Hypoglycaemia

  • See also:

    Background to condition

    • Clinical hypoglycemia is defined as a blood sugar level (BSL) low enough to cause symptoms and/or signs of impaired brain function. This is generally accepted as a BSL <2.6mmol/L.
    • Prolonged or recurrent hypoglycaemia, especially when associated with symptoms and signs can cause long term neurological damage or death. Thus, prompt recognition and treatment are essential.
    • Hypoglycaemia is the most frequent acute complication of type 1 diabetes either due to excess insulin or illnesses causing nausea, vomiting or diarrhoea and decreased oral intake.
    • Hyperinsulinism is the most common cause of persistent hypoglycaemia under 2 years. The presence of ketonuria and/or ketonaemia makes this diagnosis very unlikely.
    • Accelerated starvation (previously known as “ketotic hypoglycaemia”) is the most common cause of hypoglycemia beyond infancy, usually presenting between 18 months to 5 years.  It occurs after a prolonged fast and is usually precipitated by a relatively mild illness. It requires documenting a low BSL in association with ketonuria and/or ketonaemia, but definitive diagnosis requires exclusion of other metabolic and endocrine causes.
    • Hypoglycaemia may be an early manifestation of other serious disorders (eg. sepsis, congenital heart disease, tumours)

    How to assess

    Features on history

    Age

    • Neonates – please refer to Neonatal Hypoglycemia
    • Beyond neonatal period to 2 years: congenital hyperinsulinism, inborn errors of metabolism (eg. fatty acid oxidation defect, glycogen storage disease, galactosemia), congenital hormone deficiencies (eg. growth hormone deficiency)
    • Child: accelerated starvation, hypopituitarism
    • Adolescent: insulinoma, adrenal insufficiency

    Feeding history

    • Tolerance to fasting / illness
    • Relationship to food
      • Milk products (galactosemia)
      • Fructose e.g. juices (hereditary fructose intolerance)
      • Protein (amino acid or organic acid disorders)
    • History of toxin ingestion – in toddlers or young children consider accidental ingestion of alcohol, oral hypoglycemic agents, aspirin, beta blockers, or toxins
    • Past history
      • Neonatal history of hypoglycemia
      • Episodes suggestive of hypoglycemia eg. undiagnosed seizure disorder
      • Previous gastric surgery, fundoplication (postprandial hypoglycemia)
    • Family history
      • Consanguinity
      • Unexplained infant deaths (may be from inborn errors of metabolism)
      • Hormonal deficiencies and hyperinsulinism

    Features on investigations

    Any infant or child with first presentation, recurrent or severe hypoglycemia should be further investigated.

    Critical Blood samples

    Capillary glucometer readings are unreliable at low readings, hence it is important to confirm that true (lab) glucose is <2.6mmol/l before sampling

    Blood

    Glucose*1
    Ketones*1 (Beta hydroxybutyrate)
    Free fatty acids*1
    Cortisol*3
    Insulin & C-peptide*3
    Lactate1,3
    Carnitine / acylcarnitine2, 4
    Ammonia2
    Growth hormone3
    Amino acids2
    Electrolytes2
    Liver function tests2

    *Must be taken at time of hypoglycemia

    All tests must go immediately to the laboratory on an ice pillow.
    Minimum blood volume 5 mL


    Tubes Required:

    1. 3 x 0.5 mL fluoride oxalate
    2. 3 x 0.5 mL lithium heparin 
    3. 2 x 0.5 mL serum gel tube
    4. Newborn Screening Test (NST/Guthrie) card -  send air dried and in envelope, not in a plastic specimen bag.

    Note: A venous/capillary blood gas should have been previously performed.

    Urine (first voided urine after hypoglycaemic episode)

    Glucose
    Ketones
    Reducing substances
    Amino acids and organic acids

    Acute management

    See hypoglycemia flowchart

    When to admit/consult local paediatric team, or who/when to phone consult at RCH:

    • All patients with hypoglycaemia of unknown cause require admission.
    • The following features on examination should prompt discussion with Endocrinology or Metabolics
      • Weight and height
        • Failure to thrive (disorders of amino acid, organic acid, and carbohydrate metabolism)
        • Short stature (hypopituitarism or growth hormone deficiency)
        • Macrosomia (Beckwith-Wiedemann)
      • Hepatomegaly (Beckwith-Wiedemann, glycogen storage disease, defects in gluconeogenesis, galactosemia, hereditary fructose intolerance)
      • Midline facial defects eg. single central incisor, optic nerve hypoplasia, cleft lip or palate (hypopituitarism)
      • Appearance of genetalia (micropenis in growth hormone deficiency)
      • Skin pigmentation (adrenal insufficiency)
    • Endocrinology should be consulted if ongoing requirements exceed 5% dextrose concentration
    • A controlled fasting test should only be done after consultation with Endocrinology

    Discharge requirements

    • A cause for hypoglycemia must be known prior to discharge
    • A reasonable time between feeds/meals (at least 4 hours) must be safely tolerated without blood sugar dropping below 3 mmol/L.

    Appendix

    Interpretation of test results

    Test   Interpretation

    Blood

    Glucose <2.6mmol/l - hypoglycaemia
    Ketones
    (Beta hydroxybutyrate )
    ↓ in:
    Fatty acid oxidation defect
    Hyperinsulinaemia
    Lactate ↑ in:
    Metabolic liver disease
    Glycogen storage disorders
    Sepsis
    Prolonged convulsion
    Free fatty acids Fatty acid oxidation defect
    Carnitine / acylcarnitine Fatty acid oxidation defect
    Ammonia ↑ in:
    Organic acidaemias
    Tyrosinaemia
    Liver dysfunction
    Hyperinsulinism-Hyperammonaemia Syndrome
    Cortisol ↓ in:
    Hypoadrenalism
    Hypopituitarism
    ACTH deficiency
    Insulin & C-peptide Any detectable insulin in the presence of a BSL <2.6mmol/l is inappropriate
    Growth hormone ↓ in:
    GH deficiency
    Panhypopituitarism
    Amino acids Amino acid disorders
    Electrolytes Adrenal disorders
    Liver function tests Sepsis
    Liver disease
    Metabolic defects

    Urine

    Glucose  
    Ketones ↓ in
    Fatty acid oxidation defect
    Hyperinsulinaemia
    Reducing substances Galactosaemia
    Fructosaemia
    Amino acids and organic acids Urea cycle defect

    Last updated January 2016