Complications in Equine Surgery. Группа авторов

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Название Complications in Equine Surgery
Автор произведения Группа авторов
Жанр Биология
Серия
Издательство Биология
Год выпуска 0
isbn 9781119190158



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      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 gastrointestinal dysfunction grows when opioids are used systemically at high doses over long periods of time. Therefore, these drugs should be used judiciously and in regional routes (e.g. intra‐articular) whenever possible.

      Similarly, excessive doses of long‐acting alpha‐2 agonists given over several hours (e.g. for standing sedation) should be avoided if possible (i.e. long procedures could be staged into two shorter procedures separated by a return to feeding).

      Anticholinergics, as discussed previously, are recommended to be used with care and only when low heart rate is detrimental, reversal of agents causing bradycardia is not possible, and other methods used to improve hemodynamics have failed. They should be titrated carefully such that the lowest effective dose is used.

      Use of local anesthetic techniques may be helpful from the standpoint of prevention of post‐operative pain (thus aiding a quicker return to normal feeding behavior) as well as to reduce the dose of sedative and systemic analgesic drugs required to complete the procedure.

      There is also no conclusive recommendation as to the most appropriate pre‐operative fasting or post‐operative re‐feeding regimen to prevent post‐operative colic, though as mentioned earlier fasting does contribute to decreases in gastrointestinal motility.

       Monitoring

      In many hospitals, it is routine to monitor and record fecal output in addition to both subjective and physiological indicators of abdominal discomfort in the post‐anesthetic period. Early signs of discomfort may be subtle or masked by systemic use of analgesic drugs (e.g. phenylbutazone) in the peri‐operative period. Since the consequences of impaired gastrointestinal motility in the horse are potentially dire, observation of behavior and normal fecal production in the recovery period are essential.

       Treatment

      In‐depth discussion of the treatment of post‐anesthesia gastrointestinal dysfunction is beyond the scope of this chapter, and management strategies for post‐operative ileus have been reviewed elsewhere [147, 148].