The Poison Control Center

Iron Poisoning

Iron poisoning is a common accidental ingestion among children under 5. Iron is available as ferrous sulfate (20 percent elemental iron), ferrous fumarate (33 percent elemental iron) and ferrous gluconate (12 percent elemental iron) salts, as prenatal vitamins and in multivitamin preparations. Ingestions of less than 20 mg./kg. of elemental iron are considered non-toxic, ingestions of 20-60 mg./kg. produce mild to moderate toxicity, and ingestions of greater than 60 mg./kg. of elemental iron have the potential to produce serious toxicity.1

Acute iron poisoning produces gastrointestinal, cardiovascular, metabolic, hepatic, and central nervous system effects secondary to both the direct caustic effect of iron on the GI mucosa and to the presence of free unbound iron in the circulation.1 Symptoms seen as a result of iron's corrosive action on the GI mucosa range from abdominal pain, vomiting and diarrhea1 to intestinal necrosis, perforation and peritonitis.2 Free iron is a potent vasodilator and causes circulatory failure by a direct action on peripheral blood vessels.1 Gastrointestinal fluid and blood loss also contribute to hypovolemia. Iron enters cells and acts as a mitochondrial poison.1 The resultant metabolic acidosis is secondary to an increased anaerobic metabolism, lactic acidosis and shock. Acute hepatic failure is rare and generally occurs three to four days after a severe iron ingestion. The central nervous system effects can range from mild obtundation to coma.

Table 1: The four phases of iron poisoning
Phase I: 0 - 6 hours since ingestion
nausea, vomiting, diarrhea, abdominal pain, melena, hemetemesis, lethargy, pallor, tachycardia, hyperglycemia, leukotocytosis (presence of coma, shock and hypotension in Phase I is considered a poor prognostic sign)
Phase II: 6 - 12 hours since ingestion
intermittent lethargy
Phase III: 12 - 48 hours since ingestion
hemetemesis, melena, lethargy, coma, cyanosis, pulmonary edema, vasomotor collapse, metabolic acidosis, liver damage, coagulation defects
Phase IV: 4 - 6 weeks since ingestion
gastric scarring, pyloric stricture

Ingestions of less than 20 mg./kg. of elemental iron can be treated with observation alone while ingestions between 20-40 mg./kg. of elemental iron require Syrup of Ipecac but generally do not require a physician visit or a serum iron determination. Gastric emptying via emesis or lavage should be performed in patients who have ingested greater than 40-60 mg./kg. of elemental iron or an unknown amount.1 Activated charcoal is not useful, unless there are co-ingestants, since it does not bind metals such as iron.1 Iron tablets are radiopaque, therefore, an abdominal radiograph should be performed to determine if there is evidence of iron tablets in the stomach or small bowel. If there is evidence of iron tablets in the stomach, lavage with a 1-5 percent sodium bicarbonate solution may be instituted as it theoretically results in the formation of the less absorbable ferrous carbonate; however, clinical benefits are questionable.

It is important to remember that multivitamins with iron contain a smaller quantity of elemental iron and are therefore, less radiopaque than preparations such as ferrous sulfate and that partially dissolved tablets will not be as radiopaque as undissolved tablets. Whole bowel irrigation may be considered in a patient who has radiographic evidence of persistent iron tablets in the abdomen after initial gastrointestinal decontamination, especially if the patient has a continually rising serum iron level. The use of deferoxamine in the lavage solution is controversial.

Since iron is rapidly cleared from the plasma and taken up by hepatocytes, a serum iron (SI) level and total iron binding capacity (TIBC) determination should be drawn two to four hours after ingestion.3 Serum iron levels drawn after six hours may be misleadingly low. Other pertinent laboratory parameters to monitor are serum glucose and leukocyte count. Lacouture et al. found that a leukocyte count greater than 15,000/mm3 and a serum glucose greater than 150 mg./dl. are predictive of a serum iron concentration greater than 300 mcg./dl.4

Deferoxamine, which is the specific chelator for iron, should be instituted in patients whose SI is greater than their TIBC or in the symptomatic patient whose SI is greater than 350 mcg./dl.1 Deferoxamine binds free iron in the serum and forms ferrioxamine, a water soluble, renally excreted compound which, if present, turns the urine a characteristic reddish-orange or "vin rose" color. Treatment is given preferentially by the intravenous route in a dose of 15mg./kg./hour but may also be given intramuscularly at a dose of 40mg./kg. every four to eight hours. A deferoxamine challenge test can be given at a dose of 50 mg./kg. IM up to a maximum of 1 gm. in children and 2 gm. in adults.5 The maximum daily dose is 360 mg./kg. up to a maximum of 6 gm.1 Too rapid administration of intravenous deferoxamine has led to hypotension.1 It is important to monitor blood pressure frequently during intravenous infusions of deferoxamine and to maintain adequate urine output to help enhance the clearance of the ferrioxamine complex.1 Deferoxamine therapy should be continued until the urine loses its vin-rose color or the SI falls below 100 mcg./dl.1 When evaluating the risks versus the benefits of treating a pregnant patient with deferoxamine it should be noted that animal studies have shown no passage of deferoxamine across the placenta.6


  1. Henretig FM, Temple AR. Acute iron poisoning in children. Emerg Med Clin North Am 1984;2(1):121-32.
  2. Knott LH, Miller RC. Acute iron intoxication with intestinal infarction. J Pediatr Surg 1978 Dec;13(6D):720-1.
  3. Proudfoot AT, Simpson D, Dyson EH. Management of acute iron poisoning. Med Toxicol 1986 Mar-Apr;1(2):83-100.
  4. Lacouture PG, Wason S, Temple AR, Wallace DK, Lovejoy FH Jr. Emergency assessment of severity of iron overdose by clinical and laboratory methods. J Pediatr 1981 Jul;99(1):89-91.
  5. Goldfrank LR, Kulberg AG, Kirstein RM. Iron. In Goldfrank's Toxicologic Emergencies, 3rd ed. Norwalk, Appleton-Century-Crofts, 1982.
  6. Curry S, Bond R, Raschke R, et al. Fetal iron kinetics in a model of maternal iron poisoning with and without maternal deferoxamine therapy. Vet Hum Tox 1988;30:372 (abstract).
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