DIC in adults

DIC syndrome (disseminated intravascular coagulation syndrome) is a consumption coagulopathy that develops with the participation of the antigen-antibody reaction and is accompanied by thrombus formation in capillaries and small vessels with depletion and disruption of the formation of all factors.

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Causes DIC in adults

DIC syndrome can develop in many diseases; in this case, endotoxins, amniotic fluid, stroma or hemolysate of erythrocytes, catecholamines, developing hypovolemia, decreased blood flow, hypoxia, etc. can be responsible for the initiation of the process. In addition to hemorrhages, DIC syndrome can manifest itself as vascular hypotension and multiple organ failure.

DIC syndrome complicates many pathological conditions: all forms of shock, diseases accompanied by the development of intoxication syndrome (primarily due to damage to the liver, which produces almost all blood clotting factors), blood thickening, slowing of blood flow, with massive transfusion of protein preparations, especially blood and its components. All these conditions have in their pathogenesis factors of hematopoiesis disorders, blood thickening, activation of the reticuloendothelial and immune systems. At the same time, with the participation of the antigen-antibody reaction, thrombus formation occurs in the capillaries and small vessels. A very large number of blood clotting factors are consumed in the process, which are not produced by the liver, especially with its functional insufficiency. Therefore, in large vessels, on the contrary, hypocoagulation and a tendency to bleeding due to afibrinogenemia are observed, since it is fibrinogen that suffers to a greater extent and serves as a differential criterion in the laboratory diagnosis of DIC syndrome according to the coagulogram. The total amount of fibrinogen decreases (other factors, including prothrombin, also decrease), an increase in partial thrombin time, thrombin time, prothrombin time, and fibrinogen decay products is observed.

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Pathogenesis

The preservation of the aggregate state of blood is ensured by 3 functionally different systems that make up the biological blood coagulation system:

1. coagulating - forming a thrombus;
2. anticoagulant (anticoagulant) - preventing the formation of a blood clot;
3. fibrinolytic - dissolving an already formed thrombus.

All these factors are in a state of dynamic equilibrium.

There are two main mechanisms of hemocoagulation: primary, vascular-platelet (VPH), and secondary, enzymatic-coagulation (ECG) hemostasis.

STH is carried out at the level of microcirculation and plays an important role in the hemostasis system. Its main stages are:

• adhesion (sticking to damaged vascular endothelium) of platelets;
• platelet aggregation (sticking together);
• release of biologically active substances (BAS; mainly serotonin and thromboxane), which cause the formation of a primary hemostatic thrombus.

Activation of STH is promoted by vasoconstriction, acidosis, slowing of blood flow, increased blood viscosity, catecholamines, thrombin, ADP, etc., and it is inhibited by fibrinogen breakdown products, salicylic acid, butadion, curantyl, papaverine, euphyllin, low molecular weight dextrans.

FCG is carried out mainly in veins and arteries through the interaction of plasma (denoted by Roman numerals) and platelet (denoted by Arabic numerals) blood coagulation factors.

The blood clotting process includes 3 phases: formation of thromboplastin, thrombin and fibrin. The blood clotting process begins with damage to the vascular endothelium, vasoconstriction, activation of the Hageman factor. Stimulation of STH, formation of a primary hemostatic thrombus and formation of tissue thromboplastin (phase 1, lasts 5-8 minutes) occur. The other two phases occur quickly (in a few seconds). Thrombin, formed at the end of phase 2, converts fibrinogen into fibrin. Approximately 20 minutes after the formation of a loose fibrin clot, its retraction (compaction) begins, which is completely completed in 2.5-3 hours.

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Anticoagulant system

Primary anticoagulants include AT III, heparin, proteins C and B. AT III provides 80% of the anticoagulant activity of blood plasma. The second most important is heparin (formed in mast cells of the liver, vascular endothelium, RES cells), which, by activating AT III, blocks thrombin formation, disrupts the synthesis of blood thromboplastin, simultaneously prevents the release of serotonin from platelets, and inhibits the conversion of fibrinogen into fibrin. In small doses, it activates fibrinolysis, and in large doses, it inhibits it. The low-molecular fraction of heparin is the most active. Proteins C and B are also synthesized in the liver with the participation of vitamin K, are inhibitors of f. V and VIII, and, along with AT III, prevent thrombin formation.

Secondary anticoagulants are formed during the blood coagulation process. These properties are possessed by fibrin degradation products (FDP; they activate fibrinolysis), AT I, metafactor V, etc.

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Fibrinolytic system

Fibrinolysin (plasmin) is an active proteolytic enzyme that lyses organized fibrin and fibrinogen. It is formed from profibrinolysin (plasminogen) under the action of cellular and plasma activators. Fibrinolysis inhibitors include antiplasmin, antitrypsin I, a2-macroglobulin, as well as thrombocytes, albumin, pleural exudate, and sperm.

The anticoagulant and fibrinolytic hemostatic systems are rapidly depleted in DIC syndrome.

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Symptoms DIC in adults

DIC syndrome is caused by a sharp decrease in functionally active capillaries in all organs and tissues due to erythrocyte stasis, with the development of hypoxic syndrome of the hemic type and the formation of decompensated metabolic acidosis. Capillary blood flow in the lungs suffers to a greater extent with the development of respiratory distress syndrome and kidneys with the development of Gasser syndrome (hemolytic uremic). In these organs, arteriovenous shunts open, which disrupts gas exchange to a greater extent, and cortical necrosis develops in the kidneys. Even with timely treatment in intensive care, the mortality rate is more than 60%.

The symptoms of DIC syndrome are caused by the aggregation of formed elements of the blood, its coagulation, thrombosis of the blood and lymphatic bed, as well as the resulting ischemic and congestive phenomena. The greatest danger is generalized diffuse thrombosis at the level of the terminal microcirculatory link, which ensures transcapillary exchange: oxygenation, entry and removal of metabolic products. Blockade of organ microcirculation in cases of maximum severity is manifested by ARF, ARF, ARF, cerebral insufficiency (coma), catabolic syndrome. Bleeding into the adrenal glands in children leads to acute adrenal insufficiency with clinical symptoms of intractable collapse.

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Stages

There are 4 stages of DIC syndrome:

• I - hypercoagulation;
• II - consumption coagulopathy, in which the consumption of platelets and coagulation material in thrombi progresses, and fibrinolysis is activated;
• III - severe hypocoagulation, active fibrinolysis, afibrinogenemia;
• IV - recovery or phase of residual thrombosis and blockades.

The course of DIC syndrome can be acute, subacute and chronic; some also distinguish a fulminant form.

At stage I, the initial stage, centralization of blood circulation is observed. The skin is hyperemic or pale, cyanosis of the nails and mucous membranes is noted. At stage II, the skin becomes pale, cold, with a marbled pattern. Purpura appears. In girls, menses appears prematurely.

In stage III, the above changes become most pronounced. The skin becomes more marbling, cold, pale cyanotic, with hypostases. Purpura and bleeding from the intestines, nose, and other organs dominate. Arterial hypotension, hypothermia, anuria, and metabolic acidosis are observed. The appearance of symptoms such as "bloody tears" and "bloody sweat" in patients is considered a bad prognostic sign.

In stage IV, with effective treatment, purpura gradually subsides. Defense mechanisms provide recanalization, melting of thrombi, elimination of fibrin. The leading ones in stage IV are asthenic syndrome, vegetative-vascular dystonia, dystrophy with a decrease in MT, polyhypovitaminosis, as well as functional changes in various "shock" organs - kidneys, liver, brain, etc., maximally damaged by thrombosis, dystrophy, fatty infiltration.

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Forms

Lightning and acute forms of DIC syndrome are observed in sepsis, extensive injuries, burns accompanied by shock. The clinical picture of increasing toxicosis, cerebral and pulmonary edema, acute cardiac, cardiopulmonary, renal, hepatorenal failure prevails. The process is always accompanied by increasing tissue bleeding, profuse bleeding. Subacute and chronic thrombus formation usually occurs with a predominance of stages I and II of DIC syndrome, often detected only by laboratory diagnostic methods. The possibility of hypercoagulation and the presence of real conditions for thrombus formation can be indirectly indicated by erythrocytosis of more than 5 million in 1 μl, hemoglobin level over 160 g/l, sharply accelerated ESR, high hematocrit values, the presence of hyperfibrinogenemia, significant changes in acid-base balance.

Diagnostics DIC in adults

Laboratory diagnosis of advanced manifestations of DIC syndrome should be based on several positive tests:

1. thrombocytogenemia + prolonged blood clotting time (BCT) + positive coagulation test (PCT) + hypofibrinogenemia + AT III deficiency;
2. thrombocytopenia + prolongation of activated partial thromboplastin time (APTT) + prolongation of thrombin test + decrease in AT III level + increase in fibrin degradation products (FDP) level. The absence of hypofibrinogenemia and decrease in the concentration of other blood coagulation factors does not exclude DIC.

Depending on the stage of DIC syndrome, laboratory tests vary as follows:

• Stage I: shortening of bleeding time, ICS, APTT + hyperfibrinogenemia + hyperthrombocytosis + spontaneous platelet aggregation + increase in FDP + positive PCT.
• Stage II: thrombocytopenia + decreased platelet aggregation and PTI + prolongation of thrombin test + further increase in PDF + pronounced PCT + normal fibrinogen + decreased levels of AT III and protein C.
• Stage III: sharp prolongation of the blood clotting time + hypo- or afibrinogenemia + profound thrombocytopenia + decrease in all blood clotting factors + AT III deficiency + negative PCT.

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Treatment DIC in adults

Treatment of DIC syndrome is usually carried out in the intensive care unit and is aimed at removing existing blood clots, preventing new ones, and restoring blood circulation and hemostasis.

Active antibacterial and other etiotropic therapy. It should be taken into account that some antibiotics (ristomycin, aminoglycosides) enhance platelet aggregation, while others (ampicillin, carbenicillin, cephalosporins) weaken it.

Rapid removal of patients from a state of shock, elimination of other circulatory disorders, hypovolemia, correction of metabolic and electrolyte disturbances by IT.

Prescription of antiplatelet, anticoagulant, fibrinolytic and replacement therapy.

In stage I of DIC, heparin has therapeutic value. It is administered in a daily dose of 100-300 U/kg (4-6 injections or evenly by drip at a rate of 15-20 U/kg per hour); intradermal administration is possible. Since medium-molecular heparin does not inhibit platelet-vascular hemostasis, inhibiting mainly thrombogenesis, in case of damage to the vascular wall (septic shock), it is better to use low-molecular forms - fraxiparin (0.1-0.3 ml 1-2 times a day), calciparin, etc.

It is advisable to use antiplatelet agents (curantil, trental, euphyllin), weak fibrinolytics (nicotinic acid, complamine) and agents that improve blood rheology (rheopolyglucin), restoring the BCC (albumin). In recent years, the disaggregation activity of small doses of acetylsalicylic acid (1-3 mg / kg once a day) has been established. Thrombolytics (streptase, cabikinase, etc.) are used extremely rarely in pediatric practice, although with strictly controlled thrombogenic blockade of blood vessels using laboratory and instrumental methods, their administration is justified in the first 4 hours from the moment of thrombosis and ischemia.

In stage II of DIC syndrome, dynamic monitoring of the coagulogram is necessary (the coagulation rate should be within 10-20 min). Deficiency of plasma coagulation factors and AT III can be eliminated by transfusion of its concentrate, FFP, cryoprecipitate. In order to reduce the activity of STH, dicynone, doxium, disaggregants (curantil, angina, parmidine) are used. The greatest difficulties arise in stage III of DIC syndrome. First, FFP is administered in large doses (30 ml / kg per day or more). It is useful to divide cryoprecipitate, then transfuse a glucose solution with vitamins, a soda solution. In recent years, OPD is often carried out in a volume of up to III OCP with a repeat procedure after 12-24 hours. When performing (LDZ in young children, it is possible to use plasma from one donor.

Red blood cell mass is prescribed for replacement purposes at hemoglobin levels < 80 g/l, erythrocytes - < 2.5- 10 ¹² /l. Platelet suspension is used if their level in the blood becomes less than 30 109/l (2-6 doses per day by drip). Administration of GCS is indicated (10-30 mg/kg per day in terms of prednisolone, fractionally or by pulse therapy - metipred).

As a rule, such patients are immediately transferred to artificial ventilation. It is advisable to use proteolysis inhibitors (contrycal - 500-1000 ATE/kg, pantrypin - 5000-10,000 ATE/kg, trasylol, gordox - 10,000-20,000 ATE/kg) intravenously by drip 2-3 times a day or continuously.

ACC is used only locally (internally, intrapleurally). For local hemostasis, dressings with thrombin, dicynone, androxon, doxium, as well as fibrin film, hemostatic sponge are used.

In stage IV of DIC syndrome, angioprotectors are added to antiplatelet agents to restore microcirculation - stugeron, prodectin, and also complamin (theonikol). Nootropil series drugs (aminalon, piracetam), etc. are used.

Thus, treatment of DIC syndrome is usually actively carried out only in the case of its obvious clinical manifestations (bleeding and thrombogenic organ failure); in other cases, attention should be paid to treating the underlying disease, improving the ventilation function of the lungs and the state of central and peripheral hemodynamics.