Top 5 poisons to induce emesis in the veterinary poisoned patient
Dr. Justine Lee, DVM, DACVECC, DABT
When it comes to common toxicants that dogs and cats get into, make sure you know when to appropriately decontaminate your veterinary patient. In veterinary medicine, the primary treatment for toxicant exposure should be decontamination and detoxification of the patient. The goal of decontamination is to inhibit or minimize further toxicant absorption and to promote excretion or elimination of the toxicant from the body. Decontamination can only be performed within a narrow window of time for most substances; therefore, it is important to obtain a thorough history and time since exposure.
The five toxicants below? In VETgirl’s opinion, these are the most popular toxicants that dogs ingest. Some of these stay in the stomach for a slightly longer period of time, allowing for a more productive, effective emesis return).
Certain cardiac medications include broad categories such as calcium channel blockers, beta-blockers, and angiotensin-converting enzyme (or “ACE”) inhibitors. These medications are commonly used in both human and veterinary medicine to treat underlying cardiac disease or hypertension. Each category of cardiac medication has different margins of safety. Calcium channel blocker and beta-blocker toxicosis should be treated aggressively, as these two categories of medications have a narrow margin of safety. Toxicosis of these agents can result in myocardial failure, severe bradycardiac, and hypotension; untreated, cardiac output becomes reduced, and secondary severe hypoperfusion and AKI can potentially develop.1-3
With ACE-inhibitors, severe overdoses can cause hypotension, dizziness, weakness, and hypotension. In general, there is a wider margin of safety with ACE-inhibitors, which are typically considered much safer. Pets ingesting small amounts of ACE-inhibitors can potentially be monitored at home, unless they have underlying disease (e.g., kidney failure, cardiac disease, etc.). With ACE-inhibitors, ingestions > 10-20X a therapeutic dose are generally considered toxic, and can result in severe clinical symptoms (e.g., hypotension).3 Treatment for any cardiac medication includes decontamination (e.g., emesis induction, gastric lavage, activated charcoal administration), blood pressure monitoring, aggressive IV fluid therapy if hypotension is detected, and blood work monitoring. With severe toxicosis, the use of high-dose insulin therapy or intravenous lipid emulsion may be warranted as a potential antidote for calcium channel blocker toxicosis.
GRAPES AND RAISINS
Grapes and raisins (Vitis spp) have been recently associated with development of acute kidney injury (AKI) with ingestion. All types have been implemented with toxicosis, including organic grapes, commercial grapes, homegrown grapes, and seedless or seeded grapes. While the mechanism of toxicosis is unknown, there are several suspected hypotheses, including individual inability to metabolize certain components of the fruit (e.g., tannins, high monosaccharide content),4 the presence of mycotoxins or pesticide residues on the fruit,4 or salicylate-like chemicals within the grape or raisin. Common kitchen items also contain grapes, raisins, or currants in their active ingredient, including raisin bread, trail mix, chocolate-covered raisins, cereal with raisins, etc. Currently, grapeseed extract has not been associated with nephrotoxicity.4
Treatment for grape and raisin ingestion includes aggressive decontamination as the first-line of therapy. Grapes and raisins seem to stay in the stomach for a prolonged period of time, and are not rapidly broken down or absorbed from the gastrointestinal (GI) tract; hence, delayed emesis induction even several hours post-ingestion can still be initiated to maximize decontamination methods. One dose of activated charcoal can also be administered to prevent absorption of the unknown nephrotoxin. In general, all ingestions should be treated as potentially idiosyncratic and be appropriately decontaminated and treated. Treatment includes decontamination, aggressive intravenous (IV) fluid therapy, anti-emetics, blood pressure and urine output monitoring, and serial blood work monitoring (q. 12-24 hours for several days). In severe cases, hemodialysis or peritoneal dialysis may be necessary. Asymptomatic patients that have been adequately decontaminated and survive to discharge should have a renal panel and electrolytes monitored 48-72 hours post-ingestion. Overall, the prognosis varies from good to poor, depending on time to decontamination, response to therapy, and prevalence of oliguria or anuria. While 50% of dogs that ingest grapes and raisins never develop clinical signs or azotemia, aggressive treatment is still warranted.4
Xylitol is a natural sweetener found in small quantities in certain fruit. Xylitol has gained recent popularity because it is sugar-free, and is often found in diabetic snacks, foods, baked foods, mouthwashes, toothpastes, chewing gum, mints, candies, and chewable multivitamins.5 Sugarless products, particularly those with xylitol listed within the first 3 to 5 active ingredients (AI), can result in severe toxicosis within 15-30 minutes of ingestion. Ingestion of xylitol results in an insulin spike in non-primate species, resulting in severe hypoglycemia. Many pieces of candy and gum (e.g., Orbit™, Trident™, Ice Breakers™) contain various amounts of xylitol ranging, on average, from as low as 2 mgs up to 1.0 grams/piece (Many average 150-170 mg per piece). Unfortunately, not all sources are disclosed by the company (e.g., how many grams of xylitol may be in each piece of gum) due to a proprietary nature. With xylitol toxicosis, it is imperative to calculate whether a toxic dose has been ingested. Doses > 0.1 g/kg are considered toxic and result in profound, sudden hypoglycemia from insulin stimulation.5 Higher doses (> 0.5 g/kg) of xylitol have been associated with acute hepatic necrosis. Clinical signs of xylitol toxicosis include lethargy, weakness, vomiting, collapse, anorexia, generalized malaise, tremors, and seizures (from hypoglycemia). When hepatotoxic doses are ingested, clinical signs and clinicopathologic findings may include melena, icterus, increased liver enzymes, diarrhea, hypoglycemia, hypocholesterolemia, decreased BUN, hypoalbuminemia, etc.
When presented a patient that has ingested a toxic amount of xylitol, a blood glucose should be checked immediately upon presentation; if hypoglycemic, a bolus of 1 ml/kg of 50% dextrose, diluted with an additional amount of 0.9% NaCl (in a 1:3 ratio) should be given IV over 1-2 minutes. Emesis induction should not be performed until the patient is euglycemic. Keep in mind that activated charcoal does not reliably bind to xylitol, and is not routinely recommended for xylitol toxicosis. Hypoglycemic patients should be hospitalized for IV fluid therapy [supplemented with dextrose (2.5 to 5% dextrose, CRI, IV)] for approximately 24 hours, and frequent blood glucose check should be performed every 1-4 hours. For patients ingesting a hepatotoxic amount of xylitol, the use of hepatoprotectants (e.g., SAMe), anti-emetics, and supportive care (including frequent liver enzyme monitoring) are warranted.
Chocolate is one of the most well-known toxic foods that pet owners are aware of. Chocolate contains methylxanthines such as theobromine and caffeine (More information on caffeine specifically can be found below in the next section). Methylxanthines antagonize adenosine receptors and inhibits cellular phosphodiesterases, causing an increase in cAMP. Methylxanthines also stimulate release of catecholamines (e.g., norepinephrine) and cause an increase of calcium entry into cardiac and skeletal muscle, resulting in central nervous system (CNS) stimulation, diuresis, and myocardial contraction. When ingested in toxic doses, clinical signs may include agitation, vomiting, diarrhea, panting, tachycardia, polyuria, hyperthermia, muscle tremors, and seizures. Clinical signs of theobromine toxicosis can be seen at within a few hours, up to 10-12 hours out (as the absorption time is slow). As theobromine has a very long half-life (e.g., 17 hours), treatment may be necessary for 72-96 hours.6 Toxic doses of theobromine can be seen at:
- > 20 mg/kg: mild signs of agitation and gastrointestinal distress (e.g., vomiting, diarrhea, abdominal pain)
- > 40 mg/kg: moderate signs of cardiotoxicosis can be seen in addition to aforementioned signs (e.g., tachycardia, hypertension)
- > 60 mg/kg: severe signs of neurotoxicosis can be seen in addition to aforementioned signs (e.g., tremors, seizures)
- 250-500 mg/kg: LD50 (for dogs) 6
- 200 mg/kg: LD50 (for cats) 6
Treatment should be aimed at decontamination, administration of multiple doses of activated charcoal, antiemetic therapy, IV fluid therapy, sedation, blood pressure monitoring, and beta-blocker therapy (for sustained tachycardia).
Think you know how to treat that dog that just ingested a green or blue block of rodenticide? Well, before reaching for your bottle of Vitamin K1, make sure you identify the correct active ingredient! New mandates by the EPA (effective 2011) were created that will reduce the availability of anticoagulant rodenticide (ACR). So, before you reach for that Vitamin K1, read on! One of the most common mistakes seen in the field of veterinary toxicology is assuming that every green or blue block of rat or mouse poison is a ACR rodenticide. The active ingredient of a rodenticide cannot be identified based on physical appearance (e.g., color, shape, size, etc.). When in doubt, the EPA-Reg. number or active ingredient (and concentration) must be properly identified to ensure appropriate treatment and management of rodenticide toxicoses. Several different classes of rodenticides exist, including those that contain bromethalin, zinc phosphide, and cholecalciferol (Vitamin D3).
Bromethalin is not an anticoagulant rodenticide and should not be treated with Vitamin K1 as an antidote. Bromethalin works by uncoupling oxidative phosphorylation in the brain and liver mitochondria.7 This results in decreased ATP production, which affects sodium and potassium pumps; as a result, lipid peroxidation occurs, resulting in sodium accumulation within the cell.1 Edema of the central nervous system (CNS) may result.7
Phosphide rodenticides result in the production of phosphine gas. When zinc phosphide combines with gastric acid or moisture (or the presence of food!), liberated phosphine gas is rapidly absorbed across gastric mucosa and distributed systemically, where it exerts its toxic effect. Phosphine gas is considered a corrosive and a direct irritant to the gastrointestinal tract (GIT).8,9
Cholecalciferol, the chemical name for vitamin D3, is one of the most deadly– and costly – rodenticides to pets. Ingestion of toxic levels of cholecalciferol can result in severe hypercalcemia and hyperphosphatemia, with secondary AKI developing as a result of dystrophic mineralization to the soft tissue and kidneys.10
ACR anticoagulants result in inhibition of Vitamin K epoxide reductase, resulting in inactivation of clotting factors II, VII, IX, and X.11 Due to a new EPA mandate, many second generation anticoagulants (e.g., brodifacoum, bromadiolone, diphacinone, chlorophacinone, etc.) are now being taken off the market, as they are considered to be more toxic with a longer duration of action (requiring a longer duration of treatment compared to first generation anticoagulants).
When it comes to treating a rodenticide toxicosis patient, make sure you have confirmed the appropriate active ingredient, as treatment will vary with each different type.
When in doubt, if you think your patient ingested something poisonous, recognize that the time to decontaminate them is limited to 1-6 hours, depending on the toxicant. When in doubt, contact ASPCA Animal Poison Control Center at 888-426-4435 for life-saving advice, 24/7.
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- Syring RS, Engebretsen KM. Calcium channel blockers. In: Osweiler G, Hovda L, Brutlag A, Lee JA, eds. Blackwell’s Five-Minute Veterinary Consult Clinical Companion: Small Animal Toxicology, 1st Iowa City: Wiley-Blackwell, 2010, pp. 170-178.
- Engebretsen KM, Syring RS. Beta-blockers. In: Osweiler G, Hovda L, Brutlag A, Lee JA, eds. Blackwell’s Five-Minute Veterinary Consult Clinical Companion: Small Animal Toxicology, 1st Iowa City: Wiley-Blackwell, 2010, pp. 155-163.
- Adams CM. Angiotensin-converting enzyme (ACE) inhibitors. In: Osweiler G, Hovda L, Brutlag A, Lee JA, eds. Blackwell’s Five-Minute Veterinary Consult Clinical Companion: Small Animal Toxicology, 1st Iowa City: Wiley-Blackwell, 2010, pp. 131-135.
- Craft EM, Lee JA. Grapes and raisins. In: Osweiler G, Hovda L, Brutlag A, Lee JA, eds. Blackwell’s Five-Minute Veterinary Consult Clinical Companion: Small Animal Toxicology, 1st Iowa City: Wiley-Blackwell, 2011. pp. 429-435.
- Liu TY D, Lee JA. Xylitol. In: Osweiler G, Hovda L, Brutlag A, Lee JA, eds. Blackwell’s Five-Minute Veterinary Consult Clinical Companion: Small Animal Toxicology, 1st Iowa City: Wiley-Blackwell, 2011, pp. 470-475.
- Craft EM, Powell LL. Chocolate and Caffeine. In: Osweiler G, Hovda L, Brutlag A, Lee JA, eds. Blackwell’s Five-Minute Veterinary Consult Clinical Companion: Small Animal Toxicology, 1st Iowa City: Wiley-Blackwell, 2011, pp. 421-428.
- Adams CA. Bromethalin. The Five-Minute Veterinary Consult Clinical Companion: Small Animal Toxicology. Ames, IO: Wiley-Blackwell. pp. 769-774.
- Gray S, Lee JA, Hovda L, et al. Zinc phosphide rodenticide toxicity in dogs: 362 cases (2004-2009). J Am Vet Med Assoc 2011;239(5):646-651.
- Gray S. Phosphides. The Five-Minute Veterinary Consult Clinical Companion: Small Animal Toxicology. Ames, IO: Wiley-Blackwell. pp 781-790.
- Adams CM. Cholecalciferol. The Five-Minute Veterinary Consult Clinical Companion: Small Animal Toxicology. Ames, IO: Wiley-Blackwell. pp 775-780.
- Murphy M. Anticoagulants. The Five-Minute Veterinary Consult Clinical Companion: Small Animal Toxicology. Ames, IO: Wiley-Blackwell. pp 759-768.
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