Severe bradyarrhythmia causes a severe decrease in cardiac output, which may cause cardiovascular collapse. This is especially likely in horses with limited cardiovascular reserve capacity, such as hypovolemic animals. In these cases, it is recommended to replace the intravascular volume before an alpha‐2 adrenergic agonist agent is used.
Anaphylactoid Reaction
Definition
Anaphylactoid reactions produce a similar clinical picture as true anaphylactic reactions, but are not mediated by IgE and occur through a direct non‐immune mediated release of histamine and other mediators from mast cells and/or basophils.
Risk factors
Some opioid drugs (morphine and meperidine [pethidine])
Route, dose and rate of drug administration. The administration of a high dose of a rapid intravenous bolus of the drug leads to a greater histamine release compared with lower doses administered as a constant rate infusion [9].
Pathogenesis
Morphine and meperidine (pethidine), when injected intravenously, induce histamine release due to mast‐cell degranulation by a non‐immunological mechanism (non‐IgE mediated) [10]. The most potent at causing this effect is meperidine (pethidine) [11].
The clinical consequences of an anaphylactoid reaction are the same as those of a true anaphylactic reaction, most commonly hypotension and tachycardia, but other effects such as bronchoconstriction, pruritus, urticaria or cardiovascular collapse may also occur (non‐allergic anaphylaxis).
A retrospective study of intraoperative administration of morphine at doses of 0.1–0.17 mg/kg in horses found no significant increase in problems during or immediately after anesthesia, which included no cardiovascular side effects when compared with a similar protocol without the opioid [12]. However, a case report of two horses who received intravenous meperidine, one sedated and one anesthetized, describes the occurrence of tachycardia and profuse sweating, which may have been due to an anaphylactoid reaction [13]. Unfortunately, no blood pressure was measured in these horses. Both horses recovered uneventfully from this reaction within 10 minutes.
Prevention
An alternative route of administration such as intramuscular should be considered when drugs known to cause histamine release are administered, especially meperidine. When morphine is administered intravenously, it should be injected slowly while monitoring the horse for any possible side effects (especially heart rate and blood pressure).
Previous administration of an anti‐histaminic drug such as chlorphenamine or diphenhydramine, may be considered when these drugs are used in debilitated animals with a reduced cardiovascular reserve. However, no problems associated with the use of intravenous morphine at clinical doses are usually observed in healthy horses [12] or horses with colic (personal observation) and therefore the routine use of anti‐histaminic drugs is not recommended as they may produce other unwanted effects (e.g. sedation).
Diagnosis
Histamine release occurs within minutes of drug administration and the consequences appear quickly. The first clinical signs of histamine release are hypotension and tachycardia, which may be mild and short lasting or severe, even causing cardiovascular collapse. These signs can be easily observed if the heart rate and blood pressure are being monitored (e.g. under general anesthesia), but in conscious horses they may go unnoticed.
Treatment
Usually, treatment is not necessary. Supportive treatment of hypotension includes the administration of intravenous fluids and/or vasoconstrictors (e.g. phenylephrine). If the reaction is severe, causing bronchoconstriction and cardiovascular collapse, epinephrine (adrenaline) should be immediately administered as well as oxygen supplementation, while blood pressure, heart rate and oxygenation (pulse oximetry and/or blood gases) are being monitored.
Expected outcome
Outcome should be good if supportive treatment is instituted rapidly.
Negative Effect on Recovery from General Anesthesia
Alpha‐2 adrenergic agonists: excessive sedation and ataxia
Definition
A normally functioning body can “sense” how its joints, muscles and tendons are moving, and where all the components of the body are in relation to each other. Ataxic horses are those that are unable to control the rate, 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