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].
Treatment
No specific treatment exists for lidocaine neurotoxicity. The patients recover rapidly from the effects of lidocaine after discontinuation due to its short terminal half‐life (40 min) in the horse [26].
Expected outcome
The outcome should be good if the horse does not suffer from major injuries.
Postop complications
Opioids: Excitement
Definition
Opioids can produce excitement, seen as box walking, restlessness and dysphoria when administered alone in pain‐free horses.
Risk factors
Administration of high doses of opioids without the concurrent administration of a sedative drug
Administration of opioids in pain‐free horses
Pathogenesis
Horses possess a unique opioid receptor profile and density compared to other species and are sensitive to opioid‐induced CNS stimulatory and locomotor effects. Excitement may result indirectly from increased release of norepinephrine and dopamine. This may explain the mechanism why noradrenergic and dopaminergic blocking drugs like phenothiazines suppress the opioid induced excitement [12]. However, increased locomotor activity produced by opioids seems to be associated with opioid receptors. The propensity of an opioid analgesic to promote locomotion may be greater with mu (e.g., morphine) than with kappa agonists (e.g. butorphanol) [27]. Kappa agonism more commonly causes ataxia and staggering [28]. Opioids were studied in varying numbers of pain‐free horses in one of the most commonly cited references on opioid‐induced locomotion in horses [32]. It is important to note that there is marked individual variation in responses. The median effective dose of morphine that causes an increase in locomotion activity in pain‐free animals is 0.91 mg/kg, which is considerably higher than the doses used clinically to produce analgesia [30].
Prevention
Using appropriate clinical doses of opioids in combination with a sedative drug will prevent this excitement [30].
Diagnosis
Increased locomotor activity, box walking, head jerking, disorientation and/or ataxia
Treatment
The use of sedative agents like acepromazine or apha‐2 adrenergic agonists can calm and sedate the horse, solving the excitement and increased locomotor activity. The use of the opioid antagonist naloxone (0.015 mg/kg) entirely prevented locomotor responses to morphine and fentanyl [31]. Naloxone will revert the analgesics effects of any opioid, therefore it should be used with caution in painful horses and only in severe cases or overdose.
Expected outcome
The outcome is good as these effects are usually mild and easy to control with the administration of a sedative.
Ileus
Definition
Gastrointestinal propulsive motility depends on a complex
