Hypoglycemia. Newborns of a diabetic mother experience a rapid drop in plasma glucose concentration after delivery. This is attributed to hyperplasia of the fetal �-islet cells induced by chronic maternal hyperglycemia. Low glucose concentrationsdefined as <45 mg/dL-are particularly common in newborns of women with unstable glucose concentrations during labor (Persson, 2009). Frequent blood glucose measurements in the newborn and active early feeding practices can mitigate these complications.
Hypocalcemia. Deined as a total serum calcium concentration <8 mg/dL in term newborns, early onset hypocalcemia is one of the potential metabolic derangements in neonates of diabetic mothers. Its cause has not been explained. Theories include aberrations in magnesium-calcium economy, asphyxia, and preterm birth. In a randomized study, 137 pregnant women with type 1 diabetes were managed with strict versus customary glucose control (DeMarini, 1994). Almost a third of neonates in the customary control group developed hypocalcemia compared with only 18 percent of those in the strict-control group.
Hyperbilirubinemia and Polycythemia. he pathogenesis of hyperbilirubinemia in neonates of diabetic mothers is uncertain. A major contributing factor is newborn polycythemia, which raises the bilirubin load (Chap. 33, p. 626). Polycythemia is thought to be a fetal response to relative hypoxia. According to Hay (2012), the sources of this fetal hypoxia are hyperglycemia-mediated elevations in maternal ainity for oxygen and fetal oxygen consumption. Together with insulin-like growth factors, this hypoxia leads to elevated fetal erythropoietin levels and red cell production. Fetal renal vein thrombosis is reported to result from polycythemia.
Cardiomyopathy. Newborns of diabetic pregnancies may have hypertrophic cardiomyopathy that primarily afects the interventricular septum (Rolo, 2011). Huang and coworkers (2013) propose that pathological ventricular hypertrophy in neonates born to women with diabetes is due to insulin excess. In severe cases, this cardiomyopathy may lead to obstructive cardiac failure. Russell and coworkers (2008) performed serial echo cardiograms on fetuses of 26 women with pregestational diabetes. In the first trimester, fetal diastolic dysfunction was already evident in some. In the third trimester, the fetal interventricular septum and right ventricular wall were thicker in fetuses of diabetic mothers. Most afected newborns are asymptomatic following birth, and hypertrophy usually resolves in the months after delivery.
Long-Term Cognitive Development. Intrauterine metabolic conditions have long been linked to neurodevelopment in ofspring. In a study of more than 700,000 Swedish-born men, the intelligence quotient of those whose mothers had diabetes during pregnancy averaged 1 to 2 points lower (Fraser, 2014). DeBoer and associates (2005) demonstrated impaired memory performance in infants of diabetic mothers at age 1 year. Results from the Childhood Autism Risks from Genetics and the Environment (CHARGE) study indicated that autism spectrum disorders or developmental delay were also more common in children of diabetic women (Krakowiak, 2012). Adane and colleagues (2016) conirmed a consistent relationship between maternal diabetes and diminished cognitive and language development in studies of younger children but not older children. Because interpreting efects of the intrauterine environment on neurodevelopment is confounded by postnatal factors, the link between maternal diabetes, glycemic control, and long-term neurocognitive outcome remains unconfirmed.