INFANT OF DIABETIC MOTHER HISTORY
Category: Child Health
Abstract : 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 lea
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.
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