DIC in gynecology

In gynecological practice, disseminated intravascular coagulation syndrome is most often encountered in hemorrhagic shock caused by various reasons, bacterial toxic shock as a complication of a criminal abortion; frozen pregnancy, transfusion of incompatible blood.

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

Causes DIC

The trigger mechanism in the development of DIC syndrome is the activation of blood or tissue thromboplastin due to hypoxia and metabolic acidosis of any origin, trauma, entry of toxins of various nature into the bloodstream, etc. The formation of active thromboplastin is the first and longest phase of hemostasis, in which many coagulation factors take part, both 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 is converted into thrombin (phase II). In the presence of calcium ions and with the participation of platelet factor (4), thrombin converts fibrinogen into fibrin monomer, which, in turn, under the influence of plasma factor XIII and platelet factor (2) is converted into insoluble fibrin polymer threads (phase III).

In addition to changes in the procoagulant link of hemostasis, activation of the platelet link occurs, leading to adhesion and aggregation of platelets with the release of biologically active substances: kinins, prostaglandins, gnetamine, catecholamines, etc. These substances change the permeability of blood vessels, cause their spasm, opening of arteriovenous shunts, slow down blood flow in the microcirculation system, promote stasis, development of sludge syndrome, blood deposition, and thrombus formation. As a result of these processes, there is a disruption of the blood supply to tissues and organs, including vital ones: liver, kidneys, lungs, some parts of the brain.

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

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

Symptoms DIC

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

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

The degree of clinical manifestations depends on the stage of DIC syndrome. However, clinical diagnostics of DIC syndrome is difficult, on the one hand, because all these symptoms are not specific to this pathology, on the other hand, because the symptoms of the main diseases and conditions against which it develops are extremely diverse. Therefore, the results of laboratory studies of the hemostasis system come to the forefront in the diagnostics of acute DIC syndrome of blood.

Acute DIC is characterized by an increase in blood clotting time (more than 10 minutes), a decrease in the number of platelets and fibrinogen levels, an increase in plasma recalcification time, prothrombin and thrombin time, and an increase in the concentration of PDP and RKMP.

To determine the phase of the DIC syndrome, the following express diagnostic tests are offered: blood clotting time, spontaneous clot lysis, thrombin test, determination of FDP by ethanol test and immunoprecipitation, platelet count, thrombin time, erythrocyte fragmentation test.

Phase I is characterized by an increase in blood clotting time and thrombin time, and a positive ethanol test.

In phase II of DIC syndrome, there is a moderate decrease in the number of platelets (120-10 ⁹ /l), thrombin time is extended to 60 s or more, and PDP and damaged erythrocytes are detected.

In phase III, the blood clotting time, test thrombin and thrombin time are prolonged, the platelet count decreases to 100 • 10 ⁹ /l, and rapid lysis of the formed blood clot occurs. The following indicators are characteristic of phase IV: no clot is formed, test thrombin is more than 60 sec, the platelet count is less than 60 • 10 ⁹ /l.

The chronic form of DIC is characterized by a normal or decreased number of platelets, normal or even increased amount of fibrinogen, normal or slightly decreased prothrombin time, decreased blood clotting time, and an increase in the number of reticulocytes. Of particular importance in the diagnosis of DIC syndrome is the appearance of fibrin degradation products (FDP) and soluble fibrin/fibrinogen monomer complexes (SFMC).

[ 9 ], [ 10 ]

Stages

DIC syndrome occurs in successive phases. M.S. Machabeln identifies 4 stages:

1. stage - hypercoagulation associated with the appearance of a large amount of active thromboplastin;
2. stage - consumption coagulopathy associated with a decrease in procoagulants due to their inclusion in microthrombi, with simultaneous activation of fibrinolysis.
3. stage - a sharp decrease in all procoagulants in the blood up to the development of afibrinogenemia against the background of pronounced fibrinolysis. This stage is characterized by particularly severe hemorrhages. If the patient does not die, then the DIC syndrome of blood passes to the next stage;
4. stage - recovery, during which the state of the blood coagulation system gradually normalizes. However, sometimes at this stage the results of thrombosis and disturbances of regional perfusion of organs and tissues may appear in the form of acute renal failure, acute respiratory failure (ARF) and/or cerebrovascular accident.

It should be emphasized that in clinical practice, patients with DIC syndrome rarely manifest themselves in such a classic form. Depending on the cause that caused its development, the duration of the pathogenic effect, the state of the previous health of women, one of the stages can be prolonged and not pass into another. In some cases, there is a predominance of hypercoagulation against the background of mild fibrinolysis, in others, fibrinolysis is the leading link in the pathological process.

According to the classification, the following are distinguished:

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

In the hypercoagulation stage, the clotting time of general coagulogram tests is shortened, fibrinolytic and anticoagulant activity is reduced. In stage II, the coagulogram indicates the consumption of coagulation factors: the number of platelets, prothrombin index, and activity of blood coagulation factors - V, VII, VIII are reduced. An increase in the level of free heparin and the appearance of fibrin degradation products (FDP) 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 incoagulation is characterized by an extreme degree of hypocoagulation with extremely high fibrinolytic and anticoagulant activity.

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

Diagnostics DIC

The leading role in the diagnosis and treatment of DIC syndrome belongs to coagulation specialists. However, gynecologists are the first to come face to face with this formidable pathology, so they must have the necessary set of knowledge to begin correct, pathogenetically justified treatment before coagulation specialists are included in the provision of therapeutic and resuscitation actions.

[ 16 ]

Treatment DIC

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.

The methods used to eliminate the cause of DIC follow from the nature of the gynecological pathology. In women with a frozen pregnancy (dead fetus retention syndrome in the uterus), the uterus must be evacuated. In septic conditions, the sanitation of the infection site is indicated. The acute form of DIC caused by hemorrhagic shock due to a disrupted ectopic pregnancy, ovarian rupture, and other causes requires surgical bleeding control.

The approach to eliminating hemodynamic disturbances should also be individual. Acute forms of DIC syndrome are usually combined with hemorrhagic shock, so measures to restore central and peripheral hemodynamics in them have much in common. In such cases, preference is given to whole "warm" or freshly citrated blood for infusion-transfusion therapy, and plasma is used among its components. The controlled hemodilution regimen is carried out within limits not exceeding 15-25% of the BCC, due to gelatinol, albumin, rheopolyglucin and crystalloids such as Ringer's solution - sodium lactate, lactasol. However, it should be taken into account that the use of rheopolyglucin in the late stage of the process and in the presence of profuse bleeding requires great caution, since its excessive administration can increase bleeding. At this point, it is preferable to transfuse albumin and plasma.

The most difficult task in treating the acute form of DIC syndrome is to restore normal coagulation properties of the blood, which requires stopping intravascular coagulation, reducing fibrinolytic activity and restoring the coagulation potential of the blood. This task should be solved by a hematologist under the control of a coagulogram.

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

Fibrinolytic activity can be inhibited using inhibitors of animal origin such as contrical, trasilol, and gordox. A single dose of contrical is 20,000 U (daily dose - 60,000 U), trisilol - 25,000 U (100,000 U), gordox - 100,000 U (500,000 U). It is not recommended to use synthetic inhibitors of proteolytic enzymes intravenously (epsilon-aminocaproic acid, pamba), because they cause stabilization of blood clots in the microcirculation system, which leads to severe circulatory disorders in the kidneys and brain. These drugs can only be used locally. Fibrinolysis inhibitors are used according to strict indications, because a sharp decrease in fibrinolytic activity can lead to increased intravascular fibrin deposition. The best effect is achieved by administering these drugs in phases III and IV of DIC syndrome.

The most widely used method of restoring the coagulation properties of blood in the acute form of DIC syndrome is replacement therapy. For this purpose, "warm" donor and freshly citrated blood, dry native and antihemophilic plasma are used. Blood is transfused in initial doses of up to 500 ml. After assessing the effect of the transfusion, the blood infusion is repeated. Dry, native and/or antihemophilic plasma is used in a total amount of 250-500 ml. It is recommended to take into account the fibrinogen content in all administered drugs: in "warm" donor blood - in antihemophilic plasma - 4 g / l, in dry plasma - 1 g / l, cryoprecipitate - 10-21 g / l.

Elimination of acute manifestations of DIC syndrome should not serve as a signal for the end of intensive therapy. During the rehabilitation period, it is necessary to continue treatment aimed at eliminating possible manifestations of renal and hepatic failure, correcting respiratory disorders, restoring protein and electrolyte homeostasis, and preventing infectious complications.