May 2026
In this VETgirl online veterinary continuing education blog, Dr. Justine Lee, DACVECC, DABT discusses the growing threat of kratom poisoning in dogs and cats. Dr. Lee explains what kratom is, the variable clinical signs of toxicity from sedation to agitation, key treatment recommendations like decontamination and supportive care, and the excellent prognosis for pets who receive prompt veterinary attention.

Kratom Toxicity in Dogs and Cats: A Growing Poisoning To Know About

By Dr. Justine Lee, DACVECC, DABT, Director of Medicine/Co-founder, VETgirl


You’re working an ER shift when a 4-year-old, MN, Labrador retriever presents for acute agitation, hypersalivation, tachycardiac, and vomiting. The pet owner reports the dog got into a “natural supplement” that the pet owner uses for chronic back pain. You’re sitting there racking your brain, and the pet owner identifies the “gummy” that she purchased on Google… turns out the supplement contains kratom. You pause for a second — WTH is that?

Never heard of it? Sounds vaguely familiar? Not quite an opioid, not quite a stimulant, and definitely not something we learned about extensively in veterinary school!

Welcome to the up-and-coming world of kratom toxicosis in dogs (and less commonly, cats).

Kratom (Mitragyna speciosa), a plant indigenous to Southeast Asia, is a member of the coffee family (Rubiaceae). In some countries, the leaves have been chewed, smoked or even brewed (as a tea). More recently in the United States, it has been “advocated” for recreational use, chronic pain, and for opioid withdrawal. As a result, its use has surged in the United States for the past decade. Kratom comes in various forms: from edibles like gummies and chocolates to powders, liquids, capsules and even more concentrated extract formulations (which may be more potent). Note that since this is a “supplement,” there’s no regulation (e.g., not regulated by the FDA, etc.), quality control or monitoring of this over-the-counter product in the United States. That said, in over a dozen countries, kratom is considered a controlled substance. Thankfully, some states are now banning its use (including in alphabetical order at the time of writing this blog Alabama, Arkansas, Indiana, Louisiana, Rhode Island, Vermont, and Wisconsin).

Although kratom exposures still represent a small percentage of total toxicology calls, the ASPCA Animal Poison Control Center (APCC) based out of Urbana, Illinois recently documented nearly a 400% increase in reported veterinary cases in 2025 compared to 2024. As long as this product remains in pet households, veterinarians will continue to see these cases… especially when it comes in “edible” forms that dogs are drawn to (like chocolate, gummies, etc.).

Mechanism of Action of Kratom

So, what clinical signs do we see with kratom toxicity in dogs and cats? Kratom contains two main alkaloids: mitragynine and 7-hydroxymitragynine. Mitragynine is the most abundant alkaloid in the plant (according to ASPCA APCC, comprising approximately 12–66% of the plant’s total alkaloid content.) It is metabolized hepatically into 7-hydroxymitragynine, which is also present in the plant at low concentrations. These alkaloids result in the majority of the signs seen when ingested by dogs and cats.

These alkaloids also have an affinity for the mu-opioid receptor agonists and can result in a dose-dependent opioid-like sedation. The alkaloids are also thought to potentially affect other receptors such as the alpha-2 adrenergic receptors, along with serotonin, dopamine and adenosine receptors in the CNS.

In humans, lower doses are associated with stimulant properties, while higher doses produce sedation and euphoria. However, in veterinary patients, clinical signs can be variable – either sedative-like or paradoxical.

Toxic Dose, Onset, and Duration

Unfortunately, as with a lot of veterinary toxicants, the exact amount of ingestion is often unknown (e.g., think THC amount in brownies – it’s difficult if not impossible to calculate how much was in the product, how much ingested, how much was removed by decontamination, etc.). As a result, an exact mg/kg is often difficult to determine. Add to that, there’s variability in product concentration, formulation (especially extracts), individual metabolism, and incomplete exposure histories. Likewise, with kratom toxicity, there is a known wide variability in reported dose-response relationships (at least in humans). According to the ASPCA Animal Poison Control Center database, clinical signs have been reported at doses as low as 0.15 mg/kg. Conversely, exposures up to 5878 mg/kg have been documented without reported fatalities.

Clinical Signs of Kratom Toxicity

So, what should we expect with a kratom poisoning case in our veterinary patients? Clinical signs typically develop within a few hours of ingestion. In most cases, signs resolve within 24–48 hours with appropriate supportive care.

Kratom exposure may produce a combination of sedative and stimulatory effects.

 

While many patients exhibit mild sedation, others may present with more concerning neurologic or cardiovascular abnormalities. Because of kratom’s mixed receptor activity, clinical presentation can vary widely.

Differential Diagnoses

Given its pharmacologic profile, kratom toxicosis can resemble several other toxicologic exposures (THC, anyone?). Depending on the clinical signs, your top differentials should also include opioid intoxication, alpha-2 agonist exposure, stimulant toxicosis, serotonergic agents, cannabis intoxication, or other CNS depressants (NOTE: This list is not all inclusive – there are a lot of toxicants that show these signs!).

When in doubt, get a good history – this is imperative, as if you don’t ask about “supplement” ingestion, the owner is unlikely to remember or admit to this. When in doubt, consult with the ASPCA APCC, as this can be invaluable when presentation is atypical.

Decontamination

As with many oral toxicants, early decontamination may be appropriate in select patients. Emesis induction should ONLY be considered with recent ingestion in asymptomatic patients who are presenting shortly after ingestion (provided there are no contraindications such as laryngeal paralysis, BOAS, megaesophagus, etc.). Those patients with profound clinical signs, excessive sedation or neurologic impairment should NOT have emesis induction due to high risk for aspiration secondary to a decreased gag reflex.

Likewise, activated charcoal may be considered after emesis IF appropriate, particularly in cases involving concentrated extracts or uncertain dose exposure. While ASPCA APCC often doesn’t advocate for the use of charcoal, this VETgirl is still old school and will consider one dose of charcoal, if appropriate. As always, the decision to pursue decontamination should consider time since ingestion, product formulation, and the patient’s neurologic status.

Treatment for Kratom Toxicity

In general, the determination on whether to hospitalize or treat on an outpatient basis will depend on several factors, including severity of clinical signs, amount ingested, success of decontamination (if performed), owner compliance/finances, etc. Hospitalization is warranted for patients with moderate to severe CNS depression, persistent agitation or tremors, cardiovascular instability, or inability to maintain hydration (e.g., persistent vomiting, etc.).

When in doubt, patients should be carefully monitored, particularly during the first 12–24 hours. Cardiovascular parameters should be closely observed, including heart rate, rhythm, and blood pressure. ECG monitoring is reasonable in patients with bradycardia, tachycardia, or other rhythm abnormalities. If hyperactivity, tachycardia and hypertension are noted, the use of acepromazine can be considered. If bradycardia is detected, a stat blood pressure and ECG should ideally be performed.

Neurologic status should be reassessed serially to detect progression from mild sedation to more profound CNS depression or escalating agitation. Body temperature should also be monitored, particularly in patients with tremors or hyperactivity. Intravenous fluid therapy may be indicated to maintain hydration and support perfusion, if indicated.

As with most toxicants, kratom toxicity does not have a specific antidote. Management is primarily symptomatic supportive care and directed at controlling clinical signs.

Prognosis for Kratom Poisoning

Thankfully, the prognosis for kratom toxicosis in dogs and cats is generally excellent with appropriate supportive care. Most patients recover fully within 24–48 hours.. When in doubt, early recognition, supportive care, and appropriate monitoring remain the cornerstones of successful management. When in doubt, contact the ASPCA Animal Poison Control Center at (888) 426-4435 for expert consultation and life-saving care.

As kratom continues to gain popularity among pet owners, we veterinarians and veterinary technicians need to be aware of this ever-so-common toxicity in our canine and (less commonly) feline patients!


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