ABSTRACT
Following attachment of the human blastocyst to the uterine luminal epithelium, syncytiotrophoblasts invade the underlying stroma then breach endometrial capillaries and venules. This process initiates development of the primordial utero-placental circulation, thus providing the embryo with essential oxygen and nutrients prior to placentation (Moore, 1988). It is accompanied by a rapid rise in circulating human chorionic gonadotropin (hCG) signifying that the trophoblast has gained access to maternal blood. That decidual hemorrhage can disrupt this event is suggested by the phenomenon of “chemical pregnancy” in which endometrial bleeding follows the transient detection of circulating hCG. Once the primordial uteroplacental circulation is established, extravillous cytotrophoblasts penetrate the uterine spiral arteries and initiate morphological changes that increase intervillous blood flow and remodel these vessels (DeWolf et al., 1973). The success of these events can be jeopardized by the occurrence of decidual hemorrhage, which can lead to spontaneous abortion, placental abruption and preterm birth (Edmonds et al., 1982; Miller et al., 1980; McCormick, 1985; Shanklin and Scott, 1975; Strobino and Pantel-Silverman, 1989).
