• Stage 1 (0 to 6 to 12 hours postingestion)
  • Direct corrosive effects of iron on gastrointestinal (GI) mucosa
  • Vomiting, diarrhea, and abdominal pain
  • Lethargy, hypotension, pallor possible
  • Metabolic acidosis, leukocytosis, hyperglycemia possible
• Stage 2 (6 to 24 hours postingestion)
  • Lasts no more than 12 to 24 hours
  • A transition stage between resolving GI symptoms and the development of systemic symptoms
• Stage 3 (12 to 48 hours postingestion)
  • Cerebral dysfunction, coma, myocardial depression, renal/hepatic failure
  • Coagulopathies, hypoglycemia, acidosis possible
• Stage 4 (2 to 6 weeks postingestion)
  • Survivors may develop GI scarring, which can lead to gastric outlet and small bowel obstructions.

• Free (unbound) iron is toxic to many cellular processes. By binding this free iron to carrier/storage proteins (e.g., transferrin, ferritin), cells are protected from its harmful effects. If a cell is exposed to excessive amounts of free iron, damage occurs as free radicals attack cellular biomolecules.
• Iron has a direct corrosive effect on the intestinal mucosa, which can lead to significant GI bleeding, perforation, ischemia, necrosis, and significant fluid losses.
• Venodilation, third spacing of fluids, hepatic dysfunction, and metabolic acidosis may occur as well.
• Humans are unable to eliminate excesses in total body iron. Thus, only by limiting the absorption of dietary iron can iron balance be regulated.

• There were more than 24,209 cases per year of exposure to iron-containing products in 1993.
• Eighty-four percent of these exposures occurred in children under 6 years of age.
• Iron exposures accounted for 2.2% of all ingestions in children under 6 years of age.

• GI bleeding
• GI perforation
• Renal failure
• Hepatic dysfunction
• Metabolic acidosis
• Shock
• Cerebral dysfunction
• Coma
• Myocardial depression
• Coagulopathy

• After an iron ingestion, a majority of children remain asymptomatic or develop only minimal toxicity.
• The children remain asymptomatic 6 hours after the ingestion, they are unlikely to develop serious toxicity.
• Shock, coma, and serum iron levels greater than 500 µg/dL are poor prognostic signs.

• Ingestion
  • Salicylates
  • Acetaminophen
  • Methanol
  • Ethylene glycol
  • Isoniazid (INH)
• Infectious
  • Sepsis
  • Bacterial gastroenteritis
• Gastrointestinal
  • GI hemorrhage

• Time since ingestion to assess staging, and degree of absorption
• Determine formulation of iron taken and calculate potential amount ingested:
  • Ferrous sulfate (20% elemental iron)
  • Ferrous gluconate (12%)
  • Ferrous fumarate (33%)
  • Ferrous chloride (28%)
• Potential milligrams of iron ingested × percentage of elemental iron = maximum potential milligrams of elemental iron ingested.
• Ask about symptoms, including vomiting, abdominal pain, and change in mental status.

• Assess vital signs.
• Assess mental status, and perform a thorough neurologic examination.
• Assess hydration status and peripheral perfusion.
• Assess abdominal examination and hematest stool.

• Iron level (serum): Peak level occurs 3 to 5 hours following ingestion. Levels of greater than 350 µg/dL are often associated with serious toxicity. However, the converse is not true.
• CBC: helps to identify significant GI bleeding. Initial studies attempted to correlate WBC greater than 15,000 cells/L with serum iron levels greater than 300 µg/dL. However, more recent studies do not confirm this correlation.
• PT/PTT: to rule out associated coagulopathy
• Electrolytes/ABG: to rule out metabolic acidosis
• Total iron binding capacity (TIBC): total amount of iron that transferrin can bind in a particular volume of serum; no longer recommended. Previously, it was felt that toxicity occurred when the serum iron level is greater than the TIBC. Recent studies have shown fault in this theory.
• Serum glucose: Initial studies attempted to correlate serum glucose greater than 150 mg/dL with serum iron levels greater than 300 µg/dL. However, more recent studies do not confirm this correlation. Current recommendations no longer use this test as a screening tool.

• Abdominal x-ray (AXR): may identify iron tablets, which are radiopaque, in the GI tract. This study is helpful if positive, but, if negative, one cannot exclude a significant iron ingestion.
• Deferoxamine challenge test: no longer recommended because it can be falsely negative. Consists of giving an IM dose of deferoxamine, and watching for the appearance of vin rose-colored urine. A positive test suggests a significantly elevated serum iron level.

• Support airway, breathing, and circulation.
• Isotonic fluid rehydration for dehydration
• Ipecac: emetigenic agent; use is controversial. It is difficult to differentiate induced emesis from emesis as a result of iron toxicity.
• Gastric lavage: should be performed in patients following intentional ingestions, if AXR shows retained iron in the GI tract, or if the amount of iron ingested is greater than 20 mg/kg.
• Whole bowel irrigation: Most often, polyethylene glycol is used to flush iron out of the GI tract. This is rarely used, because no controlled studies have been done.
• Charcoal: ineffective, because it does not bind iron
• Deferoxamine: a specific ferric iron chelator. When it binds to iron, it forms ferrioxamine. This compound is excreted by the kidneys, and may turn the patient’s urine a vin-rose color (red/orange). The dosage is usually 15 mg/kg/hr. It should be used in the following situations:
  • Symptomatic patients with more than transient, minor symptoms
  • Presence of severe symptoms: lethargy, intense abdominal pain, hypovolemia, or acidosis
  • Positive AXR
  • Serum iron level greater than 500 µg/dL

• Serum iron levels should be repeated until the level is normal.
• Any patient with positive AXR should have films repeated until all radiopacities have disappeared.

• Education about the serious nature of iron ingestions to prevent recurrence
• Counsel families on the presence of iron in vitamins (especially prenatal vitamins), and encourage their safe storage.
• Always educate parents of young children and adolescents to keep all medications in a locked, elevated cabinet.

• Relying solely on laboratory values to determine the need for therapy. Clinical symptoms alone necessitate treatment.
• Missing the diagnosis in a patient in stage 2 of iron ingestion
• Using the deferoxamine challenge test to determine if chelation therapy is indicated
• Giving prochlorperazine (Compazine) with deferoxamine. For unknown reasons, this combination of medications can lead to coma.

Q: When should deferoxamine infusion be stopped?
A: Most patients will need less than 24 hours of deferoxamine. The infusion should continue until the patient has no more signs or symptoms of iron toxicity, a repeat AXR is negative (if the initial study was positive), and the urine returns to a normal color (if the patient developed vin rose-colored urine with treatment). Ideally, a serum iron level should be normal, but this may be difficult to measure in the presence of deferoxamine.

Q: Are there any major side effects of deferoxamine therapy?
A: At rapid infusion rates (>15 mg/kg/hr), hypotension has been seen. Some studies have reported the development of ARDS with prolonged infusions. Other rarer complications include Yersinia sepsis, ocular toxicity, ototoxicity, and acute renal failure.

Q: Can deferoxamine be given in the face of renal failure?
A: Yes. Deferoxamine offers protective effects that are independent of the renal elimination of ferrioxamine. However, the doses of deferoxamine should be adjusted accordingly.

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Howland M. Risks of parenteral deferoxamine for acute iron poisoning. Clin Toxicol 1996;34(5):491–497.

McGuigan M. Acute iron poisoning. Pediatr Ann 1996;25(1):33–38.

Mills K, Curry S. Acute iron poisoning. Emerg Med Clin North Am 1994;12(2):397–413.

Tenenbein M. Benefits of parenteral deferoxamine for acute iron poisoning. Clin Toxicol 1996;34(5):485–489.