Ultrasound diagnosis of placental and umbilical cord anomalies in singleton pregnancies resulting from in-vitro fertilization.

INTRODUCTION: placental anomalies can affect fetal and maternal outcome due to severe maternal hemorrhage potentially resulting in hysterectomy and cord accident including abruption that can determine fetal damage or death. The aims of our study are to determine if the rate of placental and umbilical cord anomalies are more common in IVF singleton pregnancies compared to spontaneous pregnancies; to evaluate the role of ultrasound in screening for these anomalies and to investigate if oocyte donor fertilization is an additional risk factor for the development of these anomalies. METHODS: this was a prospective cohort study involving two tertiary centers. Patients with a singleton pregnancy conceived with IVF and patients presenting with a spontaneous conception were recruited between 1st May 2019 to 31st March 2021. A total of 634 pregnancies were enrolled in the study. All patients underwent similar antenatal care, which included ultrasound examinations at 11-14, 19-22 and 33-35 weeks. Ultrasound findings of placental and/or umbilical cord abnormalities were recorded using the same protocol for both groups and confirmed after birth. RESULTS: IVF pregnancies had a significantly higher risk of low-lying placenta, placenta previa, bilobed placenta and velamentous cord insertion (VCI) compared with spontaneous pregnancies. In the heterologous subgroup there was a significant increased incidence of placenta accreta spectrum (PAS) disorders than in spontaneous pregnancies. All these anomalies were identified prenatally on ultrasound imaging and confirmed at birth. DISCUSSION: IVF pregnancies in general and those resulting from donor oocyte in particular are at higher risk of placental and umbilical cord abnormalities compared to spontaneous pregnancies. These anomalies can be diagnosed accurately at the mid-trimester detailed fetal anomaly scan and our findings support the need for a targeted ultrasound screening of these anomalies in IVF pregnancies.

Examination of a Stillbirth Workup: A Rural Statewide Experience.

OBJECTIVE: The objective of our study was to determine whether recommended assessments were conducted on stillbirths delivered in our predominantly rural state. METHODS: This was a descriptive study of stillbirths delivered in a rural state and included in one site of the Birth Defects Study to Evaluate Pregnancy Exposures stillbirth study. Hospital and fetal death records were examined to determine whether the following areas were evaluated: genetic testing (noninvasive perinatal testing, quad screen, amniocentesis/chorionic villus sampling with karyotype, microarrays, fetal tissue specimen), placenta/membrane/cord sent for pathologic examination, examination of the stillbirth after delivery by the healthcare provider, and fetal autopsy was performed. RESULTS: From July 1, 2015 to June 30, 2020, there were 1108 stillbirths delivered in Arkansas. The most frequent assessments undertaken were placental pathology (72%), genetic testing (67%), fetal inspection (31%), and autopsy (13%). All four assessments were done in 2% of stillbirth cases, three assessments in 27%, two assessments in 47%, one assessment in 14%, and no assessment in 15%. There was no association between stillbirth assessment evaluation by gestational age (<28 weeks and > 28 weeks; P = 0.221); however, there was an overall association between hospital delivery volume with number of components completed (P < 0.0001). Hospitals with >2000 deliveries had a higher proportion of three or four completions compared with those hospitals with <1000 deliveries or 1000 to 2000 deliveries (P = 0.021 and P < 0.0001). CONCLUSIONS: Fetal stillbirth assessment is suboptimal in our rural state, with 15% of stillbirths having no assessment and only 2% having all four assessments. There is no association between stillbirth assessment and gestational age (<28 weeks vs >28 weeks), but there is a correlation between delivery volume and stillbirth assessment.

The causes of stillbirths in south Asia: results from a prospective study in India and Pakistan (PURPOSe).

BACKGROUND: South Asia contributes more than a third of all global stillbirths, yet the causes remain largely unstudied in this region. New investigations, including novel assessments of placental and fetal tissues, facilitate more precise determination of the underlying causes of stillbirth. We sought to assess underlying and contributing causes of stillbirth from settings in India and Pakistan. METHODS: In this prospective cohort study (PURPOSe), we report the cause of death in stillbirths in hospitals in central India and south Pakistan (Davangere, India [three public and private hospitals] and Karachi, Pakistan [one public maternity and one children's hospital]). Women aged 15 years or older and with a known stillbirth (defined as a pregnancy at 20 or more weeks of gestation with the in-utero death of a fetus) weighing 1000 g or more were included in the study. Maternal clinical factors, placental evaluation, fetal tissue evaluation (from minimally invasive tissue sampling), and PCR for microbial pathogens were used to identify the causes of death. An expert panel reviewed available data for all stillbirths to identify the primary and contributing maternal, placental, and fetal causes of stillbirth. FINDINGS: Between Sept 1, 2018, and Feb 12, 2020, 981 stillborns were included and, of those, 611 were reviewed by the expert panel. The primary maternal causes of stillbirth were hypertensive disease in 221 (36%) of 611 stillbirths, followed by severe anaemia in 66 (11%) stillbirths. The primary placental causes were maternal and fetal vascular malperfusion, in 289 (47%) stillbirths. The primary fetal cause of stillbirth was intrauterine hypoxia, in 437 (72%) stillbirths. We assessed the overlap of main causes and 116 (19%) stillbirths had intrauterine hypoxia, placental malperfusion, and eclampsia or pre-eclampsia indicated as primary causes of death. Infection (including of the placenta, its membranes, and in the fetus) and congenital anomalies also were causative of stillbirth. INTERPRETATION: In south Asia, fetal asphyxia is the major cause of stillbirth. Several placental lesions, especially those associated with maternal and fetal vascular malperfusion and placental abruption, have an important role in asphyxia and fetal death. Maternal hypertension, and especially pre-eclampsia, is often the primary maternal condition associated with this pathway. FUNDING: Bill & Melinda Gates Foundation.

Prenatal Diagnosis of Vasa Previa by Routine Transvaginal Color Doppler.

The prenatal diagnosis of vasa previa is essential to achieving a safe delivery in patients who suffer from the condition. Transvaginal ultrasound with color Doppler performed at the time of a routine mid-trimester ultrasound is a valuable tool in terms of achieving a timely and accurate diagnosis of vasa previa.

MRI based morphological examination of the placenta.

Ultrasound is widely used as the initial diagnostic imaging modality during pregnancy with both high spatial and temporal resolution. Although MRI in pregnancy has long focused on the fetus, its use in placental imaging has greatly increased over recent years. In addition to the possibilities of evaluating function, MRI with a wide field of view and high contrast resolution allows characterization of placental anatomy, particularly in situations that are difficult to specify with ultrasound, especially for suspected placenta accreta. MRI also appears to be a particularly useful examination for the anatomical evaluation of the placenta independent of maternal body habitus or fetal position. Indeed, surprisingly little attention is paid to the placenta in MRI when the indication for the examination is fetal. Thus, some aspects of the placenta seem to us to be important to be recognized by the radiologist and to be described on the MRI report. In this review, we will describe MRI sequences used for, and common features seen in, imaging of i) the normal placenta, ii) abnormal aspects of the placenta that should be identified on MRI performed for fetal reason, and iii) placental anomalies for which placental MRI may be indicated.

The relationship between placental characteristics and birthweight discordance in different types of selective intrauterine growth restriction in monochorionic diamniotic twins: A single-center 7 year cohort study.

OBJECTIVE: To clarify the relationships between placental characteristics and birthweight discordance in three types of selective intrauterine growth restriction (sIUGR) in monochorionic diamniotic twins. METHODS: A retrospective cohort study was conducted between april 2013 and april 2020. Associations between placental characteristics and birthweight discordance were evaluated through multiple linear regression analyses with two models for each sIUGR type. Model A was adjusted for gestational age, Model B additionally adjusted for the impact of placental characteristics interacted. RESULTS: In cases of type I sIUGR, birthweight discordance ratio was positively associated with placental territory discordance ratio [(ß = 0.181,95%CI(0.072,0.290), p < 0.05), (ß = 0.239,95%CI(0.125, 0.353), p < 0.05)] under both Model A and Model B. In-type II sIUGR [(ß = -0.012,95%CI(-0.020, -0.004), p < 0.05) (ß = -0.010,95%CI (-0.018, -0.002), p < 0.05)] and type III sIUGR [(ß = -0.011,95%CI (-0.021, -0.001), p < 0.05), (ß = -0.012,95%CI(-0.022, -0.003), p < 0.05)], birthweight discordance ratio was negatively associated with the total diameter of all the anastomoses as calculated with both Model A and Model B. CONCLUSION: Birthweight discordance is primarily related to placental territory discordance in type I sIUGR, whereas vascular anastomoses play important roles for growth-restricted fetal compensation in type II and III sIUGR.

Acretismo placentario en gestaciones tempranas. Presentación de un caso / Placental accreta in early pregnancies. Case presentation

El acretismo placentario es la invasión de las vellosidades coriales al miometrio, siendo mayor el riesgo de presentarse en casos de placenta previa o antecedente de una o más cesáreas, causando hemorragia obstétrica mayoritariamente durante el tercer trimestre. Se presenta el caso de una paciente de 39 años de edad, con hemorragia obstétrica secundaria a acretismo placentario, en un embarazo de 19 semanas resuelto mediante histerectomía, con lo que se hace énfasis en la importancia de la sospecha y diagnóstico de acretismo en embarazos tempranos, ofreciendo así un tratamiento oportuno y disminución de la morbimortalidad materna.(AU)

Placental accreta is the invasion of the chorionic villi into the myometrium. It has a higher risk of occurring in cases of placenta previa, or a history of one or more caesarean sections, causing obstetric haemorrhage mainly during the third trimester. The case is presented of a 39-year-old patient with obstetric haemorrhage secondary to placental accreta in a 19-week pregnancy. It was resolved by hysterectomy. The importance of suspicion and diagnosis of accreta in early pregnancies is emphasised, as well as offering a timely treatment and reducing the maternal morbidity and mortality.(AU)

Effects of Pparγ1 deletion on late-stage murine embryogenesis and cells that undergo endocycle.

Peroxisome proliferator-activated receptor (PPAR) γ1, a nuclear receptor, is abundant in the murine placenta during the late stage of pregnancy (E15-E16), although its functional roles remain unclear. PPARγ1 is encoded by two splicing isoforms, namely Pparγ1canonical and Pparγ1sv, and its embryonic loss leads to early (E10) embryonic lethality. Thus, we generated knockout (KO) mice that carried only one of the isoforms to obtain a milder phenotype. Pparγ1sv-KO mice were viable and fertile, whereas Pparγ1canonical-KO mice failed to recover around the weaning age. Pparγ1canonical-KO embryos developed normally up to 15.5 dpc, followed by growth delays after that. The junctional zone of Pparγ1canonical-KO placentas severely infiltrated the labyrinth, and maternal blood sinuses were dilated. In the wild-type, PPARγ1 was highly expressed in sinusoidal trophoblast giant cells (S-TGCs), peaking at 15.5 dpc. Pparγ1canonical-KO abolished PPARγ1 expression in S-TGCs. Notably, the S-TGCs had unusually enlarged nuclei and often occupied maternal vascular spaces, disturbing the organization of the fine labyrinth structure. Gene expression analyses of Pparγ1canonical-KO placentas indicated enhanced S-phase cell cycle signatures. EdU-positive S-TGCs in Pparγ1canonical-KO placentas were greater in number than those in wild-type placentas, suggesting that the cells continued to endoreplicate in the mutant placentas. These results indicate that PPARγ1, a known cell cycle arrest mediator, is involved in the transition of TGCs undergoing endocycling to the terminal differentiation stage in the placentas. Therefore, PPARγ1 deficiency, induced through genetic manipulation, leads to placental insufficiency.

Advanced maternal age causes premature placental senescence and malformation via dysregulated α-Klotho expression in trophoblasts.

Advanced maternal age (AMA) pregnancy is associated with higher risks of adverse perinatal outcomes, which may result from premature senescence of the placenta. α-Klotho is a well-known antiaging protein; however, its expression and effect on the placenta in AMA pregnancies have not yet been fully elucidated. The expression patterns of α-Klotho in mouse and human placentas from AMA pregnancies were determined by Western blotting and immunohistochemistry (IHC) staining. α-Klotho expression in JAR cells was manipulated to investigate its role in trophoblastic senescence, and transwell assays were performed to assess trophoblast invasion. The downstream genes regulated by α-Klotho in JAR cells were first screened by mRNA sequencing in α-Klotho-knockdown and control JAR cells and then validated. α-Klotho-deficient mice were generated by injecting klotho-interfering adenovirus (Ad-Klotho) via the tail vein on GD8.5. Ablation of α-Klotho resulted in not only a senescent phenotype and loss of invasiveness in JAR cells but also a reduction in the transcription of cell adhesion molecule (CAM) genes. Overexpression of α-Klotho significantly improved invasion but did not alter the expression of senescence biomarkers. α-Klotho-deficient mice exhibited placental malformation and, consequently, lower placental and fetal weights. In conclusion, AMA results in reduced α-Klotho expression in placental trophoblasts, therefore leading to premature senescence and loss of invasion (possibly through the downregulation of CAMs), both of which ultimately result in placental malformation and adverse perinatal outcomes.

Fetal Autopsy-Categories and Causes of Death at a Tertiary Care Center.

BACKGROUND: A fetus is defined from 8 weeks after conception until term while in the uterus. Fetal death is defined as death of the fetus before the complete expulsion or extraction from the mother, irrespective of the duration of pregnancy that is not an induced termination of pregnancy. The causes of fetal death determined after fetal autopsy can be categorized according to the classification proposed by Cunningham and Hollier as fetal, placental, and maternal. METHODS: All fetuses dying in utero, that is, prior to birth, regardless of the gestational age, to the mothers admitted in the Department of Obstetrics and Gynecology along with the respective placentas were received in the Department of Pathology, MGM Medical College, Aurangabad, after an informed and written consent from October 26, 2017, to October 30, 2019, and were included in this study. Clinical details along with obstetric history and antenatal ultrasonographic findings were also recorded. Anthropometric examination of the fetus was performed and evisceration was then done using the Rokitansky technique. Representative sections from each of the organs were taken and kept in tissue cassettes and processed for routine hematoxylin and eosin staining. RESULTS: This study was done on 33 cases of fetal death. Most fetal deaths occurred in the gestational age between 15 and 19 weeks (14 cases [42.42%]) and the least amount during 35 to 39 weeks (2 cases [6.06%]). The cause of death could not be ascertained in 6 cases (18.18%), whereas the maximum cases had fetal factor as the cause of death (15 cases [45.45%]). Maternal causes were seen in only 4 cases (12.12%). Gestational hypertension was seen to be the most common maternal factor associated with fetal death, which comprised 24.24% of cases (8 of 33). Thirteen of the total 33 cases did not have any associated obstetric complication. Of the total 33 fetal deaths, only 7 had associated placental defects on gross examination. Twenty-six placentas did not show any gross abnormality. Of these 7 cases, 5 were seen to have placental infarction. CONCLUSIONS: Fetal autopsy is a valuable and cost-effective modality for the confirmation of cause of fetal death. Fetal autopsy can also prove beneficial to the parents in planning for future pregnancies. Fetal autopsy can serve as the ultimate tool in diagnosing cause of fetal death in cases where no other diagnostic clue is available. Therefore, it should be encouraged and couples to be counseled regarding its importance and clinical utility.

Trisomy 8 mosaicism in the placenta: A Danish cohort study of 37 cases and a literature review.

OBJECTIVE: To evaluate the risk of fetal involvement when trisomy 8 mosaicism (T8M) is detected in chorionic villus samples (CVS). METHODS: A retrospective descriptive study of registered pregnancies in Denmark with T8M in CVS identified through a database search and a review of published cases of T8M found through a systematic literature search and inclusion of cross references. Pregnancies with T8M in CVS and no additional numerical chromosomal aberrations were included. RESULTS: A total of 37 Danish cases and 60 published cases were included. T8M detected in a CVS was associated with fetal involvement in 18 out of 97 pregnancies (18.6% [95%CI: 11.4-27.7]). Eight out of 70 (11.4% [95%CI: 5.1-21.3]) interpreted prenatally to be confined placental mosaicism (CPM) were subsequently found to be true fetal mosaicisms (TFM). CONCLUSION: T8M detected in CVS poses a significant risk of fetal involvement, and examination of amniotic fluid (AF) and/or fetal tissue should be offered. However, a normal result of AF still has a considerable residual risk of fetal involvement. Genetic counselling at an early gestational age is essential, and follow-up ultrasonography should be performed to predict fetal involvement if possible.

A double-blind randomized trial on subendometrial injection of vasopressin to control bleeding in postpartum hysterectomy due to abnormally invasive placenta.

OBJECTIVE: To investigate the effect of subendometrial vasopressin injection in patients with abnormally invasive placenta (AIP), who underwent cesarean section and hysterectomy. METHODS: This randomized double-blinded clinical trial was conducted on pregnant women diagnosed with AIP grade 4 and 5 by ultrasonography during cesarean section. Women were randomly divided into two equal groups including group 1 (vasopressin) and group 2 (control) who underwent 20 units of vasopressin and 20 cc normal saline injection, respectively. Vasopressin and placebo were injected subendometrially 1 cm medial to the uterine vessels into the lower uterine segment. The exclusion criteria include presence of myocardial infarction, cardiomyopathy, congestive heart failure, uncontrolled hypertension, chronic obstructive pulmonary disease, pelvic malignancy. The outcome of the study was total quantitative blood loss during the cesarean section. We estimated blood loss by measuring the blood volume in one of the suction bottles with addition for weight changes of mops, pads, and soaked linen savers. RESULTS: Sixty patients were recruited into the study, 30 as the vasopressin group and 30 as the controls; with no excluded case. The amount of bleeding in the vasopressin group was significantly lower compared with that in the control group (P < 0.001). In the vasopressin group, 83.4% of patients had bleeding of less than 1.5 L, while only 3.3% of the control women had bleeding of less than 1.5 L (relative risk = 5). In addition, the number of injected packed cells was lower in the vasopressin group (P < 0.001). CONCLUSION: It was shown that vasopressin injection can help prevent excess hemorrhage and the subsequent risks of anemia or blood transfusions during abdominal hysterectomy in women with AIP.

STOX1 deficiency is associated with renin-mediated gestational hypertension and placental defects.

The pathogenesis of preeclampsia and other hypertensive disorders of pregnancy remains poorly defined despite the substantial burden of maternal and neonatal morbidity associated with these conditions. In particular, the role of genetic variants as determinants of disease susceptibility is understudied. Storkhead-box protein 1 (STOX1) was first identified as a preeclampsia risk gene through family-based genetic linkage studies in which loss-of-function variants were proposed to underlie increased preeclampsia susceptibility. We generated a genetic Stox1 loss-of-function mouse model (Stox1 KO) to evaluate whether STOX1 regulates blood pressure in pregnancy. Pregnant Stox1-KO mice developed gestational hypertension evidenced by a significant increase in blood pressure compared with WT by E17.5. While severe renal, placental, or fetal growth abnormalities were not observed, the Stox1-KO phenotype was associated with placental vascular and extracellular matrix abnormalities. Mechanistically, we found that gestational hypertension in Stox1-KO mice resulted from activation of the uteroplacental renin-angiotensin system. This mechanism was supported by showing that treatment of pregnant Stox1-KO mice with an angiotensin II receptor blocker rescued the phenotype. Our study demonstrates the utility of genetic mouse models for uncovering links between genetic variants and effector pathways implicated in the pathogenesis of hypertensive disorders of pregnancy.

Diverse species-specific phenotypic consequences of loss of function sorting nexin 14 mutations.

Mutations in the SNX14 gene cause spinocerebellar ataxia, autosomal recessive 20 (SCAR20) in both humans and dogs. Studies implicating the phenotypic consequences of SNX14 mutations to be consequences of subcellular disruption to autophagy and lipid metabolism have been limited to in vitro investigation of patient-derived dermal fibroblasts, laboratory engineered cell lines and developmental analysis of zebrafish morphants. SNX14 homologues Snz (Drosophila) and Mdm1 (yeast) have also been conducted, demonstrated an important biochemical role during lipid biogenesis. In this study we report the effect of loss of SNX14 in mice, which resulted in embryonic lethality around mid-gestation due to placental pathology that involves severe disruption to syncytiotrophoblast cell differentiation. In contrast to other vertebrates, zebrafish carrying a homozygous, maternal zygotic snx14 genetic loss-of-function mutation were both viable and anatomically normal. Whilst no obvious behavioural effects were observed, elevated levels of neutral lipids and phospholipids resemble previously reported effects on lipid homeostasis in other species. The biochemical role of SNX14 therefore appears largely conserved through evolution while the consequences of loss of function varies between species. Mouse and zebrafish models therefore provide valuable insights into the functional importance of SNX14 with distinct opportunities for investigating its cellular and metabolic function in vivo.

A missense mutation of ErbB2 produces a novel mouse model of stillbirth associated with a cardiac abnormality but lacking abnormalities of placental structure.

BACKGROUND: In humans, stillbirth describes the death of a fetus before birth after 28 weeks gestation, and accounts for approximately 2.6 million deaths worldwide annually. In high-income countries, up to half of stillbirths have an unknown cause and are described as "unexplained stillbirths"; this lack of understanding impairs efforts to prevent stillbirth. There are also few animal models of stillbirth, but those that have been described usually have significant placental abnormalities. This study describes a novel mutant murine model of fetal death with atrial conduction block due to an ErbB2 missense mutation which is not associated with abnormal placental morphology. METHODS: Phenotypic characterisation and histological analysis of the mutant mouse model was conducted. The mRNA distribution of the early cardiomyocyte marker Nkx2-5 was assessed via in situ hybridisation. Cardiac structure was quantified and cellular morphology evaluated by electron microscopy. Immunostaining was employed to quantify placental structure and cell characteristics on matched heterozygous and homozygous mutant placental samples. RESULTS: There were no structural abnormalities observed in hearts of mutant embryos. Comparable Nkx2-5 expression was observed in hearts of mutants and controls, suggesting normal cardiac specification. Additionally, there was no significant difference in the weight, placenta dimensions, giant cell characteristics, labyrinth tissue composition, levels of apoptosis, proliferation or vascularisation between placentas of homozygous mutant mice and controls. CONCLUSION: Embryonic lethality in the ErbB2 homozygous mutant mouse cannot be attributed to placental pathology. As such, we conclude the ErbB2M802R mutant is a model of stillbirth with a non-placental cause of death. The mechanism of the atrial block resulting from ErbB2 mutation and its role in embryonic death is still unclear. Studying this mutant mouse model could identify candidate genes involved in stillbirth associated with structural or functional cardiac defects.

Intermittent absent and reversed umbilical artery flows in appropriately grown monochorionic diamniotic twins in relation to proximate cord insertion: A harmful combination?

OBJECTIVE: To compare the prevalence of intermittent absent or reversed end-diastolic flow (iAREDF) in the umbilical artery in appropriately grown monochorionic diamniotic (MCDA) pregnancies with and without proximate cord insertion (PCI), and to evaluate pregnancy outcome. METHODS: The prevalence of iAREDF in MCDA pregnancies with PCI (n = 11) was compared with a control group without PCI (n = 33). PCI was defined as a distance between the cord insertions below the fifth percentile. Placental sharing, number, and diameter of anastomoses were assessed by placental examination. Pregnancy outcome was evaluated. RESULTS: iAREDF was present in 7/11 PCI pregnancies, compared with 0/33 in the control group (P ≤ .01). All PCI pregnancies and 94% of controls had arterioarterial (AA)-anastomoses (P = .56), the diameter was larger in the PCI group, respectively 3.3 vs 2.1 mm (P = .03). Three cases with iAREDF had adverse outcome, two resulted in fetal death of which one with brain damage in the co-twin, another underwent early premature emergency section for fetal distress. CONCLUSION: iAREDF occurs in a large proportion of MCDA pregnancies with PCI and is related to the diameter of the AA anastomosis. We hypothesize that iAREDF in appropriately grown MCDA twin pregnancies reflects an unstable hemodynamic balance with an increased risk for fetal deterioration. Whether outcome in these pregnancies can be improved by altered management requires further investigation.

Causes of aberrant non-invasive prenatal testing for aneuploidy: A systematic review.

Non-invasive prenatal testing (NIPT) is performed worldwide to detect common chromosomal aneuploidies. The analysis of cell-free DNA (cfDNA) in maternal blood for NIPT is highly accurate for the detection of the main fetal trisomies: 21,18, and 13. However, false-positive, false-negative, and non-reportable results can occur, and these can have biological causes. Understanding the causes of unexpected NIPT results is essential to enable clinicians and genetic counselors to counsel patients comprehensively and appropriately, both prior to testing as well as after receiving the test results. The classification of non-reportable results from cfDNA analysis is important in order to provide women with precise information. In addition to technical issues, there are biological reasons for discordant results, which can be either fetal or maternal in origin. Contributing fetal factors include insufficient or absent fetal fraction, fetoplacental mosaicism, and the presence of a vanishing twin. In some pregnant women that test positive for NIPT, multiple chromosome aneuploidy has been reported as a result of suspected malignancy, and cancer has been found. False-positive and false-negative results may be the result of placental biology and not a failure in the actual test platform. Explaining the placental origin of cfDNA provides the patient with a clear view of the abilities and limitations of cfDNA-based prenatal screening.

Comparison between abdominal ultrasound and nuclear magnetic resonance imaging detection of placenta accreta in the second and third trimester of pregnancy.

This study is to determine accuracy of abdominal ultrasound and nuclear magnetic resonance imaging (MRI) for placenta accreta in the second and third trimester of pregnancy and to define the most relevant features of abdominal ultrasound and MRI for placenta accreta prediction.Between September 2012 and September 2018, 245 high risk of placenta accreta in the second trimester of pregnancy were prenatal diagnosed by abdominal ultrasound and MRI and they were followed up until the end of pregnancy.Forty-six patients at the second trimester of pregnancy and 40 patients at the third trimester of pregnancy were confirmed as placenta accreta. For the second and third trimester of pregnancy, the sensitivity (Se), specificity (Sp), positive and negative predictive value (PPV and NPV) of abdominal ultrasound were 95.65% versus 97.50%, 91.78% versus 90.70%, 88% versus 83%, and 97% versus 99%, respectively, while the Se, Sp, PPV, and NPV of MRI were 89.13% versus 92.50%, 87.67% versus 8721%, 82% versus 77%, and 93% versus 96%, respectively. Five features having significant statistical differences between normal placentation women and placenta accreta patients in second or third trimester of pregnancy, including loss of the normal retroplacental clear space, thinning or disappearance of the myometrium, increased vascularization at the uterine serosa-bladder wall interface, and vascularization perpendicular to the uterine wall on abdominal ultrasound, and uterine bulging and dark intraplacental bands on MRI.Abdominal ultrasound and MRI for placenta accreta in the second and third trimester of pregnancy could provide meaningful imaging evidences.