A hallmark of twin pregnancy is a slower fetal growth rate during the third trimester, as compared with singleton pregnancies. Twin fetuses therefore have a higher proportion that are small for gestational age (SGA), that is, with a birth weight <10th percentile for gestational age. Whether this growth pattern represents a pathological or physiological adaptation is debated. This debate therefore includes whether unique growth charts should be used to measure twin growth rate, rather than the same growth chart used for singleton growth, and there is a lack of consistent guidelines for monitoring twin pregnancies. Use of twin-specific growth curves can hinder the ability of clinicians to detect twin pregnancies with true growth restriction,who are at greater risk of fetal death, whereas use of singleton curves may overdiagnose growth restriction. Therefore, this expert review describes differences in fetal growth when comparing twin and singleton pregnancies, to review current knowledge regarding mechanisms responsible for slow growth of twins, to summarize the available evidence on the diagnostic accuracy of the 2 types of charts for growth restriction in twin pregnancies, and to address whether an increased risk of fetal death exists for uncomplicated dichorionic twins when compared with singletons. Several studies comparing the fetal growth rates of twins versus singletons indicate that twins experience a reduced growth rate after 26 to 30 weeks. The use of singleton charts in these instances will lead to a relatively large proportion of suspected growth restriction in twin fetuses who "fall off the curve" and are classified as SGA. In addition, at approximately 33 weeks' gestation, the mean head-to-abdominal circumference ratio is progressively higher for twins than for singletons, which suggests not only a slower third-trimester growth pattern for twins, but also an asymmetric growth pattern when compared with singletons. The mechanisms by which twin fetal growth is slowed have long been debated: are they pathologic or physiologic in nature? Pathologic growth would merit closer monitoring, but a benign physiologic adaptation of twins that optimizes their survival through decreasing nutritional demands would indicate their growth pattern as less concerning. Potentialmechanisms of pathologic slower growth in the third trimester include a failure of the uteroplacental organ to meet late-gestational nutrition requirements of 2 fetuses or the physical constraint of the uterine size. Physiologic mechanisms could include reducing the risk of death with a physiological phenomenon resulting from early-pregnancy fetal programming. Prior studies of dichorionic twin pregnancies assessed via singleton or twin-based growth charts have indicated that twin fetuses diagnosed as SGA using twin charts experience greater risk for neonatal morbidity when compared with appropriately grown twins. This contrasts with SGA-diagnosed twins based on singleton charts, as such twins have not been shown to be at increased risk for neonatal mortality in comparison to their AGA counterparts. The authors note the observational nature of the majority of studies included in this review, which leads to an inability to rule out biases such as residual confounding. In addition, data for risk of death is hindered by the fact that most twin pregnancies are closely monitored and delivered at 37 to 38 weeks' gestation. Furthermore, the data acquired stem from academic centers accustomed to monitoring twin fetal growth and delivery, bringing into question whether the data can be broadly applied to smaller, nonacademic practices. In summary, the available data indicate that use of twin charts is not only reasonable but also preferred over the use of singleton charts for monitoring twin growth, because of the potential to avoid overdiagnoses of growth restriction and the subsequent negative effects of this diagnosis. Additional studies are required to increase our understanding of twin growth, such as slower twin growth noted through angiogenic and biochemical biomarkers, placental and fetal epigenetic marker analysis (which may demonstrate factors responsible for early pregnancy programming that leads to subsequent growth slowdown), molecular placental markers of hypoxia (and placental histopathology), and long-term neonatal outcomes.
|Number of pages||3|
|Journal||Obstetrical and Gynecological Survey|
|State||Published - 1 Jan 2023|