Infants whose weight is < the 10th percentile for gestational age are classified as small for gestational age (SGA). Complications include perinatal asphyxia, meconium aspiration, and hypoglycemia.
An infant may be small at birth because of genetic factors. Nongenetic factors that can restrict intrauterine growth usually are not apparent before 32 to 34 wk gestation; these factors include placental insufficiency from maternal disease involving the small blood vessels (as in preeclampsia, primary hypertension, renal disease, or long-standing diabetes); placental involution accompanying postmaturity; and infectious agents such as cytomegalovirus, rubella virus, or Toxoplasma gondii. An infant may also be SGA if the mother is an opioid or cocaine addict or a heavy user of alcohol or, to a lesser degree, if she smoked cigarettes during pregnancy.
Symptoms and Signs
Despite their size, SGA infants have physical characteristics (eg, skin appearance, ear cartilage, sole creases) and behavior (eg, alertness, spontaneous activity, zest for feeding) similar to those of normal-sized infants of like gestational age.
If growth restriction is caused by placental insufficiency and, therefore, undernutrition, the infant's weight is most affected, with a relative sparing of growth of the brain, cranium, and long bones (asymmetric growth restriction). In contrast, many genetic disorders and congenital infections cause symmetric growth restriction, in which height, weight, and head circumference are about equally affected.
Full-term SGA infants do not have the complications related to organ system immaturity that premature infants of similar size have. They are, however, at risk of perinatal asphyxia, meconium aspiration, and hypoglycemia.
Perinatal asphyxia is the most serious potential complication. It is a risk during labor if intrauterine growth restriction is caused by placental insufficiency (with marginally adequate placental perfusion), because each uterine contraction slows or stops maternal placental perfusion by compressing the spiral arteries. Therefore, when placental insufficiency is suspected, the fetus should be assessed before labor and the fetal heart rate monitored during labor. If fetal compromise is detected, rapid delivery, often by cesarean section, is indicated.
Meconium aspiration may occur during perinatal asphyxia. SGA infants, especially those who are postmature, may pass meconium into the amniotic sac and begin deep gasping movements. The consequent aspiration is likely to result in meconium aspiration syndrome (often most severe in growth-restricted or postmature infants, because the meconium is contained in a smaller volume of amniotic fluid—see Respiratory Disorders in Neonates, Infants, and Young Children: Meconium Aspiration Syndrome).
Hypoglycemia often occurs in the early hours and days of life due to a lack of adequate glycogen stores (see Metabolic, Electrolyte, and Toxic Disorders in Neonates: Neonatal Hypoglycemia).
Polycythemia may occur when SGA fetuses experience chronic mild hypoxia caused by placental insufficiency. Erythropoietin release is increased, leading to an increased rate of erythrocyte production. The neonate with polycythemia at birth appears ruddy and may be tachypneic or lethargic.
If asphyxia can be avoided, neurologic prognosis is quite good.
Infants who are SGA because of genetic factors, congenital infection, or maternal drug use often have a worse prognosis, depending on the specific diagnosis. If intrauterine growth restriction is caused by chronic placental insufficiency, adequate nutrition may allow SGA infants to demonstrate remarkable “catch-up” growth after delivery.
Underlying conditions and complications are treated. There is no specific intervention for the SGA state, but prevention is aided by prenatal advice on the importance of avoiding alcohol, tobacco, and illicit drugs.
Last full review/revision March 2007 by James W. Kendig, MD