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10 Emerging Poisonings Kevin T. Fitzgerald, Ph.D., D.V.M., D.A.B.V.P. Staff Veterinarian VCA Alameda East Veterinary Hospital Denver, Colorado INTRODUCTION Companion animals can frequently encounter a variety of intoxicants in or around the domestic household. The bedroom, the bathroom, the kitchen, basements and garages, and the yard all may house over-the-counter medications, prescriptions drugs, pesticides, and a myriad of other molecules capable of proving toxic. As a consequence of this proximity, veterinary emergency clinicians treat a large number of poisonings. Successful management of poisoned animals includes initial telephone triage, obtaining a thorough history from the client, initial stabilization, decontamination (if appropriate), diagnostic testing, and careful selection of effective treatment. Veterinarians must comprehend the mechanism of action of a poison, its pharmacokinetics (absorption, distribution, metabolism, and excretion), and whether a toxic dose has been ingested. A number of resources (animal poison helpline, veterinary colleges, and local toxicologists) are available to clinicians particularly if the toxic molecule is not well known, if the toxic molecule has a narrow margin of safety, or if the toxic molecule is a human medication not familiar to veterinarians. Each year thousands of new, potentially toxic, molecules receive patents and are made available to the public. In this discussion, we will look at the toxic potential for a number of toxins being seen more frequently. Veterinarians must make every effort to stay current with regard to substances potentially toxic to companion animals. 1) MARIJUANA Although for most states, possession of any marijuana is illegal and federal law bans the drug, some states allow medicinal use of marijuana under certain circumstances with more states expected to follow suit. Furthermore, a few states here decriminalized possession of marijuana for personal use. Similar legislation in other states is anticipated. As a result of the changes with regard to the legal status of marijuana making it more accessible, an increase in the number of accidental intoxications in pets (especially dogs) can be expected. Nowhere is this more probable than in the ingestion of edible marijuana products by companion animals. Marijuana: the major psychoactive constituent is delta-9tetrahydrocannabinol (THC). Mechanism of action: The precise action that THC has upon the nervous system is as yet unknown. Nevertheless, action at the cannabinoid receptor is thought to cause all clinical effects of THC. Toxic dose: THC has a wide margin of safety with the minimum lethal oral dose greater than 3g/kg. This dose is 1,000 times the amount needed to see behavioral effects. Clinical signs: In dogs, clinical signs include ataxia and incoordination, hypersalivation, disorientation, hypothermia, mydriasis, bradycardia, vomiting, depression, and tremors. Nearly half of dogs display urinary incontinence. Signs may vary with dosage, size and age of the dog, and underlying medical conditions. In dogs, onset of clinical signs is generally within one hour of ingest. Treatment: There is no specific antidote for cannabis. Prognosis: The majority of dogs ingesting THC recover completely with no long-term adverse effects. 2) ADDERALL TOXICITY (Amphetamine – Dextroamphetamine) Attention deficit hyperactivity disorder (ADHD) is the most commonly diagnosed neurobehavioral disorder affecting 3% to 7% of school-aged children in the US. Adderall (amphetamine-dexamphetamine salts) is a drug used in treating ADHA and neurolepsy. Recently, we have seen an increase in companion animals poisoned with this drug. Mechanism of Action: The primary action is the release of catecholamines (particularly dopamine and norepinephrine) for presynaptic terminals. These increases in neurotransmitters cause sympathetic nervous stimulation. Toxic dose (dogs): 9 - 11 mg/kg methamphetamine hydrochloride 20 – 27mg/kg amphetamine sulfate Clinical signs: hyperactivity, hypersalivation, hyperthermia, mydriasis, tachycardia, increased blood pressure, ataxia, seizures, repetitive stereotypical behaviors. Treatment: The mainstays of treatment of amphetamine poisoned animals are supportive care, control of behavior, management of arrhythmias, stopping seizures, and temperature reduction. Prognosis: Although the clinical signs of this toxicity are dramatic, most animals show no long-term clinical consequences of Adderall toxicity. 3) XYLITOL Xylitol is a sugar alcohol and sucrose substitute used in dietetic candies, gums, and snacks for diabetics. Mechanism of Action: For dogs, xylitol produces a rapid, dosedependent insulin release followed by a dramatic, significant hypoglycemia. Clinical Signs: Vomiting, weakness, ataxia, hypokalemia, seizures, and coma. Severe cases can lead to liver failure. Toxic Dose: This can be 0.5 – 1.0 g/kg. Each stick of gum can contain 1.0 grams. Treatment: Therapy includes dextrose containing fluids, liver protectants and antioxidants. Activated charcoal is of no use. Liver enzymes and coagulation status should be monitored closely. Prognosis: This depends upon the size of the dog, the amount ingested, and how long it has been since ingestion. 4) GRAPES AND RAISINS Some dogs appear particularly sensitive to raisin and grape ingestion. Other dogs never show clinical signs after ingestion. The smallest amount of grape/raisin ingestion leading to renal failure has been 0.7oz/kg (for grapes) and 0.11oz/kg (for raisins). This can be as little as 3 to 7 raisins. Mechanism of Action: At present, the toxic principle in grapes and raisins is unknown. Analysis of involved grapes and raisins has been negative for alcohol, fungi, heavy metals, and pesticides. Clinical Signs: Signs include anorexia, vomiting, depression, and dehydration. Signs develop in 6 to 12 hours after ingestion. Treatment: Therapy includes aggressive intravenous fluid diuresis for 48 hours at 1 1/2 to 2x maintenance. Renal values and urine output should be closely monitored. Symptomatic treatment of vomiting and renal failure may be required. Prognosis: The outlook is good for dogs with normal values at 48 to 72 hours post-ingestion. Prognosis is guarded for animals presenting already in renal failure. 5) MACADAMIA NUTS Macadamia nuts are a popular snack from trees grown primarily in Hawaii. Recently, macadamia nuts have been reported to cause toxicosis, so far only documented in dogs. Mechanism of Toxicity: Currently, the toxic agent responsible for macadamia nut toxicosis is unknown. Toxic Dosage: One roasted macadamia nut weighs between 2.1 and 3 grams. The minimum toxic dosage has been reported to be 1 nut/kg. As little as 5 to 40 nuts have been shown to be toxic in a 20 kg dog. Dogs experimentally given 20 g/kg all developed clinical signs within 6 hours. Clinical Signs: Weakness, inability to rise, ataxia, tremors, and occasionally vomiting. Treatment: Therapy is supportive and symptomatic. Most dogs can be successfully managed with intravenous fluids and antibiotics. Many dogs can be treated symptomatically at home. Prognosis: The prognosis for dogs after macadamia nut ingestion is excellent. Resolution in the vast majority of cases occurs within 24 to 48 hours. No long term sequellae have been noted. 6) PAINT BALLS Paint balls contain different colored paints inside gelatin and glycerol capsules. Recently, dogs ingesting paint balls have been shown to display clinical signs. Mechanism of Action: Ingredients in paint balls; glycerol, sorbitol, and polyethylene glycol are tremendously osmotically active agents. They cause fluid shifts from body tissue into the bowel lumen (osmotic diarrhea), and cause dehydration, increased plasma osmolality, and hypernatremia. These electrolyte disorders cause acid base imbalances that lead to weakness, ataxia, and seizures (neurological signs). Occasionally, dogs die. Clinical Signs: Vomiting, diarrhea, ataxia, weakness, tremors, and seizures. Treatment: Therapy includes emesis, if the patient is brought in early enough, and intravenous fluids with dextrose and halfstrength (0.45%) NaCl. Activated charcoal is of no value. Fluid rates may need to be high to counter the diarrhea. Warm water enemas may help stimulate paint ball movement through and out of the G.I. tract. Electrolytes should be frequently monitored. Prognosis: Prognosis for paint ball ingestion is good if animals are made to vomit the paint balls early and if they are put on intravenous fluids not long after the ingestion incident. 7) CYCAD (SAGO) PALM Decorative, tropical plants brought into the house as ornamentation. They are palm-like in appearance. Mechanism of Action: The major toxicant (Cycasin) is a gastrointestinal irritant that causes hepatic necrosis. This toxic glycoside is mutagenic, carcinogenic and teratogenic. The second toxicant (BMAA) is a neurotoxic amino acid that causes cerebellar necrosis. A third, as yet unidentified, toxin is also present. All parts of the plant are toxic, but the highest concentration of toxicants occurs in the seeds. Only female plants produce seeds. As few as two seeds can cause symptoms. Clinical Signs: Signs of sugar palm toxicosis include vomiting, diarrhea, anorexia, ataxia, liver signs, and seizures. Signs occur within 12 to 24 hours of ingestion. Lesions produce first G.I. hemorrhage, then liver cirrhosis and necrosis. Treatment: Therapy includes emesis if patient presents early enough, gastrointestinal protectants, intravenous support, and close electrolyte monitoring. Gastric hemorrhage can be severe with animals needing a transfusion. Prognosis: The outcome is good if treatment starts before clinical signs arise. If severe signs are already in place, the prognosis becomes guarded. 8) NICOTINE Animals can be exposed to various forms of nicotine in tobacco products and smoking cessation aids. Cigarettes, cigars, chewing tobacco, and snuff contain nicotine ranging from 9 – 15 mg per cigarette to 5 times that in a cigar. Chewing tobacco often has flavoring agents that make it attractive to dogs. Nicotine gum has about 4mg per stick and patches contain up to 114mg of nicotine. Mechanism of Action: Nicotine stimulates post-synaptic receptors of the CNS, sympathetic, and parasympathetic nervous systems. Initial stimulatory effects are followed by blockage of receptors due to persistent depolarization. Clinical signs develop within one hour of exposure. The median lethal dose (LD50) is 9.2mg/kg for dogs. Clinical Signs: Signs of intoxication with nicotine include salivation, vomiting, diarrhea, increased heart rate, excitement, tremors, and possibly convulsions. Eventually, depression with paralysis occurs. Death is caused by paralysis of the diaphragm and chest muscles leading to cessation of breathing. Treatment: Therapy begins with emesis, if the patient is seen soon enough, and activated charcoal. The heart rate should be monitored and abnormalities treated. Antacids should not be given as they can increase G.I. absorption of nicotine. Oxygen may be necessary if respiratory paralysis is a possibility. Seizures can be controlled with anticonvulsants. Prognosis: Patients stabilized within 4 hours of ingestion have a much better chance for survival. Exposures to very high dosages of nicotine have a poor prognosis. 9) TACROLIMUS The drug Tacrolimus (Protopic, Prograf) is a human immunosuppressant used in dogs to treat perianal fistulas. Dermal use on anal ulcers causes no toxicological signs but ingestion of a tube of the substance can cause adverse effects. Mechanism of Action: It is unknown at this time. Clinical Signs: In both experimental and clinical studies, Tacrolimus has been shown to cause vomiting and intussusceptions in dogs. Intussusceptions occur in 2 to 6 days following ingestion. Treatment: Therapy for Tacrolimus ingestion involves emesis if early enough, followed by intravenous fluids, activated charcoal and vigilance. There is no known antidote. Prognosis: The prognosis is good if emesis is carried out early and no signs of intussusceptions have developed. Surgery may be necessary to repair this intestinal condition. 10) NAPHTHALENE (MOTHBALLS) Naphthalene is most commonly associated with mothballs. Currently, paradichlorobenzene has replaced naphthalene in mothballs. Naphthalene is twice as toxic as “new” mothballs. It is dry appearing, white, and crystal. It has a characteristic odor. Mechanism of Action: G.I., dermal, and ocular effects are caused by the very irritating nature of naphthalene. It causes naphthalene induced hemolytic anemia, with Heinz body formation, and red cell lysis. It may lead to cataract formation. Each mothball has about 2.7g of naphthalene. Anemia has been reported at 411 mg/kg. Clinical Signs: Clinical signs reported include: vomiting, diarrhea, anorexia, and G.I. bleeding. Gastrointestinal signs are followed by signs of hemolytic anemia. Pale mucus membranes, dyspnea, ataxia, and collapse due to the anemia are the final signs. Treatment: Therapy includes emesis if discovered early enough, followed by activated charcoal and G.I. protectants. Blood transfusion and oxygen may be necessary. Prognosis: Clinical outcome is favorable is therapy is aggressive and started early. 11) POLYURETHANE ADHESIVES Polyurethane adhesive expanding wood glues (Gorilla Glue, Elmer’s Probond Polyurethane Adhesive, etc.) have been associated with gastric foreign bodies in dogs. Mechanism of Action: When even a small bottle (2oz of adhesive) is ingested, the adhesive polymerizes into a large friable ball that lines the gastric lumen. The adhesive absorbs water, expands, and continues to expand due to the heat of the stomach environment. Clinical Signs: Signs resulting from polyurethane adhesive ingestion are those of a G.I. foreign body. Anorexia, vomiting, and depression are common. Treatment: Therapy involves radiographs to visualize the presence of the foreign body in the stomach and no emesis due to the risk of the glue expanding into the esophagus. Evidence of a foreign body may be visible on stomach films at 4 hours but may take 24 hours to maximally show up. The only therapy for this condition is surgical removal of the glue ball. Prognosis: Prognosis depends upon how much glue has been ingested, the size of the animal, and how long the condition has gone on. Surgical excision of the foreign body should be curative. CONCLUSION Each year 3,400 new molecules are licensed for use in American homes. Detergents, glues, and cleansers, and this does not begin to list the new plant species, new drugs, etc. that become available. People (and animals) are constantly bombarded by new substances and the potential for these new substances to be toxic. We must be ever vigilant and strive to provide a safe environment both for ourselves and our companion animals.