Development of hemostasis in the fetus

The fetal hemostatic system is unique in many respects. Many coagulation proteins are expressed early in embryonic development and play roles outside of coagulation in cell proliferation and differentiation. Coagulation mRNA and protein can be detected within hepatic and endothelial cells within the first month of gestation and in fetal plasma during the third month. However, development of levels of most coagulation proteins is halted from mid-gestation until shortly before term onset of labor. The reason for this developmental arrest in plasma protein levels is unknown. The fetus demonstrates an unique balance of procoagulant, anticoagulant and fibrinolytic proteins concentrations which persists for several months postnatally. Fetal coagulation proteins are identical to adult proteins in structure and function with a few notable exceptions. Platelets are expressed early in fetal development and platelet concentrations are within the adult range by mid-gestation. Functional differences can be detected in fetal platelet function but rarely cause bleeding in the healthy fetus and newborn infant. Hemostasis in the fetus and newborn infants is functionally intact and spontaneous bleeding or clotting is rare. However, the neonatal hemostatic system appears to lack reserve capacity, and bleeding and clotting complications are common in the stressed infant, particularly the sick preterm infant.