What is the pathogenesis of preeclampsia?

Updated: Jun 12, 2018
  • Author: Michael P Carson, MD; Chief Editor: Edward H Springel, MD, FACOG  more...
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Although the exact pathophysiologic mechanism is not clearly understood, preeclampsia is primarily a disorder of placental dysfunction leading to a syndrome of endothelial dysfunction with associated vasospasm. In most cases, pathology evaluation demonstrates evidence of placental insufficiency with associated abnormalities such as diffuse placental thrombosis, an inflammatory placental decidual vasculopathy, and/or abnormal trophoblastic invasion of the endometrium. These findings support abnormal placental development or placental damage from diffuse microthrombosis as being central to the development of this disorder. There is also evidence to indicate an altered maternal immune response to fetal/placental tissue may contribute to the development of preeclampsia.

The widespread endothelial dysfunction may manifest as a maternal syndrome, fetal syndrome, or both. The pregnant woman may manifest dysfunction of multiple organ systems, including the central nervous, hepatic, pulmonary, renal, and hematologic systems. Endothelial damage leads to pathologic capillary leak that can present in the mother as rapid weight gain, nondependent edema (face or hands), pulmonary edema, hemoconcentration, or a combination thereof. The diseased placenta can also affect the fetus via decreased uteroplacental blood flow. This decrease in perfusion can manifest clinically as nonreassuring fetal heart rate testing, low scores on a biophysical profile, oligohydramnios, or as fetal growth restriction.

The hypertension occurring in preeclampsia is due primarily to vasospasm, with arterial constriction and relatively reduced intravascular volume compared with that of a normal pregnancy. The vasculature of normal pregnant women typically demonstrates decreased responsiveness to vasoactive peptides such as angiotensin-II and epinephrine.

In contrast, women who develop preeclampsia typically show a hyperresponsiveness to these hormones, an alteration that may be seen even before the hypertension and other manifestations of preeclampsia become apparent. In addition, blood pressures in preeclampsia are labile, and the normal circadian blood pressure rhythms may be blunted or reversed. One study found increased arterial stiffness in women with preeclampsia, as well as in those with gestational hypertension, compared with normotensive controls; treatment with alpha methyldopa significantly improved the vascular stiffness in preeclampsia but did not normalize it. [10]

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