INFANT OF DIABETIC MOTHER CAUSES
Category: Child Health
Abstract : Causes (infant of diabetic mother): • HbA1C levels o Complications caused
by maternal hyperglycemia during pregnancy are reflected by HbA1C levels,
particularly during the first trimester of pregnancy. o Because HbA1C is a
direct measure of glucose control in the mother, higher levels are predictive of
increased risks for congenital complications. Thus, the incidence of
co
Causes (infant of diabetic mother):
• HbA1C levels
o Complications caused
by maternal hyperglycemia during pregnancy are reflected by HbA1C levels,
particularly during the first trimester of pregnancy.
o Because HbA1C is a
direct measure of glucose control in the mother, higher levels are predictive of
increased risks for congenital complications. Thus, the incidence of
complications has been reported as 3.
4% with HbA1C levels lower than 8.5% and
22.4% with levels higher than 8.5%.
o There is speculation that birth defects
in IDMs may be related to reduced arachidonic acid and myoinositol levels and
elevated sorbitol and trace metal levels in the fetus.
o Others speculate
about the role of excess oxygen radicals and hydroperoxides in the mitochondria
of susceptible fetal tissues because these prostacyclin inhibitors may cause
disruption in the vascularization of developing tissues.
o A past history of
LGA infants, diabetes, stillbirth, hypertension, gestational diabetes, obesity,
or glycosuria, or a current history of excessive weight gain in the present
pregnancy or low socioeconomic class place the mother at an increased risk of
poor glucose control during pregnancy and increase her risk of delivering an
infant with subsequent complications.
• Fetal macrosomia
o IDMs
experience higher levels of glucose during gestation, resulting in pancreatic
beta cell hyperplasia with increased secretion of insulin and proinsulin factors
(IGF-1, IGF-BP3). Amino acid availability also is increased. All of these
factors are involved in the excessive growth observed in the infants of diabetic
mothers.
o All organ systems, aside from the kidney and brain, are sensitive
to the increased glucose and amino acid pools. Increased insulin levels result
in an increase in cell number and cell size.
• Impaired fetal growth
o
The major cause of impaired fetal growth is maternal diabetic nephropathy.
Maternal vascular disease compromises uteroplacental blood flow and impairs
fetal nutrient supply.
o IDMs are at increased risk of preterm labor,
stillbirth, neonatal death, birth injury, and perinatal asphyxia.
•
Pulmonary disease
o These infants are at increased risk for respiratory
distress syndrome, transient tachypnea of the newborn, and persistent pulmonary
hypertension.
o Insulin restricts substrate availability for surfactant
biosynthesis and interferes with the normal timing of glucocorticoid-induced
biosynthesis.
o Insulin also blocks cortisol action at the fibroblast level
by reducing production of fibroblast-pneumocyte factor, which normally would
stimulate type II cells to produce surfactant.
o Several studies agree that
the risk of respiratory distress syndrome in well-managed diabetic women
delivered at term is no higher than in the general population.
•
Electrolyte abnormalities
o These infants are at high risk for hypoglycemia,
especially within the early hours after birth.
o High levels of fetal insulin
with cessation of continued maternal glucose supply take place after birth. The
neonatal shift to gluconeogenesis with fatty acid use may provide an
insufficient supply of substrate, and, thus, the infant may experience
hypoglycemia (<20-40 mg/dL), which may be asymptomatic. Alternatively, the
infant may display such symptoms as jitteriness, irritability, lethargy, poor
feeding tolerance, and seizures. With hypoglycemia, the body responds with
increased counterregulatory hormones and production of ketones for use as an
energy source. With continued hyperinsulinemia, this production of ketones is
inhibited, thus lowering the source of energy for these infants even
further.
o Hypocalcemia, with or without hypomagnesemia, also may be present
and is believed to be secondary to parathyroid hormone suppression.
o
Postnatal parathormone response of IDMs is decreased compared to their
gestationally matched controls. The associated hypomagnesemia has been
speculated to be secondary to increased urinary losses associated with a more
severe diabetic state. This maternal hypomagnesemia is reflected in the fetus
also.
• Cardiovascular anomalies
o Cardiac hypertrophy may be observed
in as many as 30% of IDMs.
o Fetal growth is regulated by insulin binding to
cell receptors. Compared to the adult, the fetus has an increased number of
receptors. Because the fetal heart is particularly rich in receptors, this may
lead to increased myocardial protein, glycogen, and fat synthesis with
hyperplasia and hypertrophy of myocardial cells.
• Congenital
malformations
o Some speculate that many of the congenital anomalies in IDMs
may arise from an insult to the developing somite mesoderm and cephalic neural
crest cells.
o Metabolic disturbances, such as hyperglycemia, hypoglycemia,
hyperketonemia, and hypoxia, also may be involved. o Glucose-induced free
radicals of oxygen also have been implicated.
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