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Anaesthesia Mythbusters!
The VetEducation Online Veterinary Conference 2011
The Veteducation International Online Veterinary
Conference 2011
Part of the Veteducation Live Online Web-Seminar Series
“Anaesthetic Mythbusters!”
With Dr Roz Machon
BVSc (Hons) MVSc MS MANZCVSc Dipl. ACVA
New Zealand
August 2011
Vet Education is proudly supported by
© Dr. Roz Machon 2011 – Distributed with Permission by Veterinary Education Australia
Anaesthesia Mythbusters!
The VetEducation Online Veterinary Conference 2011
ANAESTHETIC “MYTHBUSTERS”
Small Animal Anaesthetic Myths: Fact or Fiction?
Roz Machon BVSc (Hons), MVSc, MS, MANZCVS, DACVA
Introduction
Anaesthesia textbooks often state acepromazine is contraindicated in patients with a history of seizures, and many of us
were taught not to administer this agent to Boxer dogs. Likewise, many veterinarians would consider the maintenance
period the time of greatest risk for anaesthetic-related death. But are you sure? What evidence is there to support – or
refute – these statements? Are they fact or fiction? This seminar will attempt to provide some perspective on these and
other current anaesthetic “beliefs” by means of an evidence-based literature review. The inspiration for this seminar
stems directly from the excellent paper – “Myths and Misconceptions in Small Animal Anesthesia” – published by Dr’s
Wagner, Wright and Hellyer in 2003.1. While this publication debunked many interesting anaesthetic “folktales”,
advances in clinical practice and the widespread use of the Internet (both as a means of disseminating and obtaining
information), has lead to the development of new beliefs that also warrant critique. Likewise, publication of new, peerreviewed information justifies re-visiting one or two of the “myths and misconceptions” previously reviewed by Wagner
et al.
Evidence based medicine (EBM – also known as evidence based practice) is a term coined to describe a process whereby
practitioners aim to apply the best available scientific evidence to clinical decision-making. In essence, EBM is a process
of systematically reviewing, appraising and employing clinically relevant research as an adjunct to optimal patient care.
This process seeks to assess the strength or validity of the available evidence – which may range from high powered
meta-analyses and systematic reviews of large, prospective, double-blinded, placebo-controlled clinical trials, through to
conventional “wisdom” or views posted on the Internet – and combine this with the clinician’s personal clinical acumen
to best manage a given patient.2, 3. In an ideal world, treatment decisions would be based on the evidence gleaned from
large scale, peer-reviewed meta-analyses of high quality clinical trials investigating specific aspects of small animal
anaesthetic management, with evidence from “weaker” studies rejected. In reality, the veterinary literature contains a
relative paucity of such material – the vast majority of small animal anaesthetic studies are performed in controlled
research environments using healthy, often purpose-bred, dogs or cats. Study design and methodology often vary,
making comparisons between experimental trials difficult. Investigations performed in dogs may not be repeated in cats:
results may be conflicting and do not necessarily translate across species.4, 5. For these reasons, “real world” decisions
must often be based on “best level” information – such as that gleaned from textbooks, review articles, conference
proceedings, web-based information systems (e.g. VIN), the advice of colleagues, or our own personal experience –
understanding that “best level” may fall well short of high quality, rigorously critiqued evidence. 4.
References
1.
Wagner AE, Wright BD and Hellyer PW. Myths and Misconceptions in Small Animal Anesthesia. Journal of the American
Veterinary Medical Association 223(10): 1426-1432, 2003
2.
Sackett D. What is EBM? http://www.cebm.net
3.
Emergency Dept, Manchester Royal Infirmary. BestBETS (Best Evidence Topics). http://www.bestbets.org
4.
Muir W. Trauma: non est vivere sed valere vita est (life is more than staying alive). Editorial. J Vet Emerg Crit Care 16(4): 251252, 2006.
5.
Foex BA, Dark P and Rees Davies R. Commentary: Fluid replacement via the rectum for treatment of hypovolaemic shock in an
animal model. Emerg Med J 24: 3-4, 2007.
© Dr. Roz Machon 2011 – Distributed with Permission by Veterinary Education Australia
Anaesthesia Mythbusters!
The VetEducation Online Veterinary Conference 2011
BELIEF No. 1:
The maintenance phase is the time of greatest risk for anaesthetic-related death in cats and dogs: Fact
or fiction?
Relatively few studies examine this statement. Until recently, most of our knowledge of small animal anaesthetic-related
mortality came from a 20-plus year-old British study published by Clarke and Hall in 1990.1. These investigators
conducted a survey of 53 veterinary practices in which nearly 42,000 animals were anaesthetized over a two-year period
in the mid-1980’s. In this study, the majority of anaesthetic-related deaths (55% of deaths in dogs and 39% of those in
cats) occurred during the maintenance phase of anaesthesia. A similar – although much smaller – survey of private
veterinary hospitals in Ontario, Canada, reported similar findings, with the majority of anaesthetic-related deaths
occurring intraoperatively.2. But is this still the case? Is the maintenance phase still the period of greatest risk?
A number of recently published studies collectively form the Confidential Enquiry into Perioperative Small Animal
Fatalities (CEPSAF) – a large scale, multi-centre cohort investigation evaluating the risks of anaesthetic and sedationrelated mortality in small animals.3-7. One hundred and seventeen private, referral, and university teaching practices in
the United Kingdom collected data from more than 98,000 dogs and 79,000 cats over a two-year period from 2002 to
2004. Anaesthetic and sedation-related death was defined as “perioperative death within 48 hours of termination of
the procedure, except where death was due solely to inoperable surgical or pre-existing medical conditions (i.e.
anaesthesia and sedation could not reasonably be excluded from contributing to death).”6. Compared to the previous
studies, CEPSAF revealed a clear shift in the timing of anaesthetic death with more than 50% of all deaths (47% of
deaths in dogs and 61% of deaths in cats) occurring during the recovery phase – often within the first three hours.
Although difficult to pinpoint a definitive cause of death in every case, many of the postoperative deaths were thought
to be due to respiratory or cardiovascular complications, often occurring during periods when patients were unobserved.
The last 20 years has seen the introduction of new anaesthetic agents and techniques, and – perhaps more importantly –
employment of trained veterinary nurses/technicians and the use of advanced monitoring devices such as non-invasive
blood pressure (NIBP) monitors and pulse oximetry, which tend to reduce the risks of intraoperative death. 4.
Improvements in one area of practice invariably highlight deficiencies in another. Although CEPSAF showed a notable
reduction in the overall mortality rate compared to the Clarke and Hall study, the timing of death has now moved to the
recovery period. These findings clearly identify the recovery period as the time of greatest risk for anaesthetized cats and
dogs, and highlight the importance of continued, vigilant monitoring and support during this phase of anaesthesia.
References
1.
Clarke KW and Hall LW. A survey of anaesthesia in small animal practice. AVA/BSAVA report. Journal of Veterinary
Anaesthesia 17: 4-10, 1990.
2.
Dyson DH, Maxie MG and Schnurr D. Morbidity and mortality associated with anesthetic management in small animal
veterinary practice in Ontario. Journal of the American Animal Hospital Association 34: 325-335, 1998.
3.
Brodbelt DC, Hammond RA, Tuminaro D et al. Risk factors for anaesthetic-related death in referred dogs. Veterinary Record
158: 563-564, 2006.
4.
Brodbelt DC, Pfeifer DU, Young L, and Wood JLN. Risk factors for anaesthetic-related death in cats: results from the
confidential enquiry into perioperative small animal fatalities (CEPSAF). British Journal of Anaesthesia 99: 617-623, 2007.
5.
Brodbelt DC, Pfeifer DU, Young L, and Wood JLN. Results of the confidential enquiry into perioperative small animal fatalities
regarding risk factors for anesthetic-related death in dogs. Journal of the American Veterinary Medical Association 233(7):
1096-1004, 2008.
6.
Brodbelt DC. Perioperative mortality in small animal anaesthesia. The Veterinary Journal, 2008.
7.
Brodbelt DC, Blissitt KJ, and Hammond RA et al. The risk of death: the confidential enquiry into perioperative small animal
fatalities (CEPSAF). Veterinary Anaesthesia and Analgesia, 35(5): 365-373, 2008.
© Dr. Roz Machon 2011 – Distributed with Permission by Veterinary Education Australia
Anaesthesia Mythbusters!
The VetEducation Online Veterinary Conference 2011
BELIEF No. 2:
Low doses of potent alpha2-agonists such as medetomidine produce minimal cardiovascular effects:
Fact or fiction?
Common sense suggests that as the side effects of anaesthetic agents are typically dose-dependent in nature, low doses
of potent alpha2-agonists such as medetomidine should result in minimal cardiovascular effects. But is this the case?
Can low dose medetomidine be used in patients who may be intolerant of the cardiovascular effects typical of
“standard” doses? This question was also addressed by Wagner et al1; however, increasing use of this agent and a
growing body of scientific literature addressing the cardiopulmonary effects of medetomidine justify re-visiting this issue.
The alpha2-agonist medetomidine is an equal mixture of two optical enantiomers: - dexmedetomidine and
levomedetomidine – the latter of which is considered to be pharmacologically inactive. Package insert doses vary
somewhat from country to country but are generally in the range of 10-80 micrograms/kg in dogs (with higher doses
recommended in smaller- compared to larger dogs) and 50-150 micrograms/kg in cats, with the lower end of the dose
ranges recommended when the agent is used as a premedicant. However, use of “micro-doses” of medetomidine (e.g.
1-10 micrograms/kg) has become increasingly popular. The haemodynamic effects of medetomidine in dogs have been
reviewed extensively in both the veterinary and human literature (because the dog is a common model for cardiac
research).2, 3. In contrast, there are comparatively few studies investigating the cardiovascular effects of this agent in
cats.4-6. The cardiovascular effects of the alpha2-agonists are often described as “potent”, and include a biphasic arterial
blood pressure response with decreases in heart rate and cardiac output, increases in systemic vascular resistance and
central venous pressure, and varying effects on cardiac rhythm. Studies in both dogs and cats show clinically
recommended doses of medetomidine produce these typical “alpha2-agonist” effects, although blood pressure
responses are variable (hypotension has not been reported in dogs) and it does not appear to be as arrhythmogenic as
other members of this class. But are these effects dose-dependent?
A single, small, research-based study specifically addresses this question – at least in dogs.7. Medetomidine was
administered to 25 conscious dogs at doses of 1, 2, 5, 10 and 20 micrograms/kg IV, and the haemodynamic effects
assessed. Significant haemodynamic changes (including marked reductions in heart rate and cardiac output) were noted
with all doses studied. Although the changes were slightly less severe with the two lowest doses studied, near maximal
changes were seen with doses as low as 5 micrograms/kg: increasing the dose above this increased the duration of these
effects but did little to affect their severity. The authors concluded that “a reduction of the recommended dose of up to
six times does not significantly influence the degree of cardiovascular effects and will not reduce the undesirable effects”
of medetomidine.7. These findings are supported by the results of a more recent study, investigating the haemodynamic
effects of medetomidine constant rate infusions (CRIs) in dogs. 8. The haemodynamic effects of medetomidine at doses
of 1, 2 or 3 micrograms/kg/hr were evaluated over a 60-min period in six conscious, instrumented dogs, in this small,
placebo-controlled trial. Clinically significant increases in systemic vascular resistance and decreases in heart rate and
cardiac output were detected with all doses. Although the changes trended towards a dose-dependent relationship,
dose-dependency was not demonstrated statistically.
Our best level evidence suggests that (1) the cardiovascular effects of medetomidine are not dose dependent, and (2)
that small doses may produce clinically significant changes in haemodynamic function. While these changes may be well
© Dr. Roz Machon 2011 – Distributed with Permission by Veterinary Education Australia
Anaesthesia Mythbusters!
The VetEducation Online Veterinary Conference 2011
tolerated in healthy individuals, medetomidine should be avoided or used with extreme caution in patients with
cardiovascular compromise or instability – even when employed in small doses.
References
1.
Wagner AE, Wright BD and Hellyer PW. Myths and Misconceptions in Small Animal Anesthesia. Journal of the American
Veterinary Medical Association 223(10): 1426-1432, 2003
2.
Murrell JC and Hellebrekers LJ. Medetomidine and dexmedetomidine: a review of cardiovascular effects and antinociceptive
properties in the dog. Veterinary Anaesthesia and Analgesia 32(3): 117-127, 2005.
3.
Cullen LK. Medetomidine sedation in dogs and cats: review of its pharmacology, antagonism and dose. British Veterinary
journal 152: 519-535, 1996.
4.
Lamont LA, Bulmer BJ and Sisson et al. Doppler echocardiographic effects of medetomidine on dynamic left ventricular
outflow obstruction in cats. J Am Vet Med Assoc 221(9): 1276-1281, 2002.
5.
Lamont LA, Bulmer BJ and Grimm KA et al. Cardiopulmonary evaluation of the use of medetomidine hydrochloride in cats.
Am J Vet Res 62(11): 1745-1763, 2001.
6.
Golden AL, Bright JM, and Daniel GB et al. Cardiovascular effects of the alpha -adrenergic receptor agonist medetomidine in
clinically normal cats anesthetized with isoflurane. Am J Vet Res 59: 509-513, 1998.
7.
Pypendop BH and Verstegen JP. Hemodynamic effects of medetomidine in the dog: a dose titration study. Veterinary Surgery
27: 612-622, 1998.
8.
Carter JE, Campbell NB and Posner LP et al. The hemodynamic effects of medetomidine continuous rate infusions in the dog.
Veterinary Anaesthesia and Analgesia 37(3): 197-206, 2010.
2
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Anaesthesia Mythbusters!
The VetEducation Online Veterinary Conference 2011
BELIEF No. 3:
Drug choice (i.e. the selection of an appropriate anaesthetic protocol) is the major determinant of
anaesthetic outcome in cats and dogs – particularly in compromised patients: Fact or fiction?
Selection of an anaesthetic protocol/technique should be based on consideration of the following: - (1) patient factors
(e.g. species, breed, age, temperament, and relevant history and physical examination findings), (2) the procedure to be
performed (e.g. invasive versus non-invasive and minor versus major procedure, estimated duration, body site,
anticipated pain etc), (3) the available drugs, equipment and facilities, and (4) the knowledge and experience of the
individual veterinarian. In addition, a plan for a compromised patient should also consider: - (1) the physiologic
consequences of the disease or injury process, (2) the basic pharmacology of anaesthetic agents and how this may alter
in the face of disease or dysfunction, and (3) personal familiarity with the technique. 1-5. Unfortunately, we are yet to
develop the perfect anaesthetic agent: likewise, we still lack an anaesthetic agent that is perfect for all situations. There
are relative and absolute contraindications for all commonly used anaesthetic agents, and these recommendations guide
our selection of a particular agent for a particular patient. 5. Without question, selection of an appropriate anaesthetic
protocol for a given patient is important, but is it the major determinant of anaesthetic outcome?
Few anaesthetic mortality studies have been able to identify a major association between a single anaesthetic agent or
drug-class and anaesthetic-related death in cats and dogs. Studies of this nature require large numbers to provide
sufficient statistical power for analysis, and few veterinary investigations meet these requirements. In addition, a
statistical link between a given drug and mortality does not necessarily imply cause and effect, as the causes of
anaesthetic-related death are usually complex and multifactorial.6-9. None-the-less, Clarke and Hall10 (1990) identified an
association between the alpha2-agonist xylazine and increased risk of anaesthetic-related death in both dogs and cats –
an association that was also noted (in dogs, but not in cats) by Dyson et al 6 (1998). Clarke and Hall’s small animal
anaesthetic mortality study was performed in the mid-1980s. It noted an increase in mortality in dogs receiving xylazine
as a premedicant and in cats given xylazine-ketamine combinations, in comparison to other agents. Notably, the
anaesthetic-related deaths in dogs all occurred in practices in which xylazine was used infrequently, while all anaesthetic
deaths in cats receiving xylazine-ketamine combinations occurred during periods when patients were unobserved. Other
identified risk factors in dogs included halothane and thiopentone, while those in cats included induction of anaesthesia
with a volatile agent, thiopentone, ether, ketamine and nitrous oxide.
When Dyson et al6 performed their anaesthetic mortality study about ten years later the picture had changed somewhat.
Although they also detected a link between premedication with xylazine – a known arrhythmogenic agent – and
anaesthetic-related death in dogs, most deaths occurred in dogs receiving additional arrhythmogenic agents (e.g.
thiopentone and halothane) as part of their anaesthetic protocol, or in those with likely elevations in circulating
catecholamine levels (e.g. dogs that were violently struggling at the time of death). 6. This suggested that inappropriate
use of xylazine – rather than the drug per se – was a contributing factor to mortality in these patients. No other links
between a single anaesthetic agent and death in dogs were noted. In addition, Dyson et al did not find an association
between xylazine-ketamine combinations (or any of the other, previously identified agents) and anaesthetic death in cats.
In fact, this combination was reported to be “comparable in safety to other regimens”. The authors surmised that (1)
improved anaesthetic training of veterinary graduates, (2) increased familiarity with the combination and awareness of
appropriate use (e.g. restricting use to fit healthy patients only), and (3) employment of trained veterinary
nurses/technicians to better monitor anaesthetized patients (a factor associated with a significant reduction in risk), all
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contributed to the apparent improvement in outcome associated with xylazine/ketamine combinations in cats in this
study compared to that of Clarke and Hall.
The Confidential Enquiry into Perioperative Small Animal Fatalities (CEPSAF) was performed over a two-year period from
2002-2004, an additional 10 years after Dyson et al’s work.11-14. Based on the findings outlined above, the authors
hypothesized that medetomidine – a potent, highly specific alpha2-agonist – would also be associated with an increased
risk of anaesthetic death. This did not prove to be the case. No increase in odds of death was detected when this agent
was compared to other premedicants, and in fact medetomidine trended towards reduced odds of anaesthetic-related
death in both cats and dogs. The authors deduced that specific drug differences (medetomidine is markedly less
arrhythmogenic than xylazine) and improved understanding of appropriate use of this drug class had resulted in this
“change of fortune” for alpha2-agonist use. Furthermore, CEPSAF was unable to identify a clear association between
any individual induction or maintenance agent and anaesthetic-related death in cats, suggesting that factors other than
basic drug effects were now more important with respect to outcome. 11. Interestingly, increased odds of death were
detected in dogs induced with an injectable agent and maintained with halothane and in those undergoing total
inhalational anaesthesia (isoflurane or halothane), compared to those induced with an injectable agent but maintained
with isoflurane.12. This finding also suggests that the manner in which agents are employed (i.e. technique) is more
important than choice of an individual agent (within reason), as the odds for death with isoflurane “flip-flopped”
depending on how the agent was used.
Although CEPSAF was unable to identify a clear association between a single anaesthetic agent or drug class and
anaesthetic-related death, other major risk factors were identified. Factors increasing the odds of death in both dogs
and cats included: - (1) poor health status (i.e. increasing ASA grade), (2) increasing procedural urgency, (3) procedures
of increasing complexity (4) small size, (5) low body weight, and (6) elderly patients (i.e. increasing age). Increasing the
intended duration of the procedure was also identified as a major risk factor for anaesthetic-related death in dogs.
Additional risk factors for death in cats included obesity, endotracheal intubation, and the use of fluid therapy, while
simple monitoring techniques (measurement of pulse rate and use of pulse oximetry) significantly reduced the odds of
anaesthetic-related death.11, 13, 14. It seems the picture has changed again. Selection of an appropriate protocol for a
given patient is clearly important: all agents have relative contraindications and it is important to select an appropriate
protocol (including dose rates and routes of administration) for a given patient. That aside, all modern anaesthetic
agents are extremely “safe” – at least when used appropriately.5. CEPSAF provides high quality evidence to support the
view that the manner in which those drugs are used and the overall approach to patient management have now become
the critical factors in determining outcome, rather than drug choice per se (within reason).
References
1.
Ilkiw JE. Anesthesia and disease. In Anaesthesia of the Cat. Hall and Taylor (Editors), Bailliere Tindall, 1994, Ch.11, pp224248.
2.
Campbell VL. Anesthetic protocols for common emergencies. Veterinary Clinics of North America: Small Animal Practice 35:
435-453, 2005.
3.
Garrod LA, Wetmore L. Anesthetic agents in trauma patients. Comp Cont Educ 21(9): 800-811, 1999.
4.
Perkowski S. Anesthesia for the emergency small animal patient. Veterinary Clinics of North America: Small Animal Practice
30(3): 509-530, 2000.
5.
Haskins S. Comparative cardiovascular and pulmonary effects of sedatives and anesthetic agents and anesthetic drug selection
for the trauma patient. J Vet Emerg Crit Care 16(4): 300-328, 2006.
6.
Dyson DH, Maxie MG and Schnurr D. Morbidity and mortality associated with anesthetic management in small animal
veterinary practice in Ontario. Journal of the American Animal Hospital Association 34: 325-335, 1998.
7.
Evans AT. Anesthetic emergencies and accidents. In Lumb and Jones’ Veterinary Anesthesia. 3 edition. Thurmon JC, Tranquilli
WJ and Benson GJ Editors, Williams and Wilkins, Lea and Febiger, Baltimore, 1996, Ch 25, pp849-860.
rd
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8.
9.
10.
11.
12.
13.
14.
Nitti JT and Nitti GJ. Anesthetic complications. In Clinical Anesthesiology, 4 edition. Morgan, Mikhail and Murray (Editors),
Lange Medical Books, New York, 2006, Ch 46, pp 956 – 978.
Harvey RC. Anaesthetic emergencies and complications. In British Small Animal Veterinary Association (BSAVA) Manual of
Small Animal Anaesthesia and Analgesia. Seymour and Gleed (Editors), BSAVA, Shurdington, 1999, Ch 24, pp257-263.
Clarke KW and Hall LW. A survey of anaesthesia in small animal practice. AVA/BSAVA report. Journal of Veterinary
Anaesthesia 17: 4-10, 1990.
Brodbelt DC, Pfeifer DU, Young L, and Wood JLN. Risk factors for anaesthetic-related death in cats: results from the
confidential enquiry into perioperative small animal fatalities (CEPSAF). British Journal of Anaesthesia 99: 617-623, 2007.
Brodbelt DC, Pfeifer DU, Young L, and Wood JLN. Results of the confidential enquiry into perioperative small animal fatalities
regarding risk factors for anesthetic-related death in dogs. Journal of the American Veterinary Medical Association 233(7):
1096-1004, 2008.
Brodbelt DC. Perioperative mortality in small animal anaesthesia. The Veterinary Journal, 2008.
Brodbelt DC, Blissitt KJ, and Hammond RA et al. The risk of death: the confidential enquiry into perioperative small animal
fatalities (CEPSAF). Veterinary Anaesthesia and Analgesia, 35(5): 365-373, 2008.
th
© Dr. Roz Machon 2011 – Distributed with Permission by Veterinary Education Australia
Anaesthesia Mythbusters!
The VetEducation Online Veterinary Conference 2011
BELIEF No. 4:
Sevoflurane is a superior inhalant to isoflurane. It has become the inhalant of choice in human
anaesthesia and should do likewise in small animal anaesthesia, given its superiority: Fact or fiction?
Wagner et al also reviewed this topic in their “Anesthetic Myths and Misconceptions” paper. 1. At the time (2003),
sevoflurane was a relatively new agent in Australasia – few practitioners could have chosen to use this agent routinely.
However, increasing availability and the publication of a growing body of work investigating the use of sevoflurane in
small animals justify revisiting this statement.
Sevoflurane was developed in the 1960’s but was not fully evaluated and marketed at that time, and was instead
“shelved” until its “rediscovery” in the late 1980’s. Sevoflurane was first approved for human use in Japan in 1990,
where it has become the inhalant of choice in human anaesthetic practice. It was approved for veterinary use in the US
in 1999 and has been available to veterinary practitioners in Australasia for some years.2-6. Sevoflurane is a sweetsmelling, volatile agent – not dissimilar to isoflurane − that produces classical anaesthesia and is delivered via a
conventional, agent specific vaporizer.2-4. The biggest advantage of sevoflurane is it’s low blood: gas partition coefficient
(0.69 compared to 1.4 for isoflurane) i.e. the agent is very insoluble.2-4. Theoretically, this should produce faster mask
inductions, more rapid changes in depth following a change in vaporizer setting, and more rapid recoveries than those
seen with isoflurane.4, 5. Sevoflurane has become popular in human anaesthesia because: - (1) its low blood: gas partition
coefficient, pleasant smell, and lack of airway irritability help speed mask inductions (common in both adults and
children), (2) its rapid recovery allows day-case patients to be discharged from hospital quickly (a significant cost-saver in
the human health care environment), and (3) it avoids the problems of “halothane hepatitis” – relatively common in
people, but very rare in domestic species.3, 4. But do these “advantages” translate to veterinary anaesthetic practice?
Should we consider sevoflurane a superior inhalant to isoflurane? Is there evidence in the veterinary literature to support
the view that sevoflurane should become the small animal inhalant of choice?
The single greatest disadvantage of sevoflurane in veterinary anaesthetic practice is its cost – the agent is significantly
more expensive than isoflurane on a ml per ml basis. Sevoflurane is also less potent than isoflurane with a reported
minimum alveolar concentration (MAC) of 2.1-2.58% in small animals, although values as low as 1.78% have been
reported in dogs.4-8. All other factors being equal (e.g. circuit type, fresh gas flow rate etc), higher vaporizer settings are
therefore required to maintain anaesthesia with sevoflurane compared to isoflurane. This results in further expense
because a greater volume of the liquid agent (more expensive than isoflurane to begin with) will be used on a per minute
basis.
A low blood: gas partition coefficient offers several potential benefits as outlined above. As predicted, many small
animal investigations report sevoflurane mask inductions to be faster than with isoflurane, although not markedly.9, 10, 11.
A study in 8 healthy Beagles reported induction times (to a point permitting intubation) of 5.7 min and 8.6 min for
sevoflurane versus isoflurane, respectively.9. This study employed the “low-to-high” induction method (i.e. beginning
with low concentrations of inhalant (0.5 MAC) and increasing the delivered concentration by 0.5 MAC increments every
15 sec to a final concentration of 2 MAC). These findings were supported by another speed-of-induction study
performed in 6 healthy, non-premedicated Pointers, in which both agents were initially delivered at high concentrations
(approximately 3 x MAC), rather than using the “low-to-high” technique.10. Sevoflurane induced anaesthesia more
rapidly than isoflurane in this study, the induction was considered smoother, and the dogs were noted to be more
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Anaesthesia Mythbusters!
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tolerant of the mask with sevoflurane compared to isoflurane (due, perhaps, to the agent’s low pungency). However, a
prospective clinical trial of mask inductions in 71 premedicated dogs undergoing routine de-sexing, showed no
difference in speed or quality of induction when both agents were administered at maximum vaporizer settings (i.e. 8%
(3.4 MAC) and 5% (3.8 MAC) for sevoflurane and isoflurane, respectively).6. Similar findings were also noted in a small,
research study in 8 dogs using the same “maximal vaporizer setting” induction technique. 8.
Less information is available for cats. A clinical study in 28 healthy, premedicated cats presenting for routine de-sexing,
showed mask inductions to be faster with sevoflurane (time to intubation was about 4 min with sevoflurane versus
nearly 5 min with isoflurane), although the overall quality of induction was reported to be the same with both agents. 11.
In contrast, a research-based study in 42 cats premedicated with atropine and ketamine was unable to show any
difference in the speed of mask inductions between the two agents. 12. Collectively, these studies suggest that mask
inductions with sevoflurane are generally rapid, smooth and well tolerated; however, other factors in addition to
solubility – such as induction technique, the actual concentration delivered, premedication, and individual patient factors
– also influence the speed and quality of mask inductions in the clinical environment, and may off-set some of the
perceived benefits of sevoflurane over isoflurane.
Conflicting information has also appeared about the recovery properties of sevoflurane with some studies reporting
quicker, better quality recoveries in comparison to isoflurane12; others reporting abrupt, stormy recoveries in some
species and some individuals13; others reporting a better quality of recovery with sevoflurane compared to isoflurane but
no difference in speed of recovery9, 13, 14; and still others reporting no significant differences in recovery speed or quality
between the two agents15. From a clinical perspective, it would appear that both the speed and quality of recovery in
dogs and cats are generally very good following use of either agent, and that sevoflurane offers little benefit over
isoflurane in this regard despite its lower solubility.
The introduction of isoflurane was hailed as a break through due to the clear advantages it offered over halothane,
particularly in terms of its cardiovascular effects.3. Although some contradictory results appear in the literature, the
cardiopulmonary effects of sevoflurane appear very similar to those of isoflurane. 1-5. Both agents are reported to produce
dose-dependent respiratory depression due to centrally mediated actions and impaired diaphragmatic function, resulting
in reductions in respiratory rate and tidal volume with corresponding increases in PaCO 2 levels and the production of a
respiratory acidosis.1-5. However, a recent study reported the anaesthetic index of sevoflurane in dogs (3.45) to be higher
than that of isoflurane (2.61), suggesting the former produces comparatively less ventilatory depression in this species
(although both agents produce greater ventilatory depression than halothane).8. The cardiovascular effects of the two
agents are also very similar with dose-dependent reductions in ABP, cardiac output, stroke volume and systemic vascular
resistance, and increases in heart rate, reported in dogs and cats. 4, 16-18. Clinically significant reductions in ABP are
observed with both agents when delivered in concentrations  2 MAC. These reductions were noted to be larger in dogs
receiving sevoflurane compared to isoflurane at comparable MAC values in two studies 9, 10, although the opposite effect
was seen in another study in cats.16. The arrhythmogenic potential of both agents is comparably small (and markedly less
than that of halothane).2-4, 19. A recent, prospective, multi-centre clinical trial of sevoflurane as a maintenance agent in
196 ASA grade I-III dogs undergoing a variety of diagnostic and surgical procedures, reported hypotension (defined as a
MAP less than 60 mmHg) and apnoea (defined as no ventilatory effort for greater than 30-60 sec), in 46% and 12% of
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dogs, respectively: no arrhythmias were observed.5. The authors concluded that sevoflurane appeared a safe and
effective maintenance agent in clinical canine patients.
While small animals appear relatively resistant to “halothane hepatitis”, hepatic metabolic burden and potential toxicities
should also be considered when evaluating an inhalant. About 3-5% of a total administered dose of sevoflurane
undergoes hepatic metabolism. This compares to about 20-25% for halothane and 0.17% for isoflurane (i.e. the
metabolic burden on the liver is much less than that seen with halothane but significantly greater than that seen with
isoflurane).2-4. Notably, although a larger amount of sevoflurane undergoes hepatic degradation compared to isoflurane,
sevoflurane cannot be degraded to the acyl halide molecule thought to be responsible for “halothane hepatitis” in
people.3. The effects of sevoflurane on hepatic function seem very similar to those of isoflurane – at least in those
species studied to date. An experimental study investigating the effects of 60 min of inhalational anaesthesia on hepatic
function in 24 clinically normal dogs (premedicated with xylazine and induced with propofol) reported comparable results
for isoflurane and sevoflurane.20. Both agents produced small elevations in aspartate aminotransferase (AST), alanine
aminotransferase (ALT), and gamma-glutamyl transferase (GGT) serum levels immediately after, and for a period of up to
7 days, following anaesthesia. Clinical signs of hepatic disease or dysfunction were not detected in the 14-day follow-up
period. Similar results were reported for cats receiving 90 min of sevoflurane or isoflurane anaesthesia. 12. Both agents
produced mild increases in serum AST levels 24 hr after anaesthesia but these values, along with those for ALT and BUN,
did not differ significantly from baseline for the remainder of the 7-day follow-up period.
Concerns have also been raised about the nephrotoxic potential of sevoflurane. Sevoflurane-induced nephrotoxicity may
arise via one of two main mechanisms: - (1) the degradation of the agent to fluoride ions (a similar problem to that seen
with methoxyflurane), and (2) the production of Compound A – a product that arises via interaction of sevoflurane with
CO2 absorbents (e.g. soda lime), especially in the face of low-flow anaesthesia.2-5. Despite these theoretical concerns,
nephrotoxicity has not proved a clinical problem in either human- or veterinary patients receiving sevoflurane.3, 5. Part of
the reason for this may lie in the fact that nephrotoxicity appears highly species dependent – rats are very sensitive to
these toxicoses but it appears dogs are considerably less sensitive than other species, although it is harder to find data for
relative sensitivity in cats. A study investigating the production of fluoride ions in dogs undergoing sevoflurane
anaesthesia reported small serum concentrations of the ion at levels markedly less than those seen in dogs undergoing a
comparatively shorter period of methoxyflurane anaesthesia. 5, 21, 22. In similar fashion, studies in both the human and
veterinary literature have failed to show clinically significant levels of Compound A in dogs undergoing low-flow or
closed circuit anaesthesia with sevoflurane. Although Compound A was detected, the levels were well below those
known to be nephrotoxic in rats.5, 23.
While sevoflurane offers advantages over isoflurane in human anaesthesia, it appears these factors are not as relevant in
cats and dogs. Sevoflurane is undoubtedly a safe, useful and effective inhalant in cats and dogs, and may prove the
agent of choice in some individuals under some circumstances. However, current evidence does not justify the view that
this agent is “superior” to isoflurane.
References
1.
Wagner AE, Wright BD and Hellyer PW. Myths and Misconceptions in Small Animal Anesthesia. Journal of the American
Veterinary Medical Association 223(10): 1426-1432, 2003
2.
Jones RM. Desflurane and sevoflurane: inhalation anaesthetics for this decade? Br J Anaesth 65(4): 527-536, 1990.
3.
Stoelting RK and Hillier SC. Inhaled anesthetics. In Pharmacology and Physiology in Anesthetic Practice, 4 Ed, Lippincott,
Williams and Wilkins, Philadelphia, 2006. Ch 2, pp42-86.
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4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
Steffey EP. Inhalational anesthetics. In Lumb and Jones’ Veterinary Anesthesia, 3 Ed. Thurmon, Tranquilli and Benson (editors),
Williams and Wilkins, Baltimore, 1996. Ch 11, pp297-329.
Branson KR, Quandt JE and Martinez EA et al. A multi-site case report on the clinical use of sevoflurane in dogs. JAAHA 37(5):
420-432, 2001.
Pottie RG, Dart CM and Perkins NR. Speed of induction of anaesthesia in dogs administered halothane, isoflurane, sevoflurane
or propofol in a clinical setting. Aust Vet J 86(1-2): 26-31, 2008.
Doi M, Yunoki H and Ikeda K. The minimum alveolar concentration of sevoflurane in cats. Journal of Anesthesia 2: 113-114,
1988.
Galloway DS, Ko JC and Reaugh HF et al. Anesthetic indices of sevoflurane and isoflurane in unpremedicated dogs. J Am Vet
Med Assoc 225(5): 700-704, 2004.
Johnson RA, Striler E and Sawyer DC et al. Comparison of isoflurane with sevoflurane for anesthesia induction and recovery in
adult dogs. Am J Vet Res 59(4): 478-481, 1998.
Tukey JB, Thurmon JC and Olson WA et al. Clinical comparison of mask-induced sevoflurane and isoflurane anesthesia in adult
pointer dogs (Abstract) Vet Surg 25(6): 525, 1996.
Lerche P, Muir WW and Grubb TL. Mask induction of anaesthesia with isoflurane or sevoflurane in premedicated cats. J Small
Anim Pract 43(1): 12-5, 2002.
Hikasa Y, Kawanabe H and Takase K et al. Comparisons of sevoflurane, isoflurane and halothane anesthesia in spontaneously
breathing cats. Vet Surg 25(3): 23-243, 1996.
Lozano AJ, Brodbelt DC and Borer KE et al. A comparison of the duration and quality of recovery from isoflurane, sevoflurane
and desflurane anaesthesia in dogs undergoing magnetic resonance imaging. Vet Anaesthesia and Analgesia 36(3): 220-229,
2009.
Love EJ, Holt PE and Murison PJ. Recovery characteristics following maintenance of anaesthesia with sevoflurane or isoflurane
in dogs premedicated with acepromazine. Vet Rec 161: 217-221, 2007.
Polis I, Gasthuys F and Van Ham L et al. Recovery times an evaluation of clinical hemodynamic parameters of sevoflurane,
isoflurane and halothane anaesthesia in mongrel dogs. J Vet Med A Physiol Pathol Clin Med 48: 301-411, 2001.
Hikasa Y, Ohe N and Takase K et al. Cardiopulmonary effects of sevoflurane in cats: comparison with isoflurane, halothane
and enflurane. Res Vet Sci 63(3): 205-210, 1997.
Mutoh T, Nishimura R and Kim HY et al. Cardiopulmonary effects of sevoflurane, compared with halothane, enflurane and
isoflurane in dogs. Am J Vet Res 58(8): 885-890, 1997.
Pypendop BH and Ilkiw JE. Hemodynamic effects of sevoflurane in cats. Am J Vet Res 65(1): 20-25, 2004.
Imamura S and Ikeda K. Comparison of epinephrine-induced arrhythmogenic effect of sevoflurane with isoflurane and
halothane. J Anesth 1: 62-68, 1987.
Topal A, Gul N, and Ilcol Y et al. Hepatic effects of halothane, isoflurane or sevoflurane anaesthesia in dogs. J Vet Med A
Physiol Clin Med 50(1): 530-533, 2003.
Martis L, Lynch S and Napoli MD et al. Biotransformation of sevoflurane in dogs and rats. Anesth Analg 60: 186-191, 1981.
Brunson DB, Stowe CM and McGrath CJ. Serum and urine inorganic fluoride concentration and urine oxalate concentrations
following methoxyflurane anesthesia in the dog. Am J Vet Res 40: 197-203, 1979.
Muir WW and Gadawski J. Cardiorespiratory effects of low-flow and closed circuit inhalational anesthesia, using sevoflurane
delivered with an in-circuit vaporizer and concentrations of compound A. Am J Vet Res 59: 603-614, 1998.
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BELIEF No. 5:
Acepromazine is contraindicated in patients with a history of seizures and in those undergoing
potentially seizure-genic procedures (e.g. myelography). It is also contraindicated in Boxer dogs: Fact or
fiction?
Although references are usually lacking, many anaesthetic textbooks report that acepromazine lowers the seizure
threshold in vulnerable patients and caution against the use of this agent in patients at risk for seizures.1-5.
Acepromazine is classified as an aliphatic phenothiazine – a drug class used extensively as psychotropic medicants in
people.1, 2, 5, 6. Some members of this class (most notably chlorpromazine) have been shown to reduce the seizure
threshold and induce epileptic-like EEG discharge patterns in rats and other research animals including dogs. 5-7. Clinical
use of chlorpromazine has also been linked to seizure provocation in epileptic people and dogs.7. However, analyses
suggest that psychotropic medication induced seizures are influenced by many factors including the specific drug,
dosage, rate of titration of the drug, concurrent use of other drugs (particularly those altering pharmacokinetics), and the
patient’s underlying disease and seizure history: many phenothiazines do not carry the same risk as chlorpromazine. 5-6.
Phenothiazines are anti-dopaminergic agents. Dopamine is thought to act as an inhibitory neurotransmitter, and it is
postulated that blockade/inactivation of central D2 receptors may precipitate seizure activity in vulnerable individuals.
However, while the human literature acknowledges that some phenothiazines may precipitate seizures in epileptic
patients, the precise mechanism by which this occurs is still the subject of much debate.6. Interestingly, early veterinary
textbooks note the anticonvulsant properties of acepromazine, while pre-treatment with chlorpromazine has been
documented to reduce experimentally induced seizure activity in rats.2, 6.
A recent (2006) retrospective study evaluated the effects of acepromazine administered to 36 dogs with a history of
seizures.5. In addition, acepromazine was specifically given to decrease seizure activity in a further 11 dogs also included
in this study. No seizures were seen within 16 hr of acepromazine administration in any of the 36 dogs with a seizure
history; while seizure activity was abated (1.5-8 hr), or did not recur, in 9/11 dogs that were actively fitting when they
received acepromazine (although most of these dogs also received additional anti-seizure medications). A similar study
reviewed the administration of acepromazine to 31 dogs, with a history of seizures, admitted to a specialist emergency
practice.6. “Seizure” was the presenting complaint in 28/31 dogs. 22/31 dogs had a prior history of seizures, and 15 of
these were currently receiving anti-seizure medication at the time of admission. Seizures were seen in 4 of the 31 dogs,
although in one of these, the seizure occurred > 10 hr after acepromazine administration (i.e. well outside the expected
duration of action of this drug). The authors concluded that there was no clinical evidence that acepromazine is
associated with increased seizure activity in dogs presenting with seizure disorders.6.
Acepromazine has also been contraindicated in patients undergoing potentially seizure-genic procedures – most notably,
contrast myelography.8,9. This recommendation arose from anecdotal reports of post-myelographic seizures following
the use of the now outdated contrast medium metrizamide in patients who had also received acepromazine, and was
strengthened by the results of a myelographic research-based trial in Beagles in which 5/5 of dogs anaesthetized with a
protocol that included acepromazine, convulsed on recovery.10. Since that time, at least two clinically based retrospective
reviews of post-myelographic seizures have suggested there is no link between the anaesthetic agents employed and
increased seizure risk in dogs undergoing myelography.11, 12. Despite these findings, authors continued to caution against
the use of acepromazine stating that this agent increased seizure prevalence. 13. Two retrospective analyses of contrast
myelography in small animals specifically examined the proposed link between acepromazine administration and post-
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myelographic seizures in dogs.8, 9. The first study compared clinical patients receiving iohexol with those undergoing
metrizamide or iopamidol myelography.8. Acepromazine was administered as a premedicant to 68 dogs prior to
myelography, but post-myelographic seizures were not noted in any of these dogs. Similar results were documented in a
recent (2011) retrospective study of the incidence of, and risk factors for, seizures after iohexol myelography in dogs.9.
Records for 503 dogs were reviewed. Acepromazine was administered to 145 dogs, either as premedication or as
recovery medication or both. Seizures were documented in 15/503 dogs. Although six of these dogs had received
acepromazine, 139/488 dogs that did not seizure had also received this agent. Statistical analysis failed to reveal a
causative link between use of acepromazine and post-myelographic seizures.9.
Many veterinary students are also taught that acepromazine is contraindicated in Boxer dogs. Hall and Clarke4 state that
“the Boxer dog is renowned for fainting after very small doses of acepromazine given by any route”, but do not supply
references or data to support this statement. A recent Pubmed search (August 2011) failed to find any references
supporting this view. Review of the retrospective seizure studies discussed above, showed 4/36 dogs with a history of
seizures receiving acepromazine to be Boxers: no adverse effects of acepromazine administration were noted in these
animals.5. Likewise, none of the various small animal anaesthetic complication- or morbidity and mortality studies
outlined in other sections of this paper,14-21 mentions an association between acepromazine and any anaesthetic-related
complication in Boxers – including Clarke and Hall’s own survey from the 1980’s.14.
References
1.
Thurmon JC, Tranquilli WJ and Benson GJ. Preanesthetics and adjuncts. In Lumb and Jones’ Veterinary Anesthesia, 3 Ed.
Thurmon, Tranquilli and Benson (editors), Williams and Wilkins, Baltimore, 1996. Ch 8, pp183-209.
2.
Lukasik V. Premedication and sedation. In British Small Animal Veterinary Association (BSAVA) Manual of Small Animal
Anaesthesia and Analgesia. Seymour and Gleed (Editors), BSAVA, Shurdington, 1999, Ch 7 pp71-86.
3.
Paddleford RR. Pre-anesthetic agents. In manual of small animal anesthesia. Paddleford (editor), WB Saunders, Philadelphia,
1999, pp15-17
4.
Hall LW and Clarke KW. Principles of sedation, analgesia and premedication. In Veterinary Anaesthesia 9 Ed, Hall and Clarke
(editors), Bailliere Tindall, London, 1991, Ch 4 pp51-79.
5.
Tobias KM, Marioni-Henry K and Wagner R. A retrospective study on the use of acepromazine maleate in dogs with seizures. J
Am Anim Hosp Assoc 42(4): 283-289, 2006.
6.
McConnell J, Kirby R and Rudloff E. Administration of acepromazine maleate to 31 dogs with a history of seizures. J Vet
Emerg Crit Care 17(3): 262-267, 2007.
7.
Redman HC, Wilson GL and Hogan JE. The effect of Chlorpromazine combined with intermittent light stimulation on the
electroencephalogram and clinical response of the beagle dog. Am J Vet Res 34: 929-936, 1973.
8.
Wheeler SJ and Davis JV. Iohexol myelography in the dog and cat: a series of one hundred cases, and a comparison with
metrizamide and iopamidol. J Small Anim Pract 26: 247-256, 1985.
9.
da Costa RC, Parent JM and Dobson H. Incidence and risk factors for seizures after myelography performed with iohexol in
dogs: 503 cases (2002-2004). J Am Vet Med Assoc 238(10): 1269-1300, 2011.
10.
Bartels JE, Braund KG and Redding RW. An experimental evaluation of a non-ionic agent Amipaque (Metrizamide) as a
neuroradiographic medium in the dog. J Am Vet Rad Soc 18(4): 117-123, 1977.
11.
Gray PR, Indrieri RJ and Lippert AC. Influence of anesthetic regimen on the frequency of seizures after cervical myelography in
the dog. J Am Vet Med Assoc 190(5): 527-530, 1987.
12.
Lewis DD and Hosgood G. Complications associated with the use of iohexol for myelography of the cervical vertebral column
in dogs: 66 cases (1988-1990). J Am Vet Med Assoc 200(9): 1381-1384, 1992.
13.
Barone G, Ziemer LS and Shofer FS et al. Risk factors associated with development of seizures after use of iohexol myelography
in dogs: 182 cases (1998). J Am Vet Med Assoc 220(10): 1499-1502, 2002.
14.
Clarke KW and Hall LW. A survey of anaesthesia in small animal practice. AVA/BSAVA report. Journal of Veterinary
Anaesthesia 17: 4-10, 1990.
15.
Dyson DH, Maxie MG and Schnurr D. Morbidity and mortality associated with anesthetic management in small animal
veterinary practice in Ontario. Journal of the American Animal Hospital Association 34: 325-335, 1998.
16.
Gaynor JS, Dunlop CI and Wagner AE et al. Complications and mortality associated with anesthesia in dogs and cats. JAAHA,
35: 13-17, 1999.
17.
Redondo JI, Rubio M and Soler G et al. Normal values and incidence of cardiorespiratory complications in dogs during general
anaesthesia. A review of 1281 cases. J Vet Med A 54: 470-477, 2007.
18.
Brodbelt DC, Hammond RA, Tuminaro D et al. Risk factors for anaesthetic-related death in referred dogs. Veterinary Record
158: 563-564, 2006.
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19.
20.
21.
Brodbelt DC, Pfeifer DU, Young L, and Wood JLN. Results of the confidential enquiry into perioperative small animal fatalities
regarding risk factors for anesthetic-related death in dogs. Journal of the American Veterinary Medical Association 233(7):
1096-1004, 2008.
Brodbelt DC. Perioperative mortality in small animal anaesthesia. The Veterinary Journal, 2008.
Brodbelt DC, Blissitt KJ, and Hammond RA et al. The risk of death: the confidential enquiry into perioperative small animal
fatalities (CEPSAF). Veterinary Anaesthesia and Analgesia, 35(5): 365-373, 2008.
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BELIEF No. 6:
The use of advanced monitoring techniques such as pulse oximetry, arterial blood pressure monitoring,
and capnometry significantly reduces patient morbidity and mortality: Fact or fiction?
Anaesthetic complications can only be recognised by patient monitoring (i.e. performing frequent, regular assessments of
the patient); understanding the signs and stages of anaesthesia; and being able to differentiate “normal” from
“abnormal”.1. While there is no question that simple monitoring techniques provide essential, baseline information
about anaesthetic depth and vital organ function, “hands on” methods are limited in the sense that they lack subtlety:
changes in parameters may indicate function is “inadequate” but do little to quantify the degree of impairment. In
contrast, devices such as non-invasive blood pressure (NIBP) monitors, capnometers and pulse oximeters, provide
information about respiratory and cardiovascular function that is difficult, if not impossible, to gain in anaesthetized
patients using physical techniques alone.1, 2. Common sense suggests these techniques should aid in the recognition of
anaesthetic complications, and by allowing early intervention, should reduce anaesthetic-related death – but does the
literature support this view?
Although complications of anaesthesia have been well described 3-5, few studies report the incidence of “every day”
complications in small animals. However, Dyson et al’s anaesthetic morbidity and mortality study (performed in > 16,500
small animals in the mid 1990’s), reported anaesthetic complications in 2.1% of dogs and 1.3% of cats.6. Patients in this
study were monitored at least intermittently in about 85% of cases, although monitoring was limited to fairly simple
techniques (e.g. physical assessment, stethoscope or apnoea monitor) with ABP monitoring performed in < 0.2% of
cases. In contrast, a study examining 2556 dogs and 683 cats anaesthetised by the anaesthesia service of a large
University Veterinary Teaching Hospital (also performed in the mid 1990’s), reported various complications including
hypotension, hypoxaemia and hypoventilation in 12% of dogs and 10.5% of cats, when patients were monitored with
more advanced techniques such as NIBP monitors and pulse oximetry. 7. While it could be argued that the higher
incidence of complications in the teaching hospital- versus the private practice based study was the result of a sicker
patient population (studies suggest ASA III to V patients represent only 5-10% of the caseload in private practice versus
20-40% of the caseload in referral practice) 8, a higher incidence of complications was also noted in private practice
patients that were monitored more intensively, highlighting the importance of monitoring with respect to problem
recognition.6, 7. A recent (2007) retrospective study of cardiopulmonary complications in 1281 anaesthetized dogs
undergoing a variety of diagnostic and surgical procedures, supports this view. 9. Hypoxia, bradycardia, hypotension and
hypoventilation were identified in approximately 16%, 36%, 38% and 63% of patients respectively, when monitoring
devices – including ABP monitors, pulse oximetry and capnometry – were employed. It would appear the use of
monitoring devices helps in the detection of problems, but does this translate to a reduction in anaesthetic-related
mortality?
Studies investigating critical incidents in anaesthetised people have conclusively demonstrated the use of minimum
monitoring standards (i.e. a set of published guidelines or recommendations that document the baseline level of
acceptable care) to significantly reduce patient morbidity and mortality.2, 11, 12. Routine monitoring of ABP, arterial
saturation and end-tidal CO2 values (ETCO2) is now considered a minimum standard in human anaesthesia. 2, 11. An
Australasian study of 2000 critical incidents in anaesthetised people showed a monitor of some sort was the first
indicator of a problem in 52% of reported incidents and complications. 13. The authors of this study were able to predict
the theoretical “usefulness” of various monitors in a typical anaesthetic procedure. Based on these predictions, pulse
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oximetry would have detected 82% of all problems and would have warned of nearly 60% of problems prior to the
potential for organ damage. The addition of capnography would have raised these figures to 88% and 65%
respectively, while the addition of ABP monitoring would have resulted in detection of 93% of complications – providing
warning of 65% of these – before the potential for organ damage had occurred. Based on this analysis and after
consideration of costs, the authors created a “priority sequence for monitor acquisition” for those with limited resources.
The “usefulness” ranking of the monitors (in descending order) was as follows: - (1) stethoscope, (2) NIBP monitor, (3)
pulse oximeter, and (4) capnometer, suggesting that ABP monitoring was particularly useful in detecting complications
and reducing risk in anaesthetized patients.
Dyson et al’s small animal anaesthetic morbidity and mortality investigation was the first veterinary study to demonstrate
that the presence of technician/nurse to monitor an anaesthetized patient significantly reduces the risk of anaestheticrelated death.6. More recently, the Confidential Enquiry into Perioperative Small Animal Fatalities (CEPSAF) showed a
significant (p < 0.001), 3-4-fold reduction in the odds of death when pulse rate and pulse oximetry were routinely
monitored in anaesthetized cats.10. Assessment of the success (or failure) of other monitoring devices to reduce the risk
of anaesthetic related death was not possible, because strategies such as ABP monitoring were performed in < 10% of
patients. Current evidence therefore supports the view – but does not conclusively demonstrate – that employment of
minimum anaesthetic monitoring standards (including use of monitoring devices such as NIBP monitors, pulse oximeters
and capnometers) aid in problem recognition and reduce the risk of anaesthetic-related death (understanding that use of
these methods does not guarantee outcome12).
References
1. Haskins SC. Monitoring the anesthetized patient. In Lumb and Jones’ Veterinary Anesthesia, 3 Ed. Thurmon, Tranquilli and
Benson (editors), Williams and Wilkins, Baltimore, 1996. Ch 15, pp409-424.
2. Nicholson A. Monitoring techniques and equipment for small animal anaesthesia. Aust Vet J, 74(2): 114-123, 1996. Dyson DH,
Maxie MG and Schnurr D. Morbidity and mortality associated with anesthetic management in small animal veterinary practice in
Ontario. JAAHA 34: 325-335, 1998.
3. Eicker SW. Complications in anesthesia. Seminars in Vet Med and Surg (Small An) 1(3): 2014-214, 1986.
4. Evans AT. Anesthetic emergencies and accidents. In Lumb and Jones’ Veterinary Anesthesia, 3 Ed. Thurmon, Tranquilli and
Benson (editors), Williams and Wilkins, Baltimore, 1996. Ch 25, pp849-860.
5. Harvey RC. Anaesthetic emergencies and complications. In British Small Animal Veterinary Association (BSAVA) Manual of Small
Animal Anaesthesia and Analgesia. Seymour and Gleed (Editors), BSAVA, Shurdington, 1999, Ch 24 pp257-263
6. Dyson DH, Maxie MG and Schnurr D. Morbidity and mortality associated with anesthetic management in small animal veterinary
practice in Ontario. JAAHA 34: 325-335, 1998.
7. Gaynor JS, Dunlop CI and Wagner AE et al. Complications and mortality associated with anesthesia in dogs and cats. JAAHA,
35: 13-17, 1999.
8. Brodbelt DC, Hammond R and Tuminaro D et al. Risk factors for anaesthetic-related death in referred dogs. Vet Rec 158(16):
563-564, 2006.
9. Redondo JI, Rubio M and Soler G et al. Normal values and incidence of cardiorespiratory complications in dogs during general
anaesthesia. A review of 1281 cases. J Vet Med A 54: 470-477, 2007.
10. Brodbelt DC, Pfeiffer DU and Young LE et al. Risk factors for anaesthetic-related death in cats: results from the confidential
enquiry into perioperative small animal fatalities (CEPSAF). Br J Anaesth 99(5): 606-608, 2007.
11. Nitti JT and Nitti GJ. Anesthetic complications. In Clinical Anesthesiology, 4 edition. Morgan, Mikhail and Murray (Editors),
Lange Medical Books, New York, 2006, Ch 46, pp 959-978.
12. American College of Veterinary Anesthesiologists. Suggestions for monitoring anesthetized veterinary patients. JAVMA 206(7):
936 – 937, 1995.
13. Webb RK, Van Der Walt JH and Runciman WB et al. Which monitor? An analysis of 2000 incident reports. Anaesth Intens Care,
21: 529-542, 1993.
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Conclusion
Many areas of small animal anaesthetic practice are open to debate and this paper has attempted to address just a few
of these by means of an evidence based literature review. The following statements are current, often polarizing topics,
and are provided as food for thought – you may enjoy researching these yourself, or debating these within your practice
or with other colleagues!
Statement No 1: Because isoflurane is so inert in comparison to halothane, there is no longer any need to employ
strategies for reducing staff exposure to waste anaesthetic gases when using this agent: Fact or fiction? Statement No.
2: Although it was once used routinely as a premedicant in dogs and cats, routine use of atropine is now considered
unjustified and should be avoided: Fact or fiction?
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