he absolute incidence ofVTE during pregnancy is low-1 or 2 cases per 1000 pregnancies. However, the risk is approximately ive times higher than that among women who are not pregnant (Greer, 2015). Approximately equal numbers of cases are identiied antepartum and in the puerperium. Deep-vein thrombosis alone is more frequent antepartum, and pulmonary embolism is more common in the first 6 weeks postpartum (Jacobsen, 2008). During the puerperium, the estimated incidence of a thromboembolic complication is 22 events per 100,000 deliveries. Although still elevated, the risk falls to approximately 3 cases per 100,000 deliveries during the second 6-week postpartum period (Kamel, 2014).
Rudolf Virchow (1856) postulated that stasis, local trauma to the vessel wall, and hypercoagulability predisposed to venous thrombosis. During normal pregnancy, the risk for each of these rises. Compression of the pelvic veins and inferior vena cava by the enlarging uterus renders the lower extremity venous system particularly vulnerable to stasis. From their review, Marik and Plante (2008) cite a 50-percent reduction in venous Row velocity in the legs that lasts from the early third trimester until 6 weeks postpartum. This stasis is the most constant predisposing risk factor for venous thrombosis. Venous stasis and delivery may also contribute to endothelial cell injury. Last, as listed in the Appendix (p. 1256), the synthesis of most clotting factors is markedly enhanced during pregnancy and favors coagulation.
Characteristics for developing thromboembolism during pregnancy are shown in Table 52-1. he most important of these is a personal history of thrombosis. Speciically, 15 to 25 percent of all VTE cases during pregnancy are recurrent events (American College of Obstetricians and Gynecologists, 20 17b). In one study, the magnitude of other risks was estimated from 7177 VTE cases during pregnancy and 7158 events during the postpartum period (James, 2006). Calculated risks for thromboembolism were approximately doubled in women with multifetal gestation, anemia, hyperemesis, hemorrhage, and cesarean
TABLE 52-1. Some Risk Factors Associated with an Increased Risk for Thromboembolism delivery. he risk was even greater in pregnancies complicated by postpartum infection. Waldman and associates (2013) found that the risk of VTE was slightly higher in women with advanced maternal age and approximately doubled in women with great parity, a hypertensive disorder, cesarean delivery, or obesity. Risks were signiicantly higher among women who had a stillbirth or who underwent peripartum hysterectomy.
he next most important individual risk factor is a genetically determined thrombophilia. An estimated 20 to 50 percent ofwomen who develop a venous thrombosis during pregnancy or postpartum have an identiiable underlying genetic disorder (American College ofObstetricians and Gynecologists, 2017b).
Several important regulatory proteins act as inhibitors in the coagulation cascade (Fig. 52-1). Normal values for many of these proteins during pregnancy are found in the Appendix (p. 1256). Inherited or acquired deficiencies of these inhibitory proteins are collectively referred to as thrombophilias. These can lead to hypercoagulability and recurrent TE (Connors, 2017). lthough these disorders are collectively present in approximately 15 percent ofwhite European populations, they are responsible for approximately 50 percent of all thromboembolic events during pregnancy (Lockwood, 2002; Pierangeli, alncludes May-Thurner syndrome (iliac vein compression syndrome).