Butorphanol & Isoflurane Anesthesia in Horses: A Clinical Study

Veterinary Anaesthesia and Analgesia, 2011, 38, 186–194
doi:10.1111/j.1467-2995.2011.00600.x
RESEARCH PAPER
A clinical study on the effect in horses during
medetomidine–isoflurane anaesthesia, of butorphanol
constant rate infusion on isoflurane requirements, on
cardiopulmonary function and on recovery characteristics
Regula Bettschart-Wolfensberger*, Sidonia Dicht*, Cecilia Vullo , Angela Frotzlerà, Jan M Kuemmerle§ &
Simone K Ringer*
*Section of Anaesthesiology, Equine Department, Vetsuisse Faculty University of Zurich, Zurich, Switzerland
Ospedale Veterinario Didattico, Università degli Studi di Camerino, Camerino, Italy
àParaplegikerzentrum Nottwil, Switzerland
§Section of Surgery, Equine Department, Vetsuisse Faculty University of Zurich, Zurich, Switzerland
Correspondence: Regula Bettschart-Wolfensberger, Equine Department, Section of Anaesthesiology, Vetsuisse Faculty University of Zurich,
Winterthurerstr, 260, 8057 Zurich, Switzerland. E-mail: [email protected]
Abstract
Objective To test if the addition of butorphanol by
constant rate infusion (CRI) to medetomidine–
isoflurane anaesthesia reduced isoflurane requirements, and influenced cardiopulmonary function
and/or recovery characteristics.
Study design Prospective blinded randomised clinical trial.
Animals 61 horses undergoing elective surgery.
Methods Horses were sedated with intravenous (IV)
medetomidine (7 lg kg)1); anaesthesia was induced
with IV ketamine (2.2 mg kg)1) and diazepam
(0.02 mg kg)1) and maintained with isoflurane and
a CRI of medetomidine (3.5 lg kg)1 hour)1). Group
MB (n = 31) received butorphanol CRI (25 lg kg)1
IV bolus then 25 lg kg)1 hour)1); Group M (n =
30) an equal volume of saline. Artificial ventilation
maintained end-tidal CO2 in the normal range.
Horses received lactated Ringer’s solution 5 mL
kg)1 hour)1, dobutamine <1.25 lg kg)1 minute)1
and colloids if required. Inspired and exhaled gases,
heart rate and mean arterial blood pressure (MAP)
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were monitored continuously; pH and arterial blood
gases were measured every 30 minutes. Recovery
was timed and scored. Data were analyzed using
two way repeated measures ANOVA, independent t-tests or Mann–Whitney Rank Sum test
(p < 0.05).
Results There was no difference between groups with
respect to anaesthesia duration, end-tidal isoflurane
(MB: mean 1.06 ± SD 0.11, M: 1.05 ± 0.1%), MAP
(MB: 88 ± 9, M: 87 ± 7 mmHg), heart rate (MB:
33 ± 6, M: 35 ± 8 beats minute)1), pH, PaO2 (MB:
19.2 ± 6.6, M: 18.2 ± 6.6 kPa) or PaCO2. Recovery
times and quality did not differ between groups, but
the time to extubation was significantly longer in
group MB (26.9 ± 10.9 minutes) than in group M
(20.4 ± 9.4 minutes).
Conclusion and clinical relevance Butorphanol CRI
at the dose used does not decrease isoflurane
requirements in horses anaesthetised with medetomidine–isoflurane and has no influence on cardiopulmonary function or recovery.
Keywords anaesthesia, butorphanol, horse, isoflurane,
medetomidine.
Butorphanol CRI during medetomidine–isoflurane anaesthesia R Bettschart-Wolfensberger et al.
Introduction
Complicated surgeries of >1.5 hours in horses are
performed most usually using inhalation anaesthesia
(Mee et al. 1998; Bidwell et al. 2007). All inhalant
anaesthetics impair cardiopulmonary function in a
dose dependent fashion (Steffey & Howland 1980)
and under many clinical circumstances do not
provide sufficient analgesia to prevent nociception
during surgery. Therefore the use of combination
anaesthesia has gained widespread popularity, the
aim being to reduce the concentration of the inhalant
used (Bettschart-Wolfensberger et al. 2001; Ringer
et al. 2007) and to improve cardiopulmonary function. Furthermore combination anaesthesia often
reduces nociception and provides better analgesia. As
a result, horses recovering from such ‘balanced’
anaesthesia might experience less pain and have
smoother and more coordinated recoveries.
Drugs commonly used in horses for combination
anaesthesia are lidocaine (Dzikiti et al. 2003; Valverde et al. 2005), ketamine (Yamashita et al. 2002;
Larenza et al. 2009), alpha-2 adrenoceptor agonists
(Bettschart-Wolfensberger et al. 2001; Bennett
et al. 2004; Kalchofner et al. 2006), and opioids
(Hofmeister et al. 2008; Larenza et al. 2009). All
these drugs except the opioids reduce minimum
alveolar concentration (MAC) dose dependently.
Under experimental circumstances both morphine
and butorphanol have failed consistently to reduce
the MAC of inhalation agents (Matthews & Lindsay
1990; Steffey et al. 2003). In contrast, the use of
butorphanol in clinical cases resulted in a reduced
sympathetic response to noxious stimuli and was
therefore considered a beneficial combination with
inhalation anaesthesia (Hofmeister et al. 2008).
Medetomidine, an alpha-2 adrenoceptor agonist,
has been compared to lidocaine and S-ketamine
combination anaesthesia regimes in clinical cases
(Larenza et al. 2007; Ringer et al. 2007). In both
reports, the use of medetomidine resulted in recoveries from anaesthesia of better quality. As medetomidine is an alpha-2 adrenoceptor agonist,
bradycardia, reduced cardiac output and changes
in vascular tone might be of concern. When used in
standing ponies a bolus of medetomidine was
followed by a constant rate infusion (CRI) of medetomidine, only the bolus decreased cardiac output
and heart rate (Bettschart-Wolfensberger et al.
1999a,b). At steady state, which is reached within
30 minutes following bolus application, cardiac
output did not differ from presedation values (Betts-
chart-Wolfensberger et al. 1999a). In an experimental group of horses, no difference in cardiac output
was found when lidocaine-isoflurane was compared
to lidocaine-medetomidine–isoflurane, but recovery
was of better quality in the group receiving medetomidine (Valverde et al. 2010). In contrast, lidocaine-isoflurane anaesthesia was associated with
better mean cardiopulmonary function than medetomidine–isoflurane anaesthesia (Ringer et al.
2007). However, the lowest individual heart rates,
arterial blood pressures, cardiac indices and arterial
oxygen tensions recorded in all groups were identical. It was speculated that the higher mean arterial
blood pressures and cardiac output values were
related to insufficient depth of anaesthesia rather
than to a pure result of differences in drug regimens.
Medetomidine–isoflurane was successfully used in a
further 300 equine anaesthetic procedures with a
mean duration of 149 minutes (Kalchofner et al.
2006) and in horses for fracture repair prior to pool
recovery (Bettschart-Wolfensberger et al. 2008).
Although it has been questioned whether administration of opioids to horses is useful (Bennett &
Steffey 2002) there is no doubt that their combination with alpha-2 adrenoceptor agonists is beneficial
(Clarke & Paton 1988; Schatzman et al. 2001;
Kohler et al. 2004). The combination results in
more reliable sedation and analgesia whilst using
lower dose rates of alpha-2 adrenoceptor agonists
(Taylor et al. 1988). When butorphanol was added
to an intravenous (IV) anaesthetic protocol with
alpha-2 adrenoceptor agonists and ketamine, duration of anaesthesia was prolonged (Matthews et al.
1991) and quality of anaesthesia was better (Corletto et al. 2005; Marntell et al. 2006).
The aim of the present study was to investigate
the effect of butorphanol in horses undergoing
elective surgery and anaesthetized with a combination of medetomidine and isoflurane. The hypothesis
was that with butorphanol, the dose of isoflurane
required for maintenance of anaesthesia would be
reduced and that cardiopulmonary function during
anaesthesia and recovery from anaesthesia would
be improved.
Material and methods
The study was performed according to the ethics
and animal experimentation by-law of the Vetsuisse
Faculty of the University of Zurich.
Sixty-one client-owned horses (>200 kg), ASA
(American Society of Anesthesiologists) category I
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Butorphanol CRI during medetomidine–isoflurane anaesthesia R Bettschart-Wolfensberger et al.
or II, which were to undergo elective surgical
procedures in which the eye was not covered, were
included in the study. Food but not water was
withheld for 10–16 hours prior to anaesthesia. The
horses were assigned randomly to one of the two
treatment groups, group MB (medetomidine and
butorphanol infusions) or group M (medetomidine
and saline control). All anaesthetic procedures were
performed always by the same experienced anaesthetist (RB) who was unaware of the treatment
group of any specific case.
At least 60 minutes before induction of anaesthesia
a 14 gauge · 160 mm jugular catheter (Secalon T
with flowswitch; Becton Dickinson AG, Switzerland)
was inserted using local anaesthesia with mepivacaine 2% (Mepivacain HCL 2%; Kantonsapotheke
Zurich, Switzerland). The horses were premedicated
60 minutes prior to anaesthesia with cefquinom
(Cobactan 4.5% ad us. vet.; Veterinaria AG, Switzerland), 1 mg kg)1 IV, flunixin (Flunixin ad us. vet.;
Biokema SA, Switzerland), 1 mg kg)1 for soft tissue
surgery or phenylbutazone (Butadion ad us. vet.;
Streuli AG, Switzerland), 4 mg kg)1 for orthopaedic
surgeries IV. Thirty minutes before anaesthesia
induction acepromazine (Prequillan; Arovet AG,
Switzerland), 0.03 mg kg)1 was administered intramuscularly (IM).
All horses were sedated in their stall with
3 lg kg)1 medetomidine (Dorbene; Dr. Graeub AG,
Switzerland) IV. Their mouth was flushed and they
were walked to the anaesthesia induction area. Five
minutes after the initial medetomidine bolus the
horses of group MB were given 25 lg kg)1 butorphanol (Alvegesic 1% forte ad us. vet.; Virbac AG,
Switzerland) IV, whereas horses of group M received
an equal volume of saline. This was followed
2 minutes later by an infusion of medetomidine at
a dose rate of 1 lg kg)1 minute)1. When sedation
was considered adequate (judged by the ‘blinded’
anaesthetist, RB) anaesthesia was induced with
ketamine (Narketan 10 ad us. vet.; Chassot AG,
Switzerland), 2.2 mg kg)1 IV in combination with
diazepam (Valium 10 mg; Roche Pharma Schweiz
AG, Switzerland), 0.02 mg kg)1 IV. Once the horses
were recumbent and the trachea intubated, they
were hoisted onto a surgical table and immediately
attached to a large animal circle system (LAVC2000; JD Medical distributing Co., Inc, AZ, USA).
Intermittent positive pressure ventilation (IPPV) was
commenced (Bird Mark 8; Medical solution, Switzerland) to maintain an end-tidal partial pressure of CO2
(PE¢CO2) of 6–7.3 kPa (45–55 mmHg). The initial
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fraction of inspired oxygen (FiO2) was 0.45–0.55.
When arterial oxygen tension (PaO2) dropped below
10.7 kPa (80 mmHg) FiO2 was increased to 0.9–1.
Anaesthesia was maintained with isoflurane (Isoflo
ad us. vet.; Dr. Graeub AG, Switzerland) in oxygen
and air to maintain a light but adequate plane of
anaesthesia, as judged by the experienced anaesthetist (RB). A brisk palpebral reflex and/or sporadic
spontaneous blinking was considered normal. If the
horses developed nystagmus or were breathing
against the ventilator, ketamine was administered
at a dose of 0.05–0.1 mg kg)1 IV. If the horses
moved, thiopental (Pentothal; Abbott AG, Switzerland) was administered at a dose of 0.5–1 mg kg)1
IV. Isoflurane concentration was increased following
ketamine or thiopental administration.
Immediately following anaesthesia induction all
horses were given a CRI of medetomidine 3.5 lg
kg)1 hour)1. Additionally, Group MB received a CRI
of butorphanol at 25 lg kg)1 hour)1 and group M
an equal volume of saline. Drug and saline placebo
infusions were administered by an automatic syringe
driver (Phoenix D; Schoch Electronics AG, Switzerland) and other fluids by an infusion pump (Volumed;
Arcomed AG, Switzerland). Lactated Ringer’s solution (Ringer-Lactat-Lösung; Fresenius Kabi AG,
Switzerland) was administered IV for the duration
of anaesthesia at an infusion rate of 5 mL kg)1
hour)1. Dobutamine (Dobutrex; Eli Lilly S.A.,
Switzerland) infusion was started after anaesthesia
induction at a rate of 0.63 lg kg)1 minute)1, and
consequently, infusion rates were adjusted to maintain mean arterial blood pressure (MAP) between 70
and 90 mmHg. Maximal infusion rate of dobutamine
was 1.25 lg kg)1 minute)1. If MAP remained
<70 mmHg after 1.25 lg kg)1 minute)1 dobutamine had been infused for 10 minutes, the infusion
rate of lactated Ringer’s solution was increased to
10 mL kg)1 hour)1. If MAP remained <70 mmHg
for a further 20 minutes, an infusion of hetastarch (HAES-steril 10%; Fresenius Pharma Schweiz
AG, Switzerland), 2–10 mL kg)1 hour)1 was commenced.
A urinary catheter was placed in all horses
immediately following anaesthesia induction and
was left in place until the horse had recovered from
anaesthesia.
Cardiopulmonary function was measured using a
multiparameter monitor (Datex-Ohmeda Cardiocap/
5; Anandic AVL, Switzerland). Electrocardiogram
(ECG), systolic (SAP), diastolic (SAP) and mean
intra-arterial blood pressures were measured and
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Butorphanol CRI during medetomidine–isoflurane anaesthesia R Bettschart-Wolfensberger et al.
pulse-oximetry was performed continuously. Arterial blood pressures were measured via a 22-gauge
catheter (Suflo IV Catheter 22G · 1¢¢; Terumo,
Medical Solution Gmbh, Switzerland) inserted into
the facial artery. The zero reference point was
determined from the level of the manubrium sternae.
Respiratory frequency (fR) and inspiratory and expiratory concentrations of isoflurane (Fi¢Iso, FE¢Iso),
carbon dioxide and O2 were measured continuously
using side-stream spirometry (Cardiocap). The following parameters were recorded at five minute
intervals: heart rate (HR), fR, arterial blood pressures,
haemoglobin saturation, FiO2, PE¢CO2, FE¢Iso, eye
reflexes, infusion rate of dobutamine, administered
drugs and infusion rates. Arterial blood gases and pH
were measured 10 minutes following induction of
anaesthesia and every 30 minutes thereafter. For
blood gas analyses, blood was withdrawn anaerobically from the arterial catheter and analysed immediately by a portable analyser (i-STAT Analyser;
Axon Lab AG, Switzerland).
Fifteen to 20 minutes before the end of anaesthesia
morphine (Morphin HCl 10 mg; Sintetica SA, Switzerland), 0.1 mg kg)1 was administered IM. At the
end of surgery the horses were disconnected from the
rebreathing circuit and, at the same time, CRIs were
stopped. For recovery all horses were sedated with
medetomidine, 2 lg kg)1 IV. During the recovery
phase inspired air was supplemented with O2
(15 L minute)1), which was administered via the
endotracheal tube or, following extubation, via a
small tube in the nasal cavity. Horses’ tracheas were
extubated when the return of the swallowing reflex
was noted or if the horse tried to get up before this
point was reached. Before extubation each horse
received 10 mL phenylephrine 0.15% (Phenylephrini hydrochloridum 1.5 mg mL)1; G.Streuli &
Co. AG, Switzerland) into the nares. The horse’s nose
was manually raised from the floor and the phenylephrineinstilledintotheventralmeatusofthenasalcavity.
Horses were allowed to recover from anaesthesia
without assistance. Horses that were not standing
60 minutes after disconnection were stimulated by
voice. The recoveries from anaesthesia were scored
and timed by the same investigating anaesthetist
(RB). The quality of recovery was graded on a scale
of five points (Table 1) with a score of 1 representing the best recovery. Recovery timing consisted of
recording time from disconnection of the anaesthetic to extubation, duration of lateral recumbency, time to sternal recumbency, duration of
sternal recumbency and the time to standing.
Table 1 Scoring system used to assess recovery from
anaesthesia
Score
awarded
1
2
3
4
5
Description of recovery
Horse capable to stand at the first attempt,
minimal ataxia
Two attempts needed before standing
More than 2 attempts needed before
standing, horse remains calm, minimal
ataxia when standing
Horse becomes excited during recovery,
danger of injury
Recovery resulting in injury of the horse
Statistical analyses
These were performed using the software package
SigmaStat 3.5 (Systat Software GmbH, Germany).
Normality was checked by plotting data as histograms and by using a Kolomogrov–Smirnov test.
Differences between groups were tested using an
independent t-test (normally distributed data) or a
Mann–Whitney Rank Sum test (non-normally distributed data). Repeatedly measured parameters
were analysed using a two-way repeated-measures
analysis of variance (ANOVA) for differences over time
and between treatments. All pairwise multiple
comparison procedures were performed by the
Tukey post hoc test. Data from the first two hours of
anaesthesia were included in the 2-way ANOVA.
Significance was considered when p < 0.05.
Results
Data are presented as mean ± SD or median and
range. Group MB consisted of 31 horses and group
M of 30 horses. There were no differences between
the groups concerning weight (MB: 509 ± 88 kg,
M: 493 ± 101 kg), age (MB: 7.8 ± 5.01 years, M:
7.7 ± 5.09 years), and duration of anaesthesia
(MB: 115, 55–230 minutes, M: 104, 66–204 minutes). Types of surgery in both groups were: three
and six minor orthopaedic surgeries (arthroscopy of
one joint, splint bone removal), 16 and 17 major
orthopaedic surgeries (arthroscopy of several joints,
bilateral neurectomy, arthroscopy including tourniquet) and 12 and 7 soft tissue surgeries in MB and
M, respectively.
Median dose of medetomidine necessary for sedation prior to anaesthesia induction was 7 lg kg)1 in
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Butorphanol CRI during medetomidine–isoflurane anaesthesia R Bettschart-Wolfensberger et al.
160
Group M
Group MB
140
MAP (mmHg)
120
*
*
100
80
60
40
20
0
30
40
50
60
70
80
90
100
110
120
Time (minutes)
Figure 1 Mean arterial blood pressures (MAP) (mean ± SD) in horses during medetomidine–butorphanol–isoflurane (MB)
or medetomidine–isoflurane (M) anaesthesia. Both groups received a constant rate infusion (CRI) of medetomidine
(3.5 lg kg)1 hour)1). Group MB also received a CRI of butorphanol (25 lg kg)1 hour)1); group M an equal volume of
saline. Timepoints with identical symbols (*) differ significantly (p < 0.05) within groups for both groups.
both groups (ranges MB: 5–11.8 lg kg)1, M: 5–
8 lg kg)1). Four horses of group MB and two horses
of group M needed a bolus of thiopental following
induction of anaesthesia as they were swallowing,
thus preventing endotracheal intubation.
There were no differences between the groups in
mean FE¢Iso concentrations (MB: 1.06 ± 0.11%, M:
1.05 ± 0.1%) or any of the measured cardiopulmonary parameters: MAP (MB: 88 ± 9, M: 87 ±
7 mmHg), HR (MB: 33 ± 6, M: 35 ± 8 beats minute)1), pH (MB: 7.37 ± 0.03, M: 7.38 ± 0.03),
PaO2 (MB: 19.2 ± 6.6, M: 18.2 ± 6.6 kPa), PaCO2
(MB: 6.9 ± 0.6, M: 6.7 ± 0.7 kPa).
In Figs 1–4 HR, MAP, PaO2 and PaCO2 over time
are presented graphically. Within groups, there were
significant changes in HR, MAP, PaCO2 and PaO2
over time, but no differences between the groups.
From minutes 30 to 70 and minutes 70 to 100 HR
rose significantly in both groups. MAPs were significantly lower 110 minutes following anaesthesia
induction compared to MAPs at 30 minutes. PaO2
was significantly lower 60 minutes following
anaesthesia induction in comparison to values at
30 minutes. There was no difference between the
groups in the median (range) dobutamine infusion
rate [MB: 0.55 (0.28–1.17) lg kg)1 minute)1, M:
0.55 (0.3–1.36) lg kg)1 minute)1] or the amount of
lactated Ringer’s solution [MB: 8.8 (3.7–15.1)
mL kg)1 hour)1, M: 8.7 (5.8–24.2) mL kg)1 hour)1]
infused. A total of 11 horses, all in dorsal recumbency
190
(four in MB and seven in M) were given hetastarch (MB 1.5 ± 0.9 mL kg)1 hour)1, M: 1.5 ± 0.6
mL kg)1 hour)1). In group MB, seven horses were
given ketamine on 11 occasions and in group M nine
horses on 16 occasions. In group MB one horse
received thiopental during anaesthesia.
Recovery times are listed in Table 2. Time to
extubation was significantly longer in group MB. All
other times relating to recovery did not differ
between groups. Recovery scores are represented
graphically in Fig. 5. There was no difference in
recovery scores between the groups.
Discussion
The present study tested whether the addition of
butorphanol to medetomidine–isoflurane anaesthesia in horses reduced isoflurane requirements
and influenced cardiopulmonary function and
recovery characteristics. Butorphanol did not cause
any differences in cardiopulmonary function,
requirement of isoflurane to maintain anaesthesia
or recovery times and quality. However, the time to
swallowing and extubation during the recovery
phase was significantly longer in the butorphanol
group.
It is commonly agreed that in conscious horses
the use of butorphanol improves the reliability of
alpha-2 adrenoceptor agonist induced sedation at
dose rates lower than those originally recommended
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2011 Association of Veterinary Anaesthetists and the American College of Veterinary Anesthesiologists, 38, 186–194
Butorphanol CRI during medetomidine–isoflurane anaesthesia R Bettschart-Wolfensberger et al.
80
Group M
Group MB
70
Beats minute–1
60
50
*
*
40
30
20
10
0
30
40
50
60
70
80
90
100
110
120
Time (minutes)
Figure 2 Heart rates (mean ± SD) in horses during medetomidine–butorphanol–isoflurane (MB) or medetomidine–
isoflurane (M) anaesthesia. Timepoints with identical symbols (* and ) differ significantly (p < 0.05) within groups for
both groups. For dose regimens see Fig. 1.
30
*
Group M
*
Group MB
PaO2 (kPa)
25
20
15
10
5
30
60
90
120
Time (minutes)
Figure 3 Arterial PO2 tensions (mean ± SD) in horses during medetomidine–butorphanol–isoflurane (MB) or medetomidine–isoflurane (M) anaesthesia. Timepoints with identical symbols (*) differ significantly (p < 0.05) within groups for both
groups. For dose regimens see Fig. 1.
for sole use (Clarke & Paton 1988; Clarke et al.
1991). In the present study the use of butorphanol
did not reduce the dose of medetomidine necessary
to achieve sedation considered profound enough for
anaesthesia induction with ketamine. The horses
were not stimulated and sedation was not scored in
detail before anaesthesia induction in order not to
unnecessarily prolong this phase. Two recent stud-
ies (Ringer et al. 2009; Ringer et al. 2011) investigated, whether butorphanol reduces the dose of
xylazine or romifidine necessary to maintain sedation in unstimulated horses (judged only by the
position of the head) and came to the same
conclusion. The use of butorphanol in combination
with alpha-2 adrenoceptor agonists might alter
reliability of but not apparent depth of sedation.
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Butorphanol CRI during medetomidine–isoflurane anaesthesia R Bettschart-Wolfensberger et al.
10
Group M
Group MB
PaCO2 (kPa)
9
8
7
6
5
4
30
60
90
120
Time (minutes)
Figure 4 Arterial PCO2 (mean ± SD) tensions in horses during medetomidine–butorphanol–isoflurane (MB) or medetomidine–isoflurane (M) anaesthesia. The increase over time within both groups was significant (p < 0.05). For dose regimens,
see Fig. 1.
Time (minutes) to
extubation (horse
swallowing or trying
to stand up)
Duration of lateral
recumbency (minutes)
Duration of sternal
recumbency (minutes)
Time to standing,
unassisted (minutes)
Group MB
Group M
26.9 ± 10.9
20.4 ± 9.4
Group MB
Group M
15
10
5
0
1
2
3
4
5
Score
44.6 ± 11.0
6.0 (0.0–40.0)
54.6 ± 16.0
46.2 ± 12.9
1.8 (0.0–24.0)
51.2 ± 13.4
Sedation before induction of anaesthesia with
ketamine has to be sufficiently profound in order to
optimise the quality of this induction. All horses in
the present study showed deep sedation before
ketamine administration and therefore it is surprising that four horses in the MB and two in the M
groups required thiopental after recumbency in
order to enable endotracheal intubation. It is
unlikely that butorphanol influenced this, although
one study reported that the combination of romifidine with butorphanol resulted in very poor anaesthesia induction quality in two out of six horses
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20
Number of horses
Table 2 Mean (± SD) or median (range) recovery times
(minutes) from disconnection of isoflurane recorded
following combination anaesthesia with medetomidine–
butorphanol–isoflurane (Group MB n = 31) or medetomidine–isoflurane (Group M, n = 30). For dose regimens, see
Fig. 1
Figure 5 Recovery scores in horses following medetomidine–butorphanol–isoflurane (MB) or medetomidine–
isoflurane (M) anaesthesia. For dose regimens, see Fig. 1.
(Marntell & Nyman 1996). However, a larger field
study in 54 ponies was not able to show any effect
of butorphanol on the quality of anaesthesia induction (Corletto et al. 2005). Garcia Lascurain et al.
(2006) demonstrated that different dose rates of
butorphanol had the same effect on anaesthesia
induction in horses so it is unlikely that a different
dose of butorphanol in the present study would
have influenced the results.
In dogs, 0.4 mg kg)1 IV butorphanol decreased
MAC by 20% (Ko et al. 2000) and 0.2 mg kg)1 IM
butorphanol prevented a positive reaction to tail
clamping during isoflurane anaesthesia for an
average duration of 1.5 hours (Grimm et al.
2000). This effect was markedly prolonged to
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5.6 hours when butorphanol was combined with
5 lg kg)1 medetomidine (Grimm et al. 2000).
Amongst equine anaesthesia experts there is no
doubt that opioids act as analgesics in horses.
Nevertheless their usefulness in combination with
inhalation anaesthesia is under debate. Under
experimental conditions MAC of inhalants is not
reduced consistently (Matthews & Lindsay 1990;
Steffey et al. 2003). In these studies some horses
showed a decrease in MAC, others an increase and
the remainders no effect at all. One study (Thomasy
et al. 2006) showed that a relatively high dose of
fentanyl did significantly reduce MAC of isoflurane,
but when this study was repeated using the dose
previously found effective, (Knych et al. 2009),
reductions in MAC were no longer significant; nor
were they consistent at even higher doses. Additionally, following these high doses of fentanyl, very
poor quality recoveries were observed in some
horses. Clinical studies that have investigated the
use of opioids during inhalation anaesthesia are
either of retrospective nature (Hofmeister et al.
2008) or were performed in a very small number
of horses (Clark et al. 2005). Nevertheless, both
studies provide some evidence that the intraoperative use of opioids during inhalation anaesthesia in
horses is beneficial. Hofmeister et al. (2008) showed
that following the administration of butorphanol to
horses under isoflurane anaesthesia, the sympathetic response to surgical stimulation was reduced;
he considered this to be a sign of a deeper plane of
anaesthesia. In Clark et al.’s study (2005), the
horses that received a morphine bolus followed by a
morphine CRI during anaesthesia needed fewer
additional anaesthetic drugs to maintain a stable
plane of anaesthesia and prevent horses from
purposeful movements during surgery. The combination of alpha-2 adrenoceptor agonists and opioids
during inhalation anaesthesia has been previously
investigated under experimental conditions (Bennett et al. 2004). These authors demonstrated that
a bolus dose of xylazine decreased the MAC of
halothane but the addition of morphine did not
result in a further reduction. In our current study
the addition of butorphanol to medetomidine did not
result in a further reduction of isoflurane requirements when compared to medetomidine alone.
However, cardiopulmonary function was not
depressed by adding butorphanol.
Butorphanol is a very potent antitussive (Westermann et al. 2005) and it is possible that this
property led to a later reoccurrence of swallowing
reflexes. This might be advantageous in cases of
laryngeal surgery or in cases where horses need to
be recovered with the trachea intubated.
In conclusion, the addition of butorphanol to
medetomidine sedation and to a medetomidine CRI
in isoflurane anaesthetized horses did not show any
significant effects on isoflurane requirements, cardiopulmonary function, recovery times or recovery
quality. The only parameter which was influenced
was time to extubation following anaesthesia which
was longer in the butorphanol group.
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2011 The Authors. Veterinary Anaesthesia and Analgesia
2011 Association of Veterinary Anaesthetists and the American College of Veterinary Anesthesiologists, 38, 186–194