Hypoglycemia

Presented by
Dastan Hadi

Hypoglycemia
Hypoglycemia

may be considered a
biochemical symptom, indicating the
presence of an underlying cause
The exact glucose level that constitutes
hypoglycemia is debatable,
In neonates;
o
o

Older literature :(30 mg/dl)

Newer literature:(45mg/dl)

Physiolog
y

Etiology
Hyperinsulinemia
Disorders

of glucose
underproduction

Toxins

and other illnesses

Hyperinsulinemia
Maternal

diabetes in pregnancy
Persistent hyperinsulinemic
hypoglycemia of infancy
Insulin-producing tumors
Child abuse

Disorders of Glucose
Underproduction

Inadequate glucose stores ; prematurity, infants who are

small for gestational age, malnutrition
ketotic hypoglycemia; small, thin children aged 18 months to
6 years, is usually caused by disrupted food intake.
Glycogen synthase deficiency; glycogen-storage disease 0
Disorders of hepatic glucose prouction; glycogen-storage
disease type I, glycogen-storage disease type III, glycogenstorage disease type VI; glycogen synthase deficiency;
fructose 1,6 diphosphatase deficiency; phosphoenolpyruvate
deficiency; pyruvate carboxylase deficiency; galactosemia;
hereditary fructose intolerance; maple syrup urine disease.
Hormonal abnormalities; panhypopituitarism, growth
hormone deficiency, and cortisol deficiency

Toxins and other illnesses

Toxins;

ethanol, salicylates, propranolol

illnesses

; sepsis, malaria

Epidemiology
More in neonates born at less than 37 weeks'
gestation and in those born at more than 40 wks
Age;
Infants; Hyperinsulinemia, hypopituitarism, and inborn errors

of metabolism

Toddlers; ketotic hypoglycemia is most common

Adolescents; insulin-producing pancreatic tumors

Most common cause in general is acute

complication of Typ1 DM

Symptoms
Reflect 2 major clinical pathways;
Activation of the autonomic nervous
system
Neuroglycopenia
Nonspecific symptoms

Activation of the autonomic nervous system

sweating,

trembling

flushing
anxiety
heart

pounding
hunger

Neuroglycopenia
inability

to concentrate
confusion
tiredness
feeling tearful
difficulty speaking
behavioral changes
incoordination
weakness
drowsiness

Non specific symptoms

mouth

tingling,
dry mouth,
blurred vision,
headache
nausea

Symptoms in neonates
Tremulousness
Brisk Moro reflex
Lethargy
Poor feeding
Irritability
Hypothermia
Respiratory distress
Apnea
Bradycardia
Seizure
Coma
Sudden death

Whipples Triad
the

presence of symptoms likely or

known to be caused by hypoglycemia
a low plasma glucose concentration
when symptoms are present
subsequent relief of symptoms when the
hypoglycemia is corrected.

Hypoglycemia
Symptoms
Low
Glucose Levels
Relief of symptoms
on treatment

WHIPPLES TRIAD

Screening for blood sugar in

asymptomatic patient
infants

of diabetic mothers
infants who are large or small for
gestational age,
premature infants
Screening

should begin within the first

2-3 hours of life and continue through
the first 24 hours of life

Critical Sample
This

is a sample obtained at the time of hypoglycemia for;

Glucose
Insulin
growth hormone
Cortisol
lactate
Pyruvate
beta-hydroxybutyrate& free fatty acid
carnitine, branched-chain amino acid
insulinlike growth factor-binding protein-1 (IGFB-1) levels.
(A urine sample for organic acid analysis is also critical.)

Interpretation of Critical
Sample

Interpretation of Critical
Sample
A

failure of plasma free fatty acid levels to increase

to more than 0.5 mmol/L, and betahydroxybutyrate levels to more than 1 mmol/L
suggests hyperinsulinemic lipolytic suppression.
High plasma lactate levels suggest
gluconeogenesis, glycolysis, or respiratory-chain
defects
Plasma insulin levels should be suppressed
cortisol levels should be increased (>550 nmol/L)
Growth hormone levels should also be increased
(>6 mcg/L).

 IGFB1

increase during fasting in healthy

individuals but decrease or remain stable in
individuals who are hyperinsulinemic
Measuring sulfonylurea, ethanol, or
salicylate levels is appropriate if
hypoglycemia is believed to be secondary to
their ingestion
presence of a low C-peptide level with a high
insulin level suggests exogenous insulin
administration.

Treatment
Short-term

treatment consists of an
intravenous (IV) bolus of dextrose 10% 2.5
mL/kg. after withdrawing the critical sample.
Then IV infusion of 5-8 mg/kg/min in an
infant and 3-5 mg/kg/min in an older child
should be continued
Glucagon infusion or I.M can be given to
temporary treat children with
hyperinsulinism when adequate amounts of
dextrose cannot be given

Long-term care of children with hypoglycemia

varies based on the etiology.
ketotic hypoglycemia, glycogen-storage disorder,
free fatty acid metabolism defect, mild
hyperinsulinism), hypoglycemia can be prevented
with frequent feedings involving a specifically
designed diet and a rapid response with
parenteral dextrose when feeding is inadequate
Growth hormone and cortisol replacement are
specific treatments for children with hypoglycemia
and hypopituitarism or adrenal insufficiency.

Hierarchical Approach to Treat Hyperinsulinism

1.
2.
3.
4.
5.

frequent feeding
administration of diazoxide
octreotide is usually the second-line
medical therapy
calcium channel blocker nifedipine is
also useful.
surgery is recommended if these
treatments fail or if an insulin-producing
tumor is suspected.

Surgery:
#Failure of
medication
#Insulinoma

Frequent Feeding

Medication:
#Diazoxide
#Octreotide
#Ca Channel Blocker

Prognosis
Inborn

errors of metabolism and hormonal

deficiencies are lifelong diseases that
require lifelong treatment.
Ketotic hypoglycemia is generally
outgrown around age 5 years.
Prognosis in hyperinsulinism varies and
depends on the severity of the disease,
whether it is amenable to medical therapy,
and whether the lesion is focal or diffuse

Complications
Long-term

consequences of
hypoglycemia include decreased head
size, lowered IQ, and specific regional
brain abnormalities observed using
magnetic resonance imaging (MRI).