The Poisonous Garden! - Vet Education

The 2013 Online Toxicology Symposium

The 2013 International Online Toxicology Symposium November 2013

A Joint Initiative of the ASPCA Poison Control Centre and Vet Education Pty Ltd

The Poisonous Garden!

Dr. Lauran Stern DVM ASPCA Animal Poison Control Center

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The 2013 Online Toxicology Symposium

The Poisonous Garden

Dr. Laura Stern DVM ASPCA Animal Poison Control Center

Plant Identification

Accurate and timely plant identification can be one of the most important keys to evaluating and treating plant intoxications. The Latin name of the plant should always be confirmed, as the common name can be the same or similar for multiple plants, often with very different toxicity risks and treatments. Plant material and photographs can be taken to plant professionals for identification by the owners. Some good resources for plant identification include: florists, nurseries, landscapers, and horticulturalists or botanists. Plant material should also be taken to the veterinary hospital, as well. The amount and portion of the plant ingested can be evaluated, and often hospital team members can help with identification as well.

Sago Palm (Cycas or Zamia sp.)

Cycads grow wild in tropical to subtropical climates. They are often used as landscaping plants in the yard or as houseplants. There are 3 toxins in cycads: Cycasin, which is converted to aglycone methylazoxymethanol (MAM) is thought to be responsible for the hepatic and gastrointestinal signs. bmethlamino-L-alanine (BMAA) is a neurotoxic amino acid. There is also an unidentified toxin which may be the cause of the hind limb paralysis due to axonal degeneration in the central nervous system of some cattle that ingested the cycads. It is not known if this toxin affects dogs.

All parts of cycads are toxic. As few as 1-2 seeds can be fatal in dogs; therefore, any ingestion should be considered to be potentially serious and requires veterinary care and monitoring. The first signs that are typically seen are GI upset (vomiting, diarrhea, anorexia, and hemorrhagic gastroenteritis (HGE)). This may result in dehydration as well. Neurologic signs include: depression, ataxia, tremors, and seizures. The pet may also develop icterus, ascites, DIC, and hepatic necrosis. Bloodwork changes include: increased liver enzymes (especially ALT), hypoglycemia, hypoproteinemia, leukocytosis, leukopenia, thrombocytopenia, and increased clotting times. Bloodwork changes may not be evident for 48 hours post-exposure.

Decontamination includes emesis and activated charcoal. Emesis may not be needed, if the pet is already vomiting. The pet should be monitored for hypernatremia, if activated charcoal is given. Decontamination should not be attempted if significant GI or neurologic signs are present, due to the risk of aspiration. Cholestyramine can also be given to help prevent enterohepatic recirculation, if the pet is able to eat.

Treatment should be prompt and aggressive. IV fluids with a balanced crystalloid with added potassium, Vitamin B, and dextrose (which may be hepatoprotective) should be initiated, even in

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The 2013 Online Toxicology Symposium

asymptomatic pets. Gastrointestinal protectants and hepatoprotectants should be started at this time, as well. Antiemetics should be given to prevent further vomiting. Broad spectrum antibiotics are indicated in pets with HGE or leukopenia. Fresh frozen plasma and Vitamin K1 should be given to pets who are coagulopathic. Whole blood transfusions may be needed in pets with pets with significant blood loss. Animals that are hypoproteinemic may require a plasma transfusion to help prevent interstitial edema and hypovolemia. Colloids may also be used to help increase oncotic pressure, but may increase bleeding. FFP should be given first, if the pet is at risk for significant bleeding.

Bloodwork monitoring includes blood glucose, electrolytes, and protein levels as needed. Additionally, the pet will need to have hepatic enzymes monitored daily for the first 72 hours, longer if the pet is showing increases in the hepatic enzymes. CBC should be monitored for anemia, leukopenia, leukocytosis, and thrombocytopenia. Coagulation profiles should be monitored, if the liver enzymes are significantly increased, or if there is suspicion of coagulopathy.

Prognosis is good with early treatment, but guarded in symptomatic animals. Published survival rates are between 50-68%. These low rates may also reflect the fact that many owners are not able to provide aggressive care for the pets, as this can be very expensive to treat.

Brunfelsia

Brunfelsia spp. are in the nightshade family and contain convulsants. All parts of the plant are toxic. The brunfelsamidine toxin appears to be water soluble. These plants are often used as ornamental plants in landscaping. Some common Brunfelsia plants include:

Brunfelsia americana (Lady of the Night) B. australis (Paraguay jasmine, morning-noon-and-night plant, yesterday-today-and-

tomorrow plant) B grandiflora B. lantifolia (kiss-me-quick) B pauciflora (yesterday-today-tomorrow, morning-noon-and-night, yesterday-and-today)

Clinical signs initially include GI upset (vomiting diarrhea). Neurologic signs, such as hyperesthesia, rigidity, tremors, and seizures often follow quickly. Emesis is not recommended, due to the rapid onset of signs. If the animal is not showing any clinical signs, activated charcoal is indicated, but monitor closely for hypernatremia. Animals should be monitored for signs of aspiration. Treatment consists of controlling the neurologic and GI signs. Antimetics should be given to help prevent vomiting. Seizures can be controlled with benzodiazepines, barbiturates, propofol, or gas anesthesia. Minimizing stimulation from light or sound often helps decrease seizures as well. Tremors can be controlled with methocarbamol or guaifensin. IV fluids should be instituted for support and to help prevent renal damage, if myoglobinuria develops. Treatment may last for days. It may take a week or more for mild tremors to completely resolve. Prognosis is good, as long as the clinical signs can be controlled and the pet does not aspirate.

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Insoluble Calcium Oxalate Containing Plants

There are a large number of plants that have insoluble calcium oxalate crystals as their toxic principle. Many of these plants are in the family Araceae. Many of these plants have broad green or variegated leaves and produce small flowers or do not flower. All parts of the plant are toxic.

Anthurium Sp. "Flamingo Plant" Begonia Aglaonema sp. Chinese Evergreen Dieffenbachia Dumbcane Schefflera Umbrella Plant Philodendron scandens var oxycardia Heartleaf Philodendron Sansevieria trifasciata Mother-In-Law's Tongue Spathiphyllum sp. Peace Lily Epipremnum aureum Pothos

The plants contain cells known as idioblasts. The cells contain raphides, which are spicules of calcium oxalate crystals. The raphides are sharp and needle-shaped. They are packed in a gelatinous substance. When the tip of the idioblast is broken, sap from the plant or saliva from an animal, enters the cell causing the gelatin to swell. The swelling forces the raphides to shoot from the cell, rather like a bullet. The crystals penetrate the oral mucosa, tongue, and throat causing mechanical damage. The cells may continue to expel crystals for a significant amount of time, even after a piece of plant material is swallowed. Chewing, bruising, tearing, or otherwise damaging the plant is necessary to produce effects.

Clinical signs caused by these plants include: oral pain, hypersalivation, vomiting, nausea, and diarrhea. These signs are usually mild and self-limiting and rarely require veterinary treatment. A small amount of dairy products usually provides relief from the oral pain. Swelling of the mucous membranes of the oral cavity, pharynx, and tongue are generally present. If significant swelling occurs, it is possible for dyspnea to develop but actual obstruction of the airway, though theoretically possible, is rare. Animals showing respiratory signs should be monitored at a veterinary hospital.

Lily Intoxication in Cats

Prompt and aggressive treatment of lily intoxication in cats is the most important factor in a favorable outcome. The lily should be first correctly identified by its Latin name. The common name of lily plants is often misleading. Calla Lily (Zantedeschia spp.), Peace Lily (Spathiphyllum sp.), Lily of the Valley (Convallaria majalis), African Lily (Agapanthus africanus) all have the lily name in their common name, but none of them present a risk of acute renal failure to cats. (Note: most of them do still present a toxic concern, from the insoluble calcium oxalate containing plants, such as Calla Lily and Peace Lily to the cardiotoxic Lily of the Valley, but the treatment would be markedly different than for true lilies.) All

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of the lilies that are of concern for acute renal failure in cats will have a common name that starts with Lilium or Hemerocallis. These include: Daylily (Hemerocallis spp.), Asiatic lily (Lilium aratum and Lilium speciousum), Easter lily (Lilium longiflorum), and Japanese lily (Lilium speciousum) are all "true lilies".

The toxic principle of lilies is not known. Any exposure to any part of the lily, even pollen should be considered potentially toxic and treated aggressively. The toxin is water soluble and even an exposure to water that plant material from lilies was in can cause renal failure.

Lily intoxication in cats can cause vomiting and lethargy initially. Renal failure is due to necrosis of renal tubular epithelial cells. Cats will typically become azotemic within 24-72 hours post exposure. Often, the creatinine is disproportionately increased when compared to the BUN. The phosphorus and potassium may increase as well. Some cats will develop pancreatitis as well.

Decontamination consists of emesis, and then a dose of activated charcoal, if possible. A warm water enema 12 hours post exposure may help evacuate plant material, if the cat is co-operative. Treatment and monitoring includes supportive care for any GI upset, IV fluid diuresis for 48 hours, and daily rechecks of the renal values and electrolytes for 72 hours. If bloodwork is normal at 72 hours, no further signs are expect.

Postponing treatment longer than 18 hours can result in renal failure and death. If the basement membrane remains intact, and tubular epithelial cells can regenerate with prompt, aggressive treatment. However, the basement membrane in the proximal renal tubules is disrupted in some cats. If the basement membrane is intact, in some cases, renal function has been restored after weeks of treatment with peritoneal dialysis or hemodialysis.

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