Hypoglycemia is a common,but often poorly investigated and managed. If prolonged or recurrent it can result in severe neuroglycopenia, potentially irreversible brain damage and long term mental handicap, particularly in the very young.
Hypoglycemia is a common,but often poorly investigated and managed. If prolonged or recurrent it can result in severe neuroglycopenia, potentially irreversible brain damage and long term mental handicap, particularly in the very young .
Normal neonates and young children tolerate fasting less well than adults. Blood glucose levels may start to fall after periods as short as 6–12h which has implications for the preoperative management of children requiring surgery. Glucose levels appear to fall in a cyclical fashion overnight in normal children, some falling into the ‘hypoglycemic’ range before compensation.
- Neonatal symptoms are nonspecific and include
- jitteriness
- hypotonia
- feeding difficulties
- pallor
- apnea
- tachypnea
- convulsions
- coma.
- In older children, symptoms and signs are attributable to neuroglycopenia.
- confused or bizarre behavior,
- bad temper,
- irritability,
- headache,
- visual disturbances,
- hunger,
- abdominal pain,
- convulsions,
- coma
- Or to counter-regulation
- pallor,
- sweating,
- nausea,
- vomiting
Blood glucose levels below which there is arbitrarily defined hypoglycemia (e.g. 2.2mmol/L) are controversial– it is unclear whether ‘low’ but asymptomatic blood glucose levels cause short or long term problems in different age groups. Prolonged or recurrent symptomatic hypoglycemia is undoubtedly associated with permanent neurological damage.
There are many potential causes of hypoglycemia–the most important are classified by age .
Persistent neonatal hypoglycemia is usually due to
- hyperinsulinism,
- deficiency of
- a counter-regulatory hormone
- a gluconeogenic or glycogenolytic enzyme. .
Recent onset recurring hypoglycemia is most commonly due to
- hyperinsulinism
- accelerated starvation
- defective hepatic gluconeogenesis
- GH
- glucocorticoid deficiency
- Accidental or nonaccidental administration of hypoglycemic agents must be considered and hypoglycemia anticipated in any child who has ingested alcohol
Differential diagnosis
History and examination :
- family history of neonatal death or acidosis in an inherited metabolic disorder,
- short stature with micropenis in hypopituitarism,
- hepatomegaly in galactosemia or gluconeogenic or glycogenolytic disorders,
- macroglossia
- Blood and urine samples taken when there is hypoglycemia and before treatment commences.
- Bloodglucose,
- ketonebodies,
- lactate,
- free fatty acids,
- branched chain amino acids, insulin,
- GH,
- cortisol and catecholamines
- urinary ketone bodies, catecholamine metabolites and reducing substances should ideally be measured.
- If sampling is difficult the most important assays are for blood glucose, plasma insulin and cortisol and urinary ketone bodies, and samples should be deep frozen for future analysis.
- Metabolic consequences of starvation with counter-regulation are increased plasma fatty acids, glycerol, ketone bodies, and branched chain amino acids associated with high levels of cortisol, GH and catecholamines. Insulin levels will be low or undetectable.
Significant ketosis excludes hyperinsulinism as the cause for hypoglycemia but ‘ketotic hypoglycemia’ is not a diagnosis in itself and requires further elucidation to find the cause. Important endocrine causes of ketotic hypoglycemia include .
- deficiencies of counter-regulatory hormones
- GH and ACTH deficiencies,
- CAH– especially during intercurrent stress or infection
- Addison disease,
- familial glucocorticoid deficiency and
- adrenomedullary unresponsiveness.
Hyperinsulinism results in hypoglycemia with out ketonuria because insulin inhibits lipolysis. Plasma insulin levels may not be elevated but will be high for plasma glucose; plasma ketone bodies may be detectable but will be low for the glucose level.
