• The main cause of diabetic fetopathy is the mother's blood sugar dysregulation. Maternal HbAlc is indicative.
• While it causes fetal and neonatal hyperinsulinism and LGA resulting from beta cell hypertrophy, hyperplasia and hyperfunction in the pancreas due to the reflection of the mother's hyperglycemia to the fetus, placental insufficiency occurs due to vascular problems in mothers with long-term diabetes and may cause SGA.
• Macrosomia develops due to the mitogenic and anabolic effect of insulin, but the head circumference is normal.
• Mortality in infants of diabetic mothers increased >5 times compared to infants of nondiabetic mothers.
Associated congenital anomalies
• Major congenital anomalies are 2-4 times more common than babies of non-diabetic mothers. Although many anomalies occur;
The most common cardiac pathology is hypertrophic cardiomyopathy, the most common cardiac anomaly is ventricular septal defect, the most specific cardiological anomaly is transposition of the great vessels.
Hypertrichosis pinna (excessive hair growth in the ear helices) is highly specific.
Spinal agenesis (especially caudal regression syndrome), sacral agenesis, neural tube anomalies, holoprosencephaly
Gastrointestinal atresia, small left colon, microcolon or lazy colon, duodenal or anorectal atresia
Urinary system malformations (hydronephrosis, renal agenesis-dysplasia, double ureter) can be seen.
Treatment
• While periconceptional glucose control reduces the risk of anomaly and side effects, control during pregnancy prevents neonatal hypoglycemia.
• Gestational diabetes can also be treated with diet, blood sugar control and, if necessary, insulin. Glyburide, which does not cross the placenta, can also be used in patients with gestational diabetes.
• Non-insulin-dependent diabetes mellitus develops in 45% of babies of mothers with insulin-dependent DM before the age of 20.
• HbAlc levels are an important indicator that predicts the risk of developing anomaly in the baby.
