However a fetus with an EFW of p55 and a growth deceleration of 50 percentiles ends with a birth weight of p5, which does meet the definition of SGA. For example a fetus with an EFW of p85 in the second trimester ending with a birth weight of p35 has a growth deceleration of 50 percentiles but does not meet the definition of SGA.
This slowdown is independent of the actual birth weight. This approach has been suggested in previous studies and aims to approach a slowdown in fetal growth. Since there is no definition of how much a growth curve needs to decelerate before it can be designated as a decelerating growth curve we used five cut-offs to define decelerated growth a decrease in growth of at least 30, 35, 40, 45 or 50 percentiles respectively between the second trimester and birth. SGA was defined as a gestational and fetal sex adjusted birth weight under the fifth percentile (≤ 1.78 SD).īoth estimated fetal weight in the second trimester of pregnancy and birth weight were presented in a gestational age adjusted percentile. Ultrasound examinations were performed using Aloka® model SSD-1700 (Tokyo, Japan) or the ATL-Philips® Model HDI 5000 (Seattle, WA, USA). Fetal biometry (head circumference, abdominal circumference ) was measured trans abdominally. To assess estimated fetal weight (EFW) ultrasound examinations were performed in the second trimester of pregnancy (median 20.5 weeks of gestation, 90% range 18.9–22.9). We compared this method to small for gestation age (SGA) to determine whether growth velocity, independent of SGA, affects delivery outcomes, accelerated growth in infancy and cardiovascular outcomes at the age of 6 years. In this study we assessed decelerating growth based on the fetus individual growth curve, independent of birth weight. Growth velocity represents the rate of fetal growth in a specific time interval and may have more clinical utility to distinguish normal from pathological fetal growth and hence to identify fetal growth abnormalities. This is highly warranted since it is estimated that approximately 50–70% of the SGA fetuses are constitutionally small with normal perinatal outcomes. However, there is a lack of a uniform definition of decelerated growth and no golden standard exists. FGR fetuses may experience a failure to reach their biological growth potential because of a pathological slow-down (decelerating growth curve) in the fetal growth pace. Therefore FGR is not synonymous with SGA. Growth however is dynamic and can be measured only in sequential measurements. Yet, birth weight and thus one single measurement can only indicate size. Therefore, in scientific research FGR is frequently classified as a neonate born small for gestational age (SGA). FGR is difficult to assess as the biological growth potential of the fetus can, at best, be estimated and not directly measured. Although these adaptations may be beneficial for short term survival, they may have adverse consequences at delivery or in later life. The Development and Origins of Health and Disease theory (DOHaD) states that in case of adverse fetal exposure, the unborn fetus can modify its own development such that it will be prepared for survival in an environment in which resources are likely to be short. Fetal growth restriction (FGR) is considered a severe complication of pregnancy associated with substantial perinatal morbidity and mortality and contributing to disease in adulthood.
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