Russell L Deter1, Wesley Lee1, John C P Kingdom2, Roberto Romero3,4,5,6. 1. a Department of Obstetrics and Gynecology , Texas Children's Hospital, Baylor College of Medicine , Houston , TX , USA. 2. b Division of Maternal-Fetal Medicine , Mount Sinai Hospital, University of Toronto , Toronto , Ontario , Canada. 3. c Perinatology Research Branch, Program for Perinatal Research and Obstetrics, Division of Intramural Research , Eunice Kennedy Shriver National Institute of Child Health and Human Development, NIH, Bethesda, MD and Detroit , MI , USA. 4. d Department of Obstetrics and Gynecology , University of Michigan , Ann Arbor , MI , USA. 5. e Department of Epidemiology and Biostatistics , Michigan State University , East Lansing , MI , USA. 6. f Department of Molecular Obstetrics and Genetics , Wayne State University , Detroit , MI , USA.
Abstract
OBJECTIVES: To study fetal growth in pregnancies at risk for growth restriction (GR) using, for the first time, the fetal growth pathology score (FGPS1). METHODS: A retrospective cohort study of GR was carried out in 184 selected SGA singletons using a novel, composite measure of growth abnormalities termed the FGPS1. Serial fetal biometry was used to establish second trimester Rossavik size models and determine FGPS1 values prior to delivery. FGPS1 data were compared to neonatal growth outcomes assessed using growth potential realization index (GPRI) values (average negative pathological GPRI (av - pGPRI)). Growth at the end of pregnancy was evaluated from differences in negative, individual composite prenatal growth assessment scores (-icPGAS) measured at the last two ultrasound scans. The FGPS1 and av - pGPRI values were used to classify fetal growth and neonatal growth outcomes, respectively, as Normal (N) or Abnormal (A). RESULTS: The risk of neonatal GR (based on birth weight (BW)) was moderate (MR: between 5th and10th percentiles (n = 113)) or significant (SR:<5th percentile) (n = 71)). Individual pregnancies were grouped into four categories, two representing agreement (N-N (29%), A-A (40%)) and two representing discordance (N-A (11%), A-N (20%)). In the largest and most variable subgroup (A-A,<5%tile, n = 49), there was a statistically significant correlation (0.63, p < .0001) between the FGPS1 and av - pGPRI. In N-A, all 20 cases (100%) had long last-scan-to-delivery intervals (1.9 weeks or greater), suggesting late development of the growth abnormality. For A-N, in approximately equal proportions, GR was improving, progressing or unclassifiable at the end of pregnancy. CONCLUSIONS: Significant agreement between prenatal and postnatal growth assessments was found using a novel approach for quantifying fetal growth pathology (FGPS1). Discordances appear to be due to lack of appropriate prenatal scans or an inadequate set of neonatal measurements. Evidence for a quantitative relationship between assessment methods was seen in the largest and most variable subgroup. The FGPS1 has the potential for characterizing GR in the third trimester and may provide a means for predicting the severity of corresponding abnormal neonatal growth outcomes.
OBJECTIVES: To study fetal growth in pregnancies at risk for growth restriction (GR) using, for the first time, the fetal growth pathology score (FGPS1). METHODS: A retrospective cohort study of GR was carried out in 184 selected SGA singletons using a novel, composite measure of growth abnormalities termed the FGPS1. Serial fetal biometry was used to establish second trimester Rossavik size models and determine FGPS1 values prior to delivery. FGPS1 data were compared to neonatal growth outcomes assessed using growth potential realization index (GPRI) values (average negative pathological GPRI (av - pGPRI)). Growth at the end of pregnancy was evaluated from differences in negative, individual composite prenatal growth assessment scores (-icPGAS) measured at the last two ultrasound scans. The FGPS1 and av - pGPRI values were used to classify fetal growth and neonatal growth outcomes, respectively, as Normal (N) or Abnormal (A). RESULTS: The risk of neonatal GR (based on birth weight (BW)) was moderate (MR: between 5th and10th percentiles (n = 113)) or significant (SR:<5th percentile) (n = 71)). Individual pregnancies were grouped into four categories, two representing agreement (N-N (29%), A-A (40%)) and two representing discordance (N-A (11%), A-N (20%)). In the largest and most variable subgroup (A-A,<5%tile, n = 49), there was a statistically significant correlation (0.63, p < .0001) between the FGPS1 and av - pGPRI. In N-A, all 20 cases (100%) had long last-scan-to-delivery intervals (1.9 weeks or greater), suggesting late development of the growth abnormality. For A-N, in approximately equal proportions, GR was improving, progressing or unclassifiable at the end of pregnancy. CONCLUSIONS: Significant agreement between prenatal and postnatal growth assessments was found using a novel approach for quantifying fetal growth pathology (FGPS1). Discordances appear to be due to lack of appropriate prenatal scans or an inadequate set of neonatal measurements. Evidence for a quantitative relationship between assessment methods was seen in the largest and most variable subgroup. The FGPS1 has the potential for characterizing GR in the third trimester and may provide a means for predicting the severity of corresponding abnormal neonatal growth outcomes.
Entities:
Keywords:
Individualized growth assessment; SGA; longitudinal growth study
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