WSVMA Annual Conference Toxicology Spokane Convention Center Spokane, Washington October 1-3, 2010 Ahna Brutlag, DVM Pet Poison Helpline and the University of Minnesota, Bloomington, MN Ahna Brutlag, DVM Assistant Director of Veterinary Services, Pet Poison Helpline Bloomington, MN Biography: Dr. Ahna Brutlag is the Assistant Director of Veterinary Services at Pet Poison Helpline™ (PPH). She received her veterinary degree at the University of Minnesota in 2006 and is currently preparing for veterinary toxicology board certification. Dr. Brutlag has authored multiple textbook chapters and has lectured throughout the United States. The primary focus of her publications and presentations include rodenticide toxicity, toxic plants, common pharmaceutical poisonings and the safety of household products. Contact Email: [email protected] Rodenticides – An Oldie But A Goodie Ahna Brutlag, DVM Assistant Director of Veterinary Services Pet Poison Helpline Key Points • Do not assume all rodenticides are anti-coagulants. • The active ingredient of a rodenticide cannot be determined by the color or shape of the product. • Due to better absorption and less chance of reaction, the oral administration of Vitamin K1 is preferred over injectable unless the animal is coagulopathic. Long-acting anticoagulants (i.e. brodifacoum, bromadiolone, diphacinone, difenthiolone, chlorphacinone) • Determine the risk of toxicosis understanding that there is significant difference between the LAACs. • Decontaminate via emesis and consider activated charcoal if there is risk of toxicosis. • Vitamin K 1 is the antidote. Oral K1 is preferred unless the pet is coagulopathic. Treat for 3-4 weeks and then check a PT 48 hrs after the final dose to ensure sufficient duration of dosing. Give K1 with a fatty meal. • Common signs of toxicity: lethargy, exercise intolerance, pallor, difficulty breathing, weakness. Bleeding is more often cavital (into abdominal or thoracic cavities) as opposed to serosal (gums, GI tract, bladder). • Signs of toxicity appear within 2-5 days of ingestion. Cholecalciferol (Vitamin D3) • Toxicity results in elevated hypercalcemia and hyperphosphatemia within 24-48 hours. • Hypercalcemia/hyperphosphatemia lead to soft tissue mineralization which results in renal failure. Cardiac and neurologic effects are possible but rarely seen. • Multi-dose activated charcoal is indicated because the toxin re-circulates through the liver/GIT. • Treatment needs to begin before calcium and phosphorus levels rise for best prognosis. • Basic treatments of hypercalcium: saline diuresis, Lasix (furosemide), prednisone (used to decrease the body’s absorption of calcium and promote calciuresis). • Specific treatments: Aredia (pamidronate) or salmon calcitonin. Aredia is the treatment of choice and only needs to be given once or twice. However, it is more expensive than calcitonin. Bromethalin • Results in cerebral edema (swelling of the brain). • Because of the risk of CNS effects, use caution when inducing vomiting. Do not induce vomiting if the animal has any neurological abnormalities. Multiple doses of activated charcoal may be beneficial. 1 • Common signs of toxicity: staggering, ataxia, hyperexcitability or CNS depression, tremors, and seizures. • Very large ingestions result in signs within 4-6 hrs. Smaller ingestions can take up to 24 hrs to show signs. • There is no specific antidote and treatment is focused on reducing cerebral edema (head elevation, mannitol, etc). Steroid use is considered controversial. Phosphides (zinc, aluminum, calcium) • Phosphine gas is released when this product contacts stomach acid and is the agent of toxicosis. The metal (i.e. zinc) does not contribute to toxicosis. • To reduce the formation of phosphine gas, administration of an oral antacid should be done as quickly as possible (at home or in the clinic). • Phosphine gas has a fishy or garlicky odor and may cause severe respiratory irritation in humans. Advise pet owners to roll down the car windows if the pet vomits and decontaminate these animals outdoors if possible. • Decontamination via emesis or activated charcoal alone is often not sufficient and gastric lavage (with a 5% sodium bicarbonate solution) if often necessary. • Common signs of toxicosis: vomiting, agitation, abdominal distention/ pain, dyspnea, collapse and shock. Signs often begin within 15-30 minutes of ingestion. • The end result is multi-organ damage (renal and hepatic) or death from circulatory collapse. • There is no antidote; provide supportive are as needed. Treatment is focused on decontamination due to the serious toxic effects. Poison Control Resources For assistance managing a potentially poisoned patient, a number of resources are available. In the US and Canada, veterinarians or pet owners may call Pet Poison Helpline ($35/case) at (800) 213-6680 or the ASPCA’s Animal Poison Control Center ($65/case) at (888) 426-4435. Both of these services are available 24/7 and are staffed with experts in the field of veterinary toxicology. Pet Poison Helpline is also staffed with veterinary specialists in emergency and critical care and internal medicine, as well as PharmDs. In order to obtain the most accurate and current veterinary-specific clinical advice, the use of these services is highly recommended. 2 From the Planter to the Carpet: Toxic Plants and the Small Animal Patient Ahna Brutlag, DVM Assistant Director of Veterinary Services Pet Poison Helpline INTRODUCTION For curious dogs or cats, it’s difficult to resist the allure of plants. Pet Poison Helpline receives multiple calls on a daily basis from concerned pet owners and veterinarians about plant ingestions. While many plants are simple gastrointestinal irritants, some have the potential to cause life-threatening toxicity. Thus, it is helpful for technicians and veterinarians to be familiar with common plants that have the potential to cause severe toxicosis in small animals. PLANTS CAUSING SERIOUS SYSTEMIC DISEASE Plant name: Lily (Lilium spp. and Hemerocallis spp.) Other common name(s): Easter lily, tiger lily, Japanese show lily, stargazer lily, rubrum lily, day lily Species of concern: Cats Toxic dose: 1-2 leaves or petals Toxic portion of plant: All, even pollen Onset/duration of clinical signs: Hours/days Clinical signs: Early onset vomiting, depression, anorexia. Acute anuric renal failure in 1-3 days. Azotemia, epithelial cats (12-18 hrs post ingestion) proteinuria, and glucosuria. Treatment: Aggressive decontamination and IV fluid therapy x 48 hrs. Peritoneal or hemodialysis has been successful. Prognosis: Good if treated early and aggressively; poor if treatment is delayed 18-24 hr or anuria has developed. Stargazer Lily (Lillium spp.) Plant name: Foxglove (Digitalis lannata and D. purpuea), Oleander (Nerium oleander), Lily of the Valley (Convallaria majalis), Kalanchoe (Kalanchoe spp.) Other common name(s): Yellow Oleander, Lucky Nut, Be-Still Tree Species of concern: All 3 Toxic dose: 2-3 oleander leaves; 1.5 gm dried foxglove toxic to children Toxic portion of plant: All, even oleander nectar/honey (“mad honey”) Onset/duration of clinical signs: 45 min/4-5 days Clinical signs: These plants contain cardiac glycosides. Signs may include vomiting and abdominal pain within 45 min, hyperkalemia, bradycardia with 1st, 2nd or 3rd degree AV block, ventricular arrhythmias, and asystole. Kalanchoe may also cause neurological signs. Treatment: Early emesis and activated charcoal. ECG monitoring x 24 hrs. Atropine, beta- blockers, lidocaine, a temporary pacemaker and digoxin antibody fragments (Digibind®, 1-2 vials needed, $600/vial). Prognosis: Poor unless treated early and aggressively. Foxglove (Digitalis purpuea Plant name: Rhododendrons and azaleas (Rhododendron spp.), Laurels (Kalmia spp.) Other common name(s): Mountain Laurel, Sheep Laurel Species of concern: All Toxic dose: >0.2 % of animal’s body weight. An adult human can eat 3 leaves/flowers without developing clinical signs. Toxic portion of plant: All. Onset/duration of clinical signs: As early as 1 hr, more typical 4-12 hrs/1-3 days Clinical signs: These plants contain grayanotoxin glycosides which bind to sodium channels causing a prolonged depolarization. This may lead to bradycardia or tachycardia, arrythymias, and hypotension. May also cause cholinergic signs such as vomiting, diarrhea, salivation, and dyspnea. Treatment: Aggressive decontamination, monitor an ECG and blood pressure, sodium channel blockers, atropine, aggressive IV fluids to maintain perfusion. Prognosis: Good with early intervention. 4 Plant name: Cycad palm (Cycas spp., Macrozamia spp.) Other common name(s): Sago palm, leatherleaf palm, and Japanese fern palm. These are not true palms. Species of concern: Dogs Toxic dose: 1-2 seeds are fatal in a medium sized dog. A “few bites” can cause toxicity. Toxic portion of plant: All, especially the seeds. Onset/duration of clinical signs: Variable (hours to days) Clinical signs: Common: Vomiting and diarrhea (+/- blood), lethargy, depression, liver failure, death. CNS signs possible and often related to liver failure. Treatment: Aggressive decontamination with multiple doses of activated charcoal, supportive care for GI signs and liver failure. Liver protectants such as SAMe and/or silymarin. Prognosis: Good if treated prior to the onset of liver failure. Plant name: Cyanobacteria or blue-green algae (Microcystis, Nodularia, Anabena, Aphanizomenon, Lyngbya, and Oscillatoria) Species of concern: All Toxic dose: A few mouthfuls of contaminated water.