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Most Common Canine Poisons in or Around the Home
Article copyright by: Karen Clark, Versailles Kennels, UK

Most Common Canine Poisons in or Around The Home. 

Rat / Mice / Rodent Poison 

The most important issue is identification of type of poison contained within the blue blocks or pellets etc… Several different classes of rodenticides exist, including those that contain bromethalin, zinc phosphide, cholecalciferol (Vitamin D3), and LAACs. Pet owners should be appropriately educated on how to pet-proof the house, and be trained on what common household products and kitchen items are poisonous. Pet owners should also be appropriately educated on crate training to help minimize toxin exposure. Once a pet is exposed to a toxicant, it is imperative to determine if emesis is appropriate, and to understand when it may be contraindicated (e.g., symptomatic patient, delayed time since exposure, hydrocarbons, etc.). Knowledge of the underlying mechanism of action, the pharmacokinetics (including absorption, distribution, metabolism, and excretion), and the toxic dose of the toxicant are imperative in determining appropriate decontamination and therapy for the patient. 

Bromethalin, a neurotoxic rodenticide, 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. 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. Edema of the central nervous system (CNS) may result. Lethal dose in dogs is 2.38-3.65 mg/kg, cats far worse (0.54 mg/kg) With recent ingestion in an asymptomatic patient, the use of decontamination (e.g., emesis induction, activated charcoal) is warranted. As bromethalin undergoes enterohepatic recirculation, the use of multiple doses of activated charcoal (without a cathartic) can be administered q 6 hours for 24 hours.

Rodenticides have been used since the 1930’s and are still readily available on the market. Formulations of phosphides have a unique, distinctive odor similar to rotten fish, garlic, or acetylene. The toxic dose of zinc phosphide in dogs is approximately 20-40 mg/kg, but up to 300 mg/kg on empty stomachs. Emesis – whether intentionally induced or occurring due to clinical signs - can result in poisoning to the pet owner or the veterinary professional secondary to exposure of phosphine gas. Clinical signs of nausea and difficulty breathing have been reported in humans exposed. To minimize these risks, emesis induction should always be performed in a well-ventilated area (e.g., opening the car window if the patient vomits or inducing emesis outside or in a well-ventilated area). Pet owners should be appropriately educated on the toxic gas exposure to themselves also. Pet owners should be informed not to feed their pet to prevent further production of phosphine gas. In addition, the administration of an antacid (e.g., aluminum hydroxide) prior to emesis induction may help decrease the presence of phosphine gas. With recent ingestion in an asymptomatic patient, the use of emesis induction (following antacid administration) and one dose of activated charcoal with a cathartic is warranted to minimize toxic effects of zinc phosphide. Symptomatic supportive care, including anti-emetic therapy, IV fluid therapy, gastric protectants, and analgesics are warranted.

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 ARF developing as a result of dystrophic mineralization to the soft tissue and kidneys. Common sources of Vitamin D3 include over-the-counter (OTC) or prescription vitamins (typically found in a calcium/Vitamin D3 combination), psoriasis creams (in the form of calcipotriene), and rodenticides. In dogs, cholecalciferol has an LD50 of 85 mg/kg (based on the rodenticide concentration of 0.075%).9 Doses of Vitamin D3 > 0.1-0.5 mg/kg can result in clinical signs and hypercalcemia, respectively. renal failure can occur within 12-36 hours following toxic ingestion. Clinical signs and clinicopathologic findings include increased thirst and urination, weakness, lethargy, anorexia, vomiting, generalized malaise, uremic halitosis, dehydration, hypercalcemia, hyperphosphatemia, azotemia, melena, hemorrhagic diarrhea, and death. Decontamination should include emesis induction, if ingestion was recent and the patient is asymptomatic. As cholecalciferol undergoes enterohepatic recirculation, the. administration of multiple doses of activated charcoal (without a cathartic) is warranted q 6 hours X 24 hours. Additional treatment includes the aggressive use of IV fluid therapy to promote calciuresis (e.g., 0.9% NaCl), calcium monitoring, gastrointestinal support (e.g., anti-emetics, H2 blockers, sucralfate, phosphate binders, etc.), and the use of medications to increase calciuresis (e.g., prednisone, furosemide) and prevent hypercalcemia (e.g., pamidronate, calcitonin). Treatment is often expensive, and requires hospitalization for an extended period of time. Most patients are continued on oral furosemide and prednisone for weeks, following discharge from the hospital. Frequent monitoring of renal function and electrolytes is imperative. Calcium, phosphorous, BUN, creatinine, and ionized calcium should be evaluated every 12-24 hours while hospitalized, and then every 2-3 days thereafter for the next 2-4 weeks. 

First and second generation LAAC anticoagulants result in inhibition of Vitamin K epoxide reductase, resulting in inactivation of clotting factors II, VII, IX, and X. First generation rodenticides (e.g., warfarin, pindone) have been largely replaced by more potent second generation anticoagulants (e.g., brodifacoum, bromadiolone, diphacinone, chlorophacinone, etc.) keep in mind that species differences exist; cats are much more resistant to the effects of LAAC as compared to dogs. 

Canine LD50                  Feline LD50 

Difethialone: 4 mg/kg >            16 mg/kg 

Brodifacoum: 0.25-4 mg/kg>    25 mg/kg 

Bromadiolone: 11-20 mg/kg >   25 mg/kg 

Diphacinone: 3-7.5 mg/kg >      15 mg/kg 

The most common clinical signs include lethargy, exercise intolerance, inappetence, pallor, dyspnea, coughing, hemoptysis, etc. Hemoabdomen, hemothorax, pericardial effusion may also occur. Rarer clinical signs include gingival bleeding, epistaxis, ecchymoses, petecchia, hematuria, bleeding into the subcutaneous space or joint space, and melena.

When treating LAAC rodenticides, two considerations for treatments should be utilized. With an acute, one-time ingestion of a LAAC, one can decontaminate and check a PT 48 hours post-initial ingestion. If the PT is prolonged at 48 hours, 3-4 weeks of Vitamin K1 therapy should be initiated (3-5 mg/kg PO, divided SID-BID X 4 weeks). A recheck PT should be performed 48 hours after the last dose; if prolonged, an additional 2 weeks of therapy is indicated, with another PT performed 48 hours after the last dose OR 1. With an acute one-time ingestion of a LAAC, one can just prophylatically treat with Vitamin K1 therapy, particularly if the patient is young, debilitated, geriatric, or has underlying liver pathology. Treatment includes Vitamin K1 therapy (3-5 mg/kg PO, divided SID-BID X 4 weeks), with a recheck PT being performed 48 hours after the last dose; if prolonged, an additional 2 weeks of therapy is indicated, with another PT performed 48 hours after the last dose. 

Chocolate, a naturally occurring alkaloid found primarily in the Theobrema cacao plant, contains methylated xanthine derivatives (e.g., theobromine, methylxanthine). As chocolate is prevalent in pet owners’ households, this is a very common toxicosis. 
Depending on the type of chocolate ingested, clinical signs may include vomiting, diarrhea, hyperactivity, polyuria, and hyperthermia (secondary to hyperactivity, tremoring, anxiety, etc.). With severe cases, cardiotoxicity (e.g., ventricular premature contractions, tachyarrhythmias, etc.) may be seen, along with neurotoxicity (e.g., tremors, seizures, etc.). With chocolate toxicosis, clinical signs can be seen when the amount of theobromine ingested is > 20 mg/kg (e.g., vomiting, diarrhea). With higher doses (> 40 mg/kg), cardiotoxicity may be seen, while doses > 60 mg/kg can result in neurotoxicity. As chocolate often stays in the GI tract for a prolonged period of time, emesis induction up to 4-6 hours post-ingestion may be of benefit, provided the patient remains asymptomatic. Treatment includes multiple doses of activated charcoal, as chocolate undergoes enterohepatic recirculation. Depending on the severity of clinical signs and onset of decontamination (e.g., emesis induction with administration of activated charcoal), treatment may include fluid therapy (either subcutaneously or intravenously), anti-emetic therapy, sedation (if the patient is agitated, tachycardiac, and hypertensive), cardiovascular monitoring (e.g., continuous electrocardiogram monitoring, blood pressure monitoring), and potential beta-blocker therapy (if the heart rate is persistently over 180 beats per minute – canine). As methylxanthines may be reabsorbed through the bladder, frequent walks outside to urinate (or even urinary catheter collection) can be used. As chocolate has a long half-life (approximately 17 hours), clinical signs can be seen for up to 72 hours, and treatment should be continued until clinical signs resolve. Overall, the prognosis is excellent with supportive care. Some patients may develop secondary pancreatitis from chocolate ingestion, particularly if other ingredients were involved (e.g., macadamia nuts). 

Grapes and raisins (Vitis spp.) have been recently associated with development of acute renal failure (ARF) 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), the presence of mycotoxins or pesticide residues on the fruit, 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. 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 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. As there is no current veterinary peer-reviewed, scientific published toxic dose of grapes and raisins, all ingestions should be treated as potentially idiosyncratic and be appropriately 
decontaminated and treated. Initially, vomiting may be observed within the first 24 hours of ingestion.2 Within the next 12-24 hours, clinical signs of lethargy, dehydration, vomiting, diarrhea, anorexia, abdominal pain, uremic breath, and diarrhea may be seen. Azotemia may develop within 24 hours, with hypercalcemia and hyperphosphatemia occurring first. Oliguria and anuria may develop. 48-72 hours post-ingestion, at which point the prognosis is poorer. Treatment includes decontamination, aggressive IV fluid therapy, anti-emetics, blood pressure and urine output monitoring, and serial blood work monitoring (q. 12-24 hours). In severe cases, hemodialysis or peritoneal dialysis may be necessary. 

NSAIDs are competitive inhibitors of prostaglandin synthesis (cyclooxygenase or “COX” inhibitors) and result in decreased prostaglandin, which is important for normal homeostatic function (including maintaining renal blood flow, maintaining mucous production in the stomach, etc.). Common OTC human NSAIDs include active ingredients such as ibuprofen and naproxen sodium. Common prescription veterinary NSAIDs can also result in toxicosis, particularly when available in the chewable, palatable formulation. Examples of veterinary NSAIDs include carprofen, deracoxib, etogesic, previcoxib, etc. With NSAID toxicosis, the GI tract, kidneys, CNS, and platelets can be affected. Cats and certain breeds of dogs (e.g., German shepherds) seem to be more sensitive to NSAIDs, and should be treated aggressively. With cats, severe ARF is often more clinically seen with NSAID toxicosis at lower doses (as compared to dogs). With dogs, signs secondary to GI ulceration (e.g., vomiting, diarrhea, melena, hematemesis, etc.) are more commonly seen initially, followed by secondary ARF. With NSAID toxicosis, it is important to keep in mind that each NSAID has a different toxic dose, margin of safety, half-life, and route of excretion, and an animal poison helpline should be contacted to identify what specific NSAID and toxic dose was ingested. For example, in dogs, ibuprofen results in GI signs at doses as low as 16-50 mg/kg, while severe GI signs may be seen at 50-100 mg/kg. Renal compromise may be seen at doses of 100-250 mg/kg (resulting in potential ARF), and fatalities have been reported at doses > 300 mg/kg. This differs tremendously from naproxen sodium (dogs), where severe clinical signs can be seen at doses as low as 5 mg/kg. With naproxen, experimental canine doses of 22 mg/kg orally once a day for 3 days have resulted in perforation of the GI tract with secondary septic peritonitis occurring. Clinical signs of NSAID toxicosis include anorexia, vomiting, hematemesis, diarrhea, melena, abdominal pain, lethargy, malaise, uremic halitosis, dehydration, etc. Treatment includes decontamination, the use of activated charcoal (often multiple doses due to enterohepatic recirculation, if appropriate), GI protectants (e.g., H2 blockers, sucralfate), aggressive IV fluid therapy (to help maintain renal blood flow) for 24-72 hours, anti-emetic therapy, and symptomatic and supportive care. With high doses, anti-convulsants may also be necessary if CNS signs develop. 

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. 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.4 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, etc. 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.

Acetaminophen (N-acetyl-p-aminophenol), a cyclooxygenase (COX)-3 inhibitor, is a popular over-the-counter (OTC) analgesic and antipyretic medication used frequently in humans. It is not considered a true NSAID as it lacks anti-inflammatory properties. While this drug is very safe for human use, it has a narrow margin of safety in dogs and cats; the severity of toxicosis and development of clinical signs is species-dependent. Cats have an altered glucuronidation pathway and a decreased ability to metabolize acetaminophen, making them much more susceptible to toxicosis. In cats, red blood cell injury is more likely to occur in the form of methemoglobinemia (metHb), and toxicity can develop at doses as low as 10 mg/kg. In cats, lethargy, swelling of the face or paws, respiratory distress, brown mucous membranes, cyanosis, vomiting, and anorexia may be seen secondary to metHb. In dogs, hepatic injury is more likely to occur; acetaminophen toxicosis can occur at doses > 100 mg/kg, while metHb can develop at doses of > 200 mg/kg. Dogs may develop clinical signs of keratoconjunctivitis sicca (dry eye), malaise, anorexia, hepatic encephalopathy, vomiting, melena, and icterus secondary to hepatotoxicity. Treatment includes decontamination, administration of one dose of activated charcoal with a cathartic, IV fluid therapy, antioxidant therapy (Vitamin C), provision of a glutathione source (S-adenosyl-methionine or SAMe), and N-acetylcysteine to limit formation of the toxic metabolite NAPQI by providing additional glutathione substrate. Baseline blood work and follow-up biochemical panels should be performed to monitor for hepatotoxicity. Generally, prognosis is fair with therapy. Those with severe hepatic failure have a poorer prognosis.

It is IMPORTANT that all pups going to new homes should not be given full access to any new home, more-so a new home that is new to dogs. Most good breeders will advise the use of a pen and crate system to ensure that a pup remains safe whilst new owners adapt to life with a new 4 legged little one. I have attended many an emergency to prevent death of both young pups and even much older young dogs when owners have simply not put prescription drugs out of reach of these investigative animals. One day they cant jump onto kitchen cupboards the next they sire can, breeders know their dogs very well so it is important no matter how well you think you know dogs to listen and take in the advice. IT MAY SAVE YOUR PETS LIFE ONE DAY!

How to establish fast or slow heart rate:

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How to Induce Vomiting in emergency care of dogs and cats: 

There are two products commonly found in the home that can help induce vomiting, 3 percent Hydrogen Peroxide or good old table salt. The general rule for peroxide is 5mls (or 1 teaspoon) per 10 pounds, orally. Repeat every 15-20 minutes, up to three times, until the animal vomits. 

When Should You NOT Induce Vomiting? 

Circumstances in which you should not make your pet throw up include: 

• When he's already throwing up. Don't induce more vomiting in an already vomiting animal, because you can incite a worse vomition response. 

• If your pet has lost consciousness and/or if she's very weak or has trouble standing. Do not induce vomiting in this situation because aspiration pneumonia, which can result when an animal inhales vomit into its lungs, can become a secondary problem. 

• If your pet has swallowed bleach, a drain cleaner, or a petroleum distillate. These chemicals can cause burning as they are swallowed, and secondary additional burns as they come back up. Don't induce vomiting if your pet has swallowed a caustic substance. 

• If it has been over two hours since your pet ingested a potential toxin. Once a substance enters your pet's small intestine, vomiting will not clear the stomach of that toxin. Inducing vomiting in a dog or cat that has already digested a potential toxin won't be effective in ridding her body of the substance. 

When Should You Absolutely Induce Vomiting? 

• When your pet has consumed antifreeze (#3) within the last two hours. 

• When you've called your veterinarian, discussed the specific circumstances around your pet's swallowing a potential toxin, and your vet instructs you to induce vomiting. 

Hydrogen Peroxide to Induce Vomiting 

I recommend (and probably your own veterinarian will as well) the only substance you use at home to make your pet throw up is hydrogen peroxide. 

I'm talking about three percent hydrogen peroxide – the kind you purchase at any pharmacy. Do not use the stronger, concentrated peroxide found in hair color, use only the three percent kind. 

The dose is one teaspoon (five milliliters, or cc's) for every 10 pounds of body weight. 

The hydrogen peroxide must be given orally to your pet. At my clinic, especially if the patient is a dog, we mix it with a little vanilla ice cream to make it palatable. I don't advocate feeding ice cream to dogs, of course, but in a situation where it's necessary to make a pet vomit, hydrogen peroxide hidden in sugary ice cream usually gets gobbled up with no argument. 

You can also try using a little bit of honey if there's no ice cream on hand. 

Sometimes, however, we just syringe the stuff down an animal's throat. With kitty patients, it's usually easier and more effective to syringe it. 

If your pet is a dog, after you get the hydrogen peroxide down, you should walk her around for a few minutes to get her moving, which will help the hydrogen peroxide do its work. 

Cats, of course, are a little harder to get moving, but getting them in motion will encourage absorption of the hydrogen peroxide. 

Hydrogen peroxide is an irritant to the gastrointestinal tract, so it typically induces vomiting of stomach contents within 15 minutes of use. If your pet doesn't vomit within 15 minutes, you can give him a second dose. However, if another 15 minutes pass and he still hasn't vomited, don't give him a third dose of the hydrogen peroxide. It's time to call your veterinarian. 

Veterinarians use specific drugs to induce vomiting in pets – apomorphine is used for dogs, and xylazine is used for kitties. 

These medications are by prescription only and can only be administered by a veterinarian. They can be much more effective at inducing vomiting than hydrogen peroxide. So if your pet isn't throwing up from your at-home hydrogen peroxide treatment, you should seek veterinary care immediately. 

DO NOT induce vomiting if the animal is having difficulty breathing, having seizures/convulsions, seems depressed, in shock or unconscious. 

DO NOT induce vomiting if the animal's heart rate is very slow, if the object eaten was pointed or sharp, or when the poison container says not to. 

I hope this helps. 

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