Kratom Exposure & Treatment for Pets

Kratom (Mitragyna speciosa) is a plant that is indigenous to Southeast Asia and is a part of the coffee family (Rubiaceae). Kratom has some physiologic effects similar to opioids (pain relief and euphoria); however, it also has stimulant effects. 

Background

Kratom has been used in traditional medicine in areas where it is endemic. Traditionally, the leaves are smoked, chewed or brewed into teas for consumption. In recent years, kratom has gained increasing popularity in the Western world, being used for chronic pain, opioid withdrawal and recreational use. With this increase in popularity, there has been an increase in the available forms including capsules, liquids, gummies and chocolates. Some of these forms include extracts that increase the potency over the leaf form of kratom. 

While kratom is a controlled substance in 16 different countries, it is available over the counter in much of the United States with little to no regulation for quality or side effects. However, as of January 2026, there are 7 states with bans on kratom (Alabama, Arkansas, Indiana, Wisconsin, Rhode Island, Vermont and Louisiana) and multiple cities and counties with local bans.

Kratom Popularity Impacts on Pets 

As the popularity of kratom has increased over the last 10+ years in the US, so have the incidents of exposure to our veterinary patients. While kratom exposures only account for a small fraction of the cases reported to ASPCA Poison Control, a nearly 400% increase in cases was seen in 2025 when compared 2024. Increased exposures to kratom are expected to continue as long as it is in the pet’s environments. Because of this, it is important to increase awareness of kratom, and its potential adverse effects.

What Is The Mechanism Of Action?

Kratom contains over 40 different alkaloids, with mitragynine and 7-hydroxymitragynine being the most clinically relevant. Mitragynine is the most abundant, comprising 12-66% of the total alkaloids present in the plant material. Mitragynine is biotransformed in the liver to the active metabolite 7-hydroxymitragynine. 7-hydroxymitragynine is also present in plant material, but at less than 2% of the total alkaloids present. However, 7-hydroxymitragynine is thought to be more important toxicologically, as it likely causes the majority of the clinical signs.   

Both mitragynine and 7-hydroxymitragynine act as Mu opioid receptor agonists, though some studies suggest they act more like partial agonists. Mitragynine has less opioid receptor affinity than morphine. 7-hydroxymitragynine, however, has 46 times the receptor affinity when compared to mitragynine and 13 times the affinity when compared to morphine. In addition to effects on opioid receptors, kratom alkaloids have effects on many other receptors. Effects on alpha-2 adrenergic receptors, blockade of Ca 2+ channels and inhibition of COX-2 receptors are thought to contribute to its analgesic properties. Some affinity for serotonin, dopamine and adenosine receptors in the CNS have also been identified, but the full significance is still undetermined. 

Clinical Effects

In humans, kratom has dose-dependent effects where at low doses it acts more like a stimulant and at higher doses it has more opioid-like effects. Common signs associated with kratom use in humans include agitation, altered mentation, CNS depression/sedation, nausea and tachycardia. In dogs and cats, the most common signs include lethargy/sedation, vocalization, hypersalivation and vomiting. Though some cases can present with cardiovascular effects (tachycardia, bradycardia and hypertension) or stimulatory signs (hyperactivity, agitation, hyperesthesia and tremors).  Signs are often seen within a few hours of exposure. While many cases do not have an established dose due to lack of information, doses as low as 0.15 mg/kg have been noted to cause clinical signs. However, doses up to 5878 mg/kg have been seen without reported deaths. Treatment is generally recommended if more than mild sedation is noted or if there are any stimulatory or cardiovascular effects present. While many cases lack outcomes to determine the exact duration of effects, clinical signs are generally expected to resolve in less than 24-48 hours.

Management

There is no antidote for kratom. Treatment is largely supportive, managing the clinical signs present in the patient. Treatments may include fluids to maintain normal hydration and cardiovascular support, benzodiazepines for agitation/tremors, acepromazine for agitation, methocarbamol for tremors, cyproheptadine for serotonin syndrome, atropine for bradycardia, propranolol for tachycardia and naloxone for severe CNS depression.

Please contact the ASPCA Poison Center at (888) 426-4435 if you suspect that a patient has been exposed to one of these products.