Iron is a commonly used pharmaceutical agent and supplement found in prenatal vitamins and multivitamins. The toxic dose depends on the quantity of elemental iron in the preparation, which in turn depends on the iron formulation. While the minimum toxic dose remains controversial, ingestion of more than 40 mg/kg of elemental iron may result in toxicity, while ingestion of more than 60 mg/kg of elemental iron is associated with severe morbidity and possible mortality.
Iron toxicity is classically described as a four-stage process. Stage I develops within the first few hours of ingestion and reflects the direct caustic effects of iron on the GI tract. Signs and symptoms may include abdominal pain and GI bleeding. Stage II, variably present, is a redistributive or quiescent phase; although the initial GI symptoms resolve during this phase, acidosis and end-organ toxicity may still develop. With significant toxicity, individuals may progress directly from stage I to stage III. Stage III is the phase of overt shock, metabolic acidosis, and end-organ dysfunction (including delayed hepatic failure). Individuals who survive stage III may rarely progress to stage IV—gastric outlet obstruction secondary to the initial caustic insult of stage I.
Management and Disposition
Activated charcoal does not bind iron. Whole-bowel irrigation has been advocated for substantial ingestions and for patients with evidence of iron tablets on abdominal radiographs. Serum iron levels peak between 2 and 6 hours after ingestion. Levels obtained more than 6 hours after ingestion are unreliable due to tissue redistribution. Patients with evidence of iron toxicity (eg, persistent vomiting, acidosis, altered mental status, and hypotension) or a 4- to 6-hour postingestion serum level more than 500 µg/dL should receive chelation with deferoxamine.
Acute iron ingestion and the risk for toxicity must be assessed based on the quantity of elemental iron ingested, not the total amount of iron ingested.
The absence of radiopaque materials on abdominal radiographs is not a reliable indicator to exclude potential iron toxicity; liquid and pediatric (chewable) formulations are not typically radiopaque.
Despite the potential for anaphylactoid reactions and hypotension, patients requiring chelation therapy should receive deferoxamine via the intravenous route.
Radiopaque Iron. KUB radiograph of a patient with an acute iron ingestion, demonstrating radiopaque foreign bodies as noted in the left mid-quadrant and right lower pelvis. (Photo contributor: Saralyn R. Williams, MD.)
Vin Rose Urine—Iron Poisoning. A rare example of the progression of coloration of vin rose urine (from the excreted ferrioxamine complex) over 15 hours of chelation with deferoxamine is shown. Deferoxamine chelates free iron (but not iron present in the transferrin, hemoglobin, hemosiderin, or ferritin). (Reproduced with permission from Strange GR, Ahrens WR, Schafermeyer RW, et al. Pediatric Emergency Medicine. 3rd ed. New York, NY: McGraw Hill; 2009: ...