Blackwell's Five-Minute Veterinary Consult Clinical Companion. Группа авторов

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Название Blackwell's Five-Minute Veterinary Consult Clinical Companion
Автор произведения Группа авторов
Жанр Биология
Серия
Издательство Биология
Год выпуска 0
isbn 9781119671534



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       The main goal of therapy would be to remove the marijuana source from the environment.

       Gastric lavage for any horse that has recently ingested a large quantity of marijuana.

       Activated charcoal.

      Appropriate Health Care

       Monitor for CNS signs.

       Most common sign is depression which generally is not treated.

       Sedation may be required if hazardous behavior occurs due to CNS stimulation.

      Antidotes

       None.

      Drugs of Choice

       IV fluids for depressed and/or dehydrated horses.

       Di‐Tri‐Octahedral (DTO) smectite (Bio‐Sponge®)

       Sedation if needed for animals with CNS stimulation:Xylazine 1.1 mg/kg IV or 2.2 mg/kg IM prn.Detomidine 0.02–0.04 mg/kg IV or IM prn.

      Precautions/Interactions

       Marijuana compounds can interact with other medications although specifics in horses are not known.

      Surgical Considerations

       Not known specifically but if the horse is exhibiting neurologic effects, especially depression, it may be wise to delay procedures requiring anesthesia.

COMMENTS

      Client Education

       Clients should be educated on the need to remove marijuana from the horse’s environment.

       A specific withdrawal time for marijuana is not known in horses and so clients should be made aware that marijuana may be detected in drug testing of horses used for racing or showing.

      Prevention/Avoidance

       Eliminate marijuana from the environment.

      Expected Course and Prognosis

       Marijuana toxicity is rarely fatal in animals.

       Time to recovery will depend on type of exposure (ingested or inhaled) as well as quantity and potency of toxin.

       Marijuana may possibly be detected in drug tests on horses used for racing or showing after clinical signs have resolved.

      See Also

      Synthetic Cannabinoids

      Abbreviations

      See Appendix 1 for a complete list.

      1 Donaldson CW. Marijuana exposure in animals. Vet Med 2002; 97:437–441.

      2 Hovda L, Brutlag A, Poppenga R, Peterson K. Small Animal Toxicology, 2nd edn. John Wiley & Sons, Inc., 2016.

      3 Stillabower, A. Marijuana Toxicity in Pets. Available at: https://www.petpoisonhelpline.com/pet‐safety‐tips/marijuana‐toxicity‐pets/ (accessed April 3, 2021).

      4 Ujvary I, Hanus L. Human metabolites of cannabidiol: A review on their formation, biological activity, and relevance in therapy. Cannabis Cannabinoid Res 2016; 1: 90–101.

      Author: Christy Klatt, DVM

      Consulting Editor: Dionne Benson, DVM, JD

      

DEFINITION/OVERVIEW

       There is no label indication for these compounds in veterinary medicine and exposure is most commonly due to inadvertent exposure.

       Neuroexcitation, agitation, tachycardia, hypertension, and tachypnea are the most common clinical signs noted in the case of toxicity.

ETIOLOGY/PATHOPHYSIOLOGY

      Mechanism of Action

       Stimulates the release of monoamine neurotransmitters (dopamine, serotonin, and norepinephrine) from nerve endings.

       Inhibits reuptake and metabolism of catecholamines, increasing amount at nerve endings.

      Toxicokinetics

       Pharmacokinetics of methamphetamine have been described in horses.

       Absorption, T max: 15–30 minutes following transmucosal exposure.

       Distribution, V ss: 4.44 ± 0.648 L/kg

       Metabolism: amphetamine is a minor metabolite of methamphetamine.

       Both methamphetamine and amphetamine (at lesser concentrations) are found in urine.

       Terminal half‐life: 0.5–1.7 hours

       Urinary alkalization in humans prolongs drug elimination. In horses, urine pH does not appear to affect elimination (10 mg methamphetamine exposure).

      Toxicity

       Amphetamine:LD50 in rats and mice is 10–30 mg/kg.

       Methamphetamine:LD50 (oral) in dogs is 9–11 mg/kg.Ingestion of 1.3 mg/kg in humans – death.

      Systems Affected

       Nervous – agitation, ataxia.

       Cardiovascular – tachycardia, hypertension.

       Respiratory – tachypnea.

SIGNALMENT/HISTORY

      Historical Findings

       History of exposure and clinical signs.

      Location and Circumstances of Poisoning

       Most likely exposure is from environment including inadvertent by animal handler.

CLINICAL FEATURES

       Clinical signs include hyperactivity, tremors, ataxia,