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 to 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