Accuracy of Estimated Fetal Weight by Ultrasound Versus Leopold Maneuver.

ABSTRACT: Estimated fetal weight (EFW) is frequently used for clinical decision-making in obstetrics. The goals of this study were to determine the accuracy of EFW assessments by Leopold and ultrasound and to investigate any associations with maternal characteristics. Postgraduate years 1 and 2 obstetrics and gynecology resident physicians from Harbor-UCLA Medical Center from 2014 to 2020 performed EFW assessments on 10 preterm (<37 weeks' gestational age) fetuses by ultrasound biometry and 10 full-term (≥37 weeks' gestational age) fetuses by ultrasound biometry and Leopold maneuver. Assessments were included if the patients delivered within 2 weeks of the assessments. One thousand six hundred ninety-seven EFW assessments on 1183 patients performed by 33 residents were analyzed; 72.6% of sonographic full-term EFWs, 69% of Leopold full-term EFWs, and 61.5% of sonographic preterm EFWs were within 10% of the neonatal birth weight (BW). The lowest estimation error in our study occurred when actual BW was 3600 to 3700 g. After adjusting for BW, residents were found to have lower accuracy when the mother had a higher body mass index (BMI) for full-term estimation methods (Leopold and ultrasound, ß = 0.13 and 0.12, P = 0.001 and 0.002, respectively). Maternal BMI was not related to estimation error for preterm fetuses ( ß = 0.01, P = 0.75). Clinical and sonographic EFW assessments performed by obstetrics and gynecology junior residents are within 10% of neonatal BW much of the time. In our cohort, they tended to overestimate EFWs of lower-BW infants and underestimate EFWs of higher-BW infants. Accuracy of full-term EFW assessments seems to decrease with increasing maternal BMI.

Predictive Ability of Ultrasound on Neonatal Diagnoses and Consequences on Prenatal Care Utilization.

ABSTRACT: Fetal anomalies suspected on fetal ultrasound may cause significant stress for patients. Some findings resolve or have minimal clinical significance for the neonate. Our purpose is to evaluate fetal ultrasound accuracy and false-positive results and determine the clinical impact on maternal counseling. A retrospective review was performed on electronic medical records for women receiving prenatal care at Harbor-UCLA Medical Center who had abnormal findings on fetal ultrasounds between January 2015 and December 2018. Corresponding neonatal medical records were reviewed for the suspected condition(s). χ2 and Fisher exact tests were conducted to assess associations between fetal ultrasounds and neonatal outcomes. Two hundred eight mothers and 237 babies (including all 29 sets of twins) were included in the final analysis. Fetal ultrasounds were significantly associated with neonatal findings for the following conditions (sensitivity, specificity): anatomical disorder of extremities (0.72, 0.97), anatomical disorder of the face/skull/brain (0.67, 0.91), congenital anomaly of gastrointestinal tract (0.75, 0.98), congenital heart disease (0.75, 0.91), genetic disorder (0.72, 1.00), growth restriction (1.00, 0.85), kidney disorder (0.55, 0.98), and large for gestational age (0.80, 0.98). The highest false-positive rates occurred in congenital heart disease (65.4%), anatomical disorder of the face/skull/brain (64.3%), and growth restriction (54%). Fetal ultrasound highly correlates with neonatal findings for many congenital conditions. However, it can also be associated with a high false-positive rate for certain diagnoses; maternal counseling should include the limitations of ultrasound, including the potential for false-positive results.

Maternal bisphenol A exposure alters rat offspring hepatic and skeletal muscle insulin signaling protein abundance.

BACKGROUND: The obesogenic and diabetogenic effects of the environmental toxin bisphenol A during critical windows of development are well recognized. Liver and skeletal muscle play a central role in the control of glucose production, utilization, and storage. OBJECTIVES: We hypothesized that maternal bisphenol A exposure disrupts insulin signaling in rat offspring liver and skeletal muscle. We determined the protein expression of hepatic and skeletal muscle insulin signaling molecules including insulin receptor beta, its downstream target insulin receptor substrate 1 and glucose transporters (glucose transporter 2, glucose transporter 4), and hepatic glucose-regulating enzymes phosphoenolpyruvate carboxykinase and glucokinase. STUDY DESIGN: Rat dams had ad libitum access to filtered drinking water (control) or drinking water with bisphenol A from 2 weeks prior to mating and through pregnancy and lactation. Offspring litters were standardized to 4 males and 4 females and nursed by the same dam. At weaning, bisphenol A exposure was removed from all offspring. Glucose tolerance was tested at 6 weeks and 6 months. Liver and skeletal muscle was collected from 3 week old and 10 month old offspring for protein expression (Western blot) of insulin receptor beta, insulin receptor substrate 1, glucose transporter 2, glucose transporter 4, phosphoenolpyruvate carboxykinase, and glucokinase. RESULTS: Male, but not female, bisphenol A offspring had impaired glucose tolerance at 6 weeks and 6 months. Both male and female adult offspring had higher glucose-stimulated insulin secretion as well as the ratio of stimulated insulin to glucose. Male bisphenol A offspring had higher liver protein abundance of the 200 kDa insulin receptor beta precursor (2-fold), and insulin receptor substrate 1 (1.5-fold), whereas glucose transporter 2 was 0.5-fold of the control at 3 weeks of age. In adult male bisphenol A offspring, the abundance of insulin receptor beta was higher (2-fold) and glucose transporter 4 was 0.8-fold of the control in skeletal muscle. In adult female bisphenol A offspring, the skeletal muscle protein abundance of glucose transporter 4 was 0.4-fold of the control. CONCLUSION: Maternal bisphenol A had sex- and tissue-specific effects on insulin signaling components, which may contribute to increased risk of glucose intolerance in offspring. Glucose transporters were consistently altered at both ages as well as in both sexes and may contribute to glucose intolerance. These data suggest that maternal bisphenol A exposure should be limited during pregnancy and lactation.