Critically appraise available evidence in the literature to determine whether during lameness evaluation administration of alpha-2 adrenergic agonists (α2 agonists) reduces the accuracy of interpreting diagnostic analgesia compared with no administration of α2 agonists. Establishing the location of lameness in difficult, fractious or sensitive horses can be a significant challenge for the equine veterinary surgeon, especially with the increasing demands of clients to localise the lameness source. The 2013 British Equine Veterinary Association accident survey highlighted the dangers of our occupation and the types of situations equine veterinarians regularly find themselves in. Diagnostic analgesia has become a mainstay of equine lameness investigation, and is seen as a cost-effective and valid method of localising potential sources of pain. Physical restraint, via use of a twitch, bridle or stocks, in most cases is successful, but often chemical restraint, through sedation, may be required. Although, the use of sedation is not a new method, a lot of its use in equine lameness evaluation is anecdotal in its evidence. There is concern that the use of sedation may influence the lameness examination via analgesic effects and ataxia. Many historical research papers and texts (Dyson and Kidd 1993; Barr 2010; Ross and Dyson 2011) elude to the use of sedation, in particular α2 agonists, in aiding with diagnostic analgesia and base their use on handler safety and improved patient tolerance. CAB abstracts were searched using the following terms: (Equine*/Horse*/Equus*/Foal*/Colt*) AND (Alpha-2 Agonists*/Alpha-2 Adrenergic Agonist*). Of 79 results, screening was based on the title and abstract in regards to question relevancy. Although all addressed use of α2 agonists in equines and illustrated the major pharmacology of α2 agonists, none reported use of sedation in equine lameness exams. A further screen on PubMed (using Equine* AND Lameness* AND Sedation*) obtained three relevant results. Although a relatively dated article, the paper set out to evaluate the locomotion patterns in both sound and lame horses after administering detomidine and antagonising with atipamezole prior to lameness assessment. In total, 17 horses (nine sound, eight chronically forelimb lame) were used in the study, with a repeated measures design. Horses were seen trotting on a treadmill at various time points post-sedation, focusing particularly on stride length and hoof movements in the forelimbs. Level of sedation was based on heart rate and head height. The same exercise was performed the following day; with sedation being antagonised with atipamezole after 15 min. Results showed that detomidine-sedated horses at 15 min develop a longer stride length, which could be reversed with atipamezole. The authors report no difference in perceived lameness using a head acceleration asymmetry system, and when using α2 antagonists, there was no relapse into sedation. The authors suggest that detomidine administration does not decrease the lameness grade, but does change the locomotor pattern. This may make assessment of response to diagnostic analgesia difficult in mild cases. Additionally, α2 antagonists may be useful, but can be expensive. A more recent article evaluated the effects of low dose xylazine on fore- and hindlimb lameness by using body mounted inertial sensors. In total, 44 horses of various comfort levels were divided into xylazine treatment and saline control groups. Degree of sedation was assessed by head height and ataxia grade. Horses were then assessed on a straight line, focusing on vertical head height and vertical pelvic movement asymmetry. There was no significant difference in head movement and pelvic movement asymmetry between time 0 and 20 min, and time 0 and 60 min in both treatment groups. Although, some horses with forelimb lameness changed their lameness grade, this was not significant between treatments. This was not the case with hindlimb lameness. This study provided some supportive evidence that the use of α2 agonists does not mask lameness. This study had a similar protocol to Rettig et al. using inertial sensors, but compared the difference between xylazine and acepromazine in lameness evaluation. Interestingly, no analgesic effect of xylazine was found at low doses, with no significant difference in lameness before and after xylazine. All studies (Buchner et al. 1999; Da Silva Azevedo et al. 2015; Rettig et al. 2016) provide support for α2 agonists use in lameness investigations, although the long action of effect with detomidine may prevent its use in fast-acting nerve and synovial blocks (Clarke et al. 2014). The use of short-acting xylazine does not appear to mask lameness, although, care must be taken in interpreting diagnostic analgesia in mild forelimb lameness after sedation. During the appraisal, a few questions were raised, including ridden assessment of horses after sedation with α2 agonist, opioid combinations and the potential side effects of α2 antagonists. Moreover, the possibility of species variation in the pharmacology of α2 agonists, which was raised, has some evidence (Latzel 2012). No conflicts of interest have been declared. Not applicable. None.
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Mar 28, 2019
E L Hoaglund + 4
Open Access