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restore serum pH to normal. In treating seizures, effective anticonvulsants include
the benzodiazepines or phenobarbital (both of which are GABA agonists). Either
diazepam (0.1 to 0.3 mg/kg), lorazepam (0.1 mg/kg), or midazolam (0.1 mg/kg)
should be administered IV to terminate seizures. Midazolam can be administered
effectively via the IM route at a dose of 0.2 mg/kg (max 10 mg).
Administration of pyridoxine provides specific antidotal therapy for INH
poisoning. After administration of vitamin B6 , seizures and metabolic acidosis
promptly resolve. Pyridoxine is given as an IV dose that equals the estimated
dose of INH in milligrams. In cases in which the ingested amount is unknown, a
single dose of 5 g (70 mg/kg in children) of pyridoxine is administered. Rarely,
repeat administration is necessary.
Although INH clearance can be enhanced by hemodialysis or hemoperfusion,
these techniques are rarely necessary if pyridoxine, activated charcoal, and
aggressive supportive care are provided.
Oral Hypoglycemics
Current Evidence. Although almost all pediatric patients with diabetes mellitus
require insulin therapy for control, the frequent prescription of oral hypoglycemic
agents for patients with non–insulin-dependent, adult-onset diabetes has made the
availability and, consequently, the ingestion of these medications commonplace
among toddlers. The scenario typically involves visits to a grandparent’s home (or
conversely, a visit by the grandparent to the child’s home).
Clinical Considerations. The sulfonylureas (chlorpropamide, glipizide, glyburide,
glimepiride) are capable of inducing significant hypoglycemia in a toddler after
the ingestion of a single tablet. In addition, the onset of hypoglycemia may be
delayed up to 16 to 24 hours after ingestion. Thus, prudent management of such
exposures generally implies prolonged close observation and a challenge period
of fasting. Although chlorpropamide is rarely used today, it may be enhanced by
urinary alkalinization. The biguanides (e.g., metformin) are unlikely to create
hypoglycemia but may promote metabolic acidosis.
Maintenance of euglycemia is usually accomplished in symptomatic patients
with the infusion of glucose in 10% to 20% solutions, supplemented as necessary

by bolus doses, for acute management. Glucose cannot be used as the sole
therapy, however, because the dextrose causes hyperglycemia that then leads to
insulin release with resultant hypoglycemia, and a vicious cycle of unstable blood
sugars ensues. Octreotide, a somatostatin analog that antagonizes insulin release,