Marijuana and tetrahydrocannabinol (THC), its intoxicating component, are now found in many forms and in many households. These substances are frequently ingested by pets and can result in GI signs, ataxia, lethargy, trembling, and urinary incontinence. Treatment is supportive; signs are self-limiting within 1–3 days, and death is extremely rare.
Marijuana refers to the Cannabis sativa or C indica plant or portions of the plant with a tetrahydrocannabinol (THC) content commonly ranging from 0.4% to 20% or potentially higher. The Agriculture Improvement Act of 2018, also known as the 2018 Farm Bill, removed hemp-derived cannabis from the definition of marijuana.
Researchers have identified over 540 phytochemicals (1) and more than 150 phytocannabinoids (2). Of these, delta-9-THC is the primary intoxicating phytocannabinoid.
Marijuana and THC can be encountered in many forms and concentrations:
The marijuana plant contains an average of 4–20% THC. Sinsemilla, or the seedless unpollinated female plant, carries a higher THC concentration.
Hash and hash oil are non–solvent-based THC extracts that contain 20–50% THC.
Concentrates are collected by solvent extraction and contain up to 80–90% THC. Concentrates, often referred to as dabs, can include butters, budders, shatter, wax, and oils (3, 4).
Varying THC concentrations can also be found in edibles (baked goods, gummies, candy, etc), oils, tinctures, topicals, capsules, and vaping liquids.
The FDA has not approved any THC, cannabidiol (CBD) with THC, or full-spectrum products for use in veterinary patients. Dronabinol, a THC-based medication, and nabilone, a THC analogue, are FDA-approved for use in humans to treat nausea and inappetence in chemotherapy and in AIDS (5). Nabiximols is a 1:1 ratio of THC:CBD that is approved in many countries to manage multiple sclerosis–induced spasticity; however, it remains unapproved in the US (6, 7).
Marijuana and THC remain Schedule I drugs according to the US Drug Enforcement Agency; however, their decriminalization and legal status vary by state.
Etiology and Pathogenesis of THC Toxicosis in Dogs and Cats
See the discussion of the endocannabinoid system (ECS) under the CBD topic for a more detailed mechanistic discussion. CB1 receptors are responsible for THC's intoxicating effects. CB1 receptors are well concentrated in the CNS (with lower concentrations in the peripheral nervous system) and are involved in cognitive function, emotion, motion and motor control, hunger, neuroprotection, posttraumatic events, and degenerative diseases. Their presence in the sensory and autonomic nervous systems influences cardiovascular, GI, and respiratory function and pain perception.
THC is 4–20 times more potent than endocannabinoids and carries a longer duration of action (8). In acting as a partial agonist at the CB1 receptor, THC imparts systemic effects that are commonly referred to in human literature as the “THC tetrad” of delusions, hallucinations, paranoia, and sedation (9). Interspecies differences in endocannabinoid receptor distribution and quantity likely account for the variability in sensitivity to THC and associated clinical signs in dogs and cats. Dogs have a higher concentration of CB1 receptors in the cerebellum and medulla oblongata, which likely accounts for the ataxia and cardiovascular and respiratory effects in this species (10, 11).
Pharmacokinetics and Toxicity of THC in Dogs and Cats
Note: Pharmacokinetic data pertain to dogs unless otherwise indicated.
Dogs can develop mild clinical signs with doses of THC as low as 0.3–0.5 mg/kg; clinical signs can be moderate with doses > 2–3 mg/kg (12). The variability in product consistency and the lack of regulatory oversight make toxic doses and dose exposures difficult to assess.
The probable oral lethal dose exceeds 3–9 g of delta-9-THC-dominant plant material/kg of dog body weight (13). No published median lethal dose data exist, and lethality is extremely rare.
Delta-9-THC is absorbed rapidly when inhaled, resulting in clinical signs within a matter of minutes (14). Ingestion of THC results in clinical signs within 1–2 hours (up to 4 hours in fasted dogs) (3, 15), and time to maximum concentration (Tmax) in the dog after oral soft chew ingestion was approximately 1.7 hours. The initial plasma half-life (t1/2) was approximately 4 hours. Results were similar for oil formulations (16). Tmax in the studied cat was approximately 2 hours, and the initial t1/2 was approximately 1.6 hours (17). Bioavailability ranged from 6% to 20%. THC is highly lipophilic, has a short serum half-life, and is rapidly distributed to tissues (18).
Delta-9-THC is metabolized primarily in the liver, and a large portion undergoes first-pass metabolism. Cytochrome P450 (CYP) enzymes are responsible for THC's hydroxylation and oxidation otherwise, and the brain, intestines, and lungs will secondarily metabolize THC by their CYP enzymes as well. The metabolites vary substantially by species (18, 19).
Because of its biphasic kinetics and release from fat and tissues, THC's biological half-life, at 30 hours, is relatively long, and elimination is nonlinear. In dogs, THC is excreted primarily in the feces (85%), and 15% is eliminated in the urine. Dogs excrete 80% of THC within 5 days, and clinical signs in greatly affected cases can persist to some extent for 1–3 days (3).
Clinical Signs of THC Toxicosis in Dogs and Cats
Tetrahydrocannabinol exposures carry a high morbidity rate but an extremely low mortality rate in dogs and cats. Ataxia, rare respiratory depression, and cardiovascular depression not typically noted in humans might be more common in dogs because of increased numbers of CB1 receptors and their unique distribution to the cerebellum and brainstem (10, 11).
In descending order, the most common clinical signs reported in Pet Poison Helpline cases of THC ingestion from January 2018 through February 2023 (see ) included lethargy (30%), ataxia (21%), and vomiting (15%). Other clinical signs can include urinary incontinence, increased sensitivity to motion and sound, trembling, bradycardia, agitation and twitching, mydriasis, hyperthermia, hypothermia, head bobbing, and tremors. Rare hypotension, respiratory depression, and tachycardia have been described.
Seizures are rare with THC ingestion (20).
Death following ingestion of marijuana or delta-9-THC would be extremely rare and might result from secondary complications (20).
In the two published canine fatality cases, the cause of death was not reported. These cases involved the ingestion of baked goods made with marijuana butter, a concentrated product (21).
Diagnosis of THC Toxicosis in Dogs and Cats
Gas chromatography/mass spectrometry is effective in diagnosis of tetrahydrocannabinol intoxication; however, its clinical application is limited, given the length of time required to perform the test.
Reliable point-of-care THC tests are not available for the diagnosis of THC or marijuana-derived cannabis exposures in animals. The urine drug screens currently available are intended for use in humans. False negatives are very common when they are used in animals and might be secondary to the large number of undetectable metabolites in dog and cat urine (22, 23, 24).
Decontamination and Treatment of THC Toxicosis in Dogs and Cats
Patients often respond well to supportive care, and the prognosis is generally good in dogs and cats.
Decontamination may be considered within 1 hour of THC ingestion in clinically normal patients only. Emesis may be induced in dogs with apomorphine (0.03 mg/kg, IV, or 0.04 mg/kg, IM) or ropinirole (3.75 mg/m2, with dose range of 2.7–5.4 mg/m2, ocular application). Activated charcoal with sorbitol (1 g/kg) may also be administered.
Mildly affected cases may be monitored at home. Out of caution, it might be best to ensure animals are cardiovascularly stable, ambulatory, and able to thermoregulate for a short period of time before discharge.
Clinically affected patients might benefit from fluid treatment for hydration and perfusion (30–50 mL/kg, SC, or 75–100 mL/kg, IV, every 24 hours). Antiemetics (maropitant 1 mg/kg, SC or IV, every 24 hours or ondansetron 0.1–0.2 mg/kg, IV, every 8 hours) are beneficial to vomiting or nauseated patients. Thermoregulation and nursing care might be required in more severely affected patients, and all will benefit from low-stimulus environments when possible.
Vital signs and blood pressure should be monitored every 1–4 hours. The bradycardic patient may be treated with atropine (0.02–0.04 mg/kg, IV). Agitation can be managed with butorphanol (0.1–0.4 mg/kg, IV) or diazepam (0.25–0.5 mg/kg, IV). Rare tremors can be mitigated with methocarbamol (55–220 mg/kg, IV, PO, or per rectum) or diazepam (0.25–0.5 mg/kg, IV).
Seizures rarely occur, but are amenable to treatment with anticonvulsants: diazepam (0.5–1 mg/kg, IV), levetiracetam (60 mg/kg, followed by 20–30 mg/kg, every 6 hours, IV), or phenobarbital (2–16 mg/kg, IV).
Intralipids (intravenous lipid emulsions; ILEs) might be indicated in a large overexposure, concentrate, or severe case. Severely affected cases might benefit from the use of ILEs if the patient is responding poorly to supportive care. ILEs can be dosed with a 1.5 mL/kg bolus followed by a 0.25 mL/kg/min CRI for 30–60 minutes. The 1.5 mL/kg bolus may be repeated every 4–6 hours in nonlipemic patients for up to 24 hours or 5 doses. Alternatively, a 1.5 mL/kg bolus may be followed by a 0.5 mL/kg/h CRI in nonlipemic patients.
Key Points
Tetrahydrocannabinol (THC) intoxication in dogs and cats generally causes lethargy, ataxia, and vomiting; hyperesthesia, trembling, and urinary incontinence can also occur.
The prognosis is good and clinical signs usually resolve within 1–3 days; supportive care is indicated.
For More Information
Also see pet owner content regarding poisonings from illicit and abused drugs.
References
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