Obstetrics and Gynecology - A.M. Hromova 2000

Obstetric Hemorrhage
Hemorrhage in the Third Stage of Labor and the Early Postpartum Period
Hemorrhage Caused by Coagulation Disorders

It is now widely accepted that gestational processes induce alterations in the hemostatic system aimed at ensuring the proper functioning of the mother-Placenta-fetus unit.

Pregnancy is regarded as a hypercoagulable state, with changes occurring across all Links of the hemostatic system: vascular-platelet, procoagulant, anticoagulant, and proteolytic. Platelet counts increase, whereas their aggregation activity decreases slightly; the concentration and activity of key procoagulants and fibrinogen levels rise, while fibrinolytic activity declines. These changes are considered physiological, representing an adaptive and protective response of the body that facilitates rapid and reliable cessation of postpartum Hemorrhage.

Examination of the hemostatic system in pregnant women and laboring patients prior to hemorrhage indicates a more pronounced hypercoagulability: alongside an increase in platelet count, their aggregation activity rises, and both the level and concentration of fibrinogen increase alongside qualitative changes. Increasing amounts of fibrinogen B appear in the Blood Plasma, as indicated by positive paracoagulation tests. Its presence points to the activation of intravascular Blood Coagulation and the potential development of disseminated intravascular coagulation (DIC) syndrome. An elevated concentration of fibrin degradation products leads to the blockade of uterine contractile activity, as this can cause uterine hypotonia refractory to endogenous and exogenous oxytocic agents.

Thus, alterations in the hemostatic system during pregnancy and labor prior to hemorrhage are regarded as potential hypercoagulability associated with the chronic form of DIC syndrome.

The Essence of this phenomenon lies in the excessive activation of plasma and platelet blood coagulation factors, their recruitment into the intravascular coagulation process within the microcirculatory system, the depletion of natural anticoagulants, and the exhaustion of Fibrinolysis substrates. Consequently, the consumption of clotting factors leads to hypocoagulability while elevated thromboplastic activity persists.

Acute hemorrhages caused by blood coagulation disorders occur under the following conditions:

— complicated courses of pregnancy and labor (premature detachment of a normally situated placenta, Amniotic Fluid Embolism, intrauterine fetal demise, tears of the uterine body or cervix, infection, aggressive uterine massage);

— congenital blood disorders (thrombocytopenic purpura, von Willebrand disease, etc.);

— dysadaptation of the hemostatic system, where hypocoagulability occurs instead of the physiological adaptive hypercoagulability at the end of the third trimester of pregnancy.

Under these conditions, active thromboplastic substances can enter the general Circulation, leading to intravascular blood coagulation. This results in a progressive decrease in the concentration of fibrinogen, prothrombin, and other coagulation factors, followed by impaired blood clotting.

The Clinical presentation of coagulopathic bleeding depends on the form and phase of DIC syndrome.

Phases of DIC syndrome:

Phase I - hypercoagulability (Lee-White clotting time under 4 min).

Phase II - gradual exhaustion of hemostasis (Lee-White clotting time exceeding 10-12 min); generalized bleeding is observed, microcirculation in Organs is impaired, and antithrombin III levels drop sharply.

Phase III - decompensation of hemostasis (stage III severity Shock). The blood is non-clotting.

Phase IV - thromboembolic complications (1 to 3 weeks).

DIC syndrome may present in acute, subacute, and chronic forms.

Treatment of DIC syndrome depends on the phase of the process: in hypercoagulability - heparin 2,500 IU every 5-10 min 2-4 times, transfusion of heparinized blood; however, this stage is very difficult to identify, and hemorrhages in DIC syndrome are typically diagnosed only at the hypocoagulable phase. At this stage, fresh frozen plasma administration is required. Transfusions of packed red Blood Cells, fresh citrated plasma, dry plasma, albumin, protamine sulfate, dicynone, cryoprecipitate, gelatin solution, volecam, menadione (vikasol), and calcium chloride solution are recommended. Proteolysis inhibitors such as kontrikal, gordox, or trasylol are also administered.

In A number of cases, blood clotting does not normalize; afibrinogenemia and profuse hemorrhage develop, resulting in maternal mortality.