Patricia Pawson

Development of a behaviour-based scale to measure acute pain in dogs

A composite scale for assessing pain in dogs in a hospital setting has been developed on the basis of observations of their behaviour. Initially, 279 words and expressions suggested by 69 veterinary surgeons were reduced into 47 words and expressions which were allocated into seven behaviour categories: demeanour and response to people, posture, mobility, activity, response to touch, attention to painful area and vocalisation. Three statistical methods, hierarchical agglomerative cluster analysis, Cronbachs alpha coefficient, and analysis of variance with multiple comparisons and empirical cumulative distributions, were used to validate these procedures, and a questionnaire accompanied by a list of definitions was designed around the expressions. The new composite scale is more detailed than previously reported scales for assessing pain in dogs on the basis of their behaviour, and the methods used in its development are based on sound scientific principles.

An evaluation of anaesthetic induction in healthy dogs using rapid intravenous injection of propofol or alfaxalone

OBJECTIVE To evaluate quality of anaesthetic induction and cardiorespiratory effects following rapid intravenous (IV) injection of propofol or alfaxalone. STUDY DESIGN Prospective, randomised, blinded clinical study. ANIMALS Sixty healthy dogs (ASA I/II) anaesthetized for elective surgery or diagnostic procedures. METHODS Premedication was intramuscular acepromazine (0.03 mg kg(-1) ) and meperidine (pethidine) (3 mg kg(-1) ). For anaesthetic induction dogs received either 3 mg kg(-1) propofol (Group P) or 1.5 mg kg(-1) alfaxalone (Group A) by rapid IV injection. Heart rate (HR), respiratory rate (f(R) ) and oscillometric arterial pressures were recorded prior to induction, at endotracheal intubation and at 3 and 5 minutes post-intubation. The occurrence of post-induction apnoea or hypotension was recorded. Pre-induction sedation and aspects of induction quality were scored using 4 point scales. Data were analysed using Chi-squared tests, two sample t-tests and general linear model mixed effect anova (p < 0.05). RESULTS There were no significant differences between groups with respect to sex, age, body weight, f(R) , post-induction apnoea, arterial pressures, hypotension, SpO(2) , sedation score or quality of induction scores. Groups behaved differently over time with respect to HR. On induction HR decreased in Group P (-2 ± 28 beats minute(-1) ) but increased in Group A (14 ± 33 beats minute(-1) ) the difference being significant (p = 0.047). However HR change following premedication also differed between groups (p = 0.006). Arterial pressures decreased significantly over time in both groups and transient hypotension occurred in eight dogs (five in Group P, three in Group A). Post-induction apnoea occurred in 31 dogs (17 in Group P, 14 in Group A). Additional drug was required to achieve endotracheal intubation in two dogs. CONCLUSIONS AND CLINICAL RELEVANCE Rapid IV injection of propofol or alfaxalone provided suitable conditions for endotracheal intubation in healthy dogs but post-induction apnoea was observed commonly.

Two doses of dexmedetomidine in combination with buprenorphine for premedication in dogs; a comparison with acepromazine and buprenorphine.

OBJECTIVE To assess as premedicants, the sedative, cardiorespiratory and propofol-sparing effects in dogs of dexmedetomidine and buprenorphine compared to acepromazine and buprenorphine. STUDY DESIGN Prospective, randomised, blinded clinical study. ANIMALS Sixty healthy dogs (ASA grades I/II). Mean (SD) body mass 28.0 ± 9.1 kg, and mean age 3.4 ± 2.3 years. METHODS   Dogs were allocated randomly to receive 15 μg kg(-1) buprenorphine combined with either 30 μg kg(-1) acepromazine (group 1), 62.5 μg m(-2) dexmedetomidine (group 2), or 125 μg m(-2) dexmedetomidine (group 3) intramuscularly. After 30 minutes, anaesthesia was induced using a propofol target controlled infusion. Heart rate, respiratory rate, and oscillometric arterial blood pressure were recorded prior to induction, at endotracheal intubation and at 3 and 5 minutes post-intubation. Induction quality and pre-induction sedation were scored on 4 point scales. Propofol target required for endotracheal intubation was recorded. Data were analysed using Chi-squared tests, Kruskal-Wallis, one way and general linear model ANOVA (p<0.05). RESULTS Age was significantly lower in group 1 (1.0 (1.0-3.8) years) than group 2 (5.0 (2.0-7.0) years), (median, (IQR)). There were no significant differences in sedation or quality of induction between groups. After premedication, heart rate was significantly lower and arterial blood pressures higher in groups 2 and 3 than group 1, but there was no significant difference between groups 2 and 3. Propofol targets were significantly lower in group 3 (1.5 (1.0-2.5) μg mL(-1) ) than group 1 (2.5 (2.0-3.0) μg mL(-1) ); no significant differences existed between group 2 (2.0 (1.5-2.5) μg mL(-1) ) and the other groups (median, (interquartile range)). CONCLUSIONS AND CLINICAL RELEVANCE When administered with buprenorphine, at these doses, dexmedetomidine had no advantages in terms of sedation and induction quality over acepromazine. Both doses of dexmedetomidine produced characteristic cardiovascular and respiratory effects of a similar magnitude.

A comparison of the effects of two different doses of ketamine used for co-induction of anaesthesia with a target-controlled infusion of propofol in dogs

OBJECTIVE To assess the cardiorespiratory and hypnotic-sparing effects of ketamine co-induction with target-controlled infusion of propofol in dogs. STUDY DESIGN Prospective, randomized, blinded clinical study. ANIMALS Ninety healthy dogs (ASA grades I/II). Mean body mass 30.5 +/- SD 8.6 kg and mean age 4.2 +/- 2.6 years. METHODS All dogs received pre-anaesthetic medication with acepromazine (0.03 mg kg(-1)) and morphine (0.2 mg kg(-1)) administered intramuscularly 30 minutes prior to induction of anaesthesia. Heart rate and respiratory rate were recorded prior to pre-medication. Animals were allocated into three different groups: Group 1 (control) received 0.9% NaCl, group 2, 0.25 mg kg(-1) ketamine and group 3, 0.5 mg kg(-1) ketamine, intravenously 1 minute prior to induction of anaesthesia, which was accomplished using a propofol target-controlled infusion system. The target propofol concentration was gradually increased until endotracheal intubation was possible and the target concentration at intubation was recorded. Heart rate, respiratory rate and noninvasive blood pressure were recorded immediately prior to induction, at successful intubation and at 3 and 5 minutes post-intubation. The quality of induction was graded according to the amount of muscle twitching and paddling observed. Data were analysed using a combination of chi-squared tests, Fishers exact tests, Kruskal-Wallis, and anova with significance assumed at p < 0.05. RESULTS There were no significant differences between groups in the blood propofol targets required to achieve endotracheal intubation, nor with respect to heart rate, noninvasive blood pressure or quality of induction. Compared with the other groups, the incidence of post-induction apnoea was significantly higher in group 3, but despite this dogs in this group had higher respiratory rates overall. CONCLUSIONS AND CLINICAL RELEVANCE Under the conditions of this study, ketamine does not seem to be a useful agent for co-induction of anaesthesia with propofol in dogs.

A comparison of induction of anaesthesia using a target-controlled infusion device in dogs with propofol or a propofol and alfentanil admixture

OBJECTIVE To compare induction targets, and the haemodynamic and respiratory effects, of propofol, or as an admixture with two different concentrations of alfentanil, delivered via a propofol target-controlled infusion (TCI) system. STUDY DESIGN Prospective blinded randomized clinical study. ANIMALS Sixty client-owned dogs scheduled for elective surgery under general anaesthesia. Mean body mass (SD) 28.5 kg (8.7) and mean age (SD) 3.5 years (2.4). METHODS Dogs received pre-anaesthetic medication of acepromazine (0.03 mg kg(-1)) and morphine (0.2 mg kg(-1)) administered intramuscularly. Animals were randomly assigned to receive one of three induction protocols: propofol alone (group 1), a propofol/alfentanil (11.9 microg mL(-1)) admixture (group 2), or a propofol/alfentanil (23.8 microg mL(-1)) admixture (group 3), via a TCI system. Blood target concentrations were increased until endotracheal intubation was achieved, and induction targets were recorded. Heart rate (HR), respiratory rate (f(r)) and non-invasive arterial blood pressure were recorded pre-induction, at endotracheal intubation (time 0) and at 3 and 5 minutes post-intubation (times 3 and 5, respectively). Data were analysed using anova for normally distributed data or Kruskal-Wallis test, with significance assumed at p < 0.05. RESULTS There were no significant differences between groups with respect to age, body mass, HR, f(r), systolic and diastolic blood pressure. The blood propofol targets to achieve endotracheal intubation were significantly higher in group 1 compared with groups 2 and 3. Mean arterial blood pressure (MAP) was significantly higher in group 1 at time 0 when compared with groups 2 and 3. CONCLUSIONS AND CLINICAL RELEVANCE Induction of anaesthesia with a TCI system can be achieved at lower blood propofol targets when using a propofol/alfentanil admixture compared with using propofol alone. However, despite reduced targets with both propofol/alfentanil admixture groups, MAP was lower immediately following endotracheal intubation than when using propofol alone.

The role of nitric oxide in the responses of the ovine digital artery to vasoactive agents and modification of these responses by endotoxin and cytokines

Laminitis, an important cause of lameness in domestic ungulates, occurs as a result of altered digital perfusion. Endotoxin and cytokines may mediate the vascular derangements observed through alterations in nitric oxide production. In this study, the vascular responses of the isolated ovine digital artery were examined and the influence of endotoxin and cytokines investigated. Neither removal of the endothelium nor incubation with NG‐nitro‐L‐arginine methyl ester (L‐NAME, 300 μM) altered the response to phenylephrine (PE, 1 nM to 300 μM). Indomethacin (10 μM) decreased PE log EC50 from −6.22±0.08 to −6.55±0.07. Acetylcholine (1 nM to 1 mM) and bradykinin (BK, 100 pM to 3 μM) induced endothelium‐dependent relaxation. Bradykinin‐induced relaxation was reduced by L‐NAME, Emax falling from −61.7±7.4 to −34.0±2.1%. Addition of indomethacin further reduced BK Emax to −9.6±2.8%. Sodium nitroprusside (1 nM to 300 μM) produced endothelium‐independent relaxation that was unaffected by L‐NAME or indomethacin. Following a 6 h incubation with endotoxin (3 μg ml−1), arterial responses to PE and BK did not differ from polymyxin B‐treated controls (10 μg ml−1). Arteries incubated for 6 h with interferon‐γ (IFN‐γ, 10 ng ml−1) and tumour necrosis factor‐α (TNF‐α, 5 ng ml−1) exhibited greater relaxation to BK (Emax−50.0±5.1%) than polymyxin B‐treated controls (Emax−33.1±4.0%), but did not differ in their response to PE. Prolonged incubation (16 h) with endotoxin (3 μg ml−1) did not alter the response to PE, however incubation with IFN‐γ (10 ng ml−1), TNF‐α (5 ng ml−1) and interleukin‐1β (20 ng ml−1) for 16 h increased PE log EC50 from −6.44±0.09 to −6.10±0.11. Nitric oxide is an important mediator of endothelium‐dependent relaxation in ovine digital arteries but does not modulate PE‐induced vasoconstriction. Incubation with cytokines decreased the sensitivity of digital arteries to PE.

Changes in the Doppler waveform of the ovine femoral artery following infusion of vasoactive agents: a preliminary study.

The aim of this study was to investigate whether femoral artery pulsatility index (PI) can be used as an indicator of vasomotor tone in the digit of an ungulate species by measuring the change in PI induced by infusion of vasoactive agents in halothane-anaesthetised sheep. Intra-arterial infusion of the vasoconstrictor phenylephrine (9 microg min(-1)) tended to increase waveform PI (3.89-6.24, n=4, P=0.100). Infusion of a low dose (3 microg min(-1)) of the vasodilator sodium nitroprusside did not alter femoral artery PI, however infusion of a higher dose (30 microg min(-1)) tended to increase PI (5.39-6.70, n=5, P=0.059). During these studies heart rate, mean ABP and p(a)CO(2) did not change significantly. The tendency for PI to increase in response to vasodilation was unexpected and the mechanism involved is unclear. It appears that femoral artery PI cannot be used to predict vasomotor tone in the digit of the anaesthetised sheep.

An evaluation of a target-controlled infusion of propofol or propofol-alfentanil admixture for sedation in dogs.

OBJECTIVES To evaluate sedation quality and cardiorespiratory variables in dogs sedated using a target-controlled infusion of propofol or propofol-alfentanil admixture. METHODS A total of 60 dogs undergoing diagnostic imaging were randomly assigned to one of three sedation protocols: propofol alone; propofol with a low concentration of 12 µg of alfentanil per mL of propofol; or propofol with a higher concentration of 24 µg of alfentanil per mL of propofol. Target-controlled infusion was initiated at a propofol target concentration of 1·5 µg/mL and increased until lateral recumbency was achieved. Times to adopt lateral recumbency and recover, pulse rate, respiratory rate, oscillometric mean arterial pressure and oxygen saturation were recorded. Quality of sedation onset and recovery were scored. RESULTS Propofol target at lateral recumbency differed significantly (P=0·01) between groups with median (range) values of 3·0 (1·5 to 5·5), 2·0 (2 to 4·5) and 2·25 (1·5 to 3·5) µg/mL for propofol alone, propofol with the lower concentration of alfentanil and propofol with the higher concentration of alfentanil groups, respectively. Time to lateral recumbency was longer and quality of onset less smooth for the propofol group. Pulse rate change differed significantly (P<0·001) between groups (mean pulse rate change at onset of sedation: propofol group +2 ±24 bpm, low concentration alfentanil group -30 ±24 bpm, higher concentration alfentanil group -26 ±23 bpm). Hypoxaemia (SpO2 <90%) occurred in 1, 3 and 13 dogs, in the propofol group, the low concentration alfentanil group and the higher concentration of alfentanil group, respectively (P<0·001). CLINICAL SIGNIFICANCE Addition of alfentanil to propofol target-controlled infusion did not confer cardiovascular benefits and, at the higher concentration, alfentanil increased the incidence of hypoxaemia.