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To determine the effect of 3 distinct comparison groups on associations between placental abnormalities and neonatal hypoxic-ischemic encephalopathy (HIE).This single-center, prospective case-control study of singletons of gestational age ≥36 weeks with predefined criteria for HIE (n = 30) and 3 control groups was conducted from June 2015 to January 2018. The control groups were infants born by repeat cesarean delivery (n = 60), infants born small for gestational age (SGA; n = 80), and infants receiving positive-pressure ventilation (PPV) at birth (n = 70). One pathologist blinded to infant category reviewed placental sections using the Amsterdam Placental Workshop criteria. Logistic regression with group contrasts relative to HIE was used to analyze primary placental pathologies, and ORs with 95% CIs provided effect sizes.The odds of maternal vascular malperfusion were increased among HIE group placentas compared with placentas of the repeat cesarean delivery (OR, 4.50; 95% CI, 1.45-14.00) and PPV (3.88; 1.35-11.16) groups, but not those of the SGA group. The odds of fetal vascular malperfusion were increased in the HIE group compared with the SGA group (OR, 9.75; 95% CI, 1.85-51.51). The odds of acute chorioamnionitis were higher in the HIE group compared only with the repeat cesarean delivery group, reflecting a similar incidence of chorioamnionitis in SGA group and PPV group placentas. The absence of placental findings was lowest in the HIE group (6.7%), followed by the SGA (18.8%), PPV (31.4%), and repeat cesarean delivery (75%) groups.Associations with placental abnormalities among infants with HIE varied based on the specific placental abnormality and the control group. Potentially important associations between placental pathology and HIE may be obscured if control groups are not well designed.

Congenital heart disease (CHD) remains the most common birth defect in infants, and critical CHD is associated with significant rates of morbidity and mortality. With the advent of powerful yet noninvasive advanced fetal imaging, it is becoming increasingly evident that the presence of CHD in utero disrupts typical development and contributes to the lifelong morbidity in this population. Across healthy and high-risk populations, intrauterine influences can permanently alter fetal development that may manifest in complex morbidities later in life, the so-called fetal-onset-of-adult-disease (FOAD) phenomenon. The placenta plays a critical role in not only supporting fetal development, but also by adapting to specific intrauterine conditions. The role of placental health, adaptation and dysfunction, however, in CHD is not well understood. In this article, we will review current evidence relating placental health in CHD, appraise existing knowledge-gaps in the field and highlight promising new avenues to better understand the impact of placental function on fetal well-being. We will review evidence of ex vivo human placental studies that describe abnormal placental findings in pregnancies complicated by CHD, as well evidence for in vivo assessments of the human placenta. While overall clinical in vivo assessments of placental development are rather limited, we will also review emerging evidence from advanced quantitative and functional magnetic resonance imaging that are bringing new insights into placental structure and function throughout gestation. By providing novel information about placental development, we can now explore the maternal-fetal-placental connection in greater detail, and better understand the multi-factorial mechanisms that may contribute to adverse outcomes seen in survivors of CHD.

Placental severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is associated with a specific histiocytic intervillositis. Placental fibrin depositions can decrease the maternal-fetal interface causing fetal distress. Coronavirus disease 2019-related placental inflammation can lead to SARS-CoV-2-associated pediatric inflammatory multisystem syndrome., Background In general, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection during pregnancy is not considered to be an increased risk for severe maternal outcomes but has been associated with an increased risk for fetal distress. Maternal-fetal transmission of SARS-CoV-2 was initially deemed uncertain; however, recently a few cases of vertical transmission have been reported. The intrauterine mechanisms, besides direct vertical transmission, leading to the perinatal adverse outcomes are not well understood. Methods Multiple maternal, placental, and neonatal swabs were collected for the detection of SARS-CoV-2 using real-time quantitative polymerase chain reaction (RT-qPCR). Serology of immunoglobulins against SARS-CoV-2 was tested in maternal, umbilical cord, and neonatal blood. Placental examination included immunohistochemical investigation against SARS-CoV-2 antigen expression, with SARS-CoV-2 ribonucleic acid (RNA) in situ hybridization and transmission electron microscopy. Results RT-qPCRs of the oropharynx, maternal blood, vagina, placenta, and urine were all positive over a period of 6 days, while breast milk, feces, and all neonatal samples tested negative. Placental findings showed the presence of SARS-CoV-2 particles with generalized inflammation characterized by histiocytic intervillositis with diffuse perivillous fibrin depositions with damage to the syncytiotrophoblasts. Conclusions Placental infection by SARS-CoV-2 leads to fibrin depositions hampering fetal-maternal gas exchange with resulting fetal distress necessitating a premature emergency cesarean section. Postpartum, the neonate showed a fetal or pediatric inflammatory multisystem-like syndrome with coronary artery ectasia temporarily associated with SARS-CoV-2 for which admittance and care on the neonatal intensive care unit (NICU) were required, despite being negative for SARS-CoV-2. This highlights the need for awareness of adverse fetal and neonatal outcomes during the current coronavirus disease 2019 pandemic, especially considering that the majority of pregnant women appear asymptomatic.

Aim On December 31, 2019, an unknown outbreak of pulmonary disease was reported in China. The novel coronavirus SARS‐CoV‐2 was the etiologic agent of this disease, and responsible of the current pandemic of COVID‐19. Accumulated evidence on placental features is based most on case‐reports and small case‐series, with differing results. Methods We gathered a cohort of 29 infected pregnant mothers who delivered 32 newborns, and had placentas available for pathologic examination. Placentas were compared with a control group. Results Of the 29 mothers, clinical and radiological features were similar to what was already described in COVID‐19. Pregnancy modified some analytical parameters. One of the mothers succumbed to the disease. Of the 32 newborns, 1 developed an early infection, with positive reverse‐transcriptase polymerase chain reaction (RT‐PCR) at 48 h of life, with an initial RT‐PCR negative. SARS‐CoV‐2 presence was assessed on placental tissue with immunohistochemistry and RT‐PCR, both were negative. All newborns had good clinical outcomes. No differences in morphological placental findings were found among both groups. Conclusion Lack of statistically significant differences among case and control groups suggest that placentas from SARS‐CoV‐2 infected mothers represent a cohort of normal placentas only submitted because of maternal SARS‐CoV‐2 status. To the best of our knowledge, no irrefutable cases of vertical transmission have been yet described. Other authors have failed to demonstrate presence of viral RNA in placental tissue. Accumulated knowledge suggests that if vertical transmission is possible, it is a rare event.

Fetal hypoxic events with unclear predictive value are a common indication for placenta examination. We evaluated whether the use of CD15 immunostaining can improve the assessment of severity and duration of fetal hypoxia.We compared placentas (37-42 gestational weeks) from stillborns/newborns with birth asphyxia (BA) and non-hypoxic newborns. Placental findings were studied in following groups: (1) acute BA (n = 11) due to placental abruption, (2) non-acute BA (n = 121) due to non-acute conditions, (3) non-BA (n = 46) in pregnancies with preeclampsia and gestational diabetes, and (4) controls (n = 30).A high expression of CD15 in feto-placental resistance vessels (FRVs) was present in non-acute BA (95.9%), but absent in acute BA, non-BA and controls (p 0.0001). Furthermore, we found no causal relationship of high expression of CD15 in FRVs to coexisting placental conditions, including severity and mechanisms/patterns of placental injury, fetal erythroblastosis, and maternal conditions. According to a multivariate analysis, only a high expression of CD15 in FRVs was independently associated with severe non-acute fetal hypoxia ([OR] = 15.52; 95% [CI] = 5.92-40.67).We have defined a characteristic pattern of CD15 expression in FRVs that allows to interpret various clinical/placental conditions with respect to fetal hypoxia, with an improved predictability compared to conventional analyses. This approach represents a novel diagnostic strategy for placenta examination, which could indirectly assess severity and duration of intrauterine hypoxia in a heterogeneous population of newborns.

Histological chorioamnionitis (HC) is a common placental finding that represents acute/chronic inflammation and can affect neonatal outcomes. We aimed to examine the effect of HC on neonatal outcomes in pregnancies complicated by preeclampsia. All pregnancies with the diagnosis of preeclampsia at 24–42 weeks between 2008 and 2019 were reviewed. Placental lesions were classified according to the “Amsterdam” criteria. Composite adverse neonatal outcome included ≥1 early complication. Maternal and neonatal outcomes were compared between cases with and without HC. Multivariable regression analysis was performed to identify independent associations with adverse neonatal outcome. Compared to preeclampsia without HC (n=517), preeclampsia with HC (n=55) was characterized by a more advanced gestational age (p

Placental metastasis of maternal neoplasms is well documented in solid tumors, unlike hematologic neoplasms. We reviewed placental findings from deliveries complicated by maternal hematologic neoplasms exploring the prevalence and patterns of placental transmission and insufficiency. In the 8-yr study period, 11 cases were analyzed. Acute myeloid leukemia was the most common diagnosis (4/11, 36%). Seven cases (63%) showed no evidence of placental spread of neoplasm, while four cases (36%) showed placental spread, restricted to the maternal compartment. Maternal vascular malperfusion was documented in 8/11 (72%) cases. Neonatal follow up was available in 10 cases, all children were alive and well.

Cytomegalovirus (CMV) infection is one of the most common congenital viral infections. Classically associated placental findings include chronic villitis with plasma cells, stromal hemosiderin deposition, and identification of viral inclusions in villous endothelial and stromal cells. We present a case of confirmed congenital CMV infection that lacked these classical findings, but demonstrated massive perivillous fibrin deposition (MPVFD). This is the first report of CMV associated with MPVFD. MPVFD is an uncommon placental lesion associated with adverse fetal outcomes and a high risk of recurrence. However, the recurrence risk in patients with an infectious cause may be lower in than patients with other associated clinical conditions.

Objective To assess whether pre-eclampsia (PE)-related placental/extraplacental membrane findings are linked to moderately elevated blood pressure (BP) in pregnancy and later-life hypertension. Design Prospective cohort. Setting 52 prenatal clinics, 5 Michigan communities. Sample The POUCH Study recruited women at 16-27 weeks' gestation (1998-2004) and studied a sub-cohort in depth. This sample (n = 490) includes sub-cohort women with detailed placental assessments and cardiovascular health evaluations 7-15 years later in the POUCHmoms follow-up study. Methods PE-related placental/extraplacental membrane findings (i.e. mural hyperplasia, unaltered/abnormal vessels or atherosis in decidua; infarcts) were evaluated in relation to pregnancy BP and odds of Stage 2 hypertension at follow up using weighted polytomous regression. Follow-up hypertension odds also were compared in three pregnancy BP groups: normotensives (referent) and moderately elevated BP with or without PE-related placental/extraplacental membrane findings. Main outcome measures Stage 2 hypertension (SBP ≥140 mmHg and/or DBP ≥90 mmHg, or using antihypertensive medications) at follow up. Results After excluding women with pregnancy hypertension (i.e. chronic, PE, gestational), mural hyperplasia and unaltered/abnormal decidual vessels were each associated with Stage 2 hypertension at follow up: adjusted odds ratio (aOR) = 2.7, 95% CI 1.1-6.6, and aOR = 1.7 (95% CI 0.8-3.4), respectively. Women with moderately elevated BP in pregnancy and evidence of mural hyperplasia or unaltered/abnormal decidual vessels had greater odds of Stage 2 hypertension at follow up: aOR = 4.5 (95% CI 1.6-12.5 and aOR = 2.6, 95% CI 1.1-5.9, respectively. Conclusions PE-related placental/extraplacental membrane findings help risk-stratify women with moderately elevated BP in pregnancy for later development of hypertension. Tweetable abstract Placental findings associated with mother's risk of later-life hypertension.

Objective The aim of the current review is to present a systematic evaluation of reported human placental findings in cases of zika virus (ZIKV) infection. Data sources We reviewed the EMBASE, PUBMED, and SCIELO databases until June 2019, without language restrictions. Selection of studies The search terms placenta AND zika virus were used. The inclusion criteria of the studies were studies that reported placental findings in humans. Experimental studies, reviews, notes or editorials were excluded. A total of 436 studies were retrieved; after duplicate exclusion, 243 articles had their titles screened, and 128 had their abstract read; of those, 32 were included in the final analysis (18 case reports, 10 case series, and 4 cohorts) Data collection We collected data concerning the author, year of publication, study design, number of participants, number of placental samples, onset of symptoms, perinatal outcomes, and main findings on histological analysis. Data synthesis The placental pathologic findings were described as mild and nonspecific, similar to those of other placental infections, including chronic placentitis, chronic villitis, increased Hofbauer cells, irregular fibrin deposits, increased mononuclear cells in the villus stroma, villous immaturity, edema, hypervascularization, stromal fibrosis, calcification, and focal necrosis of syncytiotrophoblasts. Conclusion Zika infection presents unspecific placental findings, similar to other infections in the toxoplasmosis, other agents, rubella, cytomegalovirus, and herpes (TORCH)group. Characterizing and standardizing placental findings after zika virus infection is key to understanding the mechanisms of congenital diseases. Resumo Objetivo O objetivo desta revisão é apresentar uma avaliação sistemática dos achados relacionados à infecção por zika vírus (ZIKV) na placenta humana. Fontes de dados As bases de dados EMBASE, PUBMED, e SCIELO foram pesquisadas, até junho de 2019, sem qualquer restrição de língua. Seleção dos estudos Os termos placenta E zika virus foram utilizados na busca. Foram incluídos estudos que reportassem achados placentários de infecção em seres humanos, enquanto estudos experimentais, revisões, notas e editoriais foram excluídos. Um total de 436 estudos foram identificados, e 243 tiveram seus títulos lidos após a exclusão de duplicatas. Cento e vinte e oito artigos tiveram seus resumos avaliados, dos quais 32 foram incluídos na análise final (18 relatos de caso, 10 séries de casos, e 4 estudos de coorte). Dados obtidos Foram pesquisados dados relativos ao autor, ano da publicação, desenho do estudo, número de participantes, número de amostras de placenta, início dos sintomas, desfechos perinatais, e principais achados histológicos. Síntese dos dados Os principais achados placentários descritos foram leves e inespecíficos, similares a outras infecções placentárias, incluindo infecção placentária crônica, vilosite crônica, aumento das células de Hofbauer, depósitos irregulares de fibrina, aumento das células mononucleares no estroma viloso, imaturidade vilosa, edema, hipervascularização, fibrose estromal, calcificação, e necrose focal dos sincicitrofoblastos. Conclusão Infecções por ZIKV têm achados placentários inespecíficos, similares aos de outras infecções do grupo toxoplasmose, rubéola, citomegalovírus e herpes (TORCH). Caracterizar e padronizar os achados placentários após infecção por ZIKV é fundamental para entender o mecanismo das infecções congênitas.

What are the clinical characteristics of pregnancies complicated by fetal growth restriction (FGR) and preeclampsia in patients who have undergone IVF, and what is the correlation between these complications and histopathological placental findings in such pregnancies.A retrospective cohort of patients who had delivered their babies at our institution who had been diagnosed with preeclampsia, whose babies had been diagnosed with FGR, or both. Deliveries in which the placenta was sent for histopathological examination were included. Computerized files and pathological reports were reviewed, and maternal, obstetric, neonatal outcomes and placental histopathological reports were compared between pregnancies conceived by IVF and controls. Placental lesions were classified according to the Amsterdam criteria.Between December 2008 and December 2018, the placentas of 1114 singleton babies who had received a diagnosis of FGR, whose mothers had received a diagnosis of preeclampisa, or both, were examined. A total of 105 patients conceived with IVF and 1009 were conceived spontaneously. The IVF group was older, of lower parity and had a higher rate of diabetes and chronic hypertension. Deliveries occurred at an earlier gestational age, although birth weight was not significantly different between the groups. The rate of neonatal adverse composite outcome among IVF deliveries was significantly lower (59.0% versus 76.7%; P0.001). On placental examination, placental weight, maternal and fetal vascular malperfusion lesions were similar between the groups, whereas villitis of unknown etiology was significantly more common among the IVF group (16.2% versus 8.3%; P = 0.007).Neonatal outcome is relatively favourable in IVF patients with placental-related diseases. Placental chronic villitis is more common in IVF patients, pointing to an additive immunological cause.

Background: The cause of meconium passage in utero is controversial, traditionally being considered evidence of fetal stress and hypoxia, and also associated with intra-amniotic inflammation/infect...

Introduction: The placenta is infrequently examined in developing countries. This study examined the role of placental pathology in perinatal deaths at Chulalongkorn University Hospital, Bangkok. M...

Indications for placental submission are variable. Established guidelines are largely based on expert opinion, and there is a need for more evidence-based criteria. A 10-year database of term placentas was used to evaluate indications significantly associated with placental pathology. Lesions in 5 categories were separated into high- and low-grade subgroups. Two additional high-grade lesions were also evaluated. Indications associated with high-grade placental lesions were chronic monitoring abnormalities, severe preeclampsia, pregestational diabetes, maternal signs of infection, postdates pregnancy, artificial reproductive technology, drug abuse, umbilical cord entanglements, selected gross placental abnormalities, stillbirth, Apgar 5 minutes

Objectives Although neonates with moderate to severe hypoxic ischemic encephalopathy (HIE) receive therapeutic hypothermia (TH), 40–50% die or have significant neurological disability. The aim of this study is to analyse the association of placental pathology and neurodevelopmental outcome in cooled neonates with HIE at 18–24 months of age. Methods Retrospective analysis of prospectively collected data on 120 neonates registered in the Swiss National Asphyxia and Cooling Register born between 2007 and 2017. This descriptive study examines the frequency and range of pathologic findings in placentas of neonates with HIE. Placenta pathology was available of 69/120 neonates, whose results are summarized as placental findings. As neonates with HIE staged Sarnat score 1 (21/69) did not routinely undergo follow-up assessments and of six neonates staged Sarnat Score 2/3 no follow-up assessments were available, 42/48 (88%) neonates remain to assess the association between placental findings and outcome. Results Of the 42/48 (88%) neonates with available follow up 29% (12/42) neonates died. Major placenta abnormalities occurred in 48% (20/42). Major placenta abnormality was neither associated with outcome at 18–24 months of age (OR 1.75 [95% CI 0.50–6.36, p=0.381]), nor with death by 2 years of age (OR 1.96 [95% CI 0.53–7.78, p=0.320]). Conclusions In this study cohort there could not be shown an association between the placenta findings and the neurodevelopmental outcome at 18–24 months of age.

Publisher Summary This chapter focuses on the placenta of red panda. The placentas of red panda have a discoid shape and are quite unlike the completely zonary placenta of raccoons, dogs, and cats. The umbilical cord of red panda afterbirth measures 3.5 cm in length and is only slightly spiralled. The umbilical cord contains two arteries, a vein, and a large allantoic duct. Similar to the cord of raccoon placentas, it contains no omphalomesenteric duct. There are numerous small and capillary blood vessels that are remarkably concentrated around the allantoic duct; some of these smaller vessels had a considerable amount of musculature as is true of many other species, e.g., the dolphin. The allantoic duct is also accompanied by many bundles of smooth muscle; its lining is of urothelial nature. A thin amnion covers the umbilical cord and, in the free amnionic membranes, it is for the most part composed of a thin layer of squamous epithelium on loose connective tissue. The placenta of raccoons falls into the general arrangement of other carnivore placentas, but the placenta of the red panda is found to be quite different from other related canines. The filiform arrangement of villi, for instance, is lacking and the placenta does not have the ring-shaped, zonary form as is seen in numerous other carnivore species. It is rather discoid with a small central sulcus connecting the villous tissue to as trip of membranes perhaps this is the remnant of a former zonary type. The placental findings discussion indicates that there are great similarities between the Ailurus placenta and those of the Mustelidae.

Background & Methods : This is a forthcoming kind of study and establishes the clinicopathological relationship of strange placental discoveries with pregnancy related maternal morbidities and related fetal result altogether preterm and full term pregnancies. Placentae from 80 conveyances of preterm and full term incubation were gathered from work room. Result: The majority of cases (51.30%) in our study displayed low birth weight. Amongst the LBW neonates 35.50% of babies are associated with preterm deliveries and 14.47% were associated with full term pregnancy. Amongst the neonates with normal birth weight, 3.94% were associated with preterm labour and 46.05% were full term. There was no significant association between length of cord and period of gestation. The majority of cases showed eccentric attachment of cord with only 2.50% of preterm cases showing battledore insertion. Study Designed: Observational Study. Conclusion: The gross features of placenta varies significantly with period of gestation. Parameters such as weight, size, number of cotyledons and thickness of placenta decreases in preterm labour. The microscopic lesions observed in decreasing order of frequency were perivillous fibrin deposition (62.50%) followed by chorioamnionitis (26.25%), infarct (21.25%) and calcification (17.50%). Other pathological lesions includes villous oedema (12.50%) and retro placental hematoma (2.50%). All the histomorphological changes were conspicuous in preterm pregnancies. To prevent the maternal and child morbidity and mortality the community based health education, care for prevention of anaemia and personal hygiene must be promoted more vigorously in rural areas of our country. Keywords: placental, maternal, morbidities & pregnancies.

Preeclampsia (PE) is a pregnancy complication associated with increased maternal and perinatal morbidity and mortality. The disease presents with recent onset hypertension (after 20 weeks of gestation) and proteinuria, and can progress to multiple organ dysfunction, with worse outcomes among early onset preeclampsia (EOP) cases (34 weeks). The placenta is considered the root cause of PE; it represents the interface between the mother and the fetus, and acts as a macromembrane between the two circulations, due to its villous and vascular structures. Therefore, in pathological conditions, macroscopic and microscopic evaluation can provide clinically useful information that can confirm diagnosis and enlighten about outcomes and future therapeutic benefit. To perform an integrative review of the literature on pathological placental findings associated to preeclampsia (comparing EOP and late onset preeclampsia [LOP]) and its impacts on clinical manifestations. Cases of EOP presented worse maternal and perinatal outcomes, and pathophysiological and anatomopathological findings were different between EOP and LOP placentas, with less placental perfusion, greater placental pathological changes with less villous volume (villous hypoplasia), greater amount of trophoblastic debris, syncytial nodules, microcalcification, villous infarcts, decidual arteriolopathy in EOP placentas when compared with LOP placentas. Clinically, the use of low doses of aspirin has been shown to be effective in preventing PE, as well as magnesium sulfate in preventing seizures in cases of severe features. The anatomopathological characteristics between EOP and LOP are significantly different, with large morphological changes in cases of EOP, such as hypoxia, villous infarctions, and hypoplasia, among others, most likely as an attempt to ascertain adequate blood flow to the fetus. Therefore, a better understanding of the basic macroscopic examination and histological patterns of the injury is important to help justify outcomes and to determine cases more prone to recurrence and long-term consequences.INTRODUçãO: A pré-eclâmpsia (PE) é uma complicação da gravidez associada ao aumento da morbidade e mortalidade materna e perinatal. A doença se apresenta com hipertensão de início recente (após 20 semanas de gestação) e proteinúria, que pode progredir para disfunção de múltiplos órgãos, com resultados piores entre os casos de início precoce (34 semanas). A placenta é considerada a principal causa da PE, representando a interface entre a mãe e o feto, e atuando como uma macromembrana entre as duas circulações, devido às suas estruturas vilosas e vasculares, de modo que, em condições patológicas, avaliações macroscópicas e microscópicas podem fornecer informações clinicamente úteis, que podem fornecer diagnóstico, prognóstico e benefício terapêutico. OBJETIVO: Realizar uma revisão integrativa da literatura para compreender e descrever os achados placentários patológicos associados à pré-eclâmpsia e seus impactos nas manifestações clínicas. RESULTADOS: Os casos de início precoce apresentaram piores desfechos maternos e perinatais, e os achados fisiopatológicos e anatomopatológicos foram diferentes entre as placentas de início precoce e início tardio, com menor perfusão placentária, maiores alterações patológicas placentárias com menor volume viloso (hipoplasia vilosa), maior quantidade de debris trofoblásticos, nódulos sinciciais, microcalcificação, infartos vilosos, arteriolopatia decidual em placentas de início precoce quando comparadas com placentas de início tardio. Clinicamente, o uso de baixas doses de aspirina tem se mostrado significativo na prevenção da PE, assim como o sulfato de magnésio na prevenção de convulsões na doença com manifestações de gravidade. CONCLUSãO: As características anatomopatológicas entre a pré-eclâmpsia precoce e tardia são significativamente diferentes, com grandes alterações morfológicas nos casos de início precoce, como hipóxia, infartos vilosos e hipoplasia, entre outros, na tentativa de estabilizar o fluxo sanguíneo para o feto. Portanto, um entendimento comum do exame macroscópico básico e dos padrões histológicos da lesão é importante para maximizar o benefício diagnóstico, prognóstico e terapêutico do exame da placenta e, consequentemente, reduzir os riscos para a mãe e o feto.

AIM Diabetes mellitus (DM) is a major complication in pregnancy. Placental lesions with DM remain unclear and controversial. Recently, the terms of placental pathological findings, such as maternal and fetal vascular malperfusions (MVM and FVM, respectively) were introduced by the Amsterdam Placental Workshop Group Consensus Statement (APWGCS). FVM cases were classified as the partial obstruction type (global FVM) and the complete obstruction type (segmental FVM). The aim of this study was to clarify the pathological characteristics of the placenta with pregestational DM/gestational DM; GDM according to APWGCS. METHODS We studied the placentas of 182 DM women (27 pregestational DM and 155 GDM) and control placentas of 460 women without DM during 2011-2018. We excluded cases of intrauterine fetal death or multiple pregnancies. We reviewed microscopical findings including, MVM, FVM, chorioamnionitis with the slides according to the APWGCS. RESULTS Microscopically, the incidence of FVM was significantly higher in GDM patients than control (17% vs. 10%, p = 0.0138), but not significant in pregestational DM (11%, p = 0.7410). Segmental FVM (complete obstruction) was significantly more observed in GDM than control group (5% vs. 0.4%, p = 0.0013). Segmental FVM in GDM showed high incidence of light-for-dates infant (three of seven cases, 43%, p = 0.0288). In addition, several segmental FVM findings (villous stromal-vascular karyorrhexis and stem vessel occlusion) were frequently noted in 2 or 3 points positive of 75 g oral glucose tolerance test than 1 point positive GDM. CONCLUSION Our placental findings suggest disorder of carbohydrate metabolism might affect the fetal vascular damage, especially complete fetal vascular obstruction.

BACKGROUND: Although the risk for transplacental transmission of SARS-CoV-2 is rare, placental infections with adverse functional consequences have been reported. This study aims to analyse histological placental findings in pregnancies complicated by SARS-CoV-2 infection and investigate its correlation with clinical symptoms and perinatal outcomes. We want to determine which pregnancies are at-risk to prevent adverse pregnancy outcomes related to COVID-19 in the future.METHODS: A prospective, longitudinal, multicentre, cohort study. All pregnant women presenting between April 2020 and March 2021 with a nasopharyngeal RT-PCR-confirmed SARS-CoV-2 infection were included. Around delivery, maternal, foetal and placental PCR samples were collected. Placental pathology was correlated with clinical maternal characteristics of COVID-19.RESULTS: Thirty-six patients were included, 33 singleton pregnancies (n = 33, 92%) and three twin pregnancies (n = 3, 8%). Twenty-four (62%) placentas showed at least one abnormality. Four placentas (4/39, 10%) showed placental staining positive for the presence of SARS-CoV-2 accompanied by a unique combination of diffuse, severe inflammatory placental changes with massive perivillous fibrin depositions, necrosis of syncytiotrophoblast, diffuse chronic intervillositis, and a specific, unprecedented CD20+ B-cell infiltration. This SARS-CoV-2 placental signature seems to correlate with foetal distress (75% vs. 15.6%, p = 0.007) but not with the severity of maternal COVID-19 disease.CONCLUSION: We describe a unique placental signature in pregnant patients with COVID-19, which has not been reported in a historical cohort. We show that the foetal environment can be seriously compromised by disruption of placental function due to local, devastating SARS-CoV-2 infection. Maternal clinical symptoms did not predict the severity of the SARS-CoV-2-related placental signature, resulting in a lack of adequate identification of maternal criteria for pregnancies at risk. Close foetal monitoring and pregnancy termination in case of foetal distress can prevent adverse pregnancy outcomes due to COVID-19 related placental disease.

Vaccines against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) have been approved for emergency use, but, despite elevated risk of severe disease, pregnant women were excluded from the clinical trials that led to their authorization.1 Placental findings can indicate potential clinical risk and could be an early signal for rare injury seen only after widespread use in the pregnant population.2–6 Maternal SARS-CoV-2 infection has been associated with decidual arteriopathy, fetal vascular malperfusion, and chronic histiocytic intervillositis.7–9 mRNA vaccines induce an immune response through activation of TLR3, which has been linked to decidual arteriopathy, growth restriction, preterm delivery, and fetal loss in mouse models.10–14 Our objective was to evaluate the frequency of these key placental lesions in patients who received SARS-CoV-2 vaccination in pregnancy.

Neonatal lupus syndrome (NLS) is a rare, passively acquired autoimmune syndrome caused by maternal autoantibodies. We describe a case of a newborn with NLS and the accompanying placental findings. A female neonate was born by emergency cesarean delivery due to non-reassuring fetal status at 35 weeks and 3 days. This neonate had congenital erythematous and scar lesions on the face, back, and upper and lower extremities. Maternal and fetal anti-SSA and SSB antibodies were elevated and this baby was diagnosed as NLS. Histologically, the chorionic villi demonstrated capillary shrinkage. An immunohistochemical study revealed complement deposition (C4d) in the capillaries of the villi and umbilical vessels. Our findings suggest that maternal autoantibodies affect the inflammatory response of the fetus through the placenta and that C4d deposition may be useful for diagnosing NLS.

To determine if pre-specified placental abnormalities among newborns with hypoxic-ischemic encephalopathy (HIE) differ compared to newborns admitted to a NICU without encephalopathy.Retrospective case-control study of newborns with HIE (2006-2014) and controls matched for birth year, gestational age, weight, and gender. One pathologist reviewed archived placental sections using pre-specified criteria.Sixty-seven newborns had HIE, 46 had available placentas and were matched with 92 controls. HIE had more maternal vascular malperfusion (46% vs 25%, p = 0.02), fetal vascular malperfusion (13% vs 0%, p 0.001), and clinical abruption (22% vs 4%, p = 0.001). Controls had more normal placentas (29% vs 7%, p = 0.002), and chorioamnionitis (30% vs 9%, p = 0.005). Pre-specified placental lesions occurred in 87% of HIE and 65% of controls (p = 0.008) and identified90% of primary diagnoses.Pre-specified placental lesions identified nearly all abnormalities in HIE and represented both acute and chronic processes.

Placental infection by SARS-CoV-2 with various pathologic alterations reported. Inflammatory findings, such as extensive perivillous fibrin deposition and intervillous histiocytosis, have been postulated as risk factors for fetal infection by SARS-CoV-2. We describe the placental findings in a case of a 31-year-old mother with SARS-CoV-2 infection who delivered a preterm female neonate who tested negative for SAR-CoV2 infection. Placental examination demonstrated a small for gestational age placenta with extensive intervillous histiocytosis, syncytiotrophoblast karyorrhexis, and diffuse intervillous fibrin deposition. Immunohistochemical staining demonstrated infection of the syncytiotrophoblasts by SARS-CoV-2 inversely related to the presence of intervillous histiocytes and fibrin deposition. Our case demonstrates that despite extensive placental pathology, no fetal transmission of SARS-CoV-2 occurred, as well as postulates a relationship between placental infection, inflammation, and fibrin deposition.

The spectrum of placental pathology in human immunodeficiency virus (HIV) is vast. Features observed are not only limited to the effects of the virus itself but may include that of coinfections such as tuberculosis and syphilis. The presence of other comorbidities and changes as a result of antiretroviral therapy may further confound the histologic findings. There is a paucity of unbiased information of the effects of maternal HIV on the placenta and how these changes relate to birth outcomes. Antiretroviral therapy, now in widespread use, has altered the course of maternal HIV disease and it is unknown whether this has altered the pathophysiology of HIV on the placenta. HIV-associated placental findings that have been most well described include acute chorioamnionitis, low placental weight, and maternal vascular malperfusion, with a tendency towards lower rates of chronic villitis.

Objectives Placental examination in a case of stillbirth can provide insight into causative/associated factors with fetal demise. The aim of this study was to compare placental and umbilical cord pathologies in singleton stillbirth and livebirth placentas, and to find prevalence of various associated maternal and fetal clinical factors. Methods This case-control study was conducted at a tertiary-care center in India over a period of 20 months. About 250 women who delivered stillborn fetus ≥28 weeks’ gestation and 250 maternal-age-matched controls were recruited. Sociodemographic and clinical details were noted and placental gross and microscopic examination was done. Placental findings were compared between stillbirth and livebirth (overall), preterm stillbirth and preterm livebirth as well as term stillbirth and term livebirth in six categories – placenta gross, cord gross, membranes gross, maternal vascular malperfusion, fetal vascular malperfusion and inflammatory response. Prevalence of 11 maternal and fetal factors were studied in all categories of placental findings in both livebirth and stillbirth. Results Placental findings in all six categories were significantly associated with stillbirths (p Conclusions Changes in placenta are associated with development of stillbirth. Therefore, antenatal investigations to identify placental dysfunction should be investigated to determine whether these reduce stillbirth. Also, placental examination in a case of stillbirth can detect/diagnose many maternal/fetal conditions and thereby can help in preventing future stillbirths.

The consequences of SARS-CoV-2 infection in pregnancy have not been well defined. However, there have been a number of reports of poor maternal and fetal outcomes worldwide. This report presents a case of stillbirth with associated placental pathology during week 35 in an otherwise healthy pregnant woman with SARS-CoV-2 infection. Placental findings in this case showed patchy acute chorionitis and diffuse infarction/villous necrosis of the placental parenchyma resulting in extensive vascular malperfusion. Fetal autopsy was most significant for placental findings and no congenital malformations were discovered. The findings in this case are consistent with reports in the literature of pathological placental changes associated with COVID-19. This case of fetal demise in a woman with confirmed SARS-CoV-2 infection without any other medical or obstetric disorders and no alternate cause suggests that fetal death can be an outcome of COVID-19 during pregnancy. This outcome was supported by the histopathological findings in the placenta. Continued research is imperative to confirm the findings in this case and multiple similar cases. Additionally, increased screening and collection of COVID-19 data specific to pregnant women and their fetuses and infants is needed to increase knowledge, support research efforts, and create guidelines for clinical practice that will prevent potential negative outcomes and loss of life., Highlights • Describes a case of stillbirth during week 35 in an otherwise healthy pregnant woman with SARS-CoV-2 infection • Placental pathology associated with SARS-CoV-2 infection seen in the current literature is consistent in this case • This case suggests stillbirth is a potential outcome of COVID-19 infection during pregnancy • Findings warrant increased surveillance of and prevention of gaps in care for this vulnerable patient population • Findings warrant increased collection of COVID-19 data specific to pregnant women and continued placental pathology research research

ObjectivesThe coexistence of two complex physiologies such as Fontan and pregnancy is still not fully understood. We aim to add a unique and essential knowledge to help our colleagues in the management of Fontan patients that undergo pregnancy as well as the fetus and the placenta perfusion.Methods and resultsWe analyse the coexistence of Fontan and pregnancy physiology on a complex case of a woman with hypoplastic left heart syndrome palliated with a univentricular repair who became pregnant, delivered very prematurely and had atypical placental findings.ConclusionHistopathological analysis of the placenta could help us to refine the understanding of Fontan physiology adaptation during pregnancy, predict women and fetal outcomes as well as to plan a better pre-pregnancy status. However, further evidence is needed in order to reach a more solid and unified conclusion.

The detection of Zika virus (ZIKV) in immunoprivileged anatomical sites, potential sites for viral persistence, may guide the confirmation of undefined cases of ZIKV infection and also bring to light unknown pathways of viral transmission. Thus, this study aimed to characterize ZIKV infection in stratified, standardized placental samples in women with exanthematic febrile manifestations during pregnancy and compare findings to the standard investigation protocol of official health agencies. To this end, a case series of placental findings within a prospective cohort study was conducted over a period of 24 months. Serum/urine were obtained at the time of clinical case identification. Placental sampling was performed following standard investigation protocol (samples of 1.0 cm sent to a reference laboratory) and in a systematic way at various regions, such as chorionic plate, chorionic villi, basal plate, amniotic membrane, and umbilical cord, for subsequent ZIKV identification and quantification. Clinical information was obtained and histological preparation with hematoxylin–eosin staining for morphological evaluation was performed. This case series included 17 placentas systematically collected. Of these, 14 were positive by qRT-PCR for ZIKV, 5 in the umbilical cord, 7 in the amniotic membrane, 7 in the chorionic plate, 13 in the chorionic villi, and 7 in the basal plate, whereas none were reported by the reference laboratory. The most common morphological and anatomopathological findings were increased stromal cellularity, villitis, calcification, maternal vascular malperfusion, placental hypoplasia, and maternal–fetal hemorrhage (intervillous thrombi). Seven women presented positive testing for ZIKV in serological and/or molecular tests during gestation in urine. While viral quantification in urine ranged from 101 to 103 FFU eq/ml, that in different placental regions ranged from 103 to 108 FFU eq/g. Thus, ZIKV can infect different regions of the placenta and umbilical cord of pregnant women, showing that the systematic collection and adequate storage of the placenta is fundamental for the detection of ZIKV in this organ. The detection of ZIKV in the placenta after several months of initial symptoms suggests that this tissue may be a site for viral persistence during pregnancy.

Obesity and unhealthy nutrition are increasing and affect women of childbearing age and hence during pregnancy. Despite normal or even high birth weight, the offspring suffers from long-term metabolic risks. We hypothesized that fetal growth is disturbed during different intrauterine phases. Underlying molecular events remain elusive. Female mice were fed either a standard diet (SD) or a high-fat diet (HFD) after weaning until mating and during pregnancy. Pregnant mice were euthanized at gestational day (G)15.5 and G18.5, and fetuses and placentas were removed for analysis. HFD fetuses displayed intrauterine growth restriction (IUGR) at G15.5, which disappeared until G18.5, indicating intrauterine catch-up growth during that time period. Main placental findings indicate decreased canonical Wnt-GSK3β signaling and lower proliferation rates at G18.5, which goes along with a smaller placental transfer zone. On the other hand, glucose depots (glycogen cluster) in HFD placentas decreased more strongly between G15.5 and G18.5 compared with placentas from SD mothers, and the glucose transporter protein GLUT-1 was increased at G18.5 in the HFD group. Maternal diet-induced obesity causes an IUGR phenotype at the beginning of the third week (G15.5) in our mouse model. This phenotype is reversed by the end of the third week (G18.5) despite a smaller placental transfer zone, probably based on GSK3β-mediated increased glucose mobilization in the placenta and hence an increased glucose supply to the fetus.

Introduction Women with adverse pregnancy outcomes (APOs) have excess risk of later life cardiovascular disease (CVD) perhaps related to an underlying high-risk vascular phenotype. We sought to determine if placental evidence of maternal malperfusion in uncomplicated pregnancies is associated with an increased risk of APOs in subsequent pregnancies. Methods 536 women with more than one delivery and an initial uncomplicated pregnancy with placental pathology examination between 2008 and 2012 were included. APOs (small for gestational age, preterm delivery, or preeclampsia) were identified for each delivery. Multivariable log-binomial regression was used to estimate the risk of an APO in a subsequent pregnancy associated with MVM lesions in index pregnancy with adjustment for covariates. Results Placental pathology from the initial pregnancy was compared between women with no APO in any pregnancy (-APO/-APO; n = 403) and women with an initial uncomplicated pregnancy and a subsequent adverse outcome (-APO/+APO; n = 133). Women with MVM lesions had an increased risk of an APO in a subsequent pregnancy relative to women with no MVM lesions after adjusting for covariates (aOR = 1.61; 95%CI = 1.06–2.46). Decidual vasculopathy was found in 13/133 (9.8%) of -APO/+APO women compared with 16/403 (4.0%) of -APO/-APO women, with an adjusted odds ratio of 2.51 (95% CI = 1.31–4.80). Discussion MVM lesions found in placentas in uncomplicated pregnancies are associated with an increased risk of an adverse outcome in a subsequent pregnancy. Placental evidence of vascular malperfusion could offer a novel approach to risk stratification for subsequent pregnancy complications and perhaps future CVD.

AIM Fetal membranes are composed of the amnion and chorion, which fuse during the early second trimester. Persistent separation confers increased risk of adverse perinatal outcomes. This study characterizes sonographic and placental findings associated with persistent amnion-chorion (AC) membrane separation. METHODS This is a case series of 23 patients carrying singleton pregnancies with persistent AC membrane separation after 16 weeks' gestation diagnosed by ultrasound from 2010 to 2016 at our institution. Twenty placentas were available for analysis. RESULTS Obstetrical complications occurred in 13 (56.5%) cases; two (8.7%) cases resulted in intrauterine fetal demise. Fetal malformations were reported in eight (34.8%) cases. Four (17.4%) neonates were small-for-gestational age (SGA

In singletons, the pathogenesis of hypertensive disorders of pregnancy (HDP) is attributed to abnormal placentation, characterized by maternal vascular malperfusion (MVM) lesions. Whether MVM plays a similar role in twin pregnancies is unclear. The purpose of the study was to compared placental pathology findings between dichorionic-twin and singleton pregnancies complicated by HDP.Retrospective cohort study of women with dichorionic-twin or singleton pregnancies complicated by HDP who gave birth in a single tertiary center between 2001 and 2015. Placental abnormalities were classified into lesions associated with MVM, fetal vascular malperfusion, placental hemorrhage and chronic villitis. Placental findings and neonatal outcomes were compared between twin and singleton pregnancies.A total of 144 women with twins and 768 women with a singleton pregnancy met the inclusion criteria. Compared with HDP singletons, twins with HDP had higher mean birth weights, were less likely to be small for gestational age and be born at34 and at32 weeks. Twins had lower odds for placental weight below10th percentile (aOR 0.49, 95%CI 0.33-0.71), for MVM pathology (aOR 0.28, 95%CI 0.20-0.39) and for fetal vascular malperfusion pathology (aOR 0.65, 95%CI 0.45-0.93). These finding remained significant in the subpopulation of early onset HDP (34 weeks) and small for gestational newborn.Our findings support the hypothesis that MVM are less relevant to the pathogenesis of HDP in twin pregnancies and suggest that other placental or non-placental factors are responsible for the increased risk of HDP in twin pregnancies.

Introduction: Hypertensive disorders complicating pregnancy contribute significantly to maternal and perinatal morbidity and mortality. Since placenta is the functional unit between the mother and fetus examination of placenta can give an idea about prenatal experience of fetus. The aim is to observe the morphology and histopathology of placenta in pregnancy with severe preeclampsia / eclampsia between 20-42 weeks of gestation.Materials and Methods: This was a prospective, descriptive study carried out in the Department of Obstetrics and Gynaecology and Department of Pathology at Institute of Medicine, Tribhuwan University Teaching Hospital, TUTH for one year, starting from 15th May 2015 - 14th May 2016. A total 55 placentas, 48 of severe preeclampsia and 7 of eclampsia were collected and placental morphometric parameters, gross and histopathological features were examined.Results: It was found that placental morphometric parameters were significantly reduced. Histopathological study showed significant number of syncytial knots, areas of fibrinoid necrosis, hyalinization and calcification. These placental findings were associated with significantly decreased weight of fetus at birth.Conclusions: Preeclampsia and eclampsia cause significant placental morphometric and histological changes which in turn adversely affects neonatal birth weight.Nepalese Medical Journal, vol.1, No. 1, 2018, page: 32-35

Background: Intrauterine fetal demise (IUFD) is an unpredictable and challenging obstetric complication. Its etiology is multifactorial with more than 60% attributed to the placental cause. The present study was done with a primary objective of understanding the placental lesions underlying IUFD. Methods: In this retrospective observational study, IUFD cases (>22 weeks) between January 2012 and September 2015 were collected from pathology database. The clinical details with ultrasound findings were collected from mother's charts. The lesions were classified into (A) maternal vascular malperfusion (MVM) including retroplacental hematomas, (B) fetal vascular malperfusion (FVM), (C) inflammatory lesions, and (D) idiopathic. The contributor to fetal death was classified as direct, major, minor, unlikely, or unknown. Placental findings of fetal hypoxia were recorded. Results: The study included 100 cases of IUFD. The mean maternal age was 26 years (18-36 years). Primipara were 46. There were 65 early preterm (PT) ( 37 weeks) IUFD. The mean gestation age was 30 weeks. The ratio of male:female fetuses was 1:1.7. Relevant obstetric complications included preeclampsia (n = 39), intrauterine growth restriction (IUGR) (n = 7), pre-gestational diabetes (n = 7), bad obstetric history (n = 6), oligohydramnios (n = 5). The mean placental weight was 256 g. Maternal vascular malperfusion had the highest incidence (30%), followed by combined maternal and FVM (10%). Exclusive inflammatory lesions and FVM were seen in 12 and 6%, respectively. No cause was identified in 18%. Direct contributor to IUFD was identified in 51 cases and major, minor, unlikely contribution in 21, 11 and nine cases, respectively. In nine cases, it was unknown. Lesions indicating fetal hypoxia were noted in 35 cases. In both early and late PT, MVM featured more commonly (23 and 5%). In term placentas, the most common cause was idiopathic. Conclusions: Lesions of MVM were the most common cause of IUFD and served as a direct contributor to fetal demise.

The placenta is a complex organ that influences prenatal growth and development, and through fetal programming impacts postnatal health and well-being lifelong. Little information exists on placental pathology in the presence of congenital heart disease (CHD). Our objective is to characterize the placenta in CHD and investigate for distinctions based on type of malformation present. Placental pathology from singleton neonates prenatally diagnosed and delivered at > 37 weeks gestation was analyzed. Placental findings of absolute weight, placental weight-to-newborn birth weight ratio, chorangiosis, villus maturity, thrombosis, and infarction were recorded and analyzed based on four physiological categories of CHD: (1) single ventricle-aortic obstruction, (2) single ventricle-pulmonic obstruction, (3) two-ventricle anomalies, and (4) transposition of the great arteries (TGA). Associations between fetal Doppler assessments of middle cerebral/umbilical arterial flow and placental findings were investigated. A total of 120 cases of complex CHD were analyzed. Overall placental-to-birth weight ratios were

Aims This prospective observational study compared placental lesions of stillbirth cases and live birth controls, and aimed to determine the cause of stillbirth. Methods The study enrolled 85 stillbirths and 85 live births at the time of delivery. Results There was significantly increased incidence of placental abruption (p = 0.005) and gestational diabetes (p = 0.032) in mothers with stillbirths. Histopathological examination of placenta was significantly abnormal in stillbirths compared with live births (p = 0.004). Delayed villous maturation was significantly more in stillbirths (38.82 vs. 16.47%; p = 0.002). Acute (30.59 vs. 16.47%; p = 0.04) and chronic diffuse villitis (16.47 vs. 4.7%; p = 0.02), chorionic plate acute vasculitis (28.235 vs. 14.11%; p = 0.04) were significantly more in stillbirths. Foetal vascular thrombi in the chorionic plate (30.58 vs. 14.12%; p = 0.02) and avascular villi (24.7 vs. 8.23%; p = 0.006) were significantly more in stillbirths. Conclusion These abnormal placental patterns could provide information about the etiopathogenisis in stillbirths of unknown aetiology.

We assessed clinical outcomes and placental pathology among pregnancies complicated with gestational diabetes mellitus (GDM) according to their pregestational body mass index (BMI) and weight gain during pregnancy.Pregnancy outcome and placental pathological reports of all GDM deliveries, during 2009-2015, were reviewed. We compared women with pregestational BMI 30 and or gestational weight gain20 kg (high-BMI group), and women with pregestational BMI 30 and weight gain less than 20 kg (normal BMI group).Out of the 429 women with GDM, 221 (51.5%) were in the high-BMI group and 208 (48.3%) were in the normal BMI group. As compared to the normal BMI group, the high-BMI group displayed a higher rate of GDMA2 41.6 versus 30.2%, p = .01, higher birth weight, 3475 ± 508 g versus 3242 ± 503 g, p .001, more large for gestational age neonates, 33.1 versus 13.9%, p .001, and a trend for more cesarean deliveries (CD), 49.3 versus 40.8%, p = .07, respectively. By logistic regression analysis, past CD and high BMI were independently associated with CD, while GDM type and birth weight were nonsignificant. Pathological reports were available for 143 of these patients. Placental weight was increased among the high-BMI group, but did not retain significance after adjustment for birth weight, and GDM type. No differences were demonstrated in other placental histological findings.GDM pregnancies accompanied by increased weight gain or elevated pregestational BMI are associated with adverse obstetric outcomes, despite similar placental findings. Patient should be advised accordingly, as gestational weight gain may determine delivery mode.

OBJECTIVE This study aimed to report the spectrum of placental pathology findings in pregnancies complicated by SARS-CoV-2 infection. DATA SOURCES MEDLINE, Embase, Google Scholar, and the Web of Science databases were searched up to August 11, 2021. STUDY ELIGIBILITY CRITERIA Histopathologic anomalies included maternal vascular malperfusion, fetal vascular malperfusion, acute inflammatory pathology, chronic inflammatory pathology, increased perivillous fibrin, and intervillous thrombosis. Moreover, subanalyses of symptomatic women only and high-risk pregnancies were performed. METHODS: Histopathologic analysis of the placenta included gross examination, histopathology on hematoxylin and eosin, immunohistochemistry, fluorescence in situ hybridization, quantitative reverse transcription-polymerase chain reaction on placental tissue, and transmission electron microscope. Random-effect meta-analyses were used to analyze the data. RESULTS A total of 56 studies (1008 pregnancies) were included. Maternal vascular malperfusion was reported in 30.7% of placentas (95% confidence interval, 20.3–42.1), whereas fetal vascular malperfusion was observed in 27.08 % of cases (95% confidence interval, 19.2–35.6). Acute and chronic inflammatory pathologies were reported in 22.68% (95% confidence interval, 16.9–29.0) and 25.65% (95% confidence interval, 18.4–33.6) of cases, respectively. Increased perivillous fibrin was observed in 32.7% (95% confidence interval, 24.1–42.0) of placentas undergoing histopathologic analysis, whereas intervillous thrombosis was observed in 14.6% of cases (95% confidence interval, 9.7–20.2). Other placental findings, including a basal plate with attached myometrial fibers, microscopic accretism, villous edema, increased circulating nucleated red blood cells, or membranes with hemorrhage, were reported in 37.5% of cases (95% confidence interval, 28.0–47.5), whereas only 17.5% of cases (95% confidence interval, 10.9–25.2) did not present any abnormal histologic findings. The subanalyses according to maternal symptoms owing to SARS-CoV-2 infection or the presence of a high-risk pregnancy showed a similar distribution of the different histopathologic anomalies to that reported in the main analysis. Moreover, the risk of placental histopathologic anomalies was higher when considering only case-control studies comparing women with SARS-CoV-2 infection with healthy controls. CONCLUSION In pregnant women with SARS-CoV-2 infection, a significant proportion of placentas showed histopathologic findings, suggesting placental hypoperfusion and inflammation. Future multicenter prospective blinded studies are needed to correlate these placental lesions with pregnancy outcomes.

A pregnant woman undergoes increased fetal ultrasonographic surveillance during the pregnancy for an amnion-chorion separation and fetal growth restriction. At 34 weeks’ gestation, an ultrasound finding prompts the recommendation for a preterm delivery. Video 1 shows the placental finding seen after an uncomplicated delivery of a late preterm infant. This finding can increase a neonate’s risk of which of the following? Video 1 Click here to view the video. Placental findings in this case that are consistent with the presence of amniotic bands. Video 2 provides commentary of the placental findings in this case, which are consistent with the presence of amniotic bands. Amniotic bands are fibrous strands that separate from the amniotic sac. Frequently they are not visualized postnatally but may result …

Background Previous studies have shown that pregnancies complicated by placentas with an isolated single umbilical artery (iSUA) are at increased risk for small-for-gestational-age (SGA) births. The etiology of SGA in this population, however, remains unknown. Objective The primary objective of this study was to evaluate whether placental abnormalities in pregnancies with SGA births differ according to the presence of iSUA. Study design This was an observational study of all women with pathologic examination of the placenta after delivering a non-anomalous, singleton SGA neonate between January 2009 and August 2015. SGA was defined as birthweight less than 10th percentile for gestational age. Women were categorized according to whether they had an iSUA or a three-vessel cord. The following placental pathologies were compared between the groups using bivariable and multivariable analyses: SGA placenta, maternal vascular malperfusion, high grade fetal vascular malperfusion, and chronic villitis. Results 1833 women were included in the analysis: 34 with iSUA and 1799 with three-vessel cord. More than 85% of women in both groups had at least one placental abnormality. After adjusting for nulliparity and neonatal gender, the presence of iSUA was associated with increased odds of high grade fetal vascular malperfusion (adjusted odds ratio 2.8, 95% confidence interval 1.1–7.5) and decreased odds of maternal vascular malperfusion (adjusted odds ratio 0.2, 95% confidence interval 0.1–0.9). There was no significant association with other pathologic findings. Conclusion Pathologic placental findings associated with SGA birth differed based on umbilical cord composition. The presence of iSUA in an SGA birth was associated with a higher odds of high grade fetal vascular malperfusion abnormalities and lower odds of maternal vascular malperfusion abnormalities, compared to SGA birth with a 3VC.

Objective: The aim of this study was to determine the association between chronic placental inflammation and amniotic fluid (AF) markers of maternal anti-fetal rejection as well as the presence of microorganisms in the AF fluid of patients with fetal death. Study Design: This cohort study included 40 patients with fetal death whose placentas were examined for chronic inflammatory lesions and whose AF chemokine ligand (CXCL)10 and interleukin (IL)-6 concentrations were determined by immunoassays. AF was processed for bacteria, mycoplasmas and viruses using cultivation and molecular microbiologic techniques (i.e. PCR-ESI/MS). Results: (1) The most prevalent placental findings were maternal vascular underperfusion (63.2%, 24/38), followed by chronic inflammatory lesions (57.9%, 22/38); (2) chronic chorioamnionitis (18/38) was three times more frequent than villitis of unknown etiology (6/38); (3) an elevated AF CXCL10 concentration (above the 95th centile) was present in 60% of the cases, and a receiver operating characteristics (ROC)-derived cut-off of 2.9 ng/mL had a sensitivity of 73% and a specificity of 75% in the identification of chronic placental inflammatory lesions; (4) only five cases had microbial invasion of the amniotic cavity, and the presence of microorganisms did not correlate with chronic placental inflammation. Conclusion: In women with unexplained fetal death, there is an association between elevated AF CXCL10 and chronic placental inflammatory lesions. Therefore, we conclude that a subset of patients with fetal death may have endured a breakdown of maternal-fetal tolerance, which cannot be attributed to microorganisms in the amniotic cavity.

Feto-maternal hemorrhage (FMH) is not an uncommon event during pregnancy with important clinical implications for both maternal and fetal outcomes. The diagnosis is often made using Kleihauer-Betke (KB) test. As FMH occurs transplacentally, examination of the placenta may contribute to the diagnosis of FMH. This retrospective case-control study aims to examine the placental features associated FMH in patients with known positive KB test results. When compared with KB negative placentas (n=88), KB positive placentas (n=49) had significantly higher incidence of pallor (6/49 vs 0/88, p=0.0017), IVT (11/49 vs. 5/88, p=0.0032) and nRBCs (12/49 vs. 4/88, p=0.0008). Autopsy cases with fetal or neonatal death due to FMH, (n=13) compared to a cohort of 162 placentas associated with other, non-FMH causes of death also had significantly higher frequency of pallor (5/13 vs 0/162, p

Background There are limited data on the natural history of antenatal Zika virus (ZIKV) exposure in twin pregnancies, especially regarding intertwin concordance of prenatal, placental, and infant outcomes. Methods This prospective cohort study included twin pregnancies referred to a single institution from September 2015 to June 2016 with maternal ZIKV. Polymerase chain reaction (PCR) testing of maternal, placental, and neonatal samples was performed. Prenatal ultrasounds were completed for each twin, and histomorphologic analysis was performed for each placenta. Abnormal neonatal outcome was defined as abnormal exam and/or abnormal imaging. Two- to three-year follow-up of infants included physical exams, neuroimaging, and Bayley-III developmental assessment. Results Among 244 pregnancies, 4 twin gestations without coinfection were identified. Zika virus infection occurred at 16–33 weeks gestation. Zika virus PCR testing revealed discordance between dichorionic twins, between placentas in a dichorionic pair, between portions of a monochorionic placenta, and between a neonate and its associated placenta. Of the 8 infants, 3 (38%) had an abnormal neonatal outcome. Of 6 infants with long-term follow-up, 3 (50%) have demonstrated ZIKV-related abnormalities. Conclusions Neonatal PCR testing, placental findings, and infant outcomes can be discordant between co-twins with antenatal ZIKV exposure. These findings demonstrate that each twin should be evaluated independently for vertical transmission.

BACKGROUND: Preterm birth remains the leading cause of neonatal morbidity and mortality, with complex biochemical pathways requiring continued understanding and assessment. OBJECTIVE: To assess the associations between maternal cortisol and placental corticotropin releasing hormone (placental CRH) concentrations with birth outcomes when stratified by placental histopathology. MATERIALS & METHODS: We conducted an analysis of 112 singleton pregnancies who received betamethasone between 23 and 34 weeks’ gestation. Maternal blood and saliva were collected prior to betamethasone administration and samples assayed for plasma cortisol (pCort), salivary cortisol (sCort), and placental CRH levels. Placental findings were characterized as inflammatory, maternal vascular underperfusion (MVU), or no pathology, and compared for the outcomes of placental CRH, pCort and sCort levels, gestational age at birth (GAB), and birthweight percentiles (BWP). RESULTS: Thirty-six subjects were characterized as inflammatory, 38 as MVU and 38 without placental abnormalities. Histopathology groups differed significantly on placental CRH levels, GAB, and BWP. Post hoc tests suggested that the MVU group had higher placental CRH than the inflammatory or no pathology groups and, despite delivering earlier than the other two groups, the inflammatory group had infants with significantly higher BWP. No differences existed between groups in terms of mean plasma or sCort levels. Higher placental CRH and pCort levels were associated with earlier GAB in the overall sample but, when split by group, these associations remained significant only among the MVU group. Higher placental CRH was also associated with lower BWP in the overall sample but did not remain significant when split by group. Higher sCort was associated with lower BWP only in the MVU group. CONCLUSION: There is differentiation of placental CRH, cortisol and birth outcomes when evaluated by placental histopathology. This highlights the importance of evaluating birth outcomes within the context of placental histopathology.

Objective Preeclampsia is a multifactorial placental disease that can occur after delivery. The pathophysiology of postpartum preeclampsia remains unknown. The objective was to describe placental findings in postpartum preeclampsia. Study Design This is a case–control study, comparing the placental histologic findings in four groups of 30 patients with postpartum preeclampsia, early-onset preeclampsia, late-onset preeclampsia, and normotensive controls. Results Placentas of postpartum preeclampsia had a mean placental weight not different from that of late-onset preeclampsia at a similar gestational age (479.0 ± 152.7 vs. 521.3 ± 144.1 g, p = 0.07); they showed a higher rate of acute deciduitis of 42.4% than early preeclampsia (5.7%, p Conclusion There were no significant differences for decidual arteriolopathy and villous infarcts among postpartum preeclampsia, late-onset preeclampsia, and the controls. This suggests that postpartum preeclampsia is more of a maternal disease in which the placenta may act as a priming effect in predisposed mothers and becomes clinically apparent after delivery.

Background: This is a prospective type of study and constitutes the clinicopathological correlation of abnormal placental findings with pregnancy related maternal morbidities and associated foetal outcome in all preterm and full term pregnancies. Placentae from 80 deliveries of preterm and fullterm gestation were collected from labour room of Bundelkhand Medical College, Sagar during the period from June 2017 to June 2018. The gross features of placenta varies significantly with period of gestation. Parameters such as weight, size, number of cotyledons and thickness of placenta decreases in preterm labour. The microscopic lesions observed in decreasing order of frequency were perivillous fibrin deposition (62.50%) followed by chorioamnionitis (26.25%), infarct (21.25%) and calcification (17.50%). Other pathological lesions includes villous oedema (12.50%) and retro placental hematoma (2.50%). All the histomorphological changes were conspicuous in preterm pregnancies. Keywords: Foetal, Gross, Microscopic & Placental

Congenital heart disease (CHD) is an independent risk factor for brain injury, including stroke, and poor neurodevelopmental outcomes, and placental abnormalities may represent an additional risk factor for brain injury in neonates. The incidence and scope of placental pathology and relationship to fetal brain abnormalities in pregnancies complicated by fetal CHD has not been explored to our knowledge. In order to determine the prevalence of placental pathology findings and whether placental findings are associated with postnatal brain injury in pregnancies complicated by fetal CHD, we reviewed placental pathology reports for 51 pregnancies complicated by CHD and scored available postnatal, pre-operative brain MRI for brain pathology. Overall, 57% of CHD infants had abnormal placental pathology. Pregnancies complicated by CHD with aortic obstruction (AO) were significantly more likely than those with no obstruction to have abnormal placental pathology (79% vs. 44%). There was a trend toward more severe brain lesions amongst patients with brain lesions and placental abnormality (55% moderate/severe) compared to those without placental abnormality (11% moderate/severe). These data suggest that placental abnormalities are common in CHD and may have a compounding effect on brain lesions in this high-risk population.

Background: Small for gestational age (SGA) is a term to define any baby born with birth weight