Placental Examination Research Articles

Recurrence risk of villitis of unknown etiology: Analysis of a large retrospective cohort study, systematic review and meta-analysis.

Recurrence risk of villitis of unknown etiology (VUE) remains uncertain because of few studies and their methodologic limitations. We calculated recurrence risk in a large population of deliveries after minimizing important biases and compared it to others via systematic review and meta-analysis. Over 11 years of placenta pathology reports on singleton deliveries were retrieved and searched for 'villitis' or 'VUE'. Cases of acute villitis and chronic villitis from infections were eliminated via pathologist review. Reports were merged to data containing gestational age, parity and gravida. Recurrence risk of VUE per patient, per parity and per gravida was determined among patients with ≥2 placentas examined for deliveries ≥20 weeks gestation. Results were compared to those from articles and their references identified by a MEDLINE® search. Recurrence risks among methodologically similar studies were pooled using a random effects model. Among 29124 placenta pathology reports from 27087 patients, there were 2423 cases of VUE among 2382 patients, of which 153 had ≥2 placentas examined. There were 41 recurrent cases of VUE for a recurrence risk of 27% per patient, 22% per parity, and 19% per gravida. We identified 64 articles, of which 4 were retained. One examined all placentas from all births over a ∼3-year period, finding a recurrence risk of 27%. The remaining 3 studies, along with our own, used indications for placental examination and had a pooled recurrence risk of 30% (95% Confidence Interval: 0.21-0.41). In our study, which is the largest, most comprehensive, and methodologically robust to date, VUE recurrence risk was ∼30%.

Classification of stillbirth by the International Classification of Diseases for Perinatal Mortality using a sequential approach: A 20-year retrospective study from Thailand.

The International Classification of Diseases for Perinatal Mortality (ICD-PM) is a system for recording causes of perinatal death. In this system, placental pathology is considered a "maternal condition" and this category does not cover the spectrum of placental pathology that can impact on perinatal death. The aim of the study was to apply a wider spectrum of placental pathology as a separate parameter for classifying death in the ICD-PM. All autopsy reports at a single institution over a 20-year period (2001-2020) were reviewed. Causes of stillbirth were analyzed in a sequential manner: step 1, clinical history and laboratory results; step 2, placenta; and step 3, autopsy; and classified at each step according to the ICD-PM. The review identified 330 cases, including 126 antepartum and 204 intrapartum deaths. Step 1 identified a cause in 176 (86%) intrapartum deaths and 64 (51%) antepartum deaths. The addition of placental pathology (step 2) changed the cause of death in 12% of cases, with causes now identified in 190 (93%) intrapartum and 89 (71%) antepartum deaths. Adding step 3 did not identify any additional causes of death. The accuracy of the ICD-PM classification is dependent on the data available. Placental pathology made a significant difference in assigning causes of death in our series, stressing the importance of placental examination. Determination of the cause of death based on clinical history and laboratory data alone may be inaccurate, and less useful for comparative studies and planning prenatal care.

Congenital Malaria in Newborns Delivered to Malaria-infected Mothers in the Hilly Region of Northern India: Is it Deadly?

Malaria is endemic in many states of India. Though there are reports of maternal and congenital malaria from endemic areas, however, there remains a paucity of data from hilly terrains. The present study evaluated the prevalence, clinical and microbiological spectrum of maternal and congenital malaria at a tertiary health care facility in Northern India over a period of 18 months. In this observational study, mothers along with their newborns were evaluated for malaria by maternal, placental, and cord blood smear examination and rapid point-of-care diagnostic serological tests. Positive cases were confirmed by polymerase chain reaction. Mother-newborn duos were followed up till discharge from the hospital. A total of 843 mothers delivered during the study period and were screened along with their newborns and placentae. A total of Ten (1.18%) mothers had evidence of malarial parasitemia (Plasmodium vivax, n=7 and Pl. falciparum, n=3), however, none of the placental and cord blood samples were positive for malaria. Overall, 127 (15.1%) neonates required admission in neonatal intensive care unit for various morbidities. Incidence of small for gestational age (SGA) was high (n=210; 24.9%). Multivariate logistic regression analysis demonstrated maternal malaria to be an independent contributor for SGA [Odds Ratio (95% Confidence Interval), 10.7 (2.06 - 49.72)]. However, only 2% variance of SGA could be explained by maternal malaria alone. We report an encouragingly lower incidence of maternal malaria in mothers attending for delivery and a 'Zero' incidence for placental and congenital malaria during the study period as compared to national data (upto 7.4% in non-immune mothers), although maternal malaria could be a causative factor for SGA.

T2*-weighted placental magnetic resonance imaging: a biomarker of placental dysfunction in small-for-gestational-age pregnancies

The antenatal identification of placental dysfunction in small-for-gestational-age fetuses with normal fetal Doppler flows remains an obstetrical challenge. In a significant fraction of such pregnancies, placental dysfunction is revealed by clinical manifestations such as preeclampsia, preterm delivery, or severe small-for-gestational-age at birth or by abnormal findings in the postnatal placental histologic examination. Therefore, new methods to identify placental function directly in pregnancy at the time of small-for-gestational-age diagnosis is highly needed. T2*-weighted placental magnetic resonance imaging is sensitive to changes in placental morphology and oxygenation and is thereby related to placental function. Previous studies have demonstrated that pregnancies complicated by low birthweight and preeclampsia are characterized by low placental T2* values. However, the specific performance of placental T2* in the prediction of placenta-related outcomes in small-for-gestational-age pregnancies with normal fetal Doppler flows remains to be explored. In small-for-gestational-age pregnancies with normal fetal Doppler flows, we aimed to evaluate T2*-weighted placental magnetic resonance imaging as an antenatal biomarker of placental dysfunction. In addition, we aimed to investigate the correlation between placental T2* and Doppler flow measurements of fetal and uterine arteries at the time of magnetic resonance imaging. In this prospective cohort study, the inclusion criterion was suspected small-for-gestational-age (ultrasound estimated fetal weight Z-score ≤-2.0 [2.3rd centile]) with normal fetal Doppler flows (middle cerebral artery pulsatility index Z-score > -2.0 and umbilical artery pulsatility index Z-score <2.0). The T2*-weighted placental magnetic resonance imaging scan was performed at inclusion in a 1.5 T system. The outcomes was placental dysfunction at birth defined by low birthweight (Z-score ≤-2.0), preeclampsia, preterm delivery (gestational age<37 weeks), or abnormal placental histologic examination such as placental vascular malperfusion according to the Amsterdam Consensus Statement. We included 92 pregnancies at 26+5 to 39+6 weeks gestation. The median time interval between the magnetic resonance imaging scan and birth was 4.6 weeks (interquartile range, 2.7-7.8 weeks). At birth, 55% (51/92) of pregnancies revealed at least 1 sign of placental dysfunction; 49% (40/81) had abnormal placental histologic examination, 29% (27/92) were born with low birthweight, 13% (12/92) were delivered preterm, and 7% (6/92) had preeclampsia. When adjusted for gestational age at magnetic resonance imaging, the placental T2* Z-score was a significant predictor of abnormal placental histologic examination (area under the curve, 0.73; P=.001), small-for-gestational-age at birth (area under the curve, 0.63; P=.030), preeclampsia (area under the curve, 0.88; P=.005), and preterm delivery (area under the curve, 0.81; P=.001). The placental T2* was reduced in pregnancies with a combination of clinical manifestations and abnormal placental histologic examination (T2* Z-score=-1.52±1.35 [mean±standard deviation]; P=.0001) and in clinically uneventful pregnancies with abnormal placental histologic examination (T2* Z-score=-0.79±0.97; P=.045). At the time of magnetic resonance imaging, the placental T2* Z-score showed a significant linear correlation with the uterine artery pulsatility index Z-scores (r=-0.24; P=.016) and the middle cerebral artery pulsatility index Z-scores (r=0.29; P=.017) but not with the umbilical artery pulsatility index Z-scores (r=0.18; P=.17) and the cerebroplacental ratio (r=0.03; P=.77). This study indicates that placental dysfunction is frequent in small-for-gestational-age fetuses with normal fetal Doppler flows. In this cohort, T2*-weighted placental magnetic resonance imaging is a sensitive biomarker of placental dysfunction regardless of the clinical manifestations. This finding supports a paradigm shift in the conception of placental dysfunction that may cover a wide spectrum of clinical and subclinical manifestations.

Clinically Relevant Prenatal Ultrasound Diagnosis of Umbilical Cord Pathology.

Umbilical cord abnormalities are not rare, and are often associated with structural or chromosomal abnormalities, fetal intrauterine growth restriction, and poor pregnancy outcomes; the latter can be a result of prematurity, placentation deficiency or, implicitly, an increased index of cesarean delivery due to the presence of fetal distress, higher admission to neonatal intensive care, and increased prenatal mortality rates. Even if the incidence of velamentous insertion, vasa praevia and umbilical knots is low, these pathologies increase the fetal morbidity and mortality prenatally and intrapartum. There is a vast heterogeneity among societies’ guidelines regarding the umbilical cord examination. We consider the mandatory introduction of placental cord insertion examination in the first and second trimester to practice guidelines for fetal ultrasound scans. Moreover, during the mid-trimester scan, we recommend a transvaginal ultrasound and color Doppler assessment of the internal cervical os for low-lying placentas, marginal or velamentous cord insertion, and the evaluation of umbilical cord entanglement between the insertion sites whenever it is incidentally found. Based on the pathological description and the neonatal outcome reported for each entity, we conclude our descriptive review by establishing a new, clinically relevant classification of these umbilical cord anomalies.

Does COVID-19 cause pre-eclampsia?

Does COVID-19 cause pre-eclampsia?

Gestational diabetes mellitus in in-vitro fertilization pregnancies – Clinical and placental histological characteristics

We aimed to investigate obstetric and neonatal outcomes and placental histological findings in in vitro fertilization (IVF) pregnancies complicated by gestational diabetes mellitus (GDM) as compared to unassisted pregnancies. This was a retrospective cohort of deliveries at a single university affiliated center between 12/2008 and 01/2020. Included were singleton pregnancies complicated by GDM, for which placental histopathological examination was performed. Obstetric, neonatal and placental outcomes were compared between pregnancies following IVF and unassisted pregnancies. Placental lesions were categorized according to the "Amsterdam" criteria. Included were 688 deliveries with a diagnosis of GDM with placental examination - 69 IVF pregnancies (IVF group) and 619 unassisted pregnancies (control group). The IVF group was characterized by a significantly higher maternal age and higher rate of nulliparous women - 60.8% vs. 32.9%, p<0.001. There were no differences in GDM type between the study groups - about two thirds of cases were GDMA1 and on third GDMA2. A higher incidence of preeclampsia was noted in the IVF group - 17.3% vs. 9.3%, p=0.03, with no difference in cesarean deliveries and birthweight. IVF deliveries were characterized by a significantly higher rate of adverse neonatal outcomes - 18.8% vs. 8.8%, p=0.008, although this did not attain significance after adjustment to gestational age. No differences were noted in placental histology between the groups. GDM in IVF is associated with a significantly higher rate of adverse neonatal outcomes, as compared with non-assisted pregnancies complicated by GDM. Placental histology does not shed light on these clinical associations.

Routine Placental Histopathological Examination: Provides Answers in Neonatal Management

Placental abnormality may affect the fetus adversely. The purpose of this study was to identify the prevalence of placental histopathological examination in a private hospital setting and analyse the placental histopathology findings for high-risk pregnancies. A retrospective cross-sectional study was conducted at the Mater Hospital in Sydney from January 2018 to June 2020. The placental histopathology was classified as per the 2014 Amsterdam Placental Workshop Group criteria, enabling uniformity for analysis. There were 5594 live births during the study period. Of these, 5% (256/5594) were low birth weight (LBW). Placental histopathology was conducted for 8% (443/5594) of the live births and 59% (152/256) of LBW births. The LBW group was subclassified into small for gestation (SGA) (n=66) and non-SGA (n=86) to analyse differences in placental abnormalities between the two groups. Of SGA, 82% (54/66) had placental abnormality compared to 76% (65/86) for non-SGA. Intervillous fibrin deposits (<i>p=0.013</i>) and smaller placental weight (<i>p=0.008</i>) were more common in the SGA; whereas the placental inflammatory-immune process was more common in the non-SGA. Original placental histopathology reports did not employ the objective Amsterdam classification system, thereby risking subjective or variable interpretation by clinicians. In conclusion, placental histopathology plays an important role in neonatal management. A quality improvement project may improve the prevalence of placental histopathological examination.

Placental Changes in Perinatal DeathAn Observational Study from a Tertiary Care Centre in North Karnataka

Introduction: Placenta is poetically described as a diary which bears the events of intrauterine life; hence examining them, especially in perinatal death can provide valuable information regarding the cause of death and sometimes gives an idea about recurrence of such events. Aim: To describe the various placental lesions in perinatal death and compare them with equal number of normal placentae. Materials and Methods: This prospective, comparative, crosssectional study was conducted in tertiary care centre, Karnataka Institute of Medical Sciences, Hubballi, Karnataka, India. All placentae, irrespective of the gestational age, received in the Department of Pathology, from October 1st 2017 to March 31st 2019 were collected after taking an informed consent. A total of 539 cases were received in this time frame, of which 121 (22.45%) were dead and included in the study and were compared with 121 normal placentae (alive), without any maternal co-morbidities. The placentae were grossed and assessed according to Amsterdam guidelines. The significance of the difference observed was established by Chi-square test using Statistical Package for Social Sciences software (SPSS) version 21.0. Results: Of these 121 cases, 89 (73.5%) cases had placental changes, whereas 32 (26.5%) cases were devoid of placental changes. Placental infarct and increased syncytial knots were seen contributing maximum to foetal death in 31 (25.6%) cases followed by chorioamnionitis. Rare cases like Twin Reversed Arterial Perfusion (TRAP) syndrome, Persistent Right Umbilical Vein (PRUV), maternal floor infarct were also reported. Conclusion: Despite many antenatal imaging advances, placental examination still remains valuable in diagnosing cause of death and growth restriction in the foetus especially recurrent causes, favouring clinical intervention in those cases.

Роль патоморфологических изменений в плаценте в патогенезе ранней преэклампсии при многоплодии и одноплодии

Objective. To compare the features of placental pathology in twin and singleton pregnancies complicated by early preeclampsia. Materials and methods. A retrospective analysis of 211 placental pathomorphological examinations in patients with early preeclampsia was performed. The first (study) group composed of placentas obtained from patients with twin pregnancy and early pre-eclampsia (n = 108); the second (comparison) group composed of placentas obtained from patients with singleton pregnancy and early pre-eclampsia (n = 103). Placental histopathological examination was conducted according to a generally accepted method with assessing the signs of circulatory disorders in the maternal-placental-fetal system and the degree of infectious and inflammatory lesions. Results. Fetal and placental massometric parameters were higher in the study group (p &lt; 0.001); a subcompensated form of placental insufficiency, villous maturation disorders, intervillous hemorrhage and thrombosis, chorangiosis, and angiospastic arteriopathy (p &lt; 0.001) were statistically significantly more common in the comparison group. Conclusion. Maternal and fetal vascular malperfusion was more pronounced in the group of singleton pregnancy with early preeclampsia, which indicates different pathophysiological mechanisms of early pre-eclampsia as opposed to multiple pregnancy. Key words: multiple pregnancy, placental pathomorphology, maternal and fetal vascular malperfusion, early pre-eclampsia

Decoding placental pathology: Usage of a comprehensive checklist and scoring system for reporting of placentas in the hypertensive disorders of pregnancy.

Hypertensive disorders of pregnancy (HDP) are major complications of pregnancy and seen in about 5% to 10% of all pregnancies. Among these, pre-eclampsia is a leading cause of perinatal and fetal morbidity and mortality. It is a multifactorial and multisystemic disorder that results in a variety of histomorphologic features, some of which may be missed if a diligent examination is not performed. The present study aimed to propose a checklist and novel scoring system to ensure comprehensive placental examination. We also aimed to evaluate the correlation, if any, between histopathological and morphometric findings in HDP and with fetal growth. A total of 100 placentas of women diagnosed with hypertensive disorders of pregnancy were included in our cross-sectional, observational study. Morphometric features and histological features that are known to be seen in HDP were analyzed, and each of them was given a numerical score based on their severity. Pearson correlation coefficient test was applied to correlate these findings, and ANOVA test was used to assess the correlation of these findings with fetal growth restriction (FGR). More than 50% of the placentas studied recorded maximum scores for weight and volume. At least 25% of the placentas showed the presence of all histo-pathological features under study. The association of total morphometric and histological scores was not found to be statistically significant (P-value = 0.239). We found a significant difference between means of morphometric scores of cases with normal fetal growth and cases showing FGR (P-value = 0.008). Uneven distribution and presentation of the lesions in these cases may lead to the absence of correlation between morphometry and histopathology, as seen in our study. Morphometric derangements in the placenta correlate with FGR. Our proposed checklist and scoring system can be utilized to standardize reporting of placental specimens in the evaluation of placentas with HDP, in order to facilitate and standardize the placental reporting.

Placental Pathology in Maternal Ornithine Transcarbamylase Deficiency.

Ornithine transcarbamylase (OTC) deficiency is the most common urea cycle disorder, inherited in an X-linked manner. Males are severely affected. Female phenotypes vary from asymptomatic to severe, and symptoms may be triggered by high metabolic states like childbirth. Literature on OTC deficiency in pregnancy and placental pathology is limited. Pathology records were searched at a single referral center from 2000-2020 and identified three placental cases from two mothers heterozygous for OTC deficiency. Placental pathology and maternal and neonatal history were reviewed in detail. The placenta from one symptomatic mother carrying an affected male fetus showed widespread high-grade fetal vascular malperfusion (FVM) lesions of varying age. These lesions were not seen in the two placentas from the asymptomatic mother. In cases of symptomatic maternal OTC deficiency, our findings highlight the need for placental examination. Since thrombotic events in the placenta have the potential to associate with fetal and neonatal endothelial damage, a high index of suspicion for neonatal thrombosis may be warranted.

Novel optical tool for assessment of human placental oxygenation detects placental dysfunction in second trimester

Currently, no bedside tools directly assess human placental function in vivo. We recently validated a hybrid optical/ultrasound instrument, which measures oxy-Hgb (HbO2) and O2 saturation (StO2) using frequency-domain near-infrared spectroscopy (FD-NIRS). Moreover, in a pilot study, we observed significant blunting of placental ΔHbO2 and ΔStO2 response to maternal hyperoxia in 3rd trimester pregnancies that later developed an adverse pregnancy outcome (APO) or had maternal vascular malperfusion (MVM) on placental examination.

Placental acute inflammation infiltrates and pregnancy outcomes: a retrospective cohort study

Chorioamnionitis can be either an infection or a sterile inflammation. This study aims to analyze the prevalence of acute inflammatory lesions of the placenta, the association with a positive result of the microbiological examination, and the fetal-maternal outcomes. This retrospective study considered all single, consecutive pregnancies and their placental pathological examination during 2014–2017. The evidence of funisitis, chorionic vasculitis, and chorioamnionitis was assessed by a pathologist, including stage and grade. Moreover, maternal fever, placental microbiological examination, and neonatal outcomes were also recorded. Among the 5910 pregnancies in the considered period, 1770 had a placental pathological examination, and 358 (6.06%) had acute placental inflammation. Microbiological examination was performed in 125 cases, revealing 64 cases with a positive microbiological outcome. In the presence of acute placental inflammation, there was a higher rate of neonatal cardiopulmonary resuscitation, admission to neonatal intensive care unit, and postnatal death of the newborn. Multivariate analysis inferred that acute inflammation of membranes was a risk factor for neonatal cardiopulmonary resuscitation (OR 2.12; CI.95 1.36–3.31; p < 0.05), acute funisitis was a risk factor for admission to intensive neonatal care unit (OR 3.2; CI.95 1.67–6.12; p < 0.05), and chorionic vasculitis was a risk factor for postnatal death of the newborn (OR 5.38; CI.95 1.37–21.06; p < 0.05). The prevalence of chorioamnionitis was 6.06%, and about half of the cases were sterile inflammation. Chorioamnionitis was associated with higher rates of adverse fetal and neonatal outcomes; in particular, chorionic vasculitis was a risk factor for postnatal death.

Correlation between Apelin and Some Angiogenic Factors in the Pathogenesis of Preeclampsia: Apelin-13 as Novel Drug for Treating Preeclampsia and Its Physiological Effects on Placenta.

Preeclampsia (PE) is one of the commonest causes for maternal and fetal morbidity and mortality. Imbalances of angiogenic factors, oxidative stress, and inflammatory response have a role in the pathogenesis of PE. Data regarding the circulating apelin level and its role in PE remains controversial. This study was formulated to assess the serum apelin level in PE, investigate its correlation with some inflammatory, oxidative stress, and angiogenic proteins in a nitric oxide synthase inhibitor; the N (gamma)-nitro-L-arginine methyl ester (L-NAME)-induced rat model of PE and determine whether apelin administration could protect against development of PE. 40 healthy adult female albino rats and 10 adult male albino rats were used in this study. The pregnant female rats were randomly divided into three groups: group 1 (normal pregnant group), group 2 (PE-induced group), injected subcutaneously with 75 mg L-NAME/kg bodyweight/day starting from day 9 to 20 of gestation, and group 3 (PE-induced group supplemented with apelin (PE + apelin)); PE induced as before and simultaneously subcutaneously injected with apelin-13 (6 × 10−8 mol/kg bodyweight/twice daily) beginning from day 6 to 20 of gestation. In all groups, blood pressure and urine protein were determined at gestation days (GD) 0, 10, and 18. Moreover, serum apelin, placental growth factor (PLGF), vascular endothelial growth factor (VEGF), soluble fms-like tyrosine kinase-1 (sFlt-1), soluble endoglin (sEng), interferon-gamma (IFN-γ), and interleukin-10 (IL-10) levels and serum superoxide dismutase enzyme (SOD) and catalase (CAT) activities of all groups were estimated at the end of experiment. Placental histopathological examination was also performed. PE-induced rats showed significantly decreased serum apelin levels. Moreover, they showed significantly increased blood pressures, urine proteins, sFlt-1, sEng, and IFN-γ (mean arterial blood pressure, urine proteins, sFlt-1, sEng, and IFN-γ showed significant negative correlations with serum apelin level), but it showed significantly decreased VEGF, PLGF, IL-10, SOD, and CAT (VEGF, PLGF, IL-10, and SOD showed significant positive correlations with serum apelin level). In contrast, exogenous apelin administration significantly ameliorated these parameters together with improvement in the placental histoarchitecture in the apelin-supplemented PE group. This study demonstrated the protective effects of apelin administration on the pathogenesis of PE.

A prospective cohort study of confirmed severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection during pregnancy evaluating SARS-CoV-2 antibodies in maternal and umbilical cord blood and SARS-CoV-2 in vaginal swabs.

IntroductionEvidence about the consequences of severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection in pregnancy is rapidly increasing; however, data on antibody response and risk of transmission during pregnancy and delivery are still limited. The aim of this study was to evaluate if SARS‐CoV‐2 is detectable in vaginal swabs and whether antibodies against SARS‐CoV‐2 are present in maternal and umbilical cord blood of pregnant women with confirmed SARS‐CoV‐2.Material and methodsA single‐unit prospective cohort study in Denmark including pregnant women with SARS‐CoV‐2 infection confirmed by a pharyngeal swab between August 20, 2020, and March 1, 2021, who gave birth during the same period. All patients admitted to the maternity ward and antepartum clinic were screened for SARS‐CoV‐2 infection. A maternal blood sample and vaginal swabs were collected at inclusion. If included antepartum, these samples were repeated intrapartum when an umbilical cord blood sample was also collected. Swabs were analyzed for SARS‐CoV‐2 and blood samples were analyzed for SARS‐CoV‐2 total antibodies. Placental and neonatal swabs as well as placental histopathological examinations were performed on clinical indications.ResultsWe included 28 women, of whom four had serious maternal or fetal outcomes including one case of neonatal death. Within the first 8 days after confirmed SARS‐CoV‐2 infection, SARS‐CoV‐2 was detectable in two vaginal swabs (2/28) and SARS‐CoV‐2 antibodies were detected in 1 of 13 women. From 16 days after confirmed infection, antibodies were observed in 19 of 21 of women. Antibodies in cord blood were not detected during the first 16 days after confirmed infection (n = 7). However, from 26 days, antibodies were present in 16 of 17 cord blood samples of seropositive mothers. Placental examination in two cases of severe fetal outcomes preceded by reduced fetal movements revealed SARS‐CoV‐2 in swabs and severe histopathological abnormalities.ConclusionsSARS‐CoV‐2 was detected in only 2 of 28 vaginal swabs within 8 days after confirmed infection in pregnant women. Our data suggest that maternal seroconversion occurs between days 8 and 16, whereas antibodies in cord blood of seropositive mothers were present in the majority from 26 days after confirmed infection. Additional data are needed regarding timing of seroconversion for the mother and appearance of antibodies in cord blood.

Massive Perivillous Fibrin Deposition-A Cause of Recurrent Fetal Demise: A Case Report

Abstract Introduction/Objective Massive perivillous fibrin deposition (MPFD) and maternal floor infarction (MFI) are rare placental lesions reported in less than 1% of all pregnancies and have a significant risk of recurrence ranging from 12% to 78%. MPFD/MFI is associated with high rates of adverse perinatal outcomes including preterm delivery, severe intrauterine growth restriction, spontaneous abortion, cystic renal cell dysplasia, fetal metabolic disease with reported mutations in the LCHAD (long-chain 3-hydroxy acyl-CoA-dehydrogenase) gene, neonatal death and long- term neurological impairment. Methods/Case Report We report a case of MFPD in a 28-year-old female gravida 3 para 1 with one uncomplicated pregnancy and one therapeutic abortion. The current pregnancy was complicated by abruption resulting in intrauterine fetal demise at 32 weeks of gestation. The placenta was examined. Grossly, the placenta weighed 260 grams (small placenta for the dates) with an eccentrically inserted three vessel umbilical cord and a diffuse, firm pale grey cut surface with focal cystic areas. The histological examination revealed MPFD characterized by extensive transmural perivillous fibrinoid material with encasement of almost entire chorionic villi (transmural type). The villi were viable but fibrotic with focal syncytiotrophoblastic necrosis and focal mild chronic inflammation. The etiology of MPFD is not well understood, but risk factors that have been reported include maternal thrombophilia, coagulopathies, and autoimmune diseases. Given the clinical associations, MFI/MPFD should be reported promptly to the obstetrician and pediatrician. As per the current literature, a combination of thrombolytic therapy (aspirin and heparin), intravenous immunoglobulin and a statin (pravastatin) helps to correct angiogenic/antiangiogenic imbalance which has been thought to be associated with recurrent MFI/MPFD. Results (if a Case Study enter NA) N/A Conclusion In summary, we present this rare recurring entity of MPFD to emphasize the awareness of this condition and the importance of placental examination in all abortions and fetal abnormalities/demise.

Distinctive Neuroimaging Pattern in Term Newborns With Neonatal Placental Encephalopathy: A Case Series

BackgroundIdentifying antepartum versus intrapartum timing and the cause of neonatal encephalopathy (NE) often remains elusive owing to our limited understanding of the underlying pathophysiological processes and lack of appropriate biomarkers. ObjectivesThis retrospective observational study describes a case series of term newborns with NE who displayed a recognizable magnetic resonance imaging pattern of immediately postnatal brain abnormalities that rapidly evolved toward cavitation. Our aim is to (1) report this neuroimaging pattern, (2) look for placental determinants, and (3) depict the outcome. Design/MethodsThis is a unicentric retrospective case series reporting the clinical, radiological, and laboratory findings of NE associated with a distinctive neuroimaging pattern, that is, immediately postnatal extensive corticosubcortical T2 hyperintensities, followed by rapid corticosubcortical cavitation that does not match the neuroimaging picture of intrapartum hypoxic-ischemic encephalopathy (HIE). ResultsSeven term newborns presented bilateral corticosubcortical hyperintensities that were detected on T2 between day of life (DOL) 1-4, which rapidly evolved toward cystic encephalomalacia, that is, between DOL9 and DOL12. All these newborns presented with moderate/severe NE. The outcome was either neonatal death or quadriplegic cerebral palsy and epilepsy. None of the reported patients fulfilled the criteria of a high likelihood of acute intrapartum hypoxic-ischemic or quadriplegic cerebral palsy. All these newborns were exposed to chronic and/or acute placental inflammation and/or hypoxic-ischemic. ConclusionsTo further define the antepartum causes of NE, early neuroimaging and a placental examination are recommended. Brain T2 hyperintense injuries before DOL4 followed by rapid cavitation before DOL12 might be biomarkers of NE from an antepartum/placental origin.

T2* weighted placental MRI in relation to placental histology and birth weight.

Placental dysfunction may be found among normal birth weight (BW) pregnancies, as indicated by abnormal histological findings in postnatal placental examination in some of these pregnancies. T2* weighted placental MRI provides non-invasive information on placental oxygenation and thereby placental function. The aim of this study was to investigate the correlation between placental T2*, BW and placental histology. A total of 63 pregnant women underwent T2* weighted placental MRI at 15-40 week's gestation and a standardized placental histological examination (PHE). Abnormal PHE was defined by vascular malperfusion according to the Amsterdam workshop consensus. The correlation between PHE, BW z-score and T2* z-score was analyzed by logistic regression. Abnormal PHE was revealed in 28 pregnancies. Multiple logistic regression revealed a significant correlation between abnormal PHE and T2* z-score (OR=0.34, p=0.008), whereas BW z-score did not add significantly to the correlation of placental histology (OR=0.52, p=0.115). In BW z-score≥0, PHE was normal in 100% of pregnancies. In BW z-score≤-2, PHE was abnormal in 89% of pregnancies. In intermediate BW (z-score between -2 and 0), PPE was abnormal in 35% of pregnancies. In this intermediate group, placental T2* z-score was reduced (-1.52±1.22 (mean SD)) when compared to normal PHE pregnancies (-0.28±1.17), p=0.006. This study demonstrates a correlation between abnormal placental histology and low placental T2* value regardless of fetal size. This indicates that T2* provides information of placental function in vivo even when fetal size is normal. This finding highlights that fetal size alone is not a valid marker of placental dysfunction.

VP31.20: Fetal deaths in COVID‐19 infected pregnancies

Fetal death as an ultimate consequence of COVID-19 infection in pregnancy, is a complication that must not be underestimated. Maternal infection can trigger a hyper-inflammatory response, causing endothelial vascular dysfunction and coagulation abnormalities. These lesions compromise placental perfusion which consequently affects fetal perfusion and leads, in some situations, to fetal anoxia and death. Our case series report clinical, analytical and histopathological findings of four cases of in utero fetal demise in COVID-19 infected pregnant women, without any other obvious cause, managed at a tertiary hospital, in Portugal. All pregnancies were uncomplicated until the third trimester and either had obstetric history or developed obstetric conditions related to placental vascular compromise such as hypertensive disorders of pregnancy and fetal growth restriction. Three cases were asymptomatic for COVID-19 on admission, whereas the fourth presented mild symptoms and developed disseminated intravascular coagulation. All fetus were morphologically normal and two of them tested positive for COVID-19. Placental histopathological examinations revealed multiple signs of maternal and fetal vascular malperfusion, chorioangioma and increased perivillous fibrin deposition, findings that are consistent with those observed in hypertensive disorders of pregnancy and fetal growth restriction. This observation suggests that COVID-19 can place at greater risk of in utero fetal demise pregnancies that are already complicated by obstetric conditions related with impaired placental perfusion.