Complications in Equine Surgery. Группа авторов
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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 of 0.75 mg/kg intravenously, N‐methylnaltrexone partially prevented the effects of morphine on the gastrointestinal tract. Alvimopan, a peripherally acting mu‐opioid receptor antagonist, is an emerging treatment for human postoperative ileus. It partially prevents the gastrointestinal effects caused by morphine while preserving the central analgesic effects [35, 36].
Expected outcome
The prognosis of ileus is guarded. The outcome will depend on the etiology and the clinical status of the horse.
References
1 1 Yamashita, K., Tsubakishita, S., Futaok S. et al. (2000). Cardiovascular effects of medetomidine, detomidine and xylazine in horses. J. Vet. Med. Sci. 62 (10): 1025–1032.
2 2 England, G.C.W., Clarke, K.W., and Goossens, L. (1992). A comparison of the sedative effects of three α2‐adrenoceptor agonists (romifidine, detomidine and xylazine) in the horse. J. Vet. Pharmacol. Ther. 15 (2): 194–201.
3 3 Wilson, D.V., Bohart, G.V., Evans, A.T. et al. (2002). Retrospective analysis of detomidine infusion for standing chemical restraint in 51 horses. Vet. Anaesth. Analg. 29 (1): 54–57.
4 4 Singh, S., Young, S.S., McDonell, W.N. et al. (1997). Modification of cardiopulmonary and intestinal motility effects of xylazine with glycopyrrolate in horses. Can. J. Vet. Res. 61 (2): 99.
5 5 Neto, F.J.T., McDonell, W.N., Black, W.D. et al. (2004). Effects of glycopyrrolate on cardiorespiratory function in horses anesthetized with halothane and xylazine. Am. J. Vet. Res. 65 (4): 456–463.
6 6 Pimenta, E.L.M., Teixeira Neto, F.J., Sá, P.A. et al. (2011). Comparative study between atropine and hyoscine‐N‐butylbromide for reversal of detomidine induced bradycardia in horses: Hyoscine and atropine in horses. Equine Vet. J. 43 (3): 332–340.
7 7 Perotta, J.H., Canola, P.A., and Lopes, M.C. (2002). Hyoscine‐N‐butylbromide premedication on cardiovascular variables of horses sedated with medetomidine. Vet. Anaesth. Analg. 41 (4): 357–364.
8 8 Pignaton, W., Luna, S.P.L., Teixeira Neto, F.J., et al. (2016). Methadone increases and prolongs detomidine‐induced arterial hypertension in horses, but these effects are not mediated by increased plasma concentrations of arginine vasopressin or serum concentrations of catecholamines. J. Equine Vet. Sci. 37: 39–45.
9 9 Guedes, A.G., Rudé, E.P., and Rider, M.A. (2006). Evaluation of histamine release during constant rate infusion of morphine in dogs. Vet. Anaesth. Analg. 33 (1): 28–35.
10 10 Barke, K.E. and Hough, L.B. (1993). Opiates, mast cells and histamine release. Life Sci. 53 (18): 1391–1399.
11 11 Thompson, W.L. and Walton, R.P. (1964). Elevation of plasma histamine levels in the dog following administration of muscle relaxants, opiates and macromolecular polymers. J. Pharmacol. Ex. Ther. 143: 131–136.
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