DIC-Syndrome in children

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

In the development of various pathological conditions, the DIC syndrome plays an essential role. This nonspecific general biological reaction of the organism arises in response to the penetration into the bloodstream of thromboplastic substances that activate hemostasis; it is accompanied by severe disturbances in the microcirculatory bed. Bleeding at DIC-syndrome differ persistent character.

[1], [2], [3], [4], [5], [6]

Causes of the dIC-syndrome in a child

The causes of the development of DIC syndrome in children are as follows:

• severe viral and bacterial (especially 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 overwhelming majority of cases, the starting 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, secretion of tissue factor in the blood, increased amounts of interleukins 1, 6 and 8, factor activation of platelets and tumor necrosis factor.

[7], [8], [9]

Pathogenesis

The excessive activation of the coagulating blood system caused by etiological factors leads to the formation of widespread blood clots of small vessels and, as a consequence, to the development of microcirculatory blockade of the parenchymal organs, their ischemia, depletion of plasma clotting factors and platelets. Excessive activation of coagulation induces fibrinolysis, exacerbating bleeding. With depletion of coagulation factors, platelet deficiency and the development of secondary depression of fibrinolysis, profuse bleeding and complete non-folding of the blood can occur. Thus, we can distinguish the following links of the pathogenesis of DIC syndrome in children:

• "Proteolytic explosion" - excessive formation of thrombin and plasmin in the blood, vasoactive effect of kinins;
• systemic endothelial damage (acidosis, endotoxicosis, exotoxicosis, etc.);
• hypercoagulability associated with the activation of both internal and external coagulation pathways;
• blockade of microcirculation in the early stages of DIC due to the formation of soluble complexes of fibrin-fibrinogen and the development of fibrin microthrombi and further - rheological occlusion of capillaries (increase in blood viscosity, sludge, clots);
• hypoxia and destruction of cells with dysfunction of the central nervous system, kidneys, lungs, liver, heart - multi-organ failure;
• coagulopathy and thrombocytopenia of consumption with depletion in blood levels as procoagulants (factors I, II, V, VIII, XIII, Willebrand) and natural anticoagulants - inhibitors of active serine proteases (antithrombin III, proteins C, B, etc.);
• pathological fibrinolysis with a significant increase in PDF, degradation of fibrinogen, proteolysis of factors V, VIII, XII, XI, XIII, Willebrand, changes in glycoproteins of the platelet membrane, which disrupts both primary and secondary hemostasis, leading to 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, if necessary, to adequately increase the synthesis of procoagulants and anticoagulants; difficulty in maintaining adequate perfusion in small vessels; vulnerability and easy damageability of most triggers leading to DIC syndrome.

[10], [11], [12], [13], [14]

Symptoms of the dIC-syndrome in a child

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

1. The first is the phase of hypercoagulation. In the clinical picture, the symptoms of the underlying disease predominate, with the addition of signs of microcirculation disturbance: marbling of the skin, distal cyanosis, stasis stasis, hypothermia, moderate increase in liver size, spleen, tachycardia, decreased blood pressure, tachypnea, decreased diuresis.
2. The second is the phase of coagulopathy and thrombocytopathy of consumption. There are petechiae and bleeding from the injection site, the pallor of the skin and mucous membranes, suffering from the functions of vital organs in the form of acute pulmonary circulation and acute renal failure, cerebral edema, myocardial damage. At the same time there are hemorrhages, including hemorrhages in the brain; pulmonary and gastrointestinal bleeding.
3. The recovery phase. If the second phase does not lead to a lethal outcome, the DIC-syndrome goes to the third phase - recovery. This phase is accompanied by the cessation of bleeding and the gradual restoration of the functions of the affected organs.

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

[15]

Diagnostics of the dIC-syndrome in a child

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

• The time of blood coagulation and the time of bleeding are normal or slightly shortened;
• the number of platelets is within the norm;
• PV is shortened;
• TWT is truncated;
• the level of fibrinogen is increased;
• PDF is increased;
• positive ethanol test.

For the consumption phase, the following laboratory indicators are characteristic:

• the time of clotting and the time of bleeding are increased;
• the number of platelets decreased;
• PV is shortened or normal;
• TCH is increased;
• the level of fibrinogen decreased;
• PDF is increased;
• ethanol test is sharply positive;
• anemia and the appearance of fragmented erythrocytes in a blood smear.

In the third phase, laboratory indicators come back to normal.

[16], [17], [18],

Treatment of the dIC-syndrome in a child

The nature and scope of treatment depends on the phase.

The phase of hypercoagulation

The main attention should be paid to adequate therapy of the underlying disease. Compulsory replacement of bcc by the method of infusion therapy with the inclusion of freshly frozen plasma (donor of plasma coagulation factors and antithrombin III) from the calculation of 10-20 ml / kg of intravenous drip, 10% glucose solution in the volume, determined by the physiological needs of the newborn. Also, an antiaggregant pentoxifylline (trental) 0.1-0.2 ml of a 2% solution in a 5% solution of glucose is prescribed (slowly, 2-4 times a day). According to the indications, a protease inhibitor aprotinin is injected 25,000 to 50,000 units intravenously slowly. When microcirculatory blockade apply inhibitor monoaminoksidazy dopamine [5-10 mkg / kghmin), intravenously, drip].

Consumption phase

Transfusion of the factor of blood coagulation VIII every 12 hours is required, according to indications - transfusion of erythrocyte mass and thromboconcentrate. Oxygen therapy, correction of acidosis, warming of the child, replacement of bcc, heparin therapy are necessary. Heparin sodium is administered (under the control of the time of blood coagulation!) Intravenously every 4-6 hours or subcutaneously every 8 hours at an initial dose of 10-25 units / kgg, and if necessary, increase the dose to 50-150 U / kgg.

Heparin sodium is prescribed only after the transfusion of the factor of blood coagulation VIII and the restoration of the level of antithrombin III (the cofactor of the action of heparin) intravenously by drip or micro-jet. The cancellation of heparin therapy is possible only on the background of the appointment of platelet inhibitors (pyracetam or nicotinic acid, dipyridamole, etc.) and with a gradual decrease in the dose of heparin.

[19], [20], [21], [22]

Recovery phase

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