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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 www.carecentre.ca facebook.com/CARECentre p.1 standards of C.A.R.E. Issue Seventy Two – October 2013 -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 www.carecentre.ca facebook.com/CARECentre p.2 standards of C.A.R.E. 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. www.carecentre.ca facebook.com/CARECentre p.3 standards of C.A.R.E. Issue Seventy Two – October 2013 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 www.carecentre.ca facebook.com/CARECentre p.4 standards of C.A.R.E. Issue Seventy Two – October 2013 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 www.carecentre.ca facebook.com/CARECentre p.5