range or force of their movements, resulting in an inconsistent gait.
Risk factors
The degree of sedation ataxia is dependent on the route and dose of alpha‐2 adrenergic agonist administration.
The administration of a high dose of a rapid intravenous bolus of the drug leads to a longer recovery period and the chance of ataxia if the horse tries to stand up at early stages.
Pathogenesis
Alpha‐2 adrenergic agonists act centrally causing sedation, analgesia and muscle relaxation. These effects are dose related up to a maximal point, after which increasing the dose further only increases the degree of ataxia and lengthens the duration of the effects. Excessive ataxia due to excessive muscle relaxation may make it impossible to keep the horse standing. Excessive sedation and ataxia in the recovery period could result in injuries or an unsuccessful recovery.
The administration of xylazine, detomidine or romifidine to horses during the recovery period prolongs, but improves the recovery from isoflurane anesthesia, making it smoother, free of excitation and ataxia with minimal cardiopulmonary effects [14]. A study comparing the recovery quality when xylazine or romifidine were administered during the recovery period showed that a dose of 20 microg/kg of intravenous romifidine in healthy adult horses anesthetised with isoflurane for >1 hour, was associated with better recovery quality than a lower dose of romifidine or xylazine [15]. However, in a study of perioperative morbidity and mortality in horses, sedation with an alpha‐2 adrenergic agonist during recovery appeared to show some association with improved recovery scores but, in the final model, it was found to be less important than other factors [16].
Prevention
When low doses of alpha‐2 adrenergic agonists are used in the recovery period, they prolong the time of recumbency and improve the quality of recovery [14]. However, if the dose is too high, they may cause excessive ataxia. Romifidine causes a lower degree of ataxia compared with equipotent doses of xylazine and detomidine [2].
An alternative route of administration such as intramuscular may be considered as drugs are absorbed slowly and side effects, like ataxia, might be less dramatic.
An adequate dose for the weight of the patient should be used. If the horse has been on an intravenous infusion of any alpha‐2 adrenergic agonist intraoperatively, the administration of any more sedation for the recovery period should be gauged carefully, as the residual amount of drug after stopping the infusion may cause sufficient sedation during this phase.
All alpha‐2 adrenergic agonists increase diuresis, which is of similar degree and duration among agents [2]; therefore, emptying the bladder at the end of the surgical procedure before the recovery phase may improve comfort and prevent early attempts to stand up.
Diagnosis
Horses recovering from general anesthesia present some degree of ataxia due to the residual effects of anesthetic drugs. Ataxia contributes to the uncoordinated and sometimes unsuccessful attempts to stand during this phase. Once standing, ataxic horses sway from side to side and sometimes fall back down. This contributes to the high mortality and morbidity observed in horses during the recovery period.
Treatment
Partial antagonism of the alpha‐2 adrenergic agonist, with yohimbine or atipamezole, can help to improve the ataxia. However, if the horse is excessively ataxic it may be dangerous for personnel to enter the recovery room. Moreover, if antagonized excessively this may cause excitement, which can also lead to fatalities during the recovery. Keeping a quiet and dark environment while the horse is recovering is essential to avoid early attempts to stand up, when the ataxia is more pronounced.
Expected outcome
The ataxia seen in recovery due to sedation with alpha‐2 adrenergic agonists is self‐limited by the metabolism of the drug. Xylazine produces the shortest effects, lasting for about 15–20 minutes.
Excessive sedation and ataxia may be responsible for morbidity and mortality during the recovery. Horses may suffer injuries, which can range from minor wounds to fatal injuries leading to the euthanasia of the animal (e.g. fracture of a long bone).
Ketamine: excitement and emergence hallucination
Definition
Ketamine side effects include muscular tremors, rigidity, involuntary limb movements, excitement, ataxia and hallucinations, which may lead to increased morbidity and mortality during the recovery of horses [17].
Risk factors
High plasma ketamine concentrations
Length of the ketamine infusion. Accumulation of ketamine and its metabolites can lead to prolonged recoveries with poor quality [18].
Hepatic and renal disease can cause a delay in the metabolism and excretion, respectively, of ketamine and its accumulation in plasma.
Pathogenesis
Ketamine is a dissociative anesthetic with actions on several receptors, but the antagonism of the N‐methyl‐D‐aspartate (NMDA) receptors in the central nervous system (CNS) is mainly responsible for its anesthetic, analgesic, psychotomimetic and neuroprotective effects. It is widely used in horses in combination with benzodiazepines and/or alpha‐2 adrenergic agonists as an induction agent and in total intravenous anesthesia, producing rapid and smooth induction with minimal cardiovascular depression and good analgesia. Intraoperative constant rate infusions (CRI) of ketamine are used in equine anesthesia as part of the balanced anesthesia concept aiming to improve analgesia, reduce the amount of inhaled agent and preserve cardiovascular function [19].
It seems that recovery from ketamine anesthesia in the horse depends on rapid redistribution of the drug from the central compartment and this explains the abrupt recovery from ketamine anesthesia often observed in the horse.
The exact dose or circulating concentration of ketamine at which excitement or abnormal behavior occurs may vary between horses and has not been identified. Fielding et al. [29] concluded in their study that the use of subanesthetic doses of ketamine in standing horses up to 0.8 mg/kg/h for 6 hours did not cause signs of excitement, but an analgesic effect was not obtained with the method of analgesic testing used.
Prevention
The administration of a ketamine CRI intraoperatively for longer than 2 hours is not recommended. Administration of ketamine CRIs in horses with hepatic and/or renal disease should be avoided.
The administration of S‐ketamine instead of racemic ketamine (R‐/S‐ ketamine)
