The Epidemiology of Placental Infarction at Term

doi:10.1053/plac.2001.0777

Placenta

Volume 23, Issue 4, April 2002, Pages 343-351

https://doi.org/10.1053/plac.2001.0777 Get rights and content

Abstract

The incidence and associations of placental infarction at term were investigated as part of a population based case-control study of small for gestational age (SGA) infants. 509 placentas from women delivering SGA infants (SGAP) and 529 placentas from women delivering infants with birthweights appropriate for gestational age (AGAP) were examined using fixed protocols for macroscopic identification and microscopic confirmation of infarction. Other information was obtained by maternal interview and from an obstetric database.

Infarcts were found in 17.3 per cent of SGAP and 11.7 per cent of AGAP. This difference was in placentas with multiple infarcts not involving the placental margin and was significant in multivariate analysis (OR 1.66; 95 per cent CI 1.12,2.47). Multivariate analysis showed significant associations between the presence of any infarct and maternal hypertension in both SGAP (OR=4.00; 95 per cent CI 1.96,8.16) and AGAP (OR 2.99; 95 per cent CI 1.23,7.32); maternal smoking, associated with a lesser risk in SGAP only (OR=0.31; 95 per cent CI 0.13,0.73); maternal age at first pregnancy in a linear relationship with AGAP only (beta co-efficient 0.09, P=0.0034); and between some ethnic groups. We conclude that at least five factors have independent associations with the incidence of placental infarction and these associations differ by site and age of infarcts.

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Cited by (44)

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Visualization of microbes by 16S in situ hybridization in term and preterm placentas without intraamniotic infection
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Citation Excerpt :
Given the absence of blood supply in such an infarct, it is tempting to speculate that hematogenously spread bacteria would find refuge from maternal leukocytes or other phagosomes in such locations. Minor focal vascular defects, including small infarcts, are common and considered normal in ordinary pregnancy81–83 but are more common in pregnancies affected by preeclampsia and fetal growth restriction. These observations are of interest given recent reports from other investigators that suggest metagenomic distinctions in placental communities occurs in cases of preeclampsia and fetal growth restriction, where infarcts of pathologic significance co-occur.43,84
Numerous reports have documented bacteria in the placental membranes and basal plate decidua in the absence of immunopathology using histologic techniques. Similarly, independent metagenomic characterizations have identified an altered taxonomic makeup in association with spontaneous preterm birth. Here we sought to corroborate these findings by localizing presumptive intact bacteria using molecular histology within the placental microanatomy.
Here we examined for microbes in term and preterm gestations using a signal-amplified 16S universal in situ hybridization probe set for bacterial rRNA, alongside traditional histologic methods of Warthin–Starry and Gram stains, as well as clinical culture methodologies. We further sought to differentiate accompanying 16S gene sequencing taxonomic profiles from germ-free (gnotobiotic) mouse and extraction and amplicon contamination controls.
Placentas were collected from a total of 53 subjects, composed of term labored (n = 4) and unlabored cesarean deliveries (n = 22) and preterm vaginal (n = 18) and cesarean deliveries (n = 8); a placenta from a single subject with clinical and histologic evident choriomanionitis was employed as a positive control (n = 1). The preterm cohort included spontaneous preterm birth with (n = 6) and without (n = 10) preterm premature rupture of membranes, as well as medically indicated preterm births (n = 10). Placental microbes were visualized using an in situ hybridization probe set designed against highly conserved regions of the bacterial 16S ribosome, which produces an amplified stable signal using branched DNA probes. Extracted bacterial nucleic acids from these same samples were subjected to 16S rRNA metagenomic sequencing (Illumina, V4) for course taxonomic analysis, alongside environmental and kit contaminant controls. A subset of unlabored, cesarean-delivered term pregnancies were also assessed with clinical culture for readily cultivatable pathogenic microbes.
Molecular in situ hybridization of bacterial rRNA enabled visualization and localization of low-abundance microbes after systematic high-power scanning. Despite the absence of clinical or histologic chorioamnionitis in 52 of 53 subjects, instances of 16S rRNA signal were confidently observed in 13 of 16 spontaneous preterm birth placentas, which was not significantly different from term unlabored cesarean specimens (18 of 22; P > .05). 16S rRNA signal was largely localized to the villous parenchyma and/or syncytiotrophoblast, and less commonly the chorion and the maternal intervillous space. In all term and unlabored cesarean deliveries, visualization of evident placental microbes by in situ hybridization occurred in the absence of clinical or histologic detection using conventional clinical cultivation, hematoxylin–eosin, and Gram staining. In 1 subject, appreciable villous bacteria localized to an infarction, where 16S microbial detection was confirmed by Warthin–Starry stain. In all instances, parallel sample principle coordinate analysis using Bray-Cutis distances of 16S rRNA gene sequencing data demonstrated consistent taxonomic distinction from all negative or potential contamination controls (P = .024, PERMANOVA). Classification from contaminant filtered data identified a distinct taxonomic makeup among term and preterm cohorts when compared with contaminant controls (false discovery rate <0.05).
Presumptively intact placental microbes are visualized as low-abundance, low-biomass and sparse populations within the placenta regardless of gestational age and mode of delivery. Their taxonomic makeup is distinct from contamination controls. These findings further support several previously published findings, including our own, which have used metagenomics to characterize low-abundance and low-biomass microbial communities in the placenta.
The effect of air pollutants on birth weight in medium-sized towns in the state of São Paulo
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Verificar o efeito da poluição do ar sobre o peso ao nascer numa cidade de médio porte paulista.
Estudo transversal, com dados relativos a todos os nascidos vivos de mães residentes no Município de São José dos Campos nos anos de 2005 a 2009. Foram obtidos dados do Departamento de Informações e Informática do Sistema Único de Saúde. Os dados dos poluentes do ar (PM, SO e O), as médias diárias de suas concentrações, foram fornecidos pela Companhia de Tecnologia de Saneamento Ambiental. Aplicou‐se a regressão linear e a logística para a análise dos dados, realizadas nos programas Excel e STATA v.7.
A exposição materna aos poluentes do ar não se associou ao nascimento de crianças com baixo peso, com exceção do SO no último mês de gestação (OR = 1,25; IC95% 1,00‐1,56). Além disso, a exposição materna ao PM e SO no último mês levou à diminuição do peso ao nascer (0,28g e 3,15g, respectivamente) para cada 1mcg/m³ de aumento da concentração desses poluentes, porém sem significância estatística.
Este estudo não permitiu identificar associação estatística entre os níveis de concentração dos poluentes atmosféricos e o peso ao nascer, com exceção da exposição SO no último mês de gestação.
To investigate the effect of air pollution on birth weight in a medium‐sized town in the State of São Paulo, Southeast Brazil.
Cross‐sectional study using data of live births to mothers residing in São José dos Campos from 2005 to 2009. Data was obtained from the Department of Information
and Computing of the Brazilian Unified Health System. Air pollutant data (PM, SO and O) and daily averages of their concentrations were obtained from the Environmental Sanitation & Technology Company. Statistical analysis was performed by linear and logistic regressions using the Excel and STATA v.7 software programs.
Maternal exposure to air pollutants was not associated with low birth weight, with the exception of exposure to SO within the last month of pregnancy (OR = 1,25; IC95% 1,00‐1,56). Maternal exposure to PM
and SO during the last month of pregnancy led to lower weight at birth (0.28 g and 3.15 g, respectively) for each 1mg/m³ increase in the concentration of these pollutants, but without statistical significance.
This study failed to identify a statistically significant association between the levels of air pollutants and birth weight, with the exception of exposure to SO within the last month of pregnancy.
Placental pathology in early intrauterine growth restriction associated with maternal hypertension
2014, Placenta
Citation Excerpt :
Both early IUGR and maternal hypertensive disease, in particular early-onset preeclampsia, are characterized by placental pathology associated with hypoxia and reperfusion damage caused by impaired remodeling and/or obstruction of the spiral arteries [3,5]. Common lesions include infarction [7], inflammation [8,9] and lesions consistent with chronic ischemia [9,10]. Maternal hypertensive disease and/or Doppler abnormalities may coincide with early IUGR, and both are associated with poorer perinatal outcome [11,12].
To identify key pathological characteristics of placentas from pregnancies complicated by early intrauterine growth restriction, and to examine their relations with maternal hypertensive disease and umbilical artery Doppler waveform abnormalities.
Single-center retrospective cohort study of singleton pregnancies with abnormal umbilical artery Doppler flow patterns resulting in a live birth <34 weeks of a baby with a weight <10th percentile for gestational age. Umbilical artery end diastolic flow was classified as being either present or absent/reversed (AREDF). Data were stratified into intrauterine growth restriction with or without hypertensive disease and pathological characteristics were compared between these various conditions according to predefined scoring criteria.
Among 164 placentas studied, we found high rates of characteristic histopathological features that were associated with intrauterine growth restriction, including infarction (>5% in 42%), chronic villitis (21%), chronic chorioamnionitis (36%), membrane necrosis (20%), elevated nucleated red blood cells (89%), increased syncytial knotting (93%), increased villous maturation (98%), fetal thrombosis (32%) and distal villous hypoplasia (35%). Chronic inflammation of fetal membranes and syncytial knotting were more common in women with concomitant hypertensive disease as compared to women with normotensive IUGR (p < 0.05). Placentas from women with umbilical artery AREDF were more likely to show increased numbers of nucleated red blood cells and distal villous hypoplasia (p < 0.05).
Placentas of women with early IUGR show high rates of several histological aberrations. Further, concomitant maternal hypertension is associated with characteristic inflammatory changes and umbilical artery AREDF with signs of chronic hypoxia.
The effect of smoking on early chorionic villous vascularisation
2012, Placenta
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Increased villous vascular branching in smokers was reported in one study using scanning electron microscopy on the casts of the capillaries [30], but two other conventional stereological studies reported similar branching degree between smokers and non-smokers [11,13]. The incidence of placental infarction reported is controversial as well, in various studies it is reported to be decreased, similar or increased [10,34,35]. However, most studies have found that the intermediate and terminal villous vascular density is decreased in placentas of smokers as compared with non-smokers [10,11,13].
The aim of the study was to investigate whether first trimester chorionic villous vascularisation is different in women who smoked cigarettes before and during pregnancy in comparison with women who did not smoke.
Placentas of smoking (>10 cigarettes/day, n = 13) and non-smoking women (n = 13), scheduled for a legal termination of a viable first trimester pregnancy for social indications, were retrieved. Placental tissues of 3–5 mm³ were whole mount CD31 immunofluorescence stained. Images of the CD31 immunofluorescence and contour of the villi were captured using an Optical Projection Tomography scanner. An immersive BARCO virtual reality system was used to create an enlarged interactive 3-dimensional hologram of the reconstructed images. Automatic volume measurements were performed using a flexible and robust segmentation algorithm that is based on a region-growing approach in combination with a neighbourhood variation threshold. The villous volume, vascular volume and vascular density were measured for the total chorionic villous tree as well as for its central and peripheral parts. No differences in maternal age and gestational age were found between non-smoking and smoking women. No differences were found in the total, central and peripheral villous tree volume and vascular volume. The central (13.4% vs. 9.5%, p=0.03) and peripheral (8.4% vs. 6.4%, p=0.02) villous tree vascular densities were increased in the smoking women as compared with the non-smoking women.
In conclusion, chorionic villous vascularisation is already altered in first trimester of pregnancy in women who smoked cigarettes before and during pregnancy.
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^f1: To whom correspondence should be addressed at: Department of Paediatrics, University of Auckland, Private Bag 92019, Auckland, New Zealand. Tel: (64) 9-373-7599, ext 6433; Fax: (64) 9-373-7486. E-mail: [email protected]

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