Clinical signs
Iron toxicosis manifests clinically in four stages. The first stage occurs in the six hours after an iron overdose. It is
marked primarily by gastrointestinal effects, such as vomiting, diarrhea, and gastrointestinal bleeding.2,4-6 The greatest mucosal damage occurs on an empty stomach. Most animals with mild to moderate iron toxicosis do not progress
beyond this stage.5
The second stage occurs six to 24 hours after the overdose. This is referred to as a latent period, a period of apparent clinical recovery. In animals with severe iron toxicosis, this recovery period is transient and soon
progresses to the third stage.2
The third stage of iron toxicosis occurs about 12 to 96 hours after the initial clinical signs develop. This stage is marked
by lethargy, a recurrence of gastrointestinal signs, metabolic acidosis, shock, hypotension, tachycardia, cardiovascular collapse,
coagulation deficits, hepatic necrosis, and possibly death.2,5,6
The fourth stage, which may occur two to six weeks after the iron overdose,2,5 is when animals that had gastrointestinal ulcerations and survived are healing. As these ulcerations heal, scarring occurs
and strictures may develop. Even animals that had only gastrointestinal irritation in the first stage of iron toxicosis are
at risk of developing strictures.2
Other abnormalities noted when iron overdoses occur are dehydration, hypovolemia, anemia, evidence of hepatic necrosis (elevated
alanine transaminase and aspartate transaminase activities), and liver failure (hypoglycemia, hyperammonemia).2,5 In addition, iron toxicosis causes coagulation disturbances that are related to thrombocytopenia, hypoprothrombinemia, and
impaired clotting factor synthesis.5 In people, the presence of hyperglycemia and leukocytosis often indicates a serum iron concentration of greater than 30
ug/dl.2 Finally, iron toxicosis results in several central nervous system signs. Often these signs result from effects on other cellular
processes. For example, metabolic acidosis and hepatotoxicity can lead to other signs such as lethargy and hepatic encephalopathy.5 Other central nervous system signs that occur are comas, seizures, and tremors.1,2,5
Diagnosis
Testing an animal's serum iron concentration is the best method to confirm iron poisoning. It is also beneficial to measure
total iron-binding capacity, although neither test alone is sufficient to determine whether treatment is needed. Most human
hospitals offer serum iron concentration and total iron-binding capacity testing, but not all veterinary clinical pathology
laboratories do.
Since the normal serum iron concentration and normal total iron-binding capacity can vary from animal to animal, it is best
to measure both and correlate the test results with clinical observations. Serum iron concentrations can change dramatically
during the first few hours after ingestion, so repeat the serum iron test four to six hours after initial measurement. When
the serum iron concentration exceeds the total iron-binding capacity or the serum iron concentration is greater than 500 ug/dl,
severe systemic effects can be expected. Normal serum iron-binding capacity is usually about 25% to 30% saturated.2 Every laboratory is different, but an example of how the serum iron concentration and total iron-binding capacity results
are reported is Fe = 134 ug/dl and total iron-binding capacity = 436 ug/dl, or 134/436 X 100 = 30.7% saturated.
Obtaining multiple blood samples to test serum iron concentrations may be indicated, especially when the total iron dose is
unknown or the animal is symptomatic. An abdominal radiographic examination can be useful to identify metallic objects since
iron tablets are radiopaque.2,5
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