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