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

Reading

      1 Thompson J, Mirza M, Barker S, et al. Clenbuterol toxicosis in three quarter horse racehorses after administration of a compounded product. J Am Vet Med Assoc 2011; 239:842–849.

      2 Barlas S. Deaths from contaminated methylprednisolone highlight failures of compounding pharmacies: Less hospital access to outside vendors and more visits from state pharmacy boards. P T. 2013; 38(1):27–57.

      Author: Dionne Benson, DVM, JD

      Consulting Editor: Dionne Benson, DVM, JD

      section II

      Specific Toxins and Toxicants

        Drugs: Illicit and Recreational

        Drugs: Prescription

        Insecticides, Herbicides and Farm Chemicals

        Ionophores and Growth Promotants

        Metals

        Mycotoxins/Fungus

        Other Toxins

        Plants and Biotoxins

        Rodenticides

        Toxic Gases

        Trees

        Zootoxins

Drugs: Illicit and Recreational

Chapter 6 Cobalt

      

DEFINITION/OVERVIEW

       Cobalt is a trace element that is a necessary part of the equine diet.

       There are no reported cobalt deficiencies in horses.

       Cobalt is present in feed, supplements, and injectables that are marketed for equine use.

       Cobalt is also purchased from compounding pharmacies.

       Cobalt is used in the equine hindgut to make vitamin B12.

       In humans, cobalt has been used to mimic hypoxia, stimulating RBC production.

       In horses, no RBC production has been observed with IV administration of varying doses.

       Intentional administration of excessive amounts of cobalt have led to toxicosis.

       Controlled substance under ARCI rules.

ETIOLOGY/PATHOPHYSIOLOGY

      Mechanism of Action

       Unknown – in humans cobalt stabilizes HIF factors, causing increased erythropoiesis. Although studied, the same effects have not been observed in horses.

      Toxicokinetics

       Onset is rapid with effects occurring within minutes of IV administration.

       Duration of action is minutes to hours for a single exposure. Repeated exposure effects have not been studied.

       Absorption through the GI tract – in studies in sheep bioavailability varied by preparation. In horses, they are most often administered IV.

       Hepatic metabolism: horses administered cobalt often have elevated concentrations in liver tissue.

       Excretion – urinary excretion.

      Toxicity

       Highly toxic – clinical signs observed at doses as low as 0.25 mg/kg.

       Toxic effects may vary by dose with some clinical signs observed more often at higher doses.

      Systems Affected

       Neurological – anxiety, ataxia, tremors, muscle fasciculations.

       Cardiovascular – tachycardia, arrhythmias (including VT), increases in MAP, SAP, DAP.

       Gastrointestinal – colic.

       Renal – hematuria.

SIGNALMENT/HISTORY

      Risk Factors

       Iatrogenic administration.

       Exposure to cobalt salts intended for other species (e.g., goats).

      Historical Findings

       Iatrogenic administration.

       Owners or trainers may be reluctant to admit administration due to regulations.

       Incidental exposure to cobalt salt intended for another animal.

      Location and Circumstances of Poisoning

       Worldwide problem, especially in racehorses.

       Often intentional exposure in horse racing due to perceived increased erythropoietic effects.

       Unintentional exposure by placement of cobalt salts, especially when co‐mingling of horses in pasture with animals requiring cobalt supplementation.

CLINICAL FEATURES

       Variable by dose received.

       Common signs include agitation, ataxia, muscle fasciculations, tachycardia, arrhythmias, hematuria, colic.

DIFFERENTIAL DIAGNOSIS

       Colic of other etiology.

       UTI or bladder stone for hematuria