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Marijuana toxicity in dogs: Part 2 | VETgirl Veterinary Continuing Education Blog

In today's VETgirl online veterinary continuing education blog, we review marijuana toxicosis in dogs. In this 2-part blog, we'll discuss all you need to know about this up-and-coming toxicosis in veterinary medicine. Last week, we reviewed marijuana's pharmacokinetics and clinical signs seen with poisoning in dogs. Check out that article first! In today's blog, we'll review specific testing (e.g., urine drug tests - should you use them) and treatment for marijuana toxicosis in dogs.

Clinicopathologic testing
With marijuana poisoning, no significant clinicopathologic findings are noted. In patients suspected of having underlying disease (e.g., metabolic, geriatric, etc.), a baseline complete blood count and general chemistry panel can be considered. In patients suspected of hypoventilating secondary to the sedative effects of marijuana, a venous blood gas should be performed to evaluate the partial pressure of carbon dioxide (pCO2; normal reference range 30-35 mm Hg). Patients with a severe respiratory acidosis (e.g., pCO2 > 50 mm Hg) are candidates for intubation and mechanical ventilation. If hypoxemia (e.g., defined as a partial pressure of oxygen of < 80 mm Hg; normal reference range 80-100 mm Hg) is a concern, the use of an arterial blood gas as a gold standard should be considered.

While some emergency veterinary clinics often screen for marijuana poisoning with human urinary drug screen tests, the author cautions that careful interpretation of the results is imperative. False negative results can be seen with THC due to the unique metabolites in dogs as compared to humans.1 That said, a positive result (e.g., even a weak positive) is consistent with marijuana poisoning.

Treatment
Treatment for marijuana poisoning includes appropriate decontamination; however, this should be performed judiciously. Keep in mind that emesis induction is often not rewarding, due to the antiemetic effect of THC. If the patient is already symptomatic, emesis should not be induced. For example, if the patient has a decreased gag reflex or is excessively sedate, emesis should not be induced due to the risk of aspiration pneumonia. In this situation, if the marijuana is thought to still be present in the stomach (e.g., wads of buds ingested), it is safer to perform gastric lavage (with an inflated endotracheal tube to protect the airway) under sedation for gavage, followed by activated charcoal administration directly through the orogastric tube. Typically, multiple doses of activated charcoal can be administered due to enterohepatic recirculation.

Additional treatment includes gastrointestinal support. Anti-emetics (e.g., maropitant, dolasetron, ondansetron) should be considered to prevent vomiting and secondary aspiration. Fluid therapy with a balanced, maintenance crystalloid can be implemented to maintain hydration and perfusion. Symptomatic supportive care, including thermoregulation, nursing care, anxiolytics (for agitated, tachycardia, and/or hypertensive patients including acepromazine or benzodiazepines), and monitoring (e.g., electrocardiogram, blood pressure, pulse oximetry, end-tidal CO2, etc.) should be performed.

Life-threatening clinical signs are less commonly seen with marijuana toxicosis, but can potentially result in demise of the patient. In patients that are hypoventilating (e.g., respiratory rate < 6 bpm, increased end-tidal CO2, respiratory acidosis, hypercapnea, etc.), intubation and mechanical ventilation are recommended. Bradycardiac patients (canine patients with a heart rate < 40-50 bpm) may require the use of atropine (0.01 mg/kg IM, IV PRN). If tachycardiac is seen (canine patients with a HR > 180 bpm), a blood pressure should be checked. If the patient is both tachycardiac and hypertensive, the use of anxiolytics (e.g., acepromazine at 0.05 mg/kg, IV, IM PRN) or beta-blockers (e.g., propranolol 0.02 mg/kg IV, up to max dose of 0.1 mg/kg) are warranted. If the patient is both tachycardiac and hypotensive, a crystalloid fluid bolus should be considered (e.g., 20-30 ml/kg IV).

While there is no “cure” for marijuana poisoning in veterinary medicine, the prognosis is generally excellent with supportive care. One potential “antidote” that can be in severe, potentially life-threatening cases is the use of intravenous lipid emulsion (ILE). Please see “IV Lipid Therapy: Are we really giving IV fat?” proceedings more for information. Dosing for ILE in veterinary medicine is extrapolated from human medicine at:2

• 20% solution: 1.5 – 4 ml/kg IV over 1 minute, followed by 0.25 mg/kg/min, over 30-60 minutes.2
• Re-dosing of aliquots of 1.5 ml/kg q 4-6 hours can also be continued for 24 hours if needed OR follow-up CRI doses of 0.5 ml/kg/hr can be continued until clinical signs improve (not to exceed 24 hours).2

Conclusion
Thankfully, with rapid recognition of clinical signs and prompt treatment, the prognosis for marijuana toxicosis in veterinary medicine in excellent with supportive care. Veterinarians should be aware of the growing prevalence of exposure in dogs and cats due to the legalization of medical marijuana in certain states, and should be able to rapidly recognize and treat this ever-growing toxicity.

REFERENCES
1. Fitzgerald KT, Bronstein AC, New quist KL. Marijuana poisoning. Top Companion Anim Med 2013;28(1):8-12.
2. Fernandez AL, Lee JA, Rahilly LJ, et al. The use of intravenous lipid emulsion as an antidote in veterinary toxicology. J Vet Emerg Crit Care 2011;21(4):309-320.

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