eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Toxicology

Toxicity, Iron

Jennifer S Boyle, MD, PharmD, Fellow in Toxicology, University of Virginia Health System
David T Lawrence, DO, Assistant Professor, Department of Emergency Medicine, Division of Medical Toxicology, University of Virginia School of Medicine; Christopher P Holstege, MD, Associate Professor of Emergency Medicine and Pediatrics, University of Virginia; Director, Division of Medical Toxicology, Center of Clinical Toxicology; Medical Director, Blue Ridge Poison Ctr, Associate Medical Toxicology Fellowship Director, VA Dept of Health; Kathryn Clark Emery, MD, Associate Professor, Department of Pediatrics, University of Colorado Health Sciences Center; Consulting Staff, Department of Emergency Medicine, Children's Hospital of Denver

Updated: Jun 24, 2009

Introduction

Background

Iron poisoning is a common toxicologic emergency in young children. Contributing factors include the availability of iron tablets and their candylike appearance. Ferrous sulfate tablets (20% elemental iron) are routinely administered to postpartum women, many of whom have toddlers in the family. The potential severity of iron poisoning is based on the amount of elemental iron ingested. The amount of elemental iron ingested must be calculated based on the number of tablets ingested and the percentage of elemental iron in the salt.

Children may show signs of toxicity with ingestions of 10-20 mg/kg of elemental iron. Serious toxicity is likely with ingestions of more than 60 mg/kg. Iron exerts both local and systemic effects and is corrosive to the GI mucosa and can affect the heart, lungs, and liver. Excess free iron is a mitochondrial toxin that leads to derangements in energy metabolism. Although iron poisoning is a clinical diagnosis, serum iron levels are useful in predicting the clinical course of the patient. In treatment of iron poisoning, consider both bowel decontamination with whole bowel irrigation and chelation using intravenous administration of deferoxamine.

Pathophysiology

The absorption of iron is normally very tightly controlled by the GI system. However, in overdose, local damage to the GI mucosa allows unregulated absorption, which leads to potentially toxic serum levels.

Much of the pathophysiology of iron poisoning is a result of metabolic acidosis and its effect on multiple organ systems. Toxicity manifests as local and systemic effects. Typically, iron poisoning is described in 5 sequential phases. No consensus has been reached regarding the number of phases and the times assigned to those phases. Patients may not always demonstrate all of the phases.

Phase 1

Phase 1, initial toxicity, predominantly manifests as GI effects. This phase begins during the first 6 hours postingestion and is associated with hemorrhagic vomiting, diarrhea, and abdominal pain. This is predominantly due to direct local corrosive effects of iron on the gastric and intestinal mucosa. Early hypovolemia may result from GI bleeding, diarrhea, and third spacing due to inflammation. This can contribute to tissue hypoperfusion and metabolic acidosis.

Convulsions, shock, and coma may complicate this phase if the circulatory blood volume is sufficiently compromised. In these cases, the patient progresses directly to phase 3, possibly within several hours.

Phase 2

Phase 2 is known as the latent phase and typically occurs 4-12 hours postingestion. It is usually associated with an improvement in symptoms, especially when supportive care is provided during phase 1. During this time, iron is absorbed by various tissues, and systemic acidosis increases. Clinically, the patient may appear to improve, especially to nonmedical personnel, because the vomiting that occurs in phase 1 subsides. However, laboratory analysis demonstrates progressive metabolic acidosis and, potentially, the beginning of other end-organ dysfunction (ie, elevation of transaminase levels).

Phase 3

Phase 3 typically begins within 12-24 hours postingestion, although it may occur within a few hours following a massive ingestion. Following absorption, ferrous iron is converted to ferric iron, and an unbuffered hydrogen ion is liberated. Iron is concentrated intracellularly in mitochondria and disrupts oxidative phosphorylation, resulting in free radical formation and lipid peroxidation. This exacerbates metabolic acidosis and contributes to cell death and tissue injury at the organ level.

Phase 3 consists of marked systemic toxicity caused by this mitochondrial damage and hepatocellular injury. GI fluid losses lead to hypovolemic shock and acidosis. Cardiovascular symptoms include decreased heart rate, decreased myocardial activity, decreased cardiac output, and increased pulmonary vascular resistance. The decrease in cardiac output may be related to a decrease in myocardial contractility exacerbated by the acidosis and hypovolemia. Free radicals from the iron absorption may induce damage and play a role in the impaired cardiac function.

The systemic iron poisoning in phase 3 is associated with a positive anion gap metabolic acidosis. The following explanations for the acidosis have been proposed:

• Conversion of free plasma iron to ferric hydroxide is accompanied by a rise in hydrogen ion concentration.
• Free radical damage to mitochondrial membranes prevents normal cellular respiration and electron transport, with the subsequent development of lactic acidosis.
• Hypovolemia and hypoperfusion contribute to acidosis.
• Cardiogenic shock contributes to hypoperfusion.

A coagulopathy is observed and may be due to 2 different mechanisms. Free iron may exhibit a direct inhibitory effect on the formation of thrombin and thrombin's effect on fibrinogen in vitro. This may result in a coagulopathy. Later, reduced levels of clotting factors may be secondary to hepatic failure.

Phase 4

Phase 4 may occur 2-3 days postingestion. Iron is absorbed by Kupffer cells and hepatocytes, exceeding the storage capacity of ferritin and causing oxidative damage. Pathologic changes include cloudy swelling, periportal hepatic necrosis, and elevated transaminase levels. This may result in hepatic failure.

Phase 5

Phase 5 occurs 2-6 weeks postingestion and is characterized by late scarring of the GI tract, which causes pyloric obstruction or hepatic cirrhosis.

The oxidative potential of iron was first proposed by Fenton in 1894. The importance of reduced oxygen species in biological reactions became apparent with the discovery of superoxide dismutase by McCord and Fridovich in 1969. The potential role of metal ion catalysis was reported the following year. Subsequently, a plethora of evidence has accumulated linking chronic excess body iron to cardiovascular disease, carcinogenesis, aging, stroke, Alzheimer disease, and Parkinson disease. The organ damage that occurs in the hereditary iron overloading disorders is well documented and can be averted and improved by decreasing the excess iron. Acute iron overload likewise produces tissue and organ damage due to the presence of free ionic iron.

Frequency

United States

In 2007, 49,440 vitamin preparation exposures (some of which contain iron) in children younger than 5 years were reported to the American Association of Poison Control Centers (AAPCC).¹ In 2007, no pediatric deaths due to iron poisoning were reported. This reflects the trend that iron-related fatalities are becoming less common.

Mortality/Morbidity

Most exposures result in minimal toxicity. However, concentrated iron supplement overdoses can result in serious sequelae and death.

Age

Most exposures involve children younger than 6 years who have ingested pediatric multivitamin preparations. Many of the serious acute ingestions follow the pattern of ingestions in general and occur in children younger than 3 years.

Clinical

History

Most pediatric poisonings are unintentional. Specifically, in relation to iron toxicity, children may ingest the iron administered to mothers as prenatal vitamins or as postpartum supplements. Other iron exposures include ingestion of iron-fortified children's vitamins, although these tend to be less toxic. A recent study examined the effects of iron supplements in breastfed infants.² Parents may not immediately be aware of the ingestion or the specific amount of the iron tablets ingested.

• If possible, determining the number of pills ingested, how much iron was in each pill, and the formulation of iron in the supplement is important.
• Different formulations of iron contain varying amounts of elemental iron, as follows:
  • Ferrous sulfate - 20% elemental iron
  • Ferrous gluconate- 12% elemental iron
  • Ferrous fumarate - 33% elemental iron
  • Ferrous lactate - 19% elemental iron
  • Ferrous chloride - 28% elemental iron
• The following is a formula used to calculate the amount of ingested iron for a 10-kg child who consumed ten 320-mg tablets of ferrous gluconate (12% elemental iron per tablet):

  10 tablets X 38.4 mg elemental iron per tablet = 384 mg/10 kg = 38.4 mg/kg

• Carbonyl iron and iron polysaccharide complex are nonionic forms of iron that have less toxicity than ferrous salts.
• Attempt to determine the time of ingestion. This is important in determining observation periods and timing of serum levels.

Physical

As stated in Pathophysiology, iron toxicity is typically described in 5 sequential phases. Universal agreement does not exist as to the number of phases or the times assigned to those phases. Patients may not always demonstrate each of the phases.

Few, if any, physical examination findings are specific to iron toxicity.

• Phase 1 usually occurs within the first 6 hours postingestion. This phase is associated with hemorrhagic vomiting, diarrhea, and abdominal pain due to mucosal injury. The hemorrhagic GI symptoms are due to the direct effects of iron on the GI mucosa. A patient is unlikely to develop significant systemic toxicity without first having GI symptoms. In severe cases, the GI losses of blood and fluid may be massive and lead to shock and coma.
• Phase 2 usually occurs 6-12 hours postingestion and may be associated with an improvement in symptoms, especially when supportive care has been provided during phase 1. This period of apparent recovery may be confusing. In mild cases, this recovery may represent true recovery. However, in serious ingestions, it may represent only a temporary respite or may not occur at all; the patient may progress directly to phase 3. The etiology of phase 2 is unclear, but it may represent the time it takes for iron to distribute throughout the body and for systemic injury to occur. The only findings on examination may be lethargy, mild tachycardia, or tachypnea.
• Phase 3 begins after 12-24 hours postingestion and consists of multisystem damage. This may include marked metabolic acidosis, coagulopathy, shock, seizures, and altered mental status due to mitochondrial damage and hepatocellular injury.
• Phase 4 occurs 2-3 days postingestion and is characterized by hepatic injury.
• Phase 5 occurs 2-6 weeks postingestion and is characterized by late scarring of the GI tract, which causes pyloric obstruction or hepatic cirrhosis. However, these complications are rare, even in severe cases.

Causes

• As with any ingestion, the risk of ingestion increases as the availability of the medication increases.
• Childproof containers for multivitamins and prenatal vitamins may be of some assistance in decreasing exposure. In addition, some consideration has been given to changing the appearance of prenatal vitamins to make them look less like candy.
• One study found an association between iron poisoning in young children and recent birth of a sibling.³

Differential Diagnoses

Acidosis, Metabolic

Other Problems to Be Considered

Gastroenteritis
Food poisoning
Hepatic failure

Workup

Laboratory Studies

• Iron toxicity is a clinical diagnosis and any studies are simply adjuncts.
• Toxic effects of iron may occur at doses of 10-20 mg/kg of elemental iron.
• Little is known about the absorption rate of iron in an overdose, the timing of peak serum iron levels, or the rate at which serum levels fall from their peak levels. Serum iron levels generally correlate with clinical severity and are as follows:
  • Mild - Less than 300 µg/dL
  • Moderate - 300-500 µg/dL
  • Severe - More than 500 µg/dL
• Difficulties involved with interpretation of serum iron levels include the following:
  • The ideal serum iron level is a peak level at 2-6 hours postingestion, and the time from ingestion is often unknown.
  • Deferoxamine interferes with standard assays and leads to falsely decreased iron levels.
  • Serum iron levels may not be available in a timely fashion. Serum levels obtained more than 8-12 hours postingestion may not be useful because iron redistributes into the tissues and the serum level does not reflect the total body burden of iron.
• Total iron-binding capacity (TIBC) has traditionally been used to determine toxicity. Previously, a patient with a serum iron level greater than the TIBC was thought to be at risk for developing systemic toxicity. However, determining the TIBC in the presence of large amounts of iron or deferoxamine may yield a falsely elevated number. Hence, a TIBC above the iron level does not indicate sufficient binding capacity, and this test is not useful in determining the likelihood of toxicity.
• Because iron levels are not always readily available, the predictive value of other laboratory test results has been explored. Previously, a WBC count greater than 15,000/µL and a serum glucose level greater than 150 mg/dL were said to correlate with iron levels greater than 300 µg/dL. However, more recent studies do not support the predictive value of these ancillary tests, and they are not useful in the setting of iron poisoning.

Imaging Studies

• Abdominal radiography may offer information on the iron ingestion, both initially and subsequently. Do not delay treatment for radiography.
• A positive radiographic finding is one that shows radiopaque tablets or particles. This indicates that the ingested iron has not been completely absorbed. Obtaining a radiograph pre–GI decontamination and post–GI decontamination may yield information as to the success of therapy. If the radiographic findings remain positive after decontamination, additional decontamination is required.
• An initial negative radiographic finding may mean that no iron was ingested or that the ingested iron tablets or solution have dissolved. In addition, liquid preparation and chewable vitamins are not visible on radiographs.
• If the radiographic findings were initially positive and are negative after GI decontamination, this indicates that GI decontamination was successful, although iron levels should still be monitored because of iron absorption prior to initiation of therapy.

Other Tests

• The deferoxamine challenge test consists of administering a single dose of deferoxamine that binds available free iron and is excreted in the urine as the ferrioxamine complex (deferoxamine and iron).
• This complex changes the urine to a reddish (vin rosé) color, indicating the need for chelation. However, the urine does not change color reliably, even when elevated serum iron levels are present.
• This test is not reliable and does not alleviate the need for monitoring serum iron levels. Therefore, one should not rely on the  deferoxamine challenge test.

Treatment

Medical Care

The first step in treating a case of acute iron toxicity is to provide appropriate supportive care, with particular attention paid to fluid balance and cardiovascular stabilization. Initial treatment should also address the issue of preventing further absorption of iron by the GI tract.

• Ipecac-induced emesis is not recommended. This is especially true in iron ingestion. GI distress is an early finding in iron poisoning and is present in all potentially serious ingestions. Ipecac-induced vomiting may cloud the clinical picture.
• Gastric lavage is not recommended because iron tablets are relatively large and become sticky in gastric fluid, making lavage unlikely to be of benefit.
• Whole bowel irrigation has been used to speed the passage of undissolved iron tablets through the GI tract. A polyethylene glycol electrolyte solution (eg, GoLYTELY) may be administered orally or nasogastrically at a rate of 250-500 mL/h for toddlers and preschoolers and 2 L/h for adolescents. Continue irrigation until the repeat radiographic findings are negative or rectal effluent is clear.
• Deferoxamine is the iron-chelating agent of choice. Deferoxamine binds absorbed iron, and the iron-deferoxamine complex is excreted in the urine. Deferoxamine does not bind iron in hemoglobin, myoglobin, or other iron-carrying proteins. Base the indications for using deferoxamine on both clinical and laboratory parameters. Indications for treatment include shock, altered mental status, persistent GI symptoms, metabolic acidosis, pills visible on radiographs, serum iron level greater than 500 µg/dL, or estimated dose greater than 60 mg/kg of elemental iron. Initiate chelation if a serum iron level is not available and symptoms are present.
  • The administration of deferoxamine may be intramuscular or intravenous. The intramuscular route is not recommended because it is painful and less iron is excreted compared with the intravenous route. The intravenous route is administered as a continuous infusion. The standard dose is 15 mg/kg/h, with an initial dose administered for 6 hours.
  • No clear end point of therapy is noted; however, indications for cessation include significant resolution of shock and acidosis. Deferoxamine, administered 6-12 hours, has been suggested for moderate toxicity. For severe toxicity, administer deferoxamine for 24 hours. Because these end points are arbitrary, observe the patient for the recurrence of toxicity 2-3 hours after the deferoxamine has been stopped.
  • Adverse effects from deferoxamine are unusual. Pulmonary toxicity (ie, acute respiratory distress syndrome [ARDS], tachypnea) has been described, especially if patients are treated with deferoxamine for more than 24 hours. Rate-related hypotension can occur. Therefore, monitor the patient while titrating the infusion rate upward to a final rate of 15 mg/kg/h.

Surgical Care

• If retained iron tablets are evident after GI decontamination, consider endoscopy or surgery for their removal.
• Failure to remove the iron can result not only in continued iron absorption and exacerbation of systemic symptoms but also in gastric perforation and severe hemorrhage.

Consultations

• Regional poison control centers may be contacted for assistance in patient management.
• In addition, consult an intensivist for help in managing the moderately to severely ill child.

Medication

Chelation agents

Deferoxamine is a specific iron chelator. In the presence of ferric iron, deferoxamine forms the complex ferrioxamine, which is excreted by the kidneys. This complex imparts a reddish, vin rosé, color to the urine. Deferoxamine does not bind iron that is present in hemoglobin, hemosiderin, or ferritin. Deferoxamine is a parenteral iron chelator. It is administered IV or IM in the management of acute iron toxicity.

Deferoxamine mesylate (Desferal)

Freely soluble in water. Approximately 8 mg of iron is bound by 100 mg of deferoxamine. Most effective when continuously provided to the circulation by infusion. May be administered either by IM injection or by slow IV infusion. Does not effectively chelate other trace metals of nutritional importance. Provided in vials containing 500 mg or 2 g of lyophilized sterile drug. Add 2 mL or 8 mL of sterile water for injection to each vial, bringing the concentration to 250 mg/mL. For IV use, this may be diluted in 0.9% sterile saline, 5% dextrose solution, or Ringer solution.

Dosing

Adult

1000 mg may be administered IV at a rate not to exceed 15 mg/kg/h; follow with a dose of 500 mg q4h for 2 doses; administer additional IV infusion slowly over 24 h; not to exceed 6 g/24 h
Alternatively, 1000 mg IM, followed by 500 mg 4 and 8 h later; depending on response, 500 mg may be administered q4-12h IM; not to exceed 6 g/24 h; IV route preferred

Pediatric

IV route preferred: 15 mg/kg/h IV; not to exceed 6 g/24 h

Interactions

Concurrent treatment with prochlorperazine, a phenothiazine derivative, may lead to temporary impairment of consciousness

Contraindications

Documented hypersensitivity; patients who do not have acute iron poisoning; severe renal disease and anuria (dose reduction after the loading dose should be considered in these circumstances)

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Acute lung injury has recently been described (these patients received deferoxamine [15 mg/kg] for >24 h), and recent recommendations include higher doses of deferoxamine during the first 24 h and subsequently decreasing the dose of deferoxamine; tachycardia, hypotension, and shock may occur in patients receiving long-term therapy and could add to the cardiovascular collapse due to iron toxicity; GI adverse effects include abdominal discomfort, nausea, vomiting, and diarrhea, which may add to the symptoms of acute iron toxicity; flushing and fever are reported

Deferasirox (Exjade)

Tab for PO susp. PO iron chelation agent demonstrated to reduce liver iron concentration in adults and children who receive repeated RBC transfusions. Binds iron with high affinity in a 2:1 ratio. Approved to treat chronic iron overload due to multiple blood transfusions. Treatment initiation recommended upon evidence of chronic iron overload (ie, transfusion of about 100 mL/kg packed RBCs [about 20 U for 40-kg person] and serum ferritin level consistently >1000 µg/L).

Dosing

Adult

Initial: 20 mg/kg PO qd on empty stomach 30 min ac
Maintenance: Adjust dose by 5-10 mg/kg/d increments q3-6mo according to serum ferritin level trends; not to exceed 30 mg/kg/d
Note: Dissolve tab completely in water, orange juice, or apple juice, then immediately drink susp; resuspend any remaining residue in small volume of liquid and swallow

Pediatric

<2 years: Not established
>2 years: Administer as in adults

Interactions

Data limited; do not take with aluminum-containing antacids

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Common adverse effects include diarrhea, nausea, abdominal pain, headache, pyrexia, cough, and rash; may increase serum creatinine and hepatic enzyme levels; decrease dose upon persistent elevation of serum creatinine level; may cause auditory and visual disturbances; slight decreases in serum copper and zinc levels may occur; dissolve tab completely in water, orange juice, or apple juice and drink resulting susp immediately (do not swallow tab whole, do not chew or crush); measure serum ferritin levels monthly and adjust dose q3-6mo based on serum ferritin trends

Whole bowel irrigation agents

Polyethylene glycol is used to increase GI transit time, decreasing absorption. It is not absorbed and is excreted entirely through the GI tract.

Polyethylene glycol (GoLYTELY, NuLytely, Colovage, Colyte)

Laxative with strong electrolyte and osmotic effects that has cathartic actions in GI tract.

Dosing

Adult

2 L/h NG

Pediatric

Toddlers, preschoolers, children: 250-500 mL/h PO/NG
Adolescents: Administer as in adults

Interactions

Reduces effectiveness and absorption of oral medications

Contraindications

Documented hypersensitivity; colitis; megacolon; bowel perforation; gastric retention; GI obstruction

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in ulcerative colitis and hot loop polypectomy

Follow-up

Further Inpatient Care

• Patients with acute iron poisoning have developed Yersinia enterocolitica infection or sepsis as a complication of their clinical course.
• Yersinia requires iron as a growth factor. Deferoxamine acts to solubilize iron and aid in intracellular entry for Yersinia.
• Suspect Yersinia infection in patients who develop abdominal pain, fever, and diarrhea following resolution of iron toxicity.

Further Outpatient Care

• Address safeguarding of medications with parents.
• Guidelines for out-of-hospital management have been established.⁴

Transfer

• Treat patients who present with signs and symptoms of significant iron poisoning, such as metabolic acidosis, potential hemodynamic instability, and/or lethargy, in a pediatric ICU.

Deterrence/Prevention

• Many ingestions are accidental. As for any medication, preventive measures include keeping the bottles of iron supplements, with childproof tops, inaccessible to children. Changing the appearance of prenatal vitamins to make them look less like candy has been considered. This would be ideal.
• In 1997, the US Food and Drug Administration (FDA) issued a regulation requiring unit-dose packaging for iron-containing products with 30 mg or more of iron per dosage unit. Because of the time and effort to open unit-dose packages, the FDA believes this packaging limits unintentional access to children. This requirement is in addition to existing Consumer Product Safety Commission regulations that require child-resistant packaging for most iron-containing products. In 2003, this requirement was rescinded because of a lawsuit in which the National Health Alliance charged that the FDA had no jurisdiction over the packaging of dietary supplements.

Complications

• Infectious -Yersinia enterocolitica septicemia
• Pulmonary - Acute respiratory distress syndrome (ARDS)
• Gastrointestinal - Fulminant hepatic failure, hepatic cirrhosis, pyloric or duodenal stenosis

Prognosis

• If a patient does not develop symptoms of iron toxicity within 6 hours of ingestion, iron toxicity is unlikely to develop. Expect clinical toxicity following an ingestion of 20 mg/kg of elemental iron. Expect systemic toxicity with an ingestion of 60 mg/kg. Ingestion of more than 250 mg/kg of elemental iron is potentially lethal.

Patient Education

• Educate parents about the need for childproofing the home and keeping medications out of reach of children.
• For excellent patient education resources, visit eMedicine's Poisoning - First Aid and Emergency Center. Also, see eMedicine's patient education articles Iron Poisoning and Poison Proofing Your Home.

Miscellaneous

Medicolegal Pitfalls

• Do not be falsely reassured by a patient's clinical improvement. This may not represent recovery. Many patients experience a quiescent phase before progressing to profound iron toxicity.
• Do not wait for a confirmatory iron level before initiating treatment in a patient who shows signs of severe toxicity. Also, do not be falsely reassured by a level that is drawn later in the course of toxicity. Treat the patient according to their clinical situation and not according to the serum iron level.
• Be sure to include iron toxicity in the differential for unexplained metabolic acidosis, vomiting, diarrhea, and GI bleeding.

Multimedia

Media file 1: The oxidative potential of iron was first proposed by Fenton in 1894. The importance of reduced oxygen species in biological reactions became apparent with the discovery of superoxide dismutase by McCord and Fridovich in 1969. The potential role of metal ion catalysis was reported the following year. Subsequently, a plethora of evidence has accumulated linking chronic excess body iron to cardiovascular disease, carcinogenesis, aging, stroke, Alzheimer disease, and Parkinson disease. The organ damage that occurs in the hereditary iron overloading disorders is well documented and can be averted and improved by decreasing the excess iron. Acute iron overload likewise produces tissue and organ damage due to the presence of free ionic iron.

References

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4. [Guideline] Manoguerra AS, Erdman AR, Booze LL, et al. Iron ingestion: an evidence-based consensus guideline for out-of-hospital management. Clin Toxicol (Phila). 2005;43(6):553-70. [Medline].

5. Bryant SM, Leikin JB. Iron. Critical Care Toxicology. 2005;687-693.

6. Desferal (deferoxamine mesylate) [package insert]. East hanover, NJ: Novartis Pharmaceuticals Corporation; 2007. [Full Text].

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8. Engle JP, Polin KS, Stile IL. Acute iron intoxication: treatment controversies. Drug Intell Clin Pharm. Feb 1987;21(2):153-9. [Medline].

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11. Madiwale T, Liebelt E. Iron: not a benign therapeutic drug. Curr Opin Pediatr. Apr 2006;18(2):174-9. [Medline].

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15. Tenenbein M. Position statement: whole bowel irrigation. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol. 1997;35(7):753-62. [Medline].

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Keywords

iron toxicity, iron poisoning, ferrous sulfate tablets, ferrous sulfate, ferrous gluconate, ferrous fumarate, ferrous lactate, ferrous chloride, metabolic acidosis, hemorrhagic vomiting, diarrhea, abdominal pain, hepatic failure, pyloric obstruction, hepatic cirrhosis, multivitamin ingestion, treatment, diagnosis

Contributor Information and Disclosures

Author

Jennifer S Boyle, MD, PharmD, Fellow in Toxicology, University of Virginia Health System
Disclosure: Nothing to disclose.

Coauthor(s)

David T Lawrence, DO, Assistant Professor, Department of Emergency Medicine, Division of Medical Toxicology, University of Virginia School of Medicine
David T Lawrence, DO is a member of the following medical societies: American College of Emergency Physicians and American College of Medical Toxicology
Disclosure: Nothing to disclose.

Christopher P Holstege, MD, Associate Professor of Emergency Medicine and Pediatrics, University of Virginia; Director, Division of Medical Toxicology, Center of Clinical Toxicology; Medical Director, Blue Ridge Poison Ctr, Associate Medical Toxicology Fellowship Director, VA Dept of Health
Christopher P Holstege, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American Association for the Advancement of Science, American College of Emergency Physicians, American College of Medical Toxicology, American Medical Association, Medical Society of Virginia, Society for Academic Emergency Medicine, Society of Toxicology, and Wilderness Medical Society
Disclosure: Nothing to disclose.

Kathryn Clark Emery, MD, Associate Professor, Department of Pediatrics, University of Colorado Health Sciences Center; Consulting Staff, Department of Emergency Medicine, Children's Hospital of Denver
Kathryn Clark Emery, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Medical Editor

Halim Hennes, MD, MS, Pediatric Emergency Medicine Research Director, Professor, Departments of Pediatrics and Emergency Medicine, Medical College of Wisconsin
Halim Hennes, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Jeffrey R Tucker, MD, Assistant Professor, Department of Pediatrics, Division of Emergency Medicine, University of Connecticut and Connecticut Children's Medical Center
Jeffrey R Tucker, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Pediatrics, and Massachusetts Medical Society
Disclosure: Merck Salary Employment

CME Editor

Paul D Petry, DO, FACOP, FAAP, Consulting Staff, Freeman Pediatric Care, Freeman Health System
Paul D Petry, DO, FACOP, FAAP is a member of the following medical societies: American Academy of Osteopathy, American Academy of Pediatrics, American College of Osteopathic Pediatricians, and American Osteopathic Association
Disclosure: Nothing to disclose.

Chief Editor

Timothy E Corden, MD, Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin
Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, and Wisconsin Medical Society
Disclosure: Nothing to disclose.

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