Briony Alderson

A comparison of acepromazine-buprenorphine and medetomidine-buprenorphine for preanesthetic medication of dogs

OBJECTIVE To assess sedative and cardiopulmonary effects of premedication with a medetomidine-buprenorphine or acepromazine-buprenorphine combination in dogs anesthetized with propofol and isoflurane. DESIGN Randomized controlled clinical trial. ANIMALS 90 dogs undergoing routine surgical and diagnostic procedures. PROCEDURES Dogs were randomly assigned to 1 of 3 premedication groups: group 1 (acepromazine, 0.03 mg/kg [0.014 mg/lb], IM; buprenorphine, 0.02 mg/kg [0.009 mg/lb], IM), 2 (medetomidine, 5 μg/kg [2.3 μg/lb], IM; buprenorphine, 0.02 mg/kg, IM), or 3 (medetomidine, 10 μg/kg [4.5 μg/lb], IM; buprenorphine, 0.02 mg/kg, IM). Anesthesia was induced with propofol and maintained with isoflurane in oxygen. Simple descriptive scores for sedation were assigned 15 minutes (groups 2 and 3) and 30 minutes (group 1) after premedication administration. Basic cardiopulmonary data were recorded throughout the anesthetic period. Times to recovery from anesthesia were recorded. RESULTS Sedation scores did not differ significantly among groups. Mean and diastolic blood pressures were significantly lower and heart rate was significantly higher in group 1 than in the other groups. Mean end-tidal partial pressure of CO(2) was significantly lower and respiratory rate was significantly higher in group 1 than in the other groups. There were no significant differences in anesthetic recovery times between groups. CONCLUSIONS AND CLINICAL RELEVANCE Results suggested that either acepromazine or medetomidine could be used in combination with buprenorphine for premedication of dogs anesthetized with propofol and isoflurane for routine surgical and diagnostic procedures. Arterial blood pressure was better maintained with the medetomidine-buprenorphine combinations, but tissue perfusion was not investigated.

Use of rocuronium administered by continuous infusion in dogs

OBJECTIVE A clinical trial to determine whether continuous infusion administration technique was suitable for maintaining neuromuscular blockade with rocuronium bromide in dogs. ANIMALS Twenty-two dogs, 10 males and 12 females, median age 2 years 4 months, median weight 32 kg undergoing elective surgical procedures under general anaesthesia: ASA classification I or II. MATERIALS AND METHODS After induction of anaesthesia, neuromuscular function was evaluated using train-of-four (TOF) stimulation of the dorsal buccal branch of the facial nerve. A bolus dose of 0.5 mg kg-1 rocuronium was administered intravenously and an infusion of 0.2 mg kg-1 hour-1 was started immediately. Neuromuscular blockade was assessed visually by counting the number of twitches observed during TOF stimulation repeated at 10-second intervals. RESULTS The bolus dose of rocuronium abolished the response to TOF stimulation in 21 of the 22 dogs. The median onset time of neuromuscular blockade (complete loss of all four twitches) was 82 seconds (range 38-184 seconds). Median infusion duration was 76 minutes (range 20.3-146 minutes). CONCLUSIONS AND CLINICAL RELEVANCE This protocol of rocuronium administration was considered to be effective in dogs. Constant infusion of rocuronium is easily applicable to clinical practice and further work is required on infusion titration.

Therapeutic options for the treatment of chronic pain in dogs.

Chronic pain is a widely recognised problem in humans and is being increasingly recognised as a significant problem in dogs. Whilst a large number of therapies are described and utilised to treat chronic pain in dogs, there is a severe shortage of evidence to guide practitioners in selection of treatments. Until more evidence becomes available, practitioners should adopt a cautious approach, utilising licensed treatments first when possible. Non-pharmacological therapies should be incorporated into the chronic pain management plan whenever possible. Given the probable prevalence of chronic pain in dogs there is an urgent need for research to identify effective treatments.

Severe bradycardia after hypoxaemia and endotracheal intubation and cardiac arrest following glycopyrrolate in a dog

A nine-year-old neutered male Yorkshire terrier with history of chronic cough underwent bronchoscopy and bronchoalveolar lavage; general anaesthesia was maintained with a variable rate infusion of propofol, and oxygen was insufflated via a urinary catheter in the trachea. At the end of the procedure, desaturation occurred; endotracheal intubation was performed and was immediately followed by severe bradycardia and respiratory arrest. Glycopyrrolate (5 µg/kg) was administered leading to cardiac arrest. Apnoea and asystole were quickly treated with manual positive pressure ventilation, external chest compressions and intravenous administration of 0.04 mg/kg of atropine. This case describes vagally induced bradycardia after intubation, possible predisposing factors and its treatment/prevention with antimuscarinic drugs.

Hyperthermia and hypercapnia following two intravenous injections of atracurium in a dog

A three month old, 5 kg American Bulldog presented with severe dyspnoea and cyanosis seven hours after being submerged in a fresh-water paddling pool. Oxygen was supplemented using an oxygen cage, but due to worsening of the clinical signs anaesthesia was induced with 2 mg/kg of propofol and the dogs trachea was intubated. Anaesthesia was maintained with a propofol infusion and mechanical ventilation was provided with 100 per cent inspired oxygen. As the patient was consistently hypercapnic and breathing against the ventilator, atracurium was administered intravenously at 0.2 mg/kg but five minutes later, the dog became hyperthermic (40°C) and hypercapnia drastically worsened. The hyperthermia and hypercapnia slowly resolved to pre-atracurium values with active cooling. After three hours another dose of atracurium was administered and a similar hyperthermic and hypercapnic reaction developed. Due to the inability to effectively ventilate the lungs and the poor prognosis the owners elected for euthanasia.

Myoclonus and hyperalgesia following intended epidural morphine administration in a dog

A West Highland White Terrier was presented after development of hindlimb myoclonus and hyperalgesia following intended epidural administration of morphine at a referring veterinary practice. MRI was unremarkable, except for the spinal cord extending to the caudal half of the L7 vertebrae. Treatment with systemic analgesia of methadone and sedation/analgesia with medetomidine resolved the clinical signs within 24 hours. The mechanism by which morphine causes adverse neurological side effects has yet to be fully determined; the morphine-3-glucuronide (M-3-G) metabolite is suspected to be responsible for the adverse effects seen. Hypotheses include action of morphine or the M-3-G metabolite on non-opioid inhibitory (glycine) or excitatory (N-methyl D-aspartate) receptors. However, more work is needed to determine the exact pathogenesis. Neuroexcitatory side effects are rarely reported following administration of morphine in dogs and this case demonstrates successful treatment with the use of an alternative opioid, methadone.