Prenatal Diagnosis of a Placental Infarction Hematoma Associated with Fetal Growth Restriction, Preeclampsia and Fetal Death: Clinicopathological Correlation

Aurioles-Garibay, Alma; Hernández‐Andrade, Edgar; Romero, Roberto; Qureshi, Faisal; Ahn, Hyunyoung; Jacques, Suzanne M.; Garcia, Manon; Yeo, Lami; Hassan, Sonia S.

doi:10.1159/000357841

Cited by 26 publications

(13 citation statements)

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“…Similarly to others, we found no differences in fetal vascular malperfusion between the EOPE and the LOPE groups, 42 but fetal vascular malperfusion in combination with maternal vascular lesions may be more dominant in EOPE with FGR than in EOPE without FGR. 43 This analysis also confirmed that IVT (Figure 1(H)) were slightly but statistically significantly more common in PE which confirms the data from the literature on the increased frequency of IVT in pregnancies complicated by hypoxia-related conditions such as PE and FGR 44–48 and maternal diabetes mellitus. 49,50 However, no significant differences were found between severe and mild PE.…”

Section: Discussionsupporting

confidence: 87%

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

Stanek

2018

Pediatr Dev Pathol

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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.

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Section: Discussionsupporting

confidence: 87%

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

Stanek

2018

Pediatr Dev Pathol

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“…The pathologic processes implicated in fetal death include: infection 65–84 , placental abruption, 5, 37, 70, 85–92 vascular lesions of the placenta, 28, 35, 93–100 preeclampsia, 41, 101–105 fetal growth restriction 9, 106–114 , maternal anti-fetal rejection, 35, 115–120 metabolic disorders, 121–133 genetic disorders, 80, 131, 134–137 umbilical cord accident, 97, 138–145 trauma 146–148 , and placental senescence 22 ; however, most of the 47,000 stillbirths reported from developed countries in 2015 149 were classified as unknown etiology. It is currently believed that the causes of fetal loss change with gestational age: chromosomal abnormalities 150–153 and infection 75 are the most common causes during the first half of pregnancy, placental causes (abruption or vascular abnormalities) 154–156 , and maternal anti-fetal rejection 118 become the most common causes after 26 weeks until term 14 , after which the etiology of in most cases, especially after 40 weeks, is unknown 14 .…”

Section: Discussionmentioning

confidence: 99%

The prediction of fetal death with a simple maternal blood test at 24-28 weeks: a role for angiogenic index-1 (PlGF/sVEGFR-1 ratio)

Chaiworapongsa

Romero

Erez

et al. 2017

American Journal of Obstetrics and Gynecology

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Objective To determine if maternal plasma concentrations of angiogenic and anti-angiogenic factors measured at 24–28 weeks of gestation can predict subsequent fetal death. Methods A case-cohort study was designed to include 1000 randomly selected subjects and all remaining fetal deaths (cases) from a cohort of 4006 women with a singleton pregnancy, enrolled at 6–22 weeks of gestation, in a pregnancy biomarker cohort study. The placentas of all fetal deaths were histologically examined by pathologists who used a standardized protocol and were blinded to patient outcomes. Placental growth factor (PlGF), soluble endoglin (sEng), and soluble vascular endothelial growth factor receptor-1 (sVEGFR-1) concentrations were measured by ELISA assays. Quantiles of the analyte concentrations (or concentration ratios) were estimated as a function of gestational age among women who delivered live neonates but did not develop preeclampsia or deliver small-for-gestational–age (SGA) newborns. A positive test was defined as analyte concentrations (or ratios) <2.5th and 10th centiles [PlGF, PlGF/sVEGFR-1 (angiogenic index-1), and PlGF/sEng)] or >90th and 97.5th centiles (sVEGFR-1 and sEng). Inverse probability weighting was used to reflect the parent cohort when estimating the relative risk. Results There were 11 fetal deaths and 829 controls with samples available for analysis between 24–28 weeks of gestation. Three fetal deaths occurred prior to 28 weeks and eight at or after 28 weeks of gestation. The rate of placental lesions consistent with maternal vascular underperfusion was 33.3% (1/3) among those who had a fetal death before 28 weeks and 87.5% (7/8) of those who had this complication at or after 28 weeks of gestation. The maternal plasma angiogenic index-1 value was below the 10th centile in 63.6% (7/11) of the fetal death group and in 11.1% (92/829) of the controls. The angiogenic index-1 value was <2.5th centile in 54.5% (6/11) of the fetal death group and in 3.7% (31/829) of the controls. An angiogenic index-1 value <2.5th centile had the largest positive likelihood ratio for predicting fetal death >24 weeks (14.6; 95% CI, 7.7–27.7) and a relative risk of 29.1 (95% CI, 8.8–97.1), followed by sEng >97.5thcentile and PlGF/sEng <2.5th, both with a positive likelihood ratio of 13.7 (95% CI, 7.3–25.8) and a relative risk of 27.4 (95% CI, 8.2–91.2). Among women without a fetal death whose plasma angiogenic index-1 concentration ratio was below the 2.5th centile, 61% (19/31) developed preeclampsia or delivered an SGA neonate; when the 10th centile was used as the cut-off, 37% (34/92) of women had these adverse outcomes. Conclusions 1) A maternal plasma angiogenic index-1 value below the 2.5th centile (0.126) at 24–28 weeks of gestation carries a 29-fold increase in the risk of subsequent fetal death and identifies 55% of subsequent fetal deaths with a false-positive rate of 3.5%; and 2) 61% of women who have a false-positive test result will subsequently experience adverse pregnancy outcomes.

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“…In our study we found that the histopathological evidence of maternal and fetal vascular malperfusion were significantly higher in the placental tissues of the cases in comparison to controls. The presence of VI and RPH are indicative of placental hypoperfusion and are common findings in placenta of pre-eclamptic pregnancies [ 7 ]. Microthrombi, fibrin deposition and occlusion of the placental spiral arteries can lead to placental infarcts.…”

Section: Discussionmentioning

confidence: 99%

COVID-19 as an independent risk factor for subclinical placental dysfunction

Jaiswal

Puri

Agarwal

et al. 2021

European Journal of Obstetrics & Gynecology and Reproductiv

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Background: The pandemic of the severe acute respiratory distress syndrome-associated Coronavirus-2 (SARS-CoV-2) has affected millions around the world. In pregnancy the dangers to the mother and fetus are still being explored. SARS-CoV2 can potentially compromise maternal and neonatal outcomes and this may be dependent on the pregnancy stage during which the infection occurs. Objective: The present study was done to find the histopathological alterations in the placenta of SARS-CoV-2 positive pregnancies with either no symptoms or mild coronavirus disease (COVID)-19 related symptoms and its association with neonatal outcomes. Study design: This was a prospective analytical study. Twenty seven asymptomatic or mildly symptomatic SARS-CoV-2 positive pregnant women with a singleton pregnancy delivered between 1 st July 2020 and 15 th September 2020, were included as cases. An equal number of SARS-CoV-2 negative singleton pregnancies matched for maternal and gestational age during the same period were included as controls. After delivery the histopathological examination of the placenta of these women was done and the findings recorded on a predesigned proforma based on the Amsterdam consensus criteria for evidence of maternal and fetal vascular malperfusion changes. Results: The baseline characteristics were comparable between the cases and controls. The following features of maternal vascular malperfusion (MVM) were significantly higher in the placentae of COVID-19 positive pregnancies: retroplacental hematomas (RPH), accelerated villous maturation (AVM), distal villous hyperplasia (DVH), atherosis, fibrinoid necrosis, mural hypertrophy of membrane arterioles (MHMA), vessel ectasia and persistence of intramural endovascular trophoblast (PIEVT). Fetal vascular malperfusion (FVM) significantly associated with the positive pregnancies were chorioangiosis, thrombosis of the fetal chorionic plate (TFCP), intramural fibrin deposition (IMFD) and vascular ectasia. Additionally, perivillous fibrin deposition was also significantly higher in the placentae of cases. The percentage of spontaneously delivered women was comparable in the two groups. The sex and weight of the newborn and the number of live births were comparable between the two groups. Conclusions: Asymptomatic or mildly symptomatic SARS-CoV-2 positive pregnant women, with otherwise uncomplicated pregnancies, show evidence of placental injury at a microscopic level. Similar findings have been demonstrated in other studies too. This placental injury apparently does not lead to poor pregnancy outcomes. The extent of this injury in symptomatic cases of COVID-19 pregnancies and its consequences on the outcomes need to be analysed.

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Prenatal Diagnosis of a Placental Infarction Hematoma Associated with Fetal Growth Restriction, Preeclampsia and Fetal Death: Clinicopathological Correlation

Cited by 26 publications

References 63 publications

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

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

The prediction of fetal death with a simple maternal blood test at 24-28 weeks: a role for angiogenic index-1 (PlGF/sVEGFR-1 ratio)

COVID-19 as an independent risk factor for subclinical placental dysfunction

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