For eclampsia, the incidence has declined in areas where health care is more readily available. In the United States in 1998, it afected 1 in 3250 births (Ventura, 2000). Except for
Iceland, which has an extremely low rate, in countries with adequate resources the incidence averages 1 in 2000 to 3000 deliveries (Andersgaard, 2006; Jaatinen, 2016; O'Connor, 2013; Royal College of Obstetricians and Gynaecologists, 2006; Zwart, 2008).
Any satisfactory theory concerning the origins of preeclampsia must account for the observation that gestational hypertensive disorders are more likely to develop in women with the following characteristics:
Are exposed to chorionic villi for the irst time
Are exposed to a superabundance of chorionic villi, as with twins or hydatidiform mole
Have preexisting conditions associated with endothelial cell activation or inflammation, such as diabetes, obesity, cardiovascular or renal disease, immunological disorders, or hereditary inluences
Are genetically predisposed to hypertension developing during pregnancy.
A fetus is not a requisite for preeclampsia to develop. And, although chorionic villi are essential, they need not be intrauterine. For example, preeclampsia can develop with an abdominal pregnancy (Worley, 2008). Regardless of precipitating etioloy, the cascade of events leading to the preeclampsia syndrome is characterized by abnormalities that result in systemic vascular endothelial damage with resultant vasospasm, transudation ofplasma, and ischemic and thrombotic sequelae.
• Phenotypic Expression of he preeclampsia syndrome varies widely in its clinical phenotypic expression. But, at least two major subtypes are diferentiated by whether or not remodeling of uterine spiral arterioles by endovascular trophoblasts is defective. his concept has given rise to the "two-stage disorder" theory of preeclampsia pathogenesis. According to Redman and coworkers (20 15a), stage 1 is caused by faulty endovascular trophoblastic remodeling that downstream causes the stage 2 clinical syndrome. Importantly, stage 2 can be modified by preexisting maternal conditions that are also manifest by endothelial cell activation or inlammation and are listed in the third prior bullet.
Such staging is artiicial, and it seems logical that preeclampsia syndrome presents clinically as a spectrum of worsening disease. Moreover, evidence is accruing that many "isoforms" exist as discussed subsequently. Examples include diferences in
FIGURE 40-2 Schematic representation of normal placental implantation shows proliferation of extravillous trophoblasts from an anchoring villus. These trophoblasts invade the decidua and extend into the walls of the spiral arteriole to replace the endothelium and muscular wall to create a dilated low-resistance vessel. With preeclampsia, defective implantation is characterized by incomplete invasion of the spiral arteriolar wall by extravillous trophoblasts. This results in a small-caliber vessel with high resistance to flow.
maternal and fetal characteristics, placental indings, and earlyversus late-onset disease (Phillips, 2010; Valensise, 2008; van der Merwe, 2010).
n imposing number of mechanisms have been proposed to explain the cause of preeclampsia. Those currently considered important include: 1.
Placental implantation with abnormal trophoblastic invasion of uterine vessels 2.
Immunological maladaptive tolerance between maternal, paternal (placental), and fetal tissues 3.
Maternal maladaptation to cardiovascular or inlammatory changes of normal pregnancy 4.