BERNIE VAATSTRA
Loki is a lively two-year-old male neutered English Springer Spaniel with a strong interest in food of all kinds, edible or otherwise. On a Friday evening on returning from work, Loki’s owner noticed him behaving unusually. He barked sharply at the car he usually recognises and approached with a swaying, uncoordinated gait.
Clinical findings:
Closer examination revealed a horizontal head tremor, dilated pupils, sluggish pupillary reflexes, and hypermetria. Temperature was 38.5, heart rate and respiratory rates were within normal ranges.
On questioning the family members, it was ascertained that Loki had been taken for a walk around some council gardens and a local rugby club approximately three hours previously. During the walk, he was noticed to have snuffled around in a particular area and surreptitiously eaten a “strange green object”. The children walking him were unable to prevent him swallowing the item. On return home, Loki was fed his usual dry biscuits half an hour prior to clinical signs first being noticed.
Suspecting exposure to a poison, and with Loki still alert and responsive, emesis was induced with a small dose of apomorphine. A small amount of dog food was brought up but nothing to suggest what might have been ingested on the walk. Loki was then administered activated charcoal and placed in a warm cage for the night.
The following morning, Loki was extremely sedated with ongoing incoordination and head tremor. He was able to be roused and taken out for toileting, but quickly tired and stumbled. He also developed urine dribbling. Serum and urine samples were collected and further charcoal was administered.
Based on the history and clinical signs, a CNS toxicity was suspected. Differential diagnoses included tremorgenic mycotoxins, macrocyclic lactone toxicity, ethylene glycol (antifreeze) toxicity, metaldehyde (slug bait) toxicity, mushroom toxicity, and cannabis toxicity. A biochemistry panel was requested to assess for liver and renal damage and therefore help rule out ethylene glycol and metaldehyde exposure.
Laboratory results:
Biochemistry was unremarkable aside from mild increases in ALT (103 IU/L – reference interval 0-88 IU/L), AST (125 IU/L – reference interval 0-51 IU/L) and CK (918 IU/L – reference interval 0-385 IU/L) concentrations. These findings suggested subtle hepatocellular and muscle damage, possibly explained by liver metabolism of an ingested toxin and tremors and ataxia, respectively. Urinalysis was unremarkable. Overall, these findings supported a primary CNS toxin and helped exclude ethylene glycol and metaldehyde poisoning.
A urine sample was sent to a human laboratory for analysis. The carboxy-THC concentration was 23 µg/L (cut-off 15 µg/L) and the carboxy-THC:creatinine ratio was 4 µg/mmol, confirming the presence of cannabis metabolites in the urine. The final diagnosis was cannabis toxicity.
Clinical progress:
Loki’s clinical signs of incoordination and depression improved gradually over approximately 72 hours. He was noticeably hyper-reactive and hungry on the third day. After approximately four days, he seemed back to normal.
Discussion:
Cannabis (marijuana) toxicity occurs due to ingestion of leaves, flowers and products made from the Cannabis sativa plant. The plant contains hundreds of chemicals although δ-9-tetrahydrocannabinol (THC) is the major psychoactive agent. Given the widespread recreational use and increasing medicinal use of cannabis, poisoning in companion animals may increase in incidence. Fortunately, cannabis has a relatively high safety margin and deaths in dogs are rare. The minimum lethal dose of THC is >3g/kg (Fitzgerald et al, 2013).
Clinical signs of cannabis toxicosis develop within 60 minutes and may last for several days, mediated largely by cannabinoid receptors distributed throughout the brain. Common manifestations include sedation, hypersalivation, hypermetria, mydriasis, urine dribbling, head tremor, hypothermia, and bradycardia. Higher doses may cause hyperexcitability and seizures (Fitzgerald et al. 2013). Treatment is largely supportive since there is no specific antidote.
Diagnosis is through appropriate clinical signs, history of ingestion, and ruling out other causes through biochemistry, haematology and urinalysis. Detection of THC metabolites in urine may help confirm the diagnosis but many human assays have low sensitivity in dogs due to low concentrations of the specific THC metabolites in canine urine. A novel ultra-performance liquid chromatography–tandem mass spectrometer method with excellent sensitivity was recently described and may prelude more reliable diagnostic assays becoming available for domestic animals (Fitzgerald et al. 2021).
References:
Fitzgerald KT, Bronstein AC, Newquist KL. Marijuana poisoning. Top Companion Anim Med. 28:8-12, 2013
Fitzgerald AH, Zhang Y, Fritz S, Whitehouse WH, Brabson T, Pohlman L, Cernicchiaro N, Tonozzi C, Ensley S. Detecting and quantifying marijuana metabolites in serum and urine of 19 dogs affected by marijuana toxicity. J Vet Diagn Invest. 33:1002-1007, 2021.