Welcome to the Veterinary Lifeline Partner Program newsletter, brought to you by the ASPCA Animal Poison Control Center.
Opportunities for CE
CE for Veterinarians: Coming Soon
As fellow veterinary professionals, the ASPCA Animal Poison Control Center understands the challenges of fitting in meetings and Continuing Education programs into your already busy schedule. In order to make our RACE-accredited CE offerings more accessible and convenient for our valued Lifeline Partners, we will be posting free, pre-recorded sessions along with comprehensive quizzes on our website. This will allow you to take one or all of our courses any time—day or night—without worrying about scheduling or space limitations. Complete and submit the quiz at the end of the course in order to qualify for RACE-accredited CE credits. Please check our website in the upcoming weeks for more information on this new program—we hope you will find it to be convenient, fun and educational for your entire staff!
CE Conference for Veterinary Technicians
The ASPCA is pleased to announce that the 1st Annual ASPCA Continuing Education Conference for Veterinary Technicians will be held on Saturday, May 19 from 8:00 A.M. to 4:30 P.M. The conference will be held at the ASPCA’s Midwest Office in Urbana, IL. Topics will include animal behavior and veterinary toxicology.
March is Poison Prevention Month, with March 18-24 being Poison Prevention Week.
And, for a fun and educational way to learn about household hazards for pets, your clients can play our Flash Game with Cooper, the Careful Canine. Just check for the link under the Free Magnet box on the main ASPCA website.
A list of Toxicology Briefs, encompassing a wide variety of toxicants, is available in the Poison Control area of the ASPCA Professional website by clicking the link for Poison Control Resources For Vets. The newest additions to the list include:
As everyone starts to plant, and as Easter rolls around, it’s time to remind everyone of the potential hazards some plants may pose to pets. Below are some links to articles that you may find useful in answering pet owners’ questions:
How Dangerous are Winter and Spring Holiday Plants to Pets? (.pdf), December 2002, Volume 97, Number 12
Easter Lily Toxicosis in Cats (.pdf), April 1999, Volume 94, Number 4, p. 331
Spring-Blooming Bulbs: A Year-Round Problem (.pdf), August 2002, Volume 97, Number 8
Potentially Toxic Garden Plants (.pdf), May 2005, Volume 24, Number 11, p. 358
The ASPCA Professional website has an archive of our previous VLPP newsletters, which contain discussions on many agents, including isoniazid, Dovonex®, baclofen, antidepressants, amphetamines, Xylitol, bread dough, macadamia nuts, raisins, antifreeze and more.
Your clients can receive a free APCC magnet or static cling decal just by filling out the form on the ASPCA website.
Spring is a time of year we all look forward to. Common activities at this time of year may include spring cleaning, planting, opening swimming pools, de-winterizing campers or cabins, Easter celebrations, and cook outs. These activities can also lead to pets ingesting potentially toxic substances. Below is a list of the relative toxicity of various springtime hazards to which pets may be exposed.
Low Toxicity: (may cause gastrointestinal upset, but unlikely to cause serious problems unless very large amounts are ingested)
Moderate toxicity: (may cause significant signs beyond mild gastrointestinal upset)
High toxicity: (potential for very serious or life-threatening signs)
With spring comes many beautiful and potentially toxic plant exposures. Don’t forget that the ASPCA website, is an excellent starting place for owners who are looking for basic information on toxic and non toxic plants.
Our website includes both scientific and common names for plants, the family they belong to and the toxic principle if it is known. There is also a list of clinical signs caused by exposure to the plant. Photos of the plants will be helpful when trying to identify a particular plant.
Acetaminophen is a non-opiate derivative of p-aminophenol that is used to treat pain and fever. It comes in a large variety of preparations including liquids, tablets and long acting compounds, both in over-the-counter and prescription only type products. Acetaminophen is also found in a great many combination products. Peak plasma is usually reached in less than 30 minutes and up to 4 hours. There is a therapeutic dose in dogs of 10mg/kg reported in Great Britain, but use in dogs is generally not recommended.
Cats are especially sensitive to the effects of acetaminophen due to their inability to glucuronidate the drug to its non-toxic metabolite, coupled with eight reactive sulfhydryl groups on feline hemoglobin, which are targeted by the toxic acetaminophen metabolites. In cats, the primary effect seen with acetaminophen exposures is methemoglobinemia (+/- Heinz bodies), resulting in dyspnea, cyanosis, weakness, depression and death. Facial and paw edema may also occur, although the mechanism of this effect is not known. Cats can develop liver injury from acetaminophen but generally succumb to methemoglobinemia before liver damage becomes apparent.
Dogs are somewhat more resistant to the effects of acetaminophen compared to cats, but overdoses may cause serious hepatic and hematologic effects, depending on the dose ingested. Keratoconjunctivitis sicca has been reported in dogs at levels below those that are typically associated with liver toxicosis (less than 100 mg/kg). The development of KCS occurs typically within 72 hrs of exposure. At dosages of acetaminophen over 100 mg/kg, there is risk of hepatic injury from acetaminophen. Dosages over about 200 mg/kg may result in methemoglobinemia in addition to hepatic injury. Facial and paw edema may be seen in dogs but is more commonly seen in cats with acetaminophen toxicosis. Metabolic acidosis, renal damage, myocardial damage, CNS signs, thrombocytopenia and pancreatitis have occasionally been reported with large dosages of acetaminophen in dogs.
Treatment involves emesis induction (when medically safe and appropriate in a non symptomatic patient) and activated charcoal administration. Oftentimes repeated doses of activated charcoal are helpful since acetaminophen is thought to undergo enterohepatic recirculation. Monitoring of liver values and for methemoglobinemia is also of primary importance. Administration of N-acetylcysteine (140-280 mg/kg loading dose followed by 70 mg/kg q 6 hrs for minimum of 7 treatments; continue if evidence of hepatic injury, methemoglobinemia occurs) in patients at risk for methemoglobinemia and liver dysfunction is also important. Fluid therapy is usually instituted, especially in large acetaminophen exposures where nephrotoxicosis can be a concern. Monitoring of tear production in the form of a Schirmer tear test is recommended at baseline and then again at 72 hrs. Adjunctive therapies of cimetidine, ascorbic acid and SAM-E are also used in some cases.
A gentleman called the APCC and wanted to know if his dog (who was not wagging his tail and not jumping, but was otherwise normal) was going to die because he ate some bread that was buried in the back yard. The bread had been buried by the owner two days before. The owner had used an herbicide to spray the bread because there were some ants crawling on it. When the APCC veterinarian inquired if the product actually killed any ants, the owner replied, "No, but they were limping away from the bread."
You have two patients, Daisy and Dingo, both Australian Cattle dogs. They are littermates, 9 months old, both healthy, spayed females. Five days ago, Dingo presented to your clinic for anorexia, vomiting, bloody diarrhea, and liver failure. Owner reported seizures at home, which were also observed in the clinic. Despite aggressive treatment, Dingo died. Centrilobular hepatic necrosis was found on necropsy. Now Daisy is showing some of the same signs, and the owner is very worried. Daisy’s ALT is 4300. Ultrasound and liver biopsy has been scheduled, and a Leptospirosis titer is pending.
Because two young, healthy dogs from the same household have developed similar signs, you are concerned that they may have been exposed to a toxic substance. What key questions should you ask the owner before contacting the ASPCA APCC?
1. Do the dogs go outdoors unattended, and if so for how long? Are the dogs confined when outside, or do they roam?
2. What types of plants do they have access to, either indoors or outdoors?
3. Is either dog on any medications? What human medications are in the household? Had there been any evidence of chewed pill vials, chewing gums or foods containing xylitol?
4. What brand of dog food do they eat? Have they recently started a new bag/batch of dog food?
5. Are they vaccinated?
6. Could they have possibly had access to mushrooms?
The dogs have a pet door that allows them free access to the back yard anytime they want, sometimes unsupervised There is a chain linked fence around the yard. You find out that the dogs have access to the following indoor plants: peace lily, Dracaena, and jade plant, but there is no evidence of exposure to any of these plants. The owner provided a list of plants that grow in the back yard: yew, azalea, queen palm (Arecastrum romanzoffianum), and Vitis. They had seen both dogs chew on a sago palm (Cycas revoluta) that had been cut down a week ago, but the owner didn’t think much about it. Neither dog is on any medications, and the only human medications in the household are over the counter ibuprofen and ketoprofen. There was no indication that the dogs had gotten into any medications and the owners do not use xylitol-containing products in the home. The dogs eat a commercial brand of dry dog food and a new bag was opened a week before the first dog became ill. The dogs’ vaccines were up to date including Leptospirosis. The climate has been dry and no mushrooms have been seen in months.
You call the ASPCA APCC to discuss the case, and reach Dr. Michael Knight, one of our most experienced toxicologists, who will be able to discuss your differentials, as well as possible agents that cause hepatic injury. Based on this history, which of the following is the primary suspect?
b. Vitis poisoning
c. Cycasin intoxication
d. Aflatoxin intoxication
e. Yew poisoning
f. Azalea poisoning
The answer is c. Because there was a witnessed exposure to sago palm, at this point, cycasin intoxication is the most likely diagnosis. However, aflatoxicosis in dogs can present as acute hepatic injury as well, so testing the food was recommended by Dr. Knight (results were negative). Because two dogs were affected, ruling out infectious etiologies (bacterial, rickettsial, mycotic, protozoal), including leptospirosis, is important. Vitis (grapes) cause acute renal failure. Yew and azalea are cardiotoxic, not hepatotoxic, plants. None of the indoor plants mentioned would be expected to cause hepatic damage.
Discussion:Sago palm, Cycas, and Macrozamia species (i.e., Zamia floridana, Cycas revoluta, C cirinalis) are found wild in tropical to subtropical climates. They can also be used as an ornamental outdoor plant, or be grown as a houseplant.
There are three toxins in cycads: 1. cycasin, which is thought to be responsible for the hepatic damage (centrilobular necrosis). Cycasin is also carcinogenic, mutagenic and teratogenic. 2. Beta-methylamino-L-alanine (BMAA), a neurotoxic amino acid implicated in Guam disease of humans. 3. An unidentified toxin, which has caused hind limb paralysis due to axonal degeneration of the CNS in cattle, but this syndrome is not reported in dogs. All plant parts are toxic, but the nuts (seeds) contain a higher amount of cycasin than do other plant parts.
The most common signs are vomiting (+/- blood), diarrhea (+/- blood), depression, anorexia, and liver failure. Seizures and death are also possible.
Treatment includes decontamination (emesis, repeated doses of activated charcoal), depending on signs, and if exposure was recent enough, baseline blood work, monitoring liver enzymes, GI protectants, and fluids (Dextrose). The patient should also be monitored for seizures which may be controlled with diazepam. Blood transfusions may be necessary if gastrointestinal tract hemorrhage is severe. Additional treatments may include denosyl and silymarin for liver support, and a low protein diet such as K/D. The prognosis is good if caught early, but guarded in cases where the patient is showing signs.
In additional to cycad, what are some other agents that can cause centrilobular hepatic necrosis?
Acetaminophen, aflatoxin, mushrooms (Amanita, Galerina, Lepiota), blue green algae (microcystin), xylitol, castor bean, and iron.