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Rudolph's Pediatrics, 22e

Chapter 48. Infant of a Diabetic Mother

Infant of a Diabetic Mother: Introduction

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 obesity­related type 2 diabetes.2

The infant of the diabetic mother (IDM) is at increased risk for periconceptional, fetal, neonatal, and long­term 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.

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Infant of a Diabetic Mother: Introduction, Heather Morein French; Rebecca A. Simmons Page 1 / 1
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