A comparison of equine recovery characteristics after isoflurane or isoflurane followed by a xylazine–ketamine infusion

Veterinary Anaesthesia and Analgesia, 2008, 35, 154–160

doi:10.1111/j.1467-2995.2007.00368.x

RESEARCH PAPER

A comparison of equine recovery characteristics after isoflurane or isoflurane followed by a xylazine–ketamine infusion Ann E Wagner DVM, MS, Diplomate ACVP, Diplomate ACVA*, Khursheed R Mama DVM, Diplomate ACVA*, Eugene P Steffey VMD, PhD, Diplomate ACVA, Diplomate ECVAA  & Peter W Hellyer DVM, MS, Diplomate ACVA* *Department of Clinical Sciences, Colorado State University, Fort Collins, CO, USA  Department of Surgical and Radiological Sciences, School of Veterinary Medicine, University of California, Davis, CA, USA

Correspondence: Ann Wagner, Department of Clinical Sciences, Colorado State University, Fort Collins, CO 80523, USA. E-mail: [email protected] Presented in abstract form at the 8th World Congress of Veterinary Anesthesia, Knoxville, Tennessee, 2003.

Abstract Objective To determine whether infusion of xylazine (XYL) and ketamine (KET) for 30 minutes after isoflurane administration in horses would result in improved quality of recovery from anesthesia, without detrimental cardiopulmonary changes. Study design Randomized, blinded experimental trial. Animals Seven healthy adult horses aged 6.4 ± 1.9 years and weighing 506 ± 30 kg. Methods Horses were anesthetized twice, at least 1 week apart. On both occasions, anesthesia was induced by the administration of XYL, diazepam, and KET, and maintained with isoflurane for approximately 90 minutes, the last 60 minutes of which were under steady-state conditions (1.2 times the minimum alveolar concentration isoflurane). On one occasion, horses were allowed to recover from isoflurane anesthesia, while on the other, XYL and KET were infused for 30 minutes after termination of isoflurane administration. Heart rate, respiratory rate, arterial blood pressure, pH, and blood-gases were measured and recorded at set intervals during steady-state isoflurane anesthesia and XYL–KET infusion. Recovery events were timed and subjectively scored by one nonblinded and two 154

blinded observers. Data were analyzed using a restricted maximum likelihood-based mixed effect model repeated measures analysis. Results Infusion of XYL and KET resulted in longer recovery times, but there was no significant improvement in recovery quality score. Conclusions Under the conditions of this study, infusion of XYL and KET does not positively influence recovery from isoflurane anesthesia in horses. Clinical relevance This study does not support the routine use of XYL and KET infusions in horses during the transition from isoflurane anesthesia to recovery. Keywords anesthesia recovery, equine anesthesia, isoflurane, ketamine, xylazine.

Introduction In the past 10–20 years, anesthetic management of horses undergoing surgery has improved greatly, particularly in regard to the monitoring of arterial blood pressure, treatment of hypotension, prevention of post-anesthetic myopathy, and controlled ventilation. However, recovery of horses from general anesthesia is still fraught with risk for both patients and personnel.

Xylazine–ketamine effect on equine isoflurane recovery AE Wagner et al.

Traditionally, induction of anesthesia in horses has been performed using drugs administered intravenously (IV), such as xylazine (XYL), guaifenesin or diazepam or both, and ketamine (KET), but maintenance of anesthesia for procedures longer than 45–60 minutes has been achieved using inhalation anesthetic agents such as halothane, isoflurane, and sevoflurane. An advantage of maintenance with contemporary inhalation anesthetics is that they are eliminated from the body mainly through the respiratory tract and do not accumulate during long procedures or require extensive metabolism for termination of their effects. However, equine recoveries from inhalation anesthesia are frequently less than ideal: a brief review of 1 month’s anesthesia records at our University showed that 65% were classified as ‘fair’, ‘poor’, or ‘unacceptably poor’, while in a research project involving 30 inhalation anesthetics in horses, 57% of recoveries were ranked as ‘fair’, ‘poor’, or ‘unacceptably poor’ (Wagner, unpublished data). Occasionally, poor recoveries result in serious or life-ending injuries. Reportedly, 0.2–1.6% of recoveries result in serious injuries, such as fractures (Hodgson & Dunlop 1990; Young & Taylor 1993; Johnston et al. 1995). While these figures illustrate the devastating consequences of a poor recovery from anesthesia in a few individuals, they do not reflect the overall morbidity of recovery in terms of non-terminal injuries such as lacerations, breakdown of surgical incisions, or destruction of bandages nor do they account for the time spent by, or injuries that occur to personnel who attempt to assist in these recoveries. There has been increasing interest in using injectable anesthetics, such as XYL, KET, and guaifenesin, to maintain anesthesia in horses because of reports during the 1990s that suggested superior quality of recoveries when injectable drugs were used (Young et al. 1993; Mama et al. 1998). A recent study found recovery quality to be ‘excellent’ or ‘good’ in 97% (35 out of 36 horses) of horses in which anesthesia was maintained for 1 hour using XYL and KET infusions (Mama et al. 2005). However, because of possible prolonged or stormy recoveries associated with excessive accumulation of injectable drugs and the time required for drug metabolism, long-term maintenance of anesthesia with currently available injectable drugs is still not generally recommended. Therefore, the goal of the current study was to combine ‘the best of both worlds’ by using a

traditional regime of injectable anesthetics for induction, and isoflurane for maintenance, but then returning to injectable drugs at the end to see if recovery quality would be improved. The hypotheses for this study were that: 1) terminating delivery of the inhalation agent (isoflurane), while prolonging sedation and recumbency by use of XYL and KET during the first 30 minutes after isoflurane anesthesia would result in improved quality of recoveries in horses compared with recoveries from isoflurane maintenance alone; 2) cardiopulmonary parameters would not be negatively influenced by the use of XYL and KET to modify recovery from isoflurane anesthesia; and 3) measured plasma XYL and KET concentrations would reflect the dosedependent behavioral effects of these drugs. Materials and methods The study protocol was reviewed and approved by the Colorado State University Animal Care and Use Committee. Seven adult mares [three Quarter Horses, three Thoroughbreds, one Quarter Horse cross; 6.4 ± 1.9 years of age (mean ± SD)], weighing 506 ± 30 kg, were anesthetized on two separate occasions, 1 week apart. Horses were not fasted prior to the experiments to simulate conditions at many equine practices. Following baseline vital signs [temperature, pulse rate, respiratory rate (fr)] and weight measurements, anesthesia was induced with XYL (1 mg kg-1), followed 5 minutes later by diazepam (DZ; 0.05 mg kg-1) and KET (2 mg kg-1), all administered IV via a 14-SWG catheter in the right jugular vein. Horses were placed in left lateral recumbency on a 30-cm thick foam pad in a padded recovery stall, with the left (dependent) thoracic limb advanced cranially and the right (nondependent) thoracic and pelvic limbs elevated slightly to reduce risk of potential nerve and muscle damage. Anesthesia was maintained by inhalation of isoflurane in oxygen, delivered via a standard large animal circle breathing system. The electrocardiogram was monitored continuously using a multichannel vital signs monitor (Escort II; MDE, Arleta, CA, USA). A 20-SWG catheter was placed in the transverse facial artery for continuous measurement of direct arterial blood pressure (Cobe pressure transducer, Electrocom; Denver, CO, USA) and periodic measurement of packed cell volume (PCV), plasma total protein (TP), blood-gases, and pH (ABL505; Radiometer Medical A/S, Copenhagen, Denmark). Blood-gas values were corrected for

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each horse’s actual body temperature. End-tidal isoflurane was sampled continuously from the distal end of a catheter inserted into the endotracheal tube and measured by a quartz crystal agent analyzer (Biochem 8100; Biochem International Inc., Waukesha, WI, USA). The agent analyzer was calibrated before, and checked during and after each experiment, using three appropriate isoflurane standards (Scott Medical Products; Plumsteadville, PA, USA) and ambient air as a zero reference point. As soon as the instrumentation was complete (generally within 10 minutes of endotracheal intubation), ventilation was controlled to maintain the arterial partial pressure of carbon dioxide (PaCO2) at 45 ± 10 mmHg (6 ± 1.3 kPa), and body temperature was maintained at 36.5 ± 0.5 C by use of blankets and heat lamps if necessary. Following a 30-minute period for instrumentation and equilibration, anesthesia was maintained at 1.2 times the minimum alveolar concentration (MAC) isoflurane for an additional 60 minutes (Steffey et al. 1977). Mean arterial blood pressure (MAP) was maintained at ‡70 mmHg by administration of dobutamine, if necessary. Balanced electrolyte solution was administered IV at a rate of 5–7 mL kg-1 hour-1, and an indwelling urinary catheter was placed. After 45–50 minutes of maintenance at 1.2 MAC isoflurane anesthesia, horses were weaned from controlled ventilation and resumed spontaneous breathing (SB). They were briefly hoisted so that the thick pad could be removed and then carefully replaced in left lateral recumbency on the floor of the recovery stall, and videotape recording of recovery was begun. At the end of the 60-minute maintenance period (total, 90 minutes of isoflurane anesthesia), the horses were randomly assigned in a Latin square design, either to recover from anesthesia, or receive XYL–KET to maintain anesthesia for an additional 30 minutes. The XYL–KET group received a bolus of XYL (0.15 mg kg-1) and KET (0.3 mg kg-1) at 5 minutes following discontinuation of isoflurane. At the same time, infusions of XYL (20 lg kg-1 minute-1) and KET (60 lg kg-1 minute-1) were started and continued for 30 minutes, resulting in a total anesthesia period of 120 minutes for the XYL–KET group. These doses were selected to achieve a light plane of anesthesia, based on the authors’ prior experience with XYL and KET infusions in horses, as well as a pilot study in three horses. All horses received oxygen, insufflated at 15 L minute-1 via the endotracheal tube, as long as they remained in lateral recumbency. Heart 156

rate (HR), fr, and MAP were continuously monitored until anesthetic delivery was discontinued, and were recorded just before XYL–KET boluses (5 minutes after termination of isoflurane administration) and at 15 and 30 minutes during administration of XYL–KET infusions. Horses were then allowed to recover without assistance in the same 12 · 12 ft (3.6 m2) padded recovery stall. Recoveries were continuously observed through a window in the recovery stall door, by both a non-blinded and a blinded observer experienced at observing horses recovering from anesthesia. Subjective scores for overall quality of recovery (1 = poor; 2 = marginal; 3 = fair; 4 = good; 5 = excellent) from these two observers were averaged to provide an overall recovery score. Recoveries from anesthesia were also scored by an additional blinded observer who viewed videotapes of the recoveries and used a modified version of a scoring system (Mama et al. 1996). The videotape observer assigned individual scores ranging from 1 to 5, as above, for the quality of the recovery. For example, a score of 1 was considered ‘poor’ and associated with multiple uncoordinated attempts to achieve sternal or standing posture resulting in major or life-threatening injury. Conversely, a score of 5 was considered ‘excellent’ and associated with fewer than 3 quiet, coordinated efforts to sternal or standing posture. Quantitative data, such as time to first movement, sternal recumbency, and standing (with time 0 being the time of discontinuation of isoflurane or XYL–KET delivery), and number of attempts to achieve sternal recumbency and to stand, were also recorded from observing the videotape. The endotracheal tube was removed only after the horse was standing and coordinated. On the day each horse received XYL–KET infusions, arterial blood was sampled for measurement of plasma XYL and KET concentrations (Mama et al. 2005). Heparinized blood samples were collected at the end of the isoflurane steady-state conditions before the XYL–KET infusions were begun, 15 and 30 minutes after starting XYL–KET infusions, and as soon as possible (within 5 minutes) after the horse stood successfully. Ketamine and XYL were quantitated in horse plasma by liquid chromatography/mass spectrometry according to previously described methods (Mama et al. 2005). The significance and magnitude of treatment group differences in steady-state and recovery means and mean changes over time were assessed using a restricted maximum likelihood-based mixed

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Xylazine–ketamine effect on equine isoflurane recovery AE Wagner et al.

effect model repeated measures (MMRM) analysis via PROC MIXED in SAS (Release 6.11; SAS Institute Inc., Cary, NC, USA) (Littell et al. 1996). Analyses included the categorical, fixed effects of treatment, time, sequence of treatment application, and treatment-by-time interaction. A first-degree autoregressive correlation structure was used to model the within-subject errors. Satterthwaite’s approximation was used to estimate deoniminator df. The significance of changes in means over time for the additional recovery data from the XYL–KET treatment group was assessed using a restricted maximum likelihood-based mixed effect model that included the categorical, fixed effect of time and a random animal effect via PROC MIXED in SAS (Littell et al. 1996). Satterthwaite’s approximation was used to estimate denominator df. Significance was set at p < 0.05. Plasma drug concentrations were not statistically analyzed. Results Recovery times and quality scores are summarized in Table 1. Xylazine–ketamine infusion following isoflurane anesthesia was associated with significantly longer times to first movement (11.2 ± 10.7 minutes), to first attempt to stand (32 ± 29 minutes), and to successfully stand (37 ± 27 minutes), compared with isoflurane anesthesia alone (3.7 ± 1.5, 21 ± 24, and 24 ± 22 minutes, respectively). There were no other statistically significant differences in times or number of attempts

to attain a certain posture, although horses which received XYL–KET tended to require fewer attempts to attain sternal recumbency (3 ± 2) than horses receiving isoflurane only (6 ± 5). In addition, scores for quality of attaining sternal recumbency, standing, and overall recovery, although not statistically significant, tended to be slightly better with XYL–KET infusion than without (Table 1). The ranges for mean values for cardiovascular and respiratory parameters measured at 15, 30, and 45 minutes after steady-state isoflurane conditions were: HR, 38–41 beats minute-1; fr, 5–6 breaths minute-1; MAP, 73–77 mmHg; body temperature, 36.2–37.0 C; arterial pH, 7.33–7.44; PaCO2, 43– 46 mmHg; arterial partial pressure of oxygen (PaO2), 229–289 mmHg; PCV, 34–37%; and TP, 5.5–5.6 g dL-1. During steady-state isoflurane anesthesia, there were no differences in these parameters between horses that were subsequently allowed to recover from isoflurane and those that received XYL–KET infusions. At 60 minutes of steady-state isoflurane anesthesia in both groups, after weaning from intermittent positive pressure ventilation and resumption of SB, mean PaCO2 was significantly increased to 55–60 mmHg. Plasma XYL and KET concentrations, and cardiovascular and respiratory parameters during XYL–KET infusions and after recovery to standing are summarized in Table 2. During XYL–KET infusions, MAP increased and HR decreased (Table 2). End-tidal isoflurane rapidly decreased during XYL– KET infusions, from approximately 1.85% during steady-state isoflurane anesthesia, to 0.39 ± 0.1%

Table 1 Recovery parameters (mean ± SD) from seven horses following 60 minutes of steady-state isoflurane anesthesia or isoflurane anesthesia and infusions of xylazine (20 lg kg-1 minute-1) and ketamine (60 lg kg-1 minute-1)

Time to 1st movement Time to 1st attempt to sternal Time to successfully attain sternal recumbency Number of attempts to attain sternal recumbency Score for quality to sternal recumbency (blinded video observer) Time to 1st attempt to stand Time to successfully stand Number of attempts to stand Score for quality of standing (blinded video observer) Score for overall quality of recovery (average of one blinded and one nonblinded observer, at stall)

ISO only

ISO ± XYL/KET

p-value

3.7 13 17 6 3.3 21 24 3 3.4 3.0

11.2 16 26 3 4.3 32 37 3 3.9 4.0

0.007* 0.159 0.485 0.216 0.181 0.035* <0.001* 0.357 0.508 0.178

± ± ± ± ± ± ± ± ± ±

1.5 15 13 5 1.4 24 22 1 1.3 1.2

± ± ± ± ± ± ± ± ± ±

10.7 9 27 2 1.3 29 27 3 1.1 0.9

All times are recorded in minutes from discontinuation of either isoflurane or isoflurane and xylazine–ketamine in respective groups. *Significant difference between treatments.

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Table 2 Plasma drug concentrations and cardiorespiratory parameters (mean ± sd) during spontaneous ventilation in seven horses given infusions of xylazine (20 lg kg-1 minute-1) and ketamine (60 lg kg-1 minute-1) following 60 minutes of steady-state isoflurane anesthesia. The values at 5 minutes were obtained prior to XYL–KET administration

Xylazine–ketamine administration

Plasma xylazine (lg mL-1) Plasma ketamine (lg mL-1) Heart rate (beats minute-1) Respiratory rate (breaths minute-1) Mean arterial blood pressure (mmHg) pHa PaCO2 (mmHg) PaO2 (mmHg) PCV (%) TP (g dL-1)

Pre-infusion (60 minutes steady-state isoflurane)

5 minutes

15 minutes

30 minutes

Standing

0.26 0.17 41 5 77 7.33 60 200 36 5.5

nd nd 39 ± 6a 8 ± 3a 92 ± 8a nd nd nd nd nd

0.76 2.07 28 9 109 7.44 46 62 37 5.7

1.05 2.39 32 12 115 7.46 42 57 35 5.6

0.62 0.45 nd nd nd 7.44 44 65 36 5.2

± ± ± ± ± ± ± ± ± ±

0.10 0.18 7 3 4 0.05 11 110 4 0.6

± ± ± ± ± ± ± ± ± ±

0.15 0.81 5c 8a 15b 0.05 6 9 5 0.5

± ± ± ± ± ± ± ± ± ±

0.39 1.23 7b 4a 18b 0.04 4 9 5 0.6

± 0.30 ± 0.68

± ± ± ± ±

0.02 3 7 5 0.2

For heart rate, respiratory rate, and mean arterial blood pressure during xylazine–ketamine administration, values within a row that do not share a superscript (a, b, c) are significantly different from one another. nd, not done or not measured.

at 5 minutes after terminating isoflurane delivery, to less than 0.2% by 30 minutes. There were small amounts of XYL and KET detected in plasma at the end of isoflurane anesthesia before XYL–KET infusions were started, but concentrations increased during the infusion period and decreased by the time of standing. Arterial partial pressure of oxygen markedly decreased during XYL–KET infusions (Table 2). Discussion The only statistically significant findings associated with recovery parameters in this study were that infusion of XYL–KET following isoflurane anesthesia in horses prolonged the times to first movement, to first attempt to stand, and to stand successfully. These findings were expected, as previous reports have demonstrated that bolus administration of XYL or other a2-adrenergic agonists, without KET, results in delayed recovery from inhalational anesthesia (Matthews et al. 1998; Santos et al. 2003). Even a single bolus of XYL (0.1 mg kg-1 IV) after isoflurane anesthesia delayed recovery to standing by approximately 15 minutes (Santos et al. 2003). McCarty et al. (1990) reported that single or multiple injections of XYL (0.31 mg kg-1) and KET (0.68 mg kg-1) prolonged anesthesia for approximately 12 minutes per administration; however, the horses in that study did not receive 158

any inhalant anesthetic agent (McCarty et al. 1990). In the current study, time to standing successfully was about 13 minutes longer after XYL–KET infusion (37 ± 27 minutes) compared with isoflurane-only anesthesia (24 ± 22 minutes). While isoflurane anesthesia in horses has sometimes produced less than ideal recoveries with periods of thrashing or excitement (Matthews et al. 1998), good to excellent quality recoveries (mean scores for ‘quality of recovery to standing’ ranging from 4.3 to 5.0, depending on infusion rates for XYL–KET) have been associated with XYL–KET infusions, without inhalational agent administration, in horses (Mama et al. 2005). It was our hope that administration of XYL–KET following a period of isoflurane anesthesia would result in improved quality of recoveries. There did seem to be any suggestion of improved recovery quality following XYL–KET infusions, as mean values for quality of recovery to sternal recumbency and standing, as well as mean values for overall recovery quality, were indeed numerically greater in horses receiving XYL–KET compared with those recovering from isoflurane only. However, there was no statistically significant difference between treatments in any of the comparisons of qualitative recovery data in the current study, and the mean scores for recovery to standing (3.4 and 3.9 for isoflurane-only and XYL–KET, respectively) were not as favorable as

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Xylazine–ketamine effect on equine isoflurane recovery AE Wagner et al.

those in the previously cited study of XYL–KET alone (Mama et al. 2005). This study demonstrates that it is possible to change from inhalation anesthesia to IV anesthesia without clinically detrimental effects. Cardiovascular and respiratory parameters during steady-state isoflurane anesthesia were typical of those observed in isoflurane-anesthetized horses. Cardiovascular responses following termination of isoflurane administration and institution of XYL–KET infusion included an increase in MAP and decrease in HR, neither of which was considered clinically significant. Other changes associated with switching from isoflurane to XYL–KET were decreases in PaCO2 and PaO2. The decrease in PaCO2 reflects a lesser degree of respiratory depression associated with these doses of XYL–KET compared with 1.2 MAC isoflurane. Isoflurane is known to be a profound respiratory depressant, leading to hypercapnia (PaCO2, 73– 77 mmHg) during SB (Steffey et al. 1987). Infusion of XYL–KET alone at higher doses than in the current study, resulted in a lesser degree of respiratory depression (PaCO2, 50–53 mmHg) (Mama et al. 2005) compared with 1.2 MAC isoflurane in our study. A reduction in overall anesthetic depth as well as the respiratory stimulant effects of hypoxemia might also have contributed to decreased respiratory depression in the XYL–KET horses. In the current study, PaO2 was lower than expected during isoflurane steady-state conditions (approximately 200 mmHg), suggesting marked ventilation–perfusion imbalance with physiologic shunt. Arterial partial pressure of oxygen then decreased even further once isoflurane administration was terminated, because during XYL–KET infusions, horses were no longer connected to the circle breathing circuit with its high (approximately 90%) inspired oxygen fraction. Instead, they were receiving oxygen insufflation at 15 L minute-1 via the endotracheal tube. Horses near sea level, which received oxygen insufflation at 10 L minute-1 during recovery from anesthesia, had PaO2 values in the mid-60s mmHg (Mason et al. 1987). In the current study, mean PaO2 values were 57– 62 mmHg during XYL–KET infusions (Table 2), only slightly less than those reported by Mason et al. (1987) and others (Muir et al. 1977; Wan et al. 1992; Matthews et al. 1993; Mama et al. 2005). Because of the low ambient barometric pressure of approximately 640 mmHg, PaO2 values in unsedated, standing horses breathing ambient air at our facility average 76 mmHg (Mama, unpublished

data), so it is not surprising that recumbent horses anesthetized with XYL–KET were relatively hypoxemic despite oxygen insufflation. In the current study, ventilation–perfusion imbalance from the effects of recumbency, residual isoflurane, and XYL–KET anesthesia likely combined to worsen physiologic shunt and decrease PaO2. In addition, the horses of the current study had not been fasted prior to anesthesia, which may have further contributed to ventilation–perfusion imbalance. As expected, analyses for plasma XYL and KET demonstrated that there were small concentrations of these drugs present after 60 minutes of steadystate isoflurane anesthesia from the XYL and KET that had been administered to induce anesthesia approximately 90 minutes earlier. Mean plasma XYL (0.26 lg mL-1) and KET (0.17 lg mL-1) at 90 minutes after induction (60 minutes of steadystate isoflurane) were considerably less than concentrations of those drugs reported to achieve surgical anesthesia (Mama et al. 2005). Plasma XYL and KET concentrations increased during infusion of these drugs but did not achieve steadystate concentrations during the 30-minute infusion period. However, these infusion rates were sufficient to keep the horses sedated and recumbent following discontinuation of isoflurane administration. At 30 minutes of XYL–KET infusion, plasma XYL reached about half the concentration associated with a higher infusion rate of XYL (35 lg kg1 minute-1) in a previous study, while plasma KET was nearly the same as that associated with a higher infusion rate of KET (90 lg kg-1 minute-1 (Mama et al. 2005). After termination of the drug infusions, plasma XYL and KET concentrations decreased as expected by the time horses stood. Results of this study failed to demonstrate that infusion of XYL and KET after isoflurane anesthesia in horses significantly improved the quality of recovery. Acknowledgements The authors thank Lucien Brevard and Anne Golden for their assistance in evaluating recoveries. This study was supported by a grant from Morris Animal Foundation, Englewood, Colorado. References Hodgson DS, Dunlop CI (1990) General anesthesia for horses with specific problems. In: Principles and Tech-

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