Common Toxicities Seen in the ER

Ingesting toxic foods and medications are common reasons pets come to DoveLewis for emergency care. Learn from Critical Care Specialist Erika Loftin, DVM, DACVECC, about how to recognize the symptoms of particular toxins and address each situation effectively.  This article is specifically RACE-approved for 1 DVM or 1 Technician CE credit upon completing the quiz.

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General approach to toxicities

The initial approach to the intoxicated patient should focus on obtaining an accurate exposure history from the owner, along with a rapid physical exam assessment and initiation of stabilizing therapy. Regardless of the ingested toxin, symptomatic and supportive treatment is almost always appropriate. There are a few toxins that have a known antidote, which can be administered once exposure is confirmed.

  • National Animal Poison Control Center : 888-426-4435 (consultation fee applies)

  • Pet Poison Helpline: 800-213-6680 (consultation fee applies)


Decontamination techniques

Emesis induction - For patients that present within 2-4 hours of ingestion of a known toxin, with minimal or no clinical signs, emesis induction is usually recommended. This is most safely performed by administration of apomorphine (IV or subconjunctivally) in dogs, and xylazine IM in cats (see Table 2 for doses). The recommended medications are based on the mechanism of action and species-specific receptor differences. Oral administration of hydrogen peroxide and concentrated salt solutions should be avoided due to potential for side effects. Emesis induction does not eliminate the requirement for further treatment in cases of dangerous ingestions, as many toxins are rapidly absorbed and only a portion of stomach contents are retrieved (40-70%). Emesis is contraindicated in cases of ingestion of petroleum distillates, acids, and alkalis due to the risk of aspiration or chemical burns to the esophagus. Emesis is also contraindicated in animals with altered mentation, decreased gag reflex, or seizures, as well as those that are already vomiting or have had recent abdominal surgery. Emesis induction should also be considered relatively contraindicated in patient with prior medical history that makes them at increased risk for aspiration pneumonia, such as patients with laryngeal paralysis or megaesophagus.

Gastric lavage – For patients that cannot safely have emesis induced (see above) or when emesis induction is unsuccessful, gastric lavage can be considered. General anesthesia is induced and the patient is intubated to protect the airway. The patient is positioned in lateral recumbency, and a large-bore gastric tube is measured to the last rib and marked. After lubrication, the tube is gently passed into the gastric lumen and placement confirmed via palpation or retrieval of gastric contents. Warm water is then pumped into the stomach (~5-10mL/kg at a time) and allowed to passively drain out (either use double lumen tube or periodically remove pump and allow fluid to drain). This process is repeated until the retrieved lavage fluid runs clear. A dose of activated charcoal can be administered via orogastric tube at the end of the procedure if indicated. Human studies have failed to show significant improvements in outcome with gastric lavage, but clinically it makes a big difference in the recovery time of certain veterinary patients, specifically those with ingestion of metaldehyde or other tremorogenic compounds. Risks include aspiration and iatrogenic damage to the pharynx, esophagus, or stomach. Patients should be monitored closely during anesthetic recovery, and extubation delayed until a good swallow reflex is present.

Activated charcoal (AC) – carbon compound treated to increase surface area and allow many binding sites for adsorption of toxic agents. AC is usually combined with a cathartic such as sorbitol, to speed passage of toxins through the GI tract. Not all toxins are effectively bound to AC. Charcoal can be carefully administered via syringe, although many animals will voluntarily ingest it if mixed with something palatable such as baby food or canned food. AC is most effective if administered within 1 hour of toxin ingestion. Multiple doses should be administered in cases of toxins that have a prolonged half life and/or undergo enterohepatic recirculation (every 4-8 hours for 1-3 days). A cathartic should be administered only with the first dose of charcoal, as repeated doses of cathartics can lead to diarrhea, dehydration, and hypernatremia.

Additional techniques

IV fluid diuresis – can help speed elimination of toxins that undergo primarily renal excretion. IV fluids are also indicated for rehydration and volume resuscitation in hypotensive patients, as well as part of therapeutic cooling in hyperthermic patients.

Cholestyramine is a bile acid sequestrant (binds bile in the gut), and is an effective adjunct method of decontamination for some toxicities (such as vitamin D). Can be obtained from human pharmacies. Suggested doses vary (see chart below). Can be continued for a couple of days in the event of massive vitamin D ingestion.

Magnesium hydroxide (ie milk of magnesia) - binds iron to convert to a form that cannot be absorbed from the GI tract. Available over-the-counter.

Enemas – the colon is very efficient at reabsorption, and toxins can be returned to circulation at this location. Enemas to remove toxins from the lower GI tract can be an effective route of decontamination, particularly in animals in which emesis cannot be safely induced due to clinical signs or decreased mentation. Administration of rectal charcoal can be performed, but without any proven benefit.

CRRT (continuous renal replacement therapy) or hemodialysis – can be a useful decontamination method for toxins that are not highly protein bound (ethylene glycol and metabolites, acetaminophen, etc). This therapy is expensive, not widely available, and can potential lead to complications such as hemorrhage, electrolyte abnormalities, and coagulopathy. Using special filters (charcoal hemoperfusion) can increase the amount of toxin removed in some cases.

Lipid rescue – IV lipids (such as those used in formulating parenteral nutrition) can be a useful decontamination method for toxins that are lipid soluble (local anesthetics, baclofen, ivermectin, pyrethrins, calcium channel blockers, metaldehyde, marijuana, etc). This therapy is relatively inexpensive, can often be obtained from human hospital pharmacies, and few complications have been reported. The mechanism of action is not completely understood, but it is believed that lipid infusion creates a "lipid sink" into which lipophilic drugs can partition for removal from the body. Lipid infusion may also move fatty acids into mitochondria to provide ATP, thus decreasing the risk of cell death. Many of the common commercial lipid preparations are isotonic and can be given through a peripheral catheter. Protocols are adapted from human literature without any supportive experimental evidence in veterinary patients. Lipid protocols vary, but typically suggest that with a 20% lipid emulsion, give a bolus of 1.5mL/kg over 5-15 minute IV, then start a continuous rate infusion at 0.25mL/kg per minute for 30-120 minutes. This is considerably higher than recommended rates when using lipids for parenteral nutrition, and risk vs benefit should be considered. For less severe toxicities (patient not in cardiovascular collapse), consider administering the lipids at RER (30xkg + 70, caloric density of lipids is 2kcal/mL) over a longer period of time. Side effects with lipid infusions are uncommon, but theoretically can include allergic reactions (soy), fluid overload, lipid emboli (pulmonary, etc), transient immunosuppression (typically only seen with chronic lipid dosing), and potentially pancreatitis in at risk-patients.  A “fat overload syndrome” has been documented in humans, including hepatomegaly, icterus, and hemolysis. The lipid dose can be repeated if clinically indicated and serum is not significantly lipemic. Lipid rescue should be used with, not instead of traditional supportive therapy, and in some cases other medications that are indicated (such as diazepam) are lipid soluble and thus could be less effective in the presence of lipid infusion.



Common toxicities


Anticoagulants – First generation (warfarin) toxic dose is 0.5mg/kg, duration of action is approximately 2 weeks. Second generation products (brodifacoum, bromadiolone, diphacenone, chlorophacinone, etc) have a lower toxic dose (0.02mg/kg) and a longer duration of action (21-30 days or more). All products in this category act by inhibiting the enzyme vitamin K epoxide reductase, thus preventing the recycling of the active form of vitamin K1. This leads to a loss of clotting factors 2, 7, 9, and 10, which results in hemorrhage several days after ingestion. Hemorrhage can occur in any location, including intrathoracic, intrapulmonary, gastrointestinal, into the urinary bladder, or into joints or subcutaneous areas. The diagnosis is made via evaluation of clotting times (PT will become prolonged prior to PTT because factor 7 has the shortest half life). Treatment includes administration of vitamin K at a dose of 3-5mg/kg/day for up to 3-6 weeks depending on the compound and dose ingested. It is recommended that coagulation times be checked 48-72 hours after finishing the prescribed vitamin K course to ensure that further treatment is not necessary. If the animal is actively hemorrhaging, plasma transfusions are required as it will take at least 12 hours for the vitamin K to result in restoration of clotting factors. Additional supportive care (oxygen, thoracocentesis, pRBC tranfusions) may also be required in some cases.  If the animal is presented within 2-4 hours of ingestion, decontamination and monitoring coagulation times for 72 hours may be sufficient therapy. Prognosis is good for animals that are treated prior to the onset of hemorrhage, fair to guarded once hemorrhage occurs. New EPA regulations prohibit use of second generation anticoagulants in consumer products (effective June 2011), and this may lead to an increase in the number of pets presenting with bromethalin or cholecalciferol intoxications (see below).

Bromethalin - Toxic dose = 0.46 mg/kg in dogs, 0.24 mg/kg in cats.  LD50 = 3.65mg/kg in dogs, 0.54mg/kg in cats. The commercial pellets and bait bars are 0.01% bromethalin. This toxin acts by uncoupling oxidative phosphorylation which results in decreased ATP production. This can cause two different clinical syndromes depending on the dose ingested. At a high dose, animals will display a “convulsant syndrome”,  leading to hyperesthesia, tremors, seizures, circling, CNS depression, hyperthermia, and death (seen acutely within 24 hours  following ingestion). At a lower dose, animals may display a delayed “paralytic syndrome”, with signs including ataxia, CNS depression, and ascending hindlimb paresis/paralysis (seen within 7-14 days). There is no specific antidote for bromethalin – treatment includes decontamination, close monitoring, and symptomatic therapy for CNS signs (mannitol, furosemide, corticosteroids). Due to a long half life and enterohepatic recirculation, repeated doses of activated charcoal are recommended for substantial ingestions. ASPCA recommends emesis induction and 1 dose of charcoal for canine ingestions 0.1-0.49mg/kg, three doses of charcoal q8 hours for doses 0.5-0.75 mg/kg, and 6 doses of charcoal q8 hours for doses >0.75mg/kg. Prognosis is poor once signs develop, although some animals with less severe signs can recover with supportive care.

Cholecalciferol (vitamin D) – Toxic dose = 0.1-0.5 mg/kg for dogs. Cholecalciferol is metabolized to calcitriol, which acts by increasing calcium uptake from the GI tract, as well as mobilizing it from bone and enhancing resorption from the kidneys. A similar toxicity can be seen with ingestion of psoriasis creams or vitamin overdose. As hypercalcemia progresses, it leads to tissue mineralization and acute renal failure. Phosphorus will increase first (usually within 12 hours), followed by calcium elevation within 24 hours. Azotemia usually develops 24-72 hours post-ingestion. Treatment includes decontamination via emesis induction , activated charcoal (repeat dosing due to enterohepatic recirculation) and potentially cholestyramine.  Blood calcium and phosphorus monitoring every 12-24 hours until 3-4 days post-exposure is recommended. If values become elevated, IV fluid diuresis and treatment for hypercalcemia should be started. 0.9% NaCl is considered the fluid of choice as sodium ions can enhance excretion of calcium via the kidneys. Additional strategies include administration of furosemide, steroids, and pamidronate (bisphosphonate that inhibits calcium reabsorption from bone). Because cholecalciferol has a long half-life, treatment may need to be continued (often on an out-patient basis) for several weeks. In these cases, feeding a diet low in calcium and phosphorus may also be recommended. Prognosis is guarded if renal failure develops.

NSAIDS – Toxic dose is dependent on the specific drug as well as the species affected (see below). In addition, susceptible patients (pediatrics, geriatrics, those with pre-existing renal, hepatic, or GI disease) may have clinical consequences at doses lower than those generally considered toxic. There are a variety of human and veterinary approved drugs that fit into this class. NSAIDS block the cyclooxygenase enzymes and thereby inhibit production of prostaglandins, which are molecules that can contribute to pain and inflammation, but are also necessary to maintain GI mucosal health and renal blood flow. In addition, NSAIDS can cause cellular injury via direct irritation of GI mucosa. In general, GI signs (vomiting, diarrhea, ulceration, hemorrhage) are seen at lower NSAID doses, and renal failure at higher doses. At very high doses, NSAID toxicity can lead to neurologic signs (seizures, coma). Treatment involves decontamination (if acute ingestion), and supportive therapy for the GI and renal systems. As NSAIDS undergo enterohepatic recirculation, repeat doses of charcoal are typically recommended. GI supportive medications include acid blockers (famotidine, omeprazole), mucosal protectants (carafate), and synthetic prostaglandins (misoprostal) for at least 7-10 days. IV fluids diuresis for a minimum of 48 hours is recommended with renal toxic doses of NSAIDS. Prognosis is guarded if acute renal failure develops or if neurologic signs are seen. High doses of aspirin can result in metabolic acidosis, and sodium bicarbonate administration may be indicated. There are also some idiosyncratic reactions that have been documented with specific NSAIDS, including carprofen-related hepatotoxicity and development of KCS in patients receiving etodolac. These reactions occur independently of the administered dose, and may be breed specific. Specific toxic doses are not well established for all available NSAIDS, but in general it has been suggested that dogs can develop GI upset at any dose, GI ulcers at 4-5x the label dose, and renal injury at 8-10x the label dose. Cats are typically 2-5x more sensitive to NSAIDS than are dogs. These guidelines may be useful for NSAID ingestions when toxicologic data is lacking, but individual risk based on age, history, and concurrent drug therapy should always be assessed and patients treated as symptoms dictate.


GI toxic dose

Renal toxic dose



Dogs 50mg/kg

Cats 25mg/kg


Metabolic acidosis at 300mg/kg


Dogs 25mg/kg

Cats – any dose

Dogs 150-175mg/kg

Cats 20-50mg/kg

Neuro signs at 400mg/kg

Lethal at 600mg/kg


Dogs 5mg/kg

Cats – any dose

Dogs 10-25mg/kg

Cats – any dose

Neuro signs at 50mg/kg


Dogs 40mg/kg




Dogs 20mg/kg

Cats 4mg/kg

Dogs 30-40mg/kg

Cats 8mg/kg



Dogs 1mg/kg

Cats – any dose # label

Dogs 2mg/kg

Cats 1.5x the label dose



Dogs 15mg/kg

Cat 4mg/kg

Dogs 20-30mg/kg

Cats 8mg/kg



Can occur at any dose

Dogs 1mg/kg




Dogs 1mg/kg


Firocoxib (previcox)

Dogs 25mg/kg




Dogs – any dose

Dogs 40mg/kg



LD50 in dogs is reported to be 332mg/kg, adverse effects seen at much lower doses

Flunixin (banamine)

“Suggested” dose for analgesia in dogs is 1mg/kg, see guidelines above for toxic dose

Acetaminophen - Toxic doses are species-dependent due to differences in metabolism. Acetaminophen is metabolized by several pathways in the liver (including the cytochrome p450 system) to both toxic and non-toxic metabolites. If the amount of acetaminophen ingested overwhelms the processing ability of the system, toxic metabolites will build up and cellular death will result. Cats have a reduced ability to metabolize acetaminophen to non-toxic metabolites, and they also possess red blood cells that are more sensitive to oxidative injury. Acute signs in cats are usually due to methemoglobin formation, whereas acute signs in dogs are more likely related to hepatic failure. Facial edema can be seen in both species with acute toxicity. KCS can also develop within 48 hours of exposure. Treatment includes decontamination if ingestion is acute, followed by medications to encourage elimination of the toxin and to protect the body from the toxic metabolites. Glutathione precursors (such as SAMe or N-acetylcysteine) are recommended to provide free radical scavenging capability and promote metabolism to non-toxic products. Vitamin C converts methemoglobin to reduced hemoglobin, and also helps with free radical scavenging. Cimetidine reduces metabolism of acetaminophen by the cytochrome p450 system and thus may decrease production of the hepatotoxic metabolites; however, it has been suggested that the concentration of cimetidine needed to achieve this effect is far higher than the recommended therapeutic dose, and treatment with cimetidine is not consistently recommended in human acetaminophen intoxication. Prognosis is guarded once clinical signs are present.

*Dogs - KCS risk at 20-30mg/kg

  Possible GI effects at 50mg/kg

  Risk of liver damage if >100mg/kg

*Any dose is considered toxic in cats

Tremorogens (metaldehyde, compost) – Toxic dose is not well established.  The hallmark of these toxicities is severe muscle tremors leading to hyperthermia. The exact mechanism is not known, but a reduction in GABA levels has been documented in patients suffering from metaldehyde toxicity. Treatment includes muscle relaxants (methocarbamol, diazepam), IV fluids, and sometimes phenobarbital or a propofol CRI in severe cases demonstrating seizure activity. Decontamination is very important, and gastric lavage should be recommended for recent ingestions if emesis induction is not possible. Enemas are also helpful to remove toxin from the colon and prevent continued reabsorption.  Lipid rescue may be useful for metaldehyde.  If severe hyperthermia has occurred, the patient should be monitored for complications including coagulopathy. Hepatic failure is possible 3-5 days after metaldehyde ingestion. A similar syndrome can be seen after ingestion of compost or moldy food.

Pyrethrins – organic esters extracted from the flower heads of Chysanthemum plants or synthetic variants. Pyrethrins work by stimulating the CNS (reversibly prolonging sodium conductance), resulting in muscular excitation and convulsions. Most veterinary exposures are due to application of topical flea medications, and cats are far more commonly affected than dogs due to species-specific sensitivity. Treatment focuses on removing the substance (bathing, potentially shaving affected fur), and supportive therapy (IV fluids, diazepam and/or methocarbamol as described above for ingested tremorogens). More severe cases with refractory tremors or seizure activity may require administration of phenobarbital or a propofol CRI to control signs. Lipid therapy may be useful for as a method of decontamination for this toxicity, although controlled studies are lacking.

Chocolate – Toxic dose is dependent on the type of chocolate (see below), and various charts and calculators are available to help with rapid determination of the potential for toxicity based on body weight and the product consumed. Chocolate toxicity is due to methylxanthines (theobromine and caffeine), which lead to catecholamine release and signs of hyperexcitability with cardiovascular and neurologic consequences. Clinical signs include tachycardia and sometimes arrhythmias, hypertension, hyperactivity, muscle tremors, and potentially seizures. Gastroenteritis and pancreatitis are also possible. Treatment is supportive – decontamination, IV fluids, sedation, and sometimes beta-blockers for tachycardia. Frequent urination should be encouraged as the toxins are reabsorbed through the bladder. In cases with severe signs including seizures and obtundation, urinary catheter placement is recommended to prevent urinary reabsorption.

20mg/kg methyxanthines (theobromine + caffeine) = mild signs

40mg/kg = moderate signs

60mg/kg = severe signs

Type of Chocolate



Milk chocolate






Dark chocolate



Baking chocolate



Cacao beans



Xylitol – Toxic dose is 0.1g/kg for hypoglycemia, 0.5-1g/kg for acute hepatic failure. Xylitol is an artificial sweetener used in sugar-free gums, sugar-free toothpaste and mouthwashes, and some candies/baked goods. In dogs, it can cause a rapid and dose-dependent increase in insulin levels and resultant drop in blood glucose. At higher doses, xylitol has been linked to acute hepatic necrosis. Xylitol is rapidly absorbed from the stomach and hypoglycemia can be seen within 30 minutes of ingestion (although occasionally delayed for up to 12 hours). Liver failure may not manifest for 8-48 hours after ingestion. Decontamination must be pursued early to be useful, as xylitol is rapidly absorbed from the stomach. Emesis induction is not likely useful if more than 30-60 minutes has passed since ingestion. Activated charcoal is not indicated for this toxicity. In asymptomatic animals, monitoring blood glucose for 12 hours and providing small/frequent meals may be adequate. Significant hypoglycemia should be treated with IV dextrose, and serum potassium and phosphorus should also be monitored. Hepatoprotectants may be useful in dogs that have ingested a large amount of xylitol, and hepatic enzymes should be monitored for 48 hours following exposure. If hepatic failure develops, supportive therapy should be provided as for any other cause, and prognosis is guarded to poor.

Grapes/raisins – Toxic dose for dogs is not clearly established, but renal failure has been documented following ingestions of very small amounts (0.7 oz/kg grapes and 0.11 oz/kg raisins). The exact nephrotoxic agent in grapes and raisins has not been identified, but theories include pesticide residues, heavy metals, or molds. This is not a predictable toxicity, as many dogs ingest grapes or raisins and have no ill effects. Due to the potential for toxicity, the recommended treatment for ingestion of these substances is decontamination (emesis induction, charcoal, +/- enema) and IV fluid diuresis for 48 hours to prevent or minimize renal tubular damage. Baseline bloodwork should be obtained, followed by repeat renal values at 24 and 48 hours following ingestion. If acute renal failure develops, additional supportive care should be instituted as clinically indicated. Grape seed extract seems to be safe (based on reports that toxicity has occurred with seedless grapes).

Lilies – Members of the genus Lilium and Hemerocallis are highly toxic to cats, and ingestion of even a small amount of any part of the plant can cause renal failure. The mechanism of toxicity is not well understood. There are other plants with “lily” in the name that are not nephrotoxic, although they can still cause gastrointestinal signs if ingested (water lily, peace lily, calla lily). With nephrotoxic lilies, signs usually develop within 12 hours of ingestion, but can be delayed up to several days in some cases. BUN, creatinine, potassium, and phosphorus typically begin rising within 24-48 hours. Treatment following ingestion includes decontamination (emesis and 1-2 doses of activated charcoal), and IV fluids at twice maintenance for at least 48 hours with bloodwork monitoring as above for grapes/raisins. Prognosis is guarded to poor if renal failure develops, so aggressive decontamination and diuresis should be strongly recommended with any exposure.

Marijuana (tetrahydrocannabinol or THC) – Toxic dose in dogs is not well established, lethal dose is >3g/kg. THC is eliminated very slowly, leading to prolonged intoxication in dogs. Onset of clinical signs is usually seen within 30-60 minutes and signs include depression, disorientation, lethargy, ataxia, bradycardia, vomiting, tremors, mydriasis, hypothermia (or less commonly hyperthermia), and urinary incontinence. Treatment is symptomatic and supportive. This is rarely a fatal toxicity, but these patients are at risk for aspiration due to recumbency, mental depression, and vomiting. Due to enterohepatic recirculation, repeated doses of activated charcoal may be required. Hospitalization should be recommended for severely affected patients. Recovery typically occurs within 24-72 hours.


Human medications

Albuterol inhaler – Usually occurs when a dog bites into an inhaler and receives a concentrated dose of albuterol. Clinical signs of toxicity are secondary to beta-2 agonist effects, and include tachycardia, hypertension or hypotension, and hypokalemia (from potassium shifting intracellularly). Treatment includes propranolol (oral or IV), and IV fluid support with potassium supplementation. Acepromazine can be used if needed for hypertension.

Amphetamines – ADHD medications (Ritalin, Adderall, Focalin, etc), some weight loss drugs – These medications stimulate the release of norepinephrine, dopamine, and serotonin, and can also directly stimulate alpha and beta receptors. Depending on the medication, clinical signs can be seen at doses as low as 0.1mg/kg (amphetamine), with seizures occurring at doses ~0.3-0.5mg/kg. Signs can occur within 20-30 minutes of ingestion. Sustained release products have a longer onset as well as duration of signs. Signs of toxicity involve CNS over stimulation and excessive sympathomimetic effects such as agitation, vocalization, hyperactivity, hypertension, head bobbing, hyperthermia, tachycardia, tremors, and seizures. Treatment is primarily symptomatic and supportive. Emesis is not often recommended due to the rapid onset of clinical signs, but should be considered with very recent ingestions (within 30 minutes, up to 2 hours with extended release products). Gastric lavage and activated charcoal may be helpful. Maintaining control of hyperthermia, tachycardia and tremors are key elements in these cases. Phenothiazines (acepromazine, chlorpromazine) are very useful both for sedative effects and to block dopamine release/binding and alpha stimulation by amphetamines. Benzodiazepines are typically avoided as they have a propensity to increase CNS excitement in these cases, and phenobarbital can be used if needed for seizure activity. Other commonly used interventions include methocarbamol, beta-blockers, and IV fluids. Stimulation should be minimized and animals kept in a quiet dark environment. In severe cases, general anesthesia is necessary. Additionally, serotonin syndrome may occur and can be treated with cyproheptadine (orally or crushed and administered rectally). Signs may last for up to 72 hours with extended release products, and supportive care and cardiovascular monitoring should continue until clinical signs resolve.

Antihistamines – Any dose over the recommended therapeutic dose has the potential to cause clinical signs, and decontamination and monitoring should be recommended. Clinical signs are typically related to the CNS, and can include depression, sedation, and potentially paradoxical excitation (panting, pacing, tremors/seizures, hyperthermia). Treatment is symptomatic, and can include diazepam, IV fluids, thermal regulation, and pressors and/or beta-blockers if cardiovascular signs occur.

Calcium channel blockers (CCBs)Verapamil, diltiazem, amlodipine, etc. These drugs block calcium channels in the heart and/or arterial smooth muscle. Different drug classes have different affinities for the various receptors. These drugs are used for treatment of hypertension, cardiac disease (including HCM), and cardiac arrhythmias. The minimum oral toxic dose of each drug has not been well established in humans or animals. Overdoses result in severe and potentially life-threatening effects on blood pressure and cardiac conductance. Clinical signs include GI upset, weakness, collapse, hypotension, hypothermia, CNS depression, bradycardia, heart block, and occasionally reflex sinus tachycardia. Rarely CNS stimulatory signs can be seen (seizures, agitation, tremors). Non-cardiogenic pulmonary edema can develop secondary to changes in capillary and alveolar membrane permeability. Laboratory findings can include hyperglycemia due to inhibition of insulin release, hypokalemia, and metabolic acidosis (due to tissue hypoperfusion and increased lactic acid production). Treatment recommendations include decontamination, close monitoring of cardiovascular and respiratory status, and supportive therapy as clinically indicated (IV fluids, hetastarch, antiemetics, diazepam, potassium supplementation). Specific treatments that may be required include IV calcium supplementation, glucagon (may temporarily increase heart rate and contractility), sympathomimetic drugs (dopamine, dobutamine, isoproterenol, epinephrine, phenylephrine), and high dose insulin therapy with concurrent dextrose (enhances glucose uptake by myocytes, can increase intracellular calcium influx).  Severe heart block may require placement of a temporary cardiac pacemaker. Lipid rescue may be of benefit in severe cases both by the mechanisms explained above, as well as by directly activating calcium channels to reverse the intoxication.

Estrogen/progesterone – Toxic dose for bone marrow suppression is ~1mg/kg. Ingestion of human contraceptive tablets usually doesn’t result in toxicity because the amount of estrogen is very low. Topical estrogen creams are another potential route of exposure, as well as prescribed estrogen supplements for urinary incontinence. Toxicity results in pancytopenia, and treatment involves discontinuation of the medication, supportive care and monitoring CBCs. Prognosis is guarded.

Joint supplements – ASPCA database from 2008-2009 revealed 21 incidents of hepatic damage to dogs following ingestion of joint supplements. Multiple products were involved, and doses of glucosamine (183-6,667mg/kg), creatine (418-2,667mg/kg), and dimethylsulfone (45-4,000mg/kg) varied widely. Initial clinical signs developed within 30 minutes to 2 days after exposure, with most lab abnormalities occurring within 24-48 hours. Clinical outcome varied – some dogs made a full recovery with supportive therapy, some were euthanized due to the severity of disease, and some improved but required long-term therapy. The cause of hepatic damage in these cases is not known but could be a result of a contaminant, an interaction between ingredients or other medications, or preexisting health conditions. Current recommendations for joint supplement overdosages include induction of emesis followed by administration of activated charcoal in dogs recently exposed. Hepatic enzymes should be monitored and hepatoprotectants and other supportive therapy provided as indicated.

Pseudoephedrine – Potentially toxic at 2-3mg/kg, can be lethal at 10-12mg/kg. Pseudoephedrine is found in a number of OTC products both alone and in combination with other drugs. Pseudoephedrine has a rapid absorption, and onset of signs is usually within 15-30 minutes of ingestion (up to 7 hours with extended release products). Clinical signs occur secondary to stimulation of alpha (and to a lesser extent beta) receptors, and include hyperactivity, tremors, panting, mydriasis, hyperthermia, tachycardia, and hypertension. Animals with underlying cardiac disease or neurologic disease are at greater risk of complications. Treatment includes decontamination (emesis induction only if within 30 minutes of ingestion) with multiple doses of activated charcoal recommended for ingestion of extended release products, and supportive care. Therapies that may be helpful include acepromazine (for agitation, hypertension), propranolol (for tachycardia), and potentially cyproheptadine (for CNS effects). Diazepam is contraindicated as it can worsen the clinical signs. In-hospital monitoring (including EKG) is recommended, and signs can last up to 24-72 hours with large ingestion of extended release products. Excretion is enhanced with acidic urine, so in severe cases assessment of urine pH and potentially administration of ascorbic and/or ammonium chloride may be useful.

Serotonin syndrome – Antidepressants (Serotonin Reuptake Inhibitors-SSRIs, Tricyclic Antidepressants-TCAs) - Reconcile, Clomicalm, etc – A variety of medication have the potential to cause serotonin syndrome by either decreasing the reuptake of serotonin, or otherwise enhancing its activity. Toxic dose will vary based on the product. For fluoxetine (Prozac, Reconcile), treatment is recommended if ingested dose is >1-3mg/kg. Clinical signs associated with these medications include sedation and lethargy (at lower doses), vs hyperthermia, hypertension, tachycardia, agitation, and seizures (at higher doses). Treatment includes decontamination and symptomatic treatment with acepromazine (for hypertension, agitation), beta-blockers (for tachycardia), IV fluids (for cooling, hemodynamic support, and to encourage renal excretion), and cyproheptadine (oral or rectal) as a serotonin antagonist. Diazepam can be used for seizure activity, but is otherwise contraindicated as it can worsen neurologic signs (barbiturates may be more effective). Tricyclic antidepressants (such as clomipramine) can have more profound cardiac toxic effects, including bradycardia, hypotension, and arrhythmias.

Vitamins – It is relatively rare to have complications other than GI upset after a one-time overdose of a multivitamin.  The main concerns with multivitamin ingestion are vitamin D and iron toxicity. Vitamin D (cholecalciferol) toxicity can occur at doses of 0.5 mg/kg. The prevalence of this toxicity may be increasing due to the frequent recommendation for vitamin D supplementation in human medicine. Prescription products are available with doses as high as 50,000 IU per tablet (40 IU = 1 mcg). Treatment recommendations are similar to those noted above under rodenticides.  Iron toxicity can occur at doses as low as 20-40mg/kg, with serious consequences more likely if dose is >60mg/kg. Decontamination is recommended (including administration of magnesium hydroxide to complex with the iron and make it less soluble), followed by supportive care (GI protectants) as indicated. Activated charcoal is not indicated as it does not bind iron well. With larger ingestions, serum iron and total iron binding capacity (TIBC) levels should be recommended, and chelation therapy with desferoxamine considered. Many sources recommend chelation if serum iron is >300-400 mcg/dL or if serum iron is > TIBC. If iron and TIBC levels cannot be assessed in a timely manner, the decision to chelate can be made based on clinical signs (ie – consider chelation if vomiting, hematemesis, or bloody diarrhea is occurring). If deferoxamine is given and the urine turns pink in color, iron is being chelated. Treatment should be continued until the urine is clear/normal. Following significant iron overdose, monitoring liver enzymes for 24-48 hours +/- hepatoprotectants are recommended by some sources.

Iron phosphate slug baits–Available as “Sluggo” and other brand names- Toxic dose – GI signs can be seen at 20-40mg/kg elemental iron, more severe consequences including hepatotoxicity are possible at 80-100mg/kg. This product has been marketed as a safer alternative to metaldehyde. It contains 37% elemental iron, which fortunately is not well absorbed through the GI tract. It can still cause significant gastroenteritis, and at higher doses can be absorbed and cause systemic signs as well. Decontamination is recommended as above under vitamins (emesis, magnesium hydroxide, no charcoal). GI protectants are recommended for 5-7 days. If the ingested dose is >80-100mg/kg of elemental iron, serum iron and total iron binding capacity (TIBC) levels should be recommended, and chelation therapy with desferoxamine considered as described above.


TABLE 1 – systems approach to toxicities



Renal toxins

GI toxins

Cardiovascular toxins







Zinc phosphide

Molds (mycotoxins)



Cholinesterase inhibitors


Botulinum toxin


Macadamia nuts







Amanita mushrooms

Blue-green algae

Alpha lipoic acid

Sago palm


Castor beans







Ethylene glycol

Lilies (cats)

Grapes/raisins (dogs)

Vitamin D



Ant baits


Many plants


Zinc phosphide






Calcium channel blockers

Bufo toads

Albuterol inhaler

TABLE 2 – drug doses used in treating toxicities








0.03-0.04mg/kg IV

Emesis induction in dogs


0.44-1.1mg/kg IM or SQ

Emesis induction in cats

Activated charcoal

1-4g/kg, repeated q4-8 hours in some cases

Toxin adsorption


Usually in combination with charcoal

GI decontamination


0.3-1g/kg TID x4 days or 1-2g/dog BID, 1g/cat BID

Bile acid sequestrant

Magnesium hydroxide

Dose based on weight – label dose

Binds iron to prevent GI absorp


Suggested protocol - bolus of 1.5mL/kg over 5-15 minute IV, then CRI at 0.25mL/kg per minute for 30-60 minutes. Can repeat (if not severely lipemic).









Oral loading dose of 140 mg/kg (dilute to 5% in dextrose or sterile water), followed by 70 mg/kg PO four times daily (q6h) for 7 treatments. Can give orally or IV (with filter) slow over 15-20 minutes. Separate from activated charcoal by at least 2-3 hours if giving orally.


With ingestion of massive quantities, some authors suggest using a 280 mg/kg loading dose and continuing treatment for 12–17 doses.

Glutathione precursor, antioxidant


5-10mg/kg q6-8 hours PO or IV

Inhibits metabolism of acetaminophen to toxic compounds

Vitamin C (ascorbic acid)

20-30mg/kg q6 hours PO

Antioxidant, reduces methemoglobin to reduced form


20mg/kg PO SID

Glutathione precursor, antioxidant







Vitamin K

3-5mg/kg/day PO, SQ

Allows generation of endogenous clotting factors


10-20mL/kg IV

Provision of exogenous clotting factors








2-4mg/kg PO q8 hours or CRI 0.5mg/kg/hr

Enhances renal calcium excretion


2mg/kg PO BID – lower doses may be effective with fewer side effects

Suppresses bone calcium reabsorption, decreases SI calcium reabsorption, enhances renal calcium excretion


1.3-2mg/kg diluted in saline over 2 hours

Can repeat in 5-7 days if needed








1.1mg/kg q4-6 hours PO or rectal (dog)


Serotonin antagonist








50mg/kg IV up to 330mg/kg/day

Muscle relaxation


0.5mg/kg IV



4mg/kg IV increments, up to 16mg/kg total loading dose



4-6mg/kg IV titrated to effect










Beta blocker – for significant tachycardia



For agitation/hyperactivity








0.5-1mg/kg SID-BID

H2 blocker


0.7-1mg/kg SID

Proton pump inhibitor


250mg-1g PO TID

Mucosal protectant


2-5mcg/kg PO TID

Synthetic prostaglandin







Magnesium hydroxide

Q4-6 hours for 24 hours

Complexes iron into less soluble form


40mg/kg IM q4-8 hours or CRI 15mg/kg/hr IV. IV administration can be associated with arrhythmias and hypotension – monitor

Chelates iron



Current Veterinary Therapy XIV

Small Animal Toxicology, Peterson and Talcott

Small Animal Toxicology and Poisonings, Gfeller and Messonnier

Toxicology, Osweiler

Veterinary Clinics of North America March 2012: Common Toxicologic Issues in Small Animals

Veterinary Critical Care Textbook, Silverstein and Hopper

Veterinary Information Network



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