When consumptive coagulopathy is severe, the likelihood of and ibrinogen-ibrin degradation products, which includes maternal and perinatal morbidity and mortality is increased. In D-dimers. long with lower concentrations of anticoagulant one study of 49 cases, antecedent causes included those listed protein S, hypercoagulability, and decreased ibrinolysis, there above, and 59 percent received blood transfusions, 18 percent is augmented-yet compensated-intravascular coagulation underwent hysterectomy, 6 percent were dialyzed, and three that may function to maintain the utero placental interface. mothers died (Rattray, 2012). he perinatal mortality rate was 30 percent. Callaghan and associates (2012) reviewed data from • Activation of Normal Coagulation the Nationwide Inpatient Sample and found a rising prevalence Instead of the "waterfall" sequential activation of clotting, a curofDIC from 1998 to 2009. And, from 2010 to 2011, DIC was rent theory proposes that tissue factor-an integral membrane the second most common severe maternal morbidity indicator glycoprotein-serves as the principal initiator of coagulation(Creanga, 2014). Notably, DIC was associated with nearly a (Levi, 2010b). Coagulation then moves forward but incorpofourth of maternal deaths during this study period. Despite these rates a feedback loop. To begin, tissue factor forms complexesstatistics, consumptive coagulopathy as the sole cause of maternal with factor VII/VIla to activate factors IX and X. Tissue factor death is relatively uncommon and accounts for only 0.2 percent is found in highly vascularized organs such as the brain, lungs, of pregnancy-related deaths in the United States (Creanga, 2015).
(Kuczynski, 2002; 0sterud, 2006; Uszynski, 2001).
Tissue factor-factor VIla complexes ultimately generate During normal pregnancy, extensive changes in coagulation activated factor X (Xa) to initiate clotting. Subsequently, the and fibrinolysis develop to create a procoagulant state. Some previously labeled "intrinsic" pathway amplifies this process. of these include appreciable increases in the plasma concentraSpecifically, the initial thrombin produced directly activates tions of factors I (fibrinogen), VII, VIII, IX, and X. A partial factor XI by providing a feedback amplification loop. This list of these normal values is found in the Appendix (p. 1256). primary role of tissue factor-factor VIla complex in coaguAt the same time, plasminogen levels rise considerably, but lation and consequent ampliication loop of thrombin is levels of plasminogen activator inhibitor-1 and 2 (PAI-1 and depicted in Figure 41-29 (Rapaport, 1995). he end result PAI-2) also grow. hus, plasmin activiy usually declines until of this ampliied coagulation process is fibrin formation. This after delivery (Hale, 2012; Hui, 2012). he mean platelet count is then counterbalanced by the ibrinolytic system, in which drops by 10 percent during pregnancy, and platelet activation is plasminogen is activated. As shown in Figure 41-29, even enhanced (Kenny, 2015). this process is tied initially to tissue factor. he inal result is
The net results of these changes include greater levels production of fibrinogen/fibrin degradation products, which of fibrinopeptide A, �-thromboglobulin, platelet factor 4, include D-dimers.
Plasminogen ---�,