DIC in children

DIC syndrome is one of the most common causes of hemorrhagic syndrome and bleeding and is observed in 8-15% of sick newborns.

In the development of various pathological conditions, DIC syndrome plays a significant role. This non-specific general biological reaction of the body occurs in response to the penetration of thromboplastic substances into the bloodstream that activate hemostasis; it is accompanied by sharp disturbances in the microcirculatory bed. Bleeding in DIC syndrome is characterized by a persistent nature.

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Causes DIC in a child

The reasons for the development of DIC syndrome in children are the following:

• severe viral and bacterial (especially those caused by gram-negative and mixed microflora) infections;
• hypothermia;
• hypoxia/asphyxia;
• acidosis;
• shock, acute hypotension;
• trauma and destructive organ damage (severe hemolysis, leukolysis, massive trauma, burns, destruction of parenchymal organs, necrosis).

In the vast majority of cases, the initiating mechanism of DIC syndrome in newborns is cardiovascular collapse or shock, followed by activation and damage to the vascular endothelium, which leads to increased vascular expression, the release of tissue factor into the blood, increased amounts of interleukins 1, 6 and 8, platelet activating factor and tumor necrosis factor.

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Pathogenesis

Excessive activation of the blood coagulation system caused by etiologic factors leads to the formation of widespread thrombi of small vessels and, as a consequence, to the development of microcirculatory blockade of parenchymatous organs, their ischemia, depletion of reserves of plasma coagulation factors and platelets. Excessive activation of coagulation induces fibrinolysis, aggravating bleeding. With depletion of coagulation factors, platelet deficiency and development of secondary depression of fibrinolysis, profuse bleeding and complete blood coagulability may occur. Thus, the following links in the pathogenesis of DIC syndrome in children can be identified:

• "proteolytic burst" - excessive formation of thrombin and plasmin in the blood, vasoactive effect of kinins;
• systemic endothelial damage (acidosis, endotoxicosis, exotoxicosis, etc.);
• hypercoagulation associated with activation of both intrinsic and extrinsic coagulation pathways;
• blockade of microcirculation in the early stages of DIC due to the formation of soluble fibrin-fibrinogen complexes and the development of fibrin microthrombi and then rheological occlusion of capillaries (increased blood viscosity, sludge, clots);
• hypoxia and destruction of cells with dysfunction of the central nervous system, kidneys, lungs, liver, heart - multiple organ failure;
• coagulopathy and thrombocytopenia of consumption with depletion of blood levels of both procoagulants (factors I, II, V, VIII, XIII, von Willebrand) and natural anticoagulants - inhibitors of active serine proteases (antithrombin III, proteins C, B, etc.);
• pathological fibrinolysis with a significant increase in FDP, degradation of fibrinogen, proteolysis of factors V, VIII, XII, XI, XIII, von Willebrand, changes in platelet membrane glycoproteins, which disrupts both primary and secondary hemostasis, leading to the simultaneous development of thrombosis and increased bleeding. The predisposition of newborns to the development of DIC syndrome is explained by the low ability of the reticuloendothelial system to remove intermediate blood coagulation products; the inability of the liver, when necessary, to adequately increase the synthesis of procoagulants and anticoagulants; difficulty maintaining adequate perfusion in small vessels; vulnerability and easy damage of most triggers leading to DIC syndrome.

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Symptoms DIC in a child

Clinically, three phases of DIC syndrome development in children are distinguished.

1. The first is the hypercoagulation phase. The clinical picture is dominated by the symptoms of the underlying disease, with the addition of signs of microcirculation disorders: marbling of the skin, distal cyanosis, stasis spots, hypothermia, moderate enlargement of the liver, spleen, tachycardia, decreased blood pressure, tachypnea, decreased diuresis.
2. The second is the phase of coagulopathy and thrombocytopathy of consumption. Petechiae and bleeding from injection sites, pale skin and mucous membranes occur, the functions of vital organs suffer in the form of acute pulmonary circulatory and acute renal failure, cerebral edema, myocardial damage. Hemorrhages occur simultaneously, including cerebral hemorrhages; pulmonary and gastrointestinal bleeding.
3. Recovery phase. If the second phase does not result in a fatal outcome, DIC syndrome moves into the third phase - recovery. This phase is accompanied by the cessation of bleeding and gradual restoration of the functions of the affected organs.

DIC syndrome in children is a serious complication of severe diseases, leading to death in 30-50% of cases.

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Diagnostics DIC in a child

The following changes in laboratory parameters are typical for the hypercoagulation phase:

• clotting time and bleeding time are normal or slightly shortened;
• platelet count within normal limits;
• PV shortened;
• Thu is shortened;
• fibrinogen level is elevated;
• PDF increased;
• positive ethanol test.

The following laboratory parameters are characteristic of the consumption phase:

• blood clotting time and bleeding time are increased;
• platelet count is reduced;
• PV is shortened or normal;
• PTT increased;
• fibrinogen level is reduced;
• PDF increased;
• ethanol test is strongly positive;
• anemia and the appearance of fragmented red blood cells in the blood smear.

In the third phase, laboratory parameters return to normal.

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Treatment DIC in a child

The nature and scope of treatment measures depend on the phase.

Hypercoagulation phase

The main attention should be paid to adequate therapy of the underlying disease. It is necessary to replenish the BCC by infusion therapy with the inclusion of fresh frozen plasma (donor of plasma coagulation factors and antithrombin III) at the rate of 10-20 ml/kg intravenously by drip, 10% glucose solution in a volume determined by the physiological needs of the newborn. Also prescribed is the antiplatelet agent pentoxifylline (Trental) 0.1-0.2 ml of a 2% solution in a 5% glucose solution (slowly by drip, 2-4 times a day). According to indications, the protease inhibitor aprotinin is administered at 25,000-50,000 IU intravenously slowly. In case of microcirculatory blockade, the monoamine oxidase inhibitor dopamine is used [5-10 mcg/kg x min), intravenously, by drip].

Consumption phase

Transfusions of blood coagulation factor VIII are required every 12 hours, and if indicated, transfusions of red blood cell mass and platelet concentrate. Oxygen therapy, correction of acidosis, warming the child, replenishment of the circulating blood volume, and heparin therapy are required. Sodium heparin is administered (under control of blood clotting time!) intravenously every 4-6 hours or subcutaneously every 8 hours at an initial dose of 10-25 U/(kg x day); if necessary, the dose is increased to 50-150 U/(kg x day).

Sodium heparin is prescribed only after transfusion of blood coagulation factor VIII and restoration of the level of antithrombin III (cofactor of heparin action) intravenously by drip or microjet. Cancellation of heparin therapy is possible only against the background of the prescription of platelet inhibitors (piracetam or nicotinic acid, dipyridamole, etc.) and with a gradual reduction in the dose of heparin.

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Recovery phase

Syndromic therapy aimed at restoring the impaired functions of organs and systems is necessary. Thrombolytic drugs are used extremely rarely, mainly in thrombosis of large vessels.