DIC-Syndrome in Gynecology

The syndrome of disseminated intravascular coagulation in gynecological practice is most often met with hemorrhagic shock caused by various causes, bacterial-toxic shock as a complication of criminal abortion; frozen pregnancy, transfusion of incompatible blood.

[1], [2], [3], [4]

Causes of the dIC-Syndrome

The triggering mechanism in the development of the DIC syndrome is the activation of blood or tissue thromboplastin due to hypoxia and metabolic acidosis of any origin, trauma, the introduction of toxins of different nature into the bloodstream, etc. The formation of active thromboplastin is the first and longest phase of hemostasis in which involvement of many clotting factors, such as plasma (XII, XI, IX, VIII, X, IV, V), and platelet (3, I). Under the influence of active thromboplastin with the participation of calcium ions (factor IV) prothrombin passes into thrombin (II phase). In the presence of calcium ions and with the participation of the platelet factor (4), thrombin converts fibrinogen to fibrin monomer, which in turn is converted into insoluble filaments of fibrin polymer (III phase) by the influence of the XIII plasma factor and platelet factor (2).

In addition to changes in the procoagulant link of hemostasis, the platelet unit activates, leading to adhesion and aggregation of platelets with the release of biologically active substances: kinins, prostaglandins, gentamines, catecholamines, etc. These substances change the permeability of the vessels, cause their spasm, open arterio-venous shunts, slow blood flow in the microcirculation system, promote stasis, develop a sludge syndrome, deposit blood, form blood clots. As a result of these processes, blood supply to tissues and organs, including vital ones: liver, kidneys, lungs, certain parts of the brain, is disturbed.

In response to the activation of the coagulation system, protective mechanisms aimed at restoring the damaged regional tissue perfusion are included: the fibrinolytic system and the cells of the reticuloendothelial system. Thus, against the background of disseminated intravascular coagulation due to increased consumption of procoagulants and increased fibrinolysis, increased bleeding occurs, thrombohemorrhagic syndrome is formed.

[5], [6], [7], [8]

Symptoms of the dIC-Syndrome

Symptoms of acute bleeding syndrome are caused by thrombotic and hemorrhagic disorders of varying severity, which manifest:

1. hemorrhages in the skin, mucous membranes, from injection sites, injuries, surgical wounds and uterus;
2. necrosis of some areas of the skin and mucous membranes;
3. manifestations from the side of the central nervous system in the form of euphoria, disorientation, darkening of consciousness;
4. acute renal, hepatic and pulmonary insufficiency.

The degree of severity of clinical manifestations depends on the stage of the DIC syndrome. However, the clinical diagnosis of the DIC syndrome is difficult, on the one hand, because all these symptoms are not specific for this pathology, on the other - because the symptomatology of the major diseases and conditions against which it develops is extremely diverse. Therefore, the results of laboratory studies of the hemostatic system are at the forefront in the diagnosis of acute blood ICD .

For the acute form of ICE, prolongation of clotting time (more than 10 min), a decrease in the number of platelets and a level of fibrinogen, an increase in the plasma recalcification time, prothrombin and thrombin time, an increase in the concentration of PDF and RCMF are characteristic.

To establish the phase of the course of the syndrome, ICE offers the following rapid diagnostic tests: blood coagulation time, spontaneous lysis of the clot, test thrombin, determination of PDF by ethanol test and immunoprecipitation, platelet count, thrombin time, erythrocyte fragmentation test.

The first phase is characterized by an increase in clotting time and thrombin time, a positive ethanol test.

In the II phase, with a syndrome of ICE, there is a moderate decrease in the number of platelets (120-10 10 ⁹ / L), thrombin time is prolonged to 60 seconds or more, PDF and damaged red blood cells are determined.

In the III phase, the blood clotting time, test thrombin and thrombin time are prolonged, the platelet count is reduced to 100 • 10 ⁹ / l, a rapid lysis of the formed clot occurs. For the IV phase, the following indices are characteristic: a clot is not formed, test-thrombin is more than 60 s, the number of platelets is less than 60-10 10 ⁹ / L.

The chronic form of ICE is characterized by a normal or reduced number of platelets, a normal or even increased amount of fibrinogen, normal or slightly decreased prothrombin time, a decrease in clotting time, an increase in the number of reticulocytes. Particular importance in the diagnosis of ICE syndrome is given to the appearance of degradation products of fibrin (PDF) and soluble complexes of fibrin / fibrinogen monomers (RCMF).

[9], [10]

Stages

Syndrome ICE takes the form of successive successive phases. MS Machabeln distinguishes four stages:

1. stage - hypercoagulability associated with the appearance of a large amount of active thromboplastin;
2. stage - coagulopathy of consumption, associated with a decrease in procoagulants due to their inclusion in microthrombi, with simultaneous activation of fibrinolysis.
3. stage - a sharp decrease in the blood of all procoagulants up to the development of afibrinogenemia on the background of pronounced fibrinolysis. This stage is characterized by particularly severe hemorrhages. If the patient does not die, the DIC syndrome of blood passes into the next stage;
4. stage - regenerative, at which gradual normalization of the state of the coagulating system of blood occurs. However, sometimes at this stage, the results of thromboses and violations of regional perfusion of organs and tissues in the form of acute arterial hypertension, acute respiratory failure (ODN) and / or cerebral circulation disorders can occur.

It should be emphasized that in clinical practice in patients with DIC syndrome is not often manifested in such a classical form. Depending on the cause that caused its development, the duration of the pathogenic effect, the state of the preceding health of women, one of the stages can be prolonged and not change to another. In some cases, the prevalence of hypercoagulability against a background of fuzzy nonshare, in others - fibrinolysis is the leading link in the pathological process.

According to the classification, the following are distinguished:

• Stage I - hypercoagulation;
• II stage - hypocoagulation without generalized fibrinolysis activation;
• Stage III - hypocoagulation with generalized activation of fibrinolysis;
• IV stage - complete blood coagulation.

In the stage of hypercoagulation, the coagulation time of coagulogram tests was shortened, fibrinolytic and anticoagulant activity was reduced. In the II stage, the coagulogram indicates the consumption of coagulation factors: the number of platelets, the prothrombin index, the activity of coagulation factors - V, VII, VIII. Increased levels of free heparin and the appearance of fibrin degradation products (PDF) indicate local activation of fibrinolysis. Stage III is characterized by a decrease in the number of platelets, a decrease in the concentration and activity of procoagulants with a simultaneous generalized increase in fibrinolytic activity and an increase in free heparin. The phase of complete blood coagulation is characterized by an extreme degree of hypocoagulation with extremely high fibrinolytic and anticoagulant activity.

[11], [12], [13], [14], [15]

Diagnostics of the dIC-Syndrome

The leading role in the diagnosis and treatment of the syndrome of ICE belongs to doctors-coagulologists. However, gynecologists are the first to come face to face with this formidable pathology, therefore they must have the necessary complex of knowledge so that before the inclusion in the provision of therapeutic and resuscitative actions of coagulologists, to proceed to the correct, pathogenetically substantiated treatment.

[16]

Treatment of the dIC-Syndrome

Treatment of DIC syndrome should be strictly individual, aimed at:

1. elimination of the underlying cause that caused it;
2. normalization of hemodynamics;
3. normalization of blood clotting.

Methods used to eliminate the cause of ICE, stem from the nature of gynecological pathology. In women with a dead pregnancy (syndrome of delaying the dead fetus in the uterus), the emptying of the uterus is necessary. In septic conditions, the sanation of the focus of infection is shown. The acute form of ICE, caused by hemorrhagic shock due to impaired ectopic pregnancy, rupture of the ovary and other causes, requires surgical stop of bleeding.

The approach to elimination of hemodynamic disorders should also be individual. Acute forms of the syndrome of ICE, as a rule, are combined with hemorrhagic shock, therefore, measures to restore central and peripheral hemodynamics with them have much in common. For infusion-transfusion therapy in such cases, preference is given to whole "warm" or freshly citrated blood, and from its components - to plasma. The mode of controlled hemodilution is carried out within the limits not exceeding 15-25% of BCC, due to gelatin, albumin, rheopolyglucin and crystalloids such as Ringer's solution - sodium lactate, lactasol. However, it should be borne in mind that the use of rheopolyglucin in the late stage of the process and in the presence of profuse bleeding requires great care, as excessive administration of it can increase bleeding. At this time, transfusions of albumin and plasma are preferable.

The most difficult task in the treatment of the acute form of the ICE syndrome is the restoration of the normal coagulation properties of the blood, for which it is necessary to stop intravascular coagulation, reduce fibrinolytic activity and restore the coagulation potential of the blood. This task should be solved by a specialist-hematologist under the control of a coagulogram.

Heparin is administered intravenously to 100-150 ml of isotonic sodium chloride solution or 5% glucose solution at a rate of 30-50 cap / min. Heparin is dosed depending on the phase of the ICE syndrome: in the I phase it is permissible to administer up to 5000 ED (70 U / kg), in the II and III phases - 2500-3000 ED (30-50 U / kg), and in IV phase, heparin can not be administered . In case of an overdose of heparin, protamine sulfate is used: 100 units of heparin neutralizes 0.1 ml of a 1% protamine sulphate solution. It is not recommended to use heparin with extensive wound surfaces.

The inhibition of fibrinolytic activity can be achieved with the help of inhibitors of animal origin such as kontrikal, trasilol, gordoksa. A single dose of counterpart is 20,000 units (daily - 60,000 units), trisolol is 25,000 units (100,000 units), and a gourde is 100,000 units (500,000 units). It is not recommended to use intravenously synthetic inhibitors of proteolytic enzymes (epsilon-aminocaproic acid, pamba), because they cause stabilization of thrombi in the microcirculation system, which leads to severe circulatory disturbances in the kidneys and in the brain. These drugs can only be used topically. Fibrinolysis inhibitors are used according to strict indications, because a sharp decrease in fibrinolytic activity may lead to an increase in intravascular fibrin deposition. The best effect is the administration of these drugs in the III and IV phases of the ICE syndrome.

The most widely used method of reducing the coagulation properties of blood in acute form of the DIC syndrome is replacement therapy. For this purpose, "warm" donor and fresh blood citrate, dry native and antihemophilic plasma are used. Blood is poured in initial doses up to 500 ml. After evaluating the effect of blood transfusion, the blood infusion is repeated. A dry, native and / or anti-hemophilic plasma is used in a total amount of 250-500 ml. It is recommended to take into account the content of fibrinogen in all injections: in "warm" donor blood - in antigemofilnoy plasma - 4 g / l, in dry plasma - 1 g / l, cryoprecipitate - 10-21 g / l.

Elimination of acute manifestations of the DIC syndrome should not serve as a signal to the end of intensive care. During the rehabilitation period, it is necessary to continue treatment aimed at eliminating possible manifestations of renal and hepatic insufficiency, correction of respiratory disorders, restoration of protein and electrolyte homeostasis, and prevention of infectious complications.