Iron

Iron is an essential mineral, but when a large amount is ingested, it can also be lethal.  Ingestion of 20 to 40 mg of elemental iron/kg of body weight may result in toxicosis. Ingestion of > 60 mg/kg is potentially serious and oral dose of >200 mg/kg is roughly estimated to be lethal.

Sources :

• Iron is used as an anti-anaemic agent.
• Injectable iron preparations include iron carbohydrate complex like iron-dextran or irondextrin and oral preparations include ferrous sulphate, ferrous fumarate and lactate. Soluble salts of iron pose the greatest risk of toxicosis.
• It is available as over the counter (OTC) drug, in multivitamin mineral preparations and gestational iron supplements. Since most of these preparations are sugar coated, dogs have a tendency to swallow more tablets.
• Iron is also used in fortified lawn and garden fertilizers.

Factors affecting toxicity:

• Iron absorption is influenced by extraluminal (level of erythropoietic activity, body iron stores and anemia) and intraluminal factors (ascorbic acid, dicarboxylic acid, sugars increase absorption, phosphates, oxalates, phytates, bicarbonates, tannins and fibre decrease absorption).
• Ferrous salts are more bioactive and more rapidly absorbed. But the overall toxicity is more dependent on the total soluble concentration of elemental iron.
• Toxicity is usually noticed in pigs.
• Toxicity is more in piglets born to selenium and vitamin E deficient pigs.
• There is no effective mechanism for excretion of iron. So animals with enough iron in the body are susceptible than those actually requiring iron.

Mechanism of toxicity

Iron can change its valance states from ferrous to ferric and then back to ferrous very rapidly.

• It plays a major role in redox reactions.
• Anaphylactic reactions are noticed due to the release of histamine.
• True iron toxicity is due to:

 o Direct damage to the gastrointestinal epithelium as unbound iron is corrosive and a strong irritant and subsequent absorption of iron in excess

o Iron has an ability to act as and produce free radiacls. Free redicals scavenge electrons and in doing so produce additional free radiacls. This causes direct damage to the liver by depletion of glutathione and peroxidation of lipids

 o Hypotension, increased capillary permeability and vasodilatation due to ferritin

o Interference with blood coagulation

• Death is due to inadequate perfusion of vital organs.

Clinical symptoms :

• Acute anaphylactic reactions leading to stagger, collapse, cyanosis, dyspnoea and shock.
• In selenium and vitamin E deficient cases, vomiting is noticed.
• Toxicity due to orally administered iron causes emesis, bloody diarrhoea, paleness and weakness, prostration, cyanosis and other signs of circulatory collapse.
• In baby pigs pale skin, corrosion of mucosa, dark faeces, diarrhoea and tachycardia.

 PM lesion :

• Cyanosis, congestion of major organs, swelling at the site of injection, hepatic necrosis, icterus and pulmonary oedema.
• Yellowish brown discolouration and oedema of the tissues especially near the injection site.

TREATMENT :

Treatment:

• In anaphylactic reactions epinephrine, antihistaminics, oxygen and proper nursing care.
• If toxicity is due to oral administration, milk of magnesia to precipitate iron will be useful.
• Egg, water, milk and emetics are found to be useful.
• Desferrioxamine can be administered slowly by intravenous route at the rate of 40 mg/kg every 4 to 8 hours. . If given faster, there may be hypotension and shock.
• Shock should be treated symptomatically.
• Ascorbic acid administered orally with desferroxamine enhances excretion of iron. After desferroxamine treatment, urine will be reddish brown in colour due to increased excretion of iron (vin rose colour).