SGA, IUGR, and FGR: Small Babies and Important Distinctions
Annie J. Rohan, PhD APRN FAANP
Fetal growth is dependent on genetic, environmental, placental, and maternal factors. Every fetus is thought to have inherent growth potential that, under normal circumstances, is closely associated with newborn health. The size of a fetus at any gestational age is an important factor that guides obstetric decisions and helps to predict pregnancy and neonatal outcomes. There are standards for weight and linear measurements (eg, length, head and abdominal circumferences, and femur length) for the fetus at all gestational ages, as well as for neonates, infants, and children. We can find these standards in the form of growth charts in apps and other reference materials and on preprinted graphs in most any setting that cares for maternal-child populations.1,2
When a fetus does not reach its intrauterine potential for growth and development, usually as a result of compromised placental function, we say that there is fetal growth restriction (FGR).3 Previously, the terms intrauterine growth restriction (IUGR) and intrauterine growth retardation have been used to characterize this entity, but such nomenclature has fallen out of favor. FGR affects 5%-10% of pregnancies, and is positioned as an obstetrical diagnosis. The current conceptualization of FGR is more comprehensive than the previously held classic characterization of IUGR as any fetus with estimated weight below the 10th percentile for gestational age.
FGR is generally defined as fetal weight below the 10th percentile of a reference population with associated placental insufficiency.3 FGR is the leading cause of perinatal mortality, a common factor in intrapartum asphyxia, and a risk factor for neurologic and cognitive developmental delays in children.4 At present, there is no gold standard for the diagnosis of FGR, though prenatal detection of pregnancies with FGR provides an opportunity to reduce the risk of adverse perinatal events and stillbirth.
FGR is multifactorial in etiology, but can be divided into 3 broad and sometimes overlapping categories of causes: maternal factors, fetal factors, and placental factors. Common conditions in these categories include the following:4,5
Maternal factors associated with FGR include drug use and clinical, nutritional, and other conditions, such as
i. cyanotic heart disease
iii. insulin-dependent diabetes with vascular disease
iv. autoimmune disease affecting the vessels
v. severe anemia
vi. severe renal disease
vii. chronic malnutrition
viii. smoking/carbon monoxide exposure
ix. severe stress/depression.
Fetal factors associated with FGR include chromosomal alterations and genetic syndromes, intrauterine infections, multiple gestation, and inborn errors of metabolism:
i. Trisomy of chromosomes 13, 18, or 21
ii. CMV, toxoplasmosis, varicella zoster, toxoplasma gondii, or rubella
iii. Fetal viremia
iv. Multiple gestation, especially monochorionic gestations
v. twin-to-twin transfusion syndrome
vi. inborn errors of metabolism.
Placental factors associated with FGR include altered interactions between maternal and fetal circulations and inadequate/abnormal implantation:
i. uterine malformations (fibroids, bicornate)
ii. pre-eclampsia associated hypertension
iii. chronic maternal hypertension
iv. prolonged high altitude exposure.
FGR is distinct from small for gestational age (SGA). SGA is typically defined as a newborn with weight at the 10th percentile or less.5 In contrast to FGR, which is an obstetrically diagnosed condition, SGA is a pediatric physical finding. Neonates with SGA include those who are constitutionally small with causes other than compromised placental function. Approximately 70% of fetuses classified as weighing below the 10th percentile (and later identified as SGA newborns) are small due to constitutional factors, such as ethnicity. These fetuses are generally not at higher risk of perinatal morbidity and mortality.4
A considerable obstetrical challenge is differentiating between the fetus that is constitutionally small and fulfilling its growth potential and the small fetus that is not fulfilling its growth potential because of an underlying pathologic condition. The challenge is avoiding harm to the small but healthy fetus and its mother and intervening appropriately to alter and improve the outcome for the fetus that is endangered by FGR. In differentiating, a significant number of healthy but small fetuses will be subject to high-risk perinatal protocols, including serial sonography and biophysical examination, amniocentesis, and, potentially, iatrogenic prematurity. Although FGR is one of the most important obstetrical diagnoses in terms of predicting pregnancy and infant outcome, screening for growth impairment in early gestation remains poorly predictive of FGR.5 Detection rates of FGR in routine-care obstetrical settings remain generally low.5 Therefore, neonatal and pediatric providers are commonly faced with the difficulty of determining whether an SGA newborn is facing greater challenges than those posed by constitutionally small size. Most nurseries have implemented processes reflective of evidence-based clinical practice guidelines (CPGs) to provide additional screening of the SGA newborn. For example, both the American Academy of Pediatrics6 and the Pediatric Endocrine Society7 have published CPGs recommending routine glucose screening of SGA newborns within a few hours of birth and ongoing screening and management of those with glucose homeostasis issues. In particular, the Pediatric Endocrine Society guideline does not distinguish between the conditions of SGA and FGR (IUGR) in its screening recommendations, as SGA initially may be used as a proxy for undiagnosed FGR. However, it is essential that neonatal and pediatric providers are aware of the important distinctions.
1. National Center for Health Statistics: Growth Charts. https://www.cdc.gov/growthcharts/ Accessed March 16, 2017.
2. Kiserud T, Piaggio G, Carroli G, et al. The World Health Organization fetal growth charts: a multinational longitudinal study of ultrasound biometric measurements and estimated fetal weight. PLOS Med. 2017, January 24. http://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.1002220 Accessed March 16, 2017.
3. American College of Obstetricians and Gynecologists. ACOG Practice bulletin no. 134: fetal growth restriction. Obstet Gynecol. 2013;121(5):1122-33.
4. Nardozza LMM, Caetano ACR, Zamarian ACP, et al. Fetal growth restriction: Current knowledge. Arch Gynecol Obstet. 2017;1-17.
5. Crovetto F, Triunfo S, Crispi F, et al. Differential performance of first-trimester screening in predicting small-for-gestational-age neonate or fetal growth restriction. Ultrasound Obstet Gynecol 2017;49(3):349-56.
6. Adamkin DH. Postnatal glucose homeostasis in late-preterm and term infants. Pediatrics.2011;127(3):575-9.
7. Thornton PS, Stanley CA, De Leon DD, et al. Recommendations from the Pediatric Endocrine Society for Evaluation and Management of Persistent Hypoglycemia in Neonates, Infants, and Children. J Pediatr. 2015;167(2):238-45.