http://www.rch.org.

au/clinicalguide/guideline_index/Hy
poglycaemia_Guideline/
Hypoglycaemia

See also:
o

Neonatal Hypoglycemia

Diabetes Mellitus

Background to condition
o

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

o
o

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
o

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*

Ketones* (Beta hydroxybutyrate)

1

Free fatty acids*

Cortisol*

Insulin & C-peptide*

Lactate

1,3

Carnitine / acylcarnitine
Ammonia

2, 4

Growth hormone
Amino acids
Electrolytes

Liver function tests

*Must be taken at time of hypoglycemia

All tests must go immediately to the laboratory on an ice pillow.
Minimum blood volume 6ml

2 x 0.5 ml fluoride oxalate

1 x 3ml lithium heparin tube

1 x 2ml serum gel tube

Guthrie card

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
Blood

Interpretation
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

Urine

Cortisol

in:
Hypoadrenalism
Hypopituitarism
ACTH deficiency

Insulin & C-peptide

Any detectable insulin in the presence of a BSL <2.6mmol/l is i

Growth hormone

in:
GH deficiency
Panhypopituitarism

Amino acids

Amino acid disorders

Electrolytes

Adrenal disorders

Liver function tests

Sepsis
Liver disease
Metabolic defects

Glucose
Ketones

in
Fatty acid oxidation defect
Hyperinsulinaemia

Reducing substances

Galactosaemia
Fructosaemia

Amino acids and organic acids

Urea cycle defect

Last updated January 2016