Acute Iron Poisoning

  • occurs mostly in infants and children: 10- 20 iron tablets or equivalent of the liquid preparation (> 60 mg/kg iron) may cause serious toxicity
  • very rare in adults.
  • The pathological lesion à hemorrhage and inflammation in the gut which may progress to necrotizing enteritis, hepatic necrosis and brain damage.

Ferric iron is toxic to a number of cellular processes. The primary mechanism for iron-induced tissue damage is free radical production and lipid peroxidation. Toxic effects on cells include the following:

  • ●Mucosal cell necrosis
  • ●Impairment of capillary permeability
  • ●Alteration of the lipid membrane of mitochondria
  • ●Inhibition of enzymatic processes in the Krebs cycle
  • ●Uncoupling of oxidative phosphorylation
  • ●Direct vasodilation
  • ●Inhibition of serum proteases (eg, thrombin)
What form of iron was ingested?
Ferrous gluconate (12 percent elemental iron)
Ferrous sulfate (20 percent elemental iron)
Ferrous fumarate (33 percent elemental iron)
How many mg/kg of elemental iron was ingested?
When did the ingestion occur?
Clinical features: Overlapping phases of clinical manifestations
Gastrointestinal phase: (30 minutes to 6 hours) Abdominal pain, vomiting, diarrhea, hematemesis, melena, lethargy, shock (from capillary leak and third spacing), metabolic acidosis
Latent: (6 to 24 hours) Improvement in GI symptoms; may have poor perfusion, tachypnea, tachycardia
Shock and metabolic acidosis: (4 hours to 4 days) Hypovolemic, distributive, or cardiogenic shock with profound metabolic acidosis, coagulopathy, renal insufficiency/failure, pulmonary dysfunction/failure, central nervous system dysfunction
Hepatotoxicity: (within 2 days) Coma, coagulopathy, jaundice. Severity is dose dependent.
Bowel obstruction: (2 to 4 weeks) Vomiting, dehydration, abdominal pain, usually gastric outlet obstruction
Diagnostic evaluation: For all patients with systemic symptoms, those who have ingested >40 mg/kg of elemental iron, and those for whom the amount of elemental iron ingested is unknown
Serum iron concentration: Measure serum iron concentration within 4 to 6 hours after ingestion (8 hours for extended release tablets)
Arterial or venous pH
Abdominal radiograph looking for radiopaque pills
Other initial labs: Electrolytes, BUN, creatinine, glucose, liver enzyme tests, total bilirubin, prothrombin, partial thromboplastin time, CBC with differential, type and cross match
Secure airway and breathing
Treat volume depletion aggressively with isotonic infusion
Whole bowel irrigation: For all patients with a significant number of pills in stomach and small intestine on radiograph
Deferoxamine: Continuous IV infusion (can cause hypotension). Begin at 15 mg/kg/hour. May increase to 35/mg/kg/hour during first 24 hours for severe ingestions. A toxicologist and/or regional poison control center should be consulted to determine the optimum dose of deferoxamine and duration of therapy. Treat in the following circumstances:
Severe symptoms: Altered mental status, hemodynamic instability, persistent vomiting, diarrhea
Anion gap metabolic acidosis
Serum iron concentration >500 mcg/dL
Significant number of pills on x-ray

Toxic dose — The toxicity of iron depends upon the amount of elemental iron ingested. Various salt forms contain different percentages of elemental iron

●Ferrous gluconate (12 percent elemental iron)

●Ferrous sulfate (20 percent elemental iron)

●Ferrous fumarate (33 percent elemental iron)

Ingestions of more than 60 mg/kg can be associated with serious toxicity


The management of patients who have ingested toxic amounts of iron begins with aggressive supportive care. Decontamination with whole bowel irrigation may be helpful. Treatment with deferoxamine to increase iron excretion is indicated for patients with severe toxicity.

To prevent further absorption of iron from gut

(a) Induce vomiting or perform gastric lavage with sodium bicarbonate solution- to render iron insoluble.

(b) Activated charcoal does not adsorb iron.

Other forms of GI decontamination are NOT indicated for patients with iron overdose:

●Syrup of ipecac should not be prescribed.

Gastric lavage with bicarbonate or phosphate solutions is no longer recommended because of the large volume of bicarbonate necessary to achieve effect and reports of phosphate poisoning

whole bowel irrigation should be initiated for all patients with a significant number of pills in the gastrointestinal tract visualized by abdominal radiograph.

●Gastric lavage with deferoxamine is not recommended because of the large volumes required in an overdose to have any appreciable effect.

●Activated charcoal binds iron poorly and is not useful for the management of iron ingestions.

To bind and remove iron already absorbed

Deferoxamine —

  • administered intravenously,
  • antidote of choice for serious iron overdose.
  • chelating agent that, in acute iron intoxication, binds with ferric iron (Fe3+) in the blood to form water-soluble ferrioxamine that is then excreted by the kidneys.
  • Ferrioxamine gives urine the classically described “vin rosé” color, which actually is orange to reddish brown.
  • DFO must be administered early in the treatment of iron overdose because iron moves rapidly from the circulation into cells, where, in acute intoxication, it is not readily accessible for chelation.

Indications for deferoxamine include any of the following:

●Severe symptoms (hypovolemia/shock, lethargy/coma, persistent vomiting or diarrhea)

●Elevated anion gap metabolic acidosis

●Peak serum iron concentration greater than 500 mcg/dL (90 micromol/L)

●Significant number of pills on abdominal radiograph

Dose and duration of treatment —

  • intravenously at a continuous rate of 15 mg/kg per hour IV, which may be increased to a maximum of 35 mg/kg per hour, based on the severity of clinical symptoms
  • Recommendations for duration of deferoxamine therapy have used resolution of clinical symptoms such as metabolic acidosis and shock as the endpoint for stopping therapy
  • [The typical duration of therapy is about 24 hours.

Adverse effects — Significant adverse effects of intravenous deferoxamine therapy include hypotension and the development of acute respiratory distress syndrome (ARDS):


  • DTPA or calcium edetate à used if desferrioxamine is not available .
  • BAL is contra indicated because its iron chelate is also toxic.
  • Supportive measures Fluid and electrolyte balance should be maintained and
  • acidosis corrected by appropriate i.v. infusion.
  • Respiration and BP may need support.
  • Diazepam i.v. may be cautiously used to control convulsions, if occur.
  • Volume resuscitation to maintain euvolemia is essential. Hypovolemic shock is the major cause of mortality during the first phase of iron intoxication. Patients who present with severe gastrointestinal (GI) phase symptoms require urgent intensive management to maintain effective circulating blood volume
  • Intravenous access should be obtained. Normal saline should be administered in boluses of 20 cc/kg as necessary to improve perfusion, tachycardia and maintain blood pressure

Extracorporeal methods of iron removal (eg, hemodialysis) are limited in effectiveness because they only remove free circulating iron and must be started soon after ingestion before intracellular iron transport occurs.

Pregnancy —

  • Iron overdose during pregnancy is common,
  • but is unique among overdoses because the fetus is protected from the direct effects of iron.
  • Transplacental iron absorption is a saturable process.
  • Consequently, significant accumulation of fetal iron does not occur.
  • The fetus is at risk only when the mother experiences clinical decompensation, such as hypotension, liver failure, or pulmonary failure.
  • Pregnancy should not change the management of iron poisoning. Indications for deferoxamine therapy in pregnant patients are the same as those for other patients.

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