Preeclampsia is a leading cause of maternal and perinatal morbidity and mortality worldwide.1 It is a syndrome characterized by proteinuria, hypertension, and edema that occurs after 20 weeks gestation and affects 3% to 7% of all pregnancies. 2, 3 Preeclampsia usually occurs in women in their first pregnancy or in women having twins. Untreated preeclampsia leads to eclampsia, a condition defined by the presence of grand mal seizures.4 Together, preeclampsia and eclampsia are responsible for 50,000 maternal deaths annually, worldwide.4 The risk factors for preeclampsia are diabetes mellitus, hypertension, obesity, proteinuria, nulliparity, family history, multiple pregnancies, contraceptive ...view middle of the document...
Most of maternal deaths and complications in developing countries are due to inadequate prenatal care, lack of access to emergency care, and poor diagnosis and treatment of patients with preeclampsia-eclampsia.4
This review will further examine the pathophysiological phenomena of preeclampsia along with the public health context of the disease.
THE PLACENTA AND PREECLAMPSIA
Preeclampsia is characterized by poor placentation, which is the poor development of the placenta and maternal blood supply. Poor placentation results in a hypoxic placenta, leading to clinical manifestations of preeclampsia in the mother, specifically hypertension, proteinuria, clotting, and a dysfunctional liver.6
In order to provide nutrients to the fetus, the placenta needs access to the maternal blood supply. The utero-placental unit is made up of fetal tissue from the chorionic sac and maternal tissue from the endometrium.7 The fetal portion is called the chorionic plate while the maternal portion is called the basal plate. Between these two regions is the intervillous space, which contains fetal blood vessels and maternal blood vessels. Maternal blood enters this space via maternal spiral arteries. Exchange of oxygen and nutrients occurs as the maternal blood flows around the villi of fetal blood vessels.8 Deoxygenated maternal blood exits through endometrial veins back into maternal circulation. Oxygen-deficient fetal blood moves from the fetus to the villous fetal vessels. The umbilical vein carries oxygenated, nutrient-rich blood back to the fetus.8
Two theories have been proposed to explain the physiological changes that allow for maternal-placental blood circulation. The first theory holds that during the first trimester trophoblasts invade the decidua, migrate along spiral arteries, and penetrate and remodel these arteries to produce dilated vessels. This process promotes perfusion of maternal blood into the placental intervillous space.6 The second theory states that trophoblasts invade the spiral arteries and form trophoblastic plugs, blocking maternal blood flow into the intervillous space. After the first trimester, the plugs are released and allow...