Introduction

Cannabis sativa, also known as marijuana, is a plant that is recreationally ingested or smoked to produce psychoactive effects.^1–3 Marijuana contains many active metabolites known as cannabinoids, with the 2 main cannabinoids being tetrahydrocannabinol (THC) and cannabidiol (CBD). Tetrahydrocannabinol is the classic cannabinoid producing psychoactive effects of cannabis.³ Tetrahydrocannabinol toxicity in dogs is a common presentation in veterinary emergency facilities, and cases will continue to increase as legalized marijuana and its products become more readily available.⁴ However, definitive diagnosis is difficult, as owners are often unwilling to admit to the possibility of marijuana exposure and the readily available human urine multidrug test (HUMT) is unreliable in dogs.^2,3,5,6 The unwillingness to admit the possibility of exposure and lack of a sensitive drug test in dogs lead clinicians to recommend thorough diagnostic testing to rule out all possible causes of acute neurologic signs including systemic (ie, hypoglycemia, portosystemic shunt) and intracranial causes (ie, meningitis). This comprehensive testing could include CBC, chemistry, bile acids, ammonia levels, and advanced imaging, all of which could be considered an unnecessary stress to the patient and increased cost to the owner.

The most common route of exposure to THC in dogs is via ingestion, with the most common sources being homemade or commercial edibles, plant material, and medical products.³ Tetrahydrocannabinol is highly lipophilic and metabolized mostly by the liver into 2 primary metabolites. First THC is metabolized into psychoactive 11-hydroxy-Δ 9-tetrahydrocannabinol, which is then metabolized into the nonactive 11-nor-9-carboxy-Δ9-tetrahydrocannabinol (THC-COOH).⁷ About 10% to 15% of these compounds undergo enterohepatic recirculation, with 85% excreted in feces and only 15% excreted in urine in dogs (compared to 30% to 65% and 20%, respectively, in humans).^2,3,6,7 THC-COOH and its glucuronide conjugate are the major end products of biotransformation in most species.⁷ However, THC metabolites excreted in canine urine appear to be a more variable and complicated mixture and are present in much lower quantities compared to those found in human urine.^3,5,6

Currently, the gold-standard confirmatory test for diagnosis of THC toxicity is measuring THC metabolites in plasma by use of gas chromatography/mass spectrometry.^3,5,6,8,9 However, this form of testing is not ideal in the emergency setting as it is costly, not widely available, and lacks immediate results.^8,9 Therefore, veterinarians still rely on the aid of point-of-care HUMT results. The accuracy, sensitivity, and specificity of the HUMT in dogs with THC toxicity has not been published, to the authors’ knowledge. The test is considered unreliable in dogs, as it tests for THC-COOH, which is found in much higher quantities in human urine compared to dog urine.^5–9 A study⁶ evaluating the Human On-site Urine Multidrug test (QuickScreen) reported no positive HUMT test results in 25 tests that were submitted for suspected THC toxicity, and these results were validated by use of gas chromatography/mass spectrometry. Fitzgerald et al⁵ recently published that only 1 of 21 HUMT results (iScreen 2 panel drug test THC/coc; AlcoPro) were positive in dogs presenting for suspected marijuana toxicity, while the same patient serum and urine tested positive for THC metabolites via a novel ultraperformance liquid chromatography–tandem mass spectrometer method.

Until a new, more sensitive, and easily accessible urine drug screen test is developed for dogs, clinicians usually must rely solely on history, physical and neurologic examination, and clinicopathologic findings to make a diagnosis of THC toxicity. The purpose of this study was to describe the historical, physical, and neurologic examination in combination with clinicopathologic findings and frequency of electrolyte derangements in dogs with confirmed THC toxicity.

Methods

Electronic medical records of a university teaching hospital were searched for cases with the diagnosis of THC toxicity (keywords marijuana, tetrahydrocannabinol, and THC) from January 2017 to July 2021. Dogs were included if they were a true positive for THC toxicity, which was defined as known ingestion of THC products or a positive HUMT result. Urine drug screening was performed and interpreted according to package insert instructions using the Alere 4 panel iScreen Drugs of Abuse Test Card (Abbott), which tests for cocaine, amphetamines, methamphetamines, THC, opioids, benzodiazepines, barbiturates, and phencyclidine. Dogs were excluded if the HUMT test result for marijuana/THC was recorded as “slight positive” or was positive for other drugs, they ingested other neurologic toxins simultaneously (ie, chocolate), or they were diagnosed with other neurologic disease previously or within 1 month of presentation for THC toxicity. Once the cases were identified as truly positive for THC toxicity only, medical records were reviewed for signalment, history, physical and neurologic examination findings, urine drug screen results, bloodwork results, product ingested, time from ingestion to the onset of clinical signs, time from ingestion to urine testing, hospitalization and treatments, and outcome. If median biochemical values were found abnormal, the severity was categorized on the basis of previously published ranges and modified to fit the institution’s reference ranges. Hyperkalemia was defined as mild (4.8 to 5.7 mEq/L), moderate (5.8 to 6.7 mEq/L), and severe (≥ 6.8 mEq/L).¹⁰ Ionized hypercalcemia was defined as mild (> 5.3 and < 5.82 mg/dL or < 1.33 and < 1.46 mmol/L) and moderate (≥ 5.82 mg/dL or ≥ 1.46 mmol/L).¹¹

Statistical analysis

Statistical analysis was performed via commercially available software (SAS, version 9.4; SAS Institute Inc). Normality was determined using the Kolmogorov-Smirnov method and visual examination of histograms. Continuous variables are expressed as the mean ± SD (SD) when normally distributed and as the median with the minimum and maximum range (min to max) when nonnormally distributed. Categorical data are presented as absolute numbers and percent frequencies. Categorical variables were compared using the χ² test or Fisher exact test, as appropriate. Values of P < .05 were considered significant.

Results

A total of 411 cases were diagnosed with THC toxicity during the study period. Of those cases, 188 were excluded for the following reasons: diagnosis based on suspicion only (n = 142), HUMT test results recorded as “slight positive” and no known ingestion (35), HUMT positive for multiple drugs (8), ingestion of chocolate in combination with marijuana (1), and re-presentation for neurologic signs and diagnosis of central brain disease 1 week later (2). Two hundred and twenty-three cases fulfilled inclusion criteria and were reviewed.

The median age was 1 year (range, 0.08 to 12 years; IQR, 0.4 to 4 years), and median weight was 9.4 kg (range, 1.22 to 57 kg; IQR, 4.82 to 25 kg). Of the 223 dogs, 52 (23.3%) were spayed female, 36 (16.1%) were intact female, 58 (26%) were neutered male, and 77 (34.5%) were intact male. The most common breeds presented were mixed breed (n = 74), pit bull–type breed (19), German Shepherd Dog (10), Husky (9), Labrador Retriever (8), Goldendoodle/Labradoodle (8), Chihuahua (8), Golden Retriever (6), Pomeranian (6), and Blue Heeler/Cattle Dog (7). Other breeds included Pug (n = 5), Boston Terrier (5), Yorkshire Terrier (4), Rottweiler (4), Catahoula (3), Miniature Pinscher (3), Miniature/Longhaired Dachshund (4), Shih Tzu (3), Basset Hound (2), Beagle (2), Boxer (2), Corgi (2), French Bulldog (2), Mini Australian Shepherd (2), West Highland White Terrier (2), and 1 each of 23 other pure breeds.

Patients were categorized on the basis of month and year of presentation. The months with the highest number of marijuana intoxication cases were February through June (January, n = 20 [8.97%]; February, 21 [9.42%]; March, 21 [9.42%]; April, 25 [11.21%]; May, 27 [9.42%]; June, 27 [9.42%]; July, 12 [5.38%]; August, 19 [8.52%]; September, 14 [6.28%]; October, 12 [5.38%]; November, 15 [6.73%]; and December, 10 [4.48%]). When categorized on the basis of year of presentation, 108 (48.43%) presented in 2020, 56 (25.11%) presented in 2021, 21 (9.42%) presented in 2017, 19 (8.52%) presented in 2018, and 19 (8.52%) presented in 2019.

A total of 223 cases were included for having known ingestion or a positive urine drug screen. A total of 194 positive urine drug tests (8 known ingestions, 80 possible ingestions, 106 no known ingestions) and a total of 37 known ingestions were documented. Of the 37 known ingestions, 26 did not have a urine drug screen performed, 8 had a positive urine drug screen, 1 had a negative urine drug screen, and 2 had documented slight positives. The majority of owners did not admit to the dog having the possibility of marijuana ingestion, with 106 (47%) claiming no known or possible ingestion, while 80 (35%) claimed possible ingestion and 27 (16%) claimed known ingestion. When known ingestion was claimed, the THC product was recorded. The major source of THC was documented as either unknown (109 [48%]) or joint/weed (70 [31%)]), with the remaining sources documented as edibles (26 [11%], plants (6 [2.69%]), medical (5 [2.24%]), or a combination of sources (3 [1.35%]).

History

When screening history, similar “stories” that were told by the owner were documented. When asked whether marijuana was in the house, 71 (31.8%) admitted yes, 28 (12.56%) admitted “yes, but it was locked in a cabinet and there is no way the pet could access it,” and 124 (55.6%) said “absolutely no marijuana is in the house.” The top 5 stories provided by the owners included the following: “acting abnormal after going outside or to a public place” (62 [27.8%]), “visitors/workers at the house” (21 [9.4%), “clinical signs after waking up from sleep” (11 [4.93%]), “dog was home alone” (10 [4.48%]), and “acted neurologic after coming out of the crate/kennel” (7 [3.1%]).

A total of 15 of 223 cases had the chief complaint of seizures by the owner. Of the 223 cases that were presented, 10 were referrals from a primary veterinarian. Of those 10 referrals, 2 of the cases were misdiagnosed as seizures and 7 were referred with no diagnosis. Of the 223 cases, 41 (18.39%) had shown a history of dietary indiscretion with cases presenting previously for marijuana intoxication (14 [6.28%]), other drug intoxication (9 [4.04%]), foreign body or other dietary indiscretion (16 [7.17%]), or a combination (2 [0.9%]).

Time to clinical signs, presentation, and urine drug screen results

The median time from ingestion of THC product to presentation was 5.5 hours (range, 1 to 13.5 hours; n = 18). The median time from ingestion to positive urine drug screen was 5.5 hours (range, 3.5 to 8.5 hours; n = 6). Median time from ingestion to onset of any clinical signs was 1.25 hours (range, 0.5 to 12 hours; n = 22), with the majority developing clinical signs within 4 hours of ingestion. Median time from onset of clinical sign to presentation was 2 hours (range, 0.1 to 14 hours; n = 143), with the majority presenting within 6 hours of onset of clinical signs.

Vitals

Heart rate (n = 222), respiratory rate (222), body temperature (212), and blood pressure (61) were recorded when available. Median heart rate was 111 beats/min (min 50, max 200), with 129 of 22 (58%) presenting with normal heart rate (70 to 120 beats/min). When heart rate was abnormal, tachycardia was more common (82/222 [37%]) than bradycardia (11/222 [5%]). Median respiratory rate was 30 breaths/min, with the vast majority having a normal respiratory rate (181/222 [81.5%]). The majority of patients were normothermic (130/212 [61.3%]) with a median temperature of 38.55 °C (101.35 °F), 48 of 212 (22.6%) were hyperthermic, and 34 of 212 (16%) were hypothermic). Most patients were hypertensive (37/61 [60.7%]) with median systolic blood pressure of 150 mm Hg, 21 of 61 (34.4%) were normotensive, and only 3 of 61 (4.9%) were hypotensive. See Tables 1 and 2 for a full description of results.

Physical and neurologic examination findings

The 5 most common individual examination findings documented included ataxia (197/223 [88.3%]), hyperesthesia (168/223 [75.3%]), lethargy/depressed mentation (140/223 [62.8%]), urine incontinence (102/223 [45.7%]), and vomiting (58/223 [26%]). A total of 157 of 223 (70.4%) dogs had a combination of ataxia and hyperesthesia; 81 of 223 (36.3%) dogs had a combination of ataxia, hyperesthesia, and urine incontinence; and 18 of 223 (8.1%) showed all 5 of the most common examination findings. Other commonly documented examination findings included tremors/twitching/shaking (73/223 [32.7%]), mydriasis (50/223 [22.4%]), falling over/leaning to 1 side (48/223 [21.5%]), dazed/decreased responsiveness (43/223 [19.3%]), tense/distended/painful abdomen (29/223 [13%]), falling asleep during the examination (28/223 [12%]), anxious/agitated (26/223 [11.7%]), recumbency (26/223 [11.7%]), head bobbing (25/223 [11.2%]), anorexia (22/223 [9.9%]), and ptyalism (17/223 [7%]). Other reported signs included retching/gagging (11/223 [4.9%]), lameness (2/223 [0.9%]), and hiccups (1/223 [0.4%]). Only 1 (0.4%) dog presented with no signs after known ingestion.

Ultimately, a wide range of multifocal neurologic signs were documented, consistent with neurotoxicity. Some documented forebrain signs not yet mentioned included agitation/anxiousness (n = 26), excitability (16), and vocalizing (1). Cerebellar/vestibular signs included hypermetric gait (n = 7), intention tremors (3), and head tilt (1). Brainstem signs included miosis (n = 8), delayed to absent pupillary light reflexes (3), strabismus (3), and episodes of unconsciousness (2). Abnormal movements documented included collapse (n = 8), myoclonus (1), and paddling (2). Other multifocal signs included stiff limbs/gait (n = 14), hind limb paresis (9), and delayed/absent proprioception (8). See Table 3 for a comprehensive list of neurologic examination findings.

Clinicopathologic results

A PCV/total solids was documented in 41 dogs, with a mean PCV of 46% (SD ± 8.8) and mean total solids of 6.6 (SD ± 0.95). A venous blood gas was performed in 67 dogs, with a mean pH of 7.34 (SD ± 0.048) and venous partial pressure of CO² of 40 mm Hg (SD ± 8.6). Most dogs had a normal venous partial pressure of CO² (42/67 [62.7%]); however, 25 of 67 (37.3%) dogs were hypercapnic (Table 4).

Electrolytes (n = 76), ionized calcium (67), magnesium (72), blood glucose (87), lactate (68), blood urea nitrogen (76), and creatinine (75) were all recorded when available (Table 4). The only 2 values with a median outside of normal reference range were potassium and ionized calcium. The median potassium was 4.8 mmol/L (range, 3.6 to 6.1 mmol/L; SD ± 0.478; reference range, 3.0 to 4.7), and the median ionized calcium was 5.6 mg/dL (range, 3.9 to 6.2 mg/dL; SD ± 0.357; reference range, 3.4 to 5.3). A total of 76 dogs had a potassium recorded, and of those, 37 of 76 (48.7%) were within reference range, 39 of 76 (51.3%) had a documented hyperkalemia, and none had a documented hypokalemia. Of those with an increased potassium, median potassium was 5.2 mEq/L, 38 of 39 (97.4%) were considered mild (4.8 to 5.7 mEq/L), and 1 considered moderate hyperkalemia (5.8 to 6.7 mEq/L).¹⁰ A total of 67 dogs had documented ionized calcium, with 53 of 67 (79.1%) showing an ionized hypercalcemia, 14 of 67 (20.9%) had normal ionized calcium, and none had a low ionized calcium. Of those that had an increased ionized calcium, median ionized calcium was 5.6 mg/dL (1.4 mmol/L), 47 of 53 (88.7%) were mild (> 5.3 and < 5.82 mg/dL or > 1.33 and < 1.46 mmol/L) and 6 of 53 (11.3%) were moderate/severe (≥ 5.82 mg/dL or ≥ 1.46 mmol/L).¹¹ The proportion of young dogs (< 1 year old) did not differ significantly between dogs with and without ionized hypercalcemia (29/33 dogs vs 24/34 dogs, respectively; P = .13). Additionally, when excluding dogs < 2 years of age to account for all possible young and growing dogs, median ionized calcium was still elevated at 5.5 mg/dL (1.375 mmol/L).

Treatments and outcome

Most commonly, the patients received no treatment (129/223 [57.8%]). Supportive medications administered included SC fluids (53/223 [23.8%]), antiemetics (41/223 [18.4%]), and IV fluids (23/223 [10.3%]). For decontamination, apomorphine was given to 1 dog, activated charcoal was given to 3 dogs, gastric lavage was performed on 1 dog, and IV lipid therapy was given to 9 dogs. One dog was given methocarbamol for severe tremors. One dog was given hypertonic saline for suspected intracranial hypertension. Two dogs were given a midazolam constant rate infusion, 1 dog was given levetiracetam, and 1 dog was given phenobarbital. Only 22 of 223 (9.86%) cases were hospitalized. Median length of hospitalization was 24 hours (range, 6 to 72 hours). All dogs survived, and 50 of 223 (22.4%) had a follow-up examination and all clinical signs had resolved. See Table 5 for comprehensive list of treatments.

Discussion

A common presentation for definitive cases of marijuana toxicosis included young dogs with acute ataxia and hyperesthesia, with and without urinary incontinence, after going outside or to a public place. Vitals were usually normal, but hyperthermia, tachycardia, and hypertension were the more common abnormalities reported. Bloodwork was mostly normal, but mild hyperkalemia and mild ionized hypercalcemia were common.

Interestingly, most positive THC cases in this study were presented in the year 2020. This was the same year of legalization of marijuana in the state of the university, as well as the beginning of the COVID-19 pandemic. As marijuana becomes more available and less “taboo,” cases will likely continue to rise.

Clinical signs of marijuana toxicity in dogs have been previously reported^2–4,12; however, this study is the largest to date of dogs and the most recent study that also combined clinical signs with history and clinicopathologic data. When comparing to previous studies, the prevalence of clinical signs appeared to be very similar to what was previously reported, except that hyperesthesia was much more common in this study (75.2% compared to 47% in a previous study) and a lower incidence of mydriasis (22.4% compared to 48%).⁴ This study was the first that evaluated combinations of clinical signs. Cardiovascular signs of marijuana toxicity in humans appear to be more stimulatory,^13–16 while in the authors’ experience, most veterinary clinicians associate marijuana toxicity in dogs with bradycardia, hypothermia, and hypotension. However, this study found that more commonly all vitals were normal, and when they were abnormal, they were more commonly to be tachycardic, hyperthermic, and hypertensive, which aligns with the most common findings in humans.^13,15–17 It is possible these dogs were consuming lower doses of THC, as bradycardia, hypotension, and hypothermia are dose dependent.^13,18,19 The median time from ingestion to onset of clinical signs was 1.25 hours (range, 0.5 to 12 hours; SD, 2.8), with most dogs developing clinical signs within 4 hours of ingestion. The earliest positive result obtained after ingestion was 3.5 hours (median, 5.5 hours) and was similar to what is reported in humans (4 hours).⁶

Previous studies have reported that no specific biochemical abnormalities are expected to be present in dogs with marijuana intoxication.^2,3,12 To the authors’ knowledge, this study is the first to report a prevalence of mild hyperkalemia and ionized hypercalcemia in dogs with confirmed THC toxicity. Cannabis has been documented to modulate potassium and calcium receptors via the cannabinoid receptors CB1 and CB2, which are coupled with Gi/o proteins and inhibit adenylate cyclase.^1,20,21 The CB1 receptor is of particular interest in this case and is found in the brain, peripheral tissues (lungs, heart, and vasculature),²² skeletal muscle, and adipocytes.²³

In contrast to the finding of hyperkalemia in dogs with THC toxicity, in humans, marijuana induces hypokalemia via CB1-mediated activation of G protein–coupled inwardly rectifying potassium channels.²⁴ Hypokalemia-induced acute paralysis has been documented after chronic marijuana use.^1,20,24,25 Other proposed mechanisms of marijuana-induced hypokalemia in humans include potassium loss through the kidneys or excessive diarrhea, potassium shifts into cells, and binge-eating.^15,25 To the authors’ knowledge, hyperkalemia has not been documented in humans with THC toxicity, and no literature supports any mechanisms by which marijuana would induce hyperkalemia in dogs. Perhaps in dogs a different receptor is involved. One study²⁶ reported that a G-coupled protein receptor GPR55 in humans has the opposite effect of CB1 receptors and inhibits potassium current through M-type potassium channels, which could be a proposed mechanism of hyperkalemia.

Ionized hypercalcemia was prevalent among dogs in this population presenting with marijuana toxicity. Although the overall young age of the sample size (median, 1; IQR, 0.4 to 4) could potentially influence these results, there was no significant difference in the proportion of young dogs (< 1 year old) between those with and without ionized hypercalcemia (P = .13). Additionally, no giant breeds were in this study and only 7 of 53 dogs with ionized hypercalcemia were < 3 months old. However, to account for all possible young, growing dogs, dogs < 2 years of age were excluded for a secondary analysis and median ionized calcium was still elevated at 5.5 mg/dL (1.375 mmol/L). Therefore, hypercalcemia of young, growing dogs does not fully explain these findings. Hypercalcemia is a documented effect of THC and other cannabinoids, mediated by activation of the same GPR55 receptor leading to release of intracellular calcium stores.²⁶ This transient hypercalcemia does not appear to be clinically significant in humans and is not discussed in the literature. However, because no reliable urine drug screening test for dogs exists at this time, a concurrent hyperkalemia and ionized hypercalcemia in combination with the right history and clinical signs could potentially be helpful biomarkers for diagnosis of THC toxicity in dogs.

A total of 12 cases were presented as referrals from primary veterinarians, and 2 of the cases were excluded due to administration of antiepileptics before referral (which worsened clinical signs). Eleven of the referred cases were unrecognized as possible marijuana intoxication and were referred for possible seizures or severe neurologic disease. Especially as marijuana becomes legalized and more widely available, understanding the common clinical signs of marijuana toxicity is important to help primary veterinarians quickly suspect marijuana toxicity and hopefully lower the referral burden on secondary and tertiary referral hospitals.

This study had several limitations. Due to its retrospective nature, not every case had all diagnostics reported. Only 76 dogs had a documented potassium and only 67 dogs had a documented ionized calcium, likely due to machine errors. Only 62 cases had a documented blood pressure. The sensitivity of the Alere 4 panel iScreen Drugs of Abuse Test Card in dogs was low at 72%. However, this sensitivity was likely not accurate due to the small number of cases with both known ingestion and a urine drug screen test. Specificity was not calculated, as no tests were performed on normal dogs.

A total of 37 HUMT drug results were reported as “slight positive,” and 35 of these cases were excluded due to no known ingestion. A “slight positive” was defined as a barely visible line. In the hospital and in the current study, faint lines are considered negative. This decision was based on the Alere One Step Drug Screen Test card package insert recommendation that “all faint lines, including barely visible ones, should be interpreted as ‘negative.’” However, this recommendation is based on the suggested screening cutoff for positive human specimens set by the Substance Abuse and Mental Health Services Administration. The One Step Drug Screen Test Card yields a positive result when the concentration of THC-COOH in urine exceeds 50 ng/mL. It is well known that dogs produce much less of the measured metabolite in urine. Fitzgerald et al⁵ reported that in urine, while no metabolite was detected consistently in all samples via ultraperformance liquid chromatography–tandem mass spectrometry, THC-COOH was most frequently detected (16 out of 19 dogs) but the median concentration was quite low at 1.84 ng/mL. Because dogs produce low levels of the measured metabolite, this cutoff should be lower in the veterinary patient population, and perhaps “slight positive” should be acceptable as a diagnosis. In the present study, 11 dogs with known ingestion had an HUMT performed, and of those tests, 8 were positive, 2 were “slight positive,” and only 1 test was negative. If “slight positive” results were to be accepted in dogs (in combination with history and clinical signs), the sensitivity of this already existing point-of-care HUMT test could be improved (in this case example, sensitivity would increase from 72% to 90%). Regardless of whether “slight positives” were included in the study, the HUMT test seemed to perform better compared to the results from different HUMTs reported by Fitzgerald et al⁵ and Teitler et al.⁶ It is also important to note that in this study there were known ingestions that tested “slight positive.” Interestingly, when comparing “faint line results” to gas chromatography/mass spectrometry, Teitler et al⁶ confirmed all these results were truly negative. This was also a different HUMT, however, and the study did not include any known ingestion cases.

In conclusion, a common presentation for definitive cases of marijuana toxicosis included young dogs with a combination of acute ataxia and hyperesthesia with and without urine incontinence with normal vitals and bloodwork. However, hyperthermia, tachycardia, hypertension, mild hyperkalemia, and mild ionized hypercalcemia were common abnormalities. Sensitivity of the HUMT in dogs was low when interpreted according to the package insert. Marijuana should be high on the differential list with these history, physical examination, neurologic examination, and clinicopathologic findings, regardless of owner denial about the possibility of marijuana exposure or negative HUMT. The presence of hyperkalemia and/or mild ionized hypercalcemia may help increase the index of suspicion of marijuana intoxication. However, these electrolyte derangements should be further investigated at other institutions on different analyzers to confirm or dispute the prevalence of mild hyperkalemia and hypercalcemia in dogs with confirmed marijuana toxicity. Future prospective studies would be ideal to calculate the true sensitivity/specificity of the HUMT and to investigate diagnostic criteria, including potassium and ionized calcium, that would aid in a more accurate diagnosis of marijuana toxicity in dogs.

Disclosures

The authors have nothing to disclose. No AI-assisted technologies were used in the generation of this manuscript.

Funding

The authors have nothing to disclose.