The 10 Most Common Toxicoses in Dogs
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Toxicology Brief managing common poisonings in companion animals PEER-REVIEWED The 10 most common toxicoses in dogs Irina Meadows, DVM, and Sharon Gwaltney-Brant DVM, PhD ogs are usually exposed to potentially toxic house- Chocolate hold products and medications accidentally. But 2 Chocolate contains two types of Dsometimes well-intentioned owners unknowingly methylxanthine, theobromine and caf- give their dogs harmful products and medications. To help feine, with their amounts varying de- prepare you for patients with theses toxicoses, we com- pending on the type of chocolate. For piled this list of the 10 most common hazards to dogs, example, milk chocolate contains about based on the number of calls we have received at the 60 mg/oz methylxanthine, dark chocolate about 150 mg/oz, ASPCA Animal Poison Control Center (APCC) between 2001 and baking chocolate about 450 mg/oz.3 and 2005.1 Clinical signs of chocolate ingestion range from GI upset to cardiovascular effects (e.g. tachycardia, hypertension or hy- Ibuprofen potension, arrhythmias) to CNS signs (e.g. agitation, pacing, hy- 1 Ibuprofen, a nonsteroidal anti- peractivity, tremors, seizures). The toxicity depends on the inflammatory drug with analgesic, anti- type of chocolate, the amount ingested, the size of the animal, inflammatory, and antipyretic effects,2 is and the animal’s sensitivity to methylxanthines. Mild stimula- available in a variety of strengths. The tion such as hyperactivity, agitation, and restlessness may most common over-the-counter occur in dogs ingesting around 20 mg/kg methylxanthine. strength is 200 mg, but the prescription-strength tablets can Cardiotoxicosis may occur in dogs ingesting 40 mg/kg, and contain up to 800 mg ibuprofen. Ibuprofen has a narrow dogs ingesting more than 60 mg/kg may exhibit severe CNS margin of safety in dogs, and acute toxicosis is common. signs, such as tremors and seizures.3 GI signs such as vomiting Dogs are often exposed to ibuprofen accidentally when and diarrhea can occur with any amount because of choco- they chew on a medicine bottle, but sometimes owners late’s high fat and sugar content. give ibuprofen to their dogs intentionally for pain control. Treating chocolate ingestion includes inducing emesis or Ibuprofen overdose can cause GI, renal, and central nerv- performing gastric lavage, administering activated charcoal ous system (CNS) effects. Doses of 25 mg/kg or more often (multiples doses are recommended with large ingestions), lead to gastrointestinal (GI) problems and ulceration, mani- monitoring the patient’s vital signs closely, and providing sup- fested as vomiting, diarrhea, or abdominal pain. Doses ap- portive care. Continuous electrocardiogram (ECG) monitoring proaching 175 mg/kg increase a dog’s risk of developing is advisable in cases in which cardiotoxicosis is expected. Per- acute renal failure,2 but older dogs or those with preexisting forming baseline serum chemistry profiles and monitoring renal compromise may exhibit renal failure at lower doses. electrolytes in symptomatic animals are also recommended. With doses greater than 400 mg/kg, CNS effects such as de- Dogs should be stabilized before you initiate decontamination pression, seizures, and comas may occur. procedures. Administer intravenous fluids to enhance methyl- Treatment for acute ibuprofen toxicosis includes induc- xanthine excretion, beta-blockers (e.g. propranolol, metopro- ing emesis, administering activated charcoal (multiple char- lol) to reduce tachycardia, and diazepam to control agitation coal doses are indicated to reduce enterohepatic recircula- and tremors. Methylxanthines can be reabsorbed from the tion in dogs that have ingested high doses of ibuprofen) bladder, so monitor urine output and consider placing a uri- and GI protectants (H2-blockers, sucralfate, misoprostol), and nary catheter to keep the bladder empty. Signs can last 24 to inducing diuresis with intravenous fluids at twice the main- 72 hours because of the long half-life of theobromine in dogs tenance rate while monitoring renal function. With timely (17.5 hours vs. 4.5 hours for caffeine).3 and appropriate treatment, most dogs are expected to have a positive outcome. Ant and roach baits 3 The product names may vary, and the containers may be referred to as cham- “Toxicology Brief” was contributed by Irina Meadows, DVM, and Sharon Gwaltney-Brant, DVM, PhD, ASPCA Animal Poison Control bers, discs, stations, systems, traps, baits, Center, 1717 S. Philo Road, Suite 36, Urbana, IL 61802. The department or trays, but most ant and roach baits use editor is Petra A. Volmer, DVM, MS, DABVT, DABT, College of Veterinary an attractant (often peanut butter), a Medicine, University of Illinois, Urbana, IL 61802. sweetening agent, and bread. And while these baits once con- tained compounds that are relatively highly toxic to mammals 142 MARCH 2006 Veterinary Medicine Toxicology Brief continued (e.g. arsenic trioxide, lead arsenate), the most common insecti- Ingesting a bromethalin-containing rodenticide may cause cides used in ant and roach baits today are boric acid, aver- vacuolization and severe spongiosis of the white matter mectin, fipronil, hydramethylnon, propoxur, and sulfluramid.1 within the CNS and cerebral edema.6 Bromethalin ingestion Because of the low concentration of the insecticide and can cause signs ranging from tremors and seizures (convul- the small size of the bait, serious toxicosis in mammalian sant syndrome) to weakness and paralysis (paralytic syn- pets ingesting the baits is not expected.4 In many instances, drome). Convulsant syndrome usually occurs at doses of 2.3 the risk of foreign body obstruction from the plastic or metal mg/kg and higher. Paralytic syndrome is more likely when a part of the container is of greater concern than the active in- dog ingests a lower dose.6 gredients. Signs of ingestion are usually limited to mild GI Ingesting cholecalciferol-containing rodenticides can in- upset and do not require specific treatment. crease dogs’ serum calcium and phosphorus concentra- tions, potentially leading to acute renal failure and tissue Rodenticides mineralization.7 4 The three main types of rodenticides Perform gastric decontamination procedures (induce emesis are those containing anticoagulants and administer activated charcoal with a cathartic) as soon as (warfarin, brodifacoum, diphacinone possible after any rodenticide ingestion. Do not induce emesis [also called diphenadione]), those con- in symptomatic animals (e.g. bleeding or seizing animals). taining bromethalin, and those contain- Treat anticoagulant-rodenticide ingestion with vitamin K1 ing cholecalciferol. orally for 14 to 30 days, depending on the specific active in- Anticoagulant rodenticides are probably the most com- gredient. It is recommended to evaluate the one-stage pro- monly used rodenticides in the world. Ingesting an anticoag- thrombin time at 48 hours after the last dose of vitamin K1. ulant rodenticide can block vitamin K-dependent clotting fac- An alternative to treatment is to monitor the prothrombin tor synthesis by inhibiting the 2,3-epoxide reductase enzyme, time at 48 and 72 hours after ingestion, and if elevated, initi- 8 which results in a coagulopathy three to five days after in- ate vitamin K1 therapy. Animals that have developed a coag- gestion (possibly sooner in immature animals).5 ulopathy may require whole blood or plasma transfusion and oxygen. The prognosis for animals that have developed 72 to 96 hours. If hyperphosphatemia or hypercalcemia oc- a coagulopathy is guarded and depends on the bleeding site. curs, perform saline diuresis, and administer corticosteroids, Because no specific treatment for bromethalin toxicosis is furosemide, or phosphate-binding agents. Salmon calcitonin available, aggressive decontamination is critical. If clinical or pamidronate may also be needed. Pamidronate, a signs develop, they are difficult to treat, and the patient’s bisphosphonate used in people to treat hypercalcemia of prognosis is guarded. Therapy is directed at resolving cere- malignancy, is a preferred agent in treating cholecalciferol bral edema and addressing seizures, usually by administering toxicosis.7 Although expensive, a single dose of pamidronate corticosteroids, furosemide, mannitol, and diazepam. Since is often sufficient to lower calcium concentrations enough the cerebral edema from bromethalin toxicosis is intra- that the animal can be returned home with minimal addi- myelinic,6 it does not respond well to standard therapy. Man- tional treatment. nitol, corticosteroids, and furosemide may temporarily lower cerebrospinal fluid pressure, but signs often progress once Acetaminophen these treatments are discontinued. 5 Acetaminophen is available as tablets, In rats, an extract of Ginkgo biloba was shown to reduce capsules, or liquids, either alone or com- the development of cerebral edema and brain lipid peroxi- bined with other compounds such as dation when administered orally immediately after gavage opioids, aspirin, caffeine, and antihista- with a lethal dose of bromethalin.6 Whether G. biloba or its mines. Acetaminophen toxicosis can re- extracts would influence the development of clinical signs in sult in hepatotoxicosis, methemoglobinemia, and facial and dogs with bromethalin toxicosis is unknown, but you may paw edema.9 Some dogs have developed transient kerato- wish to consider it in patients in which other options have conjunctivitis sicca after ingesting acetaminophen doses well been unsuccessful. below the amounts previously