Several short-term and long-term adverse sequelae are linked with fetal-growth restriction. First, perinatal morbidity and mortality rates are substantive (see Fig. 44-3). Rates of stillbirth and adverse neonatal outcomes that include birth asphyxia, meconium aspiration, hypoglycemia, and hypothermia are all increased, as is the prevalence of abnormal neurological development. This is true for both term and preterm growth-restricted newborns. In one analysis of nearly 3000 newborns born before 27 weeks' gestation, those weighing < 10th percentile had a nearly fourfold higher risk of neonatal death or neurodevelopmental impairment and a 2.6-fold increased risk of cerebral palsy compared with non-SGA neonates (De Jesus, 2013). In another analysis of more than 91,000 uncomplicated pregnancies, newborns with weights < 5th percentile had a higher risk of low 5-minute Apgar score, respiratory distress, necrotizing enterocolitis, and neonatal sepsis than appropriate-weight neonates. The risks of stillbirth and neonatal death were sixfold and fourfold higher, respectively .\1endez-Figueroa, 2016).
The most severely growth-impaired newborns also have the worst outcomes. In one study of more that 44,561 neonates, only 14 percent of those weighing < 1st percentile at birth survived to discharge (Griin, 2015). For those infants who survive, the risks of adverse neurodevelopmental outcomes are substantial, especially for growth-impaired fetuses with either brain sparing or a major birth defect (Meher, 2015; Nelson, 2015b). Poor motor, cognitive, language and attention, and behavioral outcomes in growth-restricted newborns unfortunately persist into early childhood and adolescence (Baschat, 2014; Levine, 2015; Rogne, 2015).
Barker (1992) hypothesized that aduLt mortality and morbidity are related to fetal and infant health. This includes both under-and overgrowth. In the context of fetal-growth restriction, numerous reports describe a relationship between suboptimal fetal nutrition and an increased risk of subsequent adult hypertension, atherosclerosis, type 2 diabetes, and metabolic derangement (Burton, 2016; J ornayvaz, 2016). he degree to which low birthweight mediates adult disease is controversial, as weight gain in early life also appears important (Breij, 2014;
Kerhof, 2012; McCloskey, 2016).
Mounting evidence suggests that fetal-growth restriction may afect organ development, particularly that of the heart. Individuals with low birthweight demonstrate cardiac structural changes and dysfunction persisting through childhood, adolescence, and adulthood. In one study, 80 infants who were born SGA before 34 weeks' gestation were compared at 6 months with 80 normally grown children (Cruz-Lemini, 2016). The heart in the SGA children had a more globular ventricle that resulted in systolic and diastolic dysfunction. In another study, echocardiography in 418 adolescents showed that low birthweight was associated with a thicker let ventricular posterior wall (Hietalampi, 2012). In their review, Cohen and colleagues (2016) concluded, however, that these findings have unclear long-term signiicance.