Neonatal Hypoglycemia Clinical Presentation

Updated: Apr 16, 2017
  • Author: Hilarie Cranmer, MD, MPH, FACEP; Chief Editor: George T Griffing, MD  more...
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Presentation

History

The clinical presentation of hypoglycemia reflects decreased availability of glucose for the CNS as well as adrenergic stimulation caused by a decreasing or low blood sugar level. During the first or second day of life, symptoms vary from asymptomatic to CNS and cardiopulmonary disturbances.

High-risk groups who need screening for hypoglycemia in the first hour of life include the following [6, 7] :

  • Newborns who weigh more than 4 kg or less than 2 kg
  • Large for gestational age (LGA) infants who are above the 90th percentile, small for gestational age (SGA) infants below the 10th percentile, [8] and infants with intrauterine growth restriction
  • Infants born to insulin-dependent mothers (1:1000 pregnant women) or mothers with gestational diabetes (occurs in 2% of pregnant women)
  • Gestational age less than 37 weeks
  • Newborns suspected of sepsis or born to a mother suspected of having chorioamnionitis
  • Newborns with symptoms suggestive of hypoglycemia, including jitteriness, tachypnea, hypotonia, poor feeding, apnea, temperature instability, seizures, and lethargy

Additionally, consider hypoglycemia screening in infants with significant hypoxia, perinatal distress, 5-minute Apgar scores of less than 5, isolated hepatomegaly (possible glycogen-storage disease), microcephaly, anterior midline defects, gigantism, macroglossia or hemihypertrophy (possible Beckwith-Wiedemann Syndrome), or any possibility of an inborn error of metabolism or whose mother is on terbutaline, beta blockers, or oral hypoglycemic agents

The onset of hyperinsulinemia is from birth to age 18 months. Insulin concentrations are inappropriately elevated at the time of documented hypoglycemia. Transient neonatal hyperinsulinism occurs in macrosomic infants of diabetic mothers (who have diminished glucagon secretion and in whom endogenous glucose production is significantly inhibited). Clinically, these infants are macrosomic and have increasing demands for feeding, intermittent lethargy, jitteriness, and frank seizures. [9]

Infants with prolonged neonatal hyperinsulinism can be described by the following:

  • SGA
  • Having perinatal asphyxia
  • Born to mothers with toxemia
  • Having high rates of glucose use and often requiring dextrose infusion for a prolonged period of time

Ketotic hypoglycemia is an uncommon, but dramatic, illness. It is observed in children younger than age 5 years, who usually become symptomatic after an overnight or prolonged fast, especially with illness and poor oral intake. Children often present as inexplicably lethargic or frankly comatose, having only marked hypoglycemia with ketonuria.

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Physical Examination

Clinical manifestations are broad and can result from adrenergic stimulation or from decreased availability of glucose for the CNS. Unlike older children, infants are not able to verbalize their symptoms and are particularly vulnerable to hypoglycemia.

Infants in the first or second day of life may be asymptomatic or have life-threatening CNS and cardiopulmonary disturbances. Symptoms can include the following:

Clinical manifestations associated with activation of the autonomic nervous system include the following:

  • Anxiety, tremulousness
  • Diaphoresis
  • Tachycardia
  • Pallor
  • Hunger, nausea, and vomiting

Clinical manifestations of hypoglycorrhachia or neuroglycopenia include the following:

  • Headache
  • Mental confusion, staring, behavioral changes, difficulty concentrating
  • Visual disturbances (eg, decreased acuity, diplopia)
  • Dysarthria
  • Seizures
  • Ataxia, somnolence, coma
  • Stroke (hemiplegia, aphasia), paresthesias, dizziness, amnesia, decerebrate or decorticate posturing
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