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Iron toxicity

ISSN 2398-2950


Introduction

  • Iron Iron is an essential mineral. When not protein bound in the body, it is highly reactive, induces free radicals and is damaging to tissues.
  • There are numerous forms of iron including:
    • Iron-containing supplements and multivitamins. Injectable iron therapy is also a potential source although this is rare in dogs and cats.
    • Some moss killers contain ferrous sulfate.
    • Some slug and snail killers contain ferric phosphate, generally 1% for domestic products and 3% for professional products. Iron (III) ethylenediaminetetraacetate is also used as a slug killer in some countries.
    • Oxygen absorbers or deoxidizer sachets used as preservatives in dried foods.
    • Iron-containing hand warmers and heat patches (for pain relief).
    • The remainder of this article will discuss toxicity from ingesting excessive amount of iron.
  • There are numerous forms of iron. The soluble forms are the most toxic. Insoluble forms, such as metallic iron or iron oxide (rust), are not considered toxic. Iron oxide and hydroxides (E172) are also used in some foods and medicines as a colorant.
  • Calculate the amount of elemental iron ingested to determine if the pet ingested a toxic amount of iron.
  • Mild to moderate iron toxicity can occur when 20-60 mg/kg of elemental iron is ingested. Severe toxicity can occur when over 60 mg/kg elemental iron is ingested. Over 100 mg/kg elemental iron is considered fatal without prompt treatment. Note these toxic doses are based on soluble, bioavailable forms of iron and will greatly overestimate the toxicity of insoluble poorly bioavailable iron compounds.

All cases of ingestion of iron tablets should be assessed urgently.

Presenting signs

  • Lethargy.
  • Vomiting Vomiting.
  • Diarrhea, sometimes hemorrhagic.
  • Vomitus and feces may have a metallic odor.

Acute presentation

  • Animals usually present with an acute onset of gastrointestinal signs. However, about 6 hours following ingestion, the gastrointestinal signs may abate and the cat may appear to recover. Without treatment, diarrhea, dehydration and coma occur about 24 hours later.
  • Some cats may present with icterus.

Geographic incidence

  • Iron toxicity can occur anywhere.

Age predisposition

  • Iron toxicity can occur at any age.

Breed/Species predisposition

  • There is no breed predisposition.

Public health considerations

  • Iron can be toxic to humans if excessive amounts are ingested. Care must be taken when using products containing iron.

Cost considerations

  • Moderate to expensive: therapy and cost will depend on the amount of elemental iron ingested and how quickly therapy was instituted.

Pathogenesis

Etiology

  • Toxicity occurs following ingestion of excessive amount of soluble iron, typically in the form of supplements or multivitamins or iron-containing gardening products.
  • Iron supplement usage is common in households with pregnant women or nursing mothers.

Predisposing factors

General

  • There are no specific predisposing factors. Any animal can become intoxicated by ingesting an excessive amount of iron.

Pathophysiology

  • Normally, the amount of iron that is absorbed from ingested food is determined by the bodys requirement for iron. Absorption of iron occurs in the mucosal cells of the small intestine through an active transport system. Absorbed iron is converted to ferric iron and then bound to the glycoprotein transferrin. Iron is then transported to the bone marrow and liver, where it is stored as hemosiderin and used as needed for oxygen transport by hemoglobin and myoglobin. There is no established mechanism for excreting bound iron.
  • When an excessive amount of iron is ingested, the transport mechanism becomes overwhelmed. Transferrin becomes saturated and the excess iron circulates in serum as free iron, which is corrosive and a strong oxidant. This free iron causes direct damage to epithelial cells, resulting in gastrointestinal mucosal necrosis and ulceration. Free iron will also damage mitochondria, resulting in hepatic necrosis.

Timecourse

  • Iron toxicity typically occurs in stages. The first stage occurs within 6 hours of ingestion. Free iron will damage the gastrointestinal mucosa, further increasing iron absorption. 6-24 hours following ingestion, the animal has an apparent recovery. Unfortunately, without treatment, about 12-96 hours following ingestion, diarrhea returns along with hepatic necrosis, coagulopathy, shock and possibly coma and death. Those that survive may develop gastrointestinal obstruction weeks later. GI mucosal damage and scar formation can result in stenosis and obstruction.

Diagnosis

Presenting problems

  • Depression, vomiting, bloody diarrhea.
  • Vomitus and feces may smell metallic.

Client history

  • Recent exposure to iron containing supplements or multivitamins, or fertilizers.
  • Without known exposure, owners complain of sudden and severe gastrointestinal signs.

Clinical signs

  • Lethargy.
  • Vomiting (possible hematemesis).
  • Diarrhea (possible hematochezia or melena).
  • Abdominal pain.
  • Dehydration.
  • Shock.
  • Renal failure.
  • Cardiovascular collapse.
  • Hepatic failure.
  • Coma.
  • Convulsions.

Diagnostic investigation

  • Determine the dose of elemental iron ingested.
    Iron salt Usual strength of
    pharmaceutical
    products
    Usual elemental
    iron content
    Percentage of
    elemental iron
    Ferrous fumarate 200 mg
    210 mg
    65 mg
    68 mg
    33%
    Ferrous gluconate 300 mg 35 mg 12%
    Ferrous succinate 100 mg 35 mg 35%
    Ferrous sulfate 300 mg 60 mg 20%
    Ferrous sulfate (dried) 200 mg 65 mg 37%
  • Determine total serum iron concentration  Blood biochemistry: iron.
  • CBC Hematology: complete blood count (CBC) , biochemical profile, urinalysis and abdominal radiographs Radiography: abdomen.
  • Leukocytosis, hemoconcentration, hyperglycemia and metabolic acidosis Acid base imbalance may be present.
  • Hemoglobinuria Hemoglobinuria may be found.
  • Depending on the stage of toxicity, liver enzymes and bilirubin may be elevated. Abdominal radiographs may reveal metallic foreign objects in the gastrointestinal tract.

Confirmation of diagnosis

Discriminatory diagnostic features

  • Since undissolved iron tablets are radiopaque, abdominal radiographs can be used to help to confirm recent ingestion. A negative radiograph does not exclude ingestion.

Definitive diagnostic features

  • Determine the concentration of serum iron. To get a peak serum iron concentration, consider taking samples at 6 and 12 hours after ingestion.
  • Iron concentrations 50-100% above normal suggest toxicity. Normal iron concentrations range from 100-300 mcg/dl Blood biochemistry: iron.
  • Liver samples can be analyzed. Liver iron levels over 400 ppm are considered excessive; however, this is not conclusive. Histopathology should always be performed to evaluate other disease problems associated with excessive iron in the liver (eg extramedullary hematopoesis, hemosiderois).

Gross autopsy findings

  • The gastric and small intestinal mucosa is typically hemorrhagic and edematous. Necrosis, mucosal sloughing and GI ulceration may be present. Watery diarrhea is usually present within the GI tract.
  • Hepatomegaly and/or friability may be present.

Histopathology findings

  • Mucosal necrosis, ulceration and edema is typically observed within the gastrointestinal tract.
  • Periportal necrosis may be seen.

Differential diagnosis

Treatment

Initial symptomatic treatment

  • If ingestion occurred less than 2 hours before presentation, induce vomiting or perform gastric lavage Gastric lavage if appropriate. If ingestion occurred over 2 hours prior to presentation, do not induce emesis and begin gastric demulcents or sucralfate Sucralfate (0.25-0.5 g/cat PO BID to TID).
  • Activated charcoal Charcoal activated is not effective and should not be given. 
  • Intravenous fluids Fluid therapy: for electrolyte abnormality to correct electrolyte disturbances and to maintain urine output is important.

Standard treatment

  • Aggressive supportive care is the mainstay of treatment.
  • The antidote deferoxamine (desferrioxamine) is usually only used in severe poisoning and is of limited benefit more than 12 hours after ingestion. Administer deferoxamine (desferriozamine) as a slow intravenous infusion at a rate of 15 mg/kg/h. If an IV infusion is not possible, deferoxamine can be given at a dose of 40 mg/kg/h IV every 4- hours.
  • Serum iron levels should be monitored and treatment continued until the concentration is normal. This typically takes 2-3 days. Note that deferoxamine can interfere with analysis of iron.

Monitoring

  • Monitor serum iron concentration daily until levels normalize. Monitor liver enzymes daily until serum iron concentration is normal.
  • During deferoxamine treatment, the urine will likely be reddish brown in color (described as vin rose) due to increased iron-chelate complex.

Subsequent management

Treatment

  • Periodically monitor liver values after treatment.

Monitoring

Prevention

Control

  • Keep all supplements and multivitamins safely stored away from pets and do not administer medication without veterinary advice.
  • Keep all garden products safely stored away from pets.
  • Do not allow pets into the garden if iron-containing products have recently been used.

Outcomes

Prognosis

  • Animals that remain asymptomatic for 6 hours are unlikely to develop signs of toxicity.
  • Severe iron toxicity in companion animals is rare and usually has a poor prognosis but is highly dependent on exposure dose and extent of hepatic injury.
  • The prognosis is good for animals that are treated immediately and are not showing clinical signs of toxicity.

Expected response to treatment

  • Resolution of clinical signs.

Reasons for treatment failure

  • Inappropriate or delayed therapy.

Further Reading

Publications

Refereed papers

Other sources of information

  • Hall J D (2016) Iron. In: Blackwell's Five Minute Veterinary Consult. Smal Animal Toxicology. 2nd edn. Hovda L, Brutlag A, Poppenga R, Petersen K (eds) Wiley-Blackwell, Ames, Iowa. pp 707-715.
  • Hall J O (2013) Iron. In: Small Animal Toxicology. 3rd edn. Peterson M E, Talcott P A (eds). St Louis, Missouri: Elsevier. pp 595-600.
  • Albretsen J (2006) The toxicity of iron, an essential element. Vet Med 101 (2), 82-90 ResearchGate.
  • Plunkett S (2001) Emergency Procedures for the Small Animal Veterinarian. 2nd edn. Saunders. St. Louis. pp 341-343.
  • Gfeller R W & Messonnier S P (1998) Handbook of Small Animal Toxicology & Poisonings. Mosby. St. Louis. pp158-160.

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