Abstract
This article on the placenta includes considerations of chorioamnionitis, villitis, preeclampsia, and other low placental blood flow states and aspects of the circulating lupus anticoagulant syndrome. The author explains that, although gross and microscopic placental findings document placental features at one point in time, they also reflect ongoing pathophysiologic changes. Pathogenetic relationships between placental pathology, fetal hypoxia, intrauterine growth retardation, and cerebral palsy are, discussed. The reader will learn that low placental blood flow states and chorioamnionitis are important means by which endothelins may eventually participate in the production of placental and fetal vasoconstriction and critical hypoperfusion. The author explains means by which reduced umbilical, placental, and fetal blood flow can result from chronic fetal exposure to meconium, meconium-induced vasoactivity, and ultimate vascular necrosis. Clinically important complications therein may include anoxic-ischemic neuronal necrosis in the brain, necrotizing enterocolitis, and ischemic lesions in the fetal heart, lungs, kidneys, and liver. The article includes a review of nucleated red blood cells that most often signify chronic fetal hypoxia rather than infrequent acute intrapartum asphyxia. The reader will also find information on chorangiosis (placental villous capillary hypervascularity), an important sign of placental malperfusion and very long-standing fetal hypoxia.