Histological Features of Shallow Placental Implantation Unify Early-Onset and Late-Onset Preeclampsia

Abstract

Preeclampsia is distinguishable from other hypertensive conditions of pregnancy by its high rates of decidual arteriopathy, the uterine type of chronic hypoxic placental injury, the occurrence of villous infarctions, and clusters of multinucleate trophoblasts in the maternal floor. To retrospectively study the clinical and placental phenotypes of 230 women with early-onset preeclampsia, 261 women with late-onset preeclampsia, and 5059 women without hypertension in pregnancy (comparative group), 24 clinical and 46 placental phenotypes were statistically compared (analysis of variance, 2 with Bonferroni correction). The frequency of decidual arteriopathy (both hypertrophic and atherosis), patterns of chronic hypoxic placental injury, villous infarction, membrane laminar necrosis, membrane microscopic chorionic pseudocysts, clusters of maternal floor multinucleated trophoblasts, excessive number of extravillous trophoblasts, and intervillous thrombi was strikingly higher in both late-onset preeclampsia and early-onset preeclampsia than in the comparative group without hypertension in pregnancy. All 3 patterns of chronic hypoxic placental injury were 2-to 3-fold more common in preeclampsia. Although the preuterine pattern was as common in early-onset preeclampsia as it was in late-onset preeclampsia, the postuterine pattern was 2-fold more common in early-onset preeclampsia, and chronic villitis of unknown etiology was more common in lateonset preeclampsia than in the other 2 groups. Features of shallow placental implantation occurred at the same frequency in early-onset preeclampsia as in late-onset preeclampsia, which reflects an underlying common pathological mechanism in both subgroups of preeclampsia, while hypoxic lesions and patterns of placental injury were more common in early-onset preeclampsia than in late-onset preeclampsia, which correlates with more severe clinical outcomes of the former.

Patterns of Placental Injury in Congenital Anomalies in Second Half of Pregnancy

“…As previously reported in placentas from EXIT procedures, 26 this group featured lesions of fetal vascular malperfusion, as well as various umbilical cord abnormalities 7 and, in addition, features of shallow placental implantation. 41 The fetal vascular malperfusion might have been stasis-induced as a direct impact of compression by the malformation mass or umbilical cord compromise. We reported previously that hypoxic lesions, particularly acute-on-chronic overlap hypoxic lesions predispose to fetal vascular malperfusion.…”

Placental Findings in Postpartum Preeclampsia: A Comparative Retrospective Study

“…A recent work showed similar findings with less accelerated maturation of villi in late-onset preeclampsia compared with early-onset preeclampsia. 21 It is the most discriminative feature of the diagnosis of chronic in utero hypoxia prior term but also the most difficult to assess with a low reproducibility in full-term placentas. 20 Placenta contribution to postpartum preeclampsia might involve other mechanisms not tested by our study.…”

The etiology of preeclampsia

“…274 The frequency of VUE is higher in late-onset preeclampsia than in normal pregnancy but not in early-onset preeclampsia (Figure 12, C). 268,276 Massive perivillous fibrin deposition is characterized by extensive deposition of fibrinoid material in the intervillous space, hypoplasia, and sclerosis of the engulfed villi. 274 This lesion is associated with preeclampsia in one in five cases.…”