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 interaction between neural, hormonal, vascular and neuromuscular pathways. Disruption of this intrinsic interaction leads to absence of propulsive aboral movement of food material, also called ileus.
Risk factors
The use of high doses of either opioids or alpha‐2 adrenergic agonists
The use of opioids in pain‐free horses may predispose to ileus
Prolonged starvation (>18 h)
Recent changes in management such as exercise, diet and transport increase the risk in hospitalized horses.
Stress response to anesthesia, surgery and pain
Local inflammation and edema of the intestine
Endotoxemia
Pathogenesis
Alpha‐2 adrenergic agonists decrease intestinal motility, which may predispose to ileus. Studies in rats using clonidine showed that the activation of presynaptic alpha‐2A subtype receptors was responsible for the slower motility [33]. In horses, xylazine‐induced vasoconstriction of the cecal vasculature decreases arterial blood flow to the lateral cecal artery, decreasing normal local motility for up to 120 minutes with a full sedative dose (1.1 mg/kg, IV) and for 30 minutes with a low dose (0.275 mg/kg) [34].
The gastrointestinal effects of opioids may also predispose to post‐anesthetic colic or ileus. All opioids, including mu and kappa agonists, reduce gastrointestinal motility [30]. Morphine (0.5 and 1.0 mg/kg) and fentanyl (10 or 50 mg) intravenously initially stimulated, but then inhibited ceco‐colic electrical and mechanical activity for up to 3 hours in three pain‐free ponies [38]. A decrease in gastrointestinal motility was detected 1 to 2 hours after intramuscular administration of morphine at doses of 0.05 and 0.1 mg/kg and after intravenous administration at a dose of 0.1 mg/kg [39]. In another study, morphine administered at 0.5 mg/kg twice daily decreased propulsive motility and moisture content in the gastrointestinal tract lumen for up to 6 hours after each dose [37]. Epidural morphine has also been shown to temporarily reduce GI motility but it did not cause ileus or colic in a small group of healthy unfasted horses [40]. A single intravenous injection of butorphanol was associated with decreased borborygmi, and decreased defecation; however, the administration of butorphanol as a continuous intravenous infusion over 24 hours was associated with minimal side effects including minimal gastrointestinal effects [41].
The literature indicates a multifactorial etiology for peri‐anesthetic ileus and an equivocal contribution of morphine and other opioid analgesics. Therefore, care should be taken when extrapolating these data to clinical situations of horses with painful conditions and in which other factors may also affect GI motility.
Prevention
Continuous intravenous infusions of low doses may reduce the intensity of gastrointestinal side effects as compared with intravenous bolus administration. Avoid high doses of opioids and alpha‐2‐adrenergic agonists and reduce the dose of opioids and/or alpha‐2 adrenergic agonists to the minimum effective dose. In painful horses the effective management of pain is important and the use of clinical doses of opioids (e.g. 0.1–0.3 mg/kg of morphine) is recommended, as the analgesic effect may override theoretical concerns of decreased gastrointestinal motility. Using pain scales may help to identify the patients that are in pain and in need of analgesia, allowing a more correct dosage and avoiding overdosing.
Diagnosis
It is out of the scope of this chapter to detail the diagnosis and treatment of ileus in horses, as it is a multifactorial disease, but if high doses of opioids and/or alpha‐2 agents have been administered or they have been used for prolonged periods of time, they could be a contributing factor.
Treatment
Naloxone, a full opioid antagonist, induces a marked propulsive activity in the colonic segment producing onset diarrhea, restlessness, abdominal checking, tachycardia and tachypnea in healthy horses not pre‐treated with opioids [42]. In vitro, naloxone has prokinetic effects at the ileo‐eco‐colonic junction [43]. Naloxone also reverses the analgesic effects of opioids.
N‐methylnaltrexone, a peripheral opioid antagonist that does not cross the blood–brain barrier, therefore not reversing opioid‐induced analgesia. has been studied in horses [44]. At doses