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BACKGROUND

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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.

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EPIDEMIOLOGY

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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:

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  • 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

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CLINICAL FINDINGS

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  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

    Unremarkable examination

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LABORATORY WORKUP

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Screening is recommended as follows only for at-risk infants:

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  1. IDM and LGA infants: screen for first 24 hours

  2. LPTIs and SGA infants: screen for first 12 hours

  3. Continue screening hypoglycemic infants until maintaining preprandial GLU 45 mg/dL or more for 2–3 feeding intervals

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The definition of neonatal hypoglycemia has been debated, but most recently, the American Academy of Pediatrics (AAP) has defined it as follows:

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  • GLU less than 40 mg/dL and symptomatic

  • GLU less than 25 mg/dL from birth to 4 hours of age after initial feeding

  • GLU less than 35 mg/dL prior to subsequent feeding from 4 to 24 hours of age

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A simplified algorithm for screening is shown in Figure 75-1.

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FIGURE 75-1

Glucose (GLU) screening for at-risk asymptomatic neonates. At risk defined as gestational age 34+0 to 36+6 weeks (late-preterm infants, LPTIs). small for gestional age (SGA); infant of diabetic mother (IDM); large for gestational age (LGA). aRisk interval defined as up to 24 hours for LPTIs and SGA infants and up to 12 hours for IDMs and LGA infants. IV, intravenous.

Graphic Jump Location
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TREATMENT

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Enteral

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Initial treatment is by enteral nutrition whenever possible if the baby is asymptomatic. See Figure 75-1 for a simplified treatment algorithm for asymptomatic neonates.

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