Identification of newborns with birthweight ≥ 4,500g: Ultrasound within one- vs. two weeks of delivery.

OBJECTIVE: Our objective was to compare the diagnostic characteristics of sonographic estimated fetal weight (SEFW) done within 7 versus 8-14 days before delivery for detection of fetal macrosomia (birthweight ≥ 4500 g). STUDY DESIGN: We performed a multicenter, retrospective cohort study of all non-anomalous singletons with SEFW ≥ 4000 g by Registered Diagnostic Medical Sonographers conducted within 14 days of delivery. Cohorts were grouped by time interval between ultrasound and delivery: 0-7 days versus 8-14 days. The detection rate (DR) and false positive rate (FPR) for detection of birthweight (BW) ≥ 4500 g were compared between groups with subgroup analysis for diabetic women. Area under the receiver operator curve (AUC) was calculated to analyze all possible SEFW cutoffs within our cohort. RESULTS: A total of 330 patients met inclusion criteria with 250 (75.8 %) having SEFW within 7 days and 80 (24.2 %) with SEFW 8-14 days prior to delivery. The rate of macrosomia was 15.1 % (N = 51). The DR for macrosomia was significantly higher when SEFW was performed within 7 days of delivery compared to 8-14 days among non-diabetic (73.0 % vs 7.1 %; p < 0.001) and diabetic women (76.5 % vs 16.7 %; p = 0.02). There was no significant change in FPR in either group. The AUC for detection of macrosomia was significantly higher when SEFW was performed within 7 days versus 8-14 days (0.89 vs 0.63; p < 0.01). CONCLUSION: With SEFW ≥ 4000 g, the detection of BW ≥ 4500 g is significantly higher when the sonographic examination is within 7 days of birth irrespective of maternal diabetes.

Differences in cardiac geometry in relation to body size among neonates with abnormal prenatal growth and body size at birth.

OBJECTIVES: Both excessive and restricted fetal growth are associated with changes in cardiac geometry and function at birth. There are significant issues when indexing cardiac parameters for body size in the neonatal period. The aims of this study were to determine to what extent cardiac geometry is dependent on body size in term and preterm neonates with restricted or excessive fetal growth and how this is affected by adiposity. METHODS: This was a cross-sectional study of neonates born between 31 and 42 weeks of gestation, divided into three groups: (1) small-for-gestational age (SGA, birth weight > 2 SD below the mean); (2) large-for-gestational age (LGA, birth weight > 2 SD above the mean); and (3) appropriate-for-gestational-age controls (AGA, birth weight ≤ 2 SD from the mean). Cardiac geometry and function were compared between the study groups, adjusting for body size. The potential impact of infant adiposity and maternal disease was assessed. RESULTS: In total, 174 neonates were included, of which 39 were SGA, 45 were LGA and 90 were AGA. Body size was reflected in cardiac dimensions, with differences in cardiac dimensions disappearing between the SGA and AGA groups when indexed for body surface area (BSA) or thoracic circumference. The same was true for the differences in atrial and ventricular areas between the LGA and AGA groups. However, left ventricular inflow and outflow tract dimensions did not follow this trend as, when indexed for BSA, they were associated negatively with adiposity, resulting in diminished dimensions in LGA compared with AGA and SGA neonates. Adiposity was associated positively with left ventricular mass, right ventricular length and area and right atrial area. The SGA group showed increased right ventricular fractional area change, possibly reflecting differences in the systolic function of the right ventricle. We found evidence of altered diastolic function between the groups, with the mitral valve inflow E- to lateral E'-wave peak velocity ratio being increased in the LGA group and decreased in the SGA group. CONCLUSIONS: Cardiac geometry is explained by body size in both term and preterm AGA and SGA infants. However, the nature of the relationship between body size and cardiac dimensions may be influenced by adiposity in LGA infants, leading to underestimation of left ventricular inflow and outflow tract dimensions when adjusted for BSA. Adjustments for thoracic circumference provide similar results to those for BSA. Copyright © 2020 ISUOG. Published by John Wiley & Sons Ltd.

Development and validation of a machine-learning model for prediction of shoulder dystocia.

OBJECTIVES: To develop a machine-learning (ML) model for prediction of shoulder dystocia (ShD) and to externally validate the model's predictive accuracy and potential clinical efficacy in optimizing the use of Cesarean delivery in the context of suspected macrosomia. METHODS: We used electronic health records (EHR) from the Sheba Medical Center in Israel to develop the model (derivation cohort) and EHR from the University of California San Francisco Medical Center to validate the model's accuracy and clinical efficacy (validation cohort). Subsequent to application of inclusion and exclusion criteria, the derivation cohort included 686 singleton vaginal deliveries, of which 131 were complicated by ShD, and the validation cohort included 2584 deliveries, of which 31 were complicated by ShD. For each of these deliveries, we collected maternal and neonatal delivery outcomes coupled with maternal demographics, obstetric clinical data and sonographic fetal biometry. Biometric measurements and their derived estimated fetal weight were adjusted (aEFW) according to gestational age at delivery. A ML pipeline was utilized to develop the model. RESULTS: In the derivation cohort, the ML model provided significantly better prediction than did the current clinical paradigm based on fetal weight and maternal diabetes: using nested cross-validation, the area under the receiver-operating-characteristics curve (AUC) of the model was 0.793 ± 0.041, outperforming aEFW combined with diabetes (AUC = 0.745 ± 0.044, P = 1e-16 ). The following risk modifiers had a positive beta that was > 0.02, i.e. they increased the risk of ShD: aEFW (beta = 0.164), pregestational diabetes (beta = 0.047), prior ShD (beta = 0.04), female fetal sex (beta = 0.04) and adjusted abdominal circumference (beta = 0.03). The following risk modifiers had a negative beta that was < -0.02, i.e. they were protective of ShD: adjusted biparietal diameter (beta = -0.08) and maternal height (beta = -0.03). In the validation cohort, the model outperformed aEFW combined with diabetes (AUC = 0.866 vs 0.784, P = 0.00007). Additionally, in the validation cohort, among the subgroup of 273 women carrying a fetus with aEFW ≥ 4000 g, the aEFW had no predictive power (AUC = 0.548), and the model performed significantly better (0.775, P = 0.0002). A risk-score threshold of 0.5 stratified 42.9% of deliveries to the high-risk group, which included 90.9% of ShD cases and all cases accompanied by maternal or newborn complications. A more specific threshold of 0.7 stratified only 27.5% of the deliveries to the high-risk group, which included 63.6% of ShD cases and all those accompanied by newborn complications. CONCLUSION: We developed a ML model for prediction of ShD and, in a different cohort, externally validated its performance. The model predicted ShD better than did estimated fetal weight either alone or combined with maternal diabetes, and was able to stratify the risk of ShD and neonatal injury in the context of suspected macrosomia. Copyright © 2019 ISUOG. Published by John Wiley & Sons Ltd.

Gestational Diabetes Impairs Human Fetal Postprandial Brain Activity.

CONTEXT: Gestational diabetes (GDM) influences the fetal phenotype. OBJECTIVE: In the present study, our aim was to determine the effect of GDM specifically on fetal brain activity. DESIGN: Pregnant participants underwent an oral glucose tolerance test (OGTT, 75 g). At 0, 60, and 120 minutes, maternal metabolism was determined, and fetal auditory evoked fields were recorded with a fetal magnetoencephalographic device. SETTING: All measurements were performed at the fMEG Center in Tübingen. PARTICIPANTS: Twelve women with GDM and 28 normal glucose-tolerant (NGT) pregnant women participated on a voluntary basis. INTERVENTIONS: OGTT (75 g, 120 minutes) was used in this study. MAIN OUTCOMES AND MEASURES: Fetal auditory evoked response latencies were determined for this study. RESULTS: In the fetuses of NGT women, latencies decreased between 0 and 60 minutes from 260 ± 90 to 206 ± 74 ms (P = .008) and remained stable until 120 minutes (206 ± 74 vs 230 ± 79, P =.129). In fetuses of women with GDM, there was no change in response latencies during OGTT (P = .11). Sixty minutes after glucose ingestion, fetal latencies in the GDM group were longer than in the NGT group (296 ± 82 vs 206 ± 74 ms, P = .001). Linear regression revealed a significant effect of maternal glucose, insulin levels, and insulin sensitivity on response latencies after 60 minutes. CONCLUSIONS: Fetal postprandial brain responses were slower in the offspring of women with GDM. This might indicate that gestational diabetes directly affects fetal brain development and may lead to central nervous insulin resistance in the fetus.

Sonographic and clinical methods in the diagnosis of macrosomia.

Receiver operator characteristic curves for both clinical and sonographic predictions of macrosomia subsume areas between 0.81 and 0.95, significantly larger than the area of 0.5 that indicates a useless test. Thus, these tests are defined as useful from a statistical point of view. Prediction of macrosomia by clinical or imaging techniques, however, is limited by the substantial false-positive and false-negative rates inherent in these tests. We recommend that physicians continue to use clinical methods to estimate fetal weight, including asking women with parity to provide their own estimates. We recognize that the relative error associated with clinical or sonographic estimates of fetal weight limits their use in clinical practice. Sonographic laboratories may improve their results by performing ROC curve analysis on their own data and by selecting cutoff values that best predict macrosomia in their setting. Serial sonographic measurements that are above the limits chosen to define macrosomia increase the likelihood that a birth weight will be macrosomic. Separate ROC curves must be generated for twins and breech presentations and for patients with diabetes to answer weight-related clinical questions such as mode and timing of delivery. Three-dimensional ultrasound and magnetic resonance imaging are expected to generate ROC curves for estimates of fetal weight that are better than those for two-dimensional ultrasound or clinical estimates. Such analyses have yet to be published.

Glycemic control throughout pregnancy and fetal growth in insulin-dependent diabetes.

OBJECTIVE: To determine the time of growth acceleration in fetuses of insulin-dependent diabetic women who are large for gestational age (LGA) at birth and the relationship between growth acceleration and diabetic control throughout pregnancy. METHODS: We studied a consecutive sample of 76 women with insulin-dependent diabetes divided by those who delivered LGA or normally grown infants. Fetal abdominal circumference (AC) was measured ultrasonically at regular intervals between 20 and 34 weeks' gestation. Diabetic control was assessed by regular measurement of glycosylated hemoglobin and capillary blood glucose levels. RESULTS: A significant difference in fetal AC between groups developed between 20 and 24 weeks' gestation, and the LGA group continued to have accelerated fetal growth. Between 18 and 24 weeks glycosylated hemoglobin and capillary blood glucose concentrations were significantly higher in women who delivered LGA infants. After 28 weeks, blood glucose concentrations and glycosylated hemoglobin did not differ significantly between groups. There was a nonsignificant trend toward more vaginal deliveries in the normal group (45% versus 32%). CONCLUSION: In insulin-dependent diabetic pregnancy, although actual growth acceleration occurred from about 20 weeks' gestation, growth potential of fetuses appeared to be determined by prevailing maternal glucose concentrations before then. Excessive growth continued despite subsequent satisfactory glucose control. If strict blood glucose control is maintained during first and second trimesters, it might reduce the incidence of LGA infants.