Management of Transient Hypoglycemia

               R. S. Cohen

BACKGROUND

Serum glucose levels (GLU) in the fetus are dependent on transplacental transfer of glucose from the mother and generally reflect maternal levels. Elevated maternal GLU can cause fetal hyperglycemia and increased insulin production by the fetal pancreas, resulting in fetal macrosomia. After separation from the placenta, newborn infants have to maintain their own GLU without maternal assistance. Thus, although usually euglycemic, the newborn could be either hyperglycemic or hypoglycemic depending on the maternal serum glucose and the infant’s ability for endocrine autoregulation.

EPIDEMIOLOGY

The exact incidence of transient neonatal hypoglycemia is unknown. Studies using continuous glucose monitoring have suggested that it is more common than previously believed, but the significance of this finding in asymptomatic, otherwise-well babies is unclear. Specific subgroups of neonates have been identified as having significantly increased risk of developing hypoglycemia:

Small-for-gestational-age (SGA) infants

Large-for-gestational-age (LGA) infants

Infant of diabetic mother (IDM)

Infant of gestational diabetic mother (IGDM)

Septic infants

Late preterm infants (LPTIs) born at 34⁺⁰ to 36⁺⁶ weeks’ gestation

Postdate infants

CLINICAL FINDINGS

1. Maternal history suggestive of abnormal glucose status

Diabetes mellitus

Obesity

Intravenous glucose administration

Abnormal fetal growth

Placental abnormalities (eg, too large/small, abruption)

Fetal intolerance of labor (eg, abnormal tracing, meconium staining)

2. Neonatal findings suggestive of abnormal glucose homeostasis

Intrauterine growth restriction/SGA

Macrosomia/LGA

Jitteriness

Seizures

Lethargy/poor feeding

Apnea

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