Thromboembolic Disease and Pregnancy: Are All Women Equal?

Pregnancy primes women to form clots [1]. Circulating levels of various clotting factors-fibrinogen and factors VII, VIII, IX, X, and XII-increase during gestation. Concentrations of some inhibitors of coagulation, such as free and total protein S, decrease during pregnancy. What is truly remarkable is the rarity, given the potential for the formation of clots, of serious thromboembolic events in pregnant women. The mechanisms whereby the blood of a healthy woman remains liquid during gestation are, for the most part, obscure.

The current confusion about the clinical management of thromboembolic disease during pregnancy reflects our incomplete understanding of the molecular biology and natural history of coagulation during gestation. The discovery that vasoprotective and thromboresistant molecules are membrane constituents synthesized by endothelial cells points to the enormous surface area of the vascular endothelium as an important territory still to be explored [2, 3].

Understanding the epidemiology of thromboembolic disease during pregnancy is also made difficult by inadequate definition of clinically important events and their time course. What do we know and not know about this vexing clinical area? We know that superficial phlebitis is a common nuisance that almost never progresses to deep venous disease during gestation or the postpartum period. Deep venous thrombophlebitis is a relatively infrequent complication of pregnancy, but pulmonary embolism as a complication of deep venous thrombosis is one of the most frequent causes of maternal illness and death. The converse, however, is not true: That is, it is inaccurate to conclude that serious thromboembolic disease during pregnancy is common.

Chronic underlying venous disease …