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glucose testing is not available, a trial dosage of 0.25 to 1 g/kg glucose as 10% to
25% solution should be infused. It should be noted that drug- or toxicant-induced
hypoglycemia does not present uniformly with coma or seizures. Almost any
neuropsychiatric sequelae of hypoglycemia may predominate, including aphasia,
slurred or dysarthric speech, and focal neurologic signs. Adrenergic signs, such as
diaphoresis and tachycardia, are not uniformly present. Hypoglycemia is a
complication seen in ingestions of ethanol, oral hypoglycemics, β-blockers (BBs),
salicylates, and, of course, insulin injection. As basic as this intervention seems,
in our experience, it is still one of the most often delayed critical treatments in the
management of the poisoned patient. Empiric naloxone therapy is as important in
potentially poisoned toddlers with altered mental status as it is in adults. As
opioid prescriptions in the adult population have increased in recent years, so too
has the availability of these agents to young children. Many households contain a
variety of oral opioid analgesic agents, as well as cough medicines (codeine,
dextromethorphan), antidiarrheal agents (loperamide, diphenoxylate), and
partially naloxone-responsive antihypertensive agents such as clonidine. In
addition, the possibility of exploratory ingestion of a “stash” of illicit opioids
does exist. Thus, naloxone should be used as a therapeutic/diagnostic trial when
there is a reasonable possibility that altered mental status is drug induced.
Previous recommendations have based dosing on weight (e.g., 0.01 to 0.1 mg/kg);
however, several sources now prefer a unified pediatric dose of 1 to 2 mg for
acute overdose patients of all ages (outside the neonatal period). Such an
approach conceptualizes naloxone dosing as based on total narcotic load and
number of opioid receptors that require competition for binding sites. In general,
this latter approach is easier to remember and has not been associated with
complication in the ED. Adolescent patients with a strong clinical picture for
opioid intoxication (without habituation) may receive 2-mg bolus doses every 2
minutes, up to a total dose of 8 to 10 mg, because several congeners of morphine
(e.g., propoxyphene, illicit fentanyl derivatives, pentazocine, oxycodone,
methadone) may require these higher doses. If chronic abuse is suspected, lower
initial doses (0.04 mg) are warranted. Empiric administration of flumazenil after

an unknown drug overdose is not recommended as it may precipitate seizures and
life-threatening benzodiazepine withdrawal (see “Central Nervous System
Sedative-Hypnotics” section). Lastly, thiamine (100 mg IV), although routinely
administered to adult overdose patients who receive hypertonic glucose to obviate
precipitating Wernicke encephalopathy, is not generally necessary in the pediatric
population. Perhaps it should be considered in adolescent patients who may be