The most common poisons for pets

dvm360dvm360 March 2024
Volume 55
Issue 3
Pages: 28

Toxins reported frequently are often found in the home

Editor’s Note: Pet Poison Helpline provides toxicology and pet health advice in times of potential emergency, 24 hours, seven days a week for pet owners and veterinary professionals who require assistance treating a potentially poisoned pet. It is an independent, nationally recognized animal poison control center triple licensed by the Boards of Veterinary Medicine, Medicine and Pharmacy. Pet Poison Helpline is available in North America by calling 800-213-6680. Additional information can be found online at

Every year, Pet Poison Helpline, a 24/7 animal poison control center, compiles a list of toxins from calls received regarding potential animal exposures. The top 10 toxins change from year to year based on social trends, state and federal law updates, US Environmental Protection Agency (EPA) requirements, and FDA drug approvals. Following is a Pet Poison Helpline summary of the top 10 toxins for 2023.




Chocolate is readily available in most homes and found in candies, baked goods, and many recreational edibles. The main components of concern are the methylxanthines theobromine and caffeine.1 Chocolate contains 3 to 10 times the amount of theobromine found in caffeine, making it a larger contributor to clinical signs and the focus when calculating a toxic dose.2 Theobromine inhibits cellular adenosine receptors,3 resulting in diuresis and central nervous system (CNS) stimulation. Methylxanthines in general also increase intracellular calcium concentration by decreasing intracellular sequestration of calcium into the sarcoplasmic reticulum of striated muscles and by increasing intracellular calcium influx.3 Additional methylxanthine mechanisms of action include increasing epinephrine and norepinephrine concentrations and inhibiting phosphodiesterase, as well as increasing concentration of cyclic adenosine monophosphate.3 These lead to a sympathomimetic effect. Theobromine concentrations in chocolate vary based on the type of chocolate, with unsweetened, baker’s chocolate, and 100% cacao products containing the highest content, followed by semisweet and dark chocolate. Milk chocolate contains lower amounts of theobromine, and the theobromine content of white chocolate is minimal.2

Theobromine concentrations in chocolate vary based on the type of chocolate, with unsweetened, baker’s chocolate, and 100% cacao products containing the highest content, followed by semisweet and dark chocolate. Milk chocolate contains lower amounts of theobromine, and the theobromine content of white chocolate is minimal.2

Clinical signs of chocolate toxicosis range from mild to severe.1 Mild signs include gastrointestinal (GI) upset and low-grade agitation or restlessness. Moderate signs include those in the mild range along with more significant excitation and tachycardia. Slight tremors may also be seen. For animals consuming a dose in the severe range, the previously listed signs may progress to moderate to severe tremors, seizures, tachycardia, hypertension, and arrhythmia. Signs for all ranges may be seen within 1 to 2 hours after ingestion; however, the full extent of signs may not be present for 6 to 8 hours. Signs may persist for 24 to 48 hours, generally less with ingestions in the mild range. Pancreatitis is a concern for any chocolate ingestion, regardless of the toxic concern.

Treatment depends on the amount and specific chocolate ingested.1 Patients ingesting a low dose can normally be monitored at home and seek veterinary care if signs develop. For those ingesting a moderate range and above, emesis is recommended as it is typically rewarding and can significantly reduce the risk of clinical signs developing. Because of slow absorption, emesis up to 6 hours post ingestion may still be rewarding.1 Emesis is followed by an antiemetic and 1 dose of activated charcoal with a cathartic (ACC).

As the ingested dose increases, subcutaneous (SQ) or intravenous (IV) fluids may be of benefit because of the renal excretion of methylxanthines. Sedation with acepromazine and/or butorphanol is recommended for agitation and tachycardia and methocarbamol for tremors. Seizures may be controlled with standard anticonvulsants; β-blockers are recommended for persistent tachycardia nonresponsive to sedation. Antiarrhythmics should be provided as needed.

The prognosis is excellent with prompt and aggressive care. The prognosis is guarded for patients ingesting a high dose or when there is a delay in care resulting in significant cardiovascular and neurologic signs.

Grapes and raisins

Grapes and raisins are a known concern for causing acute kidney injury in dogs, with rare anecdotal reports in cats. There is no established toxic dose for grapes and raisins, making the determination for when to provide treatment challenging.1 The toxic component of grapes and raisins has not been confirmed; however, a recent association to tartaric acid present in grapes has been proposed as the possible toxic agent.4 Although standard grapes and raisins are obvious sources of exposure, granola bars and other food products may contain less recognizable raisin paste. Wine and grape jams/jellies have not been shown to be a concern for poisoning.

The most common clinical sign of grape and raisin toxicosis is vomiting, often occurring within a few hours after ingestion.1 This may be followed over the next 12 to 24 hours with anorexia, lethargy, and continued vomiting. Polyuria/polydipsia (PU/PD) and azotemia may develop within 24 to 96 hours after consuming grapes and/or raisins. Oliguria and anuria are considered fatal sequelae.

Treatment of grape and raisin toxicosis consists of decontamination and IV fluids.1 Emesis may be rewarding up to 6 hours post ingestion, with large ingestions often producing grapes or raisins in the emesis up to 12 hours after ingestion. Emesis should be followed by an antiemetic. ACC will not likely be of benefit if the toxic component is tartaric acid; however, it may still be of benefit. Therefore, most cases, especially those with a large ingestion, would benefit from ACC administration. Baseline blood work, including renal values and packed cell volume (PCV)/total protein should be obtained and repeated every 24 hours for 48 to 72 hours. Urinalysis (UA) and urine specific gravity (USP) are not typically necessary in young, healthy animals unless azotemia/ uremia develops and then may be a helpful tool at monitoring progression. IV fluids are recommended for 48 hours. With prompt decontamination and therapy, most patients do not develop clinical signs beyond GI upset. If care is delayed more than 18 hours, the prognosis is guarded to poor.5


Ibuprofen is a popular over the counter (OTC) nonsteroidal anti-inflammatory drug (NSAID), also available by prescription in higher concentrations. Ibuprofen may be the only ingredient in a medication or be part of a combination product including opioids, antihistamines, decongestants, and acetaminophen. Ibuprofen is a competitive inhibitor of prostaglandin (PG) synthesis through inhibition of cyclooxygenase (COX), which results in decreased production of prostaglandin I2 and prostaglandin E2.2 In the GI tract (GIT), PGs normally have a cytoprotective effect. Decreased PG production causes increased acid secretion and decreased mucus production and mucosal blood flow.2 In the kidneys, PGs normally maintain afferent arteriolar dilation and other functions. Decreased PG production results in renal papillary necrosis and disruption of normal renal blood flow and homeostatic function. High doses may also result in CNS signs including seizures and coma.2 Although it is a concern in dogs and cats, felines are far more sensitive to ibuprofen poisoning because of their limited ability for glucuronidation.

Clinical signs often occur a few hours after ingestion and progress over several days. Initial signs may include vomiting, diarrhea, with or without blood, anorexia, and lethargy. If a renal toxic dose is ingested, PU/PD, continued anorexia and vomiting, and azotemia develop.1

Treatment includes inducing emesis followed by the administration of 1 dose of ACC. Cholestyramine given for 3 days has replaced multidose administration of activated charcoal for most NSAID exposures, including ibuprofen. Cholestyramine, a resin powder, does not allow bile acids to be reabsorbed in the GIT, instead converting bile acids to an insoluble form excreted through the feces. Additional therapy includes gastroprotectants (proton pump inhibitor, sucralfate,with or without prostaglandin E1 analogue), IV fluids for 48 hours if a renal toxic dose is ingested, and monitoring of renal indices for 48 to 72 hours. UA and USP are not typically necessary in young, healthy dogs unless azotemia/uremia develops and then may be helpful in monitoring progression. Proton pump inhibitors, such as omeprazole, are the gastroprotectants of choice for ibuprofen and other NSAID toxicosis.6

Therapeutic plasma exchange (TPE) is an ideal treatment for animals ingesting amounts far beyond a renal toxic dose. It has been shown to be successful in treating ibuprofen poisoning in dogs and should be considered in renal toxic doses7; however, limited availability and cost may prohibit use. Intralipid emulsion therapy (ILE) may be considered in cases of severe overdose, but because of ibuprofen’s high protein binding, ILE would only be of benefit to circulating ibuprofen once all protein binding sites have been saturated. Prognosis with prompt decontamination and therapy is good. Animals developing azotemia may recover with aggressive care.


Xylitol is a sugar alcohol with many healthy properties in humans as well as beneficial nonhealth properties. It has a sweetness comparable to sucrose and a low glycemic index, making it an ideal sugar substitute. It also has anticariogenic properties and works as a humectant, making its use in nonfood products including lotions and skin gels a possibility.8 With its many benefits, xylitol may be found in a wide range of products including gum, candy, mints, protein bars, weight-loss foods, sugar-free foods, toothpaste, mouthwash, dry-mouth spray, oral rinses, nasal spray, skin lotions, gels, and deodorants.1 Xylitol has also been found in an increasing array of prescription and OTC medications, especially gummy, liquid, or chewable formulations, and smoking cessation products.8 Dogs exposed to such products face added risk of intoxication as poisoning may result from the active ingredient of the product in addition to xylitol. This can cause serious and unanticipated clinical signs, which can easily complicate clinical treatment and prognosis. Xylitol has been shown to be toxic to dogs, rabbits, and cattle, with dogs being the most sensitive species.8 Cats do not appear to be affected.9 When dogs ingest xylitol, it is rapidly absorbed from the stomach and quickly converted to glucose. This stimulates a surge in insulin release, resulting in hypoglycemia. With larger ingestions, acute hepatic necrosis also may occur. The exact mechanism of action is unknown; however, 2 consistent theories exist. One is that depletion of adenosine triphosphate may result in decreased energy to the hepatocytes, resulting in cellular necrosis.8 Another theory suspects xylitol metabolism produces high levels of reactive oxygen species that damage hepatocytes, leading to cell death.8

Clinical signs of xylitol toxicosis in dogs may be seen as early as 20 to 30 minutes post ingestion, with vomiting being a common first sign.1 Hypoglycemia, persisting for 12 to 48 hours, occurs within 2 hours after ingestion. In addition to hypoglycemia, lethargy, ataxia, tremors, and seizures may be seen. If acute hepatic necrosis occurs, continued lethargy, inappetence, and icterus occur. Laboratory changes include elevations to alanine aminotransferase and total bilirubin, with occasional elevations to other hepatic indices such as γ-glutamyltransferase. Dogs experiencing acute hepatic necrosis may develop a secondary coagulopathy because of depletion of clotting factors produced in the liver.

Treatment includes decontamination with emesis if the patient is stable and blood glucose within normal limits, stabilization of blood glucose concentrations, and hepatic support.1 Because of low binding properties, activated charcoal is not typically recommended. Close monitoring of blood glucose and providing dextrose supplementation when needed is critical in the early stages of management. IV fluids supplemented with 2% to 2.5% dextrose and blood glucose monitoring are needed for 12 to 24 hours, and occasionally 48 hours, in dogs that become hypoglycemic. For dogs that develop significant hepatic enzyme elevations, dextrose supplementation may also be beneficial in providing hepatic support. It is important to note that hepatic necrosis may occur without the development of hypoglycemia. The use of hepatic protectants such as S-adenosyl-Lmethionine (SAMe) and N-acetylcysteine (NAC), monitoring hepatic parameters for a minimum of 2 to 3 days, and providing supportive care are necessary for a positive outcome in overdose situations. NAC is the drug of choice for dogs with evidence of severe hepatic enzyme elevations. Additionally, NAC is effective in restoring glutathione synthesis and reducing oxidative stress in the liver. Glutathione is essential in cell detoxification and many metabolic processes.8 SAMe is given for 2 weeks in dogs with mild hepatic enzyme elevations and continued for 4 weeks in dogs that develop hepatic necrosis.

SAMe is present in 3 major biochemical pathways important to the liver.Through these pathways, SAMe is converted to glutathione and plays a role in liver mass regeneration, cell membrane structure, fluidity and function, and cell detoxification. The liver normally produces SAMe; however, in a diseased state endogenous SAMe conversion is decreased, so the administration of exogenous SAMe may increase liver glutathione concentrations and prevent its depletion.8

Coagulopathy is a common sequela to hepatic necrosis, leading to an increase in prothrombin (PT) and partial thromboplastin time (PTT). All coagulation factors, except for factor VIII, are synthesized in the liver, which is the site for vitamin K–dependent activation of factors II, VII, IX and X. Vitamin K deficiency may be seen due to altered enterohepatic circulation of bile acids, leading to malabsorption. Fresh frozen plasma treatment is successful in restoring PT and PTT values as it provides all the coagulation factors in their active form.


Bromethalin is a neurotoxic rodenticide that since 2012 has experienced increasing commercial use in the United States. In 2020, bromethalin became the No. 1 rodenticide exposure call received by Pet Poison Helpline.5 The toxic effects of bromethalin are a result of uncoupling of oxidative phosphorylation leading to myelin edema in the brain and spinal cord.2 Cats have been shown to be significantly more sensitive to bromethalin than dogs.2

Clinical signs of bromethalin toxicosis are dose dependent and include CNS depression, ataxia, tremors, seizures, paresis/ paralysis, hyperthermia, abnormal pupillary light reflex, anisocoria, nystagmus, and coma.1 Many pet owners will initially report progressive lethargy or weakness. In general, signs of poisoning are seen within 2 to 24 hours after ingestion; however, these can be delayed by 2 to 5 days with ingestions that are below the LD50 but above one-tenth of the LD50.

There is no antidote available for bromethalin, leaving aggressive GI decontamination with emesis crucial for successful outcomes in poisoning situations.1 Rodenticide bait products are not rapidly broken down in the stomach, making emesis up to s6 hours post ingestion rewarding. Emesis should be followed by 1 dose of ACC, which should then be given every 6 to 8 hours for a total of 24 hours because of enterohepatic recirculation of bromethalin and its metabolites. Monitoring sodium is recommended with administration of multidose activated charcoal, as is utilizing IV fluids to minimize the risk of hypernatremia. Supportive and symptomatic care include mannitol for cerebral edema and methocarbamol for tremors. With prompt and aggressive decontamination, clinical signs of bromethalin toxicosis are infrequent; however, when signs do occur, euthanasia is a common sequela.10

Vitamin D3 /cholecalciferol

Vitamin D3 is synonymous with cholecalciferol. When looking at supplement and food products, vitamin D3 is listed as an ingredient, whereas cholecalciferol is listed as the active ingredient in certain rodenticides. Most exposures in animals occur because of ingestion of human supplements; however, exposures to cholecalciferol rodenticides continue to rise. Vitamin D3 is found in OTC products in many stores and available in much higher strengths at pharmacies, although it is not a prescription drug. Ingestion of these products may result in severe hypercalcemia and hyperphosphatemia.1 Soft tissue metastatic mineralization, with the kidney being the more sensitive organ, results in acute kidney injury and failure.1

Initial signs of vitamin D3 toxicosis include vomiting, inappetence, and lethargy.2 Within 2 to 3 days of ingestion, PU/PD, more significant lethargy, weakness, and continued vomiting are seen. Initial lab work typically shows hypercalcemia and hyperphosphatemia, with a progression to azotemia after 24 to 72 hours.

Decontamination includes emesis and administration of a single dose of ACC, followed by cholestyramine for 3 days. Treatment involves aggressive 0.9% NaCl IV fluid therapy for 24 hours to promote calciuresis. In cases where hypercalcemia (total serum calcium > 14-15 mg/dL or ionized calcium > 1.5 mmol/L) and hyperphosphatemia (> 7-8 mg/dL) are evident, a bisphosphonate such as pamidronate disodium is recommended. Prednisone may be added to increase calciuresis if a bisphosphonate is not available. Furosemide may also be used to increase calciuresis; however, because of the likelihood of more negative effects including dehydration, it should be reserved for patients not responding to other therapies or where a bisphosphonate is not available. Bisphosphonates are the treatment of choice to decrease calcium absorption and phosphate binders are recommended to decrease hyperphosphatemia. Serum calcium is expected to decrease within 24 to 48 hours after bisphosphonate administration. If no response is seen within 3 to 4 days, repeat dosing may be needed. Symptomatic animals often require weeks to months of laboratory monitoring and medication adjustment. Animals who develop renal injury may be successfully treated as patients with chronic renal disease if there is resolution of the hypercalcemia.


Although marijuana, or its’ ∆-9-tetrahydrocannabinol (THC) component, exposures are not new to our veterinary patients, 2022 was the first year that THC appeared in the top 10 toxin list for Pet Poison Helpline.5 From 2019 through 2023, Pet Poison Helpline experienced a 735.6% increase in the number of calls regarding pet exposure to THC-containing products.5 THC is a partial agonist at cannabinoid receptor 1 (CB1) and cannabinoid receptor 2 (CB2), endogenous mammalian receptors similar to opioid receptors.2 These receptors play physiologic roles in the CNS, as well as the inflammatory and immune systems. CB1 receptors are found in the CNS, with lower concentrations in the peripheral nervous system (PNS), and are involved in cognitive function, emotion, motion/motor, hunger, neuroprotection, posttraumatic events, and degenerative diseases. They are also involved in sensory/autonomic functions including pain perception, respiratory, cardiovascular, and gastrointestinal. CB1 receptors are responsible for the psychotropic effects of THC. In contrast, CB2 receptors are primarily in the PNS, and the effects are nonpsychotropic. These receptors are involved in reducing inflammation and providing chronic pain relief.

The most common THC exposure calls to Pet Poison Helpline involve food (homemade or commercial edible goods often made with marijuana butter or cooking oils used to extract the lipid soluble THC) followed in decreasing order by plant material, medical preparations or prescription medications, and other substances, including gummies.5 The butters and oils used in baked goods can contain high concentrations of THC and pose a greater risk than ingestion of plant material alone. Coingestion of chocolate, xylitol, macadamia nuts, and other products may complicate patient care. Traditional joints typically contain THC concentrations varying from 0.4% to 30%. Dogs are reported to have a larger number of CB receptors in the brain compared with people, and thus may have increased sensitivity to the psychoactive nature of THC.

The most common clinical signs noted are lethargy, ataxia, and vomiting.1,5 Other common signs include CNS depression, ataxia, urinary incontinence, increased sensitivity to motion and sound, mydriasis, hyperesthesia, bradycardia, hypothermia, and tremors. Less common signs include hypotension, bradypnea, aggression, agitation, tachycardia, nystagmus, and, rarely, seizures. Fatalities in veterinary medicine are rare. Clinical signs often develop within 1 to 2 hours after exposure and typically resolve within 12 to 72 hours. Diagnosing marijuana exposure with human urine drug tests is usually unreliable. Patient-side tests designed for detection of THC metabolites in human urine often result in false negatives when used in dogs and cats.11 Veterinary diagnostic laboratories and other drug testing laboratories may be able to detect a range of THC metabolites in dogs, including use of an ultraperformance liquid chromatography-tandem mass spectrometer.12

Decontamination includes emesis in asymptomatic patients within 60 minutes of ingestion followed by 1 dose of ACC and SQ or IV fluids.1 Mildly affected cases may be monitored at home if kept in a safe environment. For those patients with more significant signs, monitoring vitals and providing supportive in-house care including antiemetics, IV fluids, sedation if needed, and nursing care as needed are considered appropriate. In severely affected animals nonresponsive to supportive care, IV lipid emulsion (ILE) may be effective.1 Use of ILE in most cases is not routinely recommended or necessary because of a positive response to general care.5 Although aggressive care is not generally necessary, the use of extracorporeal therapies, including charcoal hemoperfusion and hemodialysis, has been successfully reported.13 Prognosis is good to excellent with supportive care. Moderately symptomatic cases may require 24 to 36 hours of care, whereas severely affected cases may require up to 72 hours.


Foods from Allium spp include onions, garlic, shallots, chives, scallions, and leeks. Sulfur containing oxidants in Allium spp, if ingested in sufficient quantity by cats and dogs, can cause oxidative hemolysis and anemia.1 Although ingestion of fresh onions and garlic is harmful, there is a more concerning exposure source in concentrated forms such as powders, salts, and minced products.5 For example, 1 tsp of onion powder is equivalent to approximately 2 oz of fresh onion. Garlic is expected to be 3 to 5 times as toxic as onion.1 There is a narrow margin of toxicity in dogs and cats, but cats are much more sensitive.

Clinical signs of poisoning include vomiting, diarrhea, lethargy, depression, abdominal pain, diarrhea, pallor, tachycardia, tachypnea, and icterus. Signs may develop within 1 to 2 days with a large acute exposure or up to several days with smaller exposures.

When toxic quantities of onions or garlic are consumed, treatment involves early emesis followed by 1 dose of ACC. Baseline blood work, including PCV and complete blood count, should be evaluated with monitoring every 1 to 2 days for 5 to 7 days or until the anemia, if present, has stabilized. Anemia typically resolves 10 to 14 days after ingestion. Whole blood transfusions and/or packed red cells and oxygen support may be needed to stabilize the patient depending on the severity of anemia and associated signs. GI signs can be treated as needed with SQ or IV fluids, antiemetics, antidiarrheals, and a bland diet.

Anticoagulant Rodenticides

Use of anticoagulant rodenticides, more specifically longacting anticoagulants (LAACs), continues to be common in the United States despite the EPA’s 2012 ban on residential/ in-home use of second-generation LAACs. These rodenticides, including bromadiolone, brodifacoum, difenacoum, and difethialone, remain available for pest control company and agricultural facility use. Although not intended for in-home use, there is no law banning individuals from using second-generation LAACs in the home or residence, highlighting the importance of diligence in determining the specific active ingredient in products ingested by animals. LAACs are Vitamin K antagonists and interfere with the activation of Vitamin K–dependent clotting factors (factors II, VII, IX, and X).2 Although peak plasma concentrations occur within 12 hours, outward clinical signs are often delayed by several days due to timing of the natural decay of circulating clotting factors. The margin of safety for anticoagulant rodenticides for many species varies based on the active ingredient. Cats are significantly more resistant to the effects of these products than most species, especially dogs, and rarely suffer poisoning.2

The most common clinical signs of anticoagulant poisoning noted by pet owners include lethargy, exercise intolerance, inappetence, pallor, hematuria, epistaxis, localized edema, and dyspnea or wheezing.1 These signs typically begin 3 to 5 days following exposure as circulating clotting factors are depleted and clotting factor production has ceased. Otic hemorrhage has been reported as a unique finding in cats.14 Other less common signs include generalized pain, fever, lameness, or neurologic abnormalities. A rare but reported consequence of anticoagulant rodenticide toxicosis identified in smallbreed dogs is tracheal collapse.15 Massive blood loss into the thoracic and abdominal cavities is common and is frequently the cause of death. Although a diagnosis is often made based on exposure history and/or clinical signs, confirmatory laboratory findings include PT and potentially PTT. The presence of anemia and activated clotting is 2 to 10 times or more than normal along with a consistent history also support a diagnosis of poisoning. Platelets may be normal to slightly decreased; however, anticoagulants do not interfere with platelet production or function. If thrombocytopenia is present, the finding is likely secondary to blood loss or due to another cause.

Treatment includes decontamination and use of the antidote, vitamin K1 (phytonadione). Emesis is beneficial after an acute ingestion of an anticoagulant rodenticide, especially in instances where there is concern for owner adherence in administering the antidote. Lab work, including PT/ PTT, is not recommended in cases where exposure occurred less than 36 to 48 hours earlier, as not enough time has elapsed for circulating clotting factors to be reduced and changes to PT/PTT to become evident. Evaluating PT/PTT 36 to 48 hours after exposure may be considered in lieu of initiating vitamin K1 to determine whether the antidote is necessary. A PT should be obtained 48 hours after treatment is discontinued to assure proper duration of treatment. If PT is prolonged, Vitamin K1 should be reinstituted for another 21 days and rechecked 48 hours after treatment is discontinued. Vitamin K1 has no direct effect on coagulation, and it takes 6 to 12 hours to make new clotting factors once therapy is instituted.2 Animals suffering significant blood loss may need a transfusion of fresh whole blood or plasma to provide clotting factors. Animals with severely compromised respiratory systems due to hemothorax may need a thoracocentesis.


Although the Pet Poison Helpline top 10 toxin list historically has included plants, human medications, and products used in and around the home, carprofen, a cyclooxygenase 2 (COX-2) inhibitor NSAID, is the first and only veterinary-approved medication to make the list. At therapeutic doses, COX-2 inhibitors provide anti-inflammatory and analgesic properties.2 In overdose situations, carprofen also inhibits COX-1 enzymes leading to GI ulceration and renal injury.2 In severe cases, hepatic injury and neurologic effects including seizures and coma have been reported.1

Clinical signs of carprofen toxicosis include vomiting and diarrhea, both potentially containing blood, as well as lethargy and inappetence. For patients ingesting a renal toxic dose, continued lethargy and vomiting along with laboratory changes including azotemia consistent with acute kidney injury may be seen within 24 to 72 hours after exposure. Significant gastric ulceration may be present several days after the initial ingestion. Duodenal perforation has been reported in cats after carprofen ingestion, and gastric and duodenal perforation have been reported in dogs when carprofen exposure occurred along with corticosteroid use.16,17

Treatment for carprofen toxicosis is consistent with that for ibuprofen toxicosis, including decontamination and gastroprotectants for doses expected to result in GI ulceration. Additionally, IV fluid therapy and lab work monitoring for renal compromise are recommended. In severe cases, TPE has been shown to be successful in decreasing carprofen plasma concentration in dogs.18 As with ibuprofen, ILE may be of benefit in cases of severe poisoning.

Renee D. Schmid, DVM, DABT, DABVT, is senior veterinary toxicologist and director, veterinary medicine for Pet Poison Helpline. She earned a bachelor of science in agriculture and her doctorate degree at Kansas State University in Manhattan. She joined the helpline and Safety Call International in 2013.


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  11. Schmid RD. Testing for marijuana toxicity in dogs. Clinician’s Brief.May 2022. Accessed February 16, 2024. 
  12. Fitzgerald AH, Zhang Y, Fritz S, et al. Detecting and quantifying marijuana metabolites in serum and urine of 19 dogs affected by marijuana toxicity. J Vet Diagn Invest. 2021;33(5):1002-1007.
  13. Culler CA, Vigani A. Successful treatment of a severe cannabinoid toxicity using extracorporeal therapy in a dog. J Vet Emerg Crit Care (San Antonio). 2019;29(6):674-679.
  14. Kohn B, Weingart C, Giger U. Haemorrhage in seven cats with suspected anticoagulant rodenticide intoxication. J Feline Med Surg. 2003;5(5):295-304.
  15. Thomer AJ, Santoro Beer KA. Anticoagulant rodenticide toxicosis causing tracheal collapse in 4 small breed dogs. J Vet Emerg Crit Care (San Antonio). 2018;28(6):573-578.
  16. Pfeifer JM, Levy NA, Carter DL, Beal MW. Gastric or duodenal perforation and secondary septic peritonitis following therapeutic nonsteroidal anti-inflammatory drug administration. J Vet Emerg Crit Care (San Antonio). 2022;32(6):764-768.
  17. Runk A, Kyles AE, Downs MO. Duodenal perforation in a cat following the administration of nonsteroidal anti-inflammatory medication. J Am Anim Hosp Assoc. 1999;35(1):52-55.
  18. Buseman M, Blong AE, Walton RA. Successful management of severe carprofen toxicity with manual therapeutic plasma exchange in a dog. J Vet Emerg Crit Care (San Antonio). 2022;32(5):675-679.
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