Behavioural and cardiovascular effects of medetomidine constant rate infusion compared with detomidine for standing sedation in horses.

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 <0.05 indicated statistical significance. 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.

Intramuscular injection of alfaxalone in combination with butorphanol for sedation in cats.

OBJECTIVE: To assess quality of sedation following intramuscular (IM) injection of two doses of alfaxalone in combination with butorphanol in cats. STUDY DESIGN: Prospective, randomized, 'blinded' clinical study. ANIMALS: A total of 38 cats undergoing diagnostic imaging or noninvasive procedures. METHODS: Cats were allocated randomly to be administered butorphanol 0.2 mg kg-1 combined with alfaxalone 2 mg kg-1 (group AB2) or 5 mg kg-1 (group AB5) IM. If sedation was inadequate, alfaxalone 2 mg kg-1 IM was administered and cats were excluded from further analysis. Temperament [1 (friendly) to 5 (aggressive)], response to injection, sedation score at 2, 6, 8, 15, 20, 30, 40, 50 and 60 minutes, overall sedation quality scored after data collection [1 (excellent) to 4 (inadequate)] and recovery quality were assessed. Heart rate (HR), respiratory rate (fR) and arterial haemoglobin saturation (SpO2) were recorded every 5 minutes. Groups were compared using t tests and Mann-Whitney U tests. Sedation was analysed using two-way anova, and additional alfaxalone using Fisher's exact test (p < 0.05). RESULTS: Groups were similar for sex, age, body mass and response to injection. Temperament score was lower in group AB2 [2 (1-3)] compared to AB5 [3 (1-5)] (p = 0.006). Group AB5 had better sedation at 6, 8, 20 and 30 minutes and overall sedation quality was better in AB5 [1 (1-3)], compared to AB2 [3 (1-4)] (p = 0.0001). Additional alfaxalone was required for 11 cats in AB2 and two in AB5 (p = 0.005). Recovery quality, HR, fR and SpO2 were similar. Seven cats required oxygen supplementation. Complete recovery times were shorter in AB2 (81.8 ± 24.3 versus 126.6 ± 33.3 minutes; p = 0.009). Twitching was the most common adverse event. CONCLUSIONS AND CLINICAL RELEVANCE: In combination with butorphanol, IM alfaxalone at 5 mg kg-1 provided better quality sedation than 2 mg kg-1. Monitoring of SpO2 is recommended.

Effect of prewarming on the body temperature of small dogs undergoing inhalation anesthesia.

OBJECTIVE: To investigate whether prewarming affects body temperature of small dogs (weighing < 10 kg [22 lb]) undergoing inhalation anesthesia. DESIGN: Prospective, randomized, blinded clinical trial. Animals: 20 dogs weighing < 10 kg with American Society of Anesthesiologists physical status I or II. PROCEDURES: Baseline rectal temperature was recorded. Before IM administration of buprenorphine hydrochloride and acepromazine maleate, dogs were randomly assigned to be placed in a pediatric incubator at 33°C (91.4°F) for approximately 30 to 60 minutes (prewarming group) or to receive no prewarming (control group); subsequently, dogs underwent inhalation anesthesia with isoflurane in oxygen. Rectal, esophageal, and ambient temperatures were measured every 5 minutes from induction of anesthesia (IOA) for > 1 hour by an observer who was unaware of treatment. If a dog became hypothermic (esophageal temperature < 36°C [96.8°F]), it was withdrawn from the study. Variables of interest relating to dogs, anesthesia, temperatures, hypothermia, and study withdrawal were compared between groups. RESULTS: 1 dog was excluded from the prewarming group after becoming excessively excited in the incubator. Between groups, age, weight, body condition score, degree of preanesthesia sedation, interval from sedation to IOA, duration of anesthesia, baseline rectal temperature, rectal temperatures immediately prior to IOA, esophageal temperature following IOA, ambient temperature during the first 70 minutes of anesthesia, esophageal or rectal temperature during the first 90 minutes of anesthesia, and incidence of hypothermia and study withdrawal (5 dogs/group) did not differ significantly. CONCLUSIONS AND CLINICAL RELEVANCE: Prewarming in an incubator prior to IOA failed to improve or maintain body temperature of dogs weighing < 10 kg during inhalation anesthesia.

Effect of intravenous lidocaine on heart rate, systolic arterial blood pressure and cough responses to endotracheal intubation in propofol-anaesthetized dogs.

OBJECTIVE: To evaluate the effect of intravenous lidocaine on coughing and variations in heart rate (HR) and systolic arterial pressure (SAP) at endotracheal intubation in propofol-anaesthetized dogs. STUDY DESIGN: Prospective, randomized, blinded clinical study. ANIMALS: Eighty dogs, ASA grades I/II. METHODS: Dogs were randomly assigned to one of two treatments, with dogs in the lidocaine group receiving 1 mg kg(-1) lidocaine intravenously and those in the saline group receiving 0.05 mL kg(-1) saline intravenously before induction of anaesthesia with up to 6.5 mg kg(-1) propofol intravenously. An electrocardiogram was recorded continuously. Heart rate was calculated and SAP (using Doppler ultrasonic flow detection) was recorded at the following time points: pre-treatment, following lidocaine or saline administration, before and after intubation. The occurrence, number and strength of coughs were recorded. Systolic arterial pressure and HR were compared using one-sample t-tests to examine whether SAP and HR changed with test drug administration or following intubation. The number of coughs was compared between groups using t-tests. A cross tabulation and chi-square or Fisher's exact test was used to compare proportions of dogs that coughed and intensity of coughing in each group. The level of significance was set at p < 0.05. RESULTS: Heart rate did not change in either group. Systolic arterial blood pressure increased following intubation in both the lidocaine (p = 0.003) and saline groups (p = 0.001). There was no difference in the increase in SAP or in the number or intensity of coughs at intubation between groups. CONCLUSIONS AND CLINICAL RELEVANCE: Intravenous lidocaine had no effect on the occurrence or intensity of coughing or on changes in SAP at endotracheal intubation in dogs anaesthetized with propofol. The use of 1 mg kg(-1) lidocaine intravenously before intubation in dogs to attenuate cough and the pressor response was not supported.