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  • Estimation of risk of iron poisoning is based upon conversion of the ingested iron salt to elemental iron with >60 mg/kg being associated with significant toxicity.

  • Phase II of iron poisoning is the quiescent phase. The patient appears improved, which may falsely reassure the clinician.

  • Serum iron concentrations should be obtained between 4 and 6 hours after ingestion.

  • Whole bowel irrigation (WBI) should be considered if multiple radiopaque iron tablets are seen on abdominal radiography.

  • The preferred route of deferoxamine administration is intravenously at a rate of 15 mg/kg/h.

Iron is one of the most important poisons in children. It has a high potential for morbidity and mortality. According to data from the American Association of Poison Control Centers (AAPCC), from 1983 to 1990 iron was the most common cause of pediatric unintentional ingestion death, accounting for 30.2% of reported cases.1 From 1985 to 1989, there were more than 11,000 reported exposures to iron in children.

The FDA has required unit dose packaging (blister-packs) for products containing more than 30-mg elemental iron per tablet. After this change in packaging, the rate of serious iron ingestions reported has plummeted.2 Despite the repealing of this regulation,2 this positive outcome has persisted. In 2015 according to the National Poison Data System of the AAPCC there were a total of 5682 iron and iron salt ingestions. There were 11 cases with a major effect, and one death.3


Iron is absorbed through the gastrointestinal (GI) mucosa in the ferrous (Fe2+) state. It is oxidized to the ferric (Fe3+) state and is bound to transferrin. Toxicity occurs when the transferrin-binding capacity is exceeded. Iron is a potent catalyst of free radical generation, which is the chief mechanism of iron toxicity. Circulating non–transferrin-bound iron can damage blood vessels and can cause transudation of fluids from the intravascular space, resulting in hypotension. Hypotension is potentiated by the release of ferritin, a potent vasodilator. Other target organs include the GI tract, the liver, and the cardiovascular system. Autopsy findings include cloudy swelling, fatty degeneration, and necrosis of hepatocytes. Iron deposits can be found in hepatocytes and the reticuloendothelial cells of the liver and spleen.


It is important to identify the specific preparation because the content of elemental iron varies (Table 121-1). If the preparation and the number of tablets are known, the total dose of elemental iron can be calculated. A dose exceeding 60 mg of elemental iron per kilogram of body weight is associated with significant toxicity.

TABLE 121-1Iron Preparations



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