of alpha‐2 adrenergic agonists
Pathogenesis
Xylazine and detomidine have both been shown to increase urine production multi‐fold over normal in standing horses [127–129]. The mechanism by which alpha‐2 agonists increase urine production is primarily related to inhibition of anti‐diuretic hormone [37]. General anesthesia tends to reduce production [130] but it still remains above normal values of approximately 0.5 ml/kg/hour, even in water deprived animals [127].
Monitoring
Urine production can be assessed via the placement of a urinary catheter and measurement of urine output over the anesthetic period.
Treatment
There is no specific treatment, but diuresis of this magnitude may contribute to dehydration and should be considered when calculating intravenous fluid administration rates during sedation and anesthesia. In addition, horses sedated for standing procedures with alpha‐2 adrenergic agonist drugs will often shift body position or attempt to posture to void. Therefore, catheterization of the urinary bladder can be helpful for longer procedures and is especially recommended in female horses when procedures involve rectal or vaginal manipulation or when constant rate infusions of alpha‐2 agonists are used.
Blood Glucose Abnormalities
Definition
Hyperglycemia is an effect of alpha‐2 adrenergic agonist drugs, which increase blood glucose concentrations for variable durations following administration [128, 131]. On the other hand, hypoglycemia is also possible, especially in foals who are fasted or medically compromised.
Risk factors for hyperglycemia
Use of alpha‐2 adrenergic agonists
Risk factors for hypoglycemia
Neonatal or pediatric patients (especially fasted)
Pathogenesis
Alpha‐2 agonists cause hyperglycemia as a result of decreased insulin release from pancreatic beta cells [37].
Monitoring
Blood glucose concentrations are often provided by bench top blood gas analyzers. However, glucose can also be easily measured via the use of a hand‐held glucometer. Although specific brands of glucometers are not necessarily designed for use in equines, some glucometers have been evaluated in studies against bench top analyzers and laboratory standards using both equine whole blood and plasma [132, 133].
Treatment
While no untoward consequences of an alpha‐2 agonist related increase in blood glucose have been documented in horses, the anesthetist should be aware of its occurrence. While in other species hyperglycemia may result in diuresis, to date urine glucose data suggests that this is not the routine situation in the horse in this circumstance of drug induced hyperglycemia.
Blood glucose concentrations should be carefully monitored in foals during anesthesia, and hypoglycemia should be treated. Depending on the fluid administration rate, 1–5% dextrose in a balanced electrolyte solution will help correct hypoglycemia.
Decreased Gastrointestinal Motility
Definition
Many drugs used for management of sedation and anesthesia in the horse negatively influence gastrointestinal motility and may lead to post‐anesthesia colic. The reported incidence of post‐anesthetic gastrointestinal dysfunction in healthy horses undergoing elective procedures varies based on whether reduced fecal output, clinical signs of abdominal discomfort, or treatment for abdominal discomfort are used as case definitions but is estimated to be between 2.5% and 10.5% [134].
Risk factors
Use of anticholinergics
Use of opioids
Use of alpha‐2 adrenergic agonists
Pre‐anesthetic fasting
Post‐operative pain
Pathogenesis
Opioids have most notably been associated with decreased gastrointestinal motility, which is a direct effect of stimulation of opioid receptors found throughout the gastrointestinal tract (including the myenteric plexus) [135, 136]. Alpha‐2 adrenergic agonist drugs also play a role in decreasing gastrointestinal motility [137, 138]. Similar to opioids, their effect is at alpha‐2 receptors at the level of the myenteric plexus [139]. Anticholinergic drugs reduce gastrointestinal motility like opioids and alpha‐2 agonists by inhibiting contractile neural activity in all segments of the gastrointestinal tract [37]. Pre‐operative fasting, while generally considered beneficial to anesthesia management (to reduce gastrointestinal volume and improve both ventilation and oxygenation), may further reduce gastrointestinal motility via decreased colonic myoelectric activity [139].
Much of the information published about risk factors for post‐anesthetic colic in horses is conflicting, which may be a result of the retrospective nature of most studies, the lack of large numbers of horses in each study, and the variety of anesthetic and management protocols horses are subjected to.
Combining information from several studies, factors found to be associated with the development of post‐operative gastrointestinal dysfunction include being an Arabian horse [140] or racing Thoroughbred [141], orthopedic surgery [142], orthopedic surgery lasting longer than an hour [143], out‐of‐hours orthopedic surgery, administration of morphine [144], use of sodium penicillin [141, 145], use of ceftiofur, inhalant anesthesia with isoflurane, having a surgical procedure (vs. MRI) [145], increased arterial lactate, positioning in right lateral recumbency, and post‐anesthetic hypothermia [140].
At the same time, these studies also determined that certain factors (some the same as above) were not associated with or were even protective for the development of post‐operative gastrointestinal dysfunction, including the use of butorphanol [142], the use of no opioid or butorphanol [144], administration of morphine [145, 146], the use of any specific anesthetic or peri‐anesthetic drugs [140]. longer versus shorter anesthetic duration, use of romifidine as a premedication, being sedated before anesthesia on two or more occasions, and the use of procaine penicillin [145].
These differing results indicate that understanding risk factors for post‐anesthetic colic is challenging, and further studies are required with larger numbers of horses to fully elucidate causative factors.
Prevention
No specific strategy has been proven unequivocally useful in the prevention of post‐anesthesia colic, but suggestions are outlined below.
To date, studies are not conclusive with respect to the link between the use of opioids and post‐anesthetic colic [134, 141, 143, 145, 146]. However, gastrointestinal stasis is a known complication of opioid use and risk of relevant
