INFANT OF DIABETIC MOTHER HISTORY

History (infant of diabetic mother):
• Fetal congenital malformations are most common when maternal glucose control has been poor during the first trimester of pregnancy. Given that many pregnancies are unplanned, the need for preconceptional glycemic control in diabetic women cannot be overstated.

• Maternal hyperglycemia during late gestation is more likely to lead to fetal macrosomia, neonatal electrolyte abnormalities, or cardiomegaly with outflow tract obstruction.

• Fetal macrosomia
o Quality of fetal growth is determined by plotting birthweight against gestational age on standard growth curves. Infants whose weight exceeds the 90th percentile for gestational age are classified as large for gestational age (LGA). Maternal hyperglycemia during late pregnancy is commonly followed by excessive fetal growth.
o LGA infants should be routinely screened for potential hypoglycemia. This is particularly important if the mother has received large amounts of glucose-containing fluids during her labor.
o Fetal macrosomia is observed in 26% of IDMs and in 10% (by definition) of infants of nondiabetic women. While most common as a consequence of maternal hyperglycemia during late pregnancy, fetal macrosomia may occur despite maternal euglycemia.

• Impaired fetal growth
o Infants whose birthweight is below the 10th percentile, when plotted against gestational age on a standard growth curve, are considered small for gestational age (SGA).

o Impaired fetal growth may occur in as many as 20% of diabetic pregnancies, compared to a 10% incidence (by definition) for infants born to nondiabetic mothers. Maternal renovascular disease is the common cause of impaired fetal growth in pregnancies complicated by maternal diabetes.

• Pulmonary disease
o These infants are at an increased risk of respiratory distress syndrome and may present within the first few hours after birth with tachypnea, nasal or intercostal retractions, and hypoxia.
o Initially, the differential diagnosis might include transient tachypnea of the newborn, respiratory distress syndrome, pneumonia, or persistent pulmonary hypertension.

• Metabolic and electrolyte abnormalities
o Hypoglycemia may present within the first few hours of life, with such symptoms as jitteriness, irritability, apathy, poor feeding, high pitched or weak cry, hypotonia, or frank seizure activity. More commonly, the neonate is asymptomatic.
o Hypoglycemia is caused by hyperinsulinemia due to hyperplasia of fetal pancreatic beta cells consequent to maternal-fetal hyperglycemia. Because the supply of glucose is no longer continuous after birth, the neonate develops hyperglycemia substrate is insufficient. Stimulation of fetal insulin release by maternal hyperglycemia during labor significantly increases the risk of early hypoglycemia in these infants.
o The overall risk of hypoglycemia is anywhere from 25-40%, with LGA and preterm infants at highest risk.
o Hypocalcemia or hypomagnesemia also may be apparent in the first few hours after
birth; symptoms may include jitteriness or seizure activity. Hypocalcemia (levels <7 mg/dL) is believed to be associated with a failure to increase parathyroid hormone synthesis normally after birth.

• Hematologic problems:
Polycythemia, caused by increased erythropoiesis triggered by chronic fetal hypoxia, may present as a clinically "ruddy" appearance, sluggish capillary refill, or respiratory distress.

• Thrombocytopenia: Thrombopoiesis may be inhibited because of an excess of red blood cell precursors within the bone marrow as a result of chronic in utero asphyxia.

• Hyperbilirubinemia: This is common, especially in association with polycythemia. Excessive red cell hemolysis, caused by vascular sludging, leads to elevated bilirubin levels.

• Cardiovascular anomalies
o Cardiomyopathy with intraventricular hypertrophy and outflow tract obstruction may occur in as many as 30% of these infants. The cardiomyopathy may be caused by congestive failure with a weakly functioning myocardium or to a hypertrophic myocardium with significant septal hypertrophy and outflow tract obstruction. When cardiomegaly or poor perfusion and hypotension are present, it is important to obtain an echocardiogram to differentiate between these processes.
o These infants also are at an increased risk of congenital heart defects, including (most commonly) ventricular septal defect (VSD) and transposition of the great arteries (TGA).

• Congenital malformations
o Central nervous malformations are 16 times more likely in these infants. In particular, the risk of anencephaly is 13 times higher, while the risk of spina bifida is 20 times higher. The risk of caudal dysplasia is up to 600 times higher in these infants.
o Renal (eg, hydronephrosis, renal agenesis, ureteral duplication), ear, cardiovascular (eg, single umbilical artery, VSDs, atrial septal defects, TGA, coarctation of the aorta, cardiomegaly), and gastrointestinal (eg, duodenal or anorectal atresia, small left colon syndrome) anomalies are more frequent in these infants.

Physical (infant of diabetic mother):
• Fetal macrosomia (>90th percentile for gestational age or >4000 g in the term infant) occurs in 15-45% of diabetic pregnancies. When present, the infant appears puffy, fat, ruddy, and often mildly limp.

• Impaired fetal growth, secondary to poor placental blood flow, is a consequence of severe maternal diabetics with diabetic nephropathy. Perinatal asphyxia, more common in such infants, may be anticipated by prenatal history, thus stressing the importance of communication between obstetrician and pediatrician.