Anemia of Prematurity - Portal Neonatal

Increased insulin levels stimulate glycogen deposition and decrease hepatic glucose production. It
is not uncommon to recognize a decreased need for insulin in the diabetic patient in early
pregnancy. Furthermore, amino acids decrease and fatty acid triglycerides and ketones both
increase with increased fatty acid deposition. As a result, increased protein catabolism and
accelerated renal gluconeogenesis occurs. As pregnancy progresses, human placental lactogen is
released by the syncytiotrophoblast, leading to lipolysis in the mother. The subsequent release of
glycerol and fatty acids reduces maternal use of glucose and amino acid, thus preserving these
substrates for the fetus.
The release of increasing amounts of contrainsulin factors as placental growth continues causes up
to a 30% increase in maternal insulin needs as pregnancy progresses. Mothers with previous
borderline glucose control, obesity, or frank diabetes may require initiation of or increase in their
insulin requirements to maintain glucose homeostasis. Glucose and amino acids traverse the
placental membrane. On the other hand, insulin is unable to cross from maternal to fetal
circulations. Using a carrier-mediated facilitated diffusion mechanism, fetal glucose levels are
maintained at a level that is 20-30 mg/dL lower than those of the mother.
The fetus is subjected to high levels of glucose at times of maternal hyperglycemia. The fetus
responds to this with pancreatic beta-cell hyperplasia and increased insulin levels. Proinsulin (IGF-
1, IGF-BP3) also acts as a growth factor that, in the presence of increased fetal amino acids, results
in fetal macrosomia.
Frequency: In the US: The 1988 National Maternal and Infant Health Survey reported that diabetes
complicated 4% of pregnancies resulting in live births. Of these, 88% were the result of gestational
diabetes mellitus, 8% were the result of non–insulin-dependent diabetes, and 4% were from insulindependent
diabetes mellitus. Given recent estimates of 0.2-0.3% of pregnancies complicated by
preexisting diabetes and a further 1-5% complicated by gestational diabetes mellitus, approximately
50,000-150,000 infants are born to diabetic mothers every year.
Internationally: Women of Asian, Indian, or Middle-Eastern descent are at a higher risk than the
general population.
Mortality/Morbidity:
• Birth defects in infants of diabetic mothers have risen from 1-2% to 8-15% as a consequence
of increased perinatal survival. Major congenital malformations are found in 5-9% and
account for 30-50% of perinatal deaths of infants of mothers with gestational diabetes.
• In mothers with insulin-dependent diabetes, the perinatal mortality rate doubles and the
neonatal mortality rate triples when compared with that of the general population. These
infants are 3 times more likely to be born by cesarean delivery, twice as likely to suffer serious
birth injury, and 4 times as likely to be admitted to a neonatal intensive care unit.
• Major causes of morbidity include the following:
o Large or small for gestational age infants
o Hypoglycemia
o Prematurity
o Respiratory distress syndrome
o Intrapartum asphyxia
Race: Incidence is higher in Latinos and African-Americans than in whites. Diabetes occurs more
frequently in persons of American Indian descent, particularly among the Pimas of the southwestern
United States.
Sex: Frequency of involvement in boy and girl IDMs is equal.
Age: Generally, the first several hours after birth are the most critical for the development of hypogl