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Disseminated intravascular coagulation is a condition in which the normally finely tuned balance between localized clot formation and clot dissolution becomes disrupted throughout the vascular system. This may result in pathologic microvascular thrombotic obstruction and tissue ischemia, hemorrhage due to consumption of available clotting factors, or both. This condition may be encountered in a wide variety of clinical situations. However, DIC in pregnancy presents the clinician with special challenges due to profound changes in the baseline system of coagulation and fibrinolysis, the presence of potent thromboplastic initiators in placental tissue, and unique clinical considerations when dealing with a mother-fetus pair and the process of childbirth. This chapter will examine each of these issues.
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Detailed diagrammatic representations of normal coagulation pathways may be found in standard textbooks of medicine.1 Germane to this discussion however are several aspects of this clotting/fibrinolysis cascade (Figure 31-1).
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In the past, extrinsic and intrinsic coagulation pathways were described as though they were alternative modes of clotting activation. This process is now more accurately understood as beginning almost universally with the exposure of the circulation to tissue factor and activation of the traditional extrinsic pathway, with subsequent augmentation or facilitation of this process through secondary activation of the intrinsic pathway.1 Ultimately, both mechanisms are involved in most types of clotting and involve thrombin generation as a fundamental initial step.2,3,4,5
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Intrinsic to the process of clot formation via conversion of fibrinogen to fibrin is the near-simultaneous initiation of clot lysis via conversion of plasminogen to plasmin, accompanied by repair of the damaged blood vessel.2,3,4 Thrombin generation is pivotal in both clot formation, and fibrinolysis.2,3,4,5,6
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Generation of thrombin is regulated at three pivotal points in the coagulation cascade; by antithrombin (which inhibits both conversion of factor X to Xa and directly inhibits the action of thrombin itself), by activated protein C (which inhibits activation of factors V and VIII), and by tissue factor pathway inhibitor (TFPI) (which interferes with the tissue factor/factor VIIa complex; see Figure 31-1).4 This process of clot formation and dissolution is normally both localized to the site of endothelial injury and limited in effect. Such tight control and localization is vital; under normal circumstances, these two processes are finely balanced, thus limiting both bleeding and potential clot-related tissue ischemia.
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DIC represents a pathologic hyperactivation of both thrombotic and thrombolytic aspects of this system which may be initiated by a number of factors, and generally involves interference with normal thrombin generation pathway at each of ...