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http://www.rch.org.au/clinicalguide/guideline_index/Hypoglycaemia_Guideline/

Hypoglycaemia• See also:

o Neonatal Hypoglycemia

o Diabetes Mellitus

Background to condition

o Clinical hypoglycemia is defined as a blood sugar level (BSL lo! enough to cause

symptoms and"or signs of impaired brain function# $his is generally accepted as a BSL

<2.mmol/L.

o %rolonged or recurrent hypoglycaemia& especially !hen associated !ith symptoms and

signs can cause long term neurological damage or death# $hus& prompt recognition and treatment

are essential#

o Hypoglycaemia i! the mo!t "re#uent acute complication o" type $ dia%ete! either

due to e'cess insulin or illnesses causing nausea& vomiting or diarrhoea and decreased oral

intae#

o Hyperin!ulini!m  is the most common cause of persistent hypoglycaemia under ) years#

$he presence of etonuria and"or etonaemia maes this diagnosis very unliely#

o &ccelerated !tar'ation (previously no!n as *etotic hypoglycaemia+ is the most

common cause of hypoglycemia beyond infancy& usually presenting bet!een ,- months to .

years# /t occurs after a prolonged fast and is usually precipitated by a relatively mild illness# /t

re0uires documenting a lo! BSL in association !ith etonuria and"or etonaemia& but definitive

diagnosis re0uires e'clusion of other metabolic and endocrine causes#

o Hypoglycaemia may be an early manifestation of other serious disorders (eg# sepsis&

congenital heart disease& tumours

How to a!!e!!

(eature! on hi!tory

&ge

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o Neonates 1 please refer to Neonatal Hypoglycemia

o Beyond neonatal period to ) years: congenital hyperinsulinism& inborn errors of

metabolism (eg# fatty acid o'idation defect& glycogen storage disease& galactosemia& congenital

hormone deficiencies (eg# gro!th hormone deficiency

o Child: accelerated starvation& hypopituitarism

o  2dolescent: insulinoma& adrenal insufficiency

(eeding hi!tory

o $olerance to fasting " illness

o 3elationship to food

Mil products (galactosemia

4ructose e#g# 5uices (hereditary fructose intolerance

%rotein (amino acid or organic acid disorders

• History of to'in ingestion 1 in toddlers or young children consider accidental

ingestion of alcohol& oral hypoglycemic agents& aspirin& beta blocers& or to'ins

• %ast history

Neonatal history of hypoglycemia

6pisodes suggestive of hypoglycemia eg# undiagnosed sei7ure disorder 

%revious gastric surgery& fundoplication (postprandial hypoglycemia

• 4amily history

Consanguinity

8ne'plained infant deaths (may be from inborn errors of metabolism

Hormonal deficiencies and hyperinsulinism

(eature! on in'e!tigation!

 2ny infant or child !ith first presentation& recurrent or severe hypoglycemia should be further investigated#

Critical Blood samples

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Capillary glucometer readings are unreliable at lo! readings& hence it is important to confirm that true

(lab glucose is 9)#mmol"l before sampling

Blood

Glucose*1

Ketones*1 (Beta hydroxybutyrate)

Free fatty acids*1

Cortisol*2

Insulin & C-etide*2

!actate1"#

Carnitine $ acylcarnitine2" %

''onia2

Groth hor'one2

'ino acids2

lectrolytes2

!ier function tests2

;Must be taen at time of hypoglycemia

 2ll tests must go immediately to the laboratory on an ice pillo!#

Minimum blood volume ml

• ) ' <#. ml fluoride o'alate

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• , ' =ml lithium heparin tube

• , ' )ml serum gel tube

• >uthrie card

Note: 2 venous"capillary blood gas should have been previously performed#

)rine *first voided urine after hypoglycaemic episode+

Glucose

Ketones

+educin, substances

'ino acids and or,anic acids

&cute ,anagement

See hypoglycemia flowchart 

-hen to admit/con!ult local paediatric team or who/when to phone con!ult

at 0H:

•  2ll patients !ith hypoglycaemia of unno!n cause re0uire admission#

• $he follo!ing features on e'amination should prompt discussion !ith

6ndocrinology or Metabolics

?eight and height

4ailure to thrive (disorders of amino acid& organic acid& and carbohydrate

metabolism

Short stature (hypopituitarism or gro!th hormone deficiency

Macrosomia (Bec!ith@?iedemann

• Hepatomegaly (Bec!ith@?iedemann& glycogen storage disease& defects

in gluconeogenesis& galactosemia& hereditary fructose intolerance

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• Midline facial defects eg# single central incisor& optic nerve hypoplasia&

cleft lip or palate (hypopituitarism

•  2ppearance of genetalia (micropenis in gro!th hormone deficiency

•

Sin pigmentation (adrenal insufficiency

• 6ndocrinology should be consulted if ongoing re0uirements e'ceed .A de'trose

concentration

•  2 controlled fasting test should only be done after consultation !ith

6ndocrinology

1i!charge re#uirement!

•  2 cause for hypoglycemia mu!t be no!n prior to discharge

•  2 reasonable time bet!een feeds"meals (at least hours must be safely

tolerated !ithout blood sugar dropping belo! = mmol"L#

&ppendix

nterpretation o" te!t re!ult!

Test Interpretation

Blood Glucose 2./''ol$l - hyo,lycae'ia

Ketones

(Beta hydroxybutyrate )

0 in

Fatty acid oxidation defectyerinsulinae'ia

!actate 3 in

4etabolic lier disease

Glyco,en stora,e disorders

5esis6rolon,ed conulsion

Free fatty acids Fatty acid oxidation defect

Carnitine $ acylcarnitine Fatty acid oxidation defect

''onia 3 in

7r,anic acidae'ias8yrosinae'ia

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!ier dysfunction

yerinsulinis'-yera''onae'ia 5yndro'e

Cortisol 0 in

yoadrenalis'

yoituitaris'C8 deficiency

Insulin & C-etide Any detectable insulin in the presence of a BSL <2.6mm

Groth hor'one 0 inG deficiency

6anhyoituitaris'

'ino acids 'ino acid disorders

lectrolytes drenal disorders

!ier function tests 5esis

!ier disease

4etabolic defects

Urine Glucose

Ketones 0 in

Fatty acid oxidation defect

yerinsulinae'ia

+educin, substances Galactosae'ia

Fructosae'ia

'ino acids and or,anic acids 9rea cycle defect

Last updated anuary )<,