American Academy of Pediatrics Guidelines
The American Academy of Pediatrics (AAP) Committee on Fetus and Newborn published guidlines for the screening for neonatal hypoglycemia. [2] The guidelines include an algorithm for determining which infants to screen, when to screen, and clinical signs. Routine screening and monitoring of blood glucose is not recommended; only infants who have clinical manifestations of neonatal hypoglycemia or asymptomatic infants with risk factors should be screened. Clinical signs and symptoms of hypoglycemia include the following [2] :
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Jitteriness
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Cyanosis
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Seizures
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Apneic episodes
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Tachypnea
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Weak or high-pitched cry
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Floppiness
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Lethargy
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Poor feeding
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Eye-rolling
Risk factors for asymptomatic infants are as follows [2] :
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Small for gestational age
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Large for gestational age
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Born to mothers who have diabetes
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Late-preterm infants
At-risk infants should be screened with a frequency and duration related to risk factors specific to the individual infant. Screening asymptomatic at-risk infants can be performed within the first hours of birth and continued through multiple feed-fast cycles. Late-preterm infants and infants who are small for gestational age should be fed every 2 to 3 hours and screened before each feeding for at least the first 24 hours. After 24 hours, repeated screening before feedings should be continued if plasma glucose concentrations remain lower than 45 mg/dL. [2]
Thus, recommended screening of asymptomatic neonates from birth to 24 hours is as follows [2] :
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0-4 hours: Maintain blood glucose levels above 40 mg/dL before feeding
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4-24 hours: Maintain blood glucose levels above 45 mg/dL. If the neonate is symptomatic , then treat the infants if their blood glucose is below 40 mg/dL.
Pediatric Endocrine Society Guidelines
The Pediatric Endocrine Society (PES) guidelines for evaluation and management of persistent hypoglycemia in neonates, infants, and children recommend expanding the screening list beyond the American Academy of Pediatrics (AAP) recommendations to include infants that experienced perinatal stress due to the following [3] :
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Birth asphyxia/ischemia; cesarean delivery for fetal distress
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Maternal preeclampsia/eclampsia or hypertension
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Meconium aspiration syndrome, erythroblastosis fetalis, polycythemia, hypothermia
Other risk factors that should prompt screeining include the following [3] :
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Family history of a genetic form of hypoglycemia
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Congenital syndromes (eg, Beckwith-Wiedemann), abnormal physical features (eg, midline facial malformations, microphallus)
Additionally, persistent hypoglycemia should be excluded before discharge of infants with the following [3] :
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Severe hypoglycemia (eg, episode of symptomatic hypoglycemia or need for IV dextrose to treat hypoglycemia)
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Inability to consistently maintain preprandial PG concentration >50 mg/dL up to 48 hours of age and >60 mg/dL after 48 hours of age
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Family history of a genetic form of hypoglycemia
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Congenital syndromes (eg, Beckwith-Wiedemann), abnormal physical features (eg, midline facial malformations, microphallus)
For at-risk neonates without a suspected congenital hypoglycemia disorder, the goal of treatment is to maintain a plasma glucose concentration >50 mg/dL in the first 48 hours of life and >60 mg/dL after 48 hours. For neonates with a suspected congenital hypoglycemia disorder, the goal of treatment is to maintain the plasma glucose concentration >70 mg/dL. [3]
Thus, the recommended screening for neonatal hypoglycemia from birth to 24 hours is as follows [3] :
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First 48 hours: Maintain blood glucose levels above 50 mg/dL. Infants unable to maintain these levels in this time period may be at risk for a congenital hypoglycemia disorder.
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After 48 hours: Maintain blood glucose levels above 60 mg/dL. It is recommended that infants at risk of having a persistent hypoglycemia syndrome undergo a fast challenge of 6-8 hours with maintenance of blood glucose levels above 70 mg/dL
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Congenital Hyperinsulinism. Pancreatic specimen showing congenital hyperinsulinism (CHI) viewed at low power. Paler-staining cells are neuroendocrine (islet) cells, which should be arranged in discrete islands within acinar lobules. Acinar cells are exocrine cells that have denser-staining, dark eosinophilic cytoplasm. These acinar cells are arranged in acini. In CHI, more neuroendocrine cells are present, and they are arranged more diffusely throughout the lobules. Image courtesy of Phil Collins, MD.
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Congenital Hyperinsulinism. Pancreatic specimen showing diffuse congenital hyperinsulinism (CHI) viewed at medium power. Paler-staining cells are neuroendocrine (islet) cells, which should be arranged in discrete islands within acinar lobules. Acinar cells are exocrine cells that have denser-staining, dark eosinophilic cytoplasm. These acinar cells are arranged in acini. In CHI, more neuroendocrine cells are present, and they are arranged more diffusely throughout lobules. Image courtesy of Phil Collins, MD.
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Congenital Hyperinsulinism. Pancreatic specimen showing diffuse congenital hyperinsulinism (CHI) viewed at high power. Paler-staining cells are neuroendocrine (islet) cells, which should be arranged in discrete islands within acinar lobules. Acinar cells are exocrine cells that have denser-staining, dark eosinophilic cytoplasm. These acinar cells are arranged in acini. In CHI, more neuroendocrine cells are present, and they are arranged more diffusely throughout lobules. Image courtesy of Phil Collins, MD.
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Congenital Hyperinsulinism. Normal pancreas. There are fewer paler-staining neuroendocrine (islet) cells than those of patients with congenital hyperinsulinism, and the cells are arranged in more discrete islands. Image courtesy of Tom Milligan, MD, Driscoll Children's Hospital, Corpus Christi, Tex.
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Congenital Hyperinsulinism. Combined positron emission tomography (PET)/computed tomography (CT) scan of a focal lesion in the head of the pancreas of an infant with congenital hyperinsulinism. Uptake of 18F-L-DOPA glows brightly in the head of the pancreas (center), pinpointing abnormal cells in focal hyperinsulinism. The large glowing areas lower in image are the kidneys, where 18F-L-DOPA is excreted. Image courtesy of Charles Stanley, MD, Children's Hospital of Philadelphia.
