INFANT OF DIABETIC MOTHER
Category: Child Health
Abstract : Diabetes has long been associated with maternal and perinatal morbidity and mortality. Before the discovery of insulin in 1921, diabetic women rarely reached reproductive age or survived pregnancy. In fact, pregnancy termination was recommended routinely for pregnant diabetic patients because of high mortality rates. Fetal and neonatal mortality rates were as high as 65% before the development of
Diabetes has long been associated with maternal and perinatal morbidity and mortality. Before the discovery of insulin in 1921, diabetic women rarely reached reproductive age or survived pregnancy. In fact, pregnancy termination was recommended routinely for pregnant diabetic patients because of high mortality rates. Fetal and neonatal mortality rates were as high as 65% before the development of specialized maternal, fetal, and neonatal care.
Since then, infants of diabetic mothers (IDMs) have experienced a nearly 30-fold decrease in morbidity and mortality rates. Today, 3-10% of pregnancies are affected by abnormal glucose regulation and control. Of these, 80% are related to abnormal glucose control of pregnancy or gestational diabetes mellitus.
Infants born to mothers with glucose intolerance are at an increased risk of morbidity and mortality related to the following:
• Respiratory distress
• Macrosomia
• Hyperviscosity secondary to polycythemia
• Hypoglycemia
• Congenital malformations
• Hypocalcemia and hypomagnesemia
These infants are likely to be born by cesarean section for many reasons, among which are such complications as shoulder dystocia with potential brachial plexus injury related to the infant's large size. It is important for these mothers to be monitored closely throughout pregnancy. If optimal care is provided, the perinatal mortality rate, excluding congenital malformations, is nearly equivalent to that observed in normal pregnancies.
Pathophysiology (infant of diabetic mother):
It is necessary to understand the physiology of fetal glucose control to appreciate the causes of the associated complications. Increased levels of both estrogen and progesterone affect glucose homeostasis as counter-regulatory hormones in the mother early in pregnancy. As a result, beta-cell hyperplasia occurs in the pancreas, stimulating an increased release of insulin.
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 (infant of diabetic mother):
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 insulin-dependent 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 (infant of diabetic mother):
• 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 hypoglycemia
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