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Issue Seventy Two – October 2013
standards of
C.A.R.E.
CLINICAL CASE MANAGEMENT NEWSLETTER
The Calgary Animal Referral & Emergency Centre Animal Hospital
standards of
C.A.R.E.
Issue Seventy Two – October 2013
Baby Products That Are Toxic To Pets Part I
Kirsty Royle MA VetMB MRCVS
Pre-natal vitamins (Iron)
Essentially the main problem with pre-natal vitamins is the iron. Iron can be present in
multivitamins, pre-natal vitamins, iron supplements and birth control pills. Iron is also found in
some plant foods and fertilizers and some hand warmers.
Available forms of iron include ferrous fumarate (33% = elemental iron), ferric hydroxide
(63%), ferrous gluconate (12%), ferric phosphate (37%) and ferrous sulphate (anhydrous)
(37%). You need to convert to elemental iron to calculate the dose ingested in mg/kg.
E.g. 20kg dog ingests 10 x 324mg ferrous fumarate.
10 x 324 = 3240mg.
Ferrous fumarate is 33% elemental iron.
3240 x 0.33 = 1069.2mg elemental iron / 20kg = 53.5mg/kg
Estimated range of toxicosis:
< 20mg/kg elemental iron : low toxicity
20-60mg/kg elemental iron : moderate toxicity
60mg/kg elemental iron
: severe toxicity
>100mg/ke elemental iron : potentially lethal
Clinical signs
Ingestion of iron causes two main problems. The first is that iron has a direct corrosive effect on
the mucosa of the stomach and small intestine. This can be severe enough to cause necrosis,
perforation and peritonitis. In a milder toxicity it may cause haemorrhagic gastroenteritis.
The second problem is that any iron absorbed in excess of the total iron binding capacity is
distributed to tissues where it enters cells and disrupts mitochondrial function, interferes with
cellular respiration, and causes lactic acidosis. Free radical formation is enhanced by the
increased availability of free iron, which results in additional cell damage. Vasodilation and
vascular damage can result in systemic shock. Vascular damage can result in haemorrhage.
You can also get an anaphylactic reaction with injectable iron which can cause
cardiovascular collapse and acute death. We would more commonly see signs associated
with the ingestion of iron.
There are generally 4 stages of toxicity
Stage 1: Up to 6 hours post ingestion
-GI signs, vomiting and diarrhoea. GI Haemorrhage, abdominal pain.
-Lethargy
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-Mild to moderate toxicities would not generally progress beyond this point
-In general most animals that remain asymptomatic for the first 6-8 hours are unlikely to
develop toxicosis.
Stage 2: 6-24 hours post ingestion
-apparent recovery phase/ quiet phase
Stage 3: 12-96 hours post ingestion
-lethargy
-continuing GI signs
-cardiac signs: hypotension, tachycardia, CV collapse
-metabolic acidosis, shock, hepatic necrosis, death
-seizures/CNS depression, coagulopathy, oliguria or anuria secondary to acute renal
failure (from shock).
Stage 4: 2-6 weeks post ingestion
-GI ulcers can heal with scarring and stricture
Differential diagnosis
Primary GI disease – mesenteric torsion, GDV, FB obstruction, pancreatitis, peritonitis, HE, viral
enteritis, bacterial enteritis, gastroenteritis, infectious, parasitic
Secondary GI disease – hypoadrenocorticism, endotoxin ingestion from garbage, caustic/
corrosive ingestion, heat stroke, ‘shock gut’.
Primary metabolic disease – renal, hepatic, etc.
Diagnostics
- Lab testing will show elevated liver enzymes, metabolic acidosis, haemoglobinuria,
haemoconcentration, hyperproteinaemia, pre-renal azotaemia.
- Radiographs may potentially show some radiopaque material (radiodense objects or
‘sludge’ from partially digested tablets) but not all will show so don’t rule out based on lack
of radiographic evidence. Free abdominal gas and/or fluid may be seen if GI perforation
has occurred.
- Serum iron levels will be elevated – these should be checked 3 and 8-10 hours post
ingestion. Normal 94-120mcg/dL, levels > 350mcg/dL are dangerous and require chelation
therapy. Serum iron levels are often available through local hospitals (and results can be
obtained rapidly this way).
Treatment
If the ingested dose is < 20mg/kg and the patient is asymptomatic they can generally be
monitored at home for GI signs. GI medications that can be used include milk of magnesia
(e.g. magnesium hydroxide), this complexes with iron to form FeOH (less available and has
a cathartic effect. H2 blockers are also useful.
If the ingested dose is 20-60mg/kg and the patient is still asymptomatic then inducing emesis
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Issue Seventy Two – October 2013
is appropriate assuming no contraindications). Activated charcoal will not bind iron and
is therefore not indicated. Treatment would also include milk of magnesia, H2 blockers,
sucralfate and you would continue to monitor for GI signs and treat symptomatically.
If the ingested dose is >60mg/kg then if appropriate emesis induction should be performed
(be very cautious if evidence of gastric damage is already present). Radiographs can be
taken after emesis to be sure there are no pills left behind that could form a bezoar. H2
blockers should be given along with anti-emetics and sucralfate. At this dose you could
also consider gastric lavage or whole bowel irrigation, and chelation therapy. If there is
radiographic evidence of tablets remaining in the stomach after lavage then surgery would
also be warranted. Adherent tablets are more likely to cause perforation.
If the patient presents with cardiovascular signs then crystalloid fluids, hypertonic saline,
colloid and potentially whole blood may be needed in the course of treatment. IV fluids
may be needed for 24-72 hours or until clinical signs resolve and will also help to increase the
urinary elimination of chelated iron. If there is a profound acidosis with pH < 7 then sodium
bicarbonate can be used.
Chelation should be performed if serum iron levels are > 350mcg/dL. If serum iron levels
are unknown but the patient is symptomatic with signs of iron toxicosis and the dosage
ingested is > 60mg/kg then chelation should also be considered. Chelation treatment is with
Deferoxamine mesylate (desferol). Intravenous doses are available however if given IV it
can cause arrhythmias, hypotension and pulmonary oedema. Recent dosage suggestions
are 40mg/kg q 4-8 hours given intramuscular. This is most effective if given within the first 24
hours (before the iron moves into the tissues). Chelation therapy should cause the urine to
change to a reddish brown colour. The drug can be repeated as needed until the urine
changes colour back to clear. Serum iron levels if available can be checked every 4 - 6
hours. Deferoxamine is teratogenic. As it causes urinary elimination of chelated iron caution
should also be used in patients with decreased renal function. Supportive care should be
continued for 24 hours after chelation therapy is discontinued.
Gastroprotectant medications should be continued for a few weeks to try and help prevent
stricture formation during healing of any gastric irritation. Owners should monitor for potential
signs of stricture formation at home.
Other ingredients in multivitamins that can cause toxicity are Vitamin D3 and Vitamin A. The
other vitamin and minerals can cause GI signs (vomiting, diarrhoea and anorexia).
For acute Vitamin A toxicity clinical signs are usually seen when the amount ingested is more
than 10 to 1000 x the daily requirements.
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standards of
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Vitamin D
To calculate the dogs ingested: 40,000 IU of vitamin D3 = 1mg or 1IU = 0.000025mg.
In dogs toxic dose are:
>0.1mg/kg can result in clinical signs (vomiting, anorexia, weakness)
>0.5mg/kg can cause hypercalcaemia
Cats, puppies and kittens are more sensitive than adults and generally seem to show signs
at 1/10th of the adult dog toxic dose.
This is a fat soluble vitamin that concentrates in milk so nursing puppies and kittens are also
at risk for toxicosis. Animals with pre-existing liver and renal disease may show signs at much
lower levels.
Diagnosis/ clinical signs
History of ingestion. Clinical signs are vague initially: anorexia, lethargy, PU/PD. This can
progress to haemorrhagic diarrhoea, depression and death. Clinical signs usually appear
within 12-36 hours with a toxic ingestion.
Calcium and phosphorous can increase in 12-72 hours, although phosphorous can increase
up to 12 hours before the serum calcium. Azotaemia can also been seen and hyposthenuria
can develop. Metabolic acidosis and bradycardia can develop
Clinical signs can last for weeks due to the slow release of the vitamin from fat stores.
Treatment
Decontamination – induce vomiting and/ or gastric lavage if indicated. Activated charcoal
with sorbitol and 3-4 additional doses (without sorbitol) can be given every 6-8 hours.
Baseline blood work should be obtained (important to get a USG prior to fluid administration).
Electrolytes and a renal chemistry panel should be monitored every 24 hours for 96 hours. If
the calcium is normal at 96 hours no additional treatment is necessary. The goal of treatment
is to keep the calcium < 1.5mg/dl and the phosphorous < 7mg/dl.
Aggressive fluid therapy should be commenced with 0.9% NaCl at 3-4 x maintenance. Fluid
diuresis should be continued until calcium levels have stabilised. Fluids containing calcium
should be avoided. Phosphate binders can be used. GI support e.g. anti-emetics and
gastroprotectant may be needed especially if azotaemia develops.
If hypercalcaemia develops once the patient is well hydrated furosemide or prednisone
can be started to increase calcium excretion. If hypercalcaemic you can also attempt to
decrease calcium absorption with pamidronate disodium or salmon calcitonin.
Once calcium levels have been stabilised the calcium and phosphorous should be checked
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every 24 hours for 7 days and then every 2-3 days for up to 2 weeks. If the calcium starts to rise
again fluids and pamidronate should be re-started. Long term oral steroids and furosemide
may be needed for several weeks.
The long term prognosis will depend on the extent of renal tubular and myocardial damage.
If calcification has already developed in the cardiac tissue or the gastro-intestinal tract the
prognosis is guarded.
Part II available November 2013
References
• Pet Poison Helpline Webinar: What to expect when Clients are expecting. Brutlag and
Lee, 2013
• Handbook of Small Animal Toxicology and Poisonings, 2nd Edition. Gfeller and Messonnier,
2004
• Small Animal Toxicology (Blackwell’s Five Minute Veterinary Consult), Ed: Osweiler, Hovda,
Brutlag and Lee, 2011
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