Introduction

The placenta has two important functions: absorption of substrates from the maternal circulation and protection of the fetus from harmful external forces. As an absorptive organ the placenta is essentially an interhemal membrane separating maternal blood in the intervillous space from fetal blood in the umbilical-villous circulation. Given the importance of both placental blood supplies it is not surprising that many external forces exert their harmful effects via hemorrhage and thrombosis. The pathologic sequelae of these processes in the placenta will be the primary focus of this chapter. Adaptations occur during placental development to maximize blood flow and minimize the diffusion distance that substrates must traverse. These developmental adjustments can predispose to later hemorrhage or thrombosis and this will be the second major emphasis of this chapter. A schematic diagram illustrating the spectrum and anatomical site of major thrombotic and hemorrhagic lesions in the placenta is provided in Figure 8.1.

Maternal perfusion of the interhemal membrane is augmented by several mechanisms. Cardiac output increases by approximately 40% over the course of pregnancy, largely due to a 50% increase in maternal plasma volume. Large uterine arteries dilate two-fold under the influence of pregnancy hormones, many of which are secreted by the placenta. Endometrial spiral arterioles are remodeled by invading trophoblast to form funnel shaped conduits that are incapable of restricting blood flow because of dissolution of their smooth muscle wall. Blood enters the intervillous space of the placenta via 80–120 of these spiral arterioles.