of rheopolyglucin.

Reopoliglyukin at a dose of 10 ml/kg is recommended for the removal of microcirculation disorders by intravenous drip in stage I of DIC, and for the prevention of increased platelet aggregation, 0.5% curantyl solution, depending on age. Curantyl (dipyridamole) has the ability to inhibit platelet aggregation and prevent the formation of blood clots in the vessels. You should not resort to intravenous injections of chimes in precollaptoid conditions and collapse.

Newborns are prescribed chimes inside, at a daily dose of 5 mg / kg, divided into 2-3 doses. In this case side effects not observed, except for increased bleeding due to thrombocytopathy. In children with large hemangiomas and developed thrombocytopenia, a decrease in the level of blood clotting factors (consumed in hemangioma), the appointment of chimes in combination with acetylsalicylic acid (each drug at a daily dose of 5 mg / kg, divided into 3 doses, orally) leads to the normalization of platelet count and coagulogram readings.

Stages II-III of DIC are characterized by a decrease in fibrinogen in the blood plasma and a natural desire in us to compensate for it in the body of each child, especially since there is an affordable drug. Barkagan Z.S. (1988) believes that intravenous fibrinogen should be avoided in DIC.

With thrombinemia, the injected fibrinogen can undergo coagulation and increase thrombus formation in the vessels and increase the blockade of microcirculation in the organs, and increase renal and pulmonary insufficiency. A sufficient amount of fibrinogen (2-4 g per 1 liter) is contained in FFP, it is more stable than in an isolated form.

To suppress proteolysis in stage II, along with possible heparin therapy, protease inhibitors are shown - Gordox (synonymous with trasylol), contrykal. Gordox - an anti-enzymatic drug is prescribed at 5000 IU per 1 kg per day in 2-3 doses of intravenous drip in isotonic sodium chloride solution.

Kontrykal, like trasilol, inhibits the activity of trypsin, kallikrein, and plasmin; Indications for the appointment of epsilon-aminocaproic acid and its analogues in DIC are sharply limited due to the risk of aggravating the blockade of microcirculation and the development of acute kidney failure.

In stage III DIC, after correcting the level of antithrombin III and prescribing proteolytic enzymes, it is permissible to prescribe glucocorticoids in usual doses (1.5–2.0 mg/kg of prednisolone per day or other glucocorticoids in equivalent dosages). Glucocorticoids inhibit pathological processes leading to damage to the vascular wall, in addition, they inhibit the formation of serotonin, histamine, activation of the kinin system and the formation of prostaglandins, i.e. endogenous factors that increase the permeability of the vascular wall. In this regard, the process of exudation decreases. However, the appointment of glucocorticoids should be treated with caution, because. they can also reduce the formation of thromboxanes in platelets, which will slow down the process of their aggregation.

According to our and foreign colleagues, an indication for the replacement of clotting factors in DIC is bleeding in a child against the background of an increase in thrombin and prothrombin time, a decrease in platelets less than 20-50 x 10/l, or a decrease in the level of fibrinogen below 0.5-0.7 g/l . For these purposes, a platelet mass of 10 cm 3 /kg is used, to compensate for fibrinogen and factor VIII (antihemophilic globulin - AGG), cryoprecipitate 100 mg / kg is prescribed. The half-life of factor VIII is approximately 12 hours, so maintenance intravenous infusion should be given every 12-24 hours.

The main source of consumable blood coagulation factors is fresh frozen plasma (FFP), which contains all the necessary coagulation factors in an optimally balanced composition.

The dose of FFP is recommended to be increased to 50 ml/kg of body weight intravenously, to be used no later than 1.5-2 hours after defrosting and warming up to 37 0 C, bolus every 6-8 hours. FFP infusion should be started early and until complete cure.

The use of thrombolytic therapy to unblock microcirculation in organs and eliminate thrombosis with drugs such as urokinase, streptokinase, fibrinolysin in acute and subacute DIC syndromes is also not recommended, because they cause destruction not only of fibrin, but also of circulating fibrinogen, cause a sharp decrease in the activity of factors V and VIII, fibrin degradation products (FDP) increase in the blood. They are prescribed only for some forms of chronic DIC. Urokinase as a thrombolytic agent is preferred to streptokinase, with the appointment of which immune reactions due to the foreignness of the drug (obtained from streptococci, group C).

The indication for the appointment of urokinase is proven by ultrasound or angiography thrombotic vascular occlusion. It is recommended to start thrombolytic therapy with the introduction of an infusion pump for 10 minutes. 4000 IU/kg of urokinase, and then carry out maintenance therapy, administering it at a dose of 4000-6000 IU/kg per hour. The dose can be increased, the duration of thrombolytic therapy can be 24-72 hours or more, it is carried out under ultrasound control of thrombus size, fibrinogen levels, plasminogen levels, fibrinogen degradation products and fibrin in well-equipped neonatal intensive care units.

Currently, there are drugs (tissue plasminogen activator) that have a selective lytic effect only on fibrin and the drug defibrotide, which increases the blood level of tissue activator of fibrinolysis and prostocycline. They are undergoing experimental and clinical trials. Urokinase therapy is especially effective in the first hours after the development of thrombosis, major surgical interventions (performed less than 10 days before the start of therapy), as well as heavy bleeding (intracranial, pulmonary, gastrointestinal, etc.) are an absolute contraindication. Any neonatologist who chooses to use urokinase must weigh the risk of prolonged vascular occlusion against the potential benefit of thrombolytic therapy against the risk of hemorrhagic complications.

Acetylsalicylic acid in acute and subacute forms of DIC should not be used, because it dramatically increases the risk of severe gastrointestinal bleeding. But it is effective in the treatment chronic forms DIC syndrome with thrombocythemia, erythremia and other myeloproliferative diseases, which are less common in the neonatal period. In small doses, aspirin relieves manifestations of microcirculation disorders in the cerebral and terminal vessels of the extremities, stops pain etc. The effect in these cases increases if acetylsalicylic acid is combined with trental, cavinton, sermion. Heparin is ineffective or completely useless in all types of DIC caused by hyperthrombocytosis, polyglobulia and hyperaggregation of blood cells.

During the treatment of acute DIC, with the rapid restoration of circulation in ischemic parts of the body and organs, a large amount of accumulated toxic products of proteolysis, biologically active amines, tissue thromboplastin and other pathogenic metabolites enter the blood from them. As a result, the patient may experience a deterioration in the course of DIC, i.e., reinfusion syndrome. There is a second wave of tourniquet-type shock, intravascular coagulation of blood in the general circulation increases sharply. Therefore, by the time of the expected reinfusion of ischemic parts of the body, it is necessary to increase the intensity of anti-shock therapy, detoxification, increase the dose of heparin in the absence of contraindications, make a single intravenous injection of contracal, prescribe antihistamine and anti-bradykinin drugs, while a good effect is observed from plasmapheresis.

If it is impossible to eliminate the root cause of DIC, then replacement transfusions of fresh heparinized blood, especially during the neonatal period, are useful from the point of view of prevention and elimination of DIC. The positive effect of such transfusions may be due to a complex effect: the removal of fibrinogen and fibrin degradation products, which can disrupt the function of the vascular wall and hemocoagulation, inhibit the adhesive-aggregation function of platelets; removal of damaged erythrocytes, improvement of the rheological properties of blood, reduction of tissue hypoxia, sorption and removal of toxic metabolites formed in tissues during hypoxia, and microbial toxins. In the last decade in complex therapy DIC syndrome included one of the methods of extracorporeal blood purification plasmapheresis. The purpose of its use is not only to remove from the bloodstream circulating immune complexes that damage the endothelium of the vascular wall, activated coagulation factors, platelet aggregates, fibrinogen degradation products, but also to prevent possible hypervolemia due to the need to transfuse large volumes of FFP. This procedure approaches plasma exchange. In severe cases, plasmapheresis can be performed twice a day, first to unblock microcirculation, and then, after 8-12 hours, to remove tissue decay and metabolic products that have entered the circulation as a result of the drainage function of plasmapheresis. In one procedure, 30-40% of the volume of circulating plasma is usually removed, replenishment is carried out with FFP and albumin.

Plasmapheresis is especially indicated for protracted and recurrent forms of DIC due to sepsis, liver and kidney failure, as well as in patients on program hemodialysis.

With a disaggregate purpose in chronic DIC, trental is prescribed, chimes, ticlid are less effective.

Plasmacytopheresis in older children is used in complex treatment subacute and chronic forms of DIC, especially with severe toxic effects, renal failure, high plasma levels of fibrinogen and acute phase proteins, hyperthermia, immunocomplex pathology, hyperviscosity syndromes, polyglobulia (Vorobiev A. And co-authors, 1984, etc.) . Remove up to 1/5 of the BCC of plasma per day, replacing it partly with blood substitutes, partly with FFP.

During plasmacytopheresis, plasma is removed along with the upper part of the cell layer, which contains a large number of activated monocytes that produce tissue thromboplastin, activated prothrombin complex factors, and a significant part of platelet aggregates.

Plasmacytopheresis is more effective in the clinic than pure plasmapheresis and is indicated especially for purulent-destructive and septic processes and DIC syndromes that occur with renal failure or hepatorenal syndrome.

The ability to prevent the development of DIC, to recognize and correct various hypercoagulemia disorders of hemostasis in a timely manner is a real reserve for reducing both infant mortality and the chronicity of a number of diseases.

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DIC is a disease affecting the blood, its qualitative and quantitative composition. Since blood is a natural fluid of the body, and only thanks to it is the normal functioning of the organs and systems of the whole body, such a pathology has very unpleasant consequences for a person, up to death.

DIC, or (thrombotic hemorrhagic syndrome) is a significant increase in blood clotting, which leads to the formation of blood clots in the capillaries, and later on in other blood vessels. Naturally, such changes lead to a serious violation of blood flow. The blood formula changes, the number of platelets decreases, and the ability of the blood to naturally clot is lost. In fact, the normal functioning of the human body is blocked.

DIC is a disease affecting the blood, its qualitative and quantitative composition.

Why does DIC appear?

The causes of disseminated intravascular coagulation syndrome are quite extensive, consider the most common of them:

• Blood transfusion. The group and Rh affiliation are far from always correctly established, therefore, during such procedures, if the recipient receives blood of a different group or with a different Rh, such manifestations are possible.
• Pregnancy and childbirth. Under these conditions, women may experience various deviations from the norm at any stage of bearing a baby. In this case, the body of the mother and fetus suffers. The same applies to gynecological operations, forced termination of pregnancy or spontaneous miscarriages. The survival rate for DIC caused by these factors is very low.
• Any surgical intervention. The body after such effects is very weakened, so one of the complications during operations may be DIC syndrome.
• Shock conditions of different nature: from anaphylactic shock caused by an allergic reaction to any substance, to nervous breakdown caused by shock due to some tragic event.
• Blood poisoning (sepsis) and severe infections (AIDS, HIV). Diseases are severe in themselves, so DIC will be a kind of reaction of the body.
• Inflammatory processes in the digestive tract and urinary system.
• Various malignant and benign neoplasms.
• Organ transplant.

There are a fairly large number of factors provoking such a pathology. These are just the most common ones.

Any surgical intervention can cause this disease

Symptoms of DIC

Let's find out for what outward signs it is possible to assume the presence of such a disease. You need to understand that it depends on the pathology that caused such a reaction of the body, the general condition of the patient, the stage of development of the syndrome. The clinic of DIC syndrome is a combination of a pathological process on the part of the blood (formation of blood clots, impaired blood clotting, bleeding), organs, and systems of the whole organism. Consider these symptoms depending on the severity:

• Acute ICE. With this course of the disease, there is a massive appearance of foci of hemorrhage, pathological bleeding from internal organs, respectively, there is a sharp drop blood pressure, deterioration of cardiac activity and respiratory depression. The prognosis for this type of DIC is very sad. In most cases, the process ends in death.
• Pathology moderate. Sluggish DIC syndrome is detected by small bruises on the skin without apparent reason. Unusual discharge may appear - tears or pink saliva. The blood mixes with the lymph and comes out. Unusual allergic reactions appear: diathesis, urticaria and other rashes on the skin, its folds and mucous membranes. On the part of the internal organs, swelling is possible. The skin is usually pale.
• Chronic DIC. This stage of the disease manifests itself in the presence hemorrhagic diathesis, vegetative-asthenic syndrome, general weakness, lethargy, impaired recovery rate skin, suppuration of small wounds and abrasions.

Diagnosis of DIC

Since this syndrome is a disease related to circulatory system, the diagnosis is not possible without several special blood tests. The patient is assigned a general and biochemical analysis blood. The doctor needs to identify the degree of violation of blood clotting, its density, viscosity, tendency to thrombosis.

Blood clotting test

Mandatory in the diagnosis are:

• screening;
• test analyzes-markers of blood clotting;
• identification of indicators of the prothrombin index.

A hematologist assesses the frequency and amount of bleeding. With such a pathology, they are observed from several organs. Often, blood loss from the intestines, nose, and genital organs is diagnosed.

In addition to laboratory diagnosis, when clarifying the diagnosis, it becomes clear and general state person. It is important for a doctor to know how the patient's organs and systems (heart, lungs, liver) function.

Treatment

After the diagnosis is clarified, treatment of thrombohemorrhagic syndrome begins. The scheme of therapeutic actions directly depends on the stage of the process and the reasons that caused it. At acute pathology the patient is hospitalized and undergoes active treatment. With timely assistance, recovery occurs in most cases.

Active anti-shock measures are being taken, drugs are being introduced that improve blood composition - Heparin, Dipyridamole, Pentoxifylline. Patients are treated under constant monitoring laboratory research effectiveness of drug administration. If necessary, one drug is replaced by another.

Heparin-Biolik solution for injections 5000 IU/ml in 5 ml vials

The patient is given intravenously:

• donor blood plasma;
• "Cryoprecipitate";
• "Sodium chloride" (saline);
• solution of "Glucose" at a concentration of 5 or 10%;
• "Aminocaproic acid";
• donated blood.

If necessary, perform procedures such as plasmapheresis, oxygen treatment, hormone therapy. In addition, therapeutic measures are necessarily taken to restore the functioning of the brain, heart, and blood vessels.

Often patients are interested in: “Is it worth treating a sudden, sluggish DIC during pregnancy, is it dangerous for the mother and baby?”. Therapy of this pathology is mandatory, because this is the only way to save the life and health of the woman and the fetus.

Ambulance for DIC

To help a patient with such a pathology before entering the hospital, it is necessary, first of all, to eliminate the causes of this process, of course, if possible. It is necessary to make every effort to stop bleeding, normalize the main indicators of the body - respiration, cardiac activity, blood pressure.

Emergency workers administer intravenously to the patient alpha-blockers ("Phenolamine") and other drugs to restore blood volume ("Reopoliglyukin").

The disease is quite serious, so therapy should be carried out immediately. Treatment of pathology is carried out only in a hospital.

What can cause DIC syndrome in a minor patient? This question worries both the parents of a sick child and specialists involved in monitoring how the disease manifests itself and develops.

AT childhood, provided that DIC is not congenital, it can be caused by the following factors:

• Infectious diseases of a viral and bacterial nature, occurring in a severe form. Mostly those that are provoked by microorganisms of gram-negative and mixed types.
• Low body temperature - hypothermia.
• Hypoxic or asphyxic condition.
• fact of acidosis.
• Child-borne shock accompanied by hypotension.
• Traumatic injuries of organs and their destruction. It can be caused by a severe degree of hemolysis, leukemia, extensive traumatic lesions and burns, a destructive state of organs belonging to the group of parenchymal, necrotic lesions.

AT early age The mechanism for the development of DIC syndrome originates from cardiovascular collapse. There is also a state of shock. These factors entail activation and subsequent damage to the vascular endothelium. Thus, vascular expression shows an increase, and tissue factors, many interleukins, tumor necrosis, etc. enter the bloodstream.

Symptoms

From the point of view of the clinical course of the disease in the period when it is just beginning, it is possible to determine a number of characteristic signs of DIC. At the same time, on different stages The disease manifests itself in different ways. Its first signs may be as follows:

• For the 1st stage - hypercoagulability. The manifestations of the underlying disease are dominant. Additionally, symptoms of a microcirculation disorder are added here. The skin of the child is covered with a specific marble mesh. You can recognize distal cyanosis, the presence of stasis spots. Body temperature drops. At the same time, there is an increase in the liver and spleen. There is a place to be tachycardia, which is combined with low blood pressure, tachypnea and low diuresis.
• For the 2nd stage - coagulopathy and thrombocytopathy. The child can recognize petechiae. Bleeding occurs at the injection sites. The skin and mucous membranes are pale in color. The lesion affects the vital organs and this process is expressed in acute pulmonary circulatory and hepatic insufficiency. Possible swelling of the brain, internal hemorrhages.
• For the 3rd stage - recovery. If timely measures are taken to treat the disease, DIC is neutralized. Bleeding decreases until it disappears completely, and the affected organs return to their previous “mode” of functioning.

Diagnosis of DIC in a child

At the 1st stage of the development of DIC, the disease can be diagnosed by examining the results laboratory tests. The following changes indicate the presence of the problem in question:

• a slight decrease in blood clotting time and bleeding - not necessary;
• a slight deviation from the norm in the number of platelets;
• shortening of PT and PTV;
• high levels of fibrinogen and PDF;
• a positive result after an ethanol study.

At the 2nd stage of development, the diagnosis is even easier, since the deviations of the available indicators from the norm become even more obvious.

Complications

What is dangerous about DIC at an early age is the high probability of death. The lack of specialized treatment in 100 percent of cases entails the death of a patient of any age.

Treatment

It is necessary to treat a child with DIC syndrome, mainly in stationary conditions. Immediately after confirming the diagnosis, the doctor must decide what to do in order to cope with the disease as soon as possible. A prerequisite is the constant check of the blood clotting factor and other parameters.

What can you do

It is important to remember that DIC is the most serious illness, with which the child's body is extremely difficult to cope with. Approximately 30-50 percent of the total number of cases are fatal. Thus, home treatment without contacting a specialist is impossible.

What does a doctor do

In order to cure DIC, the doctor uses infusion therapy at the 1st stage, oxygen therapy and artificial warming are additionally performed. Measures are taken to replenish the BCC, drugs are prescribed that support the liver and organs of the circulatory system. At the final, recovery phase, the goal of specialists is to provide first aid in the form of restoring the disturbed natural functions of the child's body.

Prevention

It is almost impossible to prevent the development of DIC on your own. Some of the preventive measures include:

• timely and adequate treatment of infections, tumors;
• use of anticoagulants in combination with antimicrobials in the fight against infectious diseases;
• avoiding poisoning with snake venom or chemical compounds;
• prompt replenishment of the volume of blood in the child's body in case of its multiple loss using plasma and plasma substitutes.

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DIC (syn.: thrombohemorrhagic syndrome) - universal nonspecific disorder system of hemostasis, characterized by disseminated intravascular coagulation and the formation in it of many microclots of fibrin and aggregates of blood cells (platelets, erythrocytes), settling in the capillaries of organs and causing deep microcirculatory and functional-dystrophic changes in them.

The process is characterized by the activation of plasma enzyme systems (clotting, fiorinolytic and kalikrein-kinin), after which their depletion occurs, leading in severe cases to complete blood incoagulability.

ICE flow phases

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Blood clotting disorders are of a phase nature. There are four main phases of the process:

1) Increased blood clotting, blockade of microcirculation and multiple microthrombosis;

2) The transition from hyper - to hypocoagulation, when some tests reveal increased blood clotting, while others - reduced (for example, an increase in the prothrombin index with a slow clotting time of whole blood);

3) Hypocoagulation and intense bleeding;

4) Recovery period, characterized by the normalization of blood clotting and improvement in the function of the affected organs.

In the first phase pronounced hypercoagulation is detected - the blood clotting time and thromboelastogram parameters are significantly shortened. Hypercoagulability is often so pronounced that it is not possible to collect blood for research: it immediately coagulates in a needle or test tube.

Then the increased coagulability is replaced phase of progressive hypocoagulation, characterized by an increase in the clotting time of whole blood, an increase in the time parameters of the thromboelastogram and a decrease in its amplitude, a decrease in the thrombin index and an increase in the thrombin time. Thrombocytopenia progresses and in acute forms of DIC - hypofibrinogenemia.

Along with these disorders of coagulation and platelet hemostasis, starting from the first phase of the process, the reserve of antithrombin III, the most important physiological anticoagulant and plasma cofactor of hemarin, protein C, and components of the fibrinolytic system, plasminogen and its activators, is progressively depleted. These shifts are natural and it is important to take them into account when carrying out pathogenetic therapy of patients.

It is possible as an acute catastrophic course of the process (for all types of shock and terminal states), and a protracted undulating course with a repeated change in the phases of hyper- and hypocoagulation (prolonged toxicoseeptic processes, malignant neoplasms, destructive-necrotic lesions of organs, crush syndrome, etc.).

Causes of DIC

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DIC is made up of the signs of the main form of the pathology that caused its development, as well as of the clinical and laboratory manifestations of the syndrome itself.

Primary early diagnosis is always “situational”, i.e. is based on identifying those effects and types of pathology in which the development of DIC is inevitable or highly probable. First of all, they include all types of shock. The severity of DIC usually corresponds to the severity and duration of the state of shock, the depth of its characteristic circulatory disorders. There is no shock without DIC, and therefore in therapy shock conditions measures to prevent and control intravascular coagulation should be included.

Second common cause the occurrence of DIC (about 50% of all cases) - purulent-septic processes, bacteremia, septicemia. Among them, the most common forms are associated with abortions (especially criminal ones), infected burn surfaces and wounds, postoperative suppuration, staphylococcal destruction of organs, septicemia due to prolonged stay of the catheter in a vein, meningococcemia, bacterial endocarditis.

DIC is caused by both gram-positive and gram-negative pathogens, as well as some viruses and rickettsiae. These types of DIC should be considered in the development of thrombohemorrhages in patients against the background of elevated temperature body, chills, sweating, signs of lesions of organs of infectious origin (especially with abscess formation), including severe forms intestinal toxicoinfection (diarrhea, vomiting, dehydration, etc.) in combination with leukocytosis or leukopenia with a shift leukocyte formula to the left, toxigenic granularity of leukocytes and blood clotting disorders.

All acute hemolytic anemias lead to DIC, including those caused by transfusions of incompatible ABO or Rh blood groups, infected blood, and blood preparations with expired storage.

Anaphylactic reactions to blood preparations, blood substitutes and medicines. This syndrome develops in all other acute hemolytic anemias - immune, associated with hereditary inferiority of erythrocytes, etc. Acute hemolysis in a number of hemolytic anemia provoked physical activity, cooling the body, changes in atmospheric pressure (flying on airplanes, climbing mountains), taking medications (quinidine, sulfonamides, nitrofuran derivatives, etc.), certain types of food (horse beans, etc.).

Excessively massive (5 or more) transfusions of compatible canned blood (the so-called massive transfusion syndrome) also lead to the development of DIC.

DIC also develops with all acute poisoning, causing shock, hemolysis and intravascular coagulation, including in case of poisoning with snake venoms containing enzymes coagulating blood - toxins of vipers and muzzles (see Snake Bites).

In obstetric practice, acute DIC can occur with placenta previa and early abruption, with early discharge of amniotic fluid, amniotic embolism, intrauterine fetal death. The frequency and severity of DIC increase in women with late pregnancy toxicosis, as well as in secondary infection of the amniotic fluid.

DIC often complicates destructive processes in organs (myocardial infarction, cerebral stroke, acute liver dystrophy, hemorrhagic and destructive pancreatitis), skin burns and chemical burns of the esophagus and stomach.

Prolonged DIC can occur with immune and immunocomplex diseases - systemic lupus erythematosus, active hepatitis and cirrhosis of the liver, hemorrhagic microthrombovasculitis of Shenlein - Genoch, glomerulonephritis, especially with nephrotic syndrome; with malignant neoplasms, especially with extensive metastasis; leukemia; during extracorporeal circulation, hemodialysis, hemosorption, as well as during implantation of artificial heart valves.

Symptoms of DIC itself

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Symptoms of DIC itself:

• signs of microcirculation disorders in organs with more or less deep dysfunction;
• hemorrhagic and (or) thrombotic phenomena, most often of multiple localization;
• blood clotting disorders and other disorders in the hemostasis system.

The first group of manifestations includes:

• shock lung (shortness of breath, cyanosis, atelectasis, crepitus and congestive fine bubbling rales, a tendency to develop pulmonary edema),
• acute or subacute renal failure (oliguria or anuria, azotemia) or hepatorenal syndrome, characterized by a combination of renal and hepatic insufficiency (pain in the liver, increasing scleral icterus, hyperbilirubinemia, bile pigments in the urine),
• acute adrenal insufficiency with recurring collaptoid conditions, less often - myocardial ischemia and cerebrovascular accidents .

In different patients in clinical picture one or the other of these syndromes may dominate. In a later stage, acute ulcers of the stomach and intestines may occur with profuse bleeding from them; it is also possible hemorrhagic impregnation of the gastric mucosa and small intestine with profuse diapedetic bleeding. In this regard, the mucous membrane of the stomach and intestines, like the lungs, kidneys, liver and adrenal glands, belongs to the so-called target organs, especially imitated in DIC.

Thrombosis of organ vessels can lead to the development of infarcts in them (most often small-focal), and peripheral vessels of the extremities - to thrombohemorrhages under the nails, the appearance of necrosis in the area of ​​the nail phalanges. The most severe manifestation of microcirculation blockade, which gives almost 100% mortality, is bilateral cortical necrosis of the kidneys.

The phase of hypercoagulability and microthrombosis in acute DIC is short-term and can proceed secretly, in connection with which the first obvious clinical manifestations there may be hemorrhages, in most cases multiple, although bleeding of any one localization may dominate. Often there is an alternation of bleeding of different localization or their simultaneous appearance.

Distinguish between early and late hemorrhages. The former are most abundant in areas of tissue damage and destruction: during abortions and childbirth, uterine bleeding, during surgical interventions - hemorrhages in the area of ​​the surgical field, with destructive processes in the lungs - pulmonary bleeding, etc.

DIC is characterized by the fact that the outflowing blood becomes less and less clotting - the size and density of clots in it rapidly decrease; in later periods, only very small clots are formed in the secreted blood, or it generally loses its ability to clot.

Along with this, other hemorrhages are detected early - in the skin at injection sites, palpation, the application of a cuff for measuring blood pressure and a tourniquet, in places of clothing friction, and also on the mucous membrane oral cavity and language. Later, nasal and gastrointestinal bleeding, deep hematoma-type hemorrhages in subcutaneous tissue, in the lumbar region and buttocks, in the perirenal and pelvic tissues, in the peritoneum and in the intestinal wall. These hemorrhages may be accompanied by symptoms of intestinal paresis, its obstruction, acute abdomen. In some cases, in places of hemorrhages, necrosis of the intestinal wall is formed, leading to the development of peritonitis. In the late period, bleeding from acute shock ulcers of the stomach and intestines predominates.

Diagnosis of DIC

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The diagnosis of DIC is based on identifying the effects and pathological processes that cause its development, detecting symptoms of damage and dysfunction of the organs most affected by this syndrome (kidneys, lungs, liver, adrenal glands, stomach and intestines, etc.), as well as characteristic for this syndrome of signs of multiple microthrombosis of vessels in combination with systemic bleeding and phase changes in blood coagulability with thrombocytopenia.

Of additional importance is the identification of positive paracoagulation tests - the formation of clots when 50% alcohol is added to the plasma of patients (ethanol test), protamine sulfate (PST test), a mixture of beta-naphthol with 50% alcohol (beta-naphthol test or test for fibrinogen B).

Of great diagnostic value is also the test for staphylococcal adhesion with blood plasma or serum of patients, which, like the tests listed above, reveals fibrin-monomeric complexes and early products of enzymatic fibrin cleavage. All these tests are operational, easy to perform not only in medical institutions, but also in the context of specialized care for patients at home (for example, thromboembolic and cardiological emergency teams).

A positive result of paracoagulation tests indicates the presence of intravascular coagulation in patients (DIC - syndrome or massive thrombosis) and serves as a laboratory confirmation of the diagnosis. Samples may become negative in the later stages of DIC, when plasma fibrinogen levels drop below. 0-100 mg%, which is observed in the terminal phase of DIC. The transition of positive samples to negative during treatment indicates sufficient effectiveness of antithromotic therapy.

Emergency care for DIC

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Urgent care first of all, it should be aimed at eliminating the effect of the factor that caused the development of DIC, and, as soon as possible, the faster elimination of shock during its development. At the prehospital stage, first of all, measures should be taken to stop microthrombosis, bleeding, hypovolemia and arterial hypotension.

It is best to start infusion therapy with intravenous administration of rheopolyglucin (300-500 ml) and (or) 5-10% albumin solution (200-400 ml) at first intravenously harmoniously, and then after normalization of blood pressure drip. Reopoliglyukin helps to restore the volume of circulating blood, improves microcirculation in organs, and prevents the aggregation of blood cells. With early administration (in the hypercoagulable phase), it significantly reduces the loss of platelets into thrombi and aggregates, and thereby alleviates subsequent thrombocytopenia, which is important for reducing bleeding in the late stages of DIC. The dose of rheopolyglucin should be reduced to 100-200 ml at the beginning of treatment at a late stage of the process and in the presence of profuse bleeding (uterine, gastrointestinal, etc.), since its excessive administration during this period can increase bleeding.

In the period of profuse bleeding, it is preferable to transfuse albumin and plasma (preferably fresh frozen). In the absence of rheopolyglucin and 5-10% albumin, infusion therapy can be started with intravenous jet injection of crystalloid solutions (0.9% sodium chloride solution, 5% glucose solution, Ringer-Locke solution, etc.) in the amount of 1-1.5 l of native or fresh frozen donor plasma (single group or IV blood group). Before the introduction of plasma or together with it intravenously, 5000-500 BD of heparin should be administered for every 300-400 ml of plasma in patients without profuse bleeding and 2500-5000 IU in patients with profuse bleeding.

In the phase of complete or almost complete blood incoagulability, i.e. in the third phase of DIC, instead of heparin, large doses of contrical can be administered intravenously (30,000-50,000 IU per injection, repeatedly).

With very large blood loss (decrease in hematocrit - below 20%, hemoglobin - below 80 g / l, the volume of lost blood in adults - more than 1 liter, along with albumin, 300400 ml of erythrosuspension or erythromass are intravenously injected with plasma. Direct transfusions from single-group blood donors are acceptable (necessarily with the addition of the above doses of heparin to prevent its coagulation.) Preserved blood should be used only with large blood loss and the absence of erythropoiesis or erythromass; only fresh blood (up to 3 days of storage) should be used, since long-term stored blood is characterized by a sharp decrease in oxygen - transport function and content is very a large number microclots that deepen DIC and disrupt microcirculation in organs.

Massive blood transfusions (5 liters or more) in themselves cause severe DIC and sharply aggravate the existing one, therefore, maximum restraint in the use of canned blood is important, but at the same time, rapid restoration of circulating blood volume and blood pressure levels by introducing colloidal blood substitutes, crystalloid solutions, plasma.

The appointment of glucocorticoids (prednisolone hemisuccinate - 60-80 mg or hydrocortisone - 100-120 mg) facilitates the removal of the patient from shock and the relief of bleeding, but glucocorticoids without heparin should not be used, since they increase blood clotting.

To improve microcirculation and weaken platelet aggregation, it is advisable to early administration of chimes (250-500 mg 3 times a day) and especially trental (pentoxifylline) 100 mg each, and this drug is added to any infused solution (the indicated dose can be administered 2-4 times a day). day)

Acetylsalicylic acid should not be prescribed as a disaggregant, as it can dramatically increase bleeding in the second or third phase of DIC and cause life-threatening bleeding from acute gastric erosions.

In the early stages of DIC, alpha-1, an adrenoblocker phentolamine, is highly effective, which is prescribed 5 mg intravenously after removing the patient from the state of hypotension.

These methods of therapy can be started at the prehospital stage, including those with a final diagnosis of DIC that has not yet been established. If a bacterial-septic or toxic-infectious genesis of this syndrome is suspected (chills, fever, leukocytosis or leukopenia, the presence of an entrance gate for infection, vomiting, diarrhea, etc.), early antibiotics are indicated. For this purpose, the introduction of oxacillin intramuscularly at 0.5 g can be started (daily dose for adults 4-6 g, for children under 6 years old - up to 2 g). Other broad-spectrum antibiotics may be added as needed.

In the early stages of hospital treatment, the optimal basic therapy is the complex use of repeated transfusions of fresh frozen plasma (300-1000 ml / day) in combination with heparin therapy (intravenous drip infusion of 15000-20000 U / day and injection under the skin of the abdomen at 10000-25000 U / day In the phase of hypocoagulation and profuse bleeding, the dose of heparin is reduced by 2-3 times and large doses of countercal or other antiproteases of the same group are prescribed.Infusion therapy is continued according to the above rules, alpha-2-blockers and antiplatelet agents are used.

In case of shock lkgcom and acute renal failure, 2-6 ml of a 1% solution of lasix (furosemide) is additionally injected intravenously, detoxification therapy is carried out (see Poisoning), plasmapheresis. Transfusions of erythromass or erythrosuspension maintain hematocrit at the level of 1822%, hemoglobin - 80 g/l and above. Avoid transfusion overload. It is necessary to provide local hemostasis. Intravenous administration of vikasol with this type of bleeding is ineffective. Aminocaproic acid is contraindicated in most cases, since it blocks fibrinolysis, enhances intravascular coagulation and blockade of microcirculation in organs. In small doses, it can be used orally (6-8 g / day) only in the late stages of DIC - with severe hypocoagulation and profuse gastrointestinal bleeding (for local relief of hemorrhages). Intravenous injections fibrinogen should be avoided even in the phase of deep hypofibrinogenemia, since in this situation it is better to compensate fibrinogen together with the replacement of other coagulation factors and physiological anticoagulants; all of them, including a sufficient amount of fibrinogen, are contained in transfused native and fresh frozen plasma.

In case of profuse bleeding, repeated injections of counterkal, plasma transfusion (including antihemophilic), erythropoiesis, and platelet mass are indicated.
Hospitalization. Patients with DIC are subject to immediate hospitalization in intensive care units or intensive care units.

All symptoms of DIC are combined into several syndromes (a stable set of symptoms united by a single development).

• Violation of blood flow in various organs due to the formation of blood clots (blood clots) in small vessels.
  • Skin: Blue ears and tip of nose, blue toes, ulceration (deep defects).
  • Nervous system: violation of sensitivity and movements, loss of consciousness, distorted perception of reality.
  • Respiratory system: destruction of lung tissue and replacement with scar tissue. It is characterized by a pronounced increase in breathing, the risk of edema (fluid accumulation) of the lungs.
  • Digestive system - ulcers (deep defects) of the stomach and intestines.
  • Liver: the development of liver failure, accompanied by jaundice (yellow staining of the skin, eyes, mouth, etc.).
  • Blood system: destruction of erythrocytes (red blood cells), resulting in a yellow discoloration of the skin and eyes.
  • Kidneys: a decrease in the volume of urine excreted, a violation of all kidney functions.
  • Adrenal glands: development of acute adrenal insufficiency. It is characterized by lightning-fast deterioration of the condition, severe damage nervous system(loss of consciousness, convulsions), fever, drop in blood pressure, vomiting, diarrhea, dehydration, disorders of the lungs and heart.

• Hemocoagulation shock - a sharp decrease in arterial and central venous pressure (pressure in the largest veins) with a deterioration in the condition of all internal organs.

• Hemorrhagic syndrome:
  • extensive subcutaneous hemorrhages;
  • bleeding from the nasal and oral cavities;
  • vomiting blood; admixture of blood in urine and feces;
  • hemorrhages in the body cavity and internal organs;
  • bleeding from wounds resulting from operations and injuries (if any);
  • bleeding from injection sites (skin puncture sites with a syringe when administering drugs).

Forms

Depending on the cause, there are:

• severe infections;
• surgical interventions;
• malignant (that is, growing with damage to surrounding tissues) tumors;
• hypersensitivity reactions to transfusion of blood components;
• acute poisoning.

• hypercoagulation (increased blood clotting);
• transitional stage (characterized by the simultaneous presence of bleeding and blood clots inside the vessels);
• hypocoagulation (reduced blood clotting and bleeding);
• Exodus - unfavorable or recovery. It is possible to repeat the alternation of different phases, as well as long-term stabilization of the process in the first two phases.

• sharp (lightning) – development time ranges from several hours to days;
• subacute - develops over days and weeks;
• chronic (protracted) - lasts for months and years;
• wavy - periods of formation of blood clots inside the vessels are repeatedly replaced by periods of increased bleeding.

The reasons

Causes of DIC:

• severe infections (viral, bacterial, fungal, etc.);
• surgical interventions;
• malignant (that is, growing with damage to surrounding tissues) tumors (blood tumors, lung cancer, ovary, breast, etc.);
• hypersensitivity reactions to transfusion of blood components;
• acute poisoning (acids, alkalis, snake venoms).

• big blood loss;
• a long operation, especially in conditions of cardiopulmonary bypass (when the blood is pumped through the body not by the heart, but by a mechanical pump);
• a significant decrease in blood pressure for any reason;
• severe infections;
• severe diseases of any internal organs.

Diagnostics

• Analysis of the anamnesis of the disease and complaints (when (how long ago) bleeding and hemorrhage appeared, a decrease in the volume of urine excreted, a decrease in blood pressure, general weakness and other symptoms, with which the patient associates their occurrence).
• Life history analysis.
  • are revealed possible reasons DIC, such as surgery, snake bites, severe infections, and other factors.
  • Find out if the patient has any chronic diseases.
  • Are there hereditary (passed from parents to children) diseases.
  • Does the patient have bad habits?
  • Has he taken any medications for a long time?
  • Did he have tumors?
  • Has he been in contact with toxic (poisonous) substances.
• Physical examination. The color of the skin is determined (pallor and the presence of subcutaneous hemorrhages are possible). The pulse may be rapid, blood pressure - reduced.
• Blood analysis. Can be defined:
  • a decrease in the number of erythrocytes (red blood cells, the norm is 4.0-5.5x10 9 g / l);
  • a decrease in the level of hemoglobin (a special compound inside red blood cells that carries oxygen, the norm is 130-160 g / l y);
  • a change in the shape of red blood cells and the appearance of fragments of red blood cells (schistocytosis) due to cutting them with fibrin threads (the basis of blood clots);
  • the number of leukocytes (white blood cells, the norm is 4-9x10 9 g / l) depends on the underlying disease, it can be normal, less often increased or decreased;
  • the number of platelets (platelets, the adhesion of which ensures blood clotting) decreases (the norm is 150-400x10 9 g / l).
• Analysis of urine. With the development of bleeding from the kidneys or urinary tract, erythrocytes appear in the urine test.
• Blood chemistry. The level is determined:
  • cholesterol (fat-like substance);
  • glucose (simple carbohydrate);
  • creatinine (protein breakdown product);
  • uric acid (a breakdown product of substances from the cell nucleus);
  • electrolytes (potassium, sodium, calcium) to detect concomitant diseases.
• Study of the coagulation and anticoagulation (that is, dissolving blood clots) system.
  • The duration of bleeding is assessed by piercing a finger or earlobe. With DIC, this figure increases.
  • clotting time. The appearance of a clot in the blood collected from the patient's vein is evaluated. Different substances are added to stimulate blood clotting, which allows you to analyze the different stages of blood clotting. Depending on the added substance, the analysis is called differently (for example, activated partial thromboplastin time, thrombin time, etc.). The clotting time is lengthened, as a deficiency of clotting factors develops due to their increased consumption in the small vessels of the patient.
  • D-dimer and fibrin degradation products (FDP) - substances released during the breakdown of blood clots - appear when blood clots dissolve. Normally, blood clots and their decay products are absent in the blood.
  • Pinch test. The appearance of subcutaneous hemorrhages is assessed when the skin fold under the clavicle is compressed. The test is positive due to a decrease in the number of platelets and a deterioration in the condition of the vascular wall.
  • Harness test. A tourniquet is applied to the patient's shoulder for 5 minutes, then the occurrence of hemorrhages on the patient's forearm is assessed. The test is positive due to a decrease in the number of platelets and a deterioration in the condition of the vascular wall.
  • Cuff test. A blood pressure cuff is placed over the patient's upper arm. Air is injected into it to a pressure of 90-100 mm Hg. for 5 minutes. After that, the occurrence of hemorrhages on the patient's forearm is evaluated. The test is positive due to a decrease in the number of platelets and a deterioration in the condition of the vascular wall.
• Ultrasound examination (ultrasound) of internal organs with Doppler study of blood flow through the vessels. They allow assessing violations of the structure of internal organs and the appearance of blood clots in large vessels.
• Spiral CT scan(SCT) - a method based on a series of x-rays at different depths - allows you to get an accurate image of the organs under study and the possible presence of blood clots.
• Magnetic resonance imaging (MRI) - a method based on building chains of water when exposed to strong magnets on the human body - allows you to get an accurate image of the organs under study and the possible presence of blood clots.
• Consultation is also possible.

Treatment of DIC

Patients need immediate referral or transfer to the intensive care unit, the mandatory involvement of resuscitators (specialists in providing emergency assistance), transfusiologists (specialists in the transfusion of blood components) and specialists in disorders of the blood coagulation system.

• Elimination of the main cause that caused DIC, for example:
  • for infectious diseases - treatment of infection (for example, antibiotics - drugs that cause the death or cessation of growth and reproduction of bacteria, as well as antiviral, antifungal drugs);
  • in case of impossibility fast elimination reasons (for example, with a large size malignant tumor, that is, a tumor that grows with damage to surrounding tissues), long-term prevention of DIC is necessary.

• Normalization of blood flow:
  • plasma substitutes - solutions that replace the liquid part of the blood - to ensure a normal volume of circulating blood (BCC);
  • antispasmodics - drugs that dilate small vessels;
  • vasopressors - drugs that help normalize low blood pressure.

• Normalization of blood coagulation:
  • the use of direct anticoagulants (drugs that prevent blood clotting) to stop the formation of new blood clots;
  • intravenous administration of fresh frozen plasma (the liquid part of the donor's blood. Rapid freezing of plasma preserves clotting factors in it). Compensates for the deficiency of all coagulation factors, helps to stop bleeding;
  • transfusion of platelet mass (donor platelets - platelets) is performed with massive bleeding by reducing the level of platelets;
  • plasmapheresis - hardware method blood purification.

• Transfusion of erythrocyte mass (erythrocytes, that is, red blood cells, a donor) is carried out with the development of severe anemia (a significant decrease in hemoglobin, a special substance of red blood cells that carries oxygen).
• Depending on the developed damage to the internal organs, these disorders are treated (for example, artificial ventilation of the lungs - that is, breathing with the help of the apparatus - with respiratory failure).

Complications and consequences

Complications of DIC.

• Violation of the functions of all organs due to the cessation of blood flow in them through small vessels due to the presence of blood clots - blood clots.
• Hemocoagulation shock is a sharp decrease in arterial and central venous pressure (pressure in the largest veins) with a deterioration in the condition of all internal organs.
• Bleeding and hemorrhage.
• Posthemorrhagic anemia - a decrease in the level of hemoglobin (a special substance of red blood cells - red blood cells - carrying oxygen) due to a large loss of blood during bleeding and hemorrhage.
• Anemic coma - loss of consciousness with no response to external stimuli due to insufficient oxygen supply to the brain after significant blood loss.

Prevention of DIC

• Timely elimination of the causes that can lead to the development of DIC (that is, the full treatment of tumors, etc.).
• Holding surgical operations in the least traumatic way.
• In the presence of serious infectious diseases it is desirable to add anticoagulants (drugs that prevent blood clotting) to antimicrobial therapy.
• Prevent snake bites and chemical poisoning.
• With blood loss not exceeding one liter, the volume of lost blood should be replenished not with whole donor blood, but with plasma (the liquid part of the blood) or plasma substitutes (solutions that perform some of the functions of plasma).