Anemia of Prematurity - Portal Neonatal

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 wellmanaged
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 (