Pediatric emergency medicine trisk 469

of 150 to 250 mg/dL. Additional supplemental insulin may be required, depending on when
the child last received insulin and the response to simple hydration.
Note, if hyperglycemia is a coincidental finding, the diagnosis requires thoughtful
consideration. How traumatic was the blood draw? How upset was the child? What
medications or IV fluids were given to the child just before the phlebotomy? What was the
child drinking while waiting to see the physician? Are the symptoms in any way related to the
hyperglycemia? How sick is the child? The sicker the child is, the less likely it is that
hyperglycemia is reflective of diabetes. Three simple evaluations are helpful in determining
whether the hyperglycemia is circumstantial or suggestive of diabetes. Brief hyperglycemia
resulting from a stress response to phlebotomy or secondary to oral intake rarely results in
significant glucosuria; therefore, a urine dip for glucose is often helpful. Second, in the
absence of ongoing stress or input, glucose tends to fall over time. A point-of-care glucose is
rarely stressful. Therefore, repeating a glucose measurement by fingerstick 1 to 2 hours after
the original sample was sent is useful in separating disease from nondisease. Third,
hyperglycemia secondary to these factors is usually mild (150 to 250 mg/dL). More significant
hyperglycemia should raise the suspicion of diabetes, glucose intolerance, or an underlying
medical illness that is producing a significant counterregulatory response.

HYPOGLYCEMIA
Goal of Treatment
To recognize hypoglycemia, initiate a diagnostic laboratory evaluation, and begin corrective
treatment immediately if exhibiting any symptoms.
CLINICAL PEARLS AND PITFALLS
Hypoglycemia in absence of ketones is consistent with hyperinsulinism or fatty acid
oxidation enzyme deficiencies.
Every acutely ill child with an altered level of consciousness should have a rapid
bedside glucose determined.
Treat severe hypoglycemia with rapid IV administration of 0.25 g dextrose per
kilogram body weight.

Current Evidence

Hypoglycemia is generally defined as plasma glucose of less than 50 mg/dL, regardless of
whether symptoms are present. A differential diagnosis of hypoglycemia, as it may present in
the ED, is provided in Table 89.4 . Hypoglycemia may be secondary to insulin therapy for
diabetes. Excluding this category, almost all hypoglycemia in children occurs during periods
of decreased or absent oral intake, often coupled with increased energy demand (e.g., viral
gastroenteritis with fever). Postprandial hypoglycemia is unusual in children, except in those
who have had prior gastrointestinal surgery. A few select poisonings can produce
hypoglycemia. Because glucose is necessary for cellular energy production in most human
tissues, the maintenance of an adequate blood glucose concentration is important for normal
function. The plasma glucose reflects a dynamic balance among glucose input from dietary


sources, glycogenolysis and gluconeogenesis, and glucose use by muscle, heart, adipose tissue,
brain, and blood elements. The liver plays a unique role in glucose homeostasis because it
stores glucose as glycogen. With fasting, this glycogen is degraded to glucose, which is
released into the bloodstream. In addition, the liver synthesizes new glucose from glycerol,
lactate, and certain amino acids. During fasting, lipolysis occurs, and the resultant fatty acids
are used for the production of both energy and ketones (acetoacetate and β-hydroxybutyrate)
by the liver. The energy generated from the metabolism of fatty acids is essential to sustain
maximal rates of gluconeogenesis and ureagenesis in the liver. The ketones are an important
auxiliary fuel for most tissues, including the brain. Muscle contains significant quantities of
glycogen and protein. Under fasting conditions, the glycogen is degraded and used
endogenously but is not released as free glucose into the bloodstream. Certain amino acids,
particularly alanine and glycine, are released from the muscle and subsequently used by the
liver for gluconeogenesis. Muscle derives an increasing proportion of its energy requirement
from fatty acids as fasting proceeds. Brain tissue is highly dependent on glucose for its energy
requirements. Under certain circumstances, it can extract a limited proportion of its energy
requirement from other substrates (e.g., glycerol, ketones, lactate), although this process
requires a period of adaptation and does not obviate the need for a constant supply of glucose.
Insulin is the primary hormone that regulates the blood glucose level. Insulin stimulates the

uptake of glucose and amino acids into skeletal, cardiac, and adipose tissue and promotes
glycogen and protein synthesis. It inhibits lipolysis and glycogenolysis. The net effect of
insulin action is to accelerate the removal of glucose and gluconeogenic substrates from the
bloodstream. Opposing or modulating the effects of insulin are cortisol, glucagon, epinephrine,
and growth hormone. The effects of these hormones include inhibition of glucose uptake by
muscle, mobilization of amino acids for gluconeogenesis, activation of lipolysis, inhibition of
insulin secretion, and induction of gluconeogenic enzymes. The net effect is to increase the
availability of gluconeogenic substrates to the liver, and to increase the accessibility and use of
nonglucose fuels by other tissues.


TABLE 89.4
CAUSES OF CHILDHOOD HYPOGLYCEMIA
Decreased availability of glucose
Decreased intake—fasting, malnutrition, illness
Decreased absorption—acute diarrhea
Inadequate glycogen reserves—defects in enzymes of glycogen synthetic pathways
Ineffective glycogenolysis—defects in enzymes of glycogenolytic pathways
Inability to mobilize glycogen—glucagon deficiency
Ineffective gluconeogenesis—defects in enzymes of gluconeogenic pathway
Increased use of glucose
Hyperinsulinism—islet cell adenoma or hyperplasia, ingestion of oral hypoglycemic agents,
insulin therapy
Large tumors—Wilms tumor, neuroblastoma
Diminished availability of alternative fuels
Decreased or absent fat stores
Inability to oxidize fats—enzymatic defects in fatty acid oxidation
Unknown or complex mechanisms
Sepsis/shock
Reye syndrome

Salicylate ingestion
Ethanol ingestion
Adrenal insufficiency
Hypothyroidism
Hypopituitarism

Clinical Considerations
Clinical Recognition
The acutely ill child warrants a glucose determination if the level of consciousness is altered
because hypoglycemia may accompany an illness that interferes with oral intake. The
symptoms and signs of hypoglycemia are nonspecific and are often overlooked, especially in
the infant and young child. Any child presenting with a seizure, other than a breakthrough
seizure with known epilepsy, or an altered level of consciousness should have a plasma
glucose determination.
Triage
Children with known diabetes who appear ill need a rapid bedside glucose for possibility of
hypoglycemia or hyperglycemia. All children with acute alterations in consciousness,


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