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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
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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
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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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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 ...