DIC syndrome (consumptive coagulopathy): how it develops, course and clinical picture, diagnosis, treatment. Causes of occurrence and danger of disseminated intravascular coagulation syndrome Complications and consequences

The abbreviation DIC hides the name of a severe pathology - disseminated intravascular coagulation. Disease of the hematopoietic system is a complication of the underlying disease, but it is DIC syndrome in children that poses a particular danger because it causes problems with blood clotting.

DIC syndrome in children is formed against the background of various diseases and is one of the most severe complications that causes the death of infants during the neonatal period. The figure reaches 36 – 50%.

Most often it occurs in an acute or fulminant form, but a protracted, as well as latent (hidden) or worsening course is possible. Typical for children aged 1 – 4 years.

Causes of development of DIC in newborns

DIC syndrome in newborns can be caused by the following reasons:

• damage to the “children's place”;
• intrauterine death of one of the children during multiple pregnancy;
• intrauterine infection;
• condition of eclampsia and preeclampsia;
• uterine rupture;
• hydatidiform mole.

Most often, the pathology is diagnosed in premature infants. The child’s blood contains insufficient amounts of procoagulants or anticoagulants, which causes increased bleeding.

Symptoms

The clinical picture of the condition is determined by the current stage of the pathology. The primary signs can be:

1. Hypercoagulation stage. The symptoms of the leading disease become the main ones. Signs of impaired blood microcirculation are added - the appearance of a characteristic “marble” mesh on the skin, a decrease in body temperature, blue discoloration of the tips of the fingers and toes, an increase in the volume of the liver/spleen. The development of tachycardia, a drop in blood pressure, and a decrease in urination cannot be ruled out.
2. Stage of thrombocytopathy and coagulopathy. Petechiae form on the surface of the skin, the surface of the mucous membranes becomes pale. Bleeding develops in the area where medications are injected. Vital organs - lungs, kidneys, brain - are involved in the pathological process. Internal hemorrhages cannot be ruled out.
3. Recovery stage. In the case of treatment adequate to the condition, a decrease in pathological symptoms is observed. The affected organs are restored and begin to function normally.

Features of DIC syndrome in newborns

DIC syndrome in an infant can develop due to many diseases. The condition typically has a lightning-fast course, which practically excludes the possibility of using any treatment.

Diagnosis in children

At the first stage of DIC syndrome, diagnosis is based on the results of a laboratory study of blood composition. The development of pathology is indicated by:

• a slight decrease (relative to the accepted norm) of blood clotting time;
• drop in platelet count;
• reduction of prothrombin time, APTT period (clot formation time);
• increased levels of fibrogen and PDP (this is a sign of increasing intravascular coagulation);
• positive result for ethanol test.

Making a diagnosis when the second stage occurs is greatly simplified. Deviations from the norm are increasing. Signs of damage to internal organs are observed, in particular, there is an even greater decrease in the number of platelets and a deterioration in the condition of the vascular system.

Therapeutic measures

Treatment of the condition requires an integrated approach. There are several basic principles.

1. Therapy for the acute form of DIC syndrome begins immediately after the collection of biomaterial for research.
2. Measures to eliminate possible provoking factors should be carried out as soon as possible.
3. During treatment, the doctor constantly evaluates the current clinical picture and takes into account the possible negative impact of the measures taken, which can cause an increase in the symptoms of DIC syndrome and cause profuse bleeding.

The pathology treatment protocol includes statistics, classification of DIC, and data on drug interactions. It also consists of the following points:

• elimination of the underlying disease;
• anti-shock therapy, ensuring the required volume of circulating blood;
• taking heparin;
• jet infusion of fresh plasma;
• patients receiving protease inhibitors and drugs from the antibradykin group;
• the use of medications that stimulate blood microcirculation processes and reduce the loss of platelets from the general bloodstream;
• maintaining hematocrit at 22% and above;
• taking Contrikal for severe forms of hypocoagulation and bleeding;
• performing local hemostasis;
• plasmacytopheresis procedure (according to indications).

Complications and prognosis

Among the complications caused by DIC syndrome, it is worth highlighting.

1. Impaired blood microcirculation up to the development of complete/partial blockade. Lung and kidney tissues are most often affected. As a result of thrombosis of small vessels of the brain, the development of ischemic stroke cannot be ruled out.
2. Hemocoagulative shock. One of the most severe complications of the pathology. Has a bad prognosis.
3. Hemorrhagic syndrome. Characterized by hemorrhages, different types of bleeding.
4. Posthemorrhagic decrease in hemoglobin level. Anemia develops due to blood loss.

The prognosis of the syndrome is variable and depends on several factors:

• leading disease;
• severity of hemostasis disorders;
• time of therapy started.

Acute DIC syndrome can lead to the death of the patient due to significant blood loss, the development of shock, disruption of the respiratory system and numerous internal hemorrhages.

Treatment of DIC syndrome

The success of therapy for the syndrome largely depends on at what stage of the condition the patient began receiving medications and procedures.

Active intake of medications and other therapeutic measures are necessary when bleeding occurs and the functionality of internal organs is impaired. Patients are subject to mandatory hospitalization in the intensive care unit. If necessary, artificial ventilation of the lungs and anti-shock treatment are performed.

In mild cases of DIC syndrome, the underlying disease is treated and hemodynamics and organ dysfunction are corrected.

Treatment of acute DIC syndrome is based on urgent elimination of the provoking cause. For example, in case of obstetric pathology, an urgent delivery or removal of the uterus may be required; in case of septic complications, the patient is prescribed a course of antibiotics.

To eliminate hypercoagulability syndrome, treatment with the following drugs is indicated:

• anticoagulants (Heparin);
• antiplatelet agents (Pentoxifylline, Dipyridamole);
• fibrinolytics.

Replacement therapy involves transfusions:

• fresh plasma;
• red blood cell/platelet mass (with a catastrophic decrease in hemoglobin/platelets);
• cryoprecipitate (in the formation of myocardial dysfunction);
• saline solution.

In case of massive bleeding, drugs from the group of antifibrinolytics - aminocaproic acid, protease inhibitors - may be prescribed.

Treatment of skin hemorrhages and open wounds uses hemostatic sponges and dressings with ethamsylate.

According to indications the following are prescribed:

• corticosteroids;
• plasmapheresis;
• oxygen therapy;
• angioprotectors;
• nootropic drugs.

When renal failure develops, hemodialysis and hemodiafiltration are prescribed.

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

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

Phases of the internal combustion engine

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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) Transition from hyper-to hypocoagulation, when some tests reveal increased blood coagulability, and others - decreased (for example, an increase in the prothrombin index with a slow coagulation time of whole blood);

3) Hypocoagulation and intense bleeding;

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

In the first phase pronounced hypercoagulation is detected - blood clotting time and thromboelastogram parameters are significantly shortened. Hypercoagulation is often so severe that it is impossible to collect blood for testing: it immediately coagulates in a needle or tube.

Then increased coagulability is replaced by 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 also progresses in acute forms of DIC - hypofibrinogenemia.

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

Both an acute catastrophic course of the process (with all types of shock and terminal conditions) and a protracted wave-like course with repeated changes in the phases of hyper- and hypocoagulation (prolonged toxicoseptic processes, malignant neoplasms, destructive-necrotic lesions of organs, crush syndrome, etc.) are possible.

Causes of DIC syndrome

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

Primary early diagnosis is always “situational”, i.e. is based on identifying those influences and types of pathology under which the development of DIC is inevitable or highly probable. These primarily include all types of shock. The severity of DIC usually corresponds to the severity and duration of the shock state, and the depth of the circulatory disorders characteristic of it. There is no shock without DIC syndrome, and therefore the treatment of shock conditions should include measures to prevent and reduce intravascular coagulation.

The second common cause of DIC (about 50% of all cases) is 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 caused by prolonged stay of a catheter in a vein, meningococcemia, and bacterial endocarditis.

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

All acute hemolytic anemias lead to disseminated intravascular coagulation, including those caused by transfusions of ABO or Rh factor incompatible blood, infected blood, and expired hemochemicals.

Anaphylactic reactions to hemotherapy, blood substitutes and drugs also lead to the development of DIC syndrome. This syndrome also develops in all other acute hemolytic anemias - immune, associated with hereditary inferiority of erythrocytes, etc. Acute hemolysis in a number of hemolytic anemias is provoked by 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 (faba 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 syndrome.

DIC syndrome also develops in all acute poisonings that cause shock, hemolysis and intravascular coagulation, including poisoning with snake venoms containing blood coagulating enzymes - toxins of vipers and copperheads (see Snake bites).

In obstetric practice, acute disseminated intravascular coagulation syndrome can occur with previa and early placental abruption, with early rupture of amniotic fluid, amniotic embolism, and intrauterine fetal death. The frequency and severity of DIC increase in women with late toxicosis of pregnancy, as well as in cases of secondary infection of amniotic fluid.

DIC syndrome is often complicated by 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 immune complex diseases - systemic lupus erythematosus, active hepatitis and cirrhosis of the liver, hemorrhagic microthrombovasculitis of Schönlein-Henoch, glomerulonephritis, especially with nephrotic syndrome; for malignant neoplasms, especially with extensive metastasis; leukemia; during extracorporeal circulation, hemodialysis, hemosorption, as well as during implantation of artificial heart valves.

Symptoms of DIC syndrome itself

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Symptoms of DIC syndrome itself:

• signs of impaired microcirculation in organs with more or less profound dysfunction;
• hemorrhagic and (or) thrombotic phenomena, most often of multiple localization;
• bleeding 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 wheezing, tendency to develop pulmonary edema),
• acute or subacute renal failure (oliguria or anuria, azotemia) or hepatorenal syndrome, characterized by a combination of renal and liver failure (pain in the liver, increasing scleral icterus, hyperbilirubinemia, bile pigments in the urine),
• acute adrenal insufficiency with repeated collaptoid conditions, less often - myocardial ischemia and cerebrovascular accidents .

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

Thrombosis of the vessels of organs can lead to the development of infarctions in them (most often small-focal), and of 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.

Phase of hypercoagulation and microthrombosis in acute disseminated intravascular coagulation syndrome It can be short-term and can occur covertly, and therefore the first obvious clinical manifestations may be hemorrhages, in most cases multiple, although bleeding from any one localization may dominate. Often there is an alternation of bleeding of different locations or their simultaneous appearance.

There are early and late hemorrhages. The former are most abundant in places of tissue damage and destruction: during abortion and childbirth, uterine bleeding predominates, during surgical interventions - hemorrhages in the area of ​​the surgical field, during destructive processes in the lungs - pulmonary hemorrhage, etc.

DIC syndrome is characterized by the fact that the flowing blood becomes less and less coagulable - the size and density of the clots in it quickly decrease; in later periods, only very small clots form in the secreted blood or it generally loses the ability to clot.

Along with this, other hemorrhages are detected early - in the skin at the sites of injections, palpation, application of a cuff for measuring blood pressure and a tourniquet, in places where clothing rubs, as well as on the mucous membrane of the oral cavity and tongue. Later, nasal and gastrointestinal bleeding, deep hematoma-type hemorrhages in the subcutaneous tissue, in the lumbar and buttocks, in the perinephric and pelvic tissue, in the peritoneum and in the intestinal wall may occur. These hemorrhages may be accompanied by symptoms of intestinal paresis, intestinal obstruction, and a picture of an acute abdomen. In some cases, necrosis of the intestinal wall forms at the sites of hemorrhages, leading to the development of peritonitis. In the late period, bleeding from acute shock ulcers of the stomach and intestines predominates.

Diagnosis of DIC syndrome

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The diagnosis of DIC syndrome 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 there are signs of multiple microthrombosis of blood vessels in combination with systemic bleeding and phase changes in blood coagulation with thromoocytopenia.

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

The test for the adhesion of staphylococci with blood plasma or serum of patients is also of great diagnostic importance, which, like the tests listed above, detects fibrin-monomer complexes and early products of the enzymatic breakdown of fibrin. All these tests are quick and easy to perform not only in medical institutions, but also in the context of providing specialized care to patients at home (for example, thromboembolic and cardiac emergency medical teams).

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

Emergency care for DIC syndrome

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Emergency care should first of all be aimed at eliminating the effect of the factor that caused the development of DIC syndrome, and as quickly as possible eliminating shock as it develops. At the prehospital stage, first of all, measures should be taken aimed at stopping microthrombosis, bleeding, hypovolemia and arterial hypotension.

Infusion therapy is best started with intravenous administration of rheopolyglucin (300-500 ml) and (or) 5-10% albumin solution (200-400 ml), first intravenously, and then after normalization of blood pressure by drip. Reopolyglucin helps restore circulating blood volume, improves microcirculation in organs, and prevents blood cell aggregation. When administered early (in the hypercoagulation phase), it significantly reduces the loss of platelets into thrombi and aggregates and thereby mitigates subsequent thrombocytopenia, which is important for reducing bleeding in the later stages of DIC. The dose of rheopolyglucin should be reduced to 100-200 ml when starting treatment in a late stage of the process and in the presence of profuse bleeding (uterine, gastrointestinal, etc.), since its excessive administration in this period can increase bleeding.

During the period of profuse bleeding, it is preferable to perform transfusions of albumin and plasma (preferably fresh frozen). In the absence of rheopolyglucin and 5-10% albumin, infusion therapy can be started with intravenous jet administration of crystalloid solutions (0.9% sodium chloride solution, 5% glucose solution, Ringer-Locke solution, etc.) in an amount of 1-1.5 liters of native or fresh frozen donor plasma (single or IV blood group). Before administering plasma or together with it, 5000-500 BD of heparin should be administered intravenously 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 units per injection, repeatedly).

In case of very large blood loss (decrease in hematocrit - below 20%, hemoglobin - below 80 g/l, volume of lost blood in adults - more than 1 liter, along with albumin, plasma, 300-400 ml of erythromytic suspension or erythromass are administered intravenously. Direct transfusions from donors of the same blood group are acceptable (necessarily with the addition of the above doses of heparin to prevent its clotting). Canned blood should be used only in case of large blood losses and the absence of erythroid suspension or erythromass; only fresh blood should be used (up to 3 days of storage), since long-term stored blood is characterized by a sharp decrease in oxygen -transport function and the content of a very large number of microclots that deepen DIC syndrome and disrupt microcirculation in organs.

Massive blood transfusions (5 liters or more) themselves cause severe disseminated intravascular coagulation 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 administering colloidal blood substitutes, crystalloid solutions, plasma.

The administration of glucocorticoids (prednisolone hemisuccinate - 60-80 mg or hydrocortisone - 100-120 mg) makes it easier to remove the patient from shock and stop 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 administer chimes (250-500 mg 3 times a day) and especially trental (pentoxifylline) 100 mg, and this drug is added to any infused solution (the indicated dose can be administered 2-4 times per day)

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

In the early stages of DIC, the alpha-1 adrenergic blocker phentolamine is highly effective, which is prescribed 5 mg intravenously after the patient has recovered from the state of hypotension.

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

In the early stages of treatment in a hospital, 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 15,000-20,000 units/day and injection under the skin of the abdomen of 10,000-25,000 units). /day. In the phase of hypocoagulation and profuse bleeding, the dose of heparin is reduced by 2-3 times and large doses of Contrical or other antiproteases of the same group are prescribed. Infusion therapy is continued according to the above rules, alpha-2-blockers and disaggregants are used.

In case of shock lung cancer and acute renal failure, an additional 2-6 ml of 1% solution of Lasix (furosemide) is injected intravenously, detoxification therapy is carried out (see Poisoning), and plasmapheresis. Transfusions of erythromass or erythroid suspension maintain hematocrit at the level of 1822%, hemoglobin - 80 g/l and above. Avoid overloading with blood transfusions. It is necessary to ensure local hemostasis. Intravenous administration of Vikasol is ineffective for this type of bleeding. Aminocaproic acid is contraindicated in most cases, as 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 administration of fibrinogen should be avoided even in the phase of deep hypofibrinogenemia, since in this situation it is better to compensate for fibrinogen along 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 administration of contrical, transfusion of plasma (including antihemophilic plasma), erythrocyte suspension, and platelet mass are indicated.
Hospitalization. Patients with DIC syndrome are subject to immediate hospitalization in intensive care units or intensive care wards.

DIC syndrome is also called disseminated intravascular coagulation syndrome. It is not a separate pathology or nosological entity. It is a complex process consisting of several stages, during which increased thrombus formation is observed in the lumen of blood vessels. This is a fairly common situation. Most often, surgical doctors and pediatricians encounter it. Treatment of DIC syndrome is extremely complex, requiring early diagnosis of the process.

The causes of DIC syndrome are determined by the diseases that provoked it. The most common triggers are.

1. Severe infectious pathologies - sepsis, accompanied by a state of shock, viral processes.
2. Other types of shock, which is inherently the main cause of DIC. These include traumatic, hypovolemic, infectious-toxic and even painful.
3. Any terminal condition can provoke disseminated intravascular coagulation.
4. Surgical operations, especially massive ones, in which artificial blood circulation machines are used.
5. Cancer diseases.
6. Hemodialysis.
7. Excessive blood loss.
8. Against the background of massive blood transfusion, this pathology also occurs.
9. In obstetric practice, DIC syndrome occurs with placental abruption, complications of labor with amniotic fluid embolism, toxicosis, and Rh conflict.
10. Pathologies of the cardiovascular system.

Based on the above, we can conclude that disseminated intravascular coagulation is caused by severe pathological processes or terminal conditions. At the same time, pathology practically does not occur in healthy newborn babies. Here it is important to correctly differentiate it from other coagulopathies, such as hemophilia or von Willebrand disease.

Stages of development and forms of DIC syndrome

Doctors classify this condition in different ways. All these divisions are based on etiological, pathogenetic features, as well as variants of the clinical course. Taking into account the mechanisms of pathology triggering, the following stages of DIC syndrome are distinguished.

1. First, hypercoagulation occurs.
2. It gives way to the so-called consumption coagulopathy, which gradually gives way to the third stage.
3. Hypocoagulation is the terminal stage of shock; if the patient is not helped at this stage, the mortality rate will be very high.
4. Restorative, includes the process of restoring the body after correction of the shock state.

Pathogenesis

The pathogenesis of DIC syndrome is based on mechanisms that occur during all its stages. The failure of the body's hemostatic system is due to increased stimulation of blood coagulation, as well as depletion of anticoagulant and fibrinolytic mechanisms.

The pathophysiology of DIC depends on many factors that serve as activators of the coagulation process. They act independently or act as mediators of effects on the endothelium of the vascular wall. Activators of all stages of DIC include toxins, bacterial waste products, immune complexes, decreased circulating blood volume, and many others. It is they who determine the flow options of the internal combustion engine.

The pathological component is based on the stages of the process.

1. The first phase of DIC is hypercoagulation, during which cells inside the vessels begin to stick together. It is triggered by thromboplastin entering the bloodstream. Its duration is several minutes.
2. The pathophysiology of DIC syndrome includes consumption coagulopathy, in which there is a pronounced deficiency of fibrinogen and other coagulation factors due to rapid consumption, and the body does not have time to replace them.
3. Secondary fibrinolysis is accompanied by hypocoagulation, the blood clots very slowly or does not clot at all.
4. Recovery is characterized by residual effects or complications.

Clinical manifestations

The symptoms of DIC syndrome are not questioned when skin manifestations occur (they may be called hemorrhagic manifestations), decreased diuresis, or lung damage. These are the main signs of pathology.

The symptoms are due to the main link in the pathogenesis, this is increased blood clotting. Parenchymal organs and skin are the first to suffer. The severity of the condition depends on the severity of thrombus formation.

1. When the skin is involved, a hemorrhagic rash is observed, it resembles minor hemorrhages and areas of tissue necrosis.
2. The lungs react by developing acute respiratory failure. Shortness of breath occurs, severe cases are accompanied by pulmonary edema or respiratory arrest.
3. With an excess of fibrin in the blood plasma, renal problems are triggered - renal failure, the terminal stage will manifest itself as anuria and electrolyte imbalance.
4. Brain damage is determined by the presence of neurological symptoms.

In addition to the changes described above, the patient may develop massive external or internal hemorrhages and hematomas.

Diagnosis of DIC syndrome

To determine the presence of disseminated intravascular coagulation in a patient, it is necessary to carefully collect anamnestic data and establish a diagnosis that provoked this condition. DIC syndrome requires laboratory diagnostics, which includes a coagulogram, a general blood test, and a study of blood coagulation factors. A very important point is to determine the severity of the patient in order to prescribe adequate correction.

It is necessary to take into account that the patient may bleed from several places at once. Moreover, if a chronic process has developed or it is not very aggressive, then hypercoagulation can only be detected through laboratory diagnostics.

The doctor must prescribe:

• blood test to determine platelets;
• coagulogram, which will display the amount of fibrinogen, blood clotting time, thrombin level, prothrombin level, APTT.

There are specific tests - RFMC, D-dimer. They are performed by enzyme immunoassay.

Doctors consider the main criteria for DIC syndrome to be the identification of fragmented red blood cells, an insufficient number of platelets, and a decrease in fibrinogen concentration. Low activity of antithrombin-III, increased duration of aPTT and thrombin time are also noted. Weak clot formation or instability indirectly indicate a violation of hemostasis.

The doctor is obliged to check the functional performance of the organs that are first exposed to shock - the kidneys, liver, lungs.

Chronic DIC syndrome

The main characteristics of chronic DIC are:

1. Constantly increased entry into the systemic bloodstream of substances that act as activators of the hemostasis system.
2. Increased rate of fibrin formation inside blood vessels.
3. Decreased platelet consumption.
4. There is no secondary activation of fibrinolysis, as well as generalized intravascular fibrinolysis.
5. Fibrin blocks the microcirculation of parenchymal organs, causing their severe dysfunction.

The acute process is activated by thromboplastin, which enters the blood from tissues that have undergone decay due to various triggering factors. These could be injuries, burns, surgical manipulations on target organs, destructive processes, obstetric diseases. Much less often, phospholipids of the endothelium of the vascular wall or blood cells become triggers of DIC syndrome. This mechanism is more typical for bacterial processes and shock conditions. Chronic disseminated intravascular coagulation is caused by less aggression of the above activation factors, which contributes to its slow onset and a better prognosis for the patient’s life.

Treatment

Successful treatment of DIC syndrome is only possible if the condition is diagnosed in the early stages of its development. Active action by medical personnel is necessary in case of severe manifestations - bleeding, development of multiple organ failure. Emergency care for DIC is provided in an intensive care unit. The chronic process requires correction of hemodynamics, electrolyte disturbances, and symptomatic therapy.

In acute cases, it is necessary to quickly determine the cause and then eliminate it. This could be an emergency delivery or the prescription of powerful antibacterial drugs. Hypercoagulation is corrected with fibrinolytics, anticoagulants, and antiplatelet agents. Patients with such pathologies are under constant supervision of medical workers; their hemostasis system is monitored every 15-30 minutes.

Replacement therapy involves blood transfusions and antifibrolytic agents. Sometimes there is a need to use hormonal drugs, plasmapheresis, and oxygen therapy. In order to restore microcirculation and the functional state of internal organs, vascular and metabolic therapy is prescribed. The chronic process requires the administration of vasodilators, antiplatelet agents, and heparins. It is important to understand that treatment of the condition is complex, requiring certain knowledge and skills on the part of the doctor. The patient’s life depends on his skill.

DIC syndrome, or disseminated intravascular coagulation syndrome, is a complex multicomponent pathological process in the hemostatic system, manifested increased thrombus formation in the vessels of the microvasculature.

This condition occurs quite often in the practice of doctors of any specialty; obstetricians-gynecologists, resuscitators, surgeons, and emergency doctors encounter it. It is also the most common form of clotting disorders (coagulopathies) in intensive care in both adults and children.

Coagulopathies are conditions accompanied by certain changes in the. The main types of coagulopathies are congenital (genetic) and acquired, one of the variants of which is DIC syndrome. In the literature you can find data on the so-called hypercoagulable coagulopathy, or hypercoagulation syndrome, which is characterized by laboratory signs of increased blood clotting, but thrombosis is most often absent.

DIC syndrome has complex development mechanisms, various clinical manifestations, and precise diagnostic criteria for it have not yet been identified, which causes significant difficulties in its recognition and treatment. This condition always complicates any other diseases, and therefore is not an independent disease.

Thrombosis: normal or pathological?

In order to understand what the cause is and what are the mechanisms of occurrence of such a severe disorder as DIC syndrome, you need to know the main stages of blood coagulation.

A person is constantly faced with the risk of possible injuries, from minor scratches or cuts to serious wounds, so nature provides a special protective mechanism - thrombosis, that is, the formation of a blood clot at the site of vessel damage.

There are two oppositely directed systems in the body - coagulating And anticoagulant , the correct interaction of which promotes thrombus formation if necessary, as well as the liquid state of blood in the vessels in the absence of any damage. These hemostatic systems play a very important protective role.

When the integrity of the vascular wall is violated, the coagulation system is activated, a whole cascade of reactions of which leads to the formation (of a clot in the lumen of the vessel or chamber of the heart). Plasma proteins, in particular, as well as platelets, coagulation factors produced in the liver, and various enzymes are directly involved in this. The result is the formation of a blood clot that closes the defect in the vascular wall and prevents further bleeding.

To maintain the fluid state of the blood and prevent the uncontrolled formation of blood clots, there are specific antithrombotic mechanisms, realized by the action of the so-called anticoagulants– substances that prevent the occurrence of massive thrombosis (plasma proteins, proteolytic enzymes, endogenous heparin). In addition, an obstacle to thrombosis is rapid blood flow and so-called fibrinolysis, that is, the dissolution of the fibrin protein and its removal from the vascular bed with the help of enzymes circulating in the blood plasma and secreted by leukocytes, platelets and other cells. The remains of fibrin after its destruction are absorbed by leukocytes and macrophages.

When the interaction of components of the hemostatic system changes in various diseases and injuries, Discoordination occurs in the functioning of the coagulation and anticoagulation systems, which contributes to massive uncontrolled thrombus formation along with bleeding. These mechanisms form the basis of the pathogenesis of DIC syndrome, which is a life-threatening complication.

Causes of DIC syndrome

Since DIC is not an independent disease, it does not occur without some effect that activates the coagulation system. The most common causes of its occurrence:

• Infections - septic shock, severe bacterial and viral infections;
• Various types of shock (traumatic, infectious-toxic, hypovolemic, etc.), terminal conditions;
• Injuries, including traumatic surgical interventions (organ transplants, heart valve replacement), the use of artificial blood circulation and hemodialysis machines during surgical interventions;
• Oncological diseases, especially common forms of cancer;
• DIC syndrome in obstetrics - premature placental abruption;
• During pregnancy in case of occurrence (eclampsia, preeclampsia), ectopic pregnancy, etc.;
• Severe diseases of the cardiovascular system, purulent-inflammatory processes of internal organs.

Thus, DIC syndrome accompanies most severe diseases and terminal conditions(clinical death, subsequent resuscitation measures). At the stage of establishing their presence, hypercoagulation either already exists or will develop if appropriate preventive measures are not taken.

In newborns born healthy and at term, DIC syndrome is extremely rare. More often it occurs in severe birth injuries, amniotic fluid embolism (in this case, both the mother and the fetus will have symptoms), and respiratory disorders.

In children, hereditary coagulopathies are possible, in particular, and, accompanied by increased bleeding, while thrombohemorrhagic syndrome is relatively rare, and its causes can be severe infections and injuries.

Stages of development and forms of DIC syndrome

There are various approaches to the classification of thrombohemorrhagic syndrome: according to etiology, features of pathogenesis and clinical manifestations.

Based on the mechanisms of occurrence, the following stages of DIC syndrome are distinguished:

1. – characterized by the entry of thromboplastin into the blood, which triggers the process of blood clotting and thrombus formation;
2. Consumptive coagulopathy – intensive consumption of coagulation factors, subsequent increase in fibrinolytic activity (as a protective mechanism against massive thrombosis);
3. Hypocoagulation stage - as a result of the consumption of components of the coagulation system, incoagulation and platelet deficiency occur ();
4. Recovery stage.

thrombodynamics of a fibrin clot under various conditions of the coagulation system

Thus, when exposed to a damaging factor, for example, injury or bleeding, a protective mechanism is triggered - but uncontrolled consumption of coagulation factors leads to their deficiency and inevitable hypocoagulation, which is expressed in severe bleeding. If the patient is lucky and all the necessary qualified assistance is provided in a timely manner, then the recovery phase will begin with residual thrombosis.

It is worth noting that the process of thrombosis occurs in the microvasculature and is generalized in nature, therefore all organs and tissues are involved in the pathological process, which creates severe disturbances in their work.

Clinical classification of DIC syndrome implies the identification of the following forms:

• Spicy;
• Subacute;
• Chronic;
• Recurrent;
• Latent.

There is a so-called fulminant DIC syndrome, which only takes a few minutes to occur. This option is especially common in obstetrics.

Acute DIC syndrome lasts from several hours to several days and accompanies injuries, sepsis, surgical operations, transfusions of large quantities of blood and its components.

Subacute course characteristic of chronic infectious processes, autoimmune diseases (for example,) and lasts several weeks.

Chronic ICE possible in case of severe diseases of the heart and blood vessels, lungs, kidneys, and diabetes. This form can last for several years and is observed in therapeutic practice. As signs of thrombohemorrhagic syndrome increase, the disease that caused it progresses.

Clinical manifestations

In addition to these laboratory research methods, the clinic plays an important role in the diagnosis of DIC syndrome. In severe cases, when the lungs and kidneys are affected, characteristic skin changes and bleeding appear, the diagnosis is beyond doubt, however, in subacute and chronic forms of the course, diagnosis can be difficult and requires a careful assessment of clinical data.

Since the main pathogenetic link in the development of DIC syndrome is increased thrombus formation in the microcirculatory vessels, those organs in which the capillary network is well developed will suffer first of all: lungs, kidneys, skin, brain, liver. The severity of the course and prognosis depend on the degree of blockage of microcirculation by blood clots.

cutaneous manifestations of DIC syndrome are the most noticeable to a layman

The main clinical signs are quite typical and are caused by widespread thrombosis, bleeding and, as a consequence, failure of various organs.

• Leather, as a well-supplied organ, is always involved in the pathological process, a characteristic hemorrhagic rash appears in it due to minor hemorrhages, foci of necrosis (necrosis) on the face and limbs.
• Defeat lungs manifested by signs of acute respiratory failure, the symptoms of which will be severe shortness of breath up to respiratory arrest, pulmonary edema due to damage to small vessels and alveoli.
• With fibrin deposition in blood vessels kidney acute renal failure develops, manifested by impaired urine formation up to anuria, as well as serious electrolyte changes.
• Defeat brain is expressed in, leading to neurological disorders.

In addition to organ changes, there will be a tendency to external and internal bleeding: uterine, gastrointestinal, etc., as well as the formation of hematomas in internal organs and soft tissues.

In general, the clinical picture of DIC syndrome consists of symptoms of multiple organ failure and thrombohemorrhagic phenomena.

Diagnosis of DIC syndrome

To establish a diagnosis of thrombohemorrhagic syndrome, in addition to the characteristic clinical manifestations, Laboratory tests are important. Using tests, you can determine not only the presence of hemostasis disorders, but also the stage and form of DIC, and also monitor how effective the treatment is.

Laboratory diagnostics includes the so-called orientation tests, available to all medical institutions (coagulogram), and more complex and accurate confirming(determination of platelet aggregation properties, blood plasma tolerance to heparin, etc.).

In the first stage, a decrease in the number of platelets, increased coagulation and an increase in the amount of fibrinogen can be observed, while during the period of severe consumption coagulopathy there will be a significant decrease in fibrinogen, severe thrombocytopenia, a decrease in the content of coagulation factors and, accordingly, an increase in blood clotting time.

Post-mortem diagnosis of DIC syndrome through histological examination of tissues makes it possible to detect characteristic microscopic signs: accumulation of formed elements in the lumens of small vessels, thrombosis, multiple hemorrhages and necrosis in internal organs.

Since in the first hours of the development of the disease laboratory parameters may remain within normal limits, then it is important to ensure constant monitoring and monitoring of changes in hemostasis parameters, especially in patients at high risk of developing DIC. It is also necessary to monitor changes in the electrolyte composition of the blood, levels (indicators of kidney function), acid-base status, and diuresis.

Treatment

Due to the multifactorial origin of consumption coagulopathy, which complicates a variety of diseases and pathological conditions, There is currently no uniform treatment strategy for DIC syndrome.. However, taking into account the characteristic stages and features of the course, the main approaches to the prevention and treatment of such a dangerous complication have been identified.

It is important to eliminate the causative factor that caused the development of thrombohemorrhagic syndrome as early as possible, this will etiotropic direction of treatment:

1. Adequate antibiotic therapy for purulent-septic complications;
2. Timely replenishment of circulating blood volume during blood loss;
3. Maintaining the function of the cardiovascular system and blood pressure during various types of shock;
4. Prevention of complications and timely surgical care in obstetric practice;
5. Adequate pain relief in case of various injuries and traumatic shock, etc.

Main directions pathogenetic And symptomatic treatment:

• The use of fibrinolytics and antifibrinolytic drugs depending on the phase of the disease;
• Replacement infusion therapy;
• Improving the rheological properties of blood, using drugs to normalize microcirculation;
• Extracorporeal detoxification.

An important principle in the treatment of DIC syndrome is the use of anticoagulant therapy. Most often, heparin is used for these purposes, which restores normal blood clotting, prevents the formation of blood clots and helps remove existing ones, thereby improving the function of affected tissues and organs.

To eliminate the deficiency of blood coagulation factors, replacement infusion therapy is performed. The optimal drug for these purposes is fresh frozen plasma. Along with it, heparin and protease inhibitors can also be administered (they reduce enzyme activity and prevent the development of hypocoagulation, prevent the development of shock - contrical, gordox).

To improve microcirculation in tissues, aspirin, trental, chimes, etc. are used, as well as the introduction of rheological solutions (reopolyglucin, voluven).

Extracorporeal detoxification methods - plasmapheresis, cytapheresis, hemodialysis - are very important in the complex therapy of DIC syndrome.

In general, the treatment of DIC syndrome is a very difficult task., and sometimes the decision on the regimen of drugs and their dosages must be made in a matter of minutes.

It is necessary to treat DIC syndrome in stages, since the prescription of a particular drug entirely depends on the patient’s state of hemostasis at a particular point in time. In addition, constant laboratory monitoring of blood coagulation, acid-base balance, and electrolyte balance should be carried out.

Emergency care consists of relieving pain, combating shock, establishing infusion therapy, and administering heparin in the first phase of DIC.

Patients who have been diagnosed with thrombohemorrhagic syndrome or are at high risk of developing it should be immediately hospitalized and placed in the intensive care unit.

Mortality in thrombohemorrhagic syndrome, according to various sources, reaches 70% in stage III, and in chronic cases – 100%.

Prevention This dangerous complication consists, first of all, in the earliest possible treatment of the diseases that led to its occurrence, as well as in restoring blood circulation and microcirculation in organs and tissues. Only early initiation of therapy and correct tactics contribute to the normalization of hemostasis and further recovery.

Video: lecture by A.I. Vorobyova about DIC syndrome