Complications in Equine Surgery. Группа авторов

       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) decreases the adverse effects observed during the recovery phase [20].

      The quality of recovery from anesthesia was better when an intravenous infusion of S‐ketamine was used instead of racemic ketamine during isoflurane anesthesia in clinical horses undergoing arthroscopy [20].

       Diagnosis

      The presence of excitement in the recovery period with nystagmus, ataxia, restlessness and hyper‐reactivity to sound and noise. Sometimes “box‐walling” has been described.

       Treatment

      If ketamine has been administered as a CRI during anesthesia and the horse shows signs of excitement early during the recovery phase, it is recommended to sedate the horse with an alpha‐2 adrenergic agonist. Keeping the horse in a quiet and dark environment will avoid stimulation and early attempts to stand.

       Expected outcome

      With time the drug will be metabolized and the horse will recover slowly from the side effects caused by the accumulation of ketamine and its metabolites. The outcome should be good if the horse does not suffer from major injuries.

       Lidocaine: ataxia and visual dysfunction

       Definition

      Ataxia and alterations in behaviour related to visual dysfunction may be observed after overdosing with lidocaine [21]. Horses show rapid and intermittent eye blinking, anxiety and attempts to inspect closely located objects.

       Risk factors

       Lidocaine administration until the end of anesthesia has a significant negative effect on the degree of ataxia exhibited by horses in the recovery period.

       Liver disease can impair lidocaine metabolism and hepatic clearance, therefore it will not be metabolized and so accumulates.

       Pathogenesis

      Lidocaine is a local anesthetic commonly used intravenously as a CRI as part of balanced anesthetic protocols in equine anesthesia. The beneficial effects include analgesia and inhalational anaesthetic‐sparing effect [22, 23]. However, lidocaine at high plasma concentrations can cause neurotoxicity and cardiotoxicity (see Chapter 14: Complications of Loco‐Regional Anesthesia).

       Prevention

      When using lidocaine as a CRI during anesthesia, it is recommended to stop the infusion 30 minutes before the end of surgery to avoid ataxia during the recovery period [24]. This study showed that using intraoperative lidocaine as a CRI at a dose of 50 microg/kg/min and discontinuing the CRI 30 minutes before the end of surgery reduced the degree of ataxia during the recovery period [24].

       Diagnosis

      Signs of neurotoxicity caused by lidocaine include rapid eye blinking, ataxia, progressing to sedation, muscle twitching, seizures and unconsciousness [21]. Tremors and signs of visual dysfunction, including staring and inspecting the walls and floor closely, in some horses that received a CRI of lidocaine during anesthesia were observed [25].