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 concentrations: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) concentrations:

  • 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

Prognosis concentrations:

  • 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