DIC syndrome: treatment and diagnosis. Reasons for the appearance and danger of DIC syndrome DIC syndrome in hematology in children

is a disorder of the hemostasis process, which contributes to the formation of blood clots, as well as the development of various hemorrhagic and microcirculatory disorders. The full name of the disease is disseminated intravascular coagulation; you can also find such a designation of the syndrome as thrombohemorrhagic syndrome.

DIC syndrome is characterized by hemorrhagic diathesis with increased blood coagulation inside the vessels, which leads to the formation of blood clots that stop them. This, in turn, entails the development of pathological changes in organs of a dystrophic-necrotic and hypoxic nature.

DIC syndrome poses a threat to the patient's life, as there is a risk of bleeding. They can be extensive and difficult to stop. Also, internal organs may be involved in the pathological process, the functioning of which will be completely disrupted. The kidneys, liver, spleen, lungs and adrenal glands are primarily at risk.

The syndrome can occur in a variety of pathologies, but it always leads to thickening of the blood, disruption of its circulation through the capillaries, and this process is not compatible with the normal functioning of the human body.

DIC syndrome can lead to both immediate death of the patient and protracted latent fatal forms of disorders.

The statistics of DIC syndrome cannot be calculated, since in different diseases the syndrome occurs with different frequencies. Some pathologies are always accompanied by DIC syndrome, while with other diseases it occurs somewhat less frequently. This syndrome can be regarded as an abnormal protective reaction of the body, which it produces in order to suppress bleeding that occurs when blood vessels are damaged. In this way, the body seeks to protect itself from affected tissues. Thrombohemorrhagic syndrome is often encountered in the practice of doctors of various specialties. Gynecologists, surgeons, resuscitators, traumatologists, hematologists, etc. are familiar with it.

Causes of DIC syndrome

The causes of DIC are various diseases that are accompanied by damage to tissues, blood vessels and blood cells. In this case, a failure of hemostasis occurs in the body with an increase in blood clotting.

The following pathological processes can lead to the development of thrombohemorrhagic syndrome:

Septic conditions that are a complication of a viral or bacterial infection. Septic shock always provokes the development of this syndrome.

Generalized infections. In this case, the syndrome most often occurs in newborns.

Obstetric pathologies - severe gestosis, premature placental abruption or placental previa, fetal death inside the womb, manual separation of the placenta, uterine bleeding, cesarean section, anatomical fluid embolism.

Surgical interventions accompanied by an increased risk of trauma to the patient. Most often, these are operations that are performed to remove malignant tumors, interventions performed on organs that primarily consist of parenchyma, and operations on blood vessels. If at the same time the patient requires a massive blood transfusion, or he develops collapse or, then the risk of developing thrombohemorrhagic syndrome increases.

Any terminal conditions of the human body lead to the development of DIC of varying severity.

With 100% probability, DIC syndrome will develop in people against the background of intravascular hemolysis. Destruction of blood cells most often occurs when a person is transfused with blood of a different type (incompatible transfusion).

Risk factors for the development of DIC include surgical procedures such as organ transplantation, implantation of a prosthetic heart valve or blood vessels, and the need to artificially start blood circulation.

Taking certain medications increases the risk of developing the syndrome. These are diuretics, oral contraceptives, drugs from the group of fibrinolysis inhibitors and Ristomycin (an antibacterial drug).

Giant angiomas with their multiple appearance.

Bites from poisonous snakes and other acute poisonings of the human body can provoke the development of DIC syndrome.

In some cases, allergic reactions become the cause of the development of a dangerous condition.

Immune diseases such as: glomerulonephritis, etc.

Vascular pathologies, including congenital heart defects, myocardial infarction, heart failure, etc.

However, the main reason for the development of DIC is sepsis (virological and bacteriological) and shock of any etiology. These pathologies account for up to 40% of cases of all registered DIC syndromes. If we are talking about newborn children, then this figure rises to 70%. But instead of the term DIC syndrome, doctors use the designation “malignant purpura of newborns.”

With DIC syndrome, there is a failure of the complex of body reactions that are triggered in order to prevent bleeding. This process is called hemostasis. In this case, the function responsible for blood clotting is excessively stimulated, and the anticoagulant (anticoagulant) and fibrinolytic systems that balance it, on the contrary, are quickly depleted.

Enzymes produced by bacteria that enter the body, toxins, immune complexes, amniotic fluid, phospholipids, low cardiac effusion into the bloodstream, acidosis and other factors pathogenic to the body can influence the manifestation of DIC syndrome. At the same time, they will circulate either in the bloodstream or act on the vascular endothelium through mediators.

DIC always develops according to certain patterns and goes through several successive stages:

At the first stage the process of excessive blood clotting, as well as cell aggregation inside the vessels, starts. An excess amount of thromboplastin or a substance with a similar effect is released into the blood. This starts the coagulation processes. The time of the initial stage can vary widely and take from a minute to several hours if the syndrome develops acutely. The pathological process will take place from several days to several months if the syndrome is chronic.

The second stage is characterized by the launch of the process of consumption coagulopathy. At the same time, there is an increasing lack of fibrogen, platelets and other plasma factors responsible for the blood clotting process in the body.

The third stage is critical. At this time, secondary fibrinolysis occurs, blood coagulation reaches a maximum, until this process completely stops. In this case, hemostasis appears to be significantly unbalanced.

Recovery stage characterized by normalization of hemostasis. Residual dystrophic-necrotic changes are observed on organs and tissues. Another end of DIC syndrome may be acute failure of one or another organ.

The full development of DIC syndrome (its severity and mechanism of development) depends on the degree of disturbance of blood microcirculation and on the degree of damage to organs or their systems.

Symptoms of DIC syndrome

The symptoms of DIC will be determined by the clinical manifestations of the disorder that provoked its development. They also depend on how quickly the pathological process develops, in what state the mechanisms responsible for compensating hemostasis are, and also at what stage of DIC the patient is.

Symptoms of acute DIC syndrome.

In the acute form of DIC, the pathological process quickly spreads throughout the body. Most often this happens within a few hours.

The person is in a state of shock, his blood pressure drops to 100/60 or below.

The patient loses consciousness, symptoms of acute respiratory failure and pulmonary edema are observed.

Bleeding increases, profuse and massive bleeding develops. This process involves systems and organs of the human body such as the uterus, lungs, and gastrointestinal tract organs. Development is possible.

Against the background of acute DIC, destructive destruction of pancreatic tissue is observed with the development of functional failure of the organ. Possible addition of gastroenteritis of an erosive-ulcerative nature.

Foci of ischemic dystrophy appear in the myocardium.

With amniotic fluid embolism, disseminated intravascular coagulation syndrome develops at lightning speed. In a few minutes, the pathology goes through all three stages, making the condition of the mother and fetus critical. Patients undergo hemorrhagic and cardiopulmonary shock, which are difficult to stop. In this regard, the prognosis for life is unfavorable and death occurs in 80% of cases.

Symptoms of subacute DIC syndrome

The course of the syndrome in this case is more favorable.

Hemosyndrome is expressed in the occurrence of hemorrhagic rashes.

Bruises and large hematomas may appear on the skin.

Injured areas and injection sites are characterized by increased bleeding.

Mucous membranes are also susceptible to bleeding. Blood may be present in sweat and tears.

The skin is characterized by excessive pallor, even marbling. When you touch the skin, you feel an unnatural coldness.

The internal organs swell, fill with blood, necrotic areas and hemorrhages appear on them. The gastrointestinal tract, liver and kidneys, as well as the adrenal glands and lungs are susceptible to pathological changes.

As for the chronic form of DIC, it not only occurs more often than others, but in most cases it occurs hidden. The patient, due to the absence of symptoms, may not even be aware of the development of pathologies in the hemostatic system. However, as the disease that provoked DIC progresses, its symptoms will become more pronounced.

Other symptoms

Other symptoms that may indicate the development of chronic DIC syndrome:

Deterioration and prolongation of the regeneration process of any wounds.

An increase in asthenic syndrome with a corresponding symptom complex.

Attachment of a secondary purulent infection.

Formation of scars on the skin in places where there was damage.

Complications of DIC syndrome are usually very severe and threaten not only the health, but also the life of the patient.

More often than others, the following conditions develop:

Hemocoagulative shock. Organs and tissues begin to experience oxygen deficiency, since blood microcirculation is disrupted in the small vessels responsible for their nutrition. In addition, the amount of toxins in the blood itself increases. As a result, the patient’s pressure drops sharply, both arterial and venous, and organ failure, shock, etc. occur.

Acute respiratory failure. It is a borderline condition that poses a direct threat to the patient’s life. As hypoxia intensifies, loss of consciousness occurs, and hypoxic coma develops and occurs.

Acute renal failure is another most common complication of DIC syndrome. The patient stops urinating, until there is no urine output at all. The water-salt balance is disturbed, the level of urea, nitrogen, and creatinine in the blood increases. This condition is potentially reversible.

Liver necrosis.

From the gastrointestinal tract: stomach ulcer, intestinal infarction, pancronecrosis.

From the cardiovascular system -.

From the hematopoietic system – acute hemorrhagic anemia.

Diagnosis of DIC syndrome

Diagnosis of DIC syndrome is based on examining the patient, taking an anamnesis and conducting laboratory tests.

The patient needs to undergo the following tests:

Blood smear;

Blood for coagulogram, as the main method for diagnosing hemostasis (platelets, fibrogens and other important indicators are counted);

ELISA (determination of PDF, RFMC, D-dimer as the main markers of blood coagulation inside blood vessels):

Blood for paracoagulation tests (allows you to confirm or refute the diagnosis).

The doctor finds out the reason that led to the development of DIC syndrome, determines its stage and nature.

If the course of the syndrome is hidden, then hypercoagulation can be determined solely by laboratory tests. In this case, fragmented red blood cells will be present in the blood smear, thrombosed time and aPTT will increase, and the concentration of PDP will increase. A blood test will indicate a lack of fibrinogen and platelets.

If the syndrome is confirmed, then the most vulnerable organs must be examined: kidneys, liver, heart, brain, lungs, adrenal glands.

Treatment of DIC syndrome is a rather complex process, and the patient’s recovery does not occur in every case. If an acute form of the syndrome is diagnosed, then death occurs in 30% of cases, which is a fairly high rate. However, it is not always possible to accurately establish the reason why the patient died. Has DIC become a critical condition, or has the patient died as a result of the negative impact of the underlying disease?

Doctors observing DIC syndrome first of all make efforts to eliminate or minimize the factor that led to the development of the syndrome and stimulates its progression. It is important to eliminate purulent-septic conditions, which most often provoke impaired hemostasis. At the same time, there is no point in waiting for the results of bacteriological studies; therapy is carried out in accordance with the clinical signs of the disease.

Antibacterial therapy against the background of DIC syndrome is indicated in the following cases:

Previous abortion;

Premature discharge of amniotic fluid, especially when it is not clear and contains turbidity;

Increase in body temperature;

Symptoms indicating inflammation of the lungs, urinary tract, abdominal organs;

Signs of meningitis.

For treatment, broad-spectrum antibacterial drugs are used, with the inclusion of γ-globulins in the treatment regimen.

To relieve shock conditions, injections of saline solutions, plasma transfusions with Heparin, Prednisolone (intravenously), and Reopoliglucin are used. If shock syndrome is eliminated in a timely manner, it is possible to stop the development of disseminated intravascular coagulation syndrome, or to significantly mitigate its manifestations.

As for Heparin, when administered there is a risk of bleeding. It has no positive effect if used late. It should be administered as early as possible, strictly following the recommended dosage. If the patient is at the third stage of development of DIC syndrome, then the administration of Heparin is a direct contraindication. Signs indicating a prohibition on the use of this drug are: drop in pressure, bleeding (it may be hidden), hemorrhagic collapse.

If the syndrome has just begun to develop, then the administration of a-blockers is indicated: Dibenamine, Phentolamine, Thioproperazine, Mazeptil. The drugs are administered intravenously in the required concentration. They help normalize microcirculation in organs and resist the formation of blood clots inside blood vessels. You should not use adrenaline and norepinephrine drugs, as they can worsen the situation.

When renal and liver failure develops, in the early stages of development of DIC syndrome, it is also possible to use drugs such as Trental and Curantil. They are administered intravenously.

At the third stage of development of DIC syndrome, it is necessary to administer protease inhibitor drugs. The drug of choice is Contrikal, the method of administration is intravenous, the dose is no more than 100,000 units at a time. If such a need arises, the infusion can be repeated.

Local effects are reduced to treating bleeding erosions, wounds and other areas with Androxon at a 6% concentration.

To summarize, it can be noted that complex treatment of DIC syndrome comes down to the following points:

Elimination of the root cause that provoked the development of the syndrome.

Carrying out antishock therapy.

Replenishment of blood volumes with transfusion of plasma enriched with Heparin, if there are no contraindications to this.

Early use of adrenergic blockers and drugs that help reduce the number of platelets in the blood: Curantil, Trental, Ticlodipine.

Administration of Contrikal, platelet transfusion to normalize hematocrit against the background of severe bleeding.

Prescribing plasmacytapheresis, if indicated.

To normalize microcirculation in the affected organs, nootropics, angioprotectors and other syndromic drugs are used.

With the development of acute renal failure, hemodiafiltration and hemodialysis are performed.

Patients with DIC syndrome are required to be hospitalized and are under 24-hour medical supervision. They are located either in the intensive care unit or in intensive care wards.

As for the prognosis, it is very variable. To a greater extent, it depends on what caused the development of DIC syndrome, on the degree of hemostasis impairment, on how quickly first aid was provided and how adequate it was.

It is impossible to exclude a lethal outcome, since it can occur against the background of heavy blood loss, shock, or organ failure.

Doctors should pay special attention to patients belonging to risk groups - elderly people, pregnant women, newborns, people with underlying diseases.

About the doctor: From 2010 to 2016 practicing physician at the therapeutic hospital of the central medical unit No. 21, the city of Elektrostal. Since 2016 he has been working at diagnostic center No. 3.

DIC syndrome (disseminated intravascular coagulation) is a pathological nonspecific process triggered by the entry into the bloodstream of factors activating platelet aggregation (sticking) and blood clotting. Thrombin is formed in the blood, activation and rapid depletion of plasma enzyme systems (fibrinolytic, kallikrein-kinin, coagulation) occur. This causes the formation of blood cell aggregates and microclots that disrupt microcirculatory circulation in the internal organs, which leads to the development of:

• hypoxia;
• acidosis;
• thrombohemorrhages;
• intoxication of the body with protein breakdown products and other under-oxidized metabolites;
• dystrophy and deep organ dysfunction;
• secondary profuse bleeding.

Causes

The development of DIC syndrome can be complicated by many pathological conditions:

• all types of shock;
• obstetric pathology (for example, non-developing pregnancy or premature abruption of a normally located placenta);
• acute intravascular hemolysis against the background of hemolytic anemia, poisoning with hemocoagulating and snake venoms;
• destructive processes in the pancreas, kidneys or liver;
• hemolytic-uremic syndrome;
• thrombocytopenic purpura;
• generalized purulent infection, sepsis;
• malignant neoplasms;
• massive chemical or thermal burns;
• immune complex and immune diseases;
• severe allergic reactions;
• extensive surgical interventions;
• heavy bleeding;
• massive blood transfusions;
• prolonged hypoxia;
• terminal states.

DIC syndrome is an extremely life-threatening pathology; its development is accompanied by high mortality. Without treatment, almost 100% of patients die.

Signs

DIC syndrome is manifested by the development of various bleedings (from the gums, gastrointestinal tract, nose), the occurrence of massive hematomas at injection sites, etc.

In addition to pathology in the blood coagulation system, changes in DIC affect almost all organ systems. Clinically this is manifested by the following symptoms:

• disturbances of consciousness up to stupor (but there is no local neurological deficit);
• tachycardia;
• drop in blood pressure;
• pleural friction noise;
• vomiting with blood;
• scarlet blood in the stool or melena;
• uterine bleeding;
• a sharp decrease in the amount of urine excreted;
• increase in azotemia;
• cyanosis of the skin.

Diagnostics

Laboratory tests are used to diagnose DIC syndrome:

1. Measurement of antithrombin III (normal 71–115%) – its level is decreasing.
2. Paracoagulation protamine test. Allows you to determine fibrin monomers in blood plasma. In DIC syndrome it becomes positive.
3. Determination of fibrin breakdown D-dimer formed as a result of the action of plasmin on fibrin clots. The presence of the named fragment indicates fibrinolysis (presence of plasmin and thrombin). This test is very specific for confirming the diagnosis of DIC.
4. Determination of fibrinopeptide A. Allows the identification of fibrinogen breakdown products. The level of this peptide is increased in DIC syndrome, which is associated with thrombin activity.

The number of platelets in the peripheral blood is also determined and the coagulogram is examined. Main criteria for DIC syndrome:

• prothrombin time – more than 15 seconds (normal – 10–13 seconds);
• plasma fibrinogen – less than 1.5 g/l (normal – 2.0–4.0 g/l);
• platelets – less than 50 x 10 9 / l (normal – 180–360 x 10 9 / l).

DIC syndrome is manifested by the development of various bleedings (from the gums, gastrointestinal tract, nose), the occurrence of massive hematomas at injection sites, etc.

Treatment

Treatment of DIC syndrome includes:

• carrying out local hemostasis;
• antishock therapy;
• maintaining vital functions;
• heparin therapy;
• compensation for blood loss and treatment of its consequences;
• the use of drugs that improve microcirculation;
• transfusion of platelet concentrate for severe thrombocytopenia.

In severe cases of DIC, intravenous administration of antithrombin III, which inactivates plasmin, thrombin and other coagulation enzymes, is indicated.

Prevention

Prevention of the development of DIC syndrome includes:

• performing surgical interventions using the least traumatic techniques;
• timely treatment of tumors and other pathologies that can cause disseminated intravascular coagulation;
• prevention of burns, snake bites, poisoning;
• adequate therapy for blood loss exceeding 1 liter.

Consequences and complications

The main complications of DIC syndrome:

• respiratory distress syndrome;
• acute hepatorenal failure;
• hemocoagulative shock;
• massive bleeding;
• anemic coma;
• severe posthemorrhagic anemia.

DIC syndrome is an extremely life-threatening pathology; its development is accompanied by high mortality. Without treatment, almost 100% of patients with DIC die. Active intensive care can reduce the mortality rate to 20%.

The term DIC syndrome denotes a nonspecific general pathological process, which is based on scattered diffuse coagulation of blood in vessels with the formation of many microclots and aggregates of blood cells, blocking blood circulation in organs and the development of deep dystrophic changes in them.

Main pathological conditions, in which DIC of the blood develops:

Infections - sepsis, bacterial dysentery, viral hepatitis, salmonellosis, HFRS, foodborne illnesses, tropical fevers, etc.

Shock - anaphylactic, septic, traumatic, cardiogenic, hemorrhagic, burn, - with prolonged crush syndrome and others.

Acute intravascular hemolysis - transfusions of incompatible blood, crises of hemolytic anemia, poisoning with hemolytic poisons, hemolytic-uremic syndrome, etc.

Tumors- disseminated forms of cancer stage III-IV, Trousseau syndrome, acute leukemia, blast crises of chronic leukemia, etc.

Injuries- fractures of tubular bones, polytrauma, burns, frostbite, electrical trauma, crash syndrome, etc.

Traumatic surgical interventions - major abdominal and orthopedic surgeries, surgeries on the lungs, liver, pancreas, surgeries for polytrauma, etc.

Obstetric and gynecological pathology - abruption, previa and rupture of the placenta; amniotic fluid embolism; atonic uterine bleeding; antenatal fetal death; stimulation of labor and fetal destruction operations; postpartum sepsis; hydatidiform mole; criminal abortion; severe late gestosis; eclampsia.

Immune and immune complex diseases- SLE, systemic scleroderma, hemorrhagic vasculitis, acute diffuse glomerulonephritis, etc.

Cardiovascular pathology - large-focal myocardial infarction, congestive heart failure, cardiac asthma, congenital “blue” defects, deep vein thrombosis of the leg, pulmonary embolism, etc.

Acute and subacute inflammatory-necrotic and destructive processes andlevaniya - acute pancreatitis, systemic vascular lesions, nonspecific lung diseases, bronchial asthma, liver disease, kidney disease and acute renal failure, diabetes mellitus, radiation sickness.

Hyperviscosity syndrome - polyglobulinemia (polyglobulia) of various origins, paraproteinemia and cryoglobulinemia, erythrocytosis and erythremia.

Transplantation organs and tissues, prosthetics of valves and blood vessels, extracorporeal procedures, etc.

Massive blood transfusions and blood reinfusions.

Thrombotic thrombocytopenic purpura.

Poisoning with snake hemocoagulating venoms.

Iatrogenic medicinal forms - large doses of antibiotics, corticosteroids, cytostatics, α-adrenostimulants, ε-ACC, improper use of anticoagulants and fibrinolytics, oral contraceptives, etc.

The basis of the internal combustion engine in all cases is excessive (pathological) activation of hemostasis, leading to massive blood clotting, blockade of microcirculation in vital organs (lungs, kidneys, liver, adrenal glands, etc.) by loose masses of fibrin and cell aggregates, and the development of multiple organ dysfunction. DIC is characterized by a significant consumption of coagulation factors and platelets during the formation of numerous thrombi and blood clots, activation of fibrinolysis, accumulation in the bloodstream of fibrin/fibrinogen breakdown products (FDP/f) and other proteins that exhibit anticoagulant properties and have a damaging effect on the walls of blood vessels. This leads to the development hypocoagulable state , which may be accompanied by severe hemorrhagic syndrome in the form of bleeding of various locations.

DIC syndrome - pathogenesis. ICE - is such variant of coagulopathy, in which especiallythere is clearly an imbalance between the coagulation and anticoagulationand fibrinolytic systems of the body. A feature of the “tragedy” of DIC syndrome is the disseminated, scattered, multiple formation of blood clots and fibrin clots, essentially where hemostasis is not required.

Etiological factors lead to hypercoagulation, the formation of small loose fibrin clots or microthrombi in almost the entire microcirculatory system. They are immediately dissolved by the fibrinolytic system. New blood clots and new clots form and all the main factors of the coagulation system are gradually depleted - platelets, prothrombin, fibrinogen. Hypocoagulation develops due to consumption coagulopathy. If the integrity of the vascular wall is compromised somewhere, a blood clot cannot form. At the same time, there are anticoagulant substances in excess, due to which bleeding also cannot be stopped. Fibrin clots and microthrombi formed in microvessels block tissue blood flow, cause tissue ischemia, and disrupt the function of such vital organs as the heart, lungs, and kidneys.

Mechanism of development of DIC syndrome

I phase. Formation of active thromboplastin- the longest phase of hemostasis. Plasma factors take part in it. (XII, XI, IX, VIII, X, IV, V) and platelet factors (3, 1).

II phase. Conversion of prothrombin to thrombin. Occurs under the action of active thromboplastin and the participation of calcium ions (factor IV).

III phase. Formation of fibrin polymer. Thrombin (with the participation of calcium ions - factor IV and platelet factor - 4) converts fibrinogen into fibrin monomer, which, under the action of plasma factor VIII and platelet factor 2, turns into insoluble strands of fibrin polymer.

Changes in procoagulants in the hemostasis system and activation of the platelet link lead to platelet aggregation with the release of biologically active substances: kinins, prostaglandins, catecholamines and others, which affect the vascular system.

When blood flows slowly through the branches of small vessels, it is separated into plasma and red blood cells, filling different capillaries. Losing plasma, red blood cells lose their ability to move and accumulate in the form of slowly circulating and then non-circulating formations. Stasis, aggregation, and then lysis occurs, and blood thromboplastin bound to the stroma of red blood cells is released. The entry of thromboplastin into the bloodstream causes the process of intravascular coagulation. The fibrin threads that fall out entangle clumps of red blood cells, forming “sludge” - lumps that settle in the capillaries and further disrupt the homogeneity of the blood structure. An important role in the development of the “sludge” phenomenon is played by two interrelated phenomena - a decrease in blood flow and an increase in blood viscosity (M.A. Repina, 1986). There is a disruption in the blood supply to tissues and organs. In response to activation of the coagulation system, protective mechanisms are activated - the fibrinolytic system and cells of the reticuloendothelial system. Against the background of disseminated intravascular coagulation, increased bleeding develops due to increased consumption of procoagulants and increased fibrinolysis.

DIC syndrome - classification.

Clinical classification.

The clinical picture of DIC syndrome consists of signs of the underlying disease that caused intravascular coagulation and the DIC syndrome itself. According to the clinical course, it happens:

acute (up to lightning);

subacute;

chronic;

recurrent.

Stages of DIC syndrome:

Hypercoagulation and platelet aggregation.

Transitional, with increasing consumption coagulopathy, thrombocytopenia, multidirectional changes in general coagulation tests.

Deep hypocoagulation up to complete blood incoagulation.

Unfavorable outcome or recovery stage.

1. hypercoagulation stage- at this stage there is a sharp increase in platelet adhesiveness, and in connection with this, activation of the first phase of coagulation, an increase in the concentration of fibrinogen. These indicators can be determined using a coagulogram, which allows you to determine the state of the coagulation and anticoagulation systems.

Blood clots form in peripheral vessels: platelets stick together, the formation of fibrin globules begins, and blood clots form in small vessels. This thrombosis of small vessels, as a rule, does not lead to necrosis, but causes significant ischemia of the tissues of various organs.

Thrombosis occurs throughout the body, so the syndrome is called disseminated (scattered). The period of hypercoagulation is characterized by activation of plasma blood coagulation systems, intravascular aggregation of platelets and other blood cells, disruption of microcirculation in various organs as a result of blockade of the vascular bed by masses of fibrin and cell aggregates. The hypercoagulable phase can develop gradually, with the slow supply of small doses of prothrombinase. However, a slow course can end in an explosion with the rapid development of disseminated intravascular coagulation syndrome.

In addition to disseminated intravascular coagulation, in some cases only local limited intravascular coagulation and thrombus formation are observed.

2. Consumptive coagulopathy. As a result of disseminated intravascular coagulation, the main resources of blood coagulation factors (fibrinogen, prothrombin) are lost and they become scarce. This depletion of blood clotting factors leads to the development of bleeding, if it is not stopped, from the main source, and bleeding from other vessels is also possible, even with minor injuries.

Intravascular coagulation also causes activation of the fibrinolytic system, leading to the dissolution of blood clots and creating the preconditions for the development of hemorrhagic syndrome. Naturally, the activation of the mechanisms causing hypocoagulation has a certain sequence and significance throughout the entire process: depletion of blood coagulation mechanisms - accumulation of fibrin degradation products - activation of the fibrinolytic system. Based on this position, some authors detail the hypocoagulation phase, distinguishing a number of stages in it. Thus, M. S. Machabeli (1981) and V. P. Baluda (1979) distinguish between the phases of hypocoagulation and hypocoagulation with secondary fibrinolysis, A. V. Papayan (1982) - the stages of consumption coagulopathy and afibrinogenemia, or pathological fibrinolysis, 3. C Barkagan (1980) - stages of hypocoagulation and deep hypocoagulation. As already noted, for practical purposes it is possible to isolate the general phase of hypocoagulation.

The coagulogram shows signs of hypo- or afibrinogenemia, but the concentration of fibrinogen S increases even more, it is already converted into fibrin, which promotes the formation of peptidases, resulting in vascular spasm, which further increases the ischemia of various organs. Hypoprothrombinemia is characteristic, the platelet count continues to decrease. As a result, the blood loses its ability to clot. At the same stage, the fibrinolytic system is activated. This leads to the fact that the formed blood clots begin to dissolve and melt, including the melting of clots that have clogged bleeding vessels.

3. Third stage - fibrinolysis. It begins as a defensive reaction, but as a result of the melting of clots in bleeding vessels, increased bleeding occurs, which becomes profuse.

The coagulogram indicators at the stage of fibrinolysis differ slightly from the indicators at the stage of consumption coagulopathy, therefore this stage is recognized by its clinical manifestations: all tissues, like a sponge, begin to bleed.

If therapeutic measures are effective, then this process can be stopped at any stage, including sometimes at the stage of fibrinolysis. Then phase 4 develops.

4. Phase recovery. Here, signs of multiple organ failure begin to come to the fore. As a result of prolonged ischemia, cardiovascular failure occurs. Possible cerebrovascular accident.

The onset of this stage is recorded in the coagulogram: indicators may improve or normalize. Depending on the phase of DIC syndrome in which treatment is started, mortality is about 5% at the hypercoagulation stage, 10-20% at the consumption coagulopathy stage, 20-50% at the fibrinolysis stage, and up to 90% at the recovery stage.

In the fourth stage, with a favorable outcome, the function of organs is restored to one degree or another, which depends on the degree of their damage (dystrophic changes, sclerosis, etc.). The stage may end with complete recovery. It is possible to develop severe complications even in the absence of DIC syndrome as such - renal, liver failure, neurological, cardiac and other complications.

V.P. Baluda (1979) identifies several main causes of death in the acute course of DIC syndrome:

1. Death of the body can occur instantly when the main vessels of vital organs are blocked.

2. If the body does not die in the first minutes from blockage of blood vessels with blood clots, then the fatal outcome can be determined by the development of severe hemorrhagic syndrome in the form of local bleeding at the site of vascular damage (surgery, trauma), or generalized bleeding and hemorrhage in the internal organs.

3. In a later period, death is possible due to severe dysfunction of individual organs (kidneys, liver, lungs, spleen, myocardium, brain, pituitary gland, adrenal glands, digestive tract).

DIC syndrome – clinic. The course of DIC syndrome can be acute, subacute, protracted and undulating. At the same time, different variants of the course are characterized by “their” etiological factors. Acute DIC develops in conditions of shock, severe forms of sepsis, massive injuries and burns, acute intravascular hemolysis, and bites of certain types of snakes. Prolonged DIC is observed in cancer, immunocomplex and myeloproliferative processes, circulatory failure in patients with cardiomyopathies, liver cirrhosis, severe active hepatitis, and chronic hemodialysis. An undulating, recurrent course is observed during destructive processes in organs caused by virulent microflora or toxic influences.

Hemorrhagic manifestations in DIC syndrome have their own characteristics. Can be local bleeding or widespread hemorrhage. In the first case, hemorrhages from wounds due to injuries, postpartum and post-abortion uterine bleeding, and hematuria are observed. These bleeding is prolonged and does not respond to routine hemostatic therapy. In the case of common hemorrhages, a mixed “bruise-hematoma” type of bleeding is noted in combination with nasal, gastrointestinal, pulmonary, uterine bleeding, diffuse sweating of blood into the pleural and abdominal cavities, and the pericardium.

DIC syndrome is characterized by a combination of hemorrhagic disorders with a number of syndromes caused by microcirculation disorders in organs, their dystrophy and dysfunction. A “shock” lung and acute respiratory failure, acute renal failure, dyscirculatory encephalopathy, adrenal insufficiency, acute erosions and ulcers in the stomach and intestines develop.

The duration of clinical manifestations of DIC syndrome can reach 7-9 hours or more. Changes in the hemocoagulation system, determined using laboratory methods, persist longer than clinical ones. Therefore, laboratory diagnosis of DIC syndrome is of paramount importance: it allows you to more accurately determine the degree or phase of the syndrome and choose the right treatment.

Clinical manifestations of blood DIC can be diverse depending on the involvement of various organs and systems. Yes, there are signs dysfunction:

of cardio-vascular system(tachycardia, hypotension, collapse, shock);

lungs(shortness of breath, wheezing, pulmonary edema, respiratory failure);

brain(lethargy, drowsiness, sensory disturbances and motorfunctions, stroke, stupor, coma);

kidney(decreased diuresis, proteinuria, hematuria, anuria, acute renal failure);

adrenal glands(acute failure with a drop in blood pressure and hypoglycemia);

liver(hyperbilirubinemia, hepatosis, liver failure);

gastrointestinal tract(impaired motility, erosion and ulcers), etc.

Clinically I internal combustion engine phase The course is very variable: from asymptomatic forms (“laboratory disseminated intravascular coagulation”) to manifestations of thrombosis of any localization (myocardial infarction, transient cerebrovascular accidents, ischemic stroke, pulmonary embolism, thrombosis of mesenteric vessels, etc.). Possible tachycardia, muffled heart sounds, shortness of breath, drop in blood pressure, and in severe cases, the development of multiple organ failure.

InIIICE phase may be observed: tachycardia, shortness of breath, hypotension, collapse, pallor or marbling of the skin, decreased diuresis due to impaired renal function, impaired intestinal motility, depression of consciousness, etc. In severe cases, multiple organ failure syndrome (MODS) develops. In this phase, thrombosis and bleeding of any localization are possible; however, in some patients the disease may be asymptomatic (“blood disseminated intravascular coagulation without disseminated intravascular coagulation syndrome”).

IIIDIC phase of blood is often critical, mortality from acute DIC reaches 40-50%. A pronounced hemorrhagic syndrome with a mixed type of bleeding develops: nasal, gingival, uterine, gastrointestinal and hemorrhoidal bleeding, hemorrhages in the sclera and at injection sites, numerous petechiae and “bruises” on the skin, bleeding from surgical wounds, micro- and macrohematuria, hemoptysis, etc. There are pronounced symptoms of cardiovascular, respiratory, renal, and liver failure; Often there is a picture of shock with pallor or marbling of the skin, acrocyanosis and coldness of the extremities, shortness of breath, hypotension and confusion. Death can occur as a result of hemorrhages in the brain, pituitary gland, adrenal glands; acute gastrointestinal bleeding; acute renal or cardiopulmonary failure, etc.

Early diagnosis of DIC is facilitated by the identification of underlying diseases and conditions (infectious and septic processes, all types of shock and severe hypovolemia, acute intravascular hemolysis, obstetric pathology, etc.). It's important to note that DIC of blood is necessaryidentify at early stages, i.e. to DIC syndrome, There are no pronounced clinical manifestations yet, but there are already laboratory symptoms. The main task of the doctor is to interrupt DIC during phases I-II of the process (before the development of irreversible disorders), preserving the functions of the organs and systems of the patient’s body.

The most important aid for a clinician in recognizing disseminated intravascular coagulation in the early stages, before a detailed clinical picture appears, is laboratory diagnostics.

The diagnosis of chronic DIC syndrome is made on the basis of laboratory studies of the hemostatic system.

DIC syndrome - diagnostic methods.

Early diagnosis is situational in nature and is based on identifying diseases and conditions in which DIC syndrome develops naturally. In all these cases, it is necessary to begin early preventive therapy before the appearance of pronounced clinical and laboratory signs of DIC syndrome.

Diagnosis should be based on the following activities:

critical analysis of the clinic;

a thorough examination of the hemostatic system to determine the form and stage of the syndrome;

assessing the response of hemostasis to therapy with antithrombotic drugs.

Diagnosis of DIC syndrome is based on a set of studies characterizing the hemostatic system. They should be prescribed as early as possible and repeated over time. This is due to the fact that with DIC syndrome, almost all parts of hemostasis are disrupted, and often these disturbances are multidirectional.

The general trend of changes in hemocoagulation tests is as follows: the number of platelets decreases, the clotting time lengthens, the fibrinogen content decreases, the prothrombin index decreases, fibrinogen degradation products increase, and clot retraction decreases.

IN hypercoagulation phase noted shortening of blood clotting time, plasma recalcification, increased prothrombin consumption, shortening of prothrombin and thrombin time. The same information is provided by standardized tests - kaolin-kephalin time, autocoagulation test, etc. Also increased platelet adhesion.

At the end of the hypercoagulation phase, in the initial period of hypocoagulation, the following typical changes are found (3. S. Barkagan, 1980):

a) the presence of erythrocyte fragments in the peripheral blood smear (fragmentation phenomenon);

b) progressive thrombocytopenia;

c) prolongation of prothrombin time;

d) prolongation of thrombin time;

e) decrease in plasma fibrinogen levels;

f) increasing the plasma content of fibrinogen and fibrin degradation products (FDP);

g) an increase in the content of antiheparin factor (factor 4) in plasma devoid of platelets;

h) in some cases, the persistence of positive paracoagulation tests (ethanol, protamine sulfate), which are usually noted in the early stages.

Hypocoagulation phase characterized severe blood coagulation disorder, which is reflected in all low- and high-sensitivity coagulation tests. It is necessary to determine antithrombin III, as well as plasminogen.

The table shows hemostasis indicators at various stages of DIC syndrome (according to E.P. Ivanov)

DIC syndrome - treatment.

The general scheme of treatment of DIC syndrome is presented in the figure. Heparin, antiplatelet agents (aspirin), rheopolyglucin are usually administered in the early stages of the syndrome. Reopolyglucin improves the rheological properties of blood, prevents platelet adhesion and aggregation. Aspirin acts in the same direction. Heparin stops the action of plasma clotting factors and prevents the conversion of fibrinogen to fibrin. When hypocoagulation phenomena increase, the most effective is the introduction of fresh frozen plasma, which eliminates the deficiency of coagulation factors - antithrombin III, fibrinogen, plasminogen. If the amount of antithrombin III is sufficient, fibrinolysis inhibitors e-aminocaproic acid, trasylol, and contrical can be administered.

There are recommendations for differentiated treatment of DIC depending on the clinical course (A.A. Martynov). Option I - dysfunction of the shock organs, moderate hemorrhages. Transfusion of fresh frozen plasma, administration of heparin and antiplatelet agents are indicated.

Option II - severe hemorrhagic syndrome. It is advisable to administer antiproteases in large doses, small doses of heparin, fresh frozen plasma and antiplatelet agents.

Option III - massive local thrombosis and/or thromboembolism. The administration of thrombolytic agents, intermittent administration of fresh frozen plasma and the administration of antiplatelet agents are necessary.

High effectiveness of treatment is achieved by early (!) connection of jet (!) transfusions of fresh frozen plasma (up to 800-1600 ml/day in 2-4 doses). The initial dose is 600-800 ml, then 300-400 ml every 3-6 hours. Such transfusions are indicated at all stages of DIC syndrome, because they compensate for the deficiency of all components of the coagulation and anticoagulation systems, including antithrombin III and proteins C and S (the decrease in the content of which in DIC syndrome is especially intense - several times faster than all procoagulants); allow the introduction into the bloodstream of a full set of natural antiproteases and factors that restore the antiaggregation activity of the blood and thromboresistance of the endothelium.

Before each transfusion of fresh frozen plasma, 5,000-10,000 units of heparin are administered intravenously in order to activate antithrombin III administered with the plasma. This also prevents plasma clotting by circulating thrombin.

In case of DIC syndrome of an infectious-toxic nature and the development of pulmonary distress syndrome, plasmacytopheresis is indicated, since leukocytes play a significant role in the pathogenesis of these forms. Some of them begin to produce tissue thromboplastin (mononuclear cells), while others begin to produce esterases that cause interstitial pulmonary edema (neutrophils).

Methods of plasma therapy and plasma exchange increase the effectiveness of treatment of DIC and the diseases that cause it, reduce mortality several times, which allows them to be considered one of the main methods of treating patients with this disorder of hemostasis.

With significant anemia and a decrease in hematocrit, it is necessary to carry out transfusions of fresh canned blood (daily or up to 3 days of storage), red blood cells. The requirement for transfusion of fresh hemopreparations is due to the fact that microclots form in canned blood for more than 3 days of storage, the entry of which into the blood only leads to potentiation of DIC syndrome. Hematocrit must be maintained at a level of at least 22%, hemoglobin - more than 80 g/l, red blood cells - 2.5 * 10¹² / l and above.

It should be remembered that acute DIC syndrome is easily complicated by pulmonary edema, therefore significant circulatory overloads of the cardiovascular system are very undesirable, and therefore, caution and strict accounting of the amount of blood transfused, as well as blood loss, loss of body fluid, and diuresis are necessary.

In stage III of DIC syndrome and with pronounced proteolysis in tissues (lung gangrene, necrotizing pancreatitis, acute liver dystrophy, etc.), plasmapheresis and jet transfusions of fresh frozen plasma (under the cover of small doses of heparin - 2,500 units per infusion) are combined with repeated intravenous administration large doses of contrical (up to 300,000-500,000 units or more) or other antiproteases.

ANEMIA

Anemia– clinical and hematological syndrome, characterized by a decrease in hemoglobin content per unit volume of blood, which leads to the development of oxygen starvation of tissues.

Classification of anemia. There are various classifications. Of greatest interest is pathogenetic classification, the basic principles of which were developed by M.P. Konchalovsky and further improved by I.A. Kassirsky (1970), L.I. Idelson (1979), P.A. Vorobyov (1994) :

I. Anemia due to blood loss (posthemorrhagic).

Acute posthemorrhagic anemia.

Chronic posthemorrhagic anemia.

II. Anemia due to impaired formation of red blood cells and hemoglobin.

Iron-deficiency anemia.

Iron redistribution anemia.

Iron-saturated (sideroachrestic) anemia associated with impaired heme synthesis.

Megaloblastic anemia associated with impaired DNA synthesis.

6.1. B12 and folate deficiency anemia.

Hypoproliferative anemia.

Anemia associated with bone marrow failure.

1. Hypoplastic (aplastic) anemia

   Refractory anemia in myelodysplastic syndrome.

Metaplastic anemia.

1. Anemia in hemoblastoses.

   Anemia due to cancer metastases to the bone marrow.

Dyserythropoietic anemia.

III . Anemia due to increased blood destruction (hemolytic).

Hereditary.

1. Associated with a violation of the structure of the erythrocyte membrane (microspherocytic anemia of Minkowski-Chaffard, ovalocytosis, acanthocytosis).

   Associated with enzyme deficiency in red blood cells

   Associated with impaired hemoglobin synthesis (sickle cell anemia, hemoglobinosis, thalassemia).

Purchased.

1. Autoimmune.

   Paroxysmal nocturnal hemoglobinuria.

   Medicinal

   Traumatic and microangiopathic

   Due to poisoning with hemolytic poisons and bacterial toxins.

IV. Mixed anemia.

Disseminated intravascular coagulation occurs with accelerated formation of blood clots in response to shock, massive trauma, severe infection, and obstetric pathology. It is characterized by bleeding due to the massive consumption of factors responsible for stopping it.

May be asymptomatic or lead to acute respiratory and renal failure. To make a diagnosis, you need to take into account the symptoms and conduct blood tests. Treatment involves the administration of anticoagulants, antiplatelet agents, transfusion of blood or its components, and plasmapheresis. Read more in this article.

📌 Read in this article

What is DIC syndrome?

Due to the influence of pathological factors, loose thrombotic masses, microthrombi, and accumulations of platelets are formed in small vessels. They disrupt blood circulation, microcirculation, lead to oxygen starvation, and dysfunction of internal organs. Most dystrophy and cell destruction affect the parenchyma of the kidneys, lungs, liver and adrenal glands. This is explained by the developed microcirculatory vascular network in them.

The danger of thrombohemorrhagic syndrome lies in the fact that the main supply of coagulation factors and blood platelets is usually spent on the formation of clots inside the vessels. Therefore, the risk of severe bleeding, which is very difficult to stop, increases. The development of DIC syndrome can be caused by various pathologies in which the fluidity of blood and its movement in the capillaries are disrupted.

According to clinical manifestations, the disease can have a latent, protracted course, and also manifest itself with lightning-fast reactions leading to death. Damage to internal organs can be local and minor, or widespread blood coagulation occurs in all small vessels with an extremely severe course.

Causes of occurrence in adults and children

DIC syndrome is provoked by conditions in which there is destruction of the inner layer of blood vessels, blood cells, and tissue damage. This causes activation of blood clotting, disruption of blood flow in small capillaries, venules and arterioles. The reasons for this condition may be:

• infections of a viral or bacterial nature, complicated by sepsis;
• state of shock;
• toxicosis of the second half of pregnancy (preeclampsia);
• previous placental abruption;
• fetal death;
• uterine atony with profuse bleeding;
• C-section;
• metastases in malignant neoplasms;
• amniotic fluid embolism;
• prolonged compression of the limbs;
• major trauma, burns or surgery, especially under artificial circulation;
• blood transfusion, organ transplantation;
• bleeding;
• or ;
• abortions, childbirth;
• long-term presence of the catheter in the vessel;
• intravascular destruction of red blood cells during poisoning with hemolytic poisons (lead, mercury, acetic acid, snake bite);
• leukemia;
• radiation sickness;
• intensive antitumor therapy.

Forms of manifestation

Based on the rate of increase in microcirculation disorders and their complications, DIC syndrome is divided into acute, subacute and chronic.

Spicy

Occurs in patients with massive intake of substances into the blood that increase the formation of blood clots. It happens in severe, critical conditions (polytrauma, difficult childbirth, surgery, tissue compression). A feature of this form is the rapid change of phases of the disease, the absence of protective reactions of the body that prevent massive coagulation.

Subacute

It takes weeks (up to 1 month) to develop. The course is more favorable than that of the acute form, the insufficiency of the function of internal organs is less pronounced or moderate, bleeding is weak or moderate. Diagnosed with tumors of the blood, lungs, kidneys, rejection of transplanted tissues, and the use of hormonal contraceptives.

If they are accompanied by blood loss, blood transfusion, administration of hemostatic agents, stress, then it can develop into an acute process.

Chronic

Lasts several months. Organ dysfunction develops slowly and is usually characterized by chewed lesions. It is caused by chronic inflammation of the lungs, liver, tumors, autoimmune diseases, leukemia, and widespread atherosclerosis. To identify clinical signs, as a rule, it is not enough. It is necessary to confirm DIC syndrome with laboratory diagnostics.

Classification

Several types of the disease are known. Clinical variants of the course may manifest themselves depending on:

• prevalence of damage - limited (one organ) and generalized (several systems or the whole body);
• degrees of compensation - compensated (there are no symptoms, blood clots are destroyed by activation of fibrinolysis, coagulation factors are synthesized or released from reserves), subcompensated (there are moderate bleedings), decompensated (a cascade of reactions of resorption of blood clots is triggered, coagulation is impaired, severe bleeding).

Stages of progression

The peculiarity of the disease is the sequential change of symptoms. In the classic version, DIC syndrome has the following stages of progression:

1. Increased blood clotting and cell connection. Caused by the release of thromboplastin from destroyed tissues or substances similar to it. They activate thrombus formation processes. Lasts from ten minutes to several months.
2. Coagulation disorder due to a lack of fibrinogen, platelets, coagulation factors, since they were intensively consumed in the first phase, and new ones have not yet been formed.
3. Critical phase of low clotting capacity. There is no fibrinogen in the blood, red blood cells are destroyed, and coagulation properties may be completely absent.
4. Recovery or development of complications. There are either residual signs of dystrophy and destruction, followed by recovery, or acute organ failure increases.

Symptoms of blood clotting pathology

Clinical manifestations of thrombohemorrhagic syndrome consist of signs of the underlying disease, of which it is a complication, and the symptom complex of DIC syndrome.

State of shock

Associated with blood clotting, stopping microcirculation, oxygen starvation of tissues. During the formation of blood clots and their destruction, many toxic compounds enter the bloodstream, leading to disruption of systemic circulation. Most often, it is difficult to determine which changes arose due to microthrombosis and which were its cause. Manifestations of shock include:

• a sharp drop in blood pressure and a decrease in central venous pressure;
• acute microcirculation disorders;
• low functional activity of internal organs.

Complications may include renal, hepatic, respiratory failure, or combinations thereof. DIC against the background of shock always has a severe course, and with a long period - catastrophic.

In the first phase, excessive blood clotting is obvious, it can even be visual when a blood clot forms even before the analysis, immediately after collecting the material. In the second phase, against the background of excessive coagulation, insufficient coagulation also appears. At this time, some tests show an increased, and others a sharply reduced, ability to form blood clots.

Hemorrhagic syndrome

Increased bleeding most often appears during the acute course of the disease. Excessive blood loss can occur against the background of normal or slightly reduced fibrinogen concentrations. Local bleeding can be both a manifestation of DIC syndrome and diseases of the organs themselves (stomach ulcer, kidney infarction, uterine atony). Common signs of hemorrhage are:

• hemorrhages in the skin, hematomas;
• nasal, pulmonary, renal blood loss;
• hemorrhage in brain tissue, adrenal glands, pericardial sac;
• permeation of plasma and red blood cells into the chest and abdominal cavity.

Acute renal failure

Urine production decreases to the point of its absence. Protein and red blood cells are found in the urine. The balance of salts, acids and alkalis in the blood is disturbed, urea, creatinine and residual nitrogen increase. Renal dysfunction is most severe when combined with liver or pulmonary failure.

Target organ damage

The progression of DIC syndrome leads to a generalized disorder - multiple organ failure. Its symptoms:

• destruction of liver cells with jaundice and pain in the right hypochondrium;
• erosions, ulcers and bleeding on the gastric mucosa;
• ulcerative defects in the intestines;
• stopping the movements of the intestinal wall, the penetration of toxins into the blood (weakening of intestinal motility or obstruction;
• -, headache, impaired consciousness, may be;
• pituitary and adrenal insufficiency - severe, diarrhea, dehydration.

Diagnosis of DIC syndrome

To make a diagnosis, the presence of bruises on the skin, bleeding from several organs and the following laboratory signs (based on a blood test) are taken into account:

• destroyed red blood cells;
• decrease in platelets and fibrinogen;
• increase in the level of fibrin destruction products;
• low activity of antithrombin 3;
• prolongation of thrombin time and activated thromboplastin time;
• clots do not form or disintegrate quickly.

In doubtful cases, determination of paracoagulation tests and soluble fibrin complexes is prescribed.

Treatment of the disease

If there are no clinical manifestations of DIC syndrome, then its laboratory signs are corrected by influencing the underlying condition. In the acute course of the disease, it is necessary to urgently eliminate the cause of its appearance, including surgically. For drug therapy the following is used:

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