Infants of diabetic and gestational diabetic mothers often bear a surprising resemblance to each other . They tend to be large and plump as a result of increased body fat and enlarged viscera, with puffy, plethoric facies resembling that of patients who have been receiving corticosteroids. These infants may also, however, be of normal or low birthweight, particularly if delivered before term or the mother has associated vascular disease.
Hypoglycemia develops in about 25–50% of infants of diabetic mothers and 15–25% of infants of mothers with gestational diabetes, but only a small percentage of these infants become symptomatic. The probability of hypoglycemia developing in the infant increases and glucose levels are likely to be lower at higher cord or maternal fasting blood glucose levels. The nadir in an infant’s blood glucose concentration is usually reached between 1 and 3 hr; spontaneous recovery may begin by 4–6 hr.
The infants tend to be jumpy, tremulous, and hyperexcitable during the 1st 3 days of life, although hypotonia, lethargy, and poor sucking may also occur. They may have any of the diverse manifestations of hypoglycemia. Early appearance of these signs is more likely to be related to hypoglycemia and later appearance related to hypocalcemia; these abnormalities may also occur together. Perinatal asphyxia or hyperbilirubinemia may produce similar signs. Hypomagnesemia may be associated with the hypocalcemia. These manifestations may also occur in the absence of hypoglycemia, hypocalcemia, or asphyxia.
Tachypnea develops in many infants of diabetic mothers during the 1st 2 days of life and may be a manifestation of hypoglycemia, hypothermia, polycythemia, cardiac failure, transient tachypnea, or cerebral edema from birth trauma or asphyxia. Infants of diabetic mothers have a higher incidence of respiratory distress syndrome than do infants of nondiabetic mothers born at comparable gestational age; the greater incidence is possibly related to an antagonistic effect of insulin on stimulation of surfactant synthesis by cortisol.
Cardiomegaly is common (30%), and heart failure occurs in 5–10% of infants of diabetic mothers. Asymmetric septal hypertrophy may occur and become manifested similar to transient idiopathic hypertrophic subaortic stenosis. Inotropic agents worsen the obstruction and are contraindicated. Congenital heart disease is more common in infants of diabetic mothers. Birth trauma is also a common sequela of fetal macrosomia.
Neurologic development and ossification centers tend to be immature and correlate with brain size (which is not increased) and gestational age rather than total body weight. In addition, these infants have an increased incidence of hyperbilirubinemia, polycythemia, and renal vein thrombosis; the latter should be suspected in infants with a flank mass, hematuria, and thrombocytopenia.
The incidence of congenital anomalies is increased threefold in infants of diabetic mothers; cardiac malformations (ventricular or atrial septal defect, transposition of the great vessels, truncus arteriosus, double-outlet right ventricle, tricuspid atresia, coarctation of the aorta) and lumbosacral agenesis are most common. Additional anomalies include neural tube defects, hydronephrosis, renal agenesis and dysplasia, duodenal or anorectal atresia, situs inversus, double ureter, and holoprosencephaly. These infants may also develop abdominal distention caused by a transient delay in development of the left side of the colon, the small left colon syndrome.