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Abnormal maternal glucose metabolism occurs in 3% to 10% of pregnancies in the United States.1 While 90% of cases encountered during pregnancy are caused by gestational diabetes mellitus, the incidence of pregestational diabetes mellitus is rapidly increasing, in large part because of the increased incidence of obesity-related type 2 diabetes.2

The infant of the diabetic mother (IDM) is at increased risk for periconceptional, fetal, neonatal, and long-term morbidities. All of the complications faced by this fragile group of infants are the direct result of maternal glycemic control both before and during pregnancy. Before the availability of insulin to the pregnant mother, perinatal mortality rates were as high as 75%. With the addition of insulin therapy and good prenatal care, perinatal mortality rates now approach those seen in the nondiabetic population.3

Even with strict glycemic control, fetal and infant complications persist. Congenital anomalies are more frequent in the diabetic versus nondiabetic pregnancies. Macrosomia and the resulting birth injuries occur 10 times more frequently in diabetic pregnancies. Electrolyte abnormalities and the hyperviscosity syndrome can make management in the neonatal period challenging for pediatricians. Commonly encountered complications in the perinatal and neonatal period include intrauterine fetal demise, macrosomia or intrauterine growth restriction, birth trauma, perinatal depression, congenital anomalies, respiratory distress syndrome, hypoglycemia, electrolyte abnormalities such as hypocalcemia and hypomagnesemia, polycythemia and hyperviscosity syndrome, hyperbilirubinemia, and cardiomyopathy. No single pathogenic mechanism has been identified that can explain the diversity of problems encountered in the IDM. Nevertheless, most researchers agree that many of the effects can be attributed to maternal metabolic control. In 1977, the hypothesis of “hyperinsulinism” in the IDM was proposed and recognized that maternal hyperglycemia causes fetal hyperglycemia that results in fetal islet cell hypertrophy and beta cell hyperplasia due to chronic fetal pancreas stimulation.4 Insulin, an anabolic hormone, and the hyperinsulinemic state lead to visceromegaly and macrosomia. At delivery, with the sudden loss of maternal glucose supplies, hypoglycemia quickly ensues. However, this hypothesis does not tell the whole story because birth weight is not always correlated with mean maternal plasma glucose concentration.5 It is likely that control of fetal growth and fetal glucose homeostasis are multifactorial.

Major congenital anomalies are the leading cause of perinatal mortality in pregnancies complicated by pregestational diabetes, occurring in 6% to 12% of IDMs.6 The incidence of major congenital anomalies is reported to range between 6% and 9%, compared to a 2% to 3% incidence in the general population.7 Most studies support that the risk of major malformations is related to the degree of maternal glycemic control during organogenesis in the first trimester. Unfortunately, the critical window for glycemic control may occur before the pregnancy is even recognized. Glycosylated hemoglobin (Hb AIc) levels correlate directly with the frequency of anomalies. An Hb AIc of 7% to 8.5% is associated with a 5% to 6% risk of congenital anomaly. However, an Hb AIc greater ...

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