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Objective: To determine the effect of fraction of inspired oxygen (FIO2) on intrapulmonary shunt fraction as measured by F-shunt in ponies during isoflurane anaesthesia. Study design: Prospective, randomized clinical study. Animals: A group of 23 adult Shetland ponies undergoing a total of 32 anaesthetic procedures. Methods: Ponies were premedicated intravenously (IV) with detomidine (0.01 mg kg–1) and either morphine (0.1 mg kg–1) or butorphanol (0.02 mg kg–1). Anaesthesia was induced with ketamine (2.2 mg kg–1) and midazolam (0.07 mg kg–1) administered IV. Ponies were randomly allocated to maintenance of anaesthesia with isoflurane in oxygen (group TH; FIO2 = 0.95) or a mixture of oxygen and medical air (group TL; FIO2 = 0.65); all ponies were given a constant rate of infusion of detomidine. Animals were mechanically ventilated to maintain PaCO2 between 40 and 50 mmHg. Arterial blood gas analysis was performed every 30 minutes. The F-shunt equation was calculated for each time point T0, T30, T60 and T90. Data were analysed using linear mixed model analysis and presented as mean ± standard deviation (p < 0.05). Results: PaO2 was greater in group TH than in group TL (TH: 406 ± 90, 438 ± 83, 441 ± 69 and 464 ± 53 mmHg versus TL: 202 ± 90, 186 ± 84, 172 ± 85 and 191 ± 98 mmHg at T0, T30, T60 and T90, respectively; p < 0.0001). In TH, F-shunt was < TL. Significant differences were found at T60 (TH: 13.2% ± 4.3 versus TL: 19.4% ± 8.3; p = 0.016) and T90 (TH: 11.7% ± 3.5 versus TL: 18.6% ± 9.5; p = 0.036). Conclusions and clinical relevance: Our findings do not support a beneficial effect of using a reduced FIO2 to improve oxygenation in anaesthetized and mechanically ventilated Shetland ponies.

Objective To assess anesthetic induction, recovery quality and cardiopulmonary variables after intramuscular (IM) injection of three drug combinations for immobilization of horses. Study design Randomized, blinded, three-way crossover prospective design. Animals A total of eight healthy adult horses weighing 470–575 kg. Methods Horses were administered three treatments IM separated by ≥1 week. Combinations were tiletamine–zolazepam (1.2 mg kg−1), ketamine (1 mg kg−1) and detomidine (0.04 mg kg−1) (treatment TKD); ketamine (3 mg kg−1) and detomidine (0.04 mg kg−1) (treatment KD); and tiletamine–zolazepam (2.4 mg kg−1) and detomidine (0.04 mg kg−1) (treatment TD). Parametric data were analyzed using mixed model linear regression. Nonparametric data were compared using Skillings–Mack test. A p value Results All horses in treatment TD became recumbent. In treatments KD and TKD, one horse remained standing. PaO2 15 minutes after recumbency was significantly lower in treatments TD (p Conclusions and clinical relevance In domestic horses, IM injections of tiletamine–zolazepam–detomidine resulted in more reliable recumbency with a longer duration when compared with ketamine–detomidine and tiletamine–zolazepam–ketamine–detomidine. Recoveries were comparable among protocols.

To determine time to first passage of feces, total fecal piles and incidence of colic in the first 24 hours postprocedure in horses undergoing standing sedation with detomidine, or general anesthesia with or without detomidine.Retrospective cohort study.A total of 246 horses.Records of all horses that underwent standing sedation or general anesthesia between December 2012 and March 2016 were reviewed. Horses aged6 months, admitted for colic or cesarean section, with inadequate data, and those not administered xylazine and/or detomidine were excluded. Records included patient signalment, fasting duration, procedure performed, drugs administered, time to first feces, number of fecal piles during 24 hours postprocedure and mention of colic. Chi-square, Fisher's exact and Tukey's post hoc comparison tests were used. Parametric data were reported as mean ± standard deviation with significance defined as p0.05.In total, 116 and 57 horses underwent general anesthesia without detomidine (group GA) and with detomidine (group GA-D), respectively, and remaining 73 horses underwent standing sedation with detomidine (group S-D). Detomidine dose was significantly higher in group S-D than in group GA-D. Time to first feces was longer (7.1 ± 4.2 hours), and group S-D horses passed one fewer fecal pile (6.3 ± 2.4) than group GA horses. There was no interaction between detomidine treatment and preprocedure food withholding and the time to first feces or the number of fecal piles in the first 24 hours postprocedure. Overall, seven horses (2.8%) showed signs of colic (five, one and one in GA, GA-D and S-D, respectively).Detomidine administration, as part of an anesthetic protocol or for standing sedation procedures, should not be expected to contribute to postprocedural colic.

Objectives To evaluate the sedative effects and pharmacokinetics of detomidine gel administered intravaginally to alpacas in comparison with intravenously (IV) administered detomidine. Study design Randomized, crossover, blinded experiment. Animals A group of six healthy adult female Huacaya alpacas (70.3 ± 7.9 kg). Methods Alpacas were studied on two occasions separated by ≥5 days. Treatments were IV detomidine hydrochloride (70 μg kg−1; treatment DET–IV) or detomidine gel (200 μg kg−1; treatment DET–VAG) administered intravaginally. Sedation and heart rate (HR) were evaluated at intervals for 240 minutes. Venous blood was collected at intervals for 360 minutes after treatment for analysis of detomidine, carboxydetomidine and hydroxydetomidine using liquid chromatography–tandem mass spectrometry. Measured variables were compared between treatments and over time using mixed model analysis. Data are presented as the mean ± standard error of the mean, and a p value of Results Onset of sedation was faster in treatment DET–IV (1.6 ± 0.2 minutes) than in treatment DET–VAG (13.0 ± 2.5 minutes). Time to maximum sedation was shorter in treatment DET–IV (8.3 ± 1.3 minutes) than in treatment DET–VAG (25 ± 4 minutes). Duration of sedation was not different between treatments. There was a significant linear relationship between sedation score and plasma detomidine concentration. HR was less than baseline for 60 and 125 minutes for treatments DET–IV and DET–VAG, respectively. The maximal decrease in HR occurred at 15 minutes for both treatments. The mean maximum plasma concentration of detomidine, time to maximum concentration and bioavailability for treatment DET–VAG were 39.6 ng mL−1, 19.9 minutes and 20%, respectively. Conclusions and clinical relevance Detomidine administration at the doses studied resulted in moderate sedation when administered IV or intravaginally to alpacas.

Objective The aim of this study was to compare different methods to determine venous admixture (Q_s=Q_t) in anaesthetized horses. The first objective was to estimate Q_s=Q_t using jugular venous blood oxygen content (Q_s=Q_t jugular), and a fixed value for the oxygen extraction (F-shunt). The second objective was to assess the influence of blood pressure and positioning on oxygen extraction. The third objective was to perform regression analysis between jugular and mixed venous blood oxygen tensions. Study design Prospective, experimental trial. Animals The study was performed with seven warmblood horses that were anaesthetized with detomidine, butorphanol, ketamine, diazepam and isoflurane in oxygen. Methods Multiple simultaneous arterial, jugular venous and pulmonary arterial blood samples were taken under normotensive and hypotensive conditions in lateral and dorsal recumbency. Arterial, mixed venous, and end-capillary oxygen content were calculated. Results A significant correlation between Q_s=Q_t and Q_s=Q_t jugular was found [intraclass correlation coefficient (ICC) ¼ 0.68, p < 0.001], and BlandeAltman analysis showed a bias of e11.5% and wide limits of agreement (e27.7% to 4.6%). Fshunt significantly correlated with Q_s=Q_t (ICC ¼ 0.88, p < 0.001), and BlandeAltman analysis showed a lower bias (e1.97) and narrower limits of agreement (e13.8% to 9.9%). Positioning and blood pressure significantly influenced oxygen extraction. The regression formula was Y ¼ 0.80X þ 2.61 (where Y is the calculated mixed venous oxygen tension and X is the jugular venous oxygen tension) when outliers were excluded (ICC¼0.82, p < 0.001). Conclusions and clinical relevance This study shows that F-shunt provides reasonable estimates of Q_s=Q_t but can possibly be improved by using simple algorithms without the need for pulmonary arterial catheterization. These algorithms use blood pressure- and positioning-dependent oxygen extraction and regression analysis between jugular venous and pulmonary arterial oxygen tension. Although promising, the validity of these algorithms needs to be determined in future studies

Objective To compare the effects of MK-467 during isoflurane anaesthesia combined with xylazine or dexmedetomidine on global and gastrointestinal perfusion parameters. Study design Prospective, randomized experimental trial. Animals A total of 15 warmblood horses. Methods Horses were divided into two groups for administration of either dexmedetomidine (D) or xylazine (X) for premedication (D: 3.5 μg kg−1; X: 0.5 mg kg−1) and as constant rate infusion during isoflurane anaesthesia (D: 7 μg kg−1 hour−1; X: 1 mg kg−1 hour−1). During anaesthesia, heart rate, mean arterial blood pressure (MAP), systemic vascular resistance index (SVRI) and cardiac index (CI) were measured. Microperfusion of the colon, jejunum and stomach was measured using laser Doppler flowmetry. After 2 hours of stabilization, MK-467 (250 μg kg−1) was administered, and measurements were continued for another 90 minutes. For statistical analysis, the permutation test and Wilcoxon rank-sum test were used (p Results There were no differences in baseline measurements between groups. The MK-467 bolus resulted in a significant decrease in MAP (D: –58%; X: –48%) and SVRI (D: –68%; X: –65%) lasting longer in group D (90 minutes) compared to group X (60 minutes). While CI increased (D: +31%; X: +35%), microperfusion was reduced in the colon (D: –44%; X: –34%), jejunum (D: –26%; X: –33%) and stomach (D: –37%; X: –35%). Conclusions and clinical relevance Alpha-2-agonist induced vasoconstriction was reversed by the MK-467 dose used, resulting in hypotension and rise in CI. Gastrointestinal microperfusion decreased, probably as a result of insufficient perfusion pressure. An infusion rate for MK-467 as well as an ideal agonist/antagonist ratio should be determined.

Objective To compare alfaxalone as continuous intravenous (IV) infusion with intermittent IV injections for maintenance of anaesthesia in ponies undergoing castration. Study design Prospective, randomized, ‘blinded’ clinical study. Animals A group of 33 entire male Welsh ponies undergoing field castration. Methods After preanaesthetic medication with IV detomidine (10 μg kg−1) and butorphanol (0.05 mg kg−1), anaesthesia was induced with IV diazepam (0.05 mg kg−1) followed by alfaxalone (1 mg kg−1). After random allocation, anaesthesia was maintained with either IV alfaxalone 2 mg kg−1 hour−1 (group A; n = 16) or saline administered at equal volume (group S; n = 17). When necessary, additional alfaxalone (0.2 mg kg−1) was administered IV. Ponies were breathing room air. Using simple descriptive scales, surgical conditions and anaesthesia recovery were scored. Total amount of alfaxalone, ponies requiring additional alfaxalone and time to administration, time from induction to end of infusion and end of infusion to standing were noted. Indirect arterial blood pressure, pulse and respiratory rates, end-expiratory carbon dioxide partial pressure and arterial haemoglobin oxygen saturation were recorded every 5 minutes. Data were analysed using Student t, Mann–Whitney U and chi-square tests, where appropriate (p Results Total amount of alfaxalone administered after induction of anaesthesia (0.75 ± 0.27 versus 0.17 ± 0.23 mg kg−1; p Conclusion and clinical relevance Continuous IV infusion and intermittent administration of alfaxalone provided similar anaesthesia quality and surgical conditions in ponies undergoing field castration. Less alfaxalone is required when used intermittently.

To measure intraocular pressure (IOP) in horses during hoisting after induction of anesthesia.Prospective nonrandomized clinical study.Eighteen healthy adult horses aged [mean±standard deviation (SD)] 10±4.2 years and weighing 491±110 kg anesthetized for elective procedures.IOP was measured in the superior eye of each horse based on planned recumbency after induction of anesthesia. Measurements were taken directly after premedication with xylazine or detomidine with butorphanol, after induction with diazepam-ketamine, after intubation, when suspended by the hoist and on the operating table. During hoisting, the head was supported and the eye-heart height was measured to account for variations in head positioning among patients. IOPs were compared across time points using repeated-measures analysis of variance. Regression was used to compare IOP outcome with potential cofactors.Compared with measurements after premedication (17.5±2.5 mmHg) (mean±SD), hoisting significantly increased IOP (32.4±15.3 mmHg) (p0.01). The highest recorded IOP in the hoist was 80.0 (range, 16.0-80.0) mmHg. The difference in IOP between premedication and hoisting was 15.0±16.2 (range, -1.0 to 68.0) mmHg. Body weight had a significant effect on absolute IOP and change in IOP in the hoist (p0.01).Hoist IOP was significantly higher than post-premedication IOP with heavier horses having higher hoist IOPs and greater increases in IOP. The clinician should take this relationship into account when anesthetizing and hoisting larger horses where an increase in IOP could be detrimental.

Objective To record the cardiopulmonary effects of pleural CO 2 positive pressure insufflation in anesthetized horses. Study design Prospective study. Animals Seven horses (mean ± standard deviation, 530.9 ± 68.1 kg) undergoing terminal surgery. Methods Horses were sedated with xylazine. Anesthesia was induced with ketamine–propofol and maintained with isoflurane, positive pressure ventilation, detomidine infusion, and butorphanol with the horses in dorsal recumbency. Baseline measurements were cardiac output, heart rate, pulmonary and systemic arterial and right atrial blood pressures, body temperature, expired and inspired gas concentrations, and arterial and mixed venous blood gases, electrolytes, glucose, and lactate concentrations. An 18 gauge 6.6 cm needle was inserted into the right pleural cavity midway between the sternum and dorsal midline in the sixth or seventh intercostal space for pleural pressure (PP) measurement. A 14 gauge 18 cm needle placed 5 cm below the previous needle allowed CO 2 insufflation into the pleural cavity. All measurements were repeated after: needle insertion, at 2, 5, and 8 mmHg PPs, and after pleural gas removal (GR). Data were compared with baseline using one-way analysis of variance with repeated measures. p Results Actual PPs were within 1.1 mmHg of the targeted PP. Pulmonary systolic and mean arterial pressures, alveolar dead space to tidal volume ratio, and isoflurane requirements increased at 8 mmHg PP and GR. Cardiac index decreased at 5 mmHg PP. Stroke index decreased at 2 mmHg PP to GR. PaO 2 decreased at 5 mmHg PP to GR. PaCO 2 increased at 8 mmHg PP and GR. Oxygen delivery decreased at 5 and 8 mmHg PP. Intrapulmonary shunt fraction and lactate concentration increased with GR. Conclusions and clinical relevance: Severe adverse cardiopulmonary effects arise from CO 2 positive pressure insufflation into the right hemithorax in dorsally recumbent isoflurane-anesthetized horses. PP should be ≤2 mmHg.

Objective To evaluate the pharmacokinetics and selected pharmacodynamic effects of a commercially available l -methadone/fenpipramide combination administered to isoflurane anaesthetized ponies. Study design Prospective single-group interventional study. Animals A group of six healthy adult research ponies (four mares, two geldings). Methods Ponies were sedated with intravenous (IV) detomidine (0.02 mg kg–1) and butorphanol (0.01 mg kg–1) for an unrelated study. Additional IV detomidine (0.004 mg kg–1) was administered 85 minutes later, followed by induction of anaesthesia using IV diazepam (0.05 mg kg–1) and ketamine (2.2 mg kg–1). Anaesthesia was maintained with isoflurane in oxygen. Baseline readings were taken after 15 minutes of stable isoflurane anaesthesia. l -Methadone (0.25 mg kg–1) with fenpipramide (0.0125 mg kg–1) was then administered IV. Selected cardiorespiratory variables were recorded every 10 minutes and compared to baseline using the Wilcoxon signed-rank test. Adverse events were recorded. Arterial plasma samples for analysis of plasma concentrations and pharmacokinetics of l -methadone were collected throughout anaesthesia at predetermined time points. Data are shown as mean ± standard deviation or median and interquartile range (p Results Plasma concentrations of l -methadone showed a rapid initial distribution phase followed by a slower elimination phase which is best described with a two-compartment model. The terminal half-life was 44.3 ± 18.0 minutes, volume of distribution 0.43 ± 0.12 L kg–1 and plasma clearance 7.77 ± 1.98 mL minute–1 kg–1. Mean arterial blood pressure increased from 85 (±16) at baseline to 100 (±26) 10 minutes after l -methadone/fenpipramide administration (p = 0.031). Heart rate remained constant. In two ponies fasciculations occurred at different time points after l -methadone administration. Conclusions and clinical relevance Administration of a l -methadone/fenpipramide combination to isoflurane anaesthetized ponies led to a transient increase in blood pressure without concurrent increases in heart rate. Pharmacokinetics of l -methadone were similar to those reported for conscious horses administered racemic methadone.

Objective To compare the efficacy of a medetomidine constant rate infusion (CRI) with a detomidine CRI for standing sedation in horses undergoing high dose rate brachytherapy. Study design Randomized, controlled, crossover, blinded clinical trial. Animals A total of 50 horses with owner consent, excluding stallions. Methods Each horse was sedated with intravenous acepromazine (0.02 mg kg–1), followed by an α2-adrenoceptor agonist 30 minutes later and then by butorphanol (0.1 mg kg–1) 5 minutes later. A CRI of the same α2-adrenoceptor agonist was started 10 minutes after butorphanol administration and maintained for the treatment duration. Treatments were given 1 week apart. Each horse was sedated with detomidine (bolus dose, 10 μg kg–1; CRI, 6 μg kg–1 hour–1) or medetomidine (bolus dose, 5 μg kg–1; CRI, 3.5 μg kg–1 hour–1). If sedation was inadequate, a quarter of the initial bolus of the α2-adrenoceptor agonist was administered. Heart rate (HR) was measured via electrocardiography, and sedation and behaviour evaluated using a previously published scale. Between treatments, behaviour scores were compared using a Wilcoxon signed-rank test, frequencies of arrhythmias with chi-square tests, and HR with two-tailed paired t tests. A p value Results Total treatment time for medetomidine was longer than that for detomidine (p = 0.04), and ear movements during medetomidine sedation were more numerous than those during detomidine sedation (p = 0.03), suggesting there may be a subtle difference in the depth of sedation. No significant differences in HR were found between treatments (p ≥ 0.09). Several horses had arrhythmias, with no difference in their frequency between the two infusions. Conclusions and clinical relevance Medetomidine at this dose rate may produce less sedation than detomidine. Further studies are required to evaluate any clinical advantages to either drug, or whether a different CRI may be more appropriate.

Objective: To compare sedative and analgesic properties of buprenorphine or morphine for standing procedures combined with a detomidine continuous rate infusion (CRI). Study design: Blinded, prospective, randomized clinical pilot study. Animals: Ten horses presented for dental or sinus procedures. Methods: Horses received 0.02 mg kg-1 acepromazine intravenously (IV), followed 30 minutes later by detomidine 10 μg kg-1 IV. Five minutes later, buprenorphine 0.01 mg kg-1 (n = 6) or morphine 0.1 mg kg-1 (n = 4) was administered IV. Detomidine was administered by CRI (0.2 μg kg-1 minute-1) and adjusted to maintain appropriate sedation. Heart rate, respiratory frequency, gastrointestinal motility and rectal temperature were measured; pain, ataxia and sedation were scored. Sedation, pain scores and ataxia scores were analysed using a mixed linear model. Detomidine dose and procedure success scores were compared using Wilcoxon's rank sum test. Complications between groups were analysed using Fisher's exact test. Results: Two horses had incomplete data. Weights and ages were not different between groups (p = 0.15 and p = 0.42, respectively). The dose rate for detomidine was not different between groups (0.33 ± 0.02 μg kg-1 minute-1 in the buprenorphine group and 0.33 ± 0.05 μg kg-1 minute-1, in the morphine group p = 0.89). Intraoperative visual analogue scale scores were greater after buprenorphine than morphine (mean ± SD, buprenorphine 48 ± 4, morphine 40 ± 5, p = 0.0497). Procedure duration was not different between groups (buprenorphine 142 ± 33, morphine 140 ± 12 minutes). All horses treated with buprenorphine experienced complications compared with none in the morphine group (p = 0.0286). Conclusions and clinical relevance: At the doses used, buprenorphine produced greater sedation but more post-operative complications than morphine. However, Type I or Type II errors cannot be excluded and larger studies are required to confirm these findings.

Objective To compare the effects of two different doses of butorphanol combined with detomidine administered intravenously (IV) on quality of sedation, degree of ataxia and anaesthetic induction in horses. Study design Randomized, blinded, clinical study. Animals A total of 40 client-owned healthy warmblood horses scheduled for elective surgery under general anaesthesia. Methods Horses were randomly allocated to be administered 8 μg kg–1 detomidine IV plus either 20 or 50 μg kg–1 butorphanol IV, with the principal investigator blinded to group allocation. Head height was measured before drug injection and 2 minutes thereafter. Data were compared using unpaired t test. Horses were filmed and scored using Simple Descriptive Scales for sedation (2 and 15 minutes after IV injection), ataxia (at walk, immediately after the 2 minute time point) and quality of swing-door induction following diazepam and ketamine administration. Data are shown as median (and range where appropriate). Scores were compared using chi-square tests (p Results There were 14 and 17 horses in high-dose (HD) and low-dose (LD) groups respectively. Data from nine horses were excluded. Mean head height reduction did not differ between groups (p = 0.86), nor did sedation scores at 2 minutes (median = 3 in both groups; p = 0.09) or 15 minutes (median = 2 in both groups; p = 0.63). There was no significant difference in the requirement for additional detomidine (p = 0.73) or in induction quality between groups (p = 0.99), but initial ataxia was significantly greater in the HD group 2 (1–3) versus 2.5 (1–3) in the LD group (p = 0.017). Conclusions and clinical relevance: In healthy warmblood horses, simultaneous administration of 50 rather than 20 μg kg–1 butorphanol with 8 μg kg–1 detomidine does not provide greater sedation or affect induction, but it causes more pronounced ataxia shortly after IV injection.

Objectives To determine the sedative effects and pharmacokinetic profile of detomidine when administered intravaginally as a gel formulation to horses. Study design Randomized, crossover, masked experimental design. Animals A group of six healthy adult mares (494 ± 56 kg). Methods Mares were studied on two occasions and were administered either detomidine hydrochloride (10 μg kg–1) intravenously (treatment IV) or detomidine gel (40 μg kg–1) intravaginally (treatment IVG), separated by 1 week. Sedation, ataxia, muzzle–floor distance and heart rate (HR) were evaluated every 15 minutes for 240 minutes. Venous blood samples were collected at 15, 30, 45, 60, 90, 120, 150, 180, 240, 300 and 360 minutes postadministration and were analyzed for detomidine and metabolites using liquid chromatography–tandem mass spectrometry. Measured variables were compared over time and between treatments using mixed model analysis. Correlation between drug plasma concentrations and muzzle–floor distance, and sedation and ataxia scores was determined using the Spearman correlation coefficient. Data are presented as mean ± standard error of the mean and p value was set at Results Sedation was shorter with IV (119 ± 16 minutes) than with IVG (188 ± 22 minutes). Ataxia scores remained greater than baseline for 90 and 135 minutes for treatments IV and IVG, respectively. HR was lower than baseline for 45 and 30 minutes for IV and IVG, respectively, but did not differ between treatments. The mean maximum plasma concentration of detomidine, time to maximum concentration and bioavailability for treatment IVG was 8.57 ng mL–1, 0.37 hour and 25%, respectively. There was a significant correlation (r = 0.68) between plasma detomidine concentrations and sedation score. Conclusions and clinical relevance Detomidine gel administered intravaginally resulted in clinically important sedation and is a viable method for detomidine gel delivery in mares.

Objective To compare intravenous (IV) midazolam and diazepam administered with ketamine for induction of anaesthesia in ponies, already sedated with detomidine, undergoing field castration. Study design Prospective, randomised, ‘blinded’, clinical study. Animals Twenty Welsh pony yearlings. Methods After IV injection of detomidine (20 μg kg −1 ) and phenylbutazone (4.4 mg kg −1 ) ponies were allocated to receive either IV midazolam (group M) or diazepam (group D) (both 0.06 mg kg −1 ) with ketamine (2.2 mg kg −1 ) for induction of anaesthesia. Using simple descriptive scales, quality of sedation, induction, endotracheal intubation, surgical conditions and recovery were scored by observers blinded to treatment. Time from sedation to induction of anaesthesia, IV injection to lateral recumbency, induction to start of surgery, induction to first head lift and to standing, and total surgical time were measured. Cardiorespiratory function was assessed every 5 minutes. Time, number and total quantity of additional IV ketamine as well as any adverse effects were documented. Data were tested for normality and analysed using two-way anova with Bonferroni post hoc tests, unpaired t -tests and Mann–Whitney U tests as appropriate. Significance was set at p Results There were no significant group differences in any of the measured variables except bodyweight (mean ± SD: group M 163 ± 12 kg; group D 150 ± 7 kg; p = 0.01). One pony in group M required ketamine 15 minutes after induction of anaesthesia. Surgical conditions were good in all cases; time from induction to standing was 50 ± 11 minutes in group M and 48 ± 12 minutes in group D. There were no adverse effects. Recoveries were uneventful with minimal ataxia. Conclusions and clinical relevance Midazolam and diazepam at 0.06 mg kg −1 can be used interchangeably in combination with ketamine for IV induction of short term anaesthesia in ponies.

Objective To review the literature with regard to the use of different intravenous agents as supplements to inhalational anaesthesia in horses. The Part 2 of this review will focus in the use of opioids and a 2 -agonists. Databases used Pubmed and Web of Science. Search terms: horse, inhalant anaesthesia, balanced anaesthesia, partial intravenous anaesthesia, opioids, morphine, pethidine, butorphanol, methadone, fentanyl, alfentanil, remifentanil, sufentanil, xylazine, romifidine, detomidine, medetomidine and dexmedetomidine . Conclusions Different drugs and their combinations can be administered systemically in anaesthetized horses aiming to reduce the amount of the volatile agent while improving the recovery qualities and providing a multimodal analgesic approach. However, full studies as to whether these techniques improve cardiopulmonary status are not always available and potential disadvantages should also be considered.

To compare the topographic modifications and tactile sensitivity of the pharynx and larynx after administration of four sedative and analgesic protocols in standing horses.Experimental, observer-blinded, crossover study.Eight healthy mares.Five protocols were evaluated: 1) xylazine and butorphanol administered intravenously (IV); 2) detomidine and butorphanol administered IV; 3) xylazine administered IV and lidocaine topically; 4) detomidine administered IV and lidocaine topically and 5) no analgesia or sedation (control). Quality of sedation, head height and sudden head movements were recorded. The degree of arytenoid cartilage displacement, the degree of pharyngeal collapse and the occurrence of soft palate displacement were scored using standardized scales. Tactile sensitivity was tested on 10 different pharyngeal and laryngeal regions using an atraumatic transendoscopic probe. Statistical analysis was performed using linear or generalized mixed-effects models.Head height was significantly decreased in protocols with xylazine (p = 0.002). Head movements were significantly increased in protocols with butorphanol (p = 0.0001). No changes in abduction grade or degree of soft palate displacement were observed between all sedative protocols and the control group. Pharyngeal collapse was significantly more frequent in protocols with lidocaine (p 0.001) or xylazine (p = 0.017). For the pharyngeal regions, no tactile sensitivity difference was observed between the control and treatment protocols. All treatment protocols led to greater desensitization of all the laryngeal regions compared with the control protocol.All the protocols provided adequate sedation and analgesia for the manipulation of the larynx and pharynx but significant differences were noted. Xylazine produces a more profound sedation compared with detomidine, but can induce dorsal pharyngeal collapse. Lidocaine caused pharyngeal collapse and its use should be limited to the target area. Butorphanol can be added to improve analgesia in the other regions but frequent head jerking can be expected.

As a result of anatomic and physiologic differences, draft breeds may be at greater risk of developing anesthetic complications. The aim of the study was to evaluate and compare anesthetic management of draft (DR) and light (LT) horses. A case-matched retrospective study of 371 clinical case records of DR (124 cases) and LT (247 cases) horses presented for general anesthesia between 1991 and 1998 was performed. Data were tabulated and comparisons were made using Student's t-test (significance p

Alpha-2 agonists cause transient dose-related increase in urine flow in normal horses. Although important clinically, effects of these drugs in dehydrated animals are not known. The purpose of this study was to describe the influence of xylazine (XYL) and detomidine (DET) on urine flow in mares deprived of food and water for 24 hours. Six clinically normal mares [12.5 ± 3.3 (mean ± SE) years] weighing 471 ± 23 kg were each studied four times; each study was separated by at least 7 days. The morning following fasting, the urinary bladder was catheterized (Foley) and emptied. Urine was then collected for 2 hours and a composite urine sample along with a sample of jugular venous blood provided baseline values. Shortly after emptying the bladder, saline, 0.5 or 1.0 mg kg−1 XYL or 0.03 mg kg−1 DET was injected IV (treatment randomly assigned) and urine and blood samples obtained over the next 2 hours. Data were analyzed by RM anova followed by Dunnett's test for pairwise comparisons p

Horses airlifted by helicopter must be cooperative, able to support their own weight plus the weight of the rescue sling, nonreactive to helicopter approach, hovering, lift-off, and transport; and able to support their own weight without significant ataxia during delivery to safe ground. The flooding that occurs in Louisiana has given us the opportunity to be involved in airlift rescue of eight horses stranded by high water. In our experience, the effective titration of sedatives is best accomplished through an IV catheter placed in one of the jugular veins rather than by repeated IV injections. Prior to the catheter placement, we sedate the horses with either xylazine (0.4–0.5 mg kg−1 IV) or detomidine (8–10 µg kg−1 IV). The process of airlifting can be divided into four phases: (1) attachment of lift sling; (2) helicopter approach and hover during attachment of the sling to the aircraft; (3) lift and transport; and (4) delivery to safe zone. The IV administration of an additional 0.4–0.5 mg kg−1 of xylazine immediately prior to placing the horse in the lift sling produces an appropriate level of sedation without excessive ataxia. With the sling in place and the horse blindfolded, the helicopter is called. As the helicopter approaches, another 0.4–0.5 mg kg−1 xylazine administered. The IV is generally sufficient to prevent reaction to the noise and wind associated with the hovering of the helicopter. After the lift sling is connected to the helicopter, a final dose of xylazine (0.25 mg kg−1 IV) has proven effective in reducing reaction to lift and transport. This sedation protocol has proven effective for airlifts of approximately 5–10-minutes duration. Thus sedated, horses are able to support their weight without excessive ataxia when delivered to their destination. Xylazine appears to be more effective than detomidine because of its shorter latency of onset and duration of action.

Changes in cardiopulmonary function, hematology, serum chemistry and peritoneal fluid were examined in six healthy, pharmacologically restrained, mature horses during and after abdominal insufflation with CO2 (15 mm Hg) during standing laparoscopy. Each horse underwent standing left flank exploratory laparoscopy (LFL) and a sham procedure (SLFL) (cannula placement without insufflation) in a randomized cross-over design with at least 4 weeks between procedures. Heart rate (HR), respiratory rate (RR), cardiac output (thermodilution) (CO), right atrial pressure (RAP), systemic arterial blood pressures (ABP), pulmonary arterial pressure (PAP) and arterial blood gases (ABG) were measured. Cardiac index (CI), systemic vascular resistance (SVR) and pulmonary vascular resistance (PVR) were derived from measured parameters. Baseline measurements were the average of measurements taken every 15 minutes for 60 minutes. Following baseline measurements, samples for complete blood count (CBC), serum chemistry analysis (SC) and peritoneal fluid (PF) analysis were obtained. The horses were then sedated with detomidine (0.02 mg kg−1 IV) followed in 5 minutes by butorphanol (0.02 mg kg−1 IV) and the flank was prepared for laparoscopy. Cardiopulmonary data and blood gas samples were obtained 5 minutes postdetomidine sedation, 10 minutes after butorphanol administration and at 0, 5, 15, 30, 45, and 60 minutes after abdominal insufflation with CO2 (15 mm Hg) (LFL) or instrumentation without insufflation (SLFL). CBC, SC, and PF analyses were repeated at the conclusion of insufflation and desufflation and 24 hours after the conclusion of each procedure. Significant decreases in HR, CO, and CI and significant increases in MRAP, SVR and PVR occurred immediately after detomidine administration. There were no clinically significant effects of abdominal insufflation with CO2 on any measure of cardiopulmonary function, including blood gases. There was a significant increase in peritoneal fluid total nucleated cell count 24 hours following LFL. Abdominal insufflation with CO2 (15 mm Hg) for 1 hour during the standing laparoscopy does not cause significant alterations in cardiopulmonary function, but does cause a mild inflammatory response within the peritoneal cavity.

Objective To describe the effects of alpha 2 -adrenergic receptor antagonists on the pharmacodynamics of sublingual (SL) detomidine in the horse. Study design Randomized crossover design. Animals Nine healthy adult horses with an average age of 7.6 ± 6.5 years. Methods Four treatment groups were studied: 1) 0.04 mg kg −1 detomidine SL; 2) 0.04 mg kg −1 detomidine SL followed 1 hour later by 0.075 mg kg −1 yohimbine intravenously (IV); 3) 0.04 mg kg −1 detomidine SL followed 1 hour later by 4 mg kg −1 tolazoline IV; and 4) 0.04 mg kg −1 detomidine SL followed 1 hour later by 0.12 mg kg −1 atipamezole IV. Each horse received all treatments with a minimum of 1 week between treatments. Blood samples were obtained and plasma analyzed for yohimbine, atipamezole and tolazoline concentrations by liquid chromatography-mass spectrometry. Behavioral effects, heart rate and rhythm, glucose, packed cell volume (PCV) and plasma proteins were monitored. Results Chin-to-ground distance increased following administration of the antagonists, however, this effect was transient, with a return to pre-reversal values as early as 1 hour. Detomidine induced bradycardia and increased incidence of atrioventricular blocks were either transiently or incompletely antagonized by all antagonists. PCV and glucose concentrations increased with tolazoline administration, and atipamezole subjectively increased urination frequency but not volume. Conclusions and clinical relevance At the doses administered in this study, the alpha 2 -adrenergic antagonistic effects of tolazoline, yohimbine and atipamezole on cardiac and behavioral effects elicited by SL administration of detomidine are transient and incomplete.

History A 10–year old Arabian mare had a slow–growing mass on the lower right mandible and required a large partial mandibulectomy. Physical examination No abnormalities were detected apart from the mass. Management A temporary tracheostomy was performed pre–operatively. Anesthesia was induced with xylazine followed by ketamine and diazepam. For 13 hours, anesthesia was maintained using sevoflurane, dexmedetomidine and remifentanil infusions, with the exception of surgical preparation time. Intra–operatively, ventilation was delivered through the cuffed tracheotomy tube. Heart and respiratory rates, ECG, arterial pressures, inspired and expired gases, pulse oximetry values and body temperature were monitored. Dobutamine and whole blood were necessary, and romifidine was used to control recovery. Post–operatively, phenylbutazone and buprenorphine given systemically and bupivacaine administered through a wound soaker catheter were used to provide analgesia. Head–shaking from buprenorphine was controlled with acepromazine and detomidine once standing after 87 minutes in recovery. For 3 days after surgery, analgesia was provided with butorphanol, phenylbutazone and bupivacaine. The mare recovered well, appeared comfortable and started eating the following day with no signs of ileus. Follow–up Seven months later, the mare was doing well. Conclusions Sevoflurane, dexmedetomidine and remifentanil infusions were suitable for a long and invasive procedure.

Objective To investigate plasma drug concentrations and the effect of MK-467 (L-659′066) on sedation, heart rate and gut motility in horses sedated with intravenous (IV) detomidine. Study design Experimental randomized blinded crossover study. Animals Six healthy horses. Methods Detomidine (10 μg kg −1 IV) was administered alone (DET) and in combination with MK-467 (250 μg kg −1 IV; DET + MK). The level of sedation and intestinal sounds were scored. Heart rate (HR) and central venous pressure (CVP) were measured. Blood was collected to determine plasma drug concentrations. Repeated measures anova was used for HR, CVP and intestinal sounds, and the Student's t -test for pairwise comparisons between treatments for the area under the time-sedation curve (AUC sed ) and pharmacokinetic parameters. Significance was set at p Results A significant reduction in HR was detected after DET, and HR was significantly higher after DET + MK than DET alone. No heart blocks were detected in any DET + MK treated horses. DET + MK attenuated the early increase in CVP detected after DET, but later the CVP decreased with both treatments. Detomidine-induced intestinal hypomotility was prevented by MK-467. AUC sed was significantly higher with DET than DET + MK, but maximal sedations scores did not differ significantly between treatments. MK-467 lowered the AUC of the plasma concentration of detomidine, and increased its volume of distribution and clearance. Conclusions and clinical relevance MK-467 prevented detomidine induced bradycardia and intestinal hypomotility. MK-467 did not affect the clinical quality of detomidine-induced sedation, but the duration of the effect was reduced, which may have been caused by the effects of MK-467 on the plasma concentration of detomidine. MK-467 may be useful clinically in the prevention of certain peripheral side effects of detomidine in horses.

Objective The study aimed to investigate the effect of varying pulse lengths of inhaled nitric oxide (iNO), and 2.5 hours of continuous pulse-delivered iNO on pulmonary gas exchange in anaesthetized horses.Study Design Experimental study. Animals Six Standardbred horses.Methods Horses received acepromazine, detomidine, guaifenesin, thiopentone and isoflurane in oxygen, were positioned in dorsal recumbency and were breathing spontaneously. iNO was on average pulsed during the first 20, 30, 43 or 73% of the inspiration in 15 minute steps. The pulse length that corresponded to the highest (peak) partial pressure of arterial oxygen (PaO2) in the individual horses was determined and delivered for a further 1.5 hours. Data measured or calculated included arterial and mixed venous partial pressures of O2 and CO2, heart rate, respiratory rate, expired minute ventilation, pulmonary and systemic arterial mean pressures, cardiac output and venous admixture. Data (mean +/- SD) was analysed using anova with p < 0.05 considered significant.Results Although the pulse length of iNO that corresponded to peak PaO2 varied between horses, administration of all pulse lengths of iNO increased PaO2 compared to baseline. The shortest pulse lengths that resulted in the peak PaO2 were 30 and 43% of the inspiration. Administration of iNO increased PaO2 (12.6 +/- 4.1 kPa [95 +/- 31 mmHg] at baseline to a range of 23.0 +/- 8.4 to 25.3 +/- 9.0 kPa [173 to 190 mmHg]) and PaCO2 (8.5 +/- 1.2 kPa [64 +/- 9 mmHg] to 9.8 +/- 1.5 kPa [73 +/- 11 mmHg]) and decreased venous admixture from 32 +/- 6% to 25 +/- 6%. The increase in PaO2 and decrease in venous admixture was sustained for the entire 2.5 hours of iNO delivery.Conclusions The improvement in arterial oxygenation during pulsed delivery of iNO was significant and sustained throughout 2.5 hours of anaesthesia.Clinical relevance Pulsed iNO potentially could be used clinically to counteract hypoxemia in anaesthetized horses.

To elaborate constant rate infusion (CRI) protocols for xylazine (X) and xylazine/butorphanol (XB) which will result in constant sedation and steady xylazine plasma concentrations.Blinded randomized experimental study.Ten adult research horses.Part I: After normal height of head above ground (HHAG = 100%) was determined, a loading dose of xylazine (1 mg kg(-1) ) with butorphanol (XB: 18 μg kg(-1) ) or saline (X: equal volume) was given slowly intravenously (IV). Immediately afterwards, a CRI of butorphanol (XB: 25 μg kg(-1) hour(-1)) or saline (X) was administered for 2 hours. The HHAG was used as a marker of depth of sedation. Sedation was maintained for 2 hours by additional boluses of xylazine (0.3 mg kg(-1)) whenever HHAG50%. The dose of xylazine (mg kg(-1) hour(-1)) required to maintain sedation was calculated for both groups. Part II: After the initial loading dose, the calculated xylazine infusion rates were administered in parallel to butorphanol (XB) or saline (X) and sedation evaluated. Xylazine plasma concentrations were measured by HPLC-MS-MS at time points 0, 5, 30, 45, 60, 90, and 120 minutes. Data were analyzed using paired t-test, Wilcoxon signed rank test and a 2-way anova for repeated measures (p0.05).There was no significant difference in xylazine requirements (X: 0.69, XB: 0.65 mg kg(-1) hour(-1)) between groups. With treatment X, a CRI leading to prolonged sedation was developed. With XB, five horses (part I: two, part II: three) fell down and during part II four horses appeared insufficiently sedated. Xylazine plasma concentrations were constant after 45 minutes in both groups.Xylazine bolus, followed by CRI, provided constant sedation. Additional butorphanol was ineffective in reducing xylazine requirements and increased ataxia and apparent early recovery from sedation in unstimulated horses.Data were obtained on unstimulated healthy horses and extrapolation to clinical conditions requires caution.

Objective To investigate the influence of a dexmedetomidine constant rate infusion (CRI) in horses anaesthetized with isoflurane. Study design Prospective, randomized, blinded, clinical study. Animals Forty adult healthy horses (weight mean 491 ± SD 102 kg) undergoing elective surgery. Methods After sedation [dexmedetomidine, 3.5 μg kg −1 intravenously (IV)] and induction IV (midazolam 0.06 mg kg −1 , ketamine 2.2 mg kg −1 ), anaesthesia was maintained with isoflurane in oxygen/air (FiO 2 55–60%). Horses were ventilated and dobutamine was administered when hypoventilation [arterial partial pressure of CO 2 > 8.00 kPa (60 mmHg)] and hypotension [arterial pressure 70 mmHg] occurred respectively. During anaesthesia, horses were randomly allocated to receive a CRI of dexmedetomidine (1.75 μg kg −1 hour −1 ) (D) or saline (S). Monitoring included end-tidal isoflurane concentration, cardiopulmonary parameters, and need for dobutamine and additional ketamine. All horses received 0.875 μg kg −1 dexmedetomidine IV for the recovery period. Age and weight of the horses, duration of anaesthesia, additional ketamine and dobutamine, cardiopulmonary data ( anova ), recovery scores (Wilcoxon Rank Sum Test), duration of recovery ( t -test) and attempts to stand (Mann–Whitney test) were compared between groups. Significance was set at p Results Heart rate and arterial partial pressure of oxygen were significantly lower in group D compared to group S. An interaction between treatment and time was present for cardiac index, oxygen delivery index and systemic vascular resistance. End-tidal isoflurane concentration and heart rate significantly increased over time. Packed cell volume, systolic, diastolic and mean arterial pressure, arterial oxygen content, stroke volume index and systemic vascular resistance significantly decreased over time. Recovery scores were significantly better in group D, with fewer attempts to stand and significantly longer times to sternal position and first attempt to stand. Conclusions and clinical relevance A dexmedetomidine CRI produced limited cardiopulmonary effects, but significantly improved recovery quality.

Objective To examine the influence of a detomidine constant rate infusion (CRI) on cardiovascular function, isoflurane requirements and recovery quality in horses undergoing elective surgery. Study design Prospective, randomized, blinded, clinical trial. Animals Twenty adult healthy horses. Methods After sedation (detomidine, 10 μg kg−1 intravenously [IV]) and induction of anaesthesia (midazolam 0.06 mg kg−1, ketamine 2.2 mg kg−1 IV), anaesthesia was maintained with isoflurane in oxygen/air (inspiratory oxygen fraction 55%). When indicated, the lungs were mechanically ventilated. Dobutamine was administered when MAP < 70 mmHg. The horses were randomly allocated to one of two groups and throughout anaesthesia, received either a detomidine (5 μg kg−1 hour−1) (D) or saline (S) CRI, with the anaesthetist unaware of the treatment. Monitoring included end-tidal isoflurane concentration, arterial pH, PaCO2, PaO2, dobutamine administration rate, heart rate (HR), arterial pressure, cardiac index (CI), systemic vascular resistance (SVR), stroke index and oxygen delivery index ( D ˙ O2I). For recovery from anaesthesia, all horses received 2.5 μg kg−1 detomidine IV. Recovery quality and duration were recorded in each horse. For statistical analysis, anova , Pearson chi-square and Wilcoxon rank sum tests were used as relevant. Results Heart rate (p = 0.0176) and D ˙ O2I (p = 0.0084) were lower and SVR higher (p = 0.0126) in group D, compared to group S. Heart rate (p = 0.0011) and pH (p = 0.0187) increased over time. Significant differences in isoflurane requirements were not detected. Recovery quality and duration were comparable between treatments. Conclusions and clinical relevance A detomidine CRI produced cardiovascular effects typical for a2-agonists, without affecting isoflurane requirements, recovery duration or recovery quality.

Objective To evaluate the effects of a constant rate infusion (CRI) of romifidine on the requirement of isoflurane, cardiovascular performance and recovery in anaesthetized horses undergoing arthroscopic surgery. Study design Randomized blinded prospective clinical trial. Animals Thirty horses scheduled for routine arthroscopy. Methods After premedication (acepromazine 0.02 mg kg −1 , romifidine 80 μg kg −1 , methadone 0.1 mg kg −1 ) and induction (midazolam 0.06 mg kg −1 ketamine 2.2 mg kg −1 ), anaesthesia was maintained with isoflurane in oxygen. Horses were assigned randomly to receive a CRI of saline (group S) or 40 μg kg −1 hour −1 romifidine (group R). The influences of time and treatment on anaesthetic and cardiovascular parameters were evaluated using an analysis of variance. Body weight ( t ‐test), duration of anaesthesia ( t ‐test) and recovery score (Wilcoxon Rank Sum Test) were compared between groups. Significance was set at p Results All but one horse were positioned in the dorsal recumbent position and ventilated from the start of anaesthesia. End tidal isoflurane concentrations were similar in both groups at similar time points and over the whole anaesthetic period. Cardiac output was significantly lower in horses of the R group, but there were no significant differences between groups in cardiac index, body weight or age. All other cardiovascular parameters were similar in both groups. Quality of recovery did not differ significantly between groups, but more horses in group R stood without ataxia at the first attempt. One horse from group S had a problematic recovery. Conclusions and clinical relevance No inhalation anaesthetic sparing effect or side effects were observed by using a 40 μg kg −1 hour −1 romifidine CRI in isoflurane anaesthetized horses under clinical conditions. Cardiovascular performance remained acceptable. Further studies are needed to identify the effective dose of romifidine that will induce an inhalation anaesthetic sparing effect in anaesthetized horses.

Observations A 26-year-old male white rhinoceros ( Ceratotherium simum ), weighing approximately 2000 kg was anesthetized for an exploratory celiotomy. Sedation was achieved with intramuscular butorphanol (0.04 mg kg −1 ) and detomidine (0.025 mg kg −1 ) and induction of anesthesia with intravenous glyceryl guaiacolate (50 g) and three intravenous boluses of ketamine (200 mg, each); the trachea was then intubated and anesthesia maintained with isoflurane in oxygen using a circle breathing system. Positioning in dorsal recumbency for the surgery and later in sternal recumbency for the recovery represented challenges that added to the prolonged anesthesia time and surgical approach to partially correct an impaction. The rhinoceros recovered uneventfully after 10.4 hours of recumbency. Conclusions Anesthetic management for an exploratory celiotomy with a midline approach is possible in rhinoceroses, although planning and extensive staff support is necessary to adequately position the patient.

Objective To compare the analgesic efficacy of buprenorphine plus detomidine with that of morphine plus detomidine when administered epidurally in horses undergoing bilateral stifle arthroscopy. Study design Prospective, randomized, blinded clinical trial. Animals Twelve healthy adult horses participating in an orthopedic research study. Group M (n = 6) received morphine (0.2 mg kg−1) and detomidine (0.15 mg kg−1) epidurally; group B (n = 6) received buprenorphine (0.005 mg kg−1) and detomidine (0.15 mg kg−1) epidurally. Methods Horses received one of two epidural treatments following induction of general anesthesia for bilateral stifle arthroscopy. Heart rate (HR), mean arterial blood pressure (MAP), end-tidal CO2 (P e ’CO2), and end-tidal isoflurane concentrations (E’Iso%) were recorded every 15 minutes following epidural administration. Post-operative assessment was performed at 1, 2, 3, 6, 9, 12, and 24 hours after standing; variables recorded included HR, respiratory rate (fR), abdominal borborygmi, defecation, and the presence of undesirable side effects. At the same times post-operatively, each horse was videotaped at a walk and subsequently assigned a lameness score (0-4) by three ACVS diplomates blinded to treatment and who followed previously published guidelines. Nonparametric data were analyzed using Wilcoxon’s rank-sum test. Inter- and intra-rater agreement were determined using weighted kappa coefficients. Statistical significance was set at p = 0.05. Results No statistically significant differences were found between groups with respect to intra-operative HR, MAP, E’Iso%, or post-operative HR, gastrointestinal function and cumulative median lameness scores. Post-operative fR in group B [24 (12-30), median (range)] breaths per minute was significantly higher than in group M [18 (15-20)] breaths per minute, p = 0.04. Conclusions and clinical relevance In horses undergoing bilateral stifle arthroscopy, these doses of buprenorphine plus detomidine injected epidurally produced analgesia similar in intensity and duration to that of morphine plus detomidine injected epidurally.

Objective Influence of detomidine or romifidine constant rate infusion (CRI) on plasma lactate concentration and isoflurane requirements in horses undergoing elective surgery. Study design Prospective, randomised, blinded, clinical trial. Animals A total of 24 adult healthy horses. Methods All horses were administered intramuscular acepromazine (0.02 mg kg −1 ) and either intravenous detomidine (0.02 mg kg −1 ) (group D), romifidine (0.08 mg kg −1 ) (group R) or xylazine (1.0 mg kg −1 ) (group C) prior to anaesthesia. Group D was administered detomidine CRI (10 μg kg −1 hour −1 ) in lactated Ringer's solution (LRS), group R romifidine CRI (40 μg kg −1 hour −1 ) in LRS and group C an equivalent amount of LRS intraoperatively. Anaesthesia was induced with ketamine and diazepam and maintained with isoflurane in oxygen. Plasma lactate samples were taken prior to anaesthesia (baseline), intraoperatively (three samples at 30 minute intervals) and in recovery (at 10 minutes, once standing and 3 hours after end of anaesthesia). End-tidal isoflurane percentage (F e ′ Iso) was analysed by allocating values into three periods: Prep (15 minutes after the start anaesthesia–start surgery); Surgery 1 (start surgery–30 minutes later); and Surgery 2 (end Surgery 1–end anaesthesia). A linear mixed model was used to analyse the data. A value of p Results There was a difference in plasma lactate between ‘baseline’ and ‘once standing’ in all three groups ( p e ′Iso decreased significantly by 18% (to 1.03%) and by 15% (to 1.07%), respectively, during Surgery 2 compared with group C (1.26%); p p Conclusions and clinical relevance Intraoperative detomidine or romifidine CRI in horses did not result in a clinically significant increase in plasma lactate compared with control group. Detomidine and romifidine infusions decreased isoflurane requirements during surgery.

Objective To evaluate the effects of intranasal benzodiazepines (midazolam and diazepam), α2-agonists (xylazine and detomidine) and their antagonists (flumazenil and yohimbine) in canaries. Study design Prospective randomized study. Animals Twenty-six healthy adult domesticated canaries of both sexes, weighing 18.3 ± 1.0 g. Methods In Study 1 an attempt was made to determine the dose of each drug that allowed treated canaries to be laid in dorsal recumbency for at least 5 minutes, i.e. its effective dose. This involved the evaluation of various doses, during which equal volumes of the tested drug were administered slowly into each nostril. In study 2 the onset of action, duration and quality of sedation induced by each drug at its effective dose were evaluated. The efficacy of flumazenil and yohimbine in antagonizing the effects of the sedative drugs was also studied. Results In study 1 administration of 25 μL per nostril diazepam (5 mg mL−1 solution) or midazolam (5 mg mL−1 solution) to each bird caused adequate sedation within 1–2 minutes; birds did not move when placed in dorsal recumbency. After administration of 12 μL per nostril of either xylazine (20 mg mL−1) or detomidine (10 mg mL−1), birds seemed heavily sedated and assumed sternal recumbency but could not be placed in dorsal recumbency. Higher doses of xylazine (0.5 mg per nostril) or detomidine (0.25 mg per nostril) prolonged sedation but did not produce dorsal recumbency. In study 2 in all treatment groups, onset of action was rapid. Duration of dorsal recumbency was significantly longer (p Conclusion Intranasal benzodiazepines produce rapid and effective sedation in canaries. Intranasal α2 agonists produce sedation but not sustained recumbency. Specific antagonists are also effective when used by this route. Clinical relevance Intranasal sedative drug administration is an acceptable alternative method of drug delivery in canaries.

During an 8-year period of clinic improvements, an increased incidence of postanesthetic myopathy (PAM) was observed in horses undergoing anesthesia. A request was made for an independent anesthesiologist to examine possible reasons for this increase. Routine methods used for anesthesia were then compared with new methods introduced by the anesthesiologist.Investigative observations were conducted from October 1999 to April 2000. Following premedication with xylazine or detomidine, anesthesia was induced with diazepam or guiaifenesin followed by ketamine. Maintenance of anesthesia was with halothane/O(2) with mechanical ventilation. Information was gathered from observing routine anesthetics. Seventeen horses were designated group A (October-December 1999) for which hypotension was defined as mean arterial pressure (MAP)60 mmHg and managed using low-volume crystalloid fluid therapy, etilefrine, or dopamine. In the next 18 horses (group B), hypotension was redefined as MAP70 mmHg, and was managed using high-volume fluid therapy and dobutamine (January-April 2000). No other changes were made. In both groups, creatine kinase (CK) and aspartate transaminase (AST) concentrations were measured before induction, 1 and 25 hours after standing. Occurrence of PAM was defined as CK and/or AST concentrations above 1000 IU L(-1) and analyzed with Fisher's exact test between groups. Muscle enzymes increased in five horses in group A (two with clinical signs) and in one horse in group B (difference between groups: p = 0.088).Maintaining MAP70 mmHg with high-volume fluid therapy and dobutamine may help to reduce the severity of myopathy.

Objective To study the effects of morphine on haemodynamic variables, blood gas values and the requirement for additional anaesthetic drugs in horses undergoing surgery. Study design Prospective randomized study. Methods Thirty-eight client-owned horses, ASA(American Society of Anesthesiologists) category I or II, undergoing elective surgical procedures, were studied. Horses were divided between two groups, and were paired according to operation, anaesthetist, body position during surgery, mass and breed. Group M+ received morphine by intravenous (IV) injection (0.15 mg kg−1) before induction of anaesthesia and then by infusion (0.1 mg kg−1 hour−1) throughout anaesthesia. Group M− received the same anaesthetic technique (pre-anaesthetic medication with romifidine (100 µg kg−1) IV; induction with ketamine (2.2 mg kg−1) and diazepam (50 µg kg−1) IV; maintenance with halothane), except that morphine was excluded. Both groups received flunixin IV (1.1 mg kg−1) before surgery. Both groups also received 50% nitrous oxide for the first 10 minutes of anaesthesia. During anaesthesia, end-tidal halothane was maintained at 0.9% (±0.1%) in both groups. Heart rate (HR) and respiratory rate (fr), systolic, mean and diastolic arterial pressures were recorded every 5 minutes. Arterial blood samples were analysed every 20 minutes. Additional anaesthetics (ketamine and midazolam) were administered whenever the horse moved. Dobutamine was infused to maintain mean arterial pressure (MAP) > 58 mm Hg, but was discontinued when MAP reached 68 mm Hg. Mechanical ventilation was imposed when PaCO2 exceeded 9.3 kPa (70 mm Hg). Results Haemodynamic data (HR and MAP) and blood gas measurements were analysed using repeated measure analysis using a mixed covariance pattern model (SAS version 8.2). A Student's t-test was used to investigate differences between groups in the doses of additional anaesthetics required. There were no significant differences between M+ or M− groups in MAP (p = 0.65), HR (p = 0.74), PaO2 (p = 0.40) or PaCO2 (p = 0.20). Fewer horses in the M+ group received additional anaesthetics (15.8% compared to 21.1% in M− group), and the mean dose of ketamine required was higher in the M− group (mean ± SD: M−, 0.93 ± 0.70; M+, 0.45 ± 0.17). These differences were not statistically significant (p = 0.28). Conclusions Pre-anaesthetic and peri-operative morphine administration is not associated with significant haemodynamic or ventilatory changes. Horses receiving morphine tended to receive fewer and lower doses of additional anaesthetic drugs, although this was not statistically significant.

A juvenile female black rhinoceros (Diceros bicornis) was successfully treated after overdose of drugs used for chemical restraint. Subsequent general anaesthesia for surgical reduction of a recurrent rectal prolapse was uneventful. Over a 25-minute period before transportation to the veterinary hospital, the animal received a total dose of 1.225 mg etorphine, 30 mg acepromazine and 30 mg detomidine. Based on an estimated mass of 200 kg, these corresponded to doses of 6.1 microg kg(-1) etorphine, 150 microg kg(-1) acepromazine, and 150 microg kg(-1) detomidine which constitutes considerable overdose for each drug given separately, notwithstanding the synergy that probably resulted when the three drugs were present concurrently. The estimated body mass may have substantially overestimated the actual body mass and exacerbated overdosage. The animal was recumbent and apnoeic on arrival at the hospital. Heart sounds were auscultated and a weak peripheral pulse was palpated; no pulse deficits were detected, although the heart rate was low. The trachea was intubated, inspired breath was enriched with oxygen and the lungs ventilated manually. Diprenorphine (1.5 mg) was given intravenously and spontaneous breathing resumed 11 minutes later. After induction of general anaesthesia using isoflurane, emergency surgery for correction of rectal prolapse was performed, from which the animal recovered uneventfully. The case highlights some of the practical problems that may be encountered in dealing with dangerous and unfamiliar species.

Objective To assess the hormonal, metabolic and physiological effects of laparascopic surgery performed under a sedative analgesic combination of detomidine and buprenorphine in standing horses. Study design Prospective study. Animals Eight healthy adult Dutch Warmblood horses and five healthy adult ponies undergoing laparoscopy were studied. Five healthy adult horses not undergoing laparoscopy were used as a control group. Methods The sedative effect of an initial detomidine and buprenorphine injection was maintained using a continuous infusion of detomidine alone. The heart and respiratory rate, arterial blood pH and arterial oxygen and carbon dioxide tensions were monitored, while blood samples were taken for the measurement of glucose, lactate, cortisol, insulin and nonesterified fatty acids (NEFA). The same variables were monitored in a control group of horses which were sedated, but which did not undergo surgery. At the end of the sedation period the effects of detomidine were antagonized using atipamezole. Results The protocol provided suitable conditions for standing laparoscopy in horses. Laparoscopy induced obvious metabolic and endocrine responses which, with the exception of NEFA values, were not significantly different from changes found in the control group. While atipamezole did not produce detectable adverse effects, it is possible that anatagonism may not be essential. Conclusions The technique described reliably produces adequate sedation and analgesia for laparoscopic procedures. The level of sedation/analgesia was controlled by decreasing or increasing the infusion rate. Antagonism of the effects of detomidine may not be necessary in all cases.

Objectives To study in horses (1) the relationship between cardiovascular variables and muscle perfusion during propofol–ketamine anaesthesia, (2) the physiological effects of a single intravenous (IV) detomidine injection, (3) the metabolic response of muscle to anaesthesia, and (4) the effects of propofol–ketamine infusion on respiratory function. Study design Prospective experimental study. Animals Seven standardbred trotters, 5–12 years old, 416–581 kg. Methods Anaesthesia was induced with intravenous (IV) guaifenesin and propofol (2 mg kg −1 ) and maintained with a continuous IV infusion of propofol (0.15 mg kg −1 minute −1 ) and ketamine (0.05 mg kg −1 minute −1 ) with horses positioned in left lateral recumbency. After 1 hour, detomidine (0.01 mg kg −1 ) was administered IV and 40–50 minutes later anaesthesia was discontinued. Cardiovascular and respiratory variables (heart rate, cardiac output, systemic and pulmonary artery blood pressures, respiratory rate, tidal volume, and inspiratory and expiratory O 2 and CO 2 ) and muscle temperature were measured at pre-determined times. Peripheral perfusion was measured continuously in the gluteal muscles and skin using laser Doppler flowmetry (LDF). Muscle biopsy samples from the left and right gluteal muscles were analysed for glycogen, creatine phosphate, creatine, adenine nucleotides, inosine monophosphate and lactate. Arterial blood was analysed for PO 2 , PCO 2 , pH, oxygen saturation and HCO 3 . Mixed venous blood was analysed for PO 2 , PCO 2 , pH, oxygen saturation, HCO 3 , cortisol, lactate, uric acid, hypoxanthine, xanthine, creatine kinase, creatinine, aspartate aminotransferase, electrolytes, total protein, haemoglobin, haematocrit and white blood cell count. Results Circulatory function was preserved during propofol–ketamine anaesthesia. Detomidine caused profound hypertension and bradycardia and decreased cardiac output and muscle perfusion. Ten minutes after detomidine injection muscle perfusion had recovered to pre-injection levels, although heart rate and cardiac output had not. No difference in indices of muscle metabolism was found between dependent and independent muscles. Anaerobic muscle metabolism, indicated by decreased muscle and creatine phosphate levels was evident after anaesthesia. Conclusion Muscle perfusion was closely related to cardiac output but not arterial blood pressure. Total intravenous anaesthesia with propofol–ketamine deserves further study despite its respiratory depression effects, as the combination preserves cardiovascular function. Decreases in high-energy phosphate stores during recovery show that muscle is vulnerable after anaesthesia. Continued research is required to clarify the course of muscle metabolic events during recovery.

Objective To compare the arterial pH and blood gas values, heart rate and mean arterial blood pressure, in hypoxaemic anaesthetized horses, before and after treatment, with a salbutamol (albuterol) aerosol. Animal population Eighty-one client-owned horses weighing between 114 and 925 kg. Fifty-seven underwent emergency abdominal surgery and 24 were anaesthetized for elective procedures. Materials and methods Pre-anaesthetic medication included xylazine, detomidine, butorphanol and morphine, alone or in various combinations. Induction of anaesthesia was achieved with guaifenesin and ketamine, diazepam and ketamine, or guaifenesin and thiopental. The trachea of all animals was intubated and anaesthesia maintained with either halothane (33 horses) or isoflurane (48 horses) in oxygen. Heart rate and rhythm were monitored continuously. Arterial blood pressure was monitored directly, and arterial blood collected for pH and blood gas analyses. When arterial PaO2 fell below 9.3 kPa (70 mm Hg) and failed to respond to corrective measures including positive pressure ventilation and treatment of hypotension (mean arterial blood pressures Results There were no significant differences in mean arterial blood pressure, heart rate, arterial pH, base excess and bicarbonate before and after treatment. Arterial O2 tension increased significantly from a mean ± SD of 8.3 ± 1.7 kPa (62.4 ± 13.1 mm Hg) before administration to 15.9 ± 9.8 kPa (119.4 ± 57.7 mm Hg) after treatment. There was a small but significant decrease in PaCO2 from 7.4 ± 1.5 kPa (55.2 ± 11.2 mm Hg) to 7.0 ± 1.3 kPa (52.9 ± 9.8 mm Hg) between sample times. No changes in heart rhythm were observed. A high percentage (approximately 70%) of animals sweated following treatment. Conclusions Salbutamol administered at a dose of 2 μg kg−1 via the endotracheal tube of anaesthetized horses with PaO2 values less than 9.3 kPa (70 mm Hg) resulted in an almost two-fold increase in PaO2 values within 20 minutes of treatment. No changes in heart rate or mean arterial blood pressure were associated with the use of salbutamol in this study. The improvement in PaO2 may be a result of bronchodilatation and improved ventilation, increased perfusion secondary to an increase in cardiac output, or a combination of these two factors. Cardiac output and ventilation–perfusion distribution were not measured in this study; therefore, the reason for the increase in PaO2 values cannot be conclusively determined. Clinical relevance Administration of a salbutamol aerosol is a simple but effective technique that can be used to improve PaO2 values in hypoxaemic horses during inhalant anaesthesia with no apparent detrimental side effects.

Objective To assess the effectiveness of a detomidine infusion technique to provide standing chemical restraint in the horse. Design Retrospective study. Animals Fifty–one adult horses aged 9.5 ± 6.9 years (range 1–23 years) and weighing 575 ± 290.3 kg. Methods Records of horses presented to our clinic over a 3–year period in which a detomidine infusion was used to provide standing chemical restraint were reviewed. Information relating to the types of procedure performed, duration of infusion, drug dosages and adjunct drugs administered was retrieved. Results Detomidine was administered as an initial bolus loading dose (mean ± SD) of 7.5 ± 1.87 μg kg −1 . The initial infusion rate was 0.6 μg kg −1 minute −1 , and this was halved every 15 minutes. The duration of the infusion ranged from 20 to 135 minutes. Twenty horses received additional detomidine or butorphanol during the procedure. All horses undergoing surgery received local anesthesia or epidural analgesia in addition to the detomidine infusion. A wide variety of procedures were performed in these horses. Conclusions Detomidine administered by infusion provides prolonged periods of chemical restraint in standing horses. Supplemental sedatives or analgesics may be needed in horses undergoing surgery. Clinical relevance An effective method that provides prolonged periods of chemical restraint in standing horses is described. The infusion alone did not provide sufficient analgesia for surgery and a significant proportion of animals required supplemental sedatives and analgesics.