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Authors: Samuel R. Reid, MD, Staff Physician, Pediatric Emergency Medicine, Children’s Hospitals and Clinics-St. Paul, MN; Joseph D. Losek, MD, FAAP, FACEP, Director, Emergency Department, Children’s Hospitals and Clinics-St. Paul, MN.
Peer Reviewer: Raymond D. Pitetti, MD, MPH, Assistant Professor of Pediatrics, Division of Pediatric Emergency Medicine, Department of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, PA.
Children with hypoglycemia pose a diagnostic challenge because hypoglycemia is an uncommon pediatric condition and its presenting signs and symptoms may be either nonspecific or suggestive of a pathophysiology other than hypoglycemia. However, prompt recognition is of utmost importance because untreated hypoglycemia may result in permanent neurologic dysfunction.
Hypoglycemia is not a diagnosis in itself but rather a sign suggesting a more specific diagnosis. Although the causes of hypoglycemia in a child are numerous, and many may seem obscure, the clinician must have a working knowledge of the broad diagnostic categories of hypoglycemia so that a timely and appropriate diagnostic investigation can be initiated at the time of recognition and treatment.
This article reviews those aspects of pediatric hypoglycemia that are important for emergency department management.
— The Editor
While it is generally accepted that a plasma glucose concentration of less than 60 mg/dL constitutes hypoglycemia in an older child or adult, the definition of hypoglycemia in the newborn period and during infancy is controversial.1,2 Attempts to correlate clinical signs with glucose levels have depended on subjective assessments and are inconclusive.1 A review of 36 pediatric textbooks found cutoff values for hypoglycemia in newborns ranging from 18 to 72 mg/dL.2 Most authorities, however, would currently accept that a plasma glucose of less than 30 mg/dL in the first 24 hours of life and less than 45 mg/dL thereafter constitutes hypoglycemia in the newborn.3 Over time, the trend has been to accept higher and higher values of plasma glucose as constituting hypoglycemia in this age group. Some authorities have advocated abandoning a numerical definition of hypoglycemia, arguing that the plasma glucose concentration constituting euglycemia may vary from person to person and from physiologic circumstance to physiologic circumstance.1,2,4 Until consensus has been reached as to the level of plasma glucose below which neurologic injury occurs, it seems prudent that the emergency medicine physician maintain a low threshold for the diagnosis and treatment of hypoglycemia in newborns and infants.
The plasma glucose concentration is felt to closely approximate the amount of glucose available to brain tissue and is therefore considered the "gold standard" for the determination of hypoglycemia.1,2,5 Whole blood measurements of glucose underestimate the plasma glucose concentration by approximately 10-15% because erythrocytes contain relatively low concentrations of glucose.1,6 Venous samples are preferred; arterial and capillary samples may overestimate the plasma glucose concentration by 10% in non-fasting patients.1 Specimens should ideally be transported to the laboratory on ice and analyzed promptly to minimize the effect of ongoing glucose consumption by blood cells.1,7,8
Bedside glucose determination is a convenient and expeditious method for determining glucose concentration in the emergency department. However, such determinations may not be accurate at low glucose concentrations; both false positives and false negatives occur.1,7,8 Isopropyl alcohol used for skin preparation may contaminate specimens and cause erroneous results.1,7,9 A low hematocrit can result in falsely high readings, while a high hematocrit and hyperbilirubinemia can result in falsely low readings.2,6,7 Some brands of reagent strips are not intended for use in neonates.7 In a recent study of adult patients, however, bedside glucose determination using a visually interpreted reagent strip was found to be both sensitive and specific for the detection of hypoglycemia.10 Until these findings have been reproduced for pediatric patients, all children for whom hypoglycemia is a possibility (either on the basis of clinical findings or a suggestive bedside glucose determination) should be treated while awaiting the results of a confirmatory laboratory plasma glucose determination.3,6,9
Glucose homeostasis is an intricate balance between those physiologic mechanisms that reduce circulating glucose (fasting, glucose utilization, and insulin) and those that increase circulating glucose (feeding, gastrointestinal glucose absorption, catecholamines, glucagon, growth hormone, and adrenal corticosteroids).5,6,11 Figure 1 diagrams glucose homeostasis. The brain is a principal consumer of circulating glucose and for all practical purposes, is dependent on glucose alone for its metabolic needs.1,5 When the brain is deprived of glucose for prolonged periods or on multiple occasions, injury occurs.3,5,6,9
Any disorder that interferes with carbohydrate intake, intestinal absorption, glycogen formation or mobilization, gluconeogenesis, ketogenesis, or fatty acid oxidation places a child at risk for hypoglycemia. Similarly, disorders which result in excessive tissue utilization of glucose (e.g., hyperinsulinism) place a child at risk for hypoglycemia.
In the presence of hypoglycemia, epinephrine and glucagon are released and stimulate glycogenolysis, gluconeogenesis, and ketogenesis. Glycogenolysis acutely increases levels of circulating glucose; gluconeogenesis becomes important when glycogen stores are depleted. After a period of adaptation, the brain can derive a portion of its energy needs by metabolizing the products of ketogenesis and fatty acid oxidation.12 Concomitantly, increased cardiac output and systemic vascular resistance increase cerebral blood flow and the delivery of glucose to brain tissue. Glucose utilization by muscle tissue is diminished and insulin secretion is suppressed. Growth hormone, adrenal corticosteroids, and non-epinephrine catecholamines also contribute to these physiologic responses.5,6,11
A number of factors make the infant and child more vulnerable to hypoglycemia than the adult. Glucose utilization is higher, probably due to the proportionately larger brain.5 Glycogen stores are smaller and may only be sufficient to provide circulating glucose for a fast of a few hours. Available muscle mass and fat stores from which to generate precursors for gluconeogenesis and ketogenesis are smaller. Most importantly, the developing brain is more prone to hypoglycemic injury.9
Electroencephalogram and brain imaging studies in patients who have suffered hypoglycemic events demonstrate characteristic changes.13-15 Pathologically, neuronal injury primarily affecting the superficial cerebral cortex, dentate gyrus, caudate nucleus, and hippocampus has been described.3 Clinical outcomes ranging from no detectable sequelae and mild cognitive dysfunction to microcephaly, mental retardation, and epilepsy have been described.3,16-19 Symptomatic hypoglycemia, particularly that resulting in seizures, seems to be more strongly associated with more adverse neurologic sequelae than asymptomatic hypoglycemia.3,19 Neonates seem to be most vulnerable to adverse outcomes.9
History. The relationship of a hypoglycemic episode to the most recent meal can be important diagnostically. Hypoglycemia occurring after a short fast (2-3 hours) is suggestive of glycogen storage disease. Hypoglycemia occurring after a long fast (12-14 hours) suggests a disorder of gluconeogenesis. Postprandial hypoglycemia may indicate galactosemia or hereditary fructose intolerance. Hypoglycemia inconsistently related to fasting is seen in patients with hyperinsulinism.5,20 A family history of sudden infant deaths may be a clue to an unrecognized, inherited metabolic disorder. A history of ingestion of an agent known to cause hypoglycemia (e.g., sulfonylurea) should be sought but may not always be available.
Signs and Symptoms. Signs and symptoms of hypoglycemia are typically divided into two categories: adrenergic and neuroglycopenic. Adrenergic signs and symptoms result from secretion of epinephrine in response to the stress of hypoglycemia. Neuroglycopenic signs and symptoms reflect a circulating supply of glucose which is insufficient for normal brain function. Classic teaching suggests that adrenergic signs and symptoms precede neuroglycopenic signs and symptoms. Recent evidence, however, suggests that not all patients present with such a predictable evolution of symptoms and that some patients will develop no adrenergic phenomena at all. Patients with repeated episodes of hypoglycemia tend to experience similar symptoms with each event; however, their perception of these symptoms may be diminished. Certain symptoms commonly experienced by hypoglycemic patients are not explained by adrenergic stimulation or neuroglycopenia alone.21
Infants cannot describe their symptoms and have a limited repertoire of signs with which to manifest illness. Signs of hypoglycemia are therefore particularly nonspecific and may suggest dysfunction in any of several organ systems. Because infants are particularly vulnerable to hypoglycemia, the possibility of hypoglycemia should be considered for all ill patients in this age group. Table 1 summarizes hypoglycemic signs and symptoms for infants and older children. It should be remembered that hypoglycemia may be asymptomatic.
|Table 1. Signs and Symptoms of Hypoglycemia in Infants and Children|
Other described focal neurologic manifestations of hypoglycemia include cranial nerve palsies, ataxia, cortical blindness, decerebrate posturing, and choreoathetosis.26-31 Non-neurologic presentations of hypoglycemia suggestive of other disease processes include acute respiratory failure, sinus bradycardia, night terrors, psychosis, and urticaria.32-36
Hypoglycemia can also present as a complication of other disease processes such as sepsis, congestive heart failure, alcohol intoxication, dehydration, and trauma.5,37-40 The clinician should not overlook the possibility of hypoglycemia in any ill-appearing infant or child.41
Physical Examination. Certain physical findings are helpful in determining the etiology of hypoglycemia.
Hepatomegally is strong evidence for an inborn error of metabolism or primary hepatic disease. Short stature may reflect growth hormone deficiency. Macrosomia suggests hyperinsulinism. The combination of macrosomia, macroglossia, omphalocele, and organomegally is consistent with Beckwith-Wiedemann syndrome. Hyperpigmentation and ambiguous genitalia are seen with adrenal insufficiency. Cleft palate and micropenis suggest hypopituitarism.
The differential diagnosis of hypoglycemia in infants and children is broad and summarized in Table 2. Selected etiologies are discussed below. Phillip has proposed an algorithm for the diagnostic evaluation of the hypoglycemic child for whom toxin or drug ingestion, malnutrition, liver failure, and extrapancreatic tumors have been excluded.20
|Table 2. Differential Diagnosis of Hypoglycemia|
|• Infant of diabetic mother|
|• Small for gestational age|
|• Systemic illness (e.g., sepsis, respiratory distress syndrome)|
|• Adrenal hemorrhage|
|• Beckwith-Wiedemann syndrome|
|• Maternal medication (e.g., insulin, beta-blockers)|
|• Hyperinsulinism (e.g., insulinoma, nesidioblastosis)|
|• Growth hormone deficiency|
|• Adrenocortical deficiency (e.g., congenital adrenal hyperplasia)|
|• Glucagon deficiency|
|• Catecholamine deficiency (e.g., adrenal medullary unresponsiveness)|
|Inborn Errors of Metabolism|
|• Disorders of carbohydrate metabolism (e.g., galactosemia, glycogen storage diseases)|
|• Disorders of amino acid and organic acid metabolism (e.g., methylmalonic acidemia, biotinidase deficiency)|
|• Disorders of fat metabolism (e.g., carnitine deficiency)|
|• Oral hypoglycemic agents (e.g., sulfonylureas)|
|• Insulin (e.g., diabetic therapy, factitious)|
|• Antimalarial agents|
|• Unripe ackee fruit|
|• Intestinal malabsorption|
|• Idiopathic ketotic hypoglycemia|
|• Dehydrating gastroenteritis|
|• Liver failure (e.g., Reye syndrome, hepatitis)|
|• Large extrapancreatic tumor (e.g. Wilm's tumor)|
|• Cyanotic congenital heart disease|
|• Malnutrition (e.g., anorexia nervosa)|
Endocrine. Hypoglycemia is a common complication of insulin therapy in children with insulin dependent diabetes mellitus. As efforts to maintain stricter glycemic control in diabetic patients intensify, the risk of hypoglycemia increases.44,45 If a child does not consume enough glucose-containing foods or beverages following the administration of insulin, hypoglycemia will occur. Diabetic patients who experience multiple episodes of hypoglycemia may develop "hypoglycemia unawareness," a failure to perceive symptoms of hypoglycemia. The mechanism of this phenomenon is unclear but may involve a blunted neurohumoral counterregulatory response to hypoglycemia.46,47 Such patients are more likely to present with findings of profound neuroglycopenia.47
Hyperinsulinism presents as refractory hypoglycemia without ketosis and results from a defect in pancreatic beta cell regulation, pancreatic beta cell hyperplasia, or an islet cell adenoma.5,8,48 Inappropriately high levels of circulating insulin increase tissue glucose utilization and decrease rates of endogenous glucose production. Intentional misuse of insulin by a diabetic child or an abusive parent will also result in hypoglycemia and can be detected by measuring low serum levels of c-peptide in the setting of high serum levels of insulin.8 Large, non-pancreatic tumors can occasionally produce an insulin-like substance with resultant hypoglycemia.49
Several other endocrine pathways are instrumental to glucose homeostasis. Glucagon, growth hormone, and cortisol play important roles in the physiologic response to hypoglycemia; deficiency of any of them predictably predisposes a child to hypoglycemia. Hypopituitarism results in both ACTH and growth hormone deficiency; therefore, patients with this disorder are especially prone to hypoglycemia. Thyroid hormone may play a role in the production of gluconeogenic substrates and hepatic enzyme function, and its deficiency has occasionally been associated with hypoglycemia. "Adrenal medullary unresponsiveness" is a term applied to children who are found to have low levels of secreted epinephrine in response to hypoglycemia. Some authorities feel these patients constitute a subset of idiopathic ketotic hypoglycemia.6
Inborn errors of metabolism are rare, but as a group are responsible for a significant portion of childhood hypoglycemia. Most are inherited in an autosomal recessive manner. Presentations vary but hepatomegally, failure to thrive, and metabolic acidosis are common. Burton has recently reviewed the diagnosis of inborn errors of metabolism.50
Toxic. Numerous medications and toxins are associated with hypoglycemia. Ethanol causes hepatic enzyme dysfunction and impaired gluconeogenesis.5 Salicylate toxicity has been associated with hypoglycemia but the mechanism remains unclear.51 Propranolol inhibits glucagon and epinephrine secretion and the mobilization of glycogen. Beta adrenergic blockade can also mask adrenergic signs and symptoms of hypoglycemia.6,52 Sulfonylurea oral hypoglycemic agents produce a state of hyperinsulinism.53 Unripe ackee fruit contains hypoglycin, a substance that inhibits gluconeogenesis.8
Other. Idiopathic ketotic hypoglycemia is the most common cause of hypoglycemia in non-diabetic children outside the neonatal period. It characteristically occurs in a child 1-5 years of age after a relatively long fast (more than 12 hours) or when suffering a routine illness. Affected children are typically smaller than their peers and may have been small for gestational age. It is felt that these children have diminished stores of gluconeogenic substrates (low muscle mass) and thus are less tolerant of prolonged fasting. This disorder typically resolves spontaneously by age 10.5,6
Fulminant liver disease such as with Reye syndrome or infectious hepatitis may cause hypoglycemia as a result of decreased glycogen stores and impaired gluconeogenesis.6
Cyanotic congenital heart disease has been associated with hypoglycemia. Chronic hypoxia may interfere with hepatic glycogen storage and release.5 Hepatic hypoperfusion leading to impaired gluconeogenesis may be responsible for hypoglycemia in children with acyanotic congenital heart disease and congestive failure.5 However, poor oral intake and intestinal malabsorption resulting in poor glycogen stores may also contribute.38
Reports from underdeveloped nations have associated hypoglycemia with dehydrating gastroenteritis.39,54,55 Most affected children were young (younger than age 5) and suffered from bacterial gastroenteritis. Malnutrition among these patients was uncommon, suggesting that hypoglycemia was not a result of deficient glycogen stores but rather a result of impaired gluconeogenesis.39
For the infant or child with hypoglycemia not easily explained by history (e.g., a diabetic child who received insulin but failed to eat, or a clear-cut oral hypoglycemic ingestion), the emergency medicine physician plays a vital diagnostic role. While a definitive diagnosis may not be made in the emergency department, collection of appropriate laboratory tests at the time of hypoglycemia can greatly expedite diagnosis and spare the patient an uncomfortable and potentially harmful diagnostic fast. Table 3 lists diagnostic studies indicated at the time of hypoglycemia.6,8,9,12 Rather than committing this list to memory, it is helpful to develop a "hypoglycemia panel" so that the clinician need only know the quantity of blood and urine to obtain and the appropriate specimen containers in which to put them. Toxicology screening should be considered for patients in whom an unwitnessed ingestion is a possibility. If phlebotomy is unsuccessful after a few minutes, treatment should be administered without obtaining laboratory studies. A first-voided urine following the diagnosis and treatment of hypoglycemia is sufficient for initial urine studies.12
|Table 3. Laboratory Studies to Obtain at the Time of Hypoglycemia|
|Plasma glucose (confirmatory)||Urinalysis (ketones)|
|Electrolytes (anion gap)||Reducing substances|
|Free fatty acids|
When hypoglycemia is suspected, treatment should be started as quickly as possible to reduce the likelihood of permanent neurologic sequelae.8 For the patient without a clear-cut etiology by history, a few minutes can be spent obtaining the laboratory tests outlined above. Table 4 summarizes the treatment of hypoglycemia and drug dosages.
|Table 4. Treatment of Hypoglycemia|
|Juice (orange/apple)||10-20 mL/kg PO/NG/OG|
|Neonate:||D10W 5-10 mL/kg IV/IO|
|Child:||D25W 2-4 mL/kg IV/IO|
|6 mg/kg/min||D10W at (3.6 ´ weight [kg]) mL/hr|
|8 mg/kg/min||D10W at (4.8 ´ weight [kg]) mL/hr|
|10 mg/kg/min||D10W at (6 ´ weight [kg]) mL/hr|
|12 mg/kg/min||D10W at (7.2 ´ weight [kg]) mL/hr|
|Neonate:||0.3 mg/kg IV/IM/SQ|
|Child/Adolescent:||1 mg IV/IM/SQ|
|Neonate:||3-5 mg/kg PO/IV (over 30 minutes)|
|Child:||1-3 mg/kg PO/IV (over 30 minutes)|
|Adolescent:||300 mg PO/IV (over 30 minutes)|
|1 mcg/kg SQ|
|2.5 mg/kg IV (maximum 100 mg)|
|PO = oral; NG = nasogastric tube; OG = orogastric tube;|
|IV = intravenous; IO = intraosseous; SQ = subcutaneous;|
|IM = intramuscular|
For patients requiring parenteral therapy, dextrose is administered intravenously or intraosseously. Dextrose in high concentration may cause venous sclerosis and local tissue damage, particularly in newborns.3,6,11 For this reason, dextrose is administered as D10W in infants and D25W in children. The American Academy of Pediatrics and the American Heart Association recommend administering 0.5-1 g/kg of glucose (5-10 mL/kg of D10W or 2-4 mL/kg of D25W) to acutely reverse hypoglycemia.57 Other authors recommend glucose boluses as small as 0.25 g/kg (2.5 mL/kg of D10W or 1 mL/kg of D25W) to acutely reverse hypoglycemia.3,6,8,9,12 While the administration of concentrated dextrose in adult patients is thought to incur some risk of exacerbating ischemic cerebrovascular disease, no such association has been reported in children.4
Following a dextrose bolus, a continuous infusion of D10W to provide glucose at approximately 6-8 mg/kg/minute is recommended.3,6,8,11,12,33 This infusion is titrated to maintain a plasma glucose concentration above 60 mg/dL.58 Glucose determinations should be performed serially to assess the adequacy of therapy.
Patients who require more than 10-12 mg/kg/min of glucose and are not ketotic should be suspected to have hyperinsulinism.3,8,58 Diazoxide inhibits insulin release and may be initiated with close blood pressure monitoring and preferably in consultation with an endocrinologist.3,5,6,8,9,11 Octreotide is a long-acting somatostatin analog that also inhibits insulin release and has been used successfully in the management of hyperinsulinism.59
Glucagon may be used in the emergency management of hypoglycemia.60 It can be administered intravenously, intraosseously, intramuscularly, and subcutaneously. Intranasal administration of glucagon has been described, but concerns about absorption in the patient with nasal obstruction or rhinitis make it a less attractive option for emergency department care.61 Glucagon may be useful for patients for whom oral therapy is contraindicated and vascular access is difficult. Effect should be observed within 20 minutes. Administration of glucagon should not, however, end attempts for vascular access and dextrose therapy. Because glucagon requires adequate glycogen stores to be effective, children with poor glycogen stores, children with defects in glycogenolysis, and children with severe liver disease would not be expected to benefit from its administration.11
Steroids do not elevate glucose levels quickly enough to be of more than adjunctive value in the acute management of hypoglycemia. Their use in the child with hypoglycemia of unknown etiology may obscure certain endocrine diagnoses.12 A child with known hypopituitarism or adrenal insufficiency should receive hydrocortisone. Epinephrine is no longer considered appropriate for the management of hypoglycemia.3,11
Management of hypoglycemia resulting from sulfonylurea ingestion is similar to that of hyperinsulinism from other etiologies. Active charcoal is administered if the child presents within one hour of ingestion and the plasma glucose concentration is determined. Careful glucose monitoring, not empiric treatment, is recommended for the euglycemic child who may have ingested a sulfonylurea. Dextrose is administered if hypoglycemia evolves. When continuous infusion of relatively high concentrations of dextrose are not effective, an inhibitor of insulin secretion such as diazoxide or octreotide is administered.51,62
Diabetic patients who experience hypoglycemia as the result of insulin administration, who become asymptomatic after treatment, tolerate oral intake and have a care giver capable of monitoring their progress may be discharged from the emergency department. In general, all other hypoglycemic patients should be hospitalized for further monitoring, treatment, and diagnostic evaluation.
The emergency medicine physician should maintain a high index of suspicion for hypoglycemia when evaluating any ill-appearing child. Once suspected, the goals for management are to confirm the diagnosis, initiate an appropriate diagnostic evaluation, and establish euglycemia.
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A. An inborn error of metabolism
B. Ketotic hypoglycemia
D. Alcohol intoxication
D. Orange juice
B. Disorder of glycogenolysis
C. Salicylate toxicity
D. Ketotic hypoglycemia
C. Fatty acid oxidation
C. Respiratory failure
D. All of the above
A. Deficient epinephrine receptors
B. Greater insulin activity
C. Smaller glycogen stores
D. Immature response to glucagon
A. An uncommon cause of hypoglycemia in childhood
B. Affected children commonly larger than peers
C. Precursor of Type 1 diabetes mellitus
D. Commonly affects children between 1 and 10 years of age
A. serum glucose concentration < 60 mg/dL.
B. plasma glucose concentration < 60 mg/dL.
C. plasma glucose concentration < 20 mg/dL.