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Abstract

Objective—To evaluate the effect of dosing interval on the efficacy of maropitant for prevention of opioid-induced vomiting and signs of nausea in dogs.

Design—Randomized prospective clinical study.

Animals—50 client-owned dogs that underwent an elective surgical procedure.

Procedures—Dogs were randomly assigned to receive maropitant (1 mg/kg [0.45 mg/lb], SC), then hydromorphone (0.1 mg/kg [0.045 mg/lb], IM) at 0 (simultaneously; group 0; n = 10), 15 (group 15; 10), 30 (group 30; 10), 45 (group 45; 10), or 60 (group 60; 10) minutes later. Dogs were monitored for vomiting and signs of nausea for 30 minutes after hydromorphone administration. A historical control group of similar dogs (n = 9) that were administered hydromorphone (0.1 mg/kg, IM) but not maropitant served as the referent for comparison purposes.

Results—Vomiting was recorded for 6 dogs in group 0 and 2 dogs in group 15. Signs of nausea were recorded for 10 dogs in group 0, 9 dogs in group 15, 8 dogs in group 30, 6 dogs in group 45, and 1 dog in group 60. Compared with dogs in the historical control group, vomiting was significantly decreased and prevented when maropitant was administered 15 and 30 minutes, respectively, before hydromorphone; signs of nausea were significantly decreased only when maropitant was administered 60 minutes before hydromorphone.

Conclusions and Clinical Relevance—Results indicated that vomiting was significantly decreased and then prevented when maropitant was administered to dogs 15 and 30 minutes before hydromorphone. However, signs of nausea were significantly decreased only when the dosing interval was 60 minutes.

Full access
in Journal of the American Veterinary Medical Association

Abstract

Objective—To evaluate the effectiveness of orally administered maropitant citrate in preventing vomiting after hydromorphone hydrochloride administration in dogs.

Design—Randomized, blinded, prospective clinical study.

Animals—40 dogs with American Society of Anesthesiologists status of I or II, > 6 months of age, and weighing between 24 and 58.2 kg (52.8 and 128.04 lb).

Procedures—Dogs were randomly selected to receive maropitant (2.0 to 4.0 mg/kg [0.9 to 1.8 mg/lb]) or placebo (lactose monohydrate) orally 2 hours prior to receiving hydromorphone (0.1 mg/kg [0.045 mg/lb], IM). A blinded observer recorded the occurrence of vomiting or signs of nausea (eg, salivation or lip-licking) during a 30-minute period after hydromorphone administration. Two-tailed Fisher exact tests were used to compare the incidences of vomiting and signs of nausea with or without vomiting between treatment groups.

Results—Of the 20 dogs receiving maropitant, none vomited but 12 (60%) developed signs of nausea. Of the 20 dogs receiving placebo, 5 (25%) vomited and 11 (55%) developed signs of nausea; overall, 16 of 20 (80%) dogs in the placebo treatment group vomited or developed signs of nausea. Compared with the effects of placebo, maropitant significantly decreased the incidence of vomiting but not signs of nausea in dogs administered hydromorphone.

Conclusions and Clinical Relevance—Among the 40 study dogs, the incidence of vomiting associated with hydromorphone administration was 25%. Oral administration of maropitant prevented vomiting but not signs of nausea associated with hydromorphone administration in dogs.

Full access
in Journal of the American Veterinary Medical Association

Abstract

OBJECTIVE

To evaluate the effects of lidocaine as a coinduction agent with propofol on cardiopulmonary variables and administered propofol doses in healthy dogs premedicated with hydromorphone hydrochloride and acepromazine maleate and anesthetized with isoflurane.

ANIMALS

40 client-owned dogs (American Society of Anesthesiologists physical status classification I or II and age ≥ 6 months) scheduled to undergo anesthesia for elective procedures.

PROCEDURES

In a randomized, blinded, controlled clinical trial, dogs received 2% lidocaine hydrochloride solution (2.0 mg/kg [0.9 mg/lb], IV; n = 20) or buffered crystalloid solution (0.1 mL/kg [0.05 mL/lb], IV; 20; control treatment) after premedication with acepromazine (0.005 mg/kg [0.002 mg/lb], IM) and hydromorphone (0.1 mg/kg, IM). Anesthesia was induced with propofol (1 mg/kg [0.45 mg/lb], IV, with additional doses administered as needed) and maintained with isoflurane. Sedation was assessed, and anesthetic and cardiopulmonary variables were measured at various points; values were compared between treatment groups.

RESULTS

Propofol doses, total sedation scores, and anesthetic and most cardiopulmonary measurements did not differ significantly between treatment groups over the monitoring period; only oxygen saturation as measured by pulse oximetry differed significantly (lower in the lidocaine group). Mean ± SD propofol dose required for endotracheal intubation was 1.30 ± 0.68 mg/kg (0.59 ± 0.31 mg/lb) and 1.41 ± 0.40 mg/kg (0.64 ± 0.18 mg/lb) for the lidocaine and control groups, respectively.

CONCLUSIONS AND CLINICAL RELEVANCE

No propofol-sparing effect was observed with administration of lidocaine as a coinduction agent for the premedicated dogs of this study. Mean propofol doses required for endotracheal intubation were considerably lower than currently recommended doses for premedicated dogs. (J Am Vet Med Assoc 2020;256:93–101)

Full access
in Journal of the American Veterinary Medical Association

SUMMARY

Evoked potentials were induced by transcranial stimulation and recovered from the spinal cord, and the radial and sciatic nerves in six dogs. Stimulation was accomplished with an anode placed on the skin over the area of the motor cortex. Evoked potentials were recovered from the thoracic and lumbar spinal cord by electrodes placed transcutaneously in the ligamentum flavum. Evoked potentials were recovered from the radial and sciatic nerves by surgical exposure and electrodes placed in the perineurium. Signals from 100 repetitive stimuli were averaged and analyzed. Waveforms were analyzed for amplitude and latency. Conduction velocities were estimated from wave latencies and distance traveled. The technique allowed recovery of evoked potentials that had similar characteristics among all dogs. Conduction velocities of potentials recovered from the radial and sciatic nerves suggested stimulation of motor pathways; however, the exact origin and pathway of these waves is unknown.

Free access
in American Journal of Veterinary Research

Abstract

OBJECTIVE

To evaluate the analgesic and tissue effects of liposomal bupivacaine administered SC as an abaxial sesamoid nerve block in horses with experimentally induced lameness.

ANIMALS

6 healthy mature light-breed horses.

PROCEDURES

In a randomized crossover study, a circumferential hoof clamp was applied to a forelimb to induce reversible lameness. An abaxial sesamoid nerve block of the lame forelimb was performed by SC perineural injection of 10 mg of liposomal bupivacaine or bupivacaine HCl/site. Quantitative gait data were objectively obtained with a body-mounted inertial sensor system before (baseline) and at 30-minute intervals after treatment. Time to return to 85% of baseline lameness was determined. After a minimum 4-day washout period, procedures were repeated with the alternate limb and treatment. Lastly, the palmar digital nerves and perineural tissues were collected and examined histologically.

RESULTS

SC perineural injection of liposomal bupivacaine ameliorated forelimb lameness in 5 of 6 horses. The median duration of analgesia was not significantly different between liposomal bupivacaine (4.5 hours) and bupivacaine HCl (3.0 hours). Histologically, mild inflammation was noted in 3 of 10 sites injected with liposomal bupivacaine and in none of the sites injected with bupivacaine HCl.

CONCLUSIONS AND CLINICAL RELEVANCE

SC perineural injection of 10 mg of liposomal bupivacaine/site ameliorated experimentally induced forelimb lameness in some horses. At milligram-equivalent doses, liposomal bupivacaine had a similar duration of analgesia to that of bupivacaine HCl. Further investigation is required before recommending clinical use of liposomal bupivacaine for nerve blocks in horses.

Full access
in American Journal of Veterinary Research

Abstract

Objective—To evaluate the effects of various flow rates of oxygen administered via 1 or 2 nasal cannulae on the fraction of inspired oxygen concentration (Fio2) and other arterial blood gas variables in healthy neonatal foals.

Animals—9 healthy neonatal (3- to 4-day-old) foals.

Procedures—In each foal, a nasal cannula was introduced into each naris and passed into the nasopharynx to the level of the medial canthus of each eye; oxygen was administered at 4 flow rates through either 1 or both cannulae (8 treatments/foal). Intratracheal Fio2, intratracheal end-tidal partial pressure of carbon dioxide, and arterial blood gas variables were measured before (baseline) and during unilateral and bilateral nasopharyngeal delivery of 50, 100, 150, and 200 mL of oxygen/kg/min.

Results—No adverse reactions were associated with administration of supplemental oxygen except at the highest flow rate, at which the foals became agitated. At individual flow rates, significant and dose-dependent increases in Fio2, Pao2, and oxygen saturation of hemoglobin (Sao2) were detected, compared with baseline values. Comparison of unilateral and bilateral delivery of oxygen at similar cumulative flow rates revealed no differences in evaluated variables.

Conclusions and Clinical Relevance—Results indicated that administration of supplemental oxygen via nasal cannulae appeared to be a highly effective means of increasing Fio2, Pao2, and Sao2 in neonatal foals. These findings may provide guidance for implementation of oxygen treatment in hypoxemic neonatal foals. (Am J Vet Med 2010;71:1081–1088)

Full access
in American Journal of Veterinary Research