The causes and dangers of DIC syndrome. DIC syndrome in newborns Treatment of DIC syndrome in infectious diseases

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Disseminated intravascular coagulation (DIC) (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 microclots of fibrin 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.

Second common reason occurrence of DIC syndrome (about 50% of all cases) - purulent-septic processes, bacteremia, septicemia. Among them, the most common forms are associated with abortions (especially criminal ones), infected burn surfaces and wounds, postoperative suppuration, staphylococcal destruction of organs, septicemia 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 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 poisoning, causing shock, hemolysis and intravascular coagulation, including poisoning with snake venoms containing blood coagulating enzymes - toxins of viper 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; at malignant neoplasms, especially with extensive metastasis; leukemia; during extracorporeal circulation, hemodialysis, hemosorption, as well as during implantation artificial valves hearts.

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 area, 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; it is also possible hemorrhagic penetration of the gastric mucosa and small intestine with heavy diapedetic bleeding. 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 can be short-term and can occur covertly, and therefore the first obvious clinical manifestations There may be hemorrhages, in most cases multiple, although bleeding from any one localization may dominate. Alternating bleeding is often observed different localization 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 they predominate uterine bleeding, at surgical interventions ah - hemorrhages in the area surgical field, with 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 oral cavity and language. 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, 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 conditions of providing specialized assistance patients at home (for example, thromboembolic and cardiac emergency teams medical care).

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. Samples may become negative in late stages DIC syndrome, when the level of fibrinogen in plasma decreases below. 0-100 mg%, which is observed in the terminal phase of DIC syndrome. The transition positive samples negative during treatment indicates sufficient effectiveness of antithromotic therapy.

Emergency care for DIC syndrome

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Urgent Care first of all, it should be aimed at eliminating the effect of the factor that caused the development of disseminated intravascular coagulation syndrome, and the fastest possible elimination of shock during its development. On 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).

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

Massive blood transfusions (5 liters or more) themselves cause severe disseminated intravascular coagulation and sharply aggravate the existing one, so maximum restraint in the use of canned blood is important, but at the same time fast recovery circulating blood volume and blood pressure level by administering colloid 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 antibiotics may be added as needed. wide range actions.

In the early stages of hospital treatment, optimal basic therapy demonstrate the complex use of repeated transfusions 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 prescribe large doses of Contrical or other antiproteases of the same group.Infusion therapy is continued according to the above rules, using alpha-2-blockers and antiplatelet agents.

For shock pulmonary and acute renal failure additionally, 2-6 ml of a 1% solution of Lasix (furosemide) is administered 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 one of the most common and most severe, life-threatening disorders of the hemostatic system (hemostasis is a complex of body reactions aimed at preventing and stopping bleeding).

Synonyms for DIC syndrome are thrombohemorrhagic syndrome, consumption coagulopathy, hypercoagulability syndrome, defibration syndrome.

DIC syndrome (disseminated intravascular coagulation syndrome) is:

secondary pathological process, which occurs with constant and prolonged stimulation of the hemostatic system;
a pathological process that has a phase course, with initial activation and subsequent deep, increasing depletion of all parts of the hemostatic system up to the complete loss of the ability of blood to clot with the development of catastrophic uncontrolled bleeding and severe generalized hemorrhagic syndrome;
a pathological process in which progressive diffuse intravascular coagulation is noted with multiple and widespread formation of blood microclots and aggregates of its formed elements, which worsens its rheological characteristics, blocks microcirculation in tissues and organs, causes ischemic damage in them and leads to multiple organ lesions.

Kinds

Depending on the intensity of formation and entry into the blood of thromboplastin, which is formed during the destruction of cells, including blood cells, DIC syndrome has various clinical forms:

lightning;
spicy;
subacute;
protracted;
chronic;
latent;
local;
generalized;
compensated;
decompensated.

Causes

The triggering factors for DIC syndrome can be a wide variety of intense or prolonged stimuli, one way or another fitting into Virchow's triad - disturbances of blood circulation, its properties or the vascular wall.

DIC syndrome occurs:

1. In case of violation of the rheological characteristics of blood and hemodynamics

any kind of shock
blood loss,
intoxication,
sepsis,
Rhesus conflict pregnancy,
circulatory arrest and subsequent resuscitation,
uterine atony,
uterine massage

2. When blood comes into contact with damaged cells and tissues

antenatal fetal death,
oncological diseases

3. When the properties of the blood change and when thromboplastic substances enter the blood massively

leukemia,
amniotic fluid embolism,
transfusion of incompatible blood,
septic abortion,
abruption of a normally located placenta with hemorrhage into the uterus,
placenta accreta,
operations on parenchymal organs: uterus, liver, lungs, prostate, kidneys;
acute radiation sickness,
long-term compartment syndrome,
gangrene,
organ transplantation, chemotherapy, pancreatic necrosis, myocardial infarction, etc.).

Symptoms of DIC syndrome

During DIC syndrome there are 4 stages:

Stage 1 - phase of hypercoagulation and platelet hyperaggregation;

Stage 2 - transitional phase (multidirectional shifts in blood clotting both towards hyper- and hypocoagulation);

Stage 3 - deep hypocoagulation phase (blood does not clot at all);

Stage 4 - the resolving phase (either hemostasis parameters are normalized, or complications develop that lead to death).

The symptoms of disseminated intravascular coagulation syndrome depend on many factors (the cause that caused it, the clinical picture of shock, disorders of all parts of hemostasis, thrombosis, reduced volume of the vascular bed, bleeding, anemia, dysfunction and dystrophy of target organs, metabolic disorders).

In the first phase, there is increased blood clotting, immediate formation of clots in large vessels and blood clots in small ones (during surgery). It is impossible to take blood from a patient for analysis, as it immediately clots. As a rule, the first phase proceeds very quickly and goes unnoticed by doctors. There has been a sharp decline blood pressure, skin pale, covered with cold sticky sweat, pulse weak (thready). Then develops respiratory failure due to lung damage, moist cough and crepitus in the lungs, cyanosis of the skin, cold feet and hands.

In the second phase, the same symptoms persist as in the first ICE stage-syndrome, plus the process involves the kidneys (renal failure), adrenal glands, digestive tract(nausea, vomiting, abdominal pain, diarrhea). Microthrombi form in the brain (headache, dizziness, convulsions, loss of consciousness up to coma, paresis and paralysis, strokes).

The third phase (hypocoagulation stage) is characterized by massive bleeding, both from the initial focus and from other organs (intestinal and stomach bleeding due to ulceration of the mucous membrane, blood in the urine - kidney damage, sputum mixed with blood when coughing).

The development of hemorrhagic syndrome is also characteristic (the appearance of massive hemorrhages, hematomas, petechiae, unstoppable bleeding at injection sites and during surgery, bleeding gums, nosebleeds, etc.).

The fourth phase, with timely and adequate treatment, leads to the restoration of hemostasis and stopping bleeding, but often ends in death with massive damage to internal organs and bleeding.

Diagnostics

Basic laboratory tests:

determination of platelets (with DIC syndrome there is a decrease in platelets in phases 2, 3 and 4);
blood clotting time (the norm is 5 - 9 minutes, in the 1st stage the indicator is shortened, in subsequent stages the time is lengthened);
bleeding time (normal 1 - 3 minutes);
APTT (activated partial thromboplastic time - increase in phases 2 and 3 of DIC syndrome);
prothrombin time, thrombin time, determination of activated plasma recalcification time - AVR (increase in the second and third stages of DIC syndrome);
clot lysis (normally not, in phase 3 lysis is rapid, and in phase 4 a clot does not form);
fibrinogen (normal 2 - 4 g/l, decreases in stages 2, 3 and 4);
study of the phenomenon of fragmentation of erythrocytes due to damage to them by fibrin threads (normally the test is negative, positive test indicates DIC syndrome);
decreased red blood cells (anemia, decreased blood volume);
decreased hematocrit (hypovolemia);
determination of acid-base and electrolyte balance.

Treatment of DIC syndrome

Therapy for DIC syndrome is carried out by a doctor who has encountered this pathology (that is, the attending physician) together with a resuscitator. In the chronic course of DIC syndrome, its treatment is carried out by a therapist and a hematologist.

First of all, it is necessary to eliminate the cause of DIC syndrome. For example, in case of sepsis, antibacterial and transfusion therapy is prescribed ( intravenous infusion blood products) therapy, for traumatic shock - adequate pain relief, immobilization, oxygenation and early surgical intervention. Or for tumor diseases - chemotherapy and radiotherapy, for myocardial infarction - pain relief, restoration of heart rhythm and hemodynamics, for obstetric and gynecological pathology radical measures (hysterectomy, caesarean section).

Restoration of hemodynamics and rheological properties blood is carried out by infusion-transfusion infusions.

An infusion of fresh frozen plasma is indicated, which not only restores the volume of circulating blood, but also contains all coagulation factors.

Crystalloid (saline, glucose) and colloid solutions (polyglucin, rheopolyglucin) in a 4/1 ratio and protein blood products (albumin, protein) are also administered.

An anticoagulant is prescribed direct action- heparin. The dose of heparin depends on the stage of DIC syndrome (in phases 1 - 2 it is significant). In case of significant anemia, fresh (no more than 3 days) red blood cells are transfused.

In the treatment of severe generalized DIC, fibrinogen and blood clotting factor concentrates (cryoprecipetate) are used. Proteolysis inhibitors - antiproteases - are used to suppress tissue proteases that are released when cells are damaged (contrical, trasylol, gordox). Corticosteroids (hydrocortisone, dexamethasone) are also prescribed, as they increase blood clotting.

In parallel, the fight against multiple organ failure is being carried out (supporting the functions of the lungs, kidneys, gastrointestinal tract, adrenal glands). In phases 2 - 4 of DIC, a mixture of aminocaproic acid, dry thrombin, sodium ethamsylate and adroxon is used to restore local hemostasis. This mixture is introduced into abdominal cavity through drainages, orally, in the form of tampons into the uterine and vaginal cavity, and wipes moistened with the solution are applied to the wound.

The entire process of intensive therapy takes 1 - 5 days (depending on the severity of DIC syndrome), and subsequent treatment continues until complete or almost complete full recovery all multiple organ disorders.

Complications and prognosis

The main complications of DIC include:

hemocoagulation shock (critical drop in blood pressure, disorders of the respiratory and cardiac systems, etc.);
posthemorrhagic anemia;
death.

The prognosis depends on the severity, course and stage of DIC syndrome. In stages 1 and 2 the prognosis is favorable, in stage 3 it is doubtful, in stage 4 (with inadequate or absent treatment) it is lethal.

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);
spicy 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:

Measurement of antithrombin III (normal 71–115%) – its level is decreasing.
Paracoagulation protamine test. Allows you to determine fibrin monomers in blood plasma. In DIC syndrome it becomes positive.
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.
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.

At severe course DIC syndrome is indicated intravenous administration antithrombin III, which inactivates plasmin, thrombin and other coagulation enzymes.

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. Actively carried out intensive therapy allows reducing the mortality rate to 20%.

DIC syndrome is a severe pathological blood disease. The mechanisms of disease development are as follows:

stimulation of platelet function;
stimulation of coagulative properties

As a result of this process, the following changes occur:

increased thrombin synthesis;
blood clot synthesis

Small clots form and interfere with blood circulation. Thrombocytopenia is a pathology that occurs due to a decrease in coagulation factors.

In addition to thrombocytopenia, the following symptoms occur:

the phenomenon of fibrinolysis;
severe hemorrhagic syndrome

Pathological severe condition that requires emergency intervention– DIC – syndrome. Mortality rate is up to sixty-five percent.

Etiology of DIC syndrome

This pathology is a consequence of other diseases. The etiology of the disease is as follows:

infections;
purulent diseases;
artificial termination of pregnancy;
catheterization process;
injuries to the walls of blood vessels;
mechanical damage to organs;
consequence of surgery;
phenomenon of vascular prosthetics

Additional causes of the disease:

state of shock;
gynecological diseases;
pathology of pregnancy;
tumor;
malignant neoplasms;
the phenomenon of hemolysis;
acute course of hemolysis;
autoimmune pathologies;
medicines;
drugs;
toxic pathologies

Shock conditions include:

anaphylactic shock;
septic shock;
cardiogenic shock;
traumatic shock;
hemorrhagic shock

TO gynecological diseases include:

amniotic fluid embolism;
process of separation of the placenta;
placenta previa;
placental abruption;
operative delivery

Malignant neoplasms of the following types:

pulmonary system;
prostate pathology

Immune pathologies of the following nature:

hemorrhagic vasculitis;
glomerulonephritis;
systemic lupus

A common cause of this disease is generalized septicemia.

DIC - syndrome - symptoms

The clinic indicator is the main cause of the disease. The main way the disease arises is through shock situations. Symptoms of the disease in chronic stage the following:

minor bleeding;
hypovolemia;
dystrophy;
metabolic disorders

Symptoms of DIC syndrome in the acute stage are as follows:

phenomenon of increased coagulation;
decreased coagulation;
bleeding is intense;
cardiogenic shock

The provision of medical care influences the manifestation of this disease. Selected necessary treatment. This disease progresses in the following cases:

injuries;
lack of relief of hypovolemia;
insufficient blood transfusion

DIC is a syndrome that can be variable in nature. In this case, this process is facilitated by:

pancreas pathology;

Signs of hemocoagulative shock are as follows:

impaired blood flow;
oxygen starvation;
kidney failure;
liver failure

Death occurs in most percent of cases. The therapeutic effect is difficult to achieve. A severe condition occurs in patients in the following cases:

diagnosis of the disease is untimely;
untimely treatment with medications

Bleeding in this disease is profuse. The provocateur of hemorrhagic shock of a generalized type is a pathology of the hemostatic system. The intensity of bleeding varies, with gynecological diseases uterine bleeding develops.

Treatment for the disease is as follows:

hemostatic therapy;
restoration of uterine tone;
therapy for stomach ulcers

Signs of generalized hemorrhagic syndrome are:

skin bruising;
hemorrhages;
cough;
sputum;
nosebleeds;
sweating blood

Hemorrhages occur in the following areas:

pulmonary system;
brain;
spinal cord;
adrenal region;
uterus

Sweating of blood affects the following system organs:

pericardial system;
abdomen;
pleural cavity

Acute posthemorrhagic shock occurs with intense bleeding. In this case, emergency treatment is necessary. DIC, a chronic syndrome, is characterized as follows:

presence of bleeding;
permanent anemia;

For anemia, transfusion must be used. A mass transfusion of red blood cells is performed. As a result of disruption of the blood circulation process, organ function is affected. If the respiratory function is impaired, DIC syndrome is severe.

Signs of this condition are:

breathing problems;
sputum;
acrocyanosis

Pulmonary edema is aggravated by transfusion of solutions. These solutions include:

sodium;
albumen

At in a state of shock pulmonary system requires the following therapy:

mechanical ventilation event;
diuretics

The kidney system is also affected in this disease. In this case, the following symptoms arise:

accumulation of proteins in the urine;
accumulation of red blood cells in the urine;
impaired urination

With liver pathology, the following symptoms occur:

kidney failure;
liver failure;
abdominal pain;
icteric syndrome

When treated with hormones, the following symptoms occur:

hemorrhages;
bleeding;
intoxication

Intoxication is a consequence of functional intestinal disorders. Signs of impaired blood circulation in the brain:

headache;
signs of meningitis;
dizziness;
impaired consciousness

Signs of septic lesions are as follows:

platelet formation;
electrolyte disturbances;
dehydration process;
adrenal insufficiency

DIC – syndrome – stages

There are signs for each stage. The initial stage is the hypercoagulative stage. Signs of the hypercoagulable stage:

intravascular aggregation;
various blood clots;
fatal outcome

The second stage of DIC syndrome is a stage accompanied by a decrease in platelets. Their aggregation is increased. Signs of this stage:

phagocytosis;
microclot lysis process

The third stage of the disease is the fibrinolytic stage. Signs of the third stage of the disease:

restoration of blood circulation;
damage to clotting factors

The fourth stage of DIC syndrome is the recovery stage. The signs of this stage are as follows:

necrosis;
dystrophy;
restoration of tissue function

Multiple organ failure is a consequence of the lack of proper treatment. The use of medications is the basis of treatment.

In pregnant women, DIC syndrome

The process of impaired hemostasis occurs during pregnancy. Gynecological pathologies are important. Causes of death as a result of this disease:

bleeding is intense;
development of blood clots

Periods of development of DIC syndrome:

stage of pregnancy;
period after childbirth;
newborn period

Forms of development of this disease:

lightning stage of damage;
death;
sluggish defeat;

Signs of chronic disease:

pregnancy status;
cardiac pathology;
urinary system disorder

Acute blood loss is a provoking factor of DIC syndrome. The cause is intense uterine bleeding.

Possible etiological signs of the disease:

infections;
inflammatory phenomena;
embolism;
placental abruption;
inflammation of the endometrium;
purulent lesion

The duration of the hypercoagulable stage is up to three days. Signs of this stage:

redness of the skin;
cardiopalmus

Signs of the hypocoagulable stage of the disease:

uterine bleeding;
nose bleed;
presence of hemorrhages;
presence of rashes;

There are various sources of bleeding. Diagnosis of the disease in pregnant women:

use of coagulogram;
laboratory methods

Therapeutic therapy includes:

drug treatment;
non-pharmacological means

Hospitalization of a pregnant woman is necessary. A pregnant woman is hospitalized in a hospital.

The child has DIC syndrome

The risk group is children, especially the neonatal period. Children may have the following symptoms:

infections inside the womb;
viruses;
low body temperature;
oxygen starvation;
signs of acidosis

The cause of the disease in children is cardiac shock. Processes influencing DIC syndrome:

thrombin synthesis;
vascular damage;
increased coagulation;
blood clot formation;
oxygen starvation;
reduction of coagulation factors;
decrease in platelets;
impaired hemostasis process

The clinic is a reflection of the stage of the disease. The underlying disease matters. Possible signs diseases:

acrocyanosis;
increased breathing;
decreased blood pressure;
urinary disturbance;
liver enlargement;
spleen enlargement

In the coagulopathic phase, the skin turns blue. The development of hemorrhagic shock is possible. Bleeding in the brain is a dangerous consequence of this condition.

Mortality is increasing. With assistance, the outcome of the disease is favorable. The recovery phase occurs with proper treatment. The main focus of therapy in children is to exclude the underlying cause.

Blood transfusions are used. To do this, use the following means:

plasma solution;
pentoxifylline solution;
drug dopamine

Treatment of the coagulopathy phase in a child:

replacement transfusion;
platelet transfusion;
heparin

Heparin is administered under the control of a coagulogram. Treatment during the recovery period is symptomatic. Thrombolytic agents are used in this case.

Diagnosis of DIC syndrome

Distinguish the following diseases with impaired hemostasis:

sepsis;
burn;
bites

Diagnosis is complicated in the following pathologies:

leukemia signs;
lupus erythematosus;

Testing is used in this case. Methods for diagnosing this disease:

lab tests;
instrumental method;
blood clot analysis;
calculation of prothrombin time;
paracoagulation tests

For rational treatment, the following diagnostic methods are used:

antithrombin assay;
plasma research;
sensitivity determination

Basic diagnostics of the following type:

determine hematocrit;
level of hypoxemia;
electrolyte level;
biochemistry

Chronic DIC syndrome is diagnosed at the terminal stage. The signs of chronic DIC syndrome are as follows:

oncological diseases;
cardiac congestion;
myeloproliferative diseases

Signs of myeloproliferative diseases:

increased blood viscosity;
increased hematocrit;
infiltrative foci

A severe degree of DIC syndrome occurs during chronic hemodialysis.

Treatment of DIC syndrome

DIC is a syndrome treated by rheumatologists. The therapy room is intensive. The mortality rate is up to thirty percent. The basis of therapy for this disease is the exclusion of provoking factors.

Therapy for this disease is antibacterial, since it is possible purulent processes. Sensitivity to drugs is determined. There are indications for the use of antibacterial agents:

criminal abortions;
discharge of amniotic fluid;
intoxication

Intoxication symptoms are as follows:

hectic fever;
meningitis;
lung damage

The following means are also used:

intravenous infusions;
antiprotease agents

The effect of these drugs is as follows:

reduction of intoxication;
reduction of the destructive process

To reduce states of shock, it is necessary antishock therapy. Drugs used to reduce shock conditions:

drug reopolyglucin;
glucocorticosteroids

Medicines to improve blood circulation:

adrenoblockers;
phentolamine;
drug trental

Heparin is used only in the presence of laboratory control. A large dosage of heparin is used in combination with antiproteases. Heparin is not used for heavy bleeding.

Indications for discontinuation of heparin:

collapse;
decreased blood pressure;
thrombocytopenic syndrome

The effect of using transfusions:

stopping the destruction process;
coagulation correction;
increasing protective properties

Drugs used in the treatment of the hypercoagulable phase:

saline solution;
albumins

Transfusion is also performed. Indications for red blood cell transfusion:

heavy bleeding

Plasmapheresis is used for chronic disease. Consequences of plasmapheresis:

protein removal;
clotting factor is activated

Complex treatment with the following drugs is effective:

dipyridamole;
trental

Indication for surgical methods treatment - the presence of a source of bleeding. Methods of surgical treatment:

gastrofibroscope method;
hemostatic agents

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 various diseases, 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. Primary signs capable of performing.

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.
Stage of thrombocytopathy and coagulopathy. Petechiae form on the surface of the skin, the surface of the mucous membranes becomes pale. In the field of injections medicines bleeding develops. Vital organs - lungs, kidneys, brain - are involved in the pathological process. Internal hemorrhages cannot be ruled out.
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 laboratory research 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 integrated approach. There are several basic principles.

Therapy for the acute form of DIC syndrome begins immediately after the collection of biomaterial for research.
Measures to eliminate possible provoking factors should be carried out as soon as possible.
During treatment, the doctor constantly evaluates the current clinical picture and takes into account the possible negative impact of measures taken that can cause increased 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.

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.
Hemocoagulative shock. One of the most severe complications of the pathology. Has a bad prognosis.
Hemorrhagic syndrome. Characterized by hemorrhages, different types bleeding.
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 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, it may be necessary to perform an urgent delivery or remove the uterus, in case 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.