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INTRODUCTION

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The true prevalence of diabetes in pregnancy (including gestational diabetes and pregestational diabetes) is unknown, but most studies report rates as high as 10% in the United States. Whereas 90% of cases encountered during pregnancy are caused by gestational diabetes mellitus (GDM), the incidence of pregestational diabetes mellitus is rapidly increasing, in large part due to the increased incidence of obesity-related type 2 diabetes. Unfortunately, the prevalence of type 2 diabetes has been increasing in every age group and ethnicity in the United States for the past 10 years. The epidemic of childhood obesity in the United States causing a sharp increase in childhood and adolescent diabetes will have a profound impact on obstetric and pediatric practices for the next generation.

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COMPLICATIONS IN THE INFANT

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The infant of a diabetic mother (IDM) is at increased risk for development of periconceptional, fetal, neonatal, and long-term morbidities. Most, if not all, of the complications are related to maternal glycemic control, both before and during pregnancy. Before insulin was available 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.

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However, even with strict glycemic control, fetal and infant complications persist. Congenital anomalies are 3 to 4 times greater in the diabetic versus nondiabetic pregnancies. Macrosomia and related birth injuries occur 10 times more frequently in diabetic pregnancies. Hypoglycemia, electrolyte abnormalities, and hyperviscosity syndrome can render management in the neonatal period challenging for pediatricians. Commonly encountered complications in the perinatal and neonatal period include the following:

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  • Intrauterine fetal demise

  • Macrosomia or intrauterine growth restriction

  • Birth trauma

  • Perinatal depression

  • Congenital anomalies

  • Respiratory distress syndrome

  • Neonatal hypoglycemia

  • Electrolyte abnormalities such as hypocalcemia and hypomagnesemia

  • Polycythemia and hyperviscosity syndrome

  • Hyperbilirubinemia

  • Cardiomyopathy

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No single pathogenic mechanism has been identified to explain the diversity of problems encountered in the IDM. Nonetheless, 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 by Jorgen Pedersen. The hypothesis recognized that maternal hyperglycemia causes fetal hyperglycemia, which results in fetal islet cell hypertrophy and β cell hyperplasia due to chronic fetal pancreas stimulation. 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, as birth weight is not always correlated with mean maternal plasma glucose concentration. Further, the large Hyperglycemia and Adverse Pregnancy Outcome (HAPO) study found a significant association between infant adverse outcomes and higher levels of maternal glucose within what is currently considered a nondiabetic range. It is likely that control of fetal growth and fetal glucose homeostasis is multifactorial.

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Congenital Anomalies

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Major congenital ...

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