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The household medicine cabinet is filled with products that are potentially toxic, many of which have been obtained over the counter. According to the 2011 American Association of Poison Control Centers’ National Poison Data System (NPDS) Annual Report, analgesics, vitamins, antihistamines as well as cough and cold preparations account for approximately 21% of all exposures in children younger than 6 years.1 Oral hypoglycemics, which are also ubiquitous, are another common household danger that cause significant morbidity and mortality in children.


Historically, iron preparations have been a leading cause of pediatric mortality from exploratory drug overdose. In 1997, the Food and Drug Administration (FDA) issued a regulation requiring warning labels and childproof packaging for iron-containing products with 30 mg or more of iron per dosage unit.2 Since the implementation of childproof packaging and warning labels, the trend in NPDS data suggests that iron poisoning and fatalities are decreasing.3,4 In 2004, the iron packaging regulations were repealed, thus ferrous sulfate tablets and prenatal vitamins remain a toxic threat.


Different formulations of iron contain disparate amounts of elemental iron (Table 166-1). Mild toxicity, expressed in terms of milligrams of elemental iron per kilogram of body weight, is seen with doses as low as 20 mg/kg elemental iron, whereas systemic illness generally occurs with doses in the range of 40 to 60 mg/kg. The pharmacokinetics of iron in an overdose remains somewhat of a mystery.5 Peak iron levels are thought to occur between 2 and 6 hours after ingestion. Serum iron levels generally correlate with clinical severity: mild symptomatology (vomiting, diarrhea) is seen with levels less than 300 μg/dL, moderate symptoms with levels of 300 to 500 μg/dL, and severe manifestations (shock, acidosis, seizures, coma) with levels exceeding 500 μg/dL.6

TABLE 166-1Iron Formulations

Iron toxicity is described in phases. Early toxicity is caused by local irritant effects, whereas later findings are thought to be due to mitochondrial damage, particularly in the liver (Table 166-2).

TABLE 166-2Phases of Iron Toxicity

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