When you have completed this chapter, you will be able to:
1 Describe steps in the managing of poison emergencies.
2 Discuss initial management of patients with ocular and dermal toxic exposures.
3 Describe procedures used in initial management of patients with oral toxic exposures.
4 List common topical insecticides and describe signs of toxicity and initial treatment of affected patients.
5 List common hazardous food and describe signs of toxicity and initial treatment of affected patients.
6 List common household substances and describe signs of toxicity and initial treatment of affected patients.
7 List common dangerous plants and describe signs of toxicity and initial treatment of affected patients.
8 List common hazardous pesticides and describe signs of toxicity and initial treatment of affected patients.
9 List common antifreeze products and describe signs of toxicity and initial treatment of affected patients.
10 List common hazardous human medications and describe signs of toxicity and initial treatment of affected patients.
Make sure to keep your practice organized with a dedicated area for emergency management of poisoned patients. The designated area should be centralized and stocked with key emergency supplies and drugs commonly used in toxicology. Maintain a library of related references in your practice, such as a current veterinary drug formulary, a current Physician’s Desk Reference (PDR), and clinical toxicology textbooks. Be wary of using the Internet as a sole source of information because there are thousands of sites with erroneous information.
Often the first instinct of an animal owner whose animal has been exposed to a poison is to call a veterinary practice. The technician should be able to recognize what constitutes a toxicologic emergency and what does not, give basic first-aid advice, and provide clear directions to the hospital, if needed. The following questions should be asked to evaluate the situation:
1. What is the current clinical status of the animal? Severe clinical signs necessitate immediate veterinary assistance.
2. What was the animal exposed to and through what route (oral, ocular, dermal)?
3. Has the owner taken any steps to treat the animal?
4. How old is the animal, and how much does it weigh?
5. How much was ingested (milligrams or quantity)?
7. Is the animal a male or female? If female, is she lactating or pregnant?
8. Does the animal have any history of health problems?
This information can be helpful to prepare for the office visit. After reviewing this information with your staff veterinarian, basic first-aid advice or at-home decontamination recommendations may be given and/or the client told to bring the animal into the hospital. While waiting for the client’s arrival, the technician can prepare the necessary equipment and medication. In addition, the technician can help investigate the toxicant by scanning a reference in the practice library or by consulting with veterinary toxicology specialists at the American Society for the Prevention of Cruelty to Animals (ASPCA) Animal Poison Control Center (888-426-4435) or accredited veterinary diagnostic laboratories (Box 35-1).
Initial management of a potential toxicoses starts with assessing the condition of the pet. The assessment should be performed quickly and include the following: an examination of the respiratory rate, capillary refill time, mucous membrane color, heart rate, and core body temperature. Examination of a pet that is unconscious, in shock, seizing, or in cardiovascular or respiratory distress must be conducted simultaneously with stabilization measures. With stable animals, the technician should obtain a comprehensive history of the pet and the exposure and perform a thorough physical examination.
As a general rule, treat the patient not the poison (Box 35-2). Establishing stabilization of the patient is essential before attempting any type of decontamination. A patent airway should be established and artificial respiration given if the animal is dyspneic or cyanotic. Artificial respiration may be required. The cardiovascular system should be monitored closely, preferably with a constant electrocardiogram (ECG) monitor, and any cardiovascular abnormality should be corrected. The placement of an indwelling intravenous catheter may be necessary for the administration of medications and intravenous fluids.
Signalment and history are crucial when dealing with a toxicosis and often affect the manner in which the animal is treated. Always get complete and accurate data about the animal.
There is no doubt that appropriate decontamination procedures have saved many animal lives. However, depending on the particular situation, certain methods of decontamination are more beneficial than others. The patient’s age, weight, and previous medical history can affect the method of decontamination.
Ocular Irrigation: With any ocular exposure, the eyes should be flushed repeatedly with water or saline solutions for a minimum of 20 to 30 minutes. Eye flushing should begin as soon as possible and often requires treatment at the pet’s home by the pet owner. Ocular exposure to corrosive agents should be considered an emergency. The eyes should be examined for corneal damage and monitored closely for excessive redness, lacrimation, or pain. Follow-up examinations or ophthalmic consultation may be needed to establish the level of corneal damage.
Dilution: Dilution with milk or water is recommended in cases of corrosive ingestion. A dosage of 1 to 3 ml/lb is suggested.
Emesis: Emesis is the technical term for inducing vomiting. The patient’s species, length of time since ingestion, the animal’s previous and current medical condition, and the type of poison can affect the decision to induce emesis.
Dogs, cats, pigs, and ferrets are able to vomit. Emesis is contraindicated in rodents, rabbits, birds, horses, and ruminants. Emesis is usually only productive within 3 hours of ingestion and is more likely to be productive if the animal is fed a small, moist meal before inducing vomiting.
Any animal who has a previous history of cardiovascular abnormalities, epilepsy, or recent abdominal surgery or is severely debilitated is not a candidate for emesis induction. Emesis should not be induced in any animal that (1) is severely depressed or in a coma (it could lead to aspiration), (2) is hyperactive (this could trigger a seizure), or (3) has already vomited.
Another factor affecting the decision to induce emesis is the nature of the substance ingested. Emesis is contraindicated for corrosive materials, such as cationic detergents, acids, and alkali. Induction of vomiting is not recommended with corrosives because of reexposure of the esophageal tissues to the corrosive material. Dilution with milk or water in combination with demulcents and gastrointestinal (GI) protectants is recommended in cases of corrosive ingestion.
Emesis is also contraindicated with hydrocarbon ingestion; the main concern is possible aspiration. Examples of hydrocarbon-containing products include lubrication oils, fuel oil, butane, propane, kerosene, mineral spirits, and gasoline.
Emetic Agents: A 3% hydrogen peroxide solution has been shown to be an effective emetic for dogs, cats, ferrets, and pigs. The mechanism of action of hydrogen peroxide is to cause a mild irritation to the gastric mucosa. The dosage for hydrogen peroxide is 1 tsp/5 lb and should not exceed 3 tbsp. Typically, vomiting occurs within 15 or 20 minutes as long as there is food in the stomach and the peroxide is fresh. If not, peroxide can be repeated one additional time.
Syrup of ipecac (never use the fluid of ipecac) is another product that owners may have in their homes. It acts both through gastric irritation and also stimulates chemoreceptor trigger zones, but it should be used cautiously because overdosing or repeated doses may cause cardiovascular problems.
Apomorphine hydrochloride is considered to be the preferred emetic agent by most small animal clinicians. Apomorphine is available in an injectable solution and as a capsule for conjunctival use.
Salt should never be used as an emetic. Salt is not an effective agent, and there have been cases of sodium toxicities reported as a result of its use as an emetic agent.
Activated Charcoal: Activated charcoal adsorbs a chemical or toxicant and facilitates its excretion via the feces. It is administered when an animal ingests organic poisons, chemicals, or bacterial toxins or if enterohepatic circulation of metabolized toxicants can occur. The recommended dose of activated charcoal for most species of animals is 1 to 3 g/kg body weight. Repeated doses of activated charcoal every 4 to 8 hours at half of the original dose may be indicated when enterohepatic recirculation occurs.
Activated charcoal can be given orally with a large syringe or with a stomach tube. In symptomatic or uncooperative animals, anesthesia may be needed. A cuffed endotracheal tube should always be used in the sedated or clinically depressed animal to prevent aspiration.
Activated charcoal is contraindicated in animals that have ingested caustic materials. These materials are not absorbed systemically, and the charcoal may make it more difficult to see oral and esophageal burns. Other chemicals that are not effectively absorbed by activated charcoal include ethanol, methanol, fertilizer, fluoride, petroleum distillates, most heavy metals, iodides, nitrate, nitrites, sodium chloride, and chlorate.
Cathartics: Cathartics increase the clearing of intestinal contents. Cathartics are used to enhance the elimination of activated charcoal and adsorbed toxicant. Cathartics can be added to solutions of activated charcoal, or a combination of activated charcoal and cathartic can be purchased. Contraindications for using cathartics include patients with diarrhea or dehydration.
Enemas: Enemas are helpful when elimination of toxicants from the lower GI tract is desired. The general technique is to use plain warm water or soapy warm water. Premixed enema solutions for humans are contraindicated in small animals because of the potential electrolyte and/or acid-base imbalance.
Gastric Lavage: Gastric lavage is a method of gently pumping the stomach contents out of the animal. Gastric lavage should not be performed in cases of caustic or petroleum distillate ingestion and should always be performed under general anesthesia using a cuffed endotracheal tube to protect the airway and prevent aspiration. The procedure involves inserting a fenestrated lavage tube two to three times the diameter of the endotracheal tube; it should be placed to the level of the xiphoid cartilage. The stomach should be lavaged repeatedly with physiologic temperature water until the fluid drawn out of the stomach is clear in color.
Enterogastric Lavage: Enterogastric lavage, also known as the through-and-through lavage, may be necessary when potentially lethal oral exposures have occurred. Following a gastric lavage, the stomach tube is left in place. An enema is performed to eliminate large pieces of fecal matter from the colon and upper large intestines. The distal end of the enema tube is attached to a water faucet, and body temperature water is slowly allowed to fill the tube and enter the intestinal tract in a retrograde manner. Water is allowed to flow until the water flows from the stomach tube. This process is continued until the color of the fluid passing out of the stomach tube is clear.
The technician plays a critical role by routinely evaluating vital signs and any parameters likely to be affected by the toxicants. Hydration can be assessed in the pet by checking skin turgor, capillary refill time, and the moisture of the oral mucous membranes. The animal’s body temperature should also be monitored closely.
Blood samples may be needed to perform complete blood count, chemistry panels, or clotting profiles to monitor the effects of the poison. Some toxicants, such as iron, copper, acetaminophen, and arsenic, can cause liver damage, whereas others, such as estrogen, lead, and antineoplastic medications, can cause anemia.
Daily fluid requirements should be maintained with compensation made for excessive fluid loss or to correct dehydration. Debilitated animals may require additional supplementation. An infusion pump should be used to prevent overhydration. The animal should be monitored for wet lung sounds or the development of a heart murmur, which could indicate overhydration. Pets with cardiovascular disease are at a higher risk for overhydration. Closely monitor pets with indwelling catheters to prevent entanglement in the line or chewing.
Diuresis may be beneficial for exposures to toxicants that can cause kidney damage or to enhance elimination of the toxicant. Examples of toxicants that can cause kidney damage include ethylene glycol (EG) antifreeze, zinc, mercury, oxalic acids, nonsteroidal antiinflammatory drugs, diquat herbicide, and aminoglycoside antibiotics. Adverse effects associated with diuresis include pulmonary edema, cerebral edema, metabolic acidosis or alkalosis, or water intoxication. Close monitoring is necessary.
Ancillary measures, such as nutritional support, are key components for complete recovery for the pet. Anorectic cats and ferrets are at risk for developing hepatic lipidosis and hypoglycemia; therefore it is extremely important to maintain nutritional requirements. A pharyngostomy tube may be necessary to provide adequate nutrition to the animal. Good nursing care should be continued until the pet completely recovers.
Some of the guidelines discussed in this chapter can be used to aid in the management of toxicoses in pets. Assessing the condition of the pet, stabilizing the animal, preventing absorption of the toxicant, controlling the signs, and instituting ancillary measures are critical areas in which the technician plays a key role. The best way to prevent serious problems resulting from toxicosis is poison prevention. Exercising caution with harmful substances by “pet proofing” the home environment is the only safe choice. The technician can educate pet owners on ways to make their homes poison safe. However, if a pet is exposed to a toxicant, prompt action will be needed to prevent potentially life-threatening problems. Refer to Box 35-3 for a quick reference chart of treatment protocols.
Topical spot on products are the newest method of insect control for pets and are commonly used because of their effectiveness and ease of use. Most of these products are applied between the shoulder blade or striped down the animal’s back and are applied every 30 days. Topical spot on products may repel or kill fleas, ticks, and or mosquitoes. Some products prevent flea egg development.
Topical insecticides have a wide safety range when used appropriately. However, all insecticides have a potential for adverse effects. Common adverse effects seen with appropriately used topical spot on products are mild and include application-site allergy and taste reactions.
In cases where the pet may have an allergic dermal reaction (mild redness at the application site or hair loss), the animal should be bathed in a mild liquid dishwashing detergent. Baths may need to be repeated to completely remove product residue. Afterward the animal should be rinsed well with warm water. The animal should also be towel dried to prevent chilling. Fractious animals may need to be sedated by a veterinarian for the procedure. Examination by a veterinarian may be needed if skin continues to be red or painful.
Ingestion of bitter tasting topical insecticides may result in a taste reaction with a pet. Dogs and cats are physically unable to spit out a bitter taste, so when they have a bad taste in their mouth, they drool to remove the taste. If the animal is breathing while drooling, the drool gets fluffy and becomes foam. Giving the animal a tasty treat, such as a few laps of milk mixes with water or tuna juice, will help dilute the bad taste and stop the drooling.
The following information contains details concerning the most popular types of topical flea control products.
Imidacloprid (1-[(6-Chloro-3-pyridinyl) methyl]-N-nitro-2-imidazolidinimine) is a chloronicotinyl nitroguanidine insecticidal agent. Imidacloprid spot on products are labeled to kill adult fleas and their larvae in dogs and cats. Advantage is the brand name. Imidacloprid is also found in combination with permethrin in dog-only products that also kill ticks. This product is K9 Advantix. In addition to its use in veterinary medicine, imidacloprid is also used in agriculture.
The dermal LD50 for rats is greater than 2000 mg/kg. According to the manufacturer’s technical profile, topically applied Advantage spreads rapidly over the skin by translocation. The product is not systemically absorbed, but goes to the hair follicles and glands where is it shed with sebum. Ingested imidacloprid is quickly absorbed from the GI tract. Within 48 hours, 96% is eliminated via urine (70% to 80%) and feces (20% to 30%).
The mechanism of action of imidacloprid is the blocking of the nicotinic pathways. This results in a buildup of acetylcholine at the neuromuscular junction. Acetylcholine buildup results in insect hyperactivity, then paralysis, and later insect death.
There is limited published information detailing adverse effects of imidacloprid in dogs or cats; however, clinical effects from the veterinary product used appropriately would be expected to be mild. Because the drug is bitter tasting, oral contact may cause excessive salivation.
As far as diagnostic testing, some laboratories can test for imidacloprid in hair and skin samples. However, these results can only confirm the exposure since toxic levels have not been determined.
Treatment for adverse effects would be symptomatic and supportive. Hypersensitivity skin reactions could occur with any topical product. In those instances, a bath with a noninsecticidal shampoo and symptomatic care, such as hydrocortisone, antibiotics, or antihistamines, would be recommended. Treatment of ingestion of topically applied veterinary imidacloprid product should consist of dilution with milk or water.
Fipronil is a phenylpyrazole antiparasitic agent used for fleas and ticks in dogs and cats. Fipronil is available as a topical product for flea and tick control and in combination with methoprene for additional control of immature flea stages. The brand name is Frontline. In addition to being used as a topical spot on for dogs and cats, it is also available in a veterinary formulation as a 0.29% topical spray.
The reported oral LD50 in rats for veterinary product formulations are greater than 5000 mg/kg.
The manufacturer states that fipronil collects in the oils of the skin and hair follicles and continues to be released over a period of time resulting in long residual activity. Topically applied, the drug apparently spreads over the body in approximately 24 hours via translocation. In oral rat studies, 5% to 25% of the parent compound and metabolites was excreted in the urine, and 45% to 75% was excreted in the feces.
Fipronil is classified as a GABA agonist. Its mechanism of action in insects is to interfere with the passage of chloride ions in GABA-regulated chloride channels, thereby disrupting CNS activity. Blockade of the GABA receptors by fipronil results in neural excitation.
There is limited published information detailing adverse effects of fipronil in dogs or cats; however, clinical effects from the veterinary product would be expected to be mild. Ingestion of any topical products may cause a taste reaction as a result of the inert ingredient. Extralabel use in rabbits has been reported to cause anorexia, lethargy, convulsion, and death.
Some laboratories can test for fipronil in hair and skin samples. However, these results can only confirm the exposure since toxic levels have not been determined.
Treatment for adverse effects would be symptomatic and supportive. If the exposure is dermal, the treatment would include initial stabilization and bathing with a mild dishwashing detergent. Treatment of ingestion of topically applied veterinary fipronil product should consist of dilution with milk or water.
Hypersensitivity skin reactions could occur with any topical product. In those instances, a bath with a noninsecticidal shampoo and symptomatic care, such as hydrocortisone, antibiotics, or antihistamines, would be recommended.
Selamectin is a semisynthetic avermectin used to treat flea infestations, prevention of heartworm disease, and for ear mites in both dogs and cats. The brand name is Revolution. Additionally, in dogs, it is indicated for sarcoptic mange (Sarcoptes scabiei) and tick infestations (Dermacentor variabilis). In cats, it is used as a parasiticide for hookworm (Ancylostoma tubaeformis) and roundworm (Toxocara cati).
The oral LD50 of selamectin is greater than 1600 mg/kg in rats. Oral overdoses in dogs of up to 15 mg/kg did not cause adverse effects (except for ataxia in one avermectin-sensitive collie). Topical overdoses (10×) to puppies caused no adverse effects; topical overdoses to avermectin-sensitive collies caused salivation. Topical overdoses of up to 10× caused no observable adverse effects in cats.
Following dermal application, selamectin is selectively distributed from the bloodstream to sebaceous glands of the skin where it forms reservoirs against fleas, ear mites, and Sarcoptes mites. Fecal excretion is responsible for its effectiveness against intestinal worms (roundworms, hookworms). The oral bioavailability of selamectin is reported to be 100% in cats and 62% in dogs. Bioavailability after topical application is 74% in cats and 4.4% in dogs.
Like other avermectin compounds, selamectin is thought to act by enhancing chloride permeability or enhancing the release of γ-aminobutyric acid (GABA) at presynaptic neurons. GABA blocks the postsynaptic stimulation of the adjacent neuron in nematodes or the muscle fiber in arthropods and causes paralysis and eventual death of the parasite.
Clinical effects from selamectin up to 10 times the normal dose are expected to be mild. According to the package insert of Revolution, approximately 1% of cats showed a transient, localized alopecia at the area of administration. Other effects reported (less than or equal to 0.5% incidence) include diarrhea, vomiting, muscle tremors, anorexia, lethargy, salivation, and tachypnea. Contact allergy could occur in especially sensitive animals with any topical product. Oral administration of the topical formulation, which might occur accidentally, caused mild, intermittent, self-limiting salivation and vomiting in cats. There were no adverse effects in avermectin-sensitive collies or in heartworm-positive dogs.
Some laboratories can test for selamectin in hair and skin samples. However, these results can only confirm the exposure since toxic levels have not been determined.
With adverse effects and overdoses of selamectin, the treatment would include initial stabilization and bathing with a mild dishwashing detergent. Treatment of ingestion should consist of dilution with milk or water. Activated charcoal has been shown to be effective in removing avermectin compounds during enterohepatic recirculation and could be considered with selamectin overdoses, whether oral or dermal. Supportive care and close monitoring of the CNS and respiratory system are also recommended. In cases of dermal hypersensitivity, a bath with a noninsecticidal shampoo and supportive care would be recommended.
Methoprene is a synthetic insect growth regulator and is classified as a terpenoid. It is used in topical flea control products to help break the flea life cycle alone or in combination with adulticide products. Methoprene does not kill adult fleas. Methoprene is found alone in many cat topical spot on products (e.g., Hartz Control One Spot for Cats) and also can be found in combination with adulticides (e.g., Frontline Plus).
In dogs, the acute oral LD50 of methoprene is 5000 to 10000 mg/kg. The World Health Organization (WHO) has approved methoprene safe for use in drinking water to control mosquitoes because of the minimal or no risk to humans, animals, or the environment.
Methoprene is classified as an insect growth regulator; it mimics the action of an insect growth regulation hormone. It is used as an insecticide because it interferes with the normal maturation process. In a normal life cycle, an insect goes from egg to larva, to pupa, and eventually to adult. Methoprene artificially stunts the insects’ development, making it impossible for insects to mature to the adult stages, thus preventing them from reproducing. Juvenile hormones maintain the larval stage in the insect or prevent metamorphosis; when the level of juvenile hormone drops, pupal and adult developmental stages begin.
There is limited published information detailing adverse effects of methoprene in dogs or cats; however, given the mechanism of action, clinical effects would be expected to be mild. Ingestion of any topical products may cause a taste reaction as a result of the inert ingredient. Topical hypersensitivity reactions could occur with any dermal product.
Some laboratories can test for methoprene in hair and skin samples. However, these results can only confirm the exposure since toxic levels have not been determined.
If the exposure is dermal, the treatment would include initial stabilization and bathing with a mild dishwashing detergent. Treatment of ingestion should consist of dilution with milk or water.
Hypersensitivity skin reactions could occur with any topical product. In those instances, a bath with a noninsecticidal shampoo and symptomatic care, such as hydrocortisone, antibiotics, or antihistamines, would be recommended.
Pyrethrins are derived from a combination of six insecticidal esters (pyrethrins, cinerins, and jasmolins) that are extracted from dried chrysanthemum flowers. They are fat-soluble compounds that undergo rapid metabolism and excretion after oral or dermal absorption. Rapid hydrolysis of ester linkage in the digestive tract results in low oral toxicity. Pyrethroids have a wide safety range in dogs. Cats have been shown to be extremely sensitive to concentrated permethrin, a synthetic pyrethrin.
Synthetic pyrethroids may cause a paresthesia dermally, which is a tingly sensation. This may occur in especially sensitive dogs. Signs noted from paresthesia include itchy skin, scratching at the application site, and agitation. Signs usually resolve with a cool bath and rinse. A cool compress held at the application site will help those dogs that are extrasensitive to the tingly sensation. Whereas dogs tolerate synthetic pyrethroids well, cats have been shown to be extremely sensitive to concentrated permethrin compounds.
Permethrin (3-phenoxyphenl)-methyl(-)cis-trans-3-(2,2-dichloroethenls)-2,2-dimethlcyclopropanecarboxalate is a synthetic pyrethroid insecticide. Permethrin is used in agricultural and household insecticides and also in flea control preparations. Permethrin has been shown to be effective against insects and is considered to have low toxicity in most mammalian species. The mechanism of action of permethrin occurs through its effect on the sodium channel in the nerve endings. The oral LD50 is more than 2000 mg/kg in rats.
Cats have been shown to be extremely sensitive to concentrated permethrin. Currently, there are more than 20 brands of permethrin spot on products available over the counter as spot on flea control labeled “for dogs only.” Product packaging of these products will have multiple warnings not to use on cats. However, inappropriate application of concentrated permethrin products can result in seizures and tremors in cats.
The first step for treating cats exposed to permethrin compounds involves controlling seizures or tremors with methocarbamol. Methocarbamol is a centrally acting muscle relaxant. The dose ranges from 44 mg/kg for mild cases up to 55 to 220 mg/kg for moderate to severe effects. Half of the dose should be given quickly (no faster than 2 ml/minute), then the rest to effect. A total 24-hour dose of 330 mg/kg/day should not be exceeded. Other choices for seizure or tremor control include propofol, barbiturates, diazepam, or inhalant anesthetics. Atropine is not an antidote for permethrin and is not recommended. Following stabilization, the cat should be bathed using a mild liquid dishwashing detergent. Supportive care, such as thermoregulation, fluid therapy to maintain hydration, and nutritional support, should be given as needed until full recovery. Some cats may experience difficulties for up to 3 days.
Etofenprox (also called ethophenprox) is an effective insecticide with a wide margin of safety in mammals. The mechanism of action of this compound is similar to that of the pyrethroid class of pesticides.
Structurally, etofenprox includes an ether unit instead of an ester unit, commonly found in pyrethroids. This structural difference is what differentiates etofenprox from pyrethroids and provides it with a higher LD50 than other pyrethroid compounds. The rat oral LD50 is more than 42,880 mg/kg and, the mouse oral LD50 is more than 107,200 mg/kg.
Etofenprox is used to treat fleas, ticks, and mosquitoes. The British Army has deemed etofenprox a safe and effective additive to nets and screens used in controlling arthropod vectors of disease in the United Kingdom.
Hypersensitivity skin reactions could occur with any topical product. In those instances, a bath with a noninsecticidal shampoo and symptomatic care, such as hydrocortisone, antibiotics, or antihistamines, would be recommended.
Pet owners are often tempted to give table scraps to their pets as a special treat. Pets that roam may come into contact with potentially dangerous food in trash cans or dumps. Unfortunately, there are some types of human food that can be dangerously toxic to pets. However, if a pet is exposed to a dangerous food item, prompt action will be needed to prevent a potentially life-threatening problem.
It is important that the veterinary staff is aware of the possible problems associated with feeding pets the following food.
Moldy food may contain certain tremorgenic mycotoxins, such as penitrem-A and roquefortine C. Tremorgenic mycotoxins can induce muscle tremors, ataxia, and convulsions that can last for several days. Tremorgenic mycotoxins are classified as neurotoxins. Severity of signs can vary from mild to severe, depending on the particular strength of the mycotoxin ingested. Diagnosis of tremorgenic mycotoxins involves sample analysis by an accredited veterinary diagnostic laboratory (see Box 35-1). Before submitting samples, always confirm availability of tests with the laboratory director. Treatment goals following tremorgenic mycotoxin ingestion include minimizing absorption through decontamination procedures, such as emesis, lavage, and activated charcoal; controlling tremors and seizures with methocarbamol; and providing supportive care. With early aggressive treatment, prognosis is good.
Chocolate is a mixture of cocoa beans and cocoa butter. It contains theobromine and caffeine, which are both classified as methylxanthines. Unfortunately, dogs are sensitive to the effects of methylxanthines. Depending on the dose, methylxanthines can cause hyperactivity, increased heart rate, tremors, and potentially death. Other effects seen with chocolate overdose include vomiting, diarrhea, increased thirst, increased urination, and lethargy. The amount of methylxanthines present in chocolate varies with the type of chocolate (Table 35-1). The general rule is the more bitter the chocolate, the more toxic it could be. Unsweetened baking chocolate contains almost seven times more theobromine as milk chocolate, and white chocolate (a combination of cocoa butter, sugar, butterfat, milk solids, and flavorings without cocoa beans) contains negligible amounts of methylxanthines.
TABLE 35-1
Type of Chocolate | Caffeine— mg/oz | Theobromine—mg/oz |
Milk chocolate | 6 | 44-56 |
Semisweet | 22 | 138 |
Baking chocolate | 33-47 | 393 |
The mechanism of action of methylxanthines is to competitively inhibit cellular adenosine receptors, which results in CNS stimulation and tachycardia. Although theobromine and caffeine have an LD50 of 100 to 200 mg/kg, signs can be seen well below this dose. Mild signs can be seen at doses more than 20 mg/kg, moderate effects are seen more than 40 mg/kg, and severe effects are seen at doses more than 60 mg/kg. Early treatment, including decontamination procedures, such as emesis and activated charcoal; cardiovascular monitoring; and supportive care, is extremely helpful with chocolate poisoning. In addition, fluid diuresis may help enhance elimination. Caffeine can be reabsorbed by the bladder wall, which may result in extended times of clinical signs. Therefore the veterinary staff should take extra steps to keep the patient’s bladder empty either through catheterization or frequent walking.
Onions and other members of the Allium family can be harmful to dogs and cats. Other members of this genus include garlic, leek, shallot, and chive. Pieces of onion, onion powder, or even cooked onion can cause damage to red blood cells (RBCs), which could result in anemia. The primary toxic principle is n-propyl disulfide, which is thought to cause oxidative damage to erythrocytes, resulting in hemolysis. Toxicoses from fresh, dried, or powdered plant material have been reported in dogs and cats. In one study, dogs developed hemolytic anemia after being fed 30 g/kg of onions once daily for 3 days. Feeding commercial baby food containing onion powder has also been reported to cause toxicity in cats. Clinical signs associated with onion poisoning include hemolytic anemia, hemoglobinuria, vomiting, weakness, and pallor. Decontamination procedures, such as inducing emesis and administering activated charcoal, should be considered with recent ingestions. Afterward the animal should be monitored for the development of hemolysis, azotemia, and/or decreased packed-cell volume (PCV). Whole-blood transfusions or administration of oxygenated hemoglobin should be considered with critical patients. Fluid diuresis is recommended in patients with hemoglobinuria. In addition, supportive care should be administered until patient recovery.
Macadamia nuts may cause problems if ingested by dogs. According to a retrospective study, clinical signs commonly reported in dogs ingesting macadamia nuts include weakness, depression, vomiting, ataxia, tremors, and hyperthermia. The lowest dose reported to cause clinical effects is 2.4 g/kg. In most cases, dogs developed clinical signs within the first 12 hours after ingestion. These signs have only been seen in dogs, and the exact cause for their sensitivity is unknown. Treatment includes decontamination procedures, such as inducing emesis, administering activated charcoal, and administering enemas. Additional supportive care should be given as needed. The prognosis in most cases is extremely good. Most dogs return to normal within 24 to 48 hours.
Ingestion of rising bread dough can be life threatening to dogs. The animal’s body heat will cause the dough to rise in the stomach. Ethanol is produced during the rising process; the dough may expand several times its original size. Signs seen with bread dough ingestion are associated with ethanol toxicoses and foreign body obstruction and may include severe abdominal pain, bloating, vomiting, incoordination, and depression. In cases of recent ingestion in asymptomatic dogs, emesis could be induced. Analgesia is important in patients exhibiting signs of pain. Administering cool water via a stomach tube or PO may halt the rising process. In some cases, dough removal may necessitate surgery. Since ethanol can cause an acidosis, it is important to monitor the acid-base balance and correct with sodium bicarbonate, if indicated.
Some types of grapes and raisins have been shown to cause kidney failure in dogs when eaten in quantity. The basis for kidney failure following consumption of grapes or raisins is unclear, but is currently being studied in the veterinary community. The amount of grapes or raisins that may cause renal failure is not exactly known, so any amount could potentially be dangerous. As for treatment of recent ingestion, inducing vomiting and administering activated charcoal is recommended. This should be followed with fluid diuresis for 48 hours. During this time, the patient should be monitored for azotemia. If the animal shows evidence of renal failure, fluids and supportive care should be continued.
Tobacco products contain varying amounts of nicotine, with cigarettes containing 13 to 30 mg and cigars containing 15 to 40 mg. Butts contain about 25% of the total nicotine content. The minimum lethal dose in dogs and cats is reported as 20 to 100 mg. Signs often develop quickly (usually within 15 to 45 minutes) and include excitation, tachypnea, salivation, emesis, and diarrhea. Muscle weakness, twitching, depression, tachycardia, shallow respiration, collapse, coma, and cardiac arrest can follow the period of excitation. Death occurs secondary to respiratory paralysis. With recent ingestion in asymptomatic animals, emesis can be induced. Never attempt emesis in stimulated animals because it may trigger a seizure. Activated charcoal has been shown to be helpful in adsorbing nicotine. Patients should be monitored closely and treated symptomatically. Artificial respiration would be indicated in patients with respiratory paralysis.
Xylitol is a sugar alcohol that is commonly found in many human food items (gum, snacks, and beverages). It may also be found in certain dental washes intended for use in pets. Xylitol’s primary use is as a sugar substitute, but it also has plaque-blocking properties. Xylitol toxicity has been well documented in dogs. In dogs, xylitol causes severe hypoglycemia secondary to the release of insulin. There also have been reports of liver failure and coagulopathy. Hypoglycemic symptoms of xylitol poisoning in dogs occur soon after ingestion (within 30 minutes) and include weakness, depression, ataxia, and vomiting. Biochemical analysis may note increased liver enzymes (ALT, AST) and/or liver failure within 18 to 72 hours after xylitol ingestion.
All ingestion of xylitol products by a dog necessitates veterinary treatment and blood work monitoring. Emesis should be performed with recent ingestions unless contraindications are present. Alternatively, gastric lavage should be considered. It is not known if activated charcoal is of benefit in adsorbing xylitol. Following decontamination, the dog’s blood glucose should be monitored frequently for hypoglycemia. During the monitoring period, the animal should have access to tasty food and encouraged to eat. If hypoglycemia is noted, intravenous fluids with dextrose should be used to normalize the blood glucose. In addition, chemistry panel and clotting tests should be performed initially and then repeated to monitor for liver failure and coagulopathy.
Hydrochloric, sulfuric, nitric, phosphoric acids, oxalic acid, and sodium bisulfate are examples of acids. Common sources of acid include toilet bowl cleaners, drain openers, metal cleaners, antirust compounds, gun barrel cleaners, automobile battery fluid, and pool sanitizers. Acids are corrosives and can produce severe burns on contact with tissue. Acids produce tissue damage at the site of contact. Severity of tissue damage produced is directly related to the concentration. Concentrated acids may produce severe burns on contact with any part of the body and the GI tract if ingested. When acids are diluted or have higher pH, they do not cause corrosion, only irritation. Most cases of exposure to acids that are irritants usually result in mild self-limiting signs of nausea, vomiting, or diarrhea. Oxalic acids include ethanedioic and dicarboxylic acid and can also cause kidney damage.
Alkali are used as drain openers, oven cleaners, bleaches, industrial cleaners, denture cleaners, bathroom and household cleaners, radiator cleaning agents, and hair relaxers and in alkaline batteries, electric dishwasher soaps, some oven cleaner pads, and cement.
Lesions from alkalis are typically deeper and more penetrating than those from acidic compounds. The ability of alkalis to generate corrosive injury depends on the concentration, pH, viscosity, amount ingested, and the duration of contact with tissue. Serious corrosive injury is unlikely to occur from substances with a pH less than 11. Alkali with a pH of 12.5 can cause esophageal ulcers, and those with a pH of 14 or more can cause esophageal perforation.
Household bleaches are used as a bleaching or oxidizing agent, a deodorant, or disinfectants. Household bleaches mainly contain less than 5% sodium hypochlorite, and household mildew removers contain up to 5% calcium hypochlorite. Nonchlorine bleach or colorfast bleaches may contain sodium peroxide, sodium perborates, or enzymatic detergents. Commercial bleaches may also contain other bleaching agents, such as sodium peroxide, sodium perborate, sodium carbonate, or oxalic acid.
Household bleaches contain low concentrations of bleach and are mild to moderate mucosal irritants. Commercial forms of alkaline bleach contain higher concentrations, and if the pH is 11 to 12 or greater, it can produce partial-thickness chemical burns. At higher concentration, corrosive effects could be seen.
Detergents are nonsoap surfactants in combination with inorganic ingredients, such as phosphates, silicates, or carbonates. Detergents are classified according to their charge in solution: nonionic, anionic, and cationic surfactants.
Anionic and nonionic detergents are found in shampoos, dishwashing detergents, laundry detergents, and electric dishwashing detergents. Anionic and ionic detergents are irritants, and their toxicity is generally limited to cutaneous, ocular, oral, or GI irritation. They are considered to be low in toxicity. However, when used in coordination with caustic substances, such as sodium tripolyphosphate and various carbonates, they can be corrosive.
Cationic detergents can be found in fabric softeners, some potpourri oils, hair mousse, conditioners, germicides, disinfectants, and sanitizers. Cationic detergents are rapidly absorbed and may produce severe local and systemic toxicity. Oral ulcerations, stomatitis, and pharyngitis can be seen in the cat at concentrations of 1% or less.
For recent ocular exposure to corrosive acids or alkali, a minimum of 20 to 30 minutes irrigation with tepid tap water or physiologic saline is recommended. Afterward the eye should be examined by a veterinarian and closely monitored for evidence of corneal ulceration.
Following dermal exposure to corrosives, the animal should be bathed immediately with a mild liquid hand or dish detergent or a noninsecticidal shampoo. The animal should be monitored and treated as needed by a veterinarian for burns, erythema, swelling, pain, or pruritus. Veterinary treatment for skin damage may include pain medication, antiinflammatory agents, and antibiotics.
In cases of ingestion of corrosive agents, do not induce vomiting because of potential corrosive effects. Preferred initial treatment should be oral dilution with a few laps of milk or water. Following, the patient should be monitored and treated by a veterinarian for oral or esophageal burns. With ingestion of oxalic acid products, additional care with intravenous fluids is necessary to prevent kidney problems.
Heavy metals are a group of elements that lie between copper and bismuth on the periodic table that have specific gravities greater than 4. The ones most commonly associated with toxicity in pets include zinc and lead.
Zinc: Sources of zinc include hardware, such as wire, screws, bolts, and nuts, and U.S. pennies. Pennies minted since 1983 contain 99.2% zinc and 0.8% copper, and one penny contains approximately 2440 mg of elemental zinc. One penny can cause zinc poisoning in a small dog. The process of galvanization involves the coating of wire or other material with a zinc-based compound to prevent rust. Owners are often not aware of galvanization on the wire used for making bird cages. Pet food and water dishes may also be galvanized, and sufficient zinc may leak into the water or food to create toxicity. Although the exact toxicologic mechanism of zinc in animals is not known, zinc toxicosis can affect the renal, hepatic, and the hematopoietic tissues. Clinical signs of zinc toxicoses may include polyuria, polydipsia, hemoglobinuria, diarrhea, weight loss, weakness, anemia, cyanosis, seizures, and death. Hemolytic anemia is also frequently encountered.
Diagnosis: Radiography of the abdomen may reveal the presence of metallic objects in the GI tract. Serum zinc levels may be obtained using blood collected from plastic syringes (no rubber grommets) and stored in Royal blue top Vacutainers to minimize contamination with exogenous zinc. In general, blood zinc levels of greater than 200 μg/dl (2 ppm) are considered to be diagnostic in avians. Normal serum and urine zinc concentrations in dogs are 0.7 to 2 ppm, and zinc concentrations of toxicosis are usually above 10 ppm. The pancreas is considered to be the best tissue for postmortem zinc analysis. Pancreatic tissue zinc levels greater than 1000 μg/g are suggestive of a zinc toxicosis.
Treatment: It is imperative to remove the sources of zinc from the GI tract. Removal of zinc-containing foreign bodies via endoscopy or gastrotomy or enterotomy may be required. The success of the removal process can be assessed with radiographs. Activated charcoal is not indicated because it is of little benefit in binding zinc. Bulk cathartics, psyllium∗ (sodium sulfate at 125 to 250 mg/kg), peanut butter, mineral oil, and corn oil may aid in the removal of zinc objects from the GI tract. The use of chelators may not be necessary in cases where prompt removal of the zinc source is accomplished. In addition, treatment for symptomatic animals should include blood replacement therapy as needed, parenteral fluids, and good nursing care, such as forced feeding or hand feeding.
Lead: Sources of lead include paint, toys, drapery weights, linoleum, batteries, plumbing materials, galvanized wire, solder, stained glass, fishing sinkers, lead shot, foil from champagne bottles, and improperly glazed bowls. Lead affects multiple tissues, especially the GI tract, renal, and nervous system. Lead combines with erythrocytes in circulating blood increasing RBC fragility, anemia, and capillary damage. It can also cause segmental demyelination of neurons and necrosis of renal tubular epithelium, GI tract mucosa, and liver parenchyma. Clinical signs seen with lead poisoning are often vague and may include lethargy, weakness, anorexia, regurgitation, polyuria, ataxia, circling, and convulsions.
Diagnosis: Radiography of the abdomen may reveal evidence of metallic objects. Blood levels of lead are helpful to confirm lead toxicoses with suspicious radiographic changes. Whole blood levels greater than 0.6 ppm are viewed as diagnostic for lead toxicosis when accompanied by appropriate clinical signs in birds. Lead levels below 35 μg/dl are rarely associated with clinical signs in dogs. The basophilic stippling and cytoplasmic vacuolization of RBCs are not always seen with lead poisoning in avian species.
Treatment: Removal of lead particles via bulk-diet therapy, endoscopy, or surgery is recommended. Succimer and calcium ethylenediaminetetraacetic acid (Ca EDTA) are both considered to be effective chelating agents. Fluid therapy is recommended to prevent renal effects from Ca EDTA during treatment. Penicillamine and diethylenetriamine pentaacetic acid (DTPA) have also been used to treat lead toxicoses. Since lead can be immunosuppressive, broad-spectrum antibiotics may be indicated. In addition, good supportive care, including seizure control, is recommended until full recovery.
Ant Baits: Ant and roach baits are common objects found in households. The product names may vary, and they may be referred to as hotels, disks, stations, systems, traps, baits, or trays. The baits usually contain inert ingredients, such as peanut butter, breadcrumbs, sugar, and vegetable or animal oils. Insecticides used most commonly in these baits are sulfluramid, fipronil, avermectin, boric acid, and hydramethylnon. These insecticides have a wide safety range and are present in small quantities within the baits, making them a hazard of low toxicity to dogs and cats.
Silica Gel Packets: Silica gel is used as a desiccant and often comes in paper packets or plastic cylinders. They are used to absorb moisture in leather, medication, some food packaging, and some types of cat litter. Silica is considered “chemically and biologically inert” upon ingestion. However, with ingestion, it is possible to see signs of GI upset, such as nausea, vomiting, and inappetence, although signs are expected to be mild or not present with the ingestion of small amounts. Additional problems could occur if the silica gel was used as a desiccant in medication since silica is able to absorb small quantities of the medication.
Toilet Water With Tank Cleaning Drop-In Tablets: Toilet tank “drop-in” tablets typically contain corrosive agents (alkali or cationic detergents). Corrosive effects could be seen if the actual tablet was chewed. When a tank “drop-in” cleaning product is used in a toilet, the actual concentration of the cleaner is low in the toilet bowl of water. With dilution by the bowl water, the cleaning agent is just a gastric irritant. Common signs seen with ingestion include mild vomiting and nausea.
Glow Necklaces: Dibutyl phthalate, also known as n-butyl phthalate, is a liquid found in various glow-in-the-dark products. Jewelry containing dibutyl phthalate is commonly sold at fairs, carnivals, and novelty stores. Pets are often attracted to the glowing jewelry. Almost all pets that bite into glow-in-the-dark jewelry drool or foam at the mouth excessively in response to the bitter taste. Some pets will also exhibit hyperactivity and aggressive behavior most likely resulting from discomfort with the unpleasant taste.
Liquid Potpourri: Liquid potpourri may contain essential oils and cationic detergents, both of which can be harmful. Because product labels may not list ingredients, it is wise to assume any liquid potpourri contains both ingredients. Essential oils can cause mucous membrane and GI irritation, CNS depression, and dermal hypersensitivity and irritation. Severe clinical signs can be seen with potpourri products that contain cationic detergents (see discussion under Detergents). Dermal exposure to cationic detergents can result in redness of the skin, tissue swelling, intense pain, and ulceration. Ingestion of cationic detergents can lead to tissue necrosis and inflammation of the mouth, esophagus, and stomach.
Batteries: Flashlights, remote controls, battery-operated toys, watches, calculators, hearing aids, etc., all provide the opportunity for animals to be exposed to batteries. The alkaline material within a battery can cause burns that can penetrate deeply into the local tissue. In addition, battery casings may result in GI obstruction if swallowed. When batteries are chewed and the contents released, alkaline burns can result. Signs of foreign body obstruction may occur when casings are swallowed. Treatment of battery exposure is as for exposure to any alkaline product and includes observation and treatment by a veterinarian (see discussion under Alkali). Radiographs are often used to determine the location of the battery when the casing is missing.
Pennies: Ingestion of coins by pets, especially dogs, is not uncommon. Of the existing U.S. coins currently in circulation, only pennies pose a significant toxicity hazard. Pennies minted since 1983 contain 99.2% zinc and 0.8% copper, making ingested pennies a rich source of zinc; one penny can cause a zinc toxicosis. Other potential sources of zinc include hardware, such as screws, bolts, or nuts, all of which may contain varying amounts of zinc. In the stomach, gastric acids leach the zinc from its source, and the ionized zinc is readily absorbed into the circulation where it causes intravascular hemolysis (breaks apart the RBC).
Veterinary treatment is always required for ingested pennies. Treatment may include inducing vomiting or removal of zinc-containing objects using an endoscope or through surgery. Often treatment includes blood replacement therapy, as needed, intravenous fluids, and other supportive care.
Mothballs: Veterinary treatment of mothball ingestion is always required. Mothballs may be composed of either 100% naphthalene or 99% paradichlorobenzene. Naphthalene-based mothballs are approximately twice as toxic as paradichlorobenzene, and cats are especially sensitive to naphthalene. One 2.7-g mothball contains 2700 mg of naphthalene. Naphthalene causes Heinz bodies, hemolysis, and occasionally methemoglobinemia. Paradichlorobenzene primarily affects the liver and CNS, although methemoglobinemia and hemolysis have been reported in humans.
Ice or Snow Melts: The most common ingredients in ice melts are sodium chloride, potassium chloride, magnesium chloride, calcium carbonate, and calcium magnesium acetate. A few ice melts contain urea. Sodium ion toxicosis is possible after large ingestion of ice melts, salt, or rock salt. Signs reported in one dog with fatal hypernatremia (increased sodium level in blood) from salt ingestion included vomiting, increased thirst, increased urination, fine muscular fasciculation, sinus tachycardia, metabolic acidosis (acidic blood pH), and seizures.
These are a wide variety of common plants that can be poison to animals if consumed. Refer to Box 35-4 for a list of some of these plants.
Members of the Rhododendron species, including azalea and rhododendrons, contain gray anatoxins, which can lead to cardiovascular dysfunction (Figure 35-1).
FIGURE 35-1 Members of the Rhododendron species, including azaleas and rhododendrons, contain gray anatoxins that can lead to cardiovascular dysfunction.
Clinical signs in dogs and cats include vomiting, diarrhea, abdominal pain, weakness, depression, cardiac arrhythmias, hypotension, shock, cardiopulmonary arrest, pulmonary edema, dyspnea, CNS depression, and seizures. Signs generally occur within 4 to 12 hours of ingestion and may persist for several days. Poisonings have also been reported in ruminants and horses. Veterinary treatment and observation is always recommended.
Hundreds of cardiac glycosides have been identified in various plants, including oleander (Nerium oleander) (Figure 35-2), lily of the valley (Convallaria majalis) (Figure 35-3), and foxglove (Digitalis purpurea) (Figure 35-4). In most cases, all parts of the plant are toxic, and even small amounts can cause significant clinical signs.
FIGURE 35-2 A, B, Nerium oleander. There are hundreds of cardiac glycosides identified in various plants, including oleander, lily of the valley, and foxglove.
Clinical signs generally develop within several hours of ingestion, and signs may persist for several days after removal of plant material from the GI tract. Clinical signs seen most commonly involve the GI tract and cardiovascular system. Veterinary treatment and observation is always recommended.
Castor beans (Ricinus communis) are often used in jewelry, and the oil extracted from the seeds is used medicinally (castor oil). Ricin is the toxic principle of castor beans and is considered to be one of the most potent plant toxins known. All parts of the castor bean plant are toxic, but the seeds contain the highest concentration of ricin. In humans, ingestion of one seed is potentially lethal. Veterinary treatment and observation is always recommended.
Cycad palms (Cycas, Zamia) are found naturally in the sandy soils of tropical to subtropical climates, but may also be grown as houseplants in more temperate climates (Figure 35-5). Cycasin is considered to be the toxic principle that is responsible for the hepatic and GI signs generally seen with toxicosis. Most parts of the plant are toxic, but the seeds contain a higher concentration of cycasin and are more often associated with toxicosis in small animals. Ingestion of one or more seeds has resulted in liver failure and death in dogs.
Easter lilies (Lilium longiflorum) (Figure 35-6), Tiger lilies (Lilium tigrinum), Rubrum or Japanese lilies (Lilium speciosum and Lilium lancifolium), and various day lilies (Hemerocallis spp.) can cause acute renal failure and death in cats (Figures 35-6 and 35-7). The toxic principle is unknown. Even minor exposures (a few bites on a leaf, ingestion of pollen, etc.) may result in toxicosis. All feline exposures to lilies should be considered potentially life threatening.
FIGURE 35-6 Lilium longiflorum, or Easter lily. Acute renal failure and death can occur in cats that consume various lilies. These include the Easter lily, Tiger lily, Day lily, and the Rubrum or Japanese lily.
Affected cats often vomit within a few hours of exposure to lilies, but the vomiting usually subsides after a few hours, during which time the cats may appear normal or may be mildly depressed and anorexic. Within 24 to 72 hours of ingestion, oliguric to anuric renal failure develops accompanied by vomiting, depression, anorexia, and dehydration.
Elevations in kidney blood values can occur as early as 12 to 18 hours after ingestion. Death from acute kidney failure generally occurs within 3 to 6 days of ingestion.
Veterinary treatment and observation is always recommended with lily ingestion in cats. Early decontamination by a veterinarian (emesis, oral activated charcoal, and cathartic) in combination with intravenous fluid therapy has been shown to effectively prevent lily-induced kidney failure. Conversely, delaying treatment beyond 18 hours frequently results in death or euthanasia as a result of severe kidney failure. Dialysis can be of help with severely affected animals, but it is not commonly available.
Philodendron species, calla lily (Zantedeschia spp.), elephant ears (Caladium spp.), dumb cane (Dieffenbachia spp.) mother-in-law’s tongue (Monstera spp.) (Figure 35-8), peace lily (Spathiphyllum spp.), pathos (Epipremnum spp.), and certain other varieties of plants contain insoluble calcium oxalate crystals in their plant material. Chewing of the plant material can cause the crystals to be expelled into the oral cavity and can result in painful oropharyngeal edema. Clinical signs associated with these plants include oral irritation; intense burning and irritation of the mouth, lips, and tongue; excessive drooling; vomiting; and difficulty in swallowing. Airway compromise from tissue swelling could be life threatening, although severe effects are a rare occurrence.
The most dangerous forms of pesticides include snail bait containing metaldehyde, fly bait containing methomyl, systemic insecticides containing Di-Syston or disulfoton, and zinc phosphide.
Methomyl is a highly toxic carbamate insecticide that can be found in fly baits. Carbamate insecticides competitively inhibit both acetylcholinesterases and pseudocholinesterases. Acetylcholinesterase inhibitors cause muscarinic, nicotinic, and CNS system effects. Exposure to methomyl may lead to cholinergic crisis with increased salivation, lacrimation, urinary incontinence, diarrhea, GI cramping, and emesis (SLUDGE) syndrome, but the most obvious sign is severe seizures. Hypertension and slow heart rate or cardiorespiratory depression may occur. Immediate veterinary treatment and observation is always required because signs can occur within minutes of methomyl ingestion.
Metaldehyde is a polymer of acetaldehyde and is commonly found in snail or slug bait and is toxic. Onset of clinical signs is typically within 30 minutes to 3 hours. Common clinical signs seen with metaldehyde ingestion include increased heart rate, nervousness, panting, drooling, incoordination, hyperthermia, tremors, and seizures. In some cases, liver failure may occur within 2 to 3 days after exposure. Veterinary treatment and observation is always required.
Zinc phosphide is used in mole and gopher baits and is considered to be highly toxic. Following ingestion, phosphide is converted to phosphine gas by stomach acid (the conversion is enhanced with the presence of food and water). Released phosphine gas causes severe respiratory distress. Clinical signs are seen soon after ingestion, typically within 15 minutes to 4 hours. Death occurs secondary to respiratory failure. Veterinary treatment and observation is always required.
Disulfoton (also known as Di-Syston) is a selective, systemic organophosphate insecticide and is highly toxic. Systemic insecticides are applied to the soil and then are actively taken up by plant roots and translocated to all parts of the plant. Onset of clinical signs is 2 to 8 hours after ingestion, and signs can last for several days. Clinical signs seen with a toxicosis include typical cholinesterase inhibitor SLUDGE signs, but they can also have hemorrhagic diarrhea and liver and pancreatic enzyme elevations. Veterinary treatment and observation is always required. Good nursing care is essential. Prognosis is good to guarded depending on the severity of the signs. Complete recovery from acute effects may take several days or weeks.
There are three main types of rat or mouse baits available commercially: anticoagulants, bromethalin, and cholecalciferol. Other pesticides, such as strychnine, aldicarb, and zinc phosphide, may be used to control wild rat and mouse populations.
Anticoagulants (Table 35-2) include:
TABLE 35-2
Type of Anticoagulant | Minimum Duration of Therapy |
Warfarin | 14 days |
Bromadiolone | 21 days |
Brodifacoum and others | 30 days |
The anticoagulant rodenticides act by competitive inhibition of vitamin K epoxide reductase, thus halting the recycling of vitamin K. In early cases of toxicoses, the prothrombin time (PT) when checked between 36 and 72 hours will be elevated, but the animal will still appear clinically normal. Beyond 72 hours, hemorrhage is a possible effect. The presence of circulating clotting factors in normal animals is the reason for the delay in the development of signs.
Clinical signs of anticoagulant poisoning may not be observed for 5 to 10 days after ingestion and include hemorrhage, pale mucous membranes, weakness, exercise intolerance, lameness, dyspnea, coughing, and swollen joints. Often the animal is not seen by the veterinarian until signs are severe.
Animals with clinical signs should be stabilized immediately. Transfusions with whole blood or plasma may be necessary to replace clotting factors. Decontamination is only effective early; remember, clinical signs are usually delayed 5 to 10 days after ingestion. Any elevation in the PT warrants full treatment with vitamin K1. No treatment is indicated if PT remains normal; however, recent vitamin K1 administration could result in misleading PT values because new clotting factor synthesis only requires 6 to 12 hours. Oral vitamin K1 is an antidote for anticoagulants. Vitamin K1 should be given with a fatty meal to enhance absorption.
Bromethalin is an uncoupler of oxidative phosphorylation. Bromethalin causes a reduction of adenosine triphosphate (ATP). ATP is necessary to sustain the sodium-potassium ion channel pumps. When the pump mechanism is inhibited, fluid buildup occurs, which results in fluid-filled vacuoles between myelin sheaths. This leads to decreased nerve impulse conduction.
Clinical signs of bromethalin toxicosis could occur within 24 hours to 2 weeks and include muscle tremors, seizures, hyperexcitability, forelimb extensor rigidity, ataxia, CNS depression, loss of vocalization, paresis, paralysis, and death.
Aggressive decontamination is most important with bromethalin ingestion. Repeated doses of activated charcoal (every 8 to 12 hours) are recommended. Supportive care should be given, as needed, for clinical signs. The prognosis is poor for animals showing severe signs. Animals exposed at lower doses exhibiting paralysis may recover. Agents such as mannitol, furosemide, and corticosteroids may reduce the cerebral edema. Unfortunately, these drugs were of little benefit in reducing the severity of signs in experimental animals. Ginkgo biloba has been used experimentally in rats with bromethalin poisoning, although the true benefit is not known.
Cholecalciferol (vitamin D3) increases intestinal absorption of calcium, stimulates bone resorption, and enhances kidney reabsorption of calcium. This results in a serum calcium increase. This can lead to kidney failure, cardiovascular abnormalities, and tissue mineralization.
Clinical signs usually have a delay in onset and usually occur 18 to 36 hours after ingestion. The most common signs seen with cholecalciferol toxicosis include vomiting, diarrhea, inappetence, depression, polyuria, polydipsia, and cardiac arrhythmia. Kidney failure arises from the deposition of calcium in the kidney.
Aggressive decontamination is most important with cholecalciferol ingestion. Repeated doses of activated charcoal (every 8 to 12 hours for 1 to 2 days) are recommended.
Close monitoring of the serum calcium, phosphorus, creatinine, and blood urea nitrogen (BUN) is recommended.
Renal effects are treated with fluid diuresis. Prednisone and furosemide are often used with treatment. Pamidronate inhibits osteoclastic bone resorption and has been used successfully to treat cholecalciferol poisoning. Alternatively, salmon calcitonin has been used to decrease calcium levels.
Methanol (also known as methyl alcohol or wood alcohol) is found most commonly in “antifreeze” windshield washer fluid and varies in concentration from 20% to 100% (with 20% to 30% the most common form). Methanol’s metabolite, formaldehyde, is rapidly oxidized by aldehyde dehydrogenase to formic acid, which can cause metabolic acidosis if significant quantities are ingested and retinal toxicity in humans and nonhuman primates. In general, alcohols are rapidly absorbed from the GI tract. The minimum toxic dose in dogs is 8.0 g/kg (or 3 oz of 100% methanol). The most common exposures occur with dogs and usually involve chewing on containers or lapping up spills. With small exposures in dogs and cats, only mild gastric upset is seen. Recent small ingestion is treated with dilution (milk and water) that may help minimize gastric upset. Large exposure would be expected to only occur when there is no other water source available. In the case of a large ingestion, the animal should be monitored and treated for acidosis.
Propylene glycol is the main ingredient in “safer” forms of engine antifreeze or coolants. Propylene glycol is approximately three times less toxic in dogs than EG. According to a study, no clinical signs were seen when a dog was given an acute dose of 20 ml/kg.
In toxic quantities, acidosis, liver damage, and renal insufficiency are possible from propylene glycol. Clinical signs of propylene glycol toxicosis include CNS depression, weakness, ataxia, and seizures. With large ingestion, diuresis and supportive care, such as treatment for acidosis, should be given.
Ethylene glycol is the most dangerous form of antifreeze. Most commercial antifreeze products contain between 95% and 97% EG. The minimum lethal dose of undiluted EG antifreeze is 4.4 to 6.6 ml/kg in dogs and 1.4 ml/kg in cats. EG can cause metabolic acidosis and acute renal tubular necrosis. In most cases of EG poisoning, vomiting is seen within the first few hours, and within 1 to 6 hours, signs of depression, ataxia, weakness, tachypnea, polyuria, and polydipsia occur. By 18 to 36 hours, acute renal failure occurs.
Diagnosis: Peak levels of EG are reached within 1 to 4 hours after ingestion. There is one commercial EG kit available for veterinary use (EGT Kit PRN Pharmacal, 800-874-9764). EG tests can be run as early as 30 minutes after ingestion up to 12 hours. The EGT Kit is labeled for dogs and detects a level greater than 50 mg/dl. Since cats are more sensitive than dogs, the kit may not be sensitive enough to diagnose a toxicosis in the cat. Some human labs may run a quantitative EG analysis to detect levels and could be considered with feline exposures. False-positive test results can occur from propylene glycol (in some types of activated charcoal solutions and also from some injection solutions, such as pentobarbital and diazepam) or from formaldehyde.
Treatment: Induction of emesis is only helpful with recent exposures (less than 1 hour). To prevent false-positive EG tests, it is recommended to take a blood sample before administering activated charcoal since many products contain propylene glycol as inactive ingredients. Although its effectiveness is controversial, activated charcoal can be given within 1 to 3 hours of ingestion. Gastric lavage with activated charcoal could be considered, but would only be effective early.
EG is metabolized via alcohol dehydrogenase to glycoaldehyde, which is then metabolized to glycolic acid, which is then metabolized to glyoxylic acid. Glycoaldehyde is more toxic than EG. The formation of glycolic acid is thought to be responsible for causing metabolic acidosis. The goal of treatment of EG toxicoses is to slow down the metabolism.
Fomepizole (Antizole Vet by Orphan Medical, 888-8-ORPHAN) is used to inhibit alcohol dehydrogenase and is considered the preferred treatment for treating EG toxicoses in dogs, but is not effective in cats.
Ethanol can be used in cats and dogs. Ethanol also competes with EG as a substrate for alcohol dehydrogenase; however, it does have several unfavorable side effects, which include CNS depression, hyperosmolality, and metabolic acidosis. Fluid diuresis and correction of acidosis with sodium bicarbonate is also an important part of therapy. Peritoneal dialysis should be considered with anuric animals. Prognosis is good with early aggressive treatment (less than 8 hours of ingestion).
Please note that any medication can be dangerous to an animal, depending on the dose and frequency. The following is a list of potentially dangerous medications. All require veterinary consultation, treatment, and monitoring.
Acetaminophen is a synthetic nonopiate derivative of p-aminophenol. Acetaminophen toxicity can result from a single toxic dose or repeated cumulative dosages, which lead to methemoglobinemia and liver damage. In dogs, acetaminophen is used therapeutically for analgesia at a dose of 10 mg/kg q 12 hours. Clinical signs of toxicity are not typically observed in dogs unless the dose exceeds 100 mg/kg, at which dose hepatotoxicity is possible. At 200 mg/kg, methemoglobinemia is a possibility. In cats, 10 mg/kg has produced signs of toxicity.
Clinical signs of acetaminophen toxicity are related to methemoglobinemia and hepatotoxicity. Clinical signs include depression, weakness, tachypnea, dyspnea, cyanosis, icterus, vomiting, methemoglobinemia, hypothermia, facial or paw edema, hepatic necrosis, and death.
Ibuprofen is a substituted phenylalkanoic acid with nonsteroidal antiinflammatory, antipyretic, and analgesic properties. Ibuprofen has been used therapeutically in dogs at 5 mg/kg, but because it can cause gastric ulcers and perforations, it is generally not recommended.
According to studies of acute ingestion of ibuprofen in dogs, vomiting, diarrhea, nausea, anorexia, gastric ulceration, and abdominal pain can be seen with doses of 50 to 125 mg/kg; these signs in combination with renal damage can be seen at doses at or above 175 mg/kg. At doses at or above 400 mg/kg, CNS effects, such as seizure, ataxia, and coma, may occur. Cats are considered to be twice as sensitive as dogs because they have a limited glucuronyl-conjugating capacity.
The most common signs of ibuprofen toxicoses include anorexia, nausea, vomiting, lethargy, diarrhea, bloody diarrhea, ataxia, increased urination, and increased thirst. Postmortem lesions associated with ibuprofen toxicoses include perforations, erosion, ulceration, and hemorrhage of the GI tract.
The primary goal of treatment is to prevent or treat gastric ulceration, renal failure, CNS effects, and possibly hepatic effects. Prognosis is good if the animal is treated promptly and appropriately. Delay in treatment can decrease survival potential with large exposures.
Aspirin is used therapeutically in dogs and cats (acceptable daily doses [ADDs]). Aspirin must be used cautiously in cats because of their inability to rapidly metabolize and excrete salicylates. Symptoms of toxicity may occur if given doses frequently or without stringent monitoring. Aspirin should be used cautiously in neonatal animals; adult doses may lead to poisoning. Symptoms of acute aspirin overdose in dogs and cats include depression, vomiting (may be blood tinged), anorexia, hyperthermia, and increased respiratory rate. If treatment is not provided, muscular weakness, pulmonary and cerebral edema, hypernatremia, hypokalemia, ataxia, and seizures may all develop with eventual coma and death.
Ma huang is used as an herbal weight loss aid and contains the sympathomimetic alkaloids ephedrine and pseudoephedrine. Ephedrine and pseudoephedrine act as stimulants and are also found in cold and flu medications as nasal decongestants and are similar in structure to amphetamines. They can cause increased blood pressure, tachycardia, ataxia, mydriasis, hyperactivity, tremors, and seizures. Ephedrine and pseudoephedrine are eliminated by the kidneys. The half-life varies with urine pH. With an overdose, it is common to see clinical signs last for more than 24 hours.
Isoniazid (INH) is a medication used to treat tuberculosis and has a narrow margin of safety. Isoniazid is available as an elixir, injectable, syrup, and tablets in strengths of 50, 100, and 300 mg. Overdoses produce life-threatening signs: seizures, acidosis, and coma. Pyridoxine (vitamin B6) is a direct agonist of INH.
Calcipotriene is a synthetic derivative of vitamin D3. It is used as a topical ointment to treat psoriasis in humans. An overdose of calcipotriene can cause hypercalcemia that can result in kidney failure, cardiac failure, and possibly death. In most cases, dogs that have ingested toxic levels of calcipotriene start showing signs of lethargy, weakness, and inappetence within 1 to 2 days after exposure. Serum calcium levels would be expected to increase within 12 to 72 hours. Hypercalcemia, hyperphosphatemia, azotemia, proteinuria, and tissue mineralization can occur with overdoses. Bradycardia and cardiac arrhythmia are also expected.
5-Fluorouracil (5-FU) is an anticancer topical cream. It is used in human patients to treat solar and actinic keratoses and some superficial skin tumors. Topical fluorouracil is available as 1% or 5% cream (5-FU can inhibit ribonucleic acid [RNA] processing and functioning and deoxyribonucleic acid [DNA] synthesis and repair). The toxicity effects of 5-FU, as with other anticancer agents, is mainly through its destruction of rapidly dividing cell lines, such as bone marrow stem cells and the epithelial layer of the intestinal crypts.
Early effects seen with 5-FU in the dog include generalized grand mal seizures, tremors, vomiting, and ataxia. Cardiac arrhythmia, respiratory distress, and hemorrhagic gastroenteritis are also seen. Clinical signs develop within 1 hour and are usually life threatening. Often death occurs within 6 to 16 hours after exposure. In those that survive initial effects, it is possible to see bone marrow suppression with evidence of neutropenia 4 to 20 days after exposure.
Ahn, A. Introducing etofenprox: a broad-spectrum, comprehensive ectoparasiticide. Hartz Companion Anim Newsletter. 2006;4(2):1–3.
Beasley, V.R., Dorman, D. Management of toxicoses. Vet Clin North Am. 1990;20(2):307–338.
Beasley, V.R., et al. A Systems affected approach to veterinary toxicology. Urbana, Ill: University of Illinois Press; 1999.
Birckel P, Cochet P, Benard P et al: Cutaneous distribution of C-fipronil in the dog and cat following a spot on administration. In von Tscharner C, Willemse T, editors: Proceedings from the Third World Congress of Veterinary Dermatology, Edinburgh, 1996.
Bishop, B.F., et al. Selamectin: a novel broad-spectrum endectocide for dogs and cats. Vet Parasitol. 2000;23(91):3–4. 163-176
Bough, M.G. Castor bean toxicosis: one mean bean. Vet Technician. 2002;23(8):498.
Cheeke, P.R. Natural toxicants in feeds, forages, and poisonous plants, ed 2. Danville, Ill: Interstate Publishers; 1998.
Dunayer, E.K. Xylitol ingestion in dogs. Vet Med. 2006;101(12):791–796.
Dunayer, E.K., Gwaltney-Brant, S.M. Acute hepatic failure and coagulopathy associated with xylitol ingestion in eight dogs. JAVMA. 2006;229(7):1113–1117.
Foss, T. Liquid potpourri and cats. Vet Technician. 2002;23(11):686–689.
Gfeller, R., Messonier, S.M. Handbook of small animal toxicology and poisonings, ed 2. St Louis: Mosby; 2004.
Gwaltney, S.M. Chocolate intoxication. Vet Med. 2001;96(2):108–111.
Hainzl, D., Cole, L.M., Casida, J.E. Mechanisms for selective toxicity of fipronil insecticide and its sulfone metabolite and desulfinyl photoproduct. Chem Res Toxicol. 1998;11(12):1529–1535.
Hansen, S.R., et al. Macadamia nut toxicosis in dogs. Vet Med. 2002;97(2):274–276.
Hovda, L.R., Hooser, S.B. Toxicology of newer pesticides for use in dogs and cats. Vet Clin Small Anim. 2002;32:455–467.
Hull, W. Ethylene glycol testing. Vet Technician. 2001;22(4):201–206.
Krautmann, M.J., et al. Safety of selamectin in cats. Vet Parasitol. 2002;23(91):3–4. 393-403
Means, C. The Wrath of grapes. ASPCA’s Anim Watch. 2002;22(2):15.
Means, C. Bread dough toxicosis in dogs. J Vet Emerg Crit Care. 2003;13(1):39–41.
Mindy, G.B. Dermal decontamination: dealing with sticky situations. Vet Technician. 2003;24(8):538–540.
Moorman, M. Anticoagulant rodenticides now more toxic to pests and pets. Vet Technician. 2002;23(1):34–36.
Moorman, M. Bromethalin: it’s not what you think. Vet Technician. 2003;24(7):484–486.
Novotny, M.J., et al. Safety of selamectin in dogs. Vet Parasitol. 2002;23(91):3–4. 377-391
Ogawa, E., et al. Effect of onion ingestion on anti-oxidizing agents in dog erythrocytes. Jpn J Vet Sci. 1986;48(4):685–690.
Peterson, M.E., Talcott, P.A. Small animal toxicology. Moscow, Idaho: University of Idaho; 2001.
Plumlee, K.H. Nicotine. In: Peterson M.E., Talcott P.A., eds. Small animal toxicology. Philadelphia: WB Saunders, 2001.
Plumlee Konnie, P. Clinical veterinary toxicology. St Louis: Mosby; 2004.
Ramesh, C., et al. Pharmacologic profile of methoprene, an insect growth regulator, in cattle, dogs, and cats. JAVMA. 1989;194(3):410–412.
Richardson, J.A. Permethrin spot-on toxicoses in cats. J Vet Emerg Crit Care. 2000;10(2):103–106.
Richardson, J.A. Poison prevention and management primer. Vet Technician. 2002;23(3):150–156.
Richardson, J.A., et al. Managing pet bird toxicoses. Exotic DVM. 2001;3(1):23–27.
Schell, M.M. Tremorgenic mycotoxin intoxication. Vet Med. 2000;95(4):283–286.
Simmons, D.M. Onion breath. Vet Technician. 2001;22(8):424–427.
Steenbergen, V.M. Beautiful lilies: a potential cat-astrophe. Vet Technician. 2002;23(4):236–237.
Steenbergen, V.M. Acetaminophen and cats. Vet Technician. 2003;24(1):43–45.
Tamara, F. The hazards of ice melts to dogs and cats. Vet Technician. 2002;23(2):94–104.
Webster, M. Product warning, Frontline. Aust Vet J. 1999;77:202.
Wismer, T.A. Novel insecticides. In: Plumlee K.H., ed. Clinical veterinary toxicology. St Louis: Mosby, 2003.
∗Toxicology Brief is a column written by ASPCA Animal Poison Control Center veterinary technicians for Veterinary Technician, a peer-reviewed journal published monthly by Veterinary Learning Systems.