Abstract
The hemostasis system is composed of procoagulant, anticoagulant, and fibrinolytic
proteins that interact with endothelial and blood cells and with each other in a complex
system of checks and balances to maintain blood flow while preventing both hemorrhage
and thrombosis. Pregnancy is a unique physiological state in which biological alterations
predispose both mother and fetus to both bleeding and clotting. The placenta is a
vascular interface for maternal and fetal blood exchange which predisposes the mother
to hemorrhage. Maternal hemostasis presents a compensatory hypercoagulability including
elevated factor VIII, von Willebrand factor, fibrinogen and thrombin generation, decreased
thrombin regulation with resistance to activated protein C and decreased free protein
S, and decreased fibrinolysis with increased plasminogen activator inhibitors. The
placental vascular surface is of fetal trophoblastic origin that derives many characteristics
of endothelium but differs in that tissue factor is constitutively expressed. Ontogeny
of fetal hemostasis is characteristic. Platelets, von Willebrand factor, factor VIII,
and fibrinogen are expressed and mature early in gestation, while vitamin K–dependent
and contact factors exhibit delayed development. The fetal hemostatic system has a
decreased capacity to generate or regulate thrombin, resulting in a fragile balance
with little capacity to compensate under stress conditions, particularly in the infant
born prematurely. Dysfunction of the maternal/placental/fetal unit gives rise to gestational
disorders including preeclampsia, fetal growth restriction, placental abruption, and
premature delivery. Knowledge of normal hemostasis levels and function are critical
to evaluate bleeding or clotting syndromes in the pregnant woman and her fetus or
newborn infant.
Keywords
hemostasis - pregnancy - placenta - fetus - newborn Infant - hemorrhage - thrombosis
