Observer reliability in assessing placental maturity by histology.

Khong, T. Yee; Staples, Alan; Bendon, Robert W.; Chambers, Helen; Gould, Stephen J.; Knowles, S. H.; Shen‐Schwarz, Susan

doi:10.1136/jcp.48.5.420

Cited by 44 publications

(26 citation statements)

References 9 publications

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“…However, a second indicator of MV, villous infarction, was not increased. Estimation of villous maturation is highly variable among pathologists so different thresholds for diagnosis might explain the discrepancy [27]. Alternatively, our inclusion of both advanced villous maturation and villous infarction in the MV category may account for this apparent disagreement.…”

Section: Discussionmentioning

confidence: 75%

Placental Lesions Associated with Abnormal Growth in Twins

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Shah

Sakar

et al. 2001

Pediatric and Developmental Pathology

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Abnormal growth in one or both twins may contribute to the increased morbidity and mortality observed in twin gestation. Our objective in this retrospective study of all twin pregnancies delivered at our hospital (n = 240) over a 2-year period was to study the relationship between placental lesions and abnormal growth. Standardized placental examinations were performed in 192 cases (80%), which constituted the study population. Two growth abnormalities were studied: discordant growth as defined by > 15% difference in birth weight and small-for-gestational-age (SGA) birth as defined by birth weight less-than the 10th percentile for gestational age. The majority of twin pregnancies with either discordant growth (41/57 cases) or SGA birth (26/35 cases) had dichorionic placentas. In monochorionic placentas studied by injection there was no significant relationship between vascular anastomoses and discordant growth. Placental weight for small discordant and SGA twins was equivalent or increased relative to infant weight, a pattern not suggestive of maternal vascular underperfusion. Eight lesions, five considered to represent chronic placental disease and three considered to represent intrauterine adaptation, were studied as possible predictors of abnormal growth. The overall prevalence of these lesions in twin placentas was less than that seen in singleton births. Concordance between twin placentas for most lesions was higher than would be expected, based on their prevalence in singleton placentas. Two lesions were associated with discordant growth in both univariate and multivariate analyses: peripheral cord insertion (OR 3.6, 95% CI 1.7-7.6) and avascular villi (AV; OR 3.2, 95% CI 1.0-10.3). Three placental lesions were associated with SGA infants at the univariate level: peripheral cord insertion, avascular villi, and maternal vascular underperfusion. Only peripheral cord insertion (OR 9.8, 95% CI 4.1-23.4) and AV (OR 3.7, CI 1.0-13.7) were significant in the multivariate analysis. The relative increase in peripheral cord insertion and AV with abnormal growth was observed for both monochorionic and dichorionic placentas. Subgroups of discordant infants with and without SGA were both associated with peripheral cord insertion while only those with SGA had an increase in AV. Both peripheral cord insertion and AV were increased in the subgroup with SGA but no discordancy. In summary, two placental lesions, peripheral cord insertion indicating a spatially limited intrauterine compartment and AV indicating occlusion of fetal vessels in the placenta, were associated with abnormal growth in twins.

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Section: Discussionmentioning

confidence: 75%

Placental Lesions Associated with Abnormal Growth in Twins

Redline

Shah

Sakar

et al. 2001

Pediatric and Developmental Pathology

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“…It is therefore possible that the pathologic diagnosis of PVH may be biased the closer delivery is to 37 weeks. This potential bias has been studied by Khong et al [35] who have shown that the magnitude and direction of error when assessing placental maturity is actually less after 31 weeks gestation than earlier, with a relative underestimation of gestational age in later preterm deliveries [31]. Gestational age was tightly controlled in our case series [33] and the pathologist’s diagnosis was made while blinded to gestational age, which is important to reduce bias [31].…”

Section: Discussionmentioning

confidence: 92%

“…Our specific definition requiring that the PVH diagnosis be made only in preterm deliveries should make this study more reproducible, because pathologists can reliably distinguish mature term from preterm villous architecture [32]. This is important because although others have reported significant differences in placental villous architecture associated with PTB [25–30], the reproducibility of these associations has been questioned [31]. Our strict preterm definition, together with our evaluation for distal villous hypoplasia, and the strength of our tightly controlled multicenter trial, reinforces prior studies from the 1990s [20,27], suggesting that placental insufficiency may cause idiopathic PTB.…”

Section: Discussionmentioning

confidence: 99%

“…In contrast, severe early-onset IUGR shows a different histologic pattern, so-called distal villous hypomaturation [12,29], which is a developmental deficit in terminal villous differentiation [12]. Nonetheless, studies performed by specialized placental pathologists suggest the overall histologic impression of placental insufficiency is reproducible (kappa statistic 0.68) [29]; and, although pathologists may have difficulty precisely dating the gestational age of the placenta [31], they can reasonably agree on whether the placenta has preterm or term villous maturation (kappa statistic 0.58) [32]. …”

Section: Introductionmentioning

confidence: 99%

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Placental villous hypermaturation is associated with idiopathic preterm birth

Morgan¹,

Tolosa²,

Mele³

et al. 2012

The Journal of Maternal-Fetal & Neonatal Medicine

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Objective Pregnancy complications such as intra-amniotic infection, preeclampsia, and fetal intrauterine growth restriction (IUGR) account for most cases of preterm birth (PTB), but many spontaneous PTB cases do not have a clear etiology. We hypothesize that placental insufficiency may be a potential cause of idiopathic PTB. Methods Secondary analysis of 82 placental samples from women with PTB obtained from a multicenter trial of repeat versus single antenatal corticosteroids. Samples were centrally reviewed by a single placental pathologist masked to clinical outcomes. The histopathologic criterion for infection was the presence of acute chorioamnionitis defined as neutrophils marginating into the chorionic plate. Placental villous hypermaturation (PVH) was defined as a predominance of terminal villi (similar to term placenta) with extensive syncytial knotting. Idiopathic PTB comprised a group without another known etiology such as preeclampsia, IUGR or infection. Results Acute chorioamnionitis was observed in 33/82 (40%) cases. Other known causes of PTB were reported in 18/82 (22%). The remaining 31/82 (38%) were idiopathic. The frequency of PVH in idiopathic PTB (26/31=84%) was similar to cases with IUGR or preeclampsia (16/ 18=89%), but significantly more common than PVH in the group with acute chorioamnionitis (10/33=30%) (p<0.001). Conclusions PVH, which is a histologic marker of relative placental insufficiency, is a common finding in idiopathic PTB.

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“…AVM was more likely to occur after 34 weeks' gestation in our study, which raises the potential of false-positive gestational aging bias. However, Khong et al (39) found that the magnitude and direction of error when assessing placental maturity are actually less after 31 weeks' gestation, with a relative underestimation of gestational age rather than overestimation. Therefore, PTL may fall within a continuum of placental insufficiency phenotypes that also include some cases of preeclampsia and FGR.…”

Section: Placental Insufficiency and Ptlmentioning

confidence: 96%

Placental Insufficiency Is a Leading Cause of Preterm Labor

Morgan

2014

NeoReviews

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1. Intra-amniotic infection is an uncommon cause of preterm labor. 2. Placental insufficiency is a common human pregnancy complication, leading to the great obstetric syndromes: preeclampsia, fetal growth restriction, and preterm labor. AbstractPreterm labor is a multifactorial syndrome with a variety of risk factors. Intra-amniotic infection is one risk factor, but accumulating evidence suggests it is an uncommon cause of preterm labor. Instead, most cases of spontaneous preterm labor appear to be caused by placental insufficiency, similar to preeclampsia and fetal growth restriction. This review addresses the placental findings most commonly observed in preterm labor and discusses the prevalence of these features related to the gestational age at the time of delivery. The implications for clinical management and the long-term health of the infant may be profound.

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Observer reliability in assessing placental maturity by histology.

Cited by 44 publications

References 9 publications

Placental Lesions Associated with Abnormal Growth in Twins

Placental Lesions Associated with Abnormal Growth in Twins

Placental villous hypermaturation is associated with idiopathic preterm birth

Placental Insufficiency Is a Leading Cause of Preterm Labor

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