A protocol for treating iron toxicosis is described in Figure 1. Animals that have recently ingested large doses of iron will benefit from gastrointestinal decontamination. In animals that
can vomit, induce emesis with 3% hydrogen peroxide (1 to 5 ml/kg orally), apomorphine hydrochloride (0.03 mg/kg intravenously,
0.04 mg/kg intramuscularly), or other appropriate emetics.8 Gastric lavage can be performed on anesthetized animals, although it may not be effective if large pills are involved or
if the pills adhere to gastric mucosa. Place a cuffed endotracheal tube to prevent aspiration of lavage material.2 In a recent study, activated charcoal adsorbed ferrous sulfate solution at a pH environment consistent with that of the
duodenum.9 It has been suggested that iron can be precipitated to a nonabsorbable form in the digestive tract by using sodium phosphate,
sodium bicarbonate, or magnesium hydroxide; however, the clinical significance of this therapy is questionable.2,4,6
Figure 1. Management of Iron Toxicosis
Restoring fluids, electrolytes, and acid-base balance is essential to successfully treating iron toxicosis. Fluids are also
needed to prevent hypovolemic shock. Administer fluids based on the animal's maintenance and replacement needs.2 Monitor electrolytes, and correct any abnormalities. Administering gastrointestinal protectants such as sucralfate, cimetidine,
misoprostol, or other inhibitors of gastric acid secretion may also be helpful.2,10
Chelation therapy is indicated in animals at risk of or showing clinical signs of severe iron toxicosis. This includes animals
that ingest more than 60 mg/kg of elemental iron, animals that have a total iron-binding capacity that is greater than the
serum iron concentration, or animals that have a serum iron concentration greater than 500 ug/dl. Deferoxamine mesylate (Desferal—Novartis
Pharmaceuticals), the chelator of choice for excessive iron in the body, is the only chelator available that seems to be effective
at reducing serum iron concentrations. The recommended dosage of deferoxamine is 40 mg/kg given intramuscularly every four
to eight hours. Alternatively, give deferoxamine as a continuous infusion at the rate of 15 mg/kg/hr. Continue chelation therapy
until the serum iron concentrations decrease below 300 ug/dl and the clinical signs resolve. Often, iron toxicosis requires
two or three days of chelation therapy.2,4,5 Deferoxamine causes reddish-colored urine, which indicates free iron is being excreted. In people, deferoxamine therapy
is continued until the urine color returns to normal.6 Deferoxamine has not been reported to cause iron deficiency.
Calcium EDTA has also been used to reduce serum iron concentrations but has not been shown to reduce mortality in cases of
acute iron poisoning. An experimental iron chelator, N, N'-bis(2-hydroxybenzyl) ethylenediamine-N, N'-diacetic acid monosodium
salt (NaHBED), has been used to successfully treat iron overdoses in dogs and monkeys and was shown to be about twice as effective
as deferoxamine and with fewer side effects.11 If NaHBED is approved for use in people, it may also become an alternative iron chelator for animals.
Monitoring and prognosis
Monitor all treated animals for four to six weeks for evidence of gastrointestinal obstruction.2 Once signs of iron toxicosis have developed, the prognosis is guarded.
Severe iron poisoning requires a lot of time and effort to treat effectively. Thus, treatment can become costly. In addition,
it is often difficult to obtain deferoxamine. If the serum iron concentration exceeds 500 ug/dl and a chelator is unavailable,
the prognosis is poor.
Prevention is the best treatment for iron toxicosis. Teaching owners about the dangers of iron toxicosis and the importance
of keeping all medications, multivitamins, and iron supplements out of reach of animals will help avoid serious injury.