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and circling.

       Severe abdominal pain, bloody diarrhea, and gut ischemia have been reported in humans following ingestion.

DIFFERENTIAL DIAGNOSIS

       CNS stimulants – cocaine, ephedrine, pseudoephedrine, methylxanthines, strychnine.

DIAGNOSTICS

       History of exposure and clinical signs.

       Thrombocytopenia, prolonged PT and activated PTT (consistent with disseminated intravascular coagulation) reported in dogs and humans.

       Quantitation of methamphetamine or amphetamine in urine.Drug screening kits available, however, not currently validated for horses.

       LC‐MS can assist with diagnostics but may not be timely for therapy.

THERAPEUTICS

       The overall goal is to provide supportive care and allow the animal to clear the drug.

      Detoxification

       Urinary acidification with ammonium chloride or ascorbic acid has been suggested to increase the rate of elimination in some species. If this is attempted, acid–base status should be monitored. In horses, urinary acidification did not enhance elimination following transdermal administration of 10 mg.

      Appropriate Health Care

       Monitor closely to ensure animal does not injure itself due to neuroexcitation.

       Monitor blood pressure, heart rate and rhythm and respiration.

       Monitor temperature.

      Antidotes

       None available.

      Drugs of Choice

       Phenothiazines tranquilizers to control CNS signs:Animal should be monitored as seizure threshold may be lowered.Acepromazine (0.05–1 mg/kg IV).

       Diazepam and other barbiturates – for seizure activity.

       Propranolol for tachycardia (0.02–0.06 mg/kg IV).

COMMENTS

      Client Education

       Ensure animal will not be exposed in the future.

       Contact veterinarian if clinical signs return or worsen.

      Patient Monitoring

       ▪ Behavioral monitoring.

       Monitor heart rate and blood pressure.

       ECG as needed.

       Monitor electrolytes.

      Prevention/Avoidance

       Prevent inadvertent exposure by handlers.

      Possible Complications

       Self‐injury due to excitation/ataxia.

       Death.

      Expected Course and Prognosis

       Time to development of clinical signs likely within 15–30 minutes but will vary with degree of exposure and amount exposed to.

       Prognosis depends on severity of poisoning.

      Abbreviations

      See Appendix 1 for a complete list.

Suggested Reading

      1 Knych HK, Arthur RM, Kanarr KL, et al. Detection, pharmacokinetics and selected pharmacodynamic effects of methamphetamine following a single transmucosal and intravenous administration to exercised thoroughbred horses. Drug Test Anal 2019; 11:1431.

      2 Zengyang P, Zhang X. Methamphetamine intoxication in a dog: case report. BMC Veterinary Research 2014; 10:139.

      Author(s): Heather K. Knych DVM, PhD, DACVCP

      Consulting Editor: Dionne Benson, DVM, JD

Chapter 12 Opioids

      

DEFINITION/OVERVIEW

       Natural opioids are found in the seeds of the opium poppy (Papaver somniferum). Opium powder is about 10% morphine and 0.5% codeine. Oxymorphone, codeine, hydromorphone, and heroin are derived from morphine.

       There are numerous synthetic opioids on the market manufactured primarily for human and animal pain relief and tranquilization. Most are not FDA‐approved for horses.

       The exact mode of action varies slightly by drug due to different receptor activity and affinity.

       The primary effects are seen in the CNS; however, there are opioid receptors throughout the body.

       Most pain relief is via agonists binding to mu receptors in the CNS and periphery. Mu receptors vary in location and density for horses compared with other species.

       Opioids licensed for equine patients:Butorphanol (kappa agonist and mu antagonist) – schedule IV, pain management (good for equine GI pain).Pethidine (Meperidine) – schedule II, pain management, labeled for spasmodic colic.Buprenorphine (partial mu agonist) – pain management.

       Other opioids used in equine health care, but not licensed specifically for equine patients:Fentanyl (pure mu agonist).Tramadol.Morphine (pure mu agonist).Nalbuphine (partial agonist/antagonist similar to butorphanol) – not DEA.Remifentanil.Methadone (pure mu agonist).Hydromorphone.

       Opioids easily cross the blood–brain barrier allowing for receptors causing cough reflex suppression, respiratory depression, and a depressed CNS.

       Clinical findings include decreased in gut motility and increased water absorption, causing constipation and impaction. Clinically, this is usually observed at high doses.

       Existing toxicology research is in humans, dogs, and cats with variations in the lethal doses in each species.

       Use of opioids (particularly mu agonists), historically, has been limited in the horse due to adverse side effects. In horses, clinical signs of toxicosis include excitation, agitation, increased locomotor activity and decreased gut motility. Side effects are likely due to the receptors’ affinity for the medications and how densely the receptors are in their specific locations in the equine brain.