Abstract:
The pathogenesis of eclampsia can be conceptually described as a cascade
beginning with impaired immunological adaptation, compounded by underlying genetic
predispositions. These disturbances hinder normal trophoblast invasion and prevent the
physiological remodeling of the muscular layer of the spiral arteries. As a consequence, regulatory
mechanisms governing vasoconstrictors and vasodilators become disrupted, giving rise to
generalized vasospasm and profound alterations in systemic and organ-specific hemodynamics,
including the utero–placental–fetal circulation. This sequence culminates in widespread
endothelial injury.
