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Vincent W V Jaddoe - One of the best experts on this subject based on the ideXlab platform.
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Fetal Growth and prenatal exposure to bisphenol a the generation r study
Environmental Health Perspectives, 2013Co-Authors: Claudia A Snijder, Albert Hofman, Vincent W V Jaddoe, Dick Heederik, Frank H Pierik, Holger M Koch, Matthew P Longnecker, Alex BurdorfAbstract:Background: Prenatal exposure to bisphenol A (BPA) has been associated with adverse birth outcomes, but findings of previous studies have been inconsistent. Objective: We investigated the relation of prenatal BPA exposure with intrauterine Growth and evaluated the effect of the number of measurements per subject on observed associations. Methods: This study was embedded in a Dutch population-based prospective cohort study, with urine samples collected during early, mid-, and late pregnancy. The study comprised 219 women, of whom 99 had one measurement, 40 had two measurements, and 80 had three measurements of urinary BPA. Fetal Growth characteristics were repeatedly measured by ultrasound during pregnancy and combined with measurements at birth. Linear regression models for repeated measurements of both BPA and Fetal Growth were used to estimate associations between urinary concentrations of creatinine-based BPA (BPACB) and intrauterine Growth. Results: The relationship between BPACB and Fetal Growth was sensitive to the number of BPA measurements per woman. Among 80 women with three BPA measurements, women with BPACB > 4.22 μg/g crea (creatinine) had lower Growth rates for Fetal weight and head circumference than did women with BPACB < 1.54 μg/g crea, with estimated differences in mean values at birth of -683 g (20.3% of mean) and -3.9 cm (11.5% of mean), respectively. When fewer measurements were available per woman, the exposure-response relationship became progressively attenuated and statistically nonsignificant. Conclusion: Our findings suggest that maternal urinary BPA may impair Fetal Growth. Because previous studies have shown contradictory findings, further evidence is needed to corroborate these findings in the general population.
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c reactive protein levels in early pregnancy Fetal Growth patterns and the risk for neonatal complications the generation r study
American Journal of Obstetrics and Gynecology, 2011Co-Authors: Gesina D S Ernst, Albert Hofman, Eric A P Steegers, Layla L De Jonge, Jan Lindemans, Henk Russcher, Vincent W V JaddoeAbstract:Objective We sought to examine the associations of maternal C-reactive protein (CRP) levels with Fetal Growth and the risks of neonatal complications. Study Design CRP levels were measured in early pregnancy in 6016 women. Main outcome measures were Fetal Growth in each trimester and neonatal complications. Results As compared to the reference group (CRP levels Conclusion Maternal CRP levels in early pregnancy are associated with Fetal Growth restriction and increased risks of neonatal complications.
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Fetal Growth retardation and risk of febrile seizures
Pediatrics, 2010Co-Authors: Annemarie M Visser, Hein Raat, Albert Hofman, Eric A P Steegers, Henning Tiemeier, Vincent W V Jaddoe, Henriette A Moll, Monique M B Breteler, W F M ArtsAbstract:+OBJECTIVE: The goal was to examine the associations between Fetal Growth characteristics in different trimesters of pregnancy and the occurrence of febrile seizures in early childhood. METHODS: This study was embedded in a population-based, prospective, cohort study from early Fetal life onward. Fetal Growth characteristics (femur length, abdominal circumference, estimated Fetal weight, head circumference, biparietal diameter, and transverse cerebellar diameter [TCD]) were measured with ultrasonography in the second and third trimesters of pregnancy. Information on the occurrence of febrile seizures was collected with questionnaires at the ages of 12 and 24 months. Analyses were based on data for 3372 subjects. RESULTS: In the second trimester, children in the lowest tertile of TCDs were at increased risk of developing febrile seizures, compared with children in the highest tertile (odds ratio 2.87 [95% confidence interval: 1.31– 6.28]). In the third trimester, children in the lowest tertile of all general Growth characteristics (femur length, abdominal circumference, and estimated Fetal weight) were at increased risk of developing febrile seizures. This association was strongest for children in the lowest tertile of estimated Fetal weight (odds ratio: 2.57 [95% confidence interval: 1.34 – 4.96]). Children in the lowest tertile of biparietal diameter in the third trimester also were at increased risk of febrile seizures. Similar but not statistically significant tendencies were observed for head circumference and TCD. CONCLUSIONS: Fetal Growth retardation is associated with increased risk of febrile seizures in the first 2 years of life. Adverse environmental and genetic factors during pregnancy may be important in the development of febrile seizures. Pediatrics 2010;126:e919–e925
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risk factors and outcomes associated with first trimester Fetal Growth restriction
Obstetrical & Gynecological Survey, 2010Co-Authors: Dennis O Mookkanamori, Hein Raat, Albert Hofman, Eric A P Steegers, Paul H C Eilers, Vincent W V JaddoeAbstract:ABSTRACT Exposure of the fetus to an adverse environment may result in developmental adaptations that lead to Fetal Growth restriction. It has been suggested that Fetal Growth restriction may increase the risk of metabolic and cardiovascular diseases and other adverse outcomes in adulthood. Previous studies have shown that first trimester Fetal Growth restriction increased the risks of low birth weight and small size for gestational age. The effects of maternal lifestyle habits and physical characteristics on first trimester Growth and postnatal outcomes are not known. This population-based prospective cohort study investigated the associations of first trimester Growth restriction with adverse birth outcomes and postnatal outcomes in early childhood. The effect of several maternal physical characteristics and lifestyle habits on postnatal outcomes was also investigated. A self-administered questionnaire was completed by the mothers at enrollment. First trimester Fetal Growth in singleton mothers was assessed sonographically by measuring Fetal crown rump length between the gestational age of 10 weeks 0 days and 13 weeks 6 days, and then performing follow-up Growth scans in the second and third trimesters. The primary birth outcomes examined were preterm birth, low birth weight, and small size for gestational age at birth. Postnatal outcomes were studied up to the age of 2 years. Multivariate analysis showed that maternal age was positively associated with Fetal crown rump length; the difference was 0.79 mm (95% confidence interval [CI]: 0.41–1.18) per 1 standard deviation (4.68 maternal years of age) increase. Both diastolic blood pressure and the hematocrit were negatively associated with first trimester crown to rump Growth (shorter length) (differences, −0.40 mm; 95% CI: −0.74 to −0.06, and −0.52 mm; 95% CI: −0.90 to −0.14 per standard deviation increase, respectively). Mothers who smoked and did not use folic acid supplements had shorter crown rump lengths than nonsmoking mothers who used folic acid supplements; the difference was 3.84 mm; 95% CI: −5.71 to −1.98. In comparison to normal first trimester Growth, restricted first trimester Growth was associated with increased risks of prematurity (4.0% vs. 7.2%; adjusted odds ratio [OR]: 2.12; 95% CI: 1.24–3.61), small size for the gestational age at birth (4.0% vs.10.6%; OR: 2.64; 95% CI: 1.64–4.25), and low birth weight (3.5% vs. 7.5%; OR: 2.42; 95% CI: 1.41–4.16). Over the first 2 years of postnatal Growth, each standard deviation decrease in first trimester Fetal crown rump length was associated with an accelerated Growth rate in weight and height; the increase in the standard deviation score was 0.139 per 2 years; 95% CI: 0.097 to 0.181. These findings demonstrate that first trimester Fetal Growth is independently associated with a number of maternal physical characteristics and lifestyle habits. Early Fetal Growth restriction is also associated with an increased risk of adverse birth outcomes and accelerated Growth rates in early childhood.
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maternal psychological distress and Fetal Growth trajectories the generation r study
Psychological Medicine, 2010Co-Authors: Jens Henrichs, Vincent W V Jaddoe, Frank C Verhulst, Jacqueline J Schenk, Sabine J Roza, M P Van Den Berg, Henk G Schmidt, E A P Steegers, A Hofman, Henning TiemeierAbstract:Background. Previous research suggests, though not consistently, that maternal psychological distress during pregnancy leads to adverse birth outcomes. We investigated whether maternal psychological distress affects Fetal Growth during the period of mid-pregnancy until birth. Method. Pregnant women (n=6313) reported levels of psychological distress using the Brief Symptom Inventory (anxious and depressive symptoms) and the Family Assessment Device (family stress) at 20.6 weeks pregnancy and had Fetal ultrasound measurements in mid- and late pregnancy. Estimated Fetal weight was calculated using head circumference, abdominal circumference and femur length. Results. In mid-pregnancy, maternal distress was not linked to Fetal size. In late pregnancy, however, anxious symptoms were related to Fetal size after controlling for potential confounders. Anxious symptoms were also associated with a 37.73 g (95 % confidence interval (CI) x69.22 to x6.25, p=0.019) lower birth weight. When we related maternal distress to Fetal Growth curves using multilevel models, more consistent results emerged. Maternal symptoms of anxiety or depression were associated with impaired Fetal weight gain and impaired Fetal head and abdominal Growth. For example, depressive symptoms reduced Fetal weight gain by 2.86 g (95 % CI x4.48 to x1.23, p<0.001) per week. Conclusions. The study suggests that, starting in mid-pregnancy, Fetal Growth can be affected by different aspects of maternal distress. In particular, children of prenatally anxious mothers seem to display impaired Fetal Growth patterns during pregnancy. Future work should address the biological mechanisms underlying the association of maternal distress with Fetal development and focus on the effects of reducing psychological distress in pregnancy.
George R Saade - One of the best experts on this subject based on the ideXlab platform.
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altered Fetal Growth placental abnormalities and stillbirth
PLOS ONE, 2017Co-Authors: Radek Bukowski, Robert M Silver, Corette B Parker, Halit Pinar, Marian Willinger, Uma M Reddy, Donald J Dudley, Barbara J. Stoll, Nellie I Hansen, George R SaadeAbstract:Background Worldwide, stillbirth is one of the leading causes of death. Altered Fetal Growth and placental abnormalities are the strongest and most prevalent known risk factors for stillbirth. The aim of this study was to identify patterns of association between placental abnormalities, Fetal Growth, and stillbirth. Methods and findings Population-based case-control study of all stillbirths and a representative sample of live births in 59 hospitals in 5 geographic areas in the U.S. Fetal Growth abnormalities were categorized as small ( 90th percentile) for gestational age at death (stillbirth) or delivery (live birth) using a published algorithm. Placental examination by perinatal pathologists was performed using a standardized protocol. Data were weighted to account for the sampling design. Among 319 singleton stillbirths and 1119 singleton live births at ≥24 weeks at death or delivery respectively, 25 placental findings were investigated. Fifteen findings were significantly associated with stillbirth. Ten of the 15 were also associated with Fetal Growth abnormalities (single umbilical artery; velamentous insertion; terminal villous immaturity; retroplacental hematoma; parenchymal infarction; intraparenchymal thrombus; avascular villi; placental edema; placental weight; ratio birth weight/placental weight) while 5 of the 15 associated with stillbirth were not associated with Fetal Growth abnormalities (acute chorioamnionitis of placental membranes; acute chorioamionitis of chorionic plate; chorionic plate vascular degenerative changes; perivillous, intervillous fibrin, fibrinoid deposition; Fetal vascular thrombi in the chorionic plate). Five patterns were observed: placental findings associated with (1) stillbirth but not Fetal Growth abnormalities; (2) Fetal Growth abnormalities in stillbirths only; (3) Fetal Growth abnormalities in live births only; (4) Fetal Growth abnormalities in stillbirths and live births in a similar manner; (5) a different pattern of Fetal Growth abnormalities in stillbirths and live births. Conclusions The patterns of association between placental abnormalities, Fetal Growth, and stillbirth provide insights into the mechanism of impaired placental function and stillbirth. They also suggest implications for clinical care, especially for placental findings amenable to prenatal diagnosis using ultrasound that may be associated with term stillbirths.
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altered Fetal Growth placental abnormalities and stillbirth
PLOS ONE, 2017Co-Authors: Radek Bukowski, Robert M Silver, Corette B Parker, Halit Pinar, Marian Willinger, Uma M Reddy, Donald J Dudley, Barbara J. Stoll, Nellie I Hansen, George R SaadeAbstract:Worldwide, stillbirth is one of the leading causes of death. Altered Fetal Growth and placental abnormalities are the strongest and most prevalent known risk factors for stillbirth. The aim of this study was to identify patterns of association between placental abnormalities, Fetal Growth, and stillbirth.
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Fetal Growth and risk of stillbirth a population based case control study
PLOS Medicine, 2014Co-Authors: Radek Bukowski, Robert M Silver, Corette B Parker, Halit Pinar, Marian Willinger, Uma M Reddy, Donald J Dudley, Barbara J. Stoll, Nellie I Hansen, George R SaadeAbstract:Background: Stillbirth is strongly related to impaired Fetal Growth. However, the relationship between Fetal Growth and stillbirth is difficult to determine because of uncertainty in the timing of death and confounding characteristics affecting normal Fetal Growth. Methods and Findings: We conducted a population-based case–control study of all stillbirths and a representative sample of live births in 59 hospitals in five geographic areas in the US. Fetal Growth abnormalities were categorized as small for gestational age (SGA) (,10th percentile) or large for gestational age (LGA) (.90th percentile) at death (stillbirth) or delivery (live birth) using population, ultrasound, and individualized norms. Gestational age at death was determined using an algorithm that considered the time-of-death interval, postmortem examination, and reliability of the gestational age estimate. Data were weighted to account for the sampling design and differential participation rates in various subgroups. Among 527 singleton stillbirths and 1,821 singleton live births studied, stillbirth was associated with SGA based on population, ultrasound, and individualized norms (odds ratio [OR] [95% CI]: 3.0 [2.2 to 4.0]; 4.7 [3.7 to 5.9]; 4.6 [3.6 to 5.9], respectively). LGA was also associated with increased risk of stillbirth using ultrasound and individualized norms (OR [95% CI]: 3.5 [2.4 to 5.0]; 2.3 [1.7 to 3.1], respectively), but not population norms (OR [95% CI]: 0.6 [0.4 to 1.0]). The associations were stronger with more severe SGA and LGA (,5th and .95th percentile). Analyses adjusted for stillbirth risk factors, subset analyses excluding potential confounders, and analyses in preterm and term pregnancies showed similar patterns of association. In this study 70% of cases and 63% of controls agreed to participate. Analysis weights accounted for differences between consenting and non-consenting women. Some of the characteristics used for individualized Fetal Growth estimates were missing and were replaced with reference values. However, a sensitivity analysis using individualized norms based on the subset of stillbirths and live births with non-missing variables showed similar findings. Conclusions: Stillbirth is associated with both Growth restriction and excessive Fetal Growth. These findings suggest that, contrary to current practices and recommendations, stillbirth prevention strategies should focus on both severe SGA and severe LGA pregnancies. Please see later in the article for the Editors’ Summary.
K H Nicolaides - One of the best experts on this subject based on the ideXlab platform.
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screening for pre eclampsia and Fetal Growth restriction by uterine artery doppler at 11 14 weeks of gestation
Ultrasound in Obstetrics & Gynecology, 2001Co-Authors: A Martin, R Bindra, P Curcio, S Cicero, K H NicolaidesAbstract:Objective To examine the value of uterine artery Doppler at 11–14 weeks of gestation in the identification of women at risk of developing pre-eclampsia and Fetal Growth restriction. Methods Uterine artery Doppler was carried out at 11– 14 weeks in 3324 consecutive singleton pregnancies attending for routine care in three London hospitals. The right and left uterine arteries were identified using color flow mapping and velocity waveforms were obtained using pulsed Doppler. The mean pulsatility index of the two arteries was determined and the predictive value of a mean pulsatility index > the 95th centile in the prediction of pre-eclampsia and/or Fetal Growth restriction was calculated. Results Satisfactory flow velocity waveforms were obtained from both uterine arteries in 3195 (96.1%) of the 3324 pregnancies examined and complete outcome information was obtained for 3045 (95.3%) of these women. The 95th centile of the uterine artery mean pulsatility index was 2.35 and did not change significantly with gestational age. The pregnancy was complicated by pre-eclampsia in 63 (2.1%) cases and by Fetal Growth restriction in 290 (9.5%) cases. The sensitivity of a mean pulsatility index > 2.35 for pre-eclampsia (with or without Fetal Growth restriction) was 27.0% but for Fetal Growth restriction alone it was 11.7%. The respective sensitivities for these complications requiring delivery before 32 weeks of gestation were 60.0% and 27.8%, respectively. Conclusion Uterine artery Doppler at 11–14 weeks of gestation identifies a high proportion of women who develop severe pre-eclampsia and/or Fetal Growth restriction.
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multicenter screening for pre eclampsia and Fetal Growth restriction by transvaginal uterine artery doppler at 23 weeks of gestation
Ultrasound in Obstetrics & Gynecology, 2001Co-Authors: A T Papageorghiou, R Bindra, G K Pandis, K H NicolaidesAbstract:Objective To determine the value of transvaginal color Doppler assessment of the uterine arteries at 23 weeks of gestation in predicting the subsequent development of pre-eclampsia and Fetal Growth restriction. Patients and methods Women with singleton pregnancies attending for routine ultrasound examination at 23 weeks in any one of seven hospitals underwent Doppler assessment of the uterine arteries. The presence of an early diastolic notch in the waveform was noted, and the mean pulsatility index of the two arteries was calculated. Screening characteristics in the prediction of pre-eclampsia and the delivery of a low birth-weight infant were calculated. Results Doppler examination of the uterine arteries was attempted in 8335 consecutive singleton pregnancies, satisfactory waveforms were obtained from both vessels in 8202 (98.4%) cases and complete outcome data were available in 7851 (95.7%) of these. The mean gestational age was 23 (range, 22–24) weeks. The mean uterine artery pulsatility index did not change significantly with gestation (r = –0.0078; P = 0.483); the median value was 1.04 and the 95th centile was 1.63. In 9.3% of cases early diastolic notches in the waveform from both uterine arteries were present and in an additional 11.1% of cases there were notches unilaterally. Pre-eclampsia with Fetal Growth restriction occurred in 42 (0.5%) cases, pre-eclampsia without Fetal Growth restriction in 71 (0.9%) and Fetal Growth restriction without pre-eclampsia in 698 (8.9%). The sensitivity of increased pulsatility index above the 95th centile (1.63) for pre-eclampsia with Fetal Growth restriction was 69%, for pre-eclampsia without Fetal Growth restriction was 24%, for Fetal Growth restriction without pre-eclampsia was 13%, for pre-eclampsia irrespective of Fetal Growth restriction was 41% and for Fetal Growth restriction irrespective of pre-eclampsia was 16%. The sensitivity of Fetal Growth restriction defined by the 5th rather than the 10th centile was higher (19% vs. 16%). The sensitivity for both pre-eclampsia and Fetal Growth restriction was inversely related to the gestational age at delivery; when delivery occurred before 32 weeks, the sensitivity for all cases of pre-eclampsia with Fetal Growth restriction, pre-eclampsia without Fetal Growth restriction and Fetal Growth restriction without pre-eclampsia increased to 93%, 80% and 56%, respectively. The sensitivity of bilateral notches in predicting pre-eclampsia and/or Fetal Growth restriction was similar to that of increased pulsatility index but the screen-positive rate with notches (9.3%) was much higher than that with increased pulsatility index (5.1%).
Eduard Gratacos - One of the best experts on this subject based on the ideXlab platform.
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diagnosis and surveillance of late onset Fetal Growth restriction
American Journal of Obstetrics and Gynecology, 2018Co-Authors: Francesc Figueras, Javier Caradeux, Fatima Crispi, E Eixarch, Anna Peguero, Eduard GratacosAbstract:By consensus, late Fetal Growth restriction is that diagnosed >32 weeks. This condition is mildly associated with a higher risk of perinatal hypoxic events and suboptimal neurodevelopment. Histologically, it is characterized by the presence of uteroplacental vascular lesions (especially infarcts), although the incidence of such lesions is lower than in preterm Fetal Growth restriction. Screening procedures for Fetal Growth restriction need to identify small babies and then differentiate between those who are healthy and those who are pathologically small. First- or second-trimester screening strategies provide detection rates for late smallness for gestational age <50% for 10% of false positives. Compared to clinically indicated ultrasonography in the third trimester, universal screening triples the detection rate of late smallness for gestational age. As opposed to early third-trimester ultrasound, scanning late in pregnancy (around 37 weeks) increases the detection rate for birthweight <3rd centile. Contrary to early Fetal Growth restriction, umbilical artery Doppler velocimetry alone does not provide good differentiation between late smallness for gestational age and Fetal Growth restriction. A combination of biometric parameters (with severe smallness usually defined as estimated Fetal weight or abdominal circumference <3rd centile) with Doppler criteria of placental insufficiency (either in the maternal [uterine Doppler] or Fetal [cerebroplacental ratio] compartments) offers a classification tool that correlates with the risk for adverse perinatal outcome. There is no evidence that induction of late Fetal Growth restriction at term improves perinatal outcomes nor is it a cost-effective strategy, and it may increase neonatal admission when performed <38 weeks.
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long term cardiovascular consequences of Fetal Growth restriction biology clinical implications and opportunities for prevention of adult disease
American Journal of Obstetrics and Gynecology, 2018Co-Authors: Fatima Crispi, Jezid Miranda, Eduard GratacosAbstract:In the modern world, cardiovascular disease is a leading cause of death for both men and women. Epidemiologic studies consistently have suggested an association between low birthweight and/or Fetal Growth restriction and increased rate of cardiovascular mortality in adulthood. Furthermore, experimental and clinical studies have demonstrated that sustained nutrient and oxygen restriction that are associated with Fetal Growth restriction activate adaptive cardiovascular changes that might explain this association. Fetal Growth restriction results in metabolic programming that may increase the risk of metabolic syndrome and, consequently, of cardiovascular morbidity in the adult. In addition, Fetal Growth restriction is strongly associated with Fetal cardiac and arterial remodeling and a subclinical state of cardiovascular dysfunction. The cardiovascular effects ocurring in Fetal life, includes cardiac morphology changes, subclinical myocardial dysfunction, arterial remodeling, and impaired endothelial function, persist into childhood and adolescence. Importantly, these changes have been described in all clinical presentations of Fetal Growth restriction, from severe early- to milder late-onset forms. In this review we summarize the current evidence on the cardiovascular effects of Fetal Growth restriction, from subcellular to organ structure and function as well as from Fetal to early postnatal life. Future research needs to elucidate whether and how early life cardiovascular remodeling persists into adulthood and determines the increased cardiovascular mortality rate described in epidemiologic studies.
Nir Melamed - One of the best experts on this subject based on the ideXlab platform.
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defining early vs late Fetal Growth restriction by placental pathology
Acta Obstetricia et Gynecologica Scandinavica, 2019Co-Authors: Amir Aviram, Christopher Sherman, John Kingdom, Arthur Zaltz, Jon Barrett, Nir MelamedAbstract:INTRODUCTION: Although early and late Fetal Growth restriction have been suggested to be distinct entities, the optimal gestational age cut-off that differentiates the two conditions is currently unclear and has been arbitrarily set in previous studies between 32 and 37 weeks. We aimed to use placental pathology findings to determine that optimal gestational age cut-off between early and late Fetal Growth restriction. MATERIAL AND METHODS: A retrospective cohort study of all women with singleton gestation who gave birth to a neonate diagnosed as small-for-gestational age (small-for-gestational age, defined as birthweight <10th percentile for gestational age) at a tertiary referral center between January 2001 and December 2015, and for whom placental pathology was available. Placental abnormalities were classified into lesions associated with maternal vascular malperfusion (MVM), Fetal vascular malperfusion, placental hemorrhage and chronic villitis. Placental findings were analyzed as a function of gestational age at birth. The analysis was repeated in the subgroups of women without hypertensive complications of pregnancy (to reflect changes associated with isolated small-for-gestational age) and of neonates with severe small-for-gestational age (defined as birthweight <5th percentile), which are more likely to represent true Fetal Growth restriction. RESULTS: A total of 895 women met the inclusion criteria. The only histological finding that changed with gestational age was MVM pathology, which decreased in frequency with increasing gestational age. We identified a considerable drop in the rate of MVM lesions at 33 weeks of gestation. The rate of MVM pathology in placentas of infants born before 330/7 weeks was significantly higher than that observed in placentas of infants born at 330/7 weeks or longer: 71.6% vs 27.4%, P < 0.001 for ≥2 MVM lesions, and 35.5% vs 3.5%, P < 0.001 for ≥3 MVM lesions. These findings persisted in the subgroups of women without hypertensive complications of pregnancy (n = 662) and of neonates with severe small-for-gestational age (n = 464). CONCLUSIONS: Using placental pathology as a direct measure of the mechanisms underlying Fetal Growth restriction, the optimal gestational age at birth cut-off which differentiates early from late Fetal Growth restriction appears to be 330/7 weeks.
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Fetal Growth velocity and body proportion in the assessment of Growth
American Journal of Obstetrics and Gynecology, 2018Co-Authors: Liran Hiersch, Nir MelamedAbstract:Fetal Growth restriction implies failure of a fetus to meet its Growth potential and is associated with increased perinatal mortality and morbidity. Therefore, antenatal detection of Fetal Growth restriction is of major importance in an attempt to deliver improved clinical outcomes. The most commonly used approach towards screening for Fetal Growth restriction is by means of sonographic Fetal weight estimation, to detect fetuses small for gestational age, defined by an estimated Fetal weight <10th percentile for gestational age. However, the predictive accuracy of this approach is limited both by suboptimal detection rate (as it may overlook non-small-for-gestational-age Growth-restricted fetuses) and by a high false-positive rate (as most small-for-gestational-age fetuses are not Growth restricted). Here, we review 2 strategies that may improve the diagnostic accuracy of sonographic Fetal biometry for Fetal Growth restriction. The first strategy involves serial ultrasound evaluations of Fetal biometry. The information obtained through these serial assessments can be interpreted using several different approaches including Fetal Growth velocity, conditional percentiles, projection-based methods, and individualized Growth assessment that can be viewed as mathematical techniques to quantify any decrease in estimated Fetal weight percentile, a phenomenon that many care providers assess and monitor routinely in a qualitative manner. This strategy appears promising in high-risk pregnancies where it seems to improve the detection of Growth-restricted fetuses at increased risk of adverse perinatal outcomes and, at the same time, decrease the risk of falsely diagnosing healthy constitutionally small-for-gestational-age fetuses as Growth restricted. Further studies are needed to determine the utility of this strategy in low-risk pregnancies as well as to optimize its performance by determining the optimal timing and interval between exams. The second strategy refers to the use of Fetal body proportions to classify fetuses as either symmetric or asymmetric using 1 of several ratios; these include the head circumference to abdominal circumference ratio, transverse cerebellar diameter to abdominal circumference ratio, and femur length to abdominal circumference ratio. Although these ratios are associated with small for gestational age at birth and with adverse perinatal outcomes, their predictive accuracy is too low for clinical practice. Furthermore, these associations become questionable when other, potentially more specific measures such as umbilical artery Doppler are being used. Furthermore, these ratios are of limited use in determining the etiology underlying Fetal smallness. It is possible that the use of the 2 gestational-age-independent ratios (transverse cerebellar diameter to abdominal circumference and femur length to abdominal circumference) may have a role in the detection of mild-moderate Fetal Growth restriction in pregnancies without adequate dating. In addition, despite their limited predictive accuracy, these ratios may become abnormal early in the course of Fetal Growth restriction and may therefore identify pregnancies that may benefit from closer monitoring of Fetal Growth.
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does gestational diabetes affect Fetal Growth and pregnancy outcome in twin pregnancies
American Journal of Obstetrics and Gynecology, 2016Co-Authors: Carly Tward, Jon Barrett, Howard Berger, Mia Kibel, Alex Pittini, Ilana Halperin, Howard Cohen, Nir MelamedAbstract:Background Women with twin pregnancies are at increased risk for Fetal Growth restriction, which might be attributed to the limited maternal resources that are being shared by >1 fetus. Based on that, it may be hypothesized that the Fetal effects of gestational diabetes mellitus (GDM) with respect to accelerated Fetal Growth may be less pronounced in twin gestations or alternatively may even have a beneficial role in decreasing the risk of Fetal Growth restriction in these pregnancies. However, available data are conflicting and are limited by the fact that many of the complications associated with GDM are less relevant for twin gestations, and that all women with GDM included in previous studies were monitored and treated to control maternal blood glucose levels. Objective We sought to assess the impact of GDM and milder degrees of glucose intolerance on Fetal Growth and pregnancy outcome in twin pregnancies. Study Design This was a retrospective cohort study of all women with twin pregnancies who underwent screening for GDM in a single tertiary referral center from October 2003 through December 2014. The diagnosis of GDM during the study period was based on the 2008 Canadian Diabetes Association (CDA) guidelines, which involve universal screening with a 50-g glucose challenge test (GCT) followed by a diagnostic 2-hour 75-g oral glucose tolerance test (OGTT). Fetal Growth and pregnancy outcome were compared among 4 groups of women with increasing degree of glucose intolerance: (1) GCT-NEGATIVE, negative 50-g GCT; (2) OGTT-NEGATIVE, positive 50-g GCT followed by a negative 75-g OGTT; (3) GDM-IADPSG, positive 50-g GCT followed by a positive 75-g OGTT according to the International Association of the Diabetes and Pregnancy Study Groups (IADPSG) criteria but not the 2008 CDA criteria–because these women were not considered to have GDM during the study period they were not subjected to any form of treatment; and (4) GDM-CDA, positive 50-g GCT followed by a positive 75-g OGTT according to the 2008 CDA criteria. Results Overall 1393 women were eligible for the study: 1021 (73.3%) in the GCT-NEGATIVE group, 184 (13.2%) in the OGTT-NEGATIVE group, 99 (7.1%) in the GDM-IADPSG group, and 89 (6.4%) in the GDM-CDA group. There was a continuous relationship between the degree of glucose intolerance and Fetal Growth as reflected by a right shift of the distribution curve of birthweight percentiles and a greater likelihood of high birthweight percentile: OGTT-NEGATIVE = odds ratio (OR), 1.5; 95% confidence interval (CI), 1.07–2.2; GDM-IADPSG = OR, 1.7; 95% CI, 1.1–2.6; and GDM-CDA = OR, 1.9, 95% CI, 1.3–3.1 (using the GCT-NEGATIVE group as reference). Fetuses of women with glucose intolerance were more likely to experience asymmetric Growth as reflected by an elevated abdominal circumference to head circumference ratio. Conclusion GDM and milder degrees of glucose intolerance in twin pregnancies are associated with an increased risk of asymmetric overGrowth in a manner that is related to the degree of glucose intolerance.