Abnormal Placenta Research Articles

Threshold value of lactic acid and buffer excess in umbilical cord arterial blood gas during neonatal asphyxia

Objective To study the threshold values of lactic acid (Lac)and buffuer excess (BE) when neonatal umbilical arterial blood gas is at pH <7.20. Methods A total of 2 518 pregnant women admitted in Beijing New Century Women and Children′s Hospital from January 2017 to February 2019 were enrolled.The general conditions in perinatal period and labor methods were counted.Umbilical cord arterial blood was immediately collected before the first cry of newborn and was detected on the Abbott I-STAT automatic blood gas analyzer from the United States, and then the umbilical arterial blood gas was measured.We analyzed the perinatal factors affecting umbilical arterial blood gas.We studied the threshold values of Lac and BE for neonal asphyxia by receiver operating characteristic curve. Results (1)Maternal anemia, Streptococcus agalactiae infection, precipitate labour, placenta abnormalities had no significant impact on neonatal umbilical artery blood gas.The Lac value in blood gas was higher in the group of premature rupture of fetal membranes and fetal intrauterine distress.The value of BE was lower in the group with premature rupture of fetal membranes and fetal distress (P 3.97 mmol/L, the sensitivity and specificity of the diagnosis of asphyxia were 0.864 and 0.791, respectively.When BE was ≤-6 mmol/L, the diagnostic sensitivity and specificity of asphyxia were 0.613 and 0.756, respectively. Conclusion Neonatal umbilical arterial blood gas is affected by many factors.The effect of accouche on umbilical arterial blood gas is large.When there is asphyxia with pH 3.97 mmol/L and ≤-6 mmol/L, respectively. Key words: Umbilical artery; Blood gas analysis; Lactic acid; Buffuer excess; Newborn

Transcriptome-wide analysis of the SCNT bovine abnormal placenta during mid- to late gestation

The dysfunction of placenta is common in somatic cell nuclear transfer (SCNT) cloned cattle and would cause aberrant fetal development and even abortion, which occurred with highest rate at the mid- to late gestation. However, the mechanism of abnormal placentas was unclear. To analyze the transcriptome-wide characteristics of abnormal placentas in SCNT cloned cattle, the mRNA, lncRNA and miRNA of placental cotyledon tissue at day 180 after gestation were sequenced. A total of 19,055 mRNAs, 30,141 lncRNAs and 684 miRNAs were identified. Compared with control group, 362 mRNAs, 1,272 lncRNAs and nine miRNAs (six known and three novel miRNAs) were differentially expressed (fold change ≥ 2 and P-value < 0.05). The differentially expressed genes were functionally enriched in urea and ions transmembrane transport, which indicated that the maternal-fetal interactions were disturbed in impaired placentas. Furthermore, the competing endogenous RNAs (ceRNAs) networks were identified to illustrate their roles in abnormal placental morphology. The present research would be helpful to discover the mechanism of late gestational abnormality of SCNT cattle by provides important genomic information and insights.

Indicators for mode of delivery in pregnant women with uteruses scarred by prior caesarean section: a retrospective study of 679 pregnant women

BackgroundThe delivery mode for pregnant women with uteruses scarred by prior caesarean section (CS) is a controversial issue, even though the CS rate has risen in the past 20 years. We performed this retrospective study to identify the factors associated with preference for CS or vaginal birth after CS (VBAC).MethodsPregnant women (n = 679) with scarred uteruses from Moulay Ali Cherif Provincial Hospital, Rashidiya, Morocco, were enrolled. Gestational age, comorbidity, fetal position, gravidity and parity, abnormal amniotic fluid, macrosomia, placenta previa or abruptio, abnormal fetal presentation, premature rupture of fetal membrane with labor failure, poor progression in delivery, and fetal outcomes were recorded.ResultsOut of 679 pregnant women ≥28 gestational weeks, 351 (51.69%) had a preference for CS. Pregnant women showed preference for CS if they were older (95% CI 1.010–1.097), had higher gestational age (95% CI 1.024–1.286), and a shorter period had passed since the last CS (95% CI 0.842–0.992). Prior gravidity (95% CI 0.638–1.166), parity (95% CI 0.453–1.235), vaginal delivery history (95% CI 0.717–1.818), and birth weight (95% CI 1.000–1.001) did not influence CS preference. In comparison with fetal preference, maternal preference was the prior indicator for CS. Correlation analysis showed that pregnant women with longer intervals since the last CS and history of gravidity, parity, and vaginal delivery showed good progress in the first and second stages of vaginal delivery.ConclusionsWe concluded that maternal and gestational age and interval since the last CS promoted CS preference among pregnant women with scarred uteruses.

Prevalence of obstetric complications including placenta abnormality in pregnancies achieved by oocyte donation in our institution

Prevalence of obstetric complications including placenta abnormality in pregnancies achieved by oocyte donation in our institution

Outcome of Transient Hypogastric Artery Balloon Occlusion with Cesarean Hysterectomy in Abnormal Adherent Placenta: Case Series

Objective: To evaluate the outcome of pregnant women with abnormal placentation who underwent transient hypogastric artery balloon occlusion with cesarean hysterectomy.Material and Methods: Descriptive retrospective study of patients with abnormal adherent placenta who underwent transient hypogastric artery balloon occlusion with cesarean hysterectomy between January 2014 and December 2016. Data were recorded and analyzed.Results: Fourteen pregnant women with abnormal placentation were included in our series. Most patients underwent cesarean hysterectomy at less than 37 weeks of gestational age. The sonograms of 7 cases overestimated the severity of placenta adherence compared with the pathological diagnosis. The median estimated blood loss was 4,350 milliliters (mL). The median estimated blood loss in placenta accrete, increta and percreta were 3,000 mL, 5,337 mL and 5,150 mL, respectively. One case had a procedure-related complication: perforation of the small branch of the anterior division of the right hypogastric artery from the guidewire.Conclusion: Intraoperative transient balloon occlusion of the hypogastric arteries was an effective method and safe treatment for controlling the massive intraoperative bleeding of cesarean hysterectomy. This technique can be an alternative option in combination with surgery in cases of abnormal placental adherence.

Methotrexate infusion followed by uterine artery embolisation for the management of placental adhesive disorders: a case series

To evaluate the efficacy and safety of the uterine artery embolisation (UAE) in combination with methotrexate (MTX) for conservative management of placental adhesive disorders. Patients with placental adhesive disorders (including accreta, increta, and percreta lesions) that were treated with UAE in combination with MTX were identified and were followed prospectively for outcomes including uterine preservation and complications. Twenty-six patients were identified who had the diagnosis of abnormal placenta implantation during this study. Fourteen patients were excluded because they were treated by a caesarean hysterectomy. Among remaining 12 patients, the successful uterine preservation observed in seven (58%) cases. Menstruation cycles returned in all successfully treated patients, although they did not have desire to get pregnant. Five (42%) patients underwent primary or delayed hysterectomy due to severe post-partum haemorrhage in three cases, and intestinal adhesion/peritonitis and secondary post-partum haemorrhage/sepsis in two patients, respectively. Although this interventional method is relatively successful in uterine preservation, the possibility of treatment failure cannot be ignored. Given that there are too few data regarding its efficacy and safety, this method should be reserved to patients who have a strong desire to maintain the uterus and their fertility, or if it is technically difficult to perform hysterectomy due to the extent of the invasion.

Gestational exposure to PM2.5 impairs vascularization of the placenta

The placenta is the bridge that connects the developing fetus and mother and is the place where nutrient uptake, waste elimination and gas exchange occurs. Epidemiological studies indicate that fetal stress, such as gestational PM2.5 (particulate matter (PM) with diameter ≤ 2.5 μm) exposure, is a risk factor for abnormal placenta development that could induce adverse effects on the fetus. In the present study, PM samples were collected in Taiyuan. Then, pregnant C57BL/6 mice were treated with 3 mg/kg b.w. PM2.5 every other day starting on GD0.5, and were sacrificed at embryonic day 13.5 (E13.5), E15.5 and E18.5, and placentas were collected for placenta histopathological analysis and gene expression evaluation at the transcription or translation level. Our results showed that gestational exposure to PM2.5 significantly reduced the ratio of the mean area of labyrinthine (lab) layer/total area of placentas at E18.5. However, no significant difference was observed at E13.5 and E15.5. Interestingly, genes essential for this process were altered at E13.5 and E18.5 but not E15.5. Furthermore, gestational PM2.5 exposure decreased the mean area of maternal blood sinuses and fetal blood vessels and suppressed protein expression of CD31 in the PM2.5 group only at E18.5, while protein expression of CD34 in the PM2.5 group was similar to that in the control group at all time points. Finally, gestational exposure to PM2.5 activated mitogen-activated protein kinase (MAPK) pathways at E13.5 and E18.5 but not E15.5. Taking these results together, gestational exposure to PM2.5 leads to histopathological changes and vascularization injuries of the placenta, and this response may be associated with activation of the MAPK pathway.

Obesity "complements" preeclampsia.

Preeclampsia (PE) is a devastating adverse outcome of pregnancy. Characterized by maternal hypertension, PE, when left untreated, can result in death of both mother and baby. The cause of PE remains unknown, and there is no way to predict which women will develop PE during pregnancy. The only known treatment is delivery of both the fetus and placenta; therefore, an abnormal placenta is thought to play a causal role. Women with obesity before pregnancy have an increased chance of developing PE. Increased adiposity results in a heightened state of systemic inflammation that can influence placental development. Adipose tissue is a rich source of proinflammatory cytokines and complement proteins, which have been implicated in the pathogenesis of PE by promoting the expression of antiangiogenic factors in the mother. Because an aggravated inflammatory response, angiogenic imbalance, and abnormal placentation are observed in PE, we hypothesize that maternal obesity and complement proteins derived from adipose tissue play an important role in the development of PE.

In vitro fertilization alters phospholipid profiles in mouse placenta.

Studies on humans and rodents have clearly shown that in vitro fertilization (IVF) is associated with abnormal placenta formation and function. Currently, dysregulated placental lipid metabolism is one of the emerging pathogenetic pathways implicated in adverse pregnancy outcomes. The purpose of this study was to identify the effects of IVF on lipid metabolism in the mouse placenta. Two groups of mouse placentas, composed of control and IVF, were collected at embryonic day 18.5. Placental lipid profiles were measured using liquid chromatography coupled with mass spectrometry. The relative levels of individual lipid were examined and compared. The proteins and enzymes that regulate the phospholipid biosynthesis were also compared by western blot. A significant increase in levels of phosphatidylcholines, phosphatidylethanolamines, phosphatidylinositols, phosphatidylglycerols, lysophosphatidylcholines, and mitochondrial cardiolipin were found in the IVF placenta. In addition, proteins and enzymes that regulate the phospholipid biosynthesis were also altered in IVF placentas. After lipidomic analysis, we present the first detailed overview of the effect of IVF on lipid metabolism, especially phospholipid profiles in the placenta in a mouse model. The widespread lipidomic shifts identified in this study might explicate some of the placental dysfunction observed after IVF, thereby illustrating that phospholipids serve as early warning biomarkers of health risks in IVF offspring.

Risk factors and complications of small for gestational age.

Objective:The objective of this study was to find out the maternal risk factors and perinatal complications in small for gestational age (SGA) newborns.Methods:A total of 181 SGA cases and 1299 cases of appropriate for gestational age (AGA) with the same gestational age between January 2015 and December 2016 were enrolled in Linyi People’s Hospital, China. The risk factors were analyzed and the frequencies of perinatal complications were compared between the two groups.Results:The frequencies of maternal risk factors such as pregnancy-induced hypertension, abnormal placenta and twins in the SGA group were significantly higher than that in the AGA group (P<0.05). The incidence of hyperbilirubinemia and hypoglycemia in the perinatal period was also higher in the SGA newborns group (P<0.05), while there were no significant differences in the incidence of pneumonia, apnea, septicemia, intracranial hemorrhage, neonatal asphyxia, congenital malformations, hypoxic-ischemic encephalopathy, respiratory distress syndrome and necrotizing enterocolitis between the two groups.Conclusions:SGA can cause perinatal complications including neonatal hypoglycemia and hyperbilirubinemia. It is necessary to strengthen the perinatal monitoring and antenatal care to reduce SGA and the perinatal complications of SGA.

Comparison of birth weight and umbilical and placental characteristics of cloned and artificial insemination-derived piglets

Somatic cell nuclear transfer (SCNT)-derived piglets have significantly higher stillbirth rate and postnatal mortality rate than artificial insemination (AI)-generated piglets. The question whether the low survival rate of SCNT piglets was related to birth weight, umbilical cord or placenta development was investigated. In this study, stillbirth rate, neonatal death rate, birth weight, umbilical cord status, placental parameters and placental gene expression patterns were compared between SCNT and AI piglets. Results showed that mortality rates at birth and during the neonatal stage of SCNT piglets were significantly higher than those of AI piglets. The incidence of abnormal umbilical cord in SCNT and SCNT-liveborn (SCNT-LB) piglets was significantly higher than in AI and AI-liveborn (AI-LB) piglets. Birth weight, placental weight, placental surface area and placental efficiency in SCNT and SCNT-LB piglets were significantly lower than those of AI and AI-LB piglets. Placental expression profiles of imprinting, angiopoiesis and nutrient transport-related genes were defective in SCNT-LB piglets compared with those in AI-LB piglets. Thus, the low survival rate of SCNT piglets may be associated with abnormal umbilical cord and placenta development. These characteristics may have resulted from aberrant expression of angiogenesis, nutrient transport, and imprinting-related genes in the placentas.

Органосохраняющие операции при аномальной инвазии плаценты (5-летний опыт Национального медицинского исследовательского центра акушерства, гинекологии и перинатологии имени академика В.И. Кулакова)

Органосохраняющие операции при аномальной инвазии плаценты (5-летний опыт Национального медицинского исследовательского центра акушерства, гинекологии и перинатологии имени академика В.И. Кулакова)

Update on the diagnosis and management of gestational trophoblastic disease.

Gestational trophoblastic disease (GTD) arises from abnormal placenta and is composed of a spectrum of premalignant to malignant disorders. Changes in epidemiology of GTD have been noted in various countries. In addition to histology, molecular genetic studies can help in the diagnostic pathway. Earlier detection of molar pregnancy by ultrasound has resulted in changes in clinical presentation and decreased morbidity from uterine evacuation. Follow-up with human chorionic gonadotropin (hCG) is essential for early diagnosis of gestational trophoblastic neoplasia (GTN). The duration of hCG monitoring varies depending on histology type and regression rate. Low-risk GTN (FIGO Stages I-III: score <7) is treated with single-agent chemotherapy but may require additional agents; although scores 5-6 are associated with more drug resistance, overall survival approaches 100%. High-risk GTN (FIGO Stages II-III: score >7 and Stage IV) is treated with multiple agent chemotherapy, with or without adjuvant surgery for excision of resistant foci of disease or radiotherapy for brain metastases, achieving a survival rate of approximately 90%. Gentle induction chemotherapy helps reduce early deaths in patients with extensive tumor burden, but late mortality still occurs from recurrent resistant tumors.

P09.10: Abnormal placenta invasion, conservative management: additional placental lobe percreta in the uterus cavity after two months and one year after delivery

P09.10: Abnormal placenta invasion, conservative management: additional placental lobe percreta in the uterus cavity after two months and one year after delivery

P09.07: The possible application of HDlive in diagnosing and monitoring abnormal placenta

P09.07: The possible application of HDlive in diagnosing and monitoring abnormal placenta

The Role of Abnormal Placentation in Congenital Heart Disease; Cause, Correlate, or Consequence?

Congenital heart disease (CHD) is the most common birth defect, affecting ~1% of all live births (van der Linde et al., 2011). Despite improvements in clinical care, it is the leading cause of infant mortality related to birth defects (Yang et al., 2006) and burdens survivors with significant morbidity (Gilboa et al., 2016). Furthermore, CHD accounts for the largest proportion (26.7%) of birth defect-associated hospitalization costs—up to $6.1 billion in 2013 (Arth et al., 2017). Yet after decades of research with a primary focus on genetic etiology, the underlying cause of these defects remains unknown in the majority of cases (Zaidi and Brueckner, 2017). Unexplained CHD may be secondary to undiscovered roles of noncoding genetic, epigenetic, and environmental factors, among others (Russell et al., 2018). Population studies have recently demonstrated that pregnancies complicated by CHD also carry a higher risk of developing pathologies associated with an abnormal placenta including growth disturbances (Puri et al., 2017), preeclampsia (Auger et al., 2015; Brodwall et al., 2016), preterm birth (Laas et al., 2012), and stillbirth (Jorgensen et al., 2014). Both the heart and placenta are vascular organs and develop concurrently; therefore, shared pathways almost certainly direct the development of both. The involvement of placental abnormalities in congenital heart disease, whether causal, commensurate or reactive, is under investigated and given the common developmental window and shared developmental pathways of the heart and placenta and concurrent vasculature development, we propose that further investigation combining clinical data, in vitro, in vivo, and computer modeling is fundamental to our understanding and the potential to develop therapeutics.

The Placenta and Neurodevelopment in Preterm Newborns

In caring for preterm neonates, a major challenge lies in understanding the contributors to brain dysmaturation and injury, both of which serve as precursors to childhood neurodevelopmental impairment. In addition to the various adverse exposures that the preterm newborn encounters in postnatal life, the placental antecedents of preterm delivery, in and of themselves, may affect brain dysmaturation and injury. The abnormal placenta is a frequent complication of pregnancy, and placental pathologies, such as placental insufficiency and acute chorioamnionitis, often precede preterm birth. Placental insufficiency is the principal cause of fetal growth restriction and acts via chronic fetal hypoxia. During fetal hypoxia, cardiac output redistribution to the brain represents an important fetal adaptive response; however, vascular sparing of the brain does not ensure normal brain growth. Early fetal growth restriction, which is associated with a hypermature and malperfused placenta, results in neurodevelopmental impairment independent of the duration of gestation in preterm newborns. Acute chorioamnionitis is characterized by infiltration of the placenta by immune cells and often results from infection that induces an inflammatory response. Chorioamnionitis can lead to the fetal inflammatory response syndrome and preterm labor, and thus can add to subsequent neonatal brain injury. Placental health should be assessed in understanding the origins of preterm brain dysmaturation and injury, and subsequent neurodevelopmental impairment.

Hydatidiform mole coexisting with normal foetus: A rare presentation of a case report from University of Maiduguri Teaching Hospital

A twin pregnancy comprising a complete hydatidiform mole coexisting with a foetus is a rare obstetric condition with an incidence of 1 in 22,000 to 1 in 100,000 pregnancies. The management of such case is challenging due to the associated risk of maternal and foetal complications. We report a case of a 25-year-old woman, gravida 2, para 1 with a normal intrauterine pregnancy coexisting with complete hydatidiform mole. An ultrasound scan demonstrated normal foetus and placenta along with coexistent intrauterine echogenic mass with features of hydatidiform mole. The microscopic examination of the abnormal placenta confirmed complete hydatidiform mole. Although twin pregnancy with complete hydatidiform mole and coexistent foetus is associated with increased risk of developing maternal and foetal complications, continuation of pregnancy may be an acceptable option under close monitoring to detect early signs of complications.

Study of Correlation of Neonatal Outcomes with Gross Abnormalities of Placenta and Umbilical Cord

Introduction: Perinatal outcome of new-borns is greatly influenced by abnormalities of placenta and umbilical cord. In most of the deliveries, whether home or institutional, the placenta and umbilical cords are discarded without examination. Due to paucity of information on abnormalities of placenta and cord, there is hardly any correlation with foetal outcomes. The aim was to study the correlation between the foetal outcome and the different types of abnormalities of placenta and umbilical cord.Materials and Methods: A prospective, cross-sectional, descriptive, randomised study was conducted from January 2016 to December 2016 in a tertiary care hospital in North India. The study was carried out on 1000 term singleton newborns. The placenta and umbilical cords were obtained from both normal and caesarean section deliveries. A proforma was used to gather data from the patients and new-borns. Statistical analysis was done using Statistical Package for the Social Sciences (SPSS) version 20 (SPSS Inc, Chicago, IL, IBM version) along with Microsoft Excel (2010 version).Results: One thousand placentae and umbilical cords were examined of which high placental weight/birth weight ratio, gross anomalies of placenta (infarctions, calcifications and retro placental haematoma), marginal (battledore and velamentous) umbilical cord insertions, long umbilical cords and single umbilical artery were associated with negative foetal outcomes.Conclusions: There was a high incidence of adverse foetal outcome with placental and umbilical cord abnormalities. Education of our health personnel dealing with deliveries on the importance of proper examination of the placenta and umbilical cords should be emphasised and instituted upon.

THROMBOPHILIA AND ABNORMAL LOCATION OF PLACENTA

The aim of the study was to search for a connection between the abnormal location of placenta and the presence of genetic and acquired forms of thrombophilia. Materials and methods. A total of 132 women with the aggravated obstetrical history were examined: Group 1 – 42 patients with the history of placenta previa; Group 2 – 60 pregnant women diagnosed with placenta previa in the current pregnancy; Group 3 – 30 pregnant women with the history of placenta previa and the same abnormality in the current pregnancy. The control group included 120 women with no abnormalities in their obstetric history and with normal location of placenta during the current pregnancy. All patients were assessed for the antiphospholipid antibodies using an enzyme immunoassay. The presence of genetic forms of thrombophilia was tested (with polymerase chain reaction and three pairs of oligonucleotide primers) for the following mutations: the C677T mutation in the 5,10-methylenetetrafolate reductase gene, the prothrombin mutation in the G20210A gene, mutations in the Leiden factor V gene, polymorphism 675 4G/5G in the gene of the inhibitor of plasminogen activator type 1, polymorphism 455G/A in the fibrinogen gene. Results. The thrombophilia spectrum in patients with placenta previa during the current pregnancy and those with abnormal placenta location in the past did not significantly differ from each other. However, in patients with both abnormal placental locations in the past and the present pregnancy, there was a greater occurrence of both genetic and acquired forms of thrombophilia. In the control group, much fewer cases of either genetic or acquired thrombophilia were found. Conclusion. The obtained results suggest a connection between thrombophilia and the abnormal location of placenta. Women with the abnormal placenta location either in the past or during the current pregnancy should be routinely tested for the genetic markers of thrombophilia and for hemostasis abnormalities.