Pediatric emergency medicine trisk 1876 1876
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including those with dehydration and fussy or lethargic young infants, should have a point-ofcare glucose measurement.
Initial Assessment/H&P
Because hypoglycemia in children occurs after a period of fasting, a careful chronology of
dietary intake during the preceding 24 hours should be obtained, as well as a history either of
poor fasting tolerance (irritable upon awakening until feeding), or of fasting avoidance (sleeps
with bottle in crib). The possibility of a toxic ingestion should be considered because ethanol,
β-blockers, and oral hypoglycemic agents are in common use. Family history should be
explored for evidence of an undiagnosed metabolic disorder.
The clinical findings of hypoglycemia reflect both the decreased availability of glucose to
the CNS and the adrenergic stimulation caused by decreasing or low blood glucose.
Adrenergic symptoms and signs include palpitations, anxiety, tremulousness, hunger, and
sweating. Irritability, headache, fatigue, confusion, seizure, and unconsciousness are
neuroglycopenic symptoms. Any combination of these symptoms should lead to a
consideration of hypoglycemia.
Management/Diagnostic Testing
If hypoglycemia is suspected, blood should be drawn before treatment, if at all possible. An
extra tube (3 mL serum) should be obtained and refrigerated until the laboratory glucose is
known. Rapid screening should be performed using a bedside glucose meter while awaiting
definitive laboratory results. In some clinical laboratories, blood glucose can be determined
emergently with heparinized “whole” blood samples along with blood gases. Therapy should
be instituted if this screen is suggestive of hypoglycemia. This method may lead to some
overtreatment because of error of bedside devices; however, treatment holds minimal risk. It is
preferable to overtreat than to allow a child to remain hypoglycemic until definitive laboratory
results are available. If the laboratory glucose confirms that the blood glucose was less than 50
mg/dL, the reserved serum can be used for chemical (β-hydroxybutyrate, acetoacetate, amino
acid profile, acylcarnitine profile), toxicologic, and hormonal (insulin, growth hormone,
cortisol) studies, and may provide the correct diagnosis without extensive additional testing. If
adequate blood is obtained before correction, other metabolites to be considered are glucagon,
C-peptide, lactate, and pyruvate. If blood is obtained with 15 minutes of glucose
administration, it may still be helpful, although possibly not diagnostic. The first voided urine
after the hypoglycemic episode should be saved for toxicologic, organic acid evaluation, and
acylglycine profile. In the ED, the urine should also be tested immediately for ketones. With
hypoglycemia, ketones should be present. Failure to find moderate or large ketone
concentrations in the presence of hypoglycemia strongly suggests either that fats are not being
mobilized from adipose tissue, as might occur in hyperinsulinism, or that fat cannot be used
for ketone body formation, as might occur in enzymatic defects in fatty acid oxidation (e.g.,
medium-chain acyl dehydrogenase [MCAD] deficiency, and many other metabolic defects—
see Chapter 95 Metabolic Emergencies ). Both the urine and the serum results will be useful in
determining the underlying cause of hypoglycemia.
The preferred treatment for hypoglycemia is rapid IV administration of 0.25 g of dextrose
per kilogram body weight (2.5 mL/kg of 10% dextrose, 1.0 mL/kg of 25% dextrose). The
