DIC (Gynecology and Obstetrics)

Disseminated intravascular coagulation is a coagulopathy, which in obstetrics is one of the most common causes of maternal death (after thromboembolic complications). DIC is one of the most serious syndromes in which coagulopathy manifests.

Pathogenesis
There are three key moments in the pathogenesis of disseminated intravascular coagulation:


 * 1) disruption of hemocoagulation balance ;
 * 2) excessive thrombin activity;
 * 3) dysregulation of plasmin activity.

In the fully developed state of DIC, there is uncontrolled activation of thrombin caused by the release of tissue factor into the circulation. Tissue factor is released from traumatized as well as non-traumatized tissues. In traumatized tissues, it is released from hematomas, exposed tissue, endothelium and leukocytes. In non-traumatized tissues, tissue factor is released from cells into the circulation under the influence of cytokines or endotoxin. In this case, DIC is part of SIRS, in sepsis. Systemic intravasal coagulation and numerous microthrombi occur. Subsequently, thrombolysis is activated (high D-dimers ), microthrombi damage platelets and they are absorbed in the spleen. Thrombocytopenia occurs. Hemorrhagic diathesis and MODS occur.

Classification of DIC in obstetrics

 * 1) Acute DIC :
 * 2) ** the prothrombotic stage is short, goes unnoticed;
 * 3) ** nausea, shortness of breath, cyanosis ;
 * 4) ** usually manifests itself in unstoppable bleeding ;
 * 5) ** if we do not intervene immediately, there will be a breakdown of the endothelium and uncontrollable bleeding into the mucous membranes and skin.
 * 6) Chronic DIC :
 * 7) ** it can take place covertly, we can find it in the laboratory − ↓ platelets, ↓ fibrinogen, ↓ antithrombin, ↑ aPTT , ↑ D-dimers, ↑ FDP;
 * 8) ** may arise as part of SIRS or manifest as MODS;
 * 9) ** is the risk of thromboembolic complications;
 * 10) ** bleeding starts more slowly;
 * 11) ** if the cause persists ( abscess, infection), decompensation soon occurs and then acute DIC develops.

Risk factors
Risk factors mainly include:


 * eclampsia, thrombophlebitis in history;
 * HELLP syndrome ;
 * coagulation disorders, hemolytic states;
 * retention and stillbirth ;
 * repeated revisions of the uterine cavity;
 * septic birth (miscarriage), placenta accreta, amniotic fluid embolism;
 * mole hydatidosa ;
 * obesity.

Diagnostics
As a guide, we perform laboratory tests in the delivery room (Lee White, thrombin test) - if positive, we do not wait for the laboratory and deal with it.


 * Lee White test: roughly indicative, at the bedside – a coagulum forms in the test tube within 1−2 minutes.
 * Thrombin time: evidence of fibrinogen, it can also be done at the bedside - add 2 ml of blood to a tube with lyophilized thrombin, if there is fibrinogen in it, it will clot within 1 minute, if it is not, the blood will not clot.
 * Laboratory tests: INR, aPTT, antithrombin III, fibrinogen, platelets, FDP, D-dimers.
 * Differential diagnosis


 * Bleeding from a birth injury;
 * various types of thrombocytopenia;
 * von Willebrand's disease ;
 * coagulopathy in HELLP syndrome.

Prevention

 * 1) Primary prevention :
 * 2) ** ambulatory detection of all conditions where there is a coagulation disorder - especially AT III deficiency, proteins C and S, Leiden mutation of factor V, homozygous MTHFR 677TT defect, etc., also, for example, antiphospholipid syndrome.
 * 3) Secondary prevention :
 * 4) ** antenatal application of LMWH in pregnant women at higher risk (mainly in abortions and surgeries);
 * 5) ** before sc, LMWH is routinely given to women in the following conditions: obesity, age over 30 years, hereditary thrombophilia, venous thrombosis in the anamnesis, preeclampsia, DM, previous abdominal surgery, placenta praevia, placental abruption, also during spontaneous stillbirth, maternal fever.

Treatment
If DIC is suspected, energetic intensive treatment is appropriate, if possible in a team (hematologist, anesthesiologist, internist, ...). The principle is to remove the provoking cause, regulate thrombin activity, maintain hemostasis.
 * Acute DIC


 * Order frozen plasma and erysma immediately ;
 * we will take blood for hemocoagulation examination;
 * first measure – we administer AT III – a bolus of 1,000 units IV and then a continuous infusion of another 1,000 units;
 * then we give heparin ;
 * circulating plasma replacement (dextrans and plasma expanders are contraindicated - they interfere with platelets);
 * we administer fibrinogen if its plasma level falls below 1 g/l.
 * Chronic DIC


 * Combination of AT III with heparin;
 * activated human protein C is newly used.

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