neonatal hypoglycemia
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Neonatal Hypoglycemia. Definition. The numerical definition varies from institution to institution: Numbers based on population studies of plasma glucose concentrations during first 48-72 hours of life with hypoglycemia defined as a plasma glucose level more than 2 SD below the population mean

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  • The numerical definition varies from institution to institution:
    • Numbers based on population studies of plasma glucose concentrations during first 48-72 hours of life with hypoglycemia defined as a plasma glucose level more than 2 SD below the population mean
  • Most institutions use plasma glucose <40mg/dl on the 1st day of life and less than 40-50mg/dl after 24 hours of life
  • Physiologic definition: when glucose supply for cells is inadequate to meet glucose demands
  • Estimated to be 10% of live births if first feeding is delayed for more than 3-6 hours after birth
  • Percentage is even higher for at-risk populations:
    • Preterm infants
    • SGA infants
    • LGA infants
    • Infants of diabetic mothers
  • Newborns have high brain-to-body weight ratio -> higher glucose demand
  • Impaired establishment of normal glucose homeostasis during transition from intrauterine to extrauterine life -> hypoglycemia
  • Normal glucose homeostasis requires supply to meet demands
  • Supply is dependent on adequate stores of glycogen, gluconeogenesis precursors, functioning hepatic enzymes, and a functioning endocrine system
  • Demands depend on the metabolic rate of the infant, which can be increased in times of stress (i.e. sepsis, asphyxia)
clinical manifestations
Clinical Manifestations
  • Asymptomatic
  • Tachypnea
  • Apnea
  • Respiratory distress
  • Tachycardia
  • Bradycardia
  • Jitteriness
  • Lethargy
  • Hypotonia
  • Weak suck
  • Temperature instability
  • Seizures
  • Diminished glucose production
  • Increased glucose utilization from hyperinsulinemia
  • Increased glucose utilization without hyperinsulinemia
  • Metabolic Disorders
  • Endocrine Disorders
  • Other
diminished glucose production
Diminished Glucose Production
  • Premature infants have diminished reserves because glycogen is deposited during the 3rd trimester of pregnancy
  • Infants with intrauterine growth restriction (IUGR) and who are SGA have reduced glycogen stores because of:
    • Low intrauterine insulin levels
    • Chronic intrauterine hypoxia
increased glucose utilization due to hyperinsulinemia
Increased Glucose Utilization Due to Hyperinsulinemia
  • Infant of a diabetic mother
  • Maternal intrapartum treatment with glucose
  • Beckwith-Wiedemann syndrome
  • Insulinoma
infant of a diabetic mother
Infant of a Diabetic Mother
  • Intermittent maternal hyperglycemia -> fetal hyperglycemia and hyperinsulinemia -> hypoglycemia once intrauterine glucose supply from mother is interrupted
  • Hypoglycemia occurs in 27% of infants of diabetic mothers (IDMs)
  • Happens in the first few hours of life
  • Most common in macrosomic IDMs
  • Premature &/or SGA IDMs are also at higher risk
beckwith wiedemann syndrome
Beckwith-Wiedemann Syndrome
  • Fetal overgrowth syndrome with characteristic features:
    • Macroglossia
    • Growth >90%
    • Abdominal wall defects
    • Ear creases/pits
    • Renal abnormalities
    • Hemi-hyperthrophy
    • Hyperplasia of organs (such as the pancreas)
beckwith wiedemann syndrome1
Beckwith-Wiedemann Syndrome
  • Incidence: 1 in 15,000 births
  • Etiology: Sporadic mutation (85%), AD (15%)
  • 50% have transient hypoglycemia caused by hyperinsulinemia from hyperplasia of the pancreas
  • Increased risk for malignancy:
    • Wilms tumor, hepatoblastoma, neuroblastoma, gonadoblastoma
    • Monitored with abdominal US and alpha-fetoprotein q6months until 6 y/o
  • Tumor of the pancreas that produces too much insulin
  • Very rare in children
  • Most are benign tumors, only about 5-10% are malignant
  • Treatment is surgical
  • If unable to surgically remove, treat with diazoxide or octreotide to reduce insulin secretion
increased glucose utilization without hyperinsulinemia
Increased Glucose Utilization Without Hyperinsulinemia
  • States of stress such as hypothermia, perinatal asphyxia, sepsis, and heart failure increase usage and depletion of glycogen stores
  • Polycythemia - increased utilization of glucose by the increased mass of RBCs
metabolic disorders
Metabolic Disorders
  • Inborn errors of metabolism:
    • Defects in carbohydrate metabolism
      • Glycogen Storage Disease
      • Glycogen Synthase Deficiency
      • Galactosemia
      • Fructose Intolerance
    • Defects in amino acid metabolism
      • Maple Syrup Urine Disease
      • PropionicAcidemia
      • MethylmalonicAcidemia
    • Defects in ketogenesis and fatty acid oxidation
endocrine disorders
Endocrine Disorders
  • Deficiency or malfunctioning of the hormones that regulate glucose homeostasis:
    • Cortisol
    • Growth hormone
    • Glucagon
    • Epinephrine
    • Thyroid
  • These could be associated with hypothalamic, pituitary, or adrenal insufficiency
other causes
Other Causes
  • Maternal drugs such as terbutaline, labetalol, propranolol -> inhibit glycogenolysis and gluconeogenesis
  • Neurohypoglycemia:
    • GLUT1 transport protein facilitates glucose diffusion across blood vessels into the brain and CSF
    • Deficiency in GLUT1 results in low CSF glucose, but blood glucose levels are normal
    • Rare disorder that presents as 2-3 months with seizures, developmental delay, and acquired microcephaly
  • Blood glucose should be monitored for infants at risk for hypoglycemia:
    • Premature infants
    • SGA infants
    • LGA infants
    • IDMs
    • Infants whose mothers were treated with beta adrenergic agents or beta blockers
    • Infants under stress requiring more intensive care (i.e. sepsis, asphyxia)
  • Monitor glucose within first 1-2 hours of life or with signs consistent with hypoglycemia
  • Surveillance should be continued in infants with glucose <40 until feedings well established and levels have stabilized
  • Low Chemstrips (glucose oxidase reagent strips for rapid screening) should be confirmed with serum glucose level processed by the lab
  • Determining Etiology:
    • Consider prenatal/perinatal history
    • Check growth parameters
    • Perform a careful physical exam
    • Screen for sepsis if suspected
  • If hypoglycemia persists for >1 week, endocrine and metabolic disorders should be suspected
    • Consult endocrinology
    • At the time of hypoglycemia, obtain:
      • ACTH/cortisol levels
      • Growth hormone levels
      • Insulin levels
      • Free fatty acids
      • Ketones
      • Pyruvate
      • Lactate
  • The following should also be obtained, but can be obtained at anytime:
    • TSH/T4 levels
    • Serum amino acids
    • Urine organic acids
    • Acylcarnitine profile
  • Anticipation and prevention is key
  • In infants who are premature or too ill to feed, begin parenteral glucose infusion at a rate of at least 6mg/kg/min
  • Glucose (mg/kg/min) = (% glucose in solution x 10) x (rate of infusion per hour) / (60 x weight in kg)
healthy asymptomatic infants
Healthy asymptomatic infants
  • Try feeding orally with either formula, breastmilk, or D10W
  • Use of formula or breastmilk better than D10W because they provide carbohydrates as well as protein and fats that are metabolized more slowly to provide a sustained supply of substrate
  • Recheck glucose in 20-30 mins after the feeding and continue to feed q2-3 hrs
  • Blood glucose should be followed before each feed for 12-24 hours
symptomatic infants or infants with very low glucose concentrations
Symptomatic infants or infants with very low glucose concentrations
  • Start parenteral glucose infusions on:
    • Symptomatic infants
    • Infants with a glucose of <20-25
    • Infants who do not tolerate enteral feedings
    • Infants whose blood sugar remains <40 after a trial of oral feeding
symptomatic infants or infants with very low glucose concentrations1
Symptomatic infants or infants with very low glucose concentrations:
  • Start with a bolus of 2-4ml/kg of D10W
  • Then begin a glucose infusion of at least 6mg/kg/min
  • Check blood glucose 20-30 mins after bolus to determine if another bolus is needed, and adjust rate of dextrose concentration to maintain plasma glucose >45mg/dl
  • Follow blood glucose every 1-2 hours until stable, then can space out monitoring as needed
  • When the glucose concentration is stable for 12-24 hrs, the glucose infusion rate can be tapered slowly by 10-20% each time the feeds are advanced and the pre-prandial blood glucose is >50-60 mg/dl
persistent hypoglycemia 7 days
Persistent Hypoglycemia (> 7 days)
  • Corticosteroids stimulate gluconeogenesis and reduces peripheral glucose utilization
    • should be considered in infants who remain hypoglycemic after 2-3 days of glucose infusion of >12mg/kg/min
  • Glucagon can also be used during severe hypoglycemia as a temporizing measure in infants with adequate glycogen stores (i.e. NOTin SGA or premature infants)
  • Diazoxide/Somatostatin/Octreotide inhibits insulin release for those with persistent hypoglycemia and hyperinsulinemia
persistent hypoglycemia 7 days1
Persistent Hypoglycemia (> 7 days)
  • Human growth hormone for infants with growth hormone deficiency
  • Nifedipine – case reports have shown some success with few side effects
  • Subtotal pancreatectomy for hyperinsulinemia
    • hypoglycemia recurs in up to 1/3 of patients
    • 40-60% develop DM later in life
  • Symptomatic hypoglycemia can result in brain injury
  • Most common sequelae are:
    • Disturbances in neurological development and intellectual function
    • Motor deficits (spasticity and ataxia)
    • Seizures

* May be related to the underlying etiology of the hypoglycemia

  • There is inconclusive evidence on the effect of asymptomatic hypoglycemia on neurodevelopment