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Potential toxins for "homebound" pets (Proceedings)


Dogs [mostly sight breeds] have been known to exhibit severe hyperthermia following ingestion of 'raw' or spent hops [Humulus lupulus].

Dogs [mostly sight breeds] have been known to exhibit severe hyperthermia following ingestion of 'raw' or spent hops [Humulus lupulus]. Rectal temperatures are often > 108 F, and are sometimes very difficult to control. The diagnosis is most commonly made following the observation of hops in vomitus of the affected patient. Commonly reported clinical signs include restlessness and excessive salivation, vomiting, abdominal tenderness, excessive panting and weakness. Treatment should be directed at lowering the core body temperature. Techniques can include IV fluid therapy [accompanied by rectal enemas], cool towel wraps, fans and isopropyl alcohol. If dantrolene is available, one can try an initial dose of 2-3 mg/kg IV [or 3.5 mg/kg PO], followed by 3.5 mg/kg q 12 hrs as necessary.

High concentrations of sodium chloride can be found in many homemade play dough formulations. Clinical signs following ingestion may include vomiting, polydipsia, polyuria, tremors, hyperthermia and seizures. The lowest dose associated with clinical signs is reported as being 1.9 g/kg BW. Seizures are consistently seen when serum sodium concentrations exceed 180 mEq/l. Hypernatremia can be complicated by lack of available water or underlying renal insufficiency. A typical recipe consists of 2 cups of flour, 1 cup of salt, and ½ to 1 cup of water - this is roughly equivalent to 8.4 grams of sodium chloride per tablespoon. Decontamination should be initiated if the exposure has occurred within 60 minutes and the patient is asymptomatic. Serum sodium levels should be monitored. For the hypernatremic patient, the treatment involves slowly correcting the water deficit over a 48-72 interval with isotonic or hypotonic fluids. It is recommended that serum sodium levels should not decrease faster than 0.5 to 1.0 mEq/l/hr.

Dibutyl phthalate is present in many glow-in-the-dark products, and its toxicity potential is considered low. However, pets chewing these products might experience salivation, along with hyperactivity and aggressive behavior. The chemical is considered to be very unpleasant, and this characteristic often limits excessive exposures. Rinsing the mouth is usually all that is required, and most signs resolve in a few hours.

Moisture absorbents, such as dessicant packets, are found in many packages for shoeboxes, lamps, medications and electronic equipment. A common ingredient is silica gel, which can look like a white powder or granular substance. Silica gel is typically found in paper or plastic packets or cylinders. Silica gel is considered to have low toxicity, and most exposures do not result in any clinical problems. Mild gastrointestinal upset is the most common abnormality reported.

Ingestion of mothballs are not commonly reported in pets. Mothballs can contain two toxic components – naphthalene or paradichlorobenzene. Napthalene mothballs are more toxic, and cats are particularly sensitive to its toxic effect. Heinz bodies, hemolysis, and possibly methemoglobinemia [leading to brown discoloration to the blood] can be observed. Exposures greater than 400 mg/kg can lead to clinical problems in dogs [one 2.7 g mothball contains 2700 mg naphthalene]. Paradichlorobenzene causes more of a neurological condition [disorientation, excitation/depression, seizures] in addition to gastrointestinal signs [vomiting, abdominal pain]. Treatment is symptomatic and supportive.

Pets ingesting human medications are common occurrences, and it is impossible to cover all potential types of ingestions. Numerous sites are available to the practitioner that can provide helpful medical information regarding appropriate treatment plans for pets. These can include websites [http://fdb.rxlist.com/drugs/search.aspx], poison control centers [800.222.1222] and the ASPCA-APCC [888-426-4435]. Many times information from the human literature can be used and extrapolated to the situation at hand. Listed below are examples of some poisonings that can be encountered in practice.

Dogs have been known to bite into and be rapidly exposed to the contents of inhalers for asthmatics that contain selective beta2-agonists. There are several beta2-agonists on the market [metaproterenol, pirbuterol, isoetharine, terbutaline, bitolterol], but the most commonly encountered one is albuterol [salbutamol]. A typical inhaler that weighs 18 g contains 28.8 mg of albuterol; an average weight dog exposed to the entire contents would be exposed to a dose which is potentially many times greater than the reported therapeutic dose of 92 µg/kg qid. These short acting compounds are rapidly absorbed and in situations of overdosages, the drugs lose their selectivity and cause beta1 effects. Commonly observed clinical findings in exposed dogs include tachycardia and premature ventricular contractions; agitation, hyperactivity, restlessness, pacing, anxiety, apprehension and seizures; tachypnea, panting, dyspnea and labored shallow breathing; lethargy, weakness and depression; vomiting and muscle tremors. Severe hypokalemia can be seen, so this occurrence should be looked for by frequent monitoring. A rebound hyperkalemia can also occur as the drug's activity wanes and the potassium redistributes from the intracellular space to the extracellular space. Other less commonly reported abnormalities include hypophosphatemia, hyperglycemia and hypomagnesemia. Treatment should include aggressive and continuous monitoring of the heart rate, rhythm and blood pressure, along with serum potassium levels. Propranolol [0.02 mg/kg IV slowly - max. of 1 mg/kg] and metoprolol [0.2-0.4 mg/kg bid PO], beta-antagonists, and lidocaine [2-4 mg/kg slow IV to effect], can be used to control the heart rate and arrhythmias present; and diazepam [0.2-0.6 mg/kg IV to effect] can be used to resolve the anxiety, restlessness, muscle tremors and seizures. Potassium can be added to IV fluids if the patient is hypokalemic; care should be taken to monitor for a rebound hyperkalemia as the pharmacological effects of the drug wanes. Most patients are expected to recover within 12 hours, but some signs can persist for longer periods depending on exposure dose.

Antidepressant medication exposures in dogs are becoming a more and more frequent occurrence. To make the situation more complicated, there are 4 classes of antidepressants [tricyclic antidepressants, monoamine oxidase inhibitors, selective serotonin reuptake inhibitors and 'atypical' antidepressants] that can have different pharmacological effects on overexposed patients, thereby warranting different treatment plans. Tricyclic antidepressants are rapidly absorbed and widely distributed in tissues, with varying reported half-lives. Dosages > 15 mg/kg are considered potentially lethal. Overdosages in dogs have been known to result in a variety of clinical problems, and these problems can vary between drugs. One should look up each drug separately to determine the most commonly encountered adverse effects observed following overexposures. Some that have been listed include vomiting, hyperexcitability, hyperthermia, tremors and seizures; lethargy, ataxia, tachycardia/bradycardia, coma, hypotension and cardiac arrhythmias have also been observed. Emesis or gastric lavage should be performed in asymptomatic patients. Repeated administration of activated charcoal is recommended to help prevent further absorption and to potentially interrupt enterohepatic recirculation. The use of a sorbitol cathartic could be beneficial, considering the anticholinergic effects of these compounds causing decreased gastrointestinal motility. Continuous monitoring of the cardiovascular and respiratory system, along with appropriate supportive care including monitoring the acid/base and electrolyte status [maintain slight alkalotic state], is critical to a successful outcome.

Overexposure to monoamine oxidase inhibitors [MAOIs] can also lead to a variety of similar clinical signs, which include depression, ataxia, restlessness, tachycardia, arrhythmias, fever, respiratory depression, coma, hypotension/hypertension and seizures. These signs are typically seen within a few hours of exposure, but can be delayed for up to several hours. Treatment includes decontamination of the asymptomatic patient [e.g., emesis, gastric lavage, activated charcoal, sorbitol cathartic], and basic supportive care while continuous monitoring of the cardiovascular and respiratory system, and acid/base and electrolyte status. MAOIs can interfere with the hepatic metabolism of many drugs, so use of any drug should be used judiciously.

Selective serotonin reuptake inhibitors [SSRIs] are generally well absorbed following oral exposures and clinical signs of overexposures generally are observed within a few hours. Different drugs elicit different clinical signs in poisoned dogs, but the most commonly encountered problems include sedation, depression, lethargy, ataxia, hypotension, bradycardia, vomiting and tremors. Less than one 37.5-mg capsule of venlafaxine can cause mydriasis, vomiting, tachypnea, tachycardia, ataxia and agitation. Half-lives vary between drugs, but in general range between a few hours up to 15 hours or longer. Bupropion hydrochloride, an antidepressant that does not fit in any of the above categories, has been shown to cause vomiting, dyspnea, salivation, ataxia, seizures, arrhythmias, tremors, hypotension and depression. Treatment options for these drugs include aggressive decontamination in the asymptomatic patient [emesis, gastric lavage, repeated activated charcoal, sorbitol cathartic], and basic symptomatic and supportive care.

The serotonin syndrome can occur in dogs, particularly if they ingest more than one type of antidepressant medication. The syndrome was first characterized in people, and affected patients exhibit a combination of mental and behavioral changes [e.g., depression, agitation], aberrant neuromuscular activity [e.g., tremors, shivering, seizures], hyperthermia and diarrhea. In addition to the basic decontamination procedures, symptomatic and supportive care [depending on the clinical presentation of the patient] and cyproheptadine hydrochloride [1.1 mg/kg PO] can be used as a nonspecific serotonin antagonist.

Benzodiazepines as a category are used as sedatives, antianxiety agents and anticonvulsants. Alprazolam [Xanax] is a commonly used anti-anxiety agent in humans. Clinical signs observed in dogs following exposures include ataxia, disorientation, depression/hyperactivity, vomiting, weakness, tremors, vocalization, tachycardia, tachypnea, hypothermia, diarrhea and excessive salivation. The benzodiazepines are rapidly absorbed following oral exposure, are highly protein bound, and have a wide tissue distribution. Most signs develop within 30 minutes of ingestion, and most drugs in this category have relatively short half lives. Treatment goals include basic decontamination procedures and symptomatic/supportive care. Flumazenil, a benzodiazepine antagonist, can be tried to counteract severe depression.

Phenylpropanolamine is a sympathomimetic drug used to treat urinary incontinence in dogs. It is rapidly absorbed from the gastrointestinal tract and stimulates both alpha and beta adrenergic receptors, similar to ephedrine. Dosages > 20 mg/kg BW have been associated with clinical problems; the most commonly reported ones include hypertension, tachycardia and cardiac arrhythmias. Panting, agitation, hyperesthesia, tremors, seizures and depression have also been reported. Clinical signs generally start within 30 to 90 minutes of ingestion, and can last up to 3 days depending upon the exposure dose. Emesis, gastric lavage, repeated doses of activated charcoal, and a cathartic can be considered in the asymptomatic patient. Oxygen, intravenous fluids and other supportive measures should be used as indicated. Short acting barbiturates can be used to control agitation and excitement, and vasopressor agents can be used cautiously to control severe hypertension. Atropine and beta-blockers are not routinely encouraged.


Barr JM et al. 2006. Hypernatremia secondary to homemade play dough ingestion in dogs: A review of 14 cases from 1998-2001. J Vet Emer Critical Care 14(3):196-202.

Duncan KL et al. 1997. Malignant hyperthermia-like reaction secondary to ingestion of hops in five dogs. JAVMA 210(1):51-54.

Mensching D and Volmer PA. 2007. Breathe with ease when managing beta2 agonist inhaler toxicosis in dogs. Vet Med, June, 369-373.

Merola V and Dunayer E. 2006. The 10 most common toxicosis in cats. Vet Med, June, 339-342.

Oehme FW and Kore AM. 2006. Miscellaneous indoor toxicants. In Small Animal Toxicology, Ed. ME Peterson, PA Talcott, Elsevier Inc., pp. 223-243.

Plumb DC. 2005. Veterinary Drug Handbook, PharmaVet Inc., Stockholm, WI.

Rosendale ME. 1999. Glow jewelry (dibutyl phthalate) ingestion in cats. Vet Med 94(8):703.

Volmer PA. 2006. "Recreational drugs". In Small Animal Toxicology, Ed. ME Peterson, PA Talcott, Elsevier Inc., pp. 273-311.

Wismer TA 2000. Antidepressant drug overdoses in dogs. Vet Med, 95(7): 520-525.

Wismer TA. 2002. Accidental ingestion of alprazolam in 415 dogs. Vet Hum Toxicol. 44(1):22-23.

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