Sedation is an effective and safe alternative to general

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BRITISH DENTAL JOURNAL

VOLUME 188, NO. 7, APRIL 8 2000

Dental treatment for people with challenging behaviour: general anaesthesia or sedation?
M C G Manley,1 A M Skelly,2 and A G Hamilton3

The dental care of people with severe learning disability and challenging behaviour presents many problems. The maintenance of oral health by regular examination, prevention and treatment may be difficult because of the limitations in patient cooperation. In many cases the diagnosis of orofacial pain may need to be discounted as a cause of uncharacteristic and sometimes aggressive behaviour. In such cases the use of general anaesthesia for examination and treatment would seem to be the obvious option but this strategy has limitations. This paper undertakes a focused review of sedation techniques as an alternative to general anaesthesia in the treatment of people with challenging behaviour. The use of novel techniques of sedation combining intravenous with oral or intranasal routes is described with patients treated in a community dental health centre. All patients had previously received treatment using general anaesthesia. The techniques described proved effective and safe for use in the primary care setting.

In brief
Sedation is an effective and safe alternative to general anaesthesia.
Sedation enables diagnosis and treatment for people with challenging behaviour in the primary care setting.
The use of sedation extends the range of treatment options for people with challenging behaviour.
People who are medically compromised can be treated using sedation techniques.
The use of sedation can increase the availability of treatment for people with disability compared with general anaesthetic.

The provision of comprehensive dental care for people with disabilities can present difficulties. It has been shown that around 20% of people with a disability needed a general anaesthetic to receive dental treatment.1 In the present climate society requires that health professionals strive for equal access to and equal standards of care for all people.2 The dental profession should look carefully at its strategies for the treatment of people with disability.

While general anaesthesia is a useful facility and, indeed, essential in certain cases, it is not without problems. For example, unless full intubation facilities are available, restorative treatment is difficult to provide and treatment may be limited to extractions only. Even when the length and range of treatment is extended by the use of tracheal intubation, it compares poorly with that available to a conscious individual. Periodontal or endodontic treatment requiring multiple visits and other complex or time-consuming procedures cannot be provided ideally under general anaesthesia. Therefore the person with a disability often remains disadvantaged compared with his abler counterparts.

Limitations in the provision of dental treatment under general anaesthesia may result not only in impaired dental health and aesthetics, but also present difficulties to carers and dentists faced with behaviour changes caused by pain from oro-facial pathology. This is particularly a problem for those with poor communication. Self injury or aggressive physical violence may result from the individuals' inability to indicate the source of their discomfort.

It must be recognised that in proper conditions, with appropriately trained, qualified and experienced staff, the risk to patients receiving treatment under general anaesthesia is small3 unless there are complicating medical factors.4 However dentists, anaesthetists and carers may be faced with the difficult decision to proceed with general anaesthesia for diagnostic purposes in the absence of any clear symptoms. In addition, for those with severe learning disability and challenging behaviour, the ethics of regular use of general anaesthesia for a routine examination and scale and polish is questionable.


The place of conscious sedation
In view of the fact that a number of reports,5-7 have encouraged the use of conscious sedation as an alternative to general anaesthesia, this review considers whether these techniques can be applied in difficult-to manage cases such as treating people with severe learning disability or challenging behaviour. Sedation is considered to be more flexible than general anaesthesia and is also more likely to be available in the primary care setting widening treatment options.

Problems in providing sedation for people with disability

Many of the difficulties in providing sedation for this group lie in the areas of cooperation, communication and cognitive ability. For example an adult with challenging behaviour may not be sufficiently cooperative to allow venepuncture prior to the administration of intravenous drugs. A person with severe learning difficulty may not be able to understand or comply with the need to breathe continuously through the nose as a requirement of inhalation sedation. Verbal communication may not be possible as a clinical sign of conscious sedation when using intravenous sedation. It may be for these and other reasons that the standard strategy of care for such patients is the provision of treatment under general anaesthetic. This paper sets out to challenge this assumption.

Evidence from the literature

Healy et al. examined the use of local anaesthetic and intravenous diazepam, as an alternative to general anaesthesia, and found the operating conditions acceptable in 80% of cases;8 the patients were adults with mild-moderate learning disability. Manford and Roberts showed the successful use of relative analgesia as an alternative to the use of general anaesthesia in the treatment of young handicapped patients.9 Malamed et al. reviewed retrospectively 96 adults with impairments treated using a combination of intravenous drugs (diazepam, midazolam, meperidine and pentazocine) and in a small number of cases (14 uncooperative patients) the intravenous drugs were combined with intramuscular midazolam plus meperidine.10 Four patients could not be treated using these techniques and were referred for general anaesthesia. A similar drug combination was also used by Jakobs et al. with an adult group.11 Silver et al.showed the effective use of oral midazolam in 31 patients aged 3-18 years.12 The children were physiologically and neurologically handicapped and treatment success varied from 60-75% depending on dosage used. Benzodiazepines have been traditionally used in children, however oral ketamine was successfully used by Rosenberg in the case of an 'extremely combative mentally handicapped female'.13 Combinations of oral meperidine and promethazine with inhalation nitrous oxide/ oxygen sedation have also been used in medically/physically/mentally compromised children as reported by Haney et al.14 Oei-Lim et al. reported on the use of intravenous propofol for the dental treatment of adults with impairments as an alternative to inhalation sedation.15 The authors concluded that the quality and ease of sedation was good (in all but two cases) using intravenous propofol and the use of propofol was an acceptable alternative to inhalation sedation. Oei-Lim et al. used propofol given by a computer controlled infusion system in a further study on adults with impairments.16 The study group comprised 89 patients who could not be treated using inhalation sedation, their median age was 29 years and all were medically fit (ASA I or II). The quality of sedation was good or excellent in 88% of cases and it was concluded that this technique can provide safe and satisfactory sedation for this group of patients. In a double blind crossover study Stephens et al. compared intravenous midazolam against propofol in a group of patients with impairments of age range 5 to 26 years.17 Eighteen cases were involved in the study and an anaesthetist administered the drugs by continuous infusion. The authors concluded that propofol had certain advantages over midazolam used in this way, particularly the rapid recovery from sedation. Van der Bijl et al. used a combination of propofol by continuous infusion and midazolam bolus with an ASA IV 21-year-old patient with learning disability.18 The treatment provided was dental extractions and the patient was well sedated throughout the procedure,with no significant cardiovascular or respiratory effect. Two years later the same patient was sedated for further dental treatment using a propofol infusion.19 The patient remained well throughout the procedure and no adverse effects were experienced. The same authors also reported the successful use of intravenous midazolam in a 29-year-old female patient with involuntary movements.20 Two studies were carried out by Fukata et al. using midazolam administered intranasally combined with nitrous oxide/oxygen inhalation sedation.21, 22 The patients selected were those with learning disability with age range from 4 to 23 years. The first study (21 cases of patients with learning disability) showed a successful treatment outcome in 70% of cases. The second study (43 cases with challenging behaviour) compared the varying doses of 0.2 mg/kg and 0.3 mg/kg intranasal midazolam to determine the appropriate concentration for the use of this drug by this route. It was concluded that there were no clinical benefits using the higher concentration and therefore 0. 2 mg/kg was recommended.

Although the evidence presented here is not extensive, it clearly shows that conscious sedation techniques can be successfully and safely used in the treatment of people with disability. It is of particular note that conscious sedation was successfully used in a seriously medically compromised case.18, 19The use of a combination of intravenous drugs, and different routes of administration (eg intranasal) suggest that for this group there are particular problems and that a more flexible approach is required to that used when sedating people who do not have a disability.

A novel approach in clinical practice

In order to address these problems, techniques have been developed for the treatment of difficult-to-manage patients with challenging behaviour at the Canterbury Community Health Centre Dental Department.

Before the introduction of these new techniques, treatment was already being provided successfully under intravenous midazolam sedation for very anxious individuals. This sedation was provided by an experienced operator-sedationist assisted by a trained and qualified dental nurse. However this was not suitable for many patients with challenging behaviour or severe learning disability whose behaviour prevented the safe placement of a cannula. The techniques described here were designed to allow dental treatment to be provided for such patients who had previously received all their dental treatment under general anaesthesia.

Midazolam is administered either orally, in a preferred drink, or intranasally as a fine aerosol delivered from a 2 ml syringe through a spray nozzle. Oral midazolam is used in a dose of 20 mg compared with 10 mg for the intranasal route. The oral or nasal medication provides sufficient sedation to allow cannulation and appropriate monitoring to be put in place before proceeding to intravenous sedation. Intravenous midazolam is titrated to each patient's response according to the manufacturer's Data Sheet.23

A review of the introduction and development of this practice over a 6-year period is presented here. A retrospective audit of 124 patient records was made.

The oral or intranasal route alone was used for seven and ten patients respectively. When used in combination with the intravenous route, oral midazolam was used for 44 and intranasal midazolam for 21 individuals. The mean number of treatment visits per patient was two, and, over the 6-year period, midazolam was used orally 102 times and intranasally on 62 occasions. During the period audited only four patients originally selected for midazolam sedation could not be treated using one of these techniques and required referral for general anaesthesia. As the Centre is also able to provide intravenous sedation with propofol for suitable cases, when a consultant anaesthetist is present, the overall number of patients referred for general anaesthesia is much reduced by the availability of a comprehensive range of sedation techniques.

The novel approach of a combination of oral/intranasal and intravenous routes has shown that sedation with a single drug can be effectively and safely employed in a primary care setting for difficult-to-manage patients.

The use of oral midazolam is already well established in medicine24 and nursing25 and it has also been shown to be effective in dentistry.26 Intranasal midazolam has also been found to be beneficial within nursing27 and in the dental treatment of people with learning disability.21, 22

It should be noted that when midazolam is administered by either of the above routes in the United Kingdom it is used without a licence. This is permissible provided that the supplier (usually the local pharmacy) is made aware of the proposed unlicensed use of any drug.28 Specific attention should be drawn to the off-licence use of midazolam on the patient's consent/agreement to treat form and the sedationist must be up to date with current evidence supporting the use of the drug in these ways. A practitioner who chooses to use a drug outside the limits of its licence must take full responsibility for this action. If the above recommendations are followed, good clinical practice is ensured.29, 30

Conclusion

This review shows that sedation can be used both safely and effectively for people with disabilities. Conscious sedation techniques must be adapted to the special needs of this patient group and clinicians may need to be flexible in their approach to the problems presented. We suggest, however, that the techniques described in this paper should only be used by practitioners who have had appropriate experience of both intravenous sedation and in the care of people with disabilities. In order to widen access to a more comprehensive range of treatment modalities for this section of our population, further training of dentists and their teams is necessary.31

1 Holland T J, O'Mullane D M. The organisation of dental care for groups of mentally handicapped persons. Community Dent Health 1990; 7: 285-293.
2 Court Report of the Committee on Child Health. Fit for the future. London: HMSO, 1976.
3 Worthington L M, Flynn P J,Strunin L. Death in the dental chair: an avoidable carastrophe? Br J Anaesthesia 1998; 80: 131-132.
4 Moore R S, Hobson P. A classification of medically handicapping conditions and the health risks they present in the dental care of children. J Paediatr Dent 1989; 5: 73-83.
5 Poswillo D. General anaesthesia,sedation and resucitation in dentistry. Report of an Expert Working Party for the Standing Dental Advisory Committee. London Department of Health, 1990.
6 Press release and response to reports on general anaesthesia, sedation and resucitation in dentistry. Department of Health, 1991.
7 Report of a Working Party on Training in Dental Anaesthesia. Wylie, The Royal College of Surgeons of England, 1978.
8 Healey T J, Edmonson H D, Hall N. Sedation for the mentally handicapped patient. Anaesthesia 1971; 26: 308-310.
9 Manford M L M, Roberts G J. Dental treatment in young handicapped patients. An assessment of relative analgaesia as an alternative to general anaesthesia. Anaesthesia 1980; 35: 1157-1168.
10 Malamed S F, Gottschalk H W, Mulligan R, Quinn C L. Intravenous sedation for conservative dentistry for disabled patients. Anaesthesia Progress 1989; 36: 140-142.
11 Jakobs W, Lipp M, Daublander M, Jakobs-Hannegrefs E. Dental treatment of handicapped patients with conscious sedation. Anaesthesia Progress 1989; 36: 144-145.
12 Silver T, Wilson C, Webb M. Evaluation of two doses of oral midazolam as a conscious sedation for physically and neurologically compromised pediatric dental patients. Pediatr Dent 1994; 16: 350-359.
13 Rosenberg M. Oral ketamine for deep sedation of difficult-to-manage children who are mentally handicapped: case report. Pediatr Dent 1991; 13: 221-223.
14 Haney K L, McWhorter A G, Seale N S. An assessment of the sucess of meperidine and promethazine sedation in medically compromised children. ASDC J Dent Children 1993; 60: 288-294.
15 Oei-Lim L B.,Vermeulen-Cranch D E, Bouvy Berends E M. Conscious sedation with propofol in dentistry. Br Dent J 1991; 170: 340-344.
16 Oei-Lim L B, Kalkman C J, Makkes P C, Ooms W G, Hoogstraten J. Computer controlled infusion of propofol for conscious sedation in dental treatment. Br Dent J 1997; 183: 204-208.
17 Stephens A J, Sapsford D J, Curzon M E J. Intravenous sedation for handicapped dental patients: a clinical trial of midazolam and propofol. Br Dent J 1993; 175: 20-25.
18 Van der Bijl., Roelofse J A. Propofol and midazolam for conscious sedation in a mentally retarded dental patient. Anaesthesia Progress 1992; 37: 37-39.
19 Van der Bijl, Roelofse J A. Propofol for sedation in a mentally retarded dental patient. Anaesthesia Progress 1994; 41: 81-82.
20 Van der Bijl P, Roelofse J A. Conscious sedation with midazolam in a patient with a spastic nerve muscular disorder - a case report. Annals of Dent 1994; 53: 37-38.
21 Fukuta O, Braham R L, Yanase H, Atsumi N, Kurosu K. The sedative effect of intranasal midazolam in the dental treatment of patients with mental disabilities Part1 - The effect of a 0. 2 mg/kg dose. J Clin Pediatr Dent 1993; 17: 231-237.
22 Fukuta O, Braham R L, Yanasa H, Kurosu K. The sedative effect of intranasal midazolam in the dental treatment of patients with mental disabilities. Part 2 - Optimal concentrations of intranasal midazolam. J Clin Paediatr Dent 1994; 18: 259-265.
23 ABPI Compendium of Data Sheets. London: Data Pharm Publications, 1998-9: 1132.
24 McCluskey A, Meakin GH. Oral administration of midazolam as a premedicant for paediatric day-case anaesthesia. Anaesthesia 1994; 49: 782-785.
25 Taiwo B, Flowers B, Zoltie N. Reducing children's fear when undergoing painful procedures. Archives of Emergency Med 1992; 9: 306-309.
26 O'Boyle C A, Harris D, Barry H, Mccreary C, Bewley A, Fox E. Comparison of midazolam by mouth and diazepam i.v. in outpatient oral surgery. Br J Anaesthesia 1987; 59: 746-754.
27 Adrian E R. Intranasal Versed: The future of pediatric conscious sedation. Pediatr Nurs 1994; 20: 287-291.
28 Dental Practitioners' Formulary. Prescribing for dental surgeons. BDA, BMA, RPSGB. London 1998-2000. pvii.
29 Pickles H. The use of unlicensed drugs. Br J Health Care Management 1996; 2: 656-658.
30 Editorial. Unlicensed drug administration Anaesthesia 1995; 50: 189-190.
31 Maintaining standards-guidance to dentists on professional and personal conduct. London: General Dental Council. Revised November 1998. Amended May 1999.


The British Dental Journal is published by Nature Publishing Group for the British Dental Association.
© 2002 British Dental Association

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British Dental Journal 1996; Volume 180, No. 7, pages 255-258.

Dental injuries during general anaesthesia

Chadwick, RG, Lindsay, SM

Abstract

Although most anaesthetic textbooks cite dental injury as a complication of endotracheal intubation few studies have examined the extent and nature of the problem. Such damage however, formed the basis for one-third of all confirmed or potential anaesthetic claims notified to the Medical Protection Society between 1977 and 1986. This article seeks to explore the extent of the problem, outline predisposing factors, summarise current prophylactic measures and make recommendations to reduce the overall incidence. Increased awareness of the problem, by both anaesthetists and dental surgeons, coupled with appropriate prophylactic measures may result in a reduced incidence of dental injury arising from general anaesthesia. Given the high incidence of dental damage we recommend that all patients undergoing a surgical operation under endotracheal intubation should have a pre-operative dental check wherever possible. Clearly, the first dental examination would be conducted by an anaesthetist familiar with the predisposing factors. Where he/she considers there to be a higher than average risk of dental damage occurring during intubation a more specialised examination should be conducted by a dental surgeon. It may, where appropriate, be possible for remedial dental treatment to be carried out and customised mouth guards to be constructed prior to the operation. Obviously such recommendations have certain financial implications and would have to be subject to controlled cost-benefit analysis before their widespread application



Keywords
Anesthesia,General, adverse effects, Anesthesiology, Cost-Benefit Analysis, Dental Care, Female, Human, Incidence, Intubation,Intratracheal, Male, Mouth, injuries, Mouth Protectors, Patient Care Team, Risk Factors, Surgery,Oral, Tooth Injuries, etiology, prevention & control

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© 2000-2004 American Veterinary Medical Association.
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November 15, 2003 (Volume 223, No. 10)
Reference Point
Myths and misconceptions in small animal anesthesia
Ann E. Wagner, DVM, MS, DACVA, DACVP; Bonnie D. Wright, DVM, DACVA; Peter W. Hellyer, DVM, MS, DACVA *

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The perianesthetic mortality rate for dogs and cats has been reported to range from 0.1% to 0.43%, but probably varies greatly from 1 veterinary practice to the next,1-4 with many veterinarians reporting a low incidence of anesthesia-related deaths in their practices. Nevertheless, even a rare anesthesia-related death has a marked impact on clients and the veterinary staff. Veterinary anesthesia has progressed to the point that survival is no longer the only criterion for good or successful anesthesia. Modern anesthetic techniques are designed to minimize risks, not only of obvious complications but also of hidden ones, and to maximize the odds of a favorable outcome. In discussing anesthetic drug protocols and monitoring techniques with small animal veterinarians, the authors have become aware of certain myths or misconceptions shared by many practitioners. In a medical community, beliefs often arise from a combination of clinical experience and the prevailing scientific evidence. As further research is conducted, many things that were once considered fact are disproved, yet reevaluation of beliefs does not always keep pace with the rate of scientific discovery. Thus, beliefs that were once evidence-based become outmoded and fall into the realm of myth or misconception.

The following comments are intended to refute some of the myths and clarify certain misconceptions surrounding the practice of small animal anesthesia, present current understanding of commonly misunderstood issues, and aid practitioners in providing higher quality care for their small animal patients.

Myth—Many breeds of dogs are sensitive to specific anesthetics.

Reality—Although certain breeds may be predisposed to problems that affect their responses to anesthesia (eg, cardiomyopathy in Doberman Pinschers and upper airway collapse in Bulldogs), very few breed-related sensitivities to anesthetic drugs have been identified. Greyhounds do have a well-documented tendency to have prolonged recoveries from thiobarbiturate anesthesia.5,6 And by extrapolation, many veterinarians avoid the use of thiopental in all sighthounds (eg, Whippets, Afghan Hounds, and Borzois), although sighthounds other than Greyhounds have not been studied in a controlled fashion and may not be similarly affected.

In addition, there are numerous anecdotal reports of Boxers fainting or collapsing when given acepromazine, possibly from excessive vagal response. Although poorly documented, this phenomenon seems to follow a geographic distribution, being more commonly reported in England, which may indicate a familial or genetic component. The authors have administered acepromazine at doses of 0.01 to 0.04 mg/kg (0.005 to 0.018 mg/lb), SC, to Boxers in Colorado without untoward effects, but recommend caution with dose and patient selection.

Finally, many veterinarians have a clinical impression that dogs of northern breeds, such as Alaskan Malamutes, Siberian Huskies, and Samoyeds, tend to respond to opioid administration by vocalizing or evidencing dysphoric behavior. However, many northern-breed dogs respond appropriately to administration of opioids at lower dosages or to administration of opioids concurrently with a tranquilizer.

In summary, although many dog owners believe rumors that their particular breeds are sensitive to certain anesthetic drugs or that certain anesthetic drugs are contraindicated in their breeds, there is little evidence to support most of these rumors.

Myth—Preanesthetic medications should not be used because they delay recovery.

Reality—Premedications are very valuable in most cases. Tranquilizers, sedatives, and analgesics decrease anxiety and pain associated with hospitalization, restraint, injections, and other unpleasant procedures. They decrease the required doses of induction drugs and gas anesthetics, frequently resulting in less cardiovascular depression during induction and maintenance of anesthesia.7-10 While it is true that some premedications lead to prolonged sleepiness during recovery, most animals that have undergone painful procedures benefit from a quiet recovery period. After nonpainful procedures, the effects of some premedications (eg, opioids, benzodiazepines, and α2-adrenoceptor agonists) can be reversed or partially reversed, if necessary, to expedite recovery.11-15

Myth—Small doses of α2-adrenoceptor agonists have minimal cardiovascular effects.

Reality—While the manufacturer of medetomidine, an α2-adrenoceptor agonist, has recommended16 the use of doses ranging from 18 to 71 μg/kg (8.2 to 32.3 μg/lb), IV, much lower doses (1 to 10 μg/kg [0.45 to 4.5 μg/lb], IV) are sometimes useful to provide short-term sedation and analgesia. However, it has been reported that administration of medetomidine at a dose of 1 μg/kg, IV, in dogs caused cardiac output to decrease to < 40% of resting values and to remain nearly 50% below normal for at least an hour.17 In healthy young animals with good cardiovascular function, this decrease may be tolerated, but in older animals and animals with preexisting cardiac disease, such a decrease may have deleterious effects on tissue perfusion and oxygen delivery, including reduced perfusion of the myocardium itself. Interestingly, several surveys of small animal veterinary practices have suggested that use of the α2-adrenoceptor agonist xylazine is associated with a higher incidence of perianesthetic complications or death than use of any other anesthetic drug, possibly related to its detrimental cardiovascular effects.1,3 Although α2-adrenoceptor agonists can induce excellent sedation and analgesia, caution is advised with regard to patient selection, even when very low doses are used.

Myth—The fewer drugs used to anesthetize an animal, the safer.

Reality—Actually, balanced anesthesia techniques that involve administration of multiple drugs often allow smaller doses of each drug to be used, resulting in fewer or less profound adverse effects than when a large dose of a single drug is used. For instance, the induction dose of propofol in dogs premedicated with acepromazine is about half the induction dose needed in dogs that have not been premedicated.18 Morphine administration can decrease the minimum alveolar concentration (MAC) of gas anesthetics by up to 63%.10 The use of balanced anesthetic techniques that involve lower doses of relatively depressant drugs, such as gas anesthetics, which produce profound dose-dependent hypotension, may benefit many patients.

Myth—It is dangerous to use more than 1 type of analgesic at a time in an animal.

Reality—Prevention and treatment of pain should involve a multimodal or balanced technique similar to the balanced techniques used for anesthesia.19-21 Drugs used to provide perioperative analgesia include opioids, α2-adrenoceptor agonists, local anesthetics, non-steroidal anti-inflammatory drugs, and ketamine. The goal of using more than 1 drug is to provide better pain control while minimizing adverse effects. Single drug techniques can be used effectively to treat minor pain in dogs and cats. Acute pain induced by trauma or surgery generally responds better to combination drug therapy, rather than single drug treatment, in part because analgesics from different classes exert their effects in different parts of the neuroanatomic pathways giving rise to pain. Thus, combining 2 or more analgesic drugs during the perioperative period may provide additive or synergistic analgesic effects.

Myth—Opioids are dangerous because of their potential for adverse effects.

Reality—The adverse effects associated with opioids administered during the perioperative period in dogs and cats are rarely serious. The respiratory depressant effects of opioids in dogs and cats are much less profound than the effects in people, although some anesthetized animals given opioids along with other respiratory depressant induction drugs and gas anesthetics do benefit from mechanical ventilation.22 Hypoxemia may accompany respiratory depression if oxygen is not supplemented. Vomiting and defecation may occur when nonpainful animals are given an opioid, such as a preanesthetic dose of morphine, but usually this is a 1-time occurrence that does not seem to be a problem in the postoperative period or when opioids are given to an animal experiencing pain. Opioids can interfere with thermoregulation, but if necessary, body temperature can usually be maintained with appropriate heating or cooling devices. Behavioral changes, which can include agitation and dysphoria or excessive sedation, may occur in conscious animals treated with opioids; however, these effects can usually be managed by adjusting the opioid dosage, administering a tranquilizer concurrently, or administering a partial antagonist. Some of the advantages of using opioids are excellent analgesia, minimal cardiovascular depressant effects, ability to decrease doses of other anesthetic drugs such as gas anesthetics, and ability to be reversed or antagonized.

Myth—Butorphanol is an effective and long-lasting analgesic.

Reality—A study of female dogs undergoing ovariohysterectomy found that administration of butorphanol at a dose of 0.5 mg/kg (0.23 mg/lb), IM, did not provide complete analgesia in all dogs at any time, and all dogs had signs of incisional pain by 30 to 90 minutes after receiving butorphanol.23 For visceral pain (colon balloon model), butorphanol at a dose of 0.4 mg/kg (0.18 mg/lb), SC, produced analgesia for < 60 minutes, even though a dose of 0.4 mg/kg was considered optimum, with a ceiling effect occurring at doses > 0.8 mg/kg (0.36 mg/lb).24 In another study,25 butorphanol did not significantly change the MAC of halothane in dogs. Taken together, these data suggest that butorphanol is useful only for fairly mild pain and if used for pain control in dogs, it should be administered every 1 to 2 hours. In cats undergoing onychectomy, butorphanol administration improved analgesia.26 However, the efficacy of butorphanol in cats varies widely, as does the duration of its effects, which have been reported to be from 80 to 360 minutes.27

Myth—Induction of anesthesia with gas anesthetics is safer than induction with injectable anesthetics.

Reality—Struggling and excitement during mask induction are not only unpleasant for the patient and dangerous for personnel, but may also lead to higher serum catecholamine concentrations, which can predispose to arrhythmias and anesthetic overdose. Induction times with gas anesthetics, even with newer, less-soluble anesthetics such as sevoflurane, are slower than induction times with injectable anesthetics. A recent studya of cats reported that mean ± SD times to intubation with sevoflurane and isoflurane induction were 7.2 ± 1.1 and 8.6 ± 1.2 minutes, respectively. By comparison, most IV induction techniques allow intubation within 1 or 2 minutes. During the relatively prolonged induction period necessary with gas anesthetics, there is no airway control, and hypoventilation can be severe, especially in patients with preexisting respiratory compromise such as a collapsing trachea or diaphragmatic hernia. In addition, the depth of anesthesia required for endotracheal intubation of a patient is usually about 30% greater than that required for surgical incision,28 which means that by the time most patients are intubated following mask induction, they will have already experienced considerable cardiovascular and respiratory depression. At least 1 private practice has found that hypotension (systolic arterial blood pressure < 90 mm Hg) occurred more frequently in dogs and cats in which anesthesia was induced with an inhalant anesthetic delivered by mask (37%), compared with those in which anesthesia was induced with injectable drugs (14%).b In addition, the high oxygen flows and vaporizer settings required for gas induction are wasteful and result in substantial pollution that contributes to occupational health hazards.

Myth—Thiopental is a dangerous and outdated anesthetic induction drug.

Reality—Thiopental is a reliable and economical induction agent that still has a place in veterinary anesthesia. Thiopental is chemically stable and resists bacterial growth for up to 4 weeks.29 Anesthetic induction with thiopental is usually rapid, smooth, and excitement-free. In healthy dogs, thiopental may increase heart rate and decrease stroke volume, resulting in little change in blood pressure or cardiac output. Reducing the induction dose of thiopental by administering premedications reduces the cardiovascular effects.30 Ventricular dysrhythmias can occur with thiopental, but these too are less common when administration of premedications allows lower doses of thiopental to be used.31 Clinical impressions suggest that supplementing oxygen prior to and during induction also seems to reduce the incidence of dysrhythmias. A study of the use of thiopental in hypovolemic dogs concluded that thiopental had minimal deleterious effects, most cardiovascular variables improved, and neither hypotension nor respiratory depression occurred.32 Nonpremedicated dogs recovering from thiopental alone may be groggy and have difficulty standing, but tranquilizers or opioids generally help to smooth recovery, as does a period of gas anesthesia.

Myth—Acepromazine-ketamine is a good combination for surgical anesthesia in cats.

Reality—A combination of acepromazine and ketamine has commonly been used as a general anesthetic in cats undergoing routine procedures such as ovariohysterectomy, castration, and onychectomy. Acepromazine is a tranquilizer and provides no analgesia, whereas ketamine is generally thought to provide good superficial analgesia and little to no analgesia for deep or visceral pain. Administration of acepromazine (0.11 mg/kg [0.05 mg/lb], IM) and atropine (0.045 to 0.067 mg/kg [0.02 to 0.03 mg/lb], IM) 15 minutes prior to administration of ketamine (22 mg/kg [10 mg/lb], IM) has been used in cats to provide anesthesia for surgical procedures.33 Another combination cited includes acepromazine (0.2 mg/kg [0.09 mg/lb], IM), butorphanol (0.4 mg/kg, IM), and ketamine (25 mg/kg [11.4 mg/lb], IM) for elective procedures such as ovariectomy. Thus, the doses of ketamine used to provide analgesia and general anesthesia are relatively high. Lower doses of ketamine, which are frequently used to induce anesthesia in dogs and cats, are unlikely to provide anesthesia sufficient for surgical procedures. Higher doses of ketamine increase the risk of adverse cardiovascular effects, such as tachycardia, hypertension, and the associated increase in myocardial oxygen demand, and are more likely to be associated with prolonged and rough recoveries. Acepromazine and ketamine administered without supplemental oxygen increases the risk of anesthesia-related hypoxemia. Ketamine-induced CNS and cardiovascular stimulation may be particularly detrimental in the presence of hypoxemia. Although both acepromazine and ketamine are useful anesthetic drugs in cats, inducing and maintaining anesthesia with this combination places cats at undue risk for inadequate analgesia and clinically important adverse effects.

Myth—Ketamine is a safe drug in patients with failing cardiac function.

Reality—Ketamine is considered to be a relatively safe induction drug, with a therapeutic index (ie, the ratio of median lethal dose to median effective dose) of 8.5 to 16, depending on species, compared with thiopental’s therapeutic index of 4.6 to 7.34 In addition, in a survey of small animal veterinarians in Colorado, ketamine was the most popular induction drug.35 When used in healthy patients without other medications, ketamine generally increases heart rate and blood pressure as a result of a generalized increase in sympathetic tone. However, in isolated heart preparations, the direct effect of ketamine on the myocardium is depression.36 In patients with clinically important cardiac disease, patients in shock that have sympathetic neurotransmitter depletion, and patients in which ketamine is used concurrently with other drugs such as benzodiazepines, the sympathomimetic, cardiostimulatory effects of ketamine are not apparent and cardiac depression may ensue.37 Therefore, although ketamine is an excellent induction drug in many situations and may have additional benefits in regard to pain relief, caution is advised with its use in patients with heart failure.

Myth—Propofol is the safest injectable anesthetic induction drug.

Reality—The therapeutic index of propofol is similar to that of thiopental, and both are probably slightly less safe, in this regard, than ketamine.34 An increased incidence of postoperative infections has been associated with use of propofol, possibly as a result of suppression of reticuloendothelial function by the diluent.38 Cardiorespiratory effects of propofol are similar to those of thiopental, although propofol is less likely to increase heart rate or induce arrhythmias.39 Because the blood-brain equilibrium time for propofol is about 3 minutes, compared with 1 minute for most other induction drugs, it may be easier to overdose animals with propofol than with other faster-acting induction drugs. In dogs, propofol can induce substantial vasodilation,34 and at the Colorado State University Veterinary Teaching Hospital, hypotension is such a common sequela to propofol induction that a bolus of fluids (5 to 10 mL/kg [2.3 to 4.5 mL/lb]) is administered IV to almost all patients before propofol is given. Cyanosis is also reported with propofol induction unless oxygen is supplemented before, during, and after induction.34 Propofol’s biggest advantage is the rapid, smooth recovery associated with its use, and this is certainly a reason to prefer propofol for short out-patient procedures in appropriately selected patients.

Myth—Sevoflurane is superior to isoflurane, and you are out of date if you are not using sevoflurane.

Reality—While everyone is entitled to his or her personal preferences, there is no compelling reason to switch from isoflurane to sevoflurane. Sevoflurane and isoflurane induce similar dose-related cardiovascular and respiratory depression,40 and neither drug sensitizes the heart to catecholamine-induced arrhythmias. Although the lower solubility of sevoflurane should result in faster induction and recovery times, a recent studya in cats demonstrated that induction was only slightly faster when sevoflurane was used (mean, 7.2 min), compared with isoflurane (mean, 8.6 min), and recovery time was not significantly different between the 2 drugs. In addition, isoflurane does not produce toxic by-products. Although clinical use of sevoflurane has not been associated with increased renal toxicoses, sevoflurane breakdown can produce fluoride ions and small amounts of compound A, which have the potential to be toxic to the kidneys.41 Therefore, low oxygen flow rates (< 1 to 2 L/min) are not recommended when using sevoflurane. Currently, sevoflurane is considerably (approx 5 times) more expensive than isoflurane.

Myth—Intravenous administration of fluids is warranted only during long surgical procedures.

Reality—Fluids are administered IV to compensate for insensible fluid losses that occur during anesthesia and surgery. Fluid loss is generally attributed to drying of exposed tissues and evaporation from the respiratory tract, especially with the administration of oxygen. Longer surgical procedures have a greater potential than shorter procedures for clinically significant fluid losses to occur. Nevertheless, IV administration of fluids is also beneficial in patients anesthetized for short procedures. As discussed elsewhere in this text, dogs and cats anesthetized for short, routine procedures are at risk of hypotension. The withholding of food prior to anesthesia, coupled with the reluctance of some dogs and cats to drink water while at a veterinary clinic, may lead to dehydration prior to anesthesia. Even mild degrees of dehydration, which tend to be difficult to recognize clinically, increase the likelihood of hypotension during anesthesia.

Intravenous administration of fluids is 1 of the cornerstones of preventing and treating hypotension during anesthesia. Intravenous administration of fluids may decrease recovery time by helping to maintain hepatic and renal blood flow, thereby hastening the elimination of anesthetic drugs. A return to normal function after anesthesia may be slowed by dehydration, which may actually become worse during recovery if the animal is still not drinking. Overall, IV administration of fluids prevents and corrects dehydration and hypotension and facilitates the elimination of anesthetic drugs, all of which are as important with a short procedure as with a long one. Finally, placing an IV catheter provides venous access for administration of emergency drugs in the event of an untoward episode during anesthesia and surgery.

Myth—Electrocardiographic activity indicates a beating heart.

Reality—While ECG monitoring is useful in detecting changes in heart rate or rhythm, it should be recognized that the ECG indicates electrical activity only, not mechanical activity (pumping) by the heart muscle. It is possible to have relatively normal ECG activity concurrently with severe hypotension or even cardiac arrest, as evidenced by continuation of ECG activity for several minutes following administration of an overdose of pentobarbital for euthanasia. Therefore, the ECG alone should not be relied on to indicate the circulatory status of an anesthetized patient.

Myth—Respiratory depression or apnea during anesthesia is a crisis.

Reality—Apnea is rarely a crisis unless the animal cannot be intubated. Most anesthetized, intubated animals breathing 100% oxygen can remain adequately oxygenated with only 1 or 2 breaths/min.42 Pulse oximetry can help determine whether oxygenation is adequate, and capnography or measurement of arterial blood gas partial pressures, if available, can confirm severe respiratory depression. If excessive respiratory depression or apnea occurs, efforts should be made to identify and correct the cause (eg, excessive anesthetic depth, recent administration of a respiratory depressant drug, and iatrogenic hyperventilation). In the meantime, providing 1 to 2 breaths/min of 100% oxygen will sustain adequate oxygenation in most patients, although hypercapnia may persist or worsen. Animals that cannot be expected to breathe spontaneously (eg, animals with a diaphragmatic hernia or undergoing an open chest procedure) and animals in which hypercapnia would be particularly detrimental (eg, animals with a brain tumor or head trauma) should be manually or mechanically ventilated at a rate of 8 to 15 breaths/min to help maintain normal oxygen and carbon dioxide partial pressures.

Myth—Pulse oximeters measure the adequacy of ventilation during inhalant anesthesia.

Reality—During inhalant anesthesia, oxygen is almost always used as the carrier gas and often comprises > 90% of the total inspired gases. As stated previously, at this concentration of oxygen, even complete apnea will not result in hypoxemia in dogs and cats with normal lung function for upwards of 30 minutes (although this time is less in horses).42,43 Therefore, pulse oximetry cannot be expected to detect hypoventilation in oxygen-breathing patients. In patients breathing room air (21% oxygen), however, desaturation generally accompanies hypoventilation and pulse oximetry may be useful in indicating hypoventilation-induced hypoxemia in these patients.44

Myth—A strong palpable pulse indicates good blood pressure and perfusion.

Reality—While a palpable pulse does at least confirm that the heart is beating and creating some degree of circulation, a strong pulse indicates only that there is a large difference between systolic and diastolic blood pressures, not necessarily an optimal mean blood pressure or good perfusion of tissues.45 For example, a puppy with a patent ductus arteriosus may have exceptionally strong pulses, yet have low mean blood pressure and relatively poor tissue perfusion. Many anesthetized animals with palpably normal pulses are actually hypotensive, as indicated by mean arterial blood pressure < 70 mm Hg.

Myth—I would know if my anesthetized patients had low blood pressure.

Reality—As indicated previously, the only way to accurately assess blood pressure is to measure it. Many animals that are hypotensive during anesthesia appear clinically normal, with normal heart and respiratory rates, pink mucous membranes, and physical signs (eye position and reflexes and jaw tone) indicating appropriate anesthetic depth. When asked to name the biggest problem encountered when anesthetizing dogs and cats, only 1 of more than 20 small animal veterinarians interviewed cited hypotension; it is unlikely to be purely coincidental that the same veterinarian was also the only one in the group who routinely measured blood pressure in her anesthetized patients.46 Many dogs and cats that are hypotensive appear to recover from anesthesia without any overt problems. However, vital organs such as the kidneys, which require a minimum blood pressure to maintain adequate perfusion, can be damaged by hypotension. Because 75% of nephrons must be nonfunctional before BUN and creatinine concentrations increase or clinical signs appear, it is likely that substantial perianesthetic kidney damage might go unnoticed. At least 1 expert on renal disease has suggested that measurement of arterial blood pressure during anesthesia would help reduce the likelihood of renal ischemia.47

Myth—Low blood pressure during anesthesia only happens to old or sick animals.

Reality—At the Colorado State University Veterinary Teaching Hospital, blood pressure is routinely measured in all anesthetized animals. A recent survey of 1 year’s anesthesia records indicated that 32% of all anesthetized dogs were hypotensive (systolic arterial pressure < 90 mm Hg or mean arterial pressure < 60 mm Hg) at some point during anesthesia. It might be speculated that the patients anesthetized in academic veterinary hospitals tend to be sicker and therefore more susceptible to anesthetic-induced hypotension than those anesthetized in private practices for routine elective surgeries. However, a separate review of Veterinary Teaching Hospital patients undergoing only elective ovariohysterectomy indicated that 28% of these presumably healthy and young dogs were hypotensive. Given that all of these patients were administered fluids IV at a standard rate of 5 to 10 mL/kg/h during anesthesia, it is likely that the incidence of hypotension might have been even higher if fluids had not been given. In most cases, hypotension was corrected by decreasing the anesthetic vaporizer setting or administering additional fluids IV, but in 12% of anesthetized dogs, inotropes such as dobutamine or ephedrine had to be administered to increase blood pressure to an acceptable value. A separate survey of blood pressure measurements in a private small animal veterinary clinic indicated that hypotension occurred in 22% of anesthetized dogs and 33% of anesthetized cats for an overall incidence of 27%.b In that clinic, blood pressure increased when the vaporizer setting was decreased (6% of anesthetized animals) or when additional fluids were administered IV (8% of anesthetized animals), but 13% of all anesthetized animals were hypotensive and did not receive any treatment.b

Myth—Dentistry is a minor procedure that requires no special patient preparation or monitoring during anesthesia.

Reality—Many patients that undergo dental procedures are old and have other problems such as mitral regurgitation or hepatic or renal disease. Consequently, anesthesia of these patients is likely to entail greater risk than anesthesia of younger, healthier patients, and the anesthetic protocol should be planned only after careful consideration of physical examination and laboratory findings. Appropriate IV administration of fluids and monitoring of blood pressure, oxygenation, and heart rate and rhythm are especially important in older or compromised patients.

Myth—Bradycardia is a sign that the vaporizer setting should be decreased.

Reality—Although tachycardia during surgical stimulation may indicate an insufficient plane of anesthesia, deep planes of gas anesthesia as a general rule do not cause bradycardia. Increasing the depth of anesthesia with some anesthetics, such as sevoflurane, may actually cause the heart rate to increase.48 Bradycardia during anesthesia is more often associated with the use of opioids and α2-adrenoceptor agonists or with interventions that increase vagal tone (usually responsive to anticholinergics) or hypothermia (often unresponsive to anticholinergics).

Myth—Movement during anesthesia indicates conscious awareness by the patient.

Reality—One of the important benefits of general anesthesia is its ability to render a patient immobile. Immobility is helpful in many procedures and vital in a few. The MAC of an inhalant anesthetic, the primary indicator of its anesthetic potency, is defined as the MAC required to prevent movement in response to a noxious stimulus in 50% of the patients studied. In general, muscle activity is reduced in a linear fashion as anesthetic depth is increased.49 For these reasons, immobility is generally regarded as an important marker of anesthetic depth. However, when cerebral function is studied, the onset of movement is not closely associated with the onset of consciousness. In fact, a fair amount of movement can occur long before awareness is reported in people.50,51 Therefore, movement that does not interfere with the procedures being performed may not be detrimental to the patient. An understanding of this fact may prevent an overreaction to movements during anesthesia and prevent anesthetizing patients beyond what is necessary, leading to cardiovascular and respiratory depression, which may be far more detrimental.

Myth—Animals that take a long time to wake up were probably at too high a vaporizer setting.

Reality—Currently used anesthetics, such as isoflurane and sevoflurane, are relatively quickly eliminated through the respiratory system once the vaporizer is turned off, and extubation should be achieved within 10 minutes.a For animals on a circle system, periodically emptying the rebreathing bag and refilling it with pure oxygen will help prevent rebreathing of the anesthetic. Even after deep levels of anesthesia, the blood and brain concentrations of gas anesthetics should decrease sufficiently within 15 minutes that the animal will wake up. If it does not, other potential causes of prolonged anesthesia, such as hypothermia and administration of sedative drugs such as opioids, should be considered. It is important to realize that a fast recovery is not necessarily a good recovery; animals that have undergone pain-inducing procedures are likely to benefit from both the analgesia and slower, quieter recovery afforded by administration of opioids.

Myth—Administering oxygen at the end of surgery delays recovery.

Reality—The administration of oxygen has minimal to no effect on recovery time but may have benefits in preventing hypoxemia. Discontinuation of oxygen administration before extubation resulted in hypoxemia (pulse oximeter values < 90%) within 3 minutes in 5% of healthy dogs (American Society of Anesthesiologists status 1 or 2) recovering from anesthesia.c If a circle system is used, periodically emptying the breathing bag and refilling it with oxygen will help remove exhaled anesthetic from the system. Assuming a scavenging system is in use, keeping the animal connected to the anesthesia breathing circuit during recovery has the added benefit of reducing pollution in the recovery area.

Myth—I would know if my patients were in pain after surgery.

Reality—Recognizing pain in the postoperative period is often difficult in dogs and cats.52-54 Some painful dogs and cats will display behaviors that will be correctly interpreted as pain. Unfortunately, many other animals will not demonstrate behaviors that will convince the veterinary staff that are actually in pain. In fact, residual anesthetic drugs and tranquilizers such as acepromazine often prevent or mask the demonstration of behaviors suggestive of pain. Adding to the difficulty of recognizing pain is the fact that no foolproof method exists to measure and quantify pain in animals.

Diagnosing pain in animals often requires time and knowledge of the normal behavior of the species and individual. It is certainly understandable that a busy veterinary staff with no training in the evaluation of pain would frequently overlook painful patients. Since the correct diagnosis of pain in dogs and cats is often difficult, a working assumption that all surgical procedures inflict pain in animals will provide better quality of care than the assumption that the staff will be able to readily recognize those animals in need of analgesics. Proactively using analgesics to minimize postoperative pain is consistent with the fundamental principles of providing good medical care to each of our patients.



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aAmai A, Steffey EP, Ilkiw JE, et al. Quantitative characteristics of anesthetic induction with and recovery from isoflurane and sevoflurane in cats (abstr), in Proceedings. Annu Meet Am Coll Vet Anesth 2002;47.
bGordon A, Westarbor Animal Hospital, Ann Arbor, Mich: Personal communication, 2003.
cGaynor JS, Animal Emergency Care Center North, Colorado Springs, Colo: Personal communication, 2003.

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19. Hellyer PW. Management of acute and surgical pain. Semin Vet Med Surg (Small Anim) 1997;12:106–114.

20. Hellyer PW, Gaynor JS. How I treat: acute postsurgical pain in dogs and cats. Compend Contin Educ Pract Vet 1998;20:140–153.

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23. Waterman AE, Kalthum W. Use of opioids in providing postoperative analgesia in the dog: a double-blind trial of pethidine, pentazocine, buprenorphine, and butorphanol. In: Short CE, Van Poznak A, ed. Animal pain. New York: Churchill Livingstone Inc, 1992;466–476.

24. Sawyer DC, Rech RH, Durham RA, et al. Dose response to butorphanol administered subcutaneously to increase visceral nociceptive threshold in dogs. Am J Vet Res 1991;52:1826–1830.

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41. Muir WW, Gadawski J. Cardiorespiratory effects of low-flow and closed circuit inhalation anesthesia, using sevoflurane delivered with an in-circuit vaporizer and concentrations of compound A. Am J Vet Res 1998;59:603–608.

42. Draper WB, Whitehead RW. The phenomenon of diffusion respiration. Anesth Analg 1947;28:307–318.

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44. Severinghaus JW, Kelleher JF. Recent developments in pulse oximetry. Anesthesiology 1992;76:1018–1038.

45. Mazzaferro E, Wagner AE. Hypotension during anesthesia in dogs and cats: recognition, causes, and treatment. Compend Contin Educ Pract Vet 2001;23:728–737.

46. Wagner AE, Hellyer PW. Observations of private veterinary practices in Colorado, with an emphasis on anesthesia. J Vet Med Educ 2002;29:175–182.

47. Grauer GF. Prevention of acute renal failure. Vet Clin North Am Small Anim Pract 1996;26:1447–1459.

48. Steffey EP. Other new and potentially useful inhalational anesthetics. Vet Clin North Am Small Anim Pract 1992;22:335–340.

49. Antognini JF, Wang XW, Carstens E. Quantitative and qualitative effects of isoflurane on movement occurring after noxious stimulation. Anesthesiology 1999;91:1064–1071.

50. Prys-Roberts C. Anaesthesia: a practical or impractical construct? Br J Anaesth 1987;59:1341–1345.

51. Zbinden AM, Maggiorini M, Petersen-Felix S, et al. Anesthetic depth defined using multiple noxious stimuli during isoflurane/oxygen anesthesia, part I: motor reactions. Anesthesiology 1994;80:253–260.

52. Hansen BD, Hardie EM, Carroll GS. Physiological measurements after ovariohysterectomy in dogs: what’s normal? Appl Anim Behav Sci 1997;51:101–109.

53. Hardie EM, Hansen BD, Carroll GS. Behavior after ovariohysterectomy in the dog: what’s normal? Appl Anim Behav Sci 1997;51:111–128.

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Postanesthetic esophageal dysfunction in 13 dogs.
J Am Anim Hosp Assoc 40[6]:455-60 2004 Nov-Dec

Wilson DV, Walshaw R
Thirteen dogs with postanesthetic esophageal dysfunction were identified; 10 of these animals had esophageal stricture. Regurgitation was noted in six dogs during the inciting anesthetic event. Clinical problems common to all dogs included vomiting/regurgitation and weight loss. Coughing was noted in six dogs, and aspiration pneumonia was present in four of these dogs. The associated mortality rate was 23%. The duration of symptoms ranged from 17 to 150 days, and the diagnosis was often delayed (up to 76 days from onset of clinical signs to diagnosis). Postanesthetic esophageal dysfunction was a debilitating and costly problem that developed in one dog despite current preventative treatment.

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Vet Rec. 1995 Nov 11;137(20):513-6. Related Articles, Links


Gastro-oesophageal reflux during anaesthesia in the dog: the effect of age, positioning and type of surgical procedure.

Galatos AD, Raptopoulos D.

Department of Clinical Sciences, Veterinary School, University of Thessaloniki, Greece.

Lower oesophageal pH was monitored in 270 dogs under anaesthesia. There were 47 episodes of gastro-oesophageal reflux (17.4 per cent), most of which occurred shortly after the induction of anaesthesia. The refluxate was usually acid (pH < 4.0), but in four of the episodes (8.5 per cent) it was alkaline (pH > 7.5). Gastric contents with a pH below 2.5 were refluxed on 27 occasions (10 per cent) for an average period of about 44 minutes. Regurgitation occurred in two of the dogs. Increased age seemed to be associated with an increased incidence of reflux and an increased gastric acidity. Body position (sternal, dorsal and left or right lateral) and the tilt of the body during surgery (horizontal or tilted to an 8 degrees head-up or head-down position) had no influence on the incidence of gastro-oesophageal reflux. Dogs undergoing intra-abdominal surgery had significantly more reflux episodes than dogs undergoing non-abdominal surgery.

PMID: 8588277 [PubMed - indexed for MEDLINE]

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Preoperative Fasting: "Nil per Os After Midnight"--Time To Change?
World Small Animal Veterinary Association World Congress Proceedings, 2004
Dimitris Raptopoulos, DVM, PhD, DVA, DECVA, Professor; Ioannis Savvas, DVM, PhD
Clinic of Surgery, Faculty of Veterinary Medicine, Aristotle University of Thessaloniki
Thessaloniki, Greece

INTRODUCTION

In 1883, Baron Joseph Lister, an English surgeon wrote, "While it is desirable that there should be no solid matter in the stomach when chloroform is administered, it will be found very salutary to give a cup of tea or beef-tea two hours previously". Most anaesthetists and surgeons followed this advice for many years. In 1946, Mendelson published a very well known paper on high incidence of pulmonary aspiration during general anaesthesia, in obstetric patients. Shortly after this publication, the practice of "nil per os after midnight" was established (Pandit et al. 2000). Thereafter, prevention of aspiration of gastric contents became one of the cornerstones of safe anaesthetic practice in humans. About 10% of the anaesthetic mortality is related to gastro-oesophageal reflux (GOR) during induction of anaesthesia. Strict preoperative fasting rules to ensure an empty stomach at induction had been a major concern for the anaesthesiologists. However, over the past two decades, several authors have questioned the scientific basis of these rules (Morgan 1984; Spence 1989; Engelhardt and Webster 1999; Ljungqvist and Soreide 2003).

In human medicine, major risk factors for GOR include: a high ASA physical status score, emergency surgery, pregnancy, ingestion of a meal within 3 hours, opioids, obesity, and type of surgery. About 10-20% of GOR cases during induction result in aspiration pneumonitis. The incidence of aspiration pneumonitis varies among the hospitals between 0.7 and 10.2 per 10,000 of general anaesthetics. The gastric contents aspirated into the lungs may cause mechanical obstruction of the airways, chemical inflammation (very high/low pH), and infection (Harrison 1978; Hovi-Viander 1980; Gibbs and Modell 1992; Warner et al. 1993; Turner 1996; Engelhardt and Webster 1999; Ng and Smith 2001). It has been shown that in rhesus monkeys a maximum volume of 0.4 ml kg-1 with a pH of 2.5 may be aspirated without severe respiratory consequences. This corresponds to a total volume of about 25 ml in an adult woman in pregnancy. The authors had proposed that a gastric content volume of at least 25 ml with a pH less than 2.5 indicate a high risk patient (Roberts and Shirley 1974).

In veterinary medicine, there is no reference to aspiration occurring during induction of anaesthesia in dogs and cats, although this should not be assumed as impossible. However, GOR during anaesthesia is the major cause of oesophagitis (reflux oesophagitis) and oesophageal stricture. In a recent study, the overall incidence of GOR during anaesthesia was 16.3 % (39/240), in dogs. In only one of these cases regurgitation occurred, the rest of them being silent ref lux (no gastric contents were observed out of the mouth) (Galatos and Raptopoulos 1995b). In another study (Kushner and Shofer 2003), the anaesthetic complication rate for oesophageal stricture calculated retrospectively was found to be 0.13 % (30/23,295). However, mortality was high (30%) in the stricture cases. It seems that whereas GOR may occur during general anaesthesia, oesophageal stricture is rare, while it is associated with high morality rate. Interestingly, there is no report of reflux oesophagitis after anaesthesia in humans.

CURRENT RECOMMENDATIONS IN HUMAN MEDICINE

In humans, the major methods used to minimize aspiration are control of gastric contents, reduction in GOR, prevention of aspiration, and attenuation of the effects of aspiration. The first two include preoperative fasting, decrease in gastric acidity, facilitation of gastric emptying, and maintenance of a competent lower oesophageal sphincter (LOS). The latter two involve tracheal intubation or the use of other airway devices and application of cricoid pressure (Ng and Smith 2001).

Fasting before surgery is necessary to avoid the risk of regurgitation and vomiting; it is also a legal requirement (Watson and Rinomhota 2002). The fear of aspiration of gastric contents and its life-threatening consequences in patients (aspiration pneumonitis and respiratory failure), has caused many medical practitioners, particularly anaesthesiologists, to rigidly follow conservative (i.e., prolonged) preoperative fasting standards. This is the nil per os (NPO) order for clear fluids/liquids and solids overnight or six to eight hours preceding the induction of anaesthesia. However, this practice neither takes into account the differences in the rate of gastric emptying for solid food (which may exceed six hours) and clear liquids (which is one to two hours), nor the differences in scheduled times of surgery (Watson and Rinomhota 2002).

Moreover, the concept that fasting produces an "empty stomach" has been shown to be incorrect. Numerous studies demonstrate that fasting neither diminishes gastric volume nor decreases gastric acidity and the risk of pulmonary aspiration is not increased by the preoperative intake of clear liquids. Withholding fluids preoperatively is not only of no benefit to patients but may even be harmful (Dowling, Jr. 1995). A long fasting may lead to thirst, general discomfort, dehydration, and possible hypoglycaemia (Phillips et al. 1994). Preoperative fasting in man may lead to a fluid deficit of about one litre, which may contribute to perioperative discomfort and morbidity (Holte and Kehlet 2002).

Several studies have confirmed that clear liquids are rapidly emptied from the stomach. Gastric residual volume in humans who have had unlimited clear fluids up to 2 hours before induction is not different from, or may even be smaller than, that for humans who have been fasted overnight. Therefore, there is no need for excessive periods of fasting before elective surgical procedures in any patient (Cote 1999). Moreover, potential benefits of reduced thirst, better perioperative experience, improved compliance and reduced hypoglycaemia may be seen (Phillips et al. 1994).

Based on the new data available, several editorials and national anaesthesiology societies recommend a more liberal approach to preoperative fasting guidelines in otherwise healthy patients undergoing elective procedures. The newer recommendations allow the consumption of clear liquids up to two hours before elective surgery, a light breakfast six hours before the procedure, and a heavier meal eight hours beforehand (Strunin 1993; Soreide et al. 1996; Eriksson and Sandin 1996; Warner et al. 1999; Pandit et al. 2000; Ng and Smith 2001; Ljungqvist and Soreide 2003). The application of these new guidelines resulted in no increase of complications in a 3-year study in Norway (Fasting et al. 1998). It should be mentioned that some authors suggest that a light breakfast (tea and toast, for example) may be given 3-4 hours before the procedure (Miller et al. 1983). Finally, non-human milk is similar to solids in gastric emptying time (Warner et al. 1999).

CURRENT RECOMMENDATIONS IN VETERINARY MEDICINE

In dogs, factors that may influence the incidence of GOR include: volume and acidity of gastric contents, age, surgical procedure, drugs used for premedication and/or anaesthesia, and preoperative fasting. Positioning (body tilt on surgical table) does not seem to have any effect. Increased age as well as intra-abdominal surgery was associated with significantly increased incidence of reflux. Moreover, many drugs may affect LOS tone and predispose to GOR (Galatos and Raptopoulos 1995a; Galatos and Raptopoulos 1995b). In mature healthy dogs, it is usually recommended to allow free access to water up to 2 hours before anaesthesia and no food 6 (Bednarski 1996) or 12 hours (Hall et al. 2001) beforehand, although Muir et al. (2000) suggest that food and water should be withheld for approximately 6 hours before surgery. However, there is evidence that increasing the duration of preoperative fasting is associated with an increased incidence of ref lux in dogs. None of 30 dogs fasted 2-4 hours refluxed, whereas 4/30 (13.3 %) dogs fasted 12-18 hours had a reflux episode during anaesthesia (p=0.112) (Galatos and Raptopoulos 1995b). In another study, none of 31 dogs fasted 3 hours refluxed, whereas 6/29 (20.7 %) dogs fasted 10 hours had a reflux episode (p=0.009) (Savvas and Raptopoulos 2000). In the latter study, the dogs had been fed a commercial canned canine diet at the half daily rate. Furthermore, dogs fasted 3 hours had not significantly increased gastric content volume compared to dogs fasted 20 hours, while gastric acidity was reduced (Savvas 2000), which may have a beneficial effect in preventing major consequences in case of GOR during anaesthesia. In contrast, the administration of fat-free cow milk (10 ml kg-1) resulted in a significantly lower gastric content pH.

There is evidence that in otherwise healthy dogs undergoing elective surgery, allowing the consumption of water up to two hours prior to induction of anaesthesia and a light meal 3-4 hours before the procedure may be beneficial. Although the above findings have not been used in a sufficiently large number of clinical cases, it seems that the time has come to abandon the traditional "nil per os after midnight" or nil per os for 6-12 hours prior to anaesthesia, and adopt more liberal guidelines for preoperative fasting in adult healthy dogs undergoing elective procedures.

References

1. Bednarski RM (1996) Anesthesia and immobilization of specific species: dogs and cats. In: Lumb & Jones' Veterinary Anesthesia (3rd ed). Thurmon JC, Tranquilli WJ, Benson GJ (eds). Williams & Wilkins, Baltimore, pp. 591-598.

2. Cote CJ (1999) Preoperative preparation and premedication. Br J Anaesth 83, 16-28.

3. Dowling JL, Jr. (1995) "Nulls per os [NPO] after midnight" reassessed. R I Med 78, 339-341.

4. Engelhardt T and Webster NR (1999) Pulmonary aspiration of gastric contents in anaesthesia. Br J Anaesth 83, 453-460.

5. Eriksson LI and Sandin R (1996) Fasting guidelines in different countries. Acta Anaesthesiol Scand 40, 971-974.

6. Fasting S, Soreide E, Raeder JC (1998) Changing preoperative fasting policies. Impact of a national consensus. Acta Anaesthesiol Scand 42, 1188-1191.

7. Galatos AD and Raptopoulos D (1995a) Gastrooesophageal ref lux during anaesthesia in the dog: the effect of age, positioning and type of surgical procedure. Vet Rec 137, 513-516.

8. Galatos AD and Raptopoulos D (1995b) Gastrooesophageal ref lux during anaesthesia in the dog: the effect of preoperative fasting and premedication. Vet Rec 137, 479-483.

9. Gibbs CP and Modell JH (1992) Management of aspiration pneumonitis. In: Anesthesia. Miller RD (ed). Churchill Livingstone, New York, pp. 12931319.

10. Hall LW, Clarke KW, Trim CM (2001) Veterinary Anaesthesia (10th ed). W.B.Saunders, London.

11. Harrison GG (1978) Death attributable to anaesthesia. A 10-year survey (1967-1976). Br J Anaesth 50, 1041-1046.

12. Holte K and Kehlet H (2002) Compensatory fluid administration for preoperative dehydration-does it improve outcome? Acta Anaesthesiol Scand 46,1089-1093.

13. Hovi-Viander M (1980) Death associated with anaesthesia in Finland. Br J Anaesth 52, 483-489.

14. Kushner LI and Shofer FS (2003) Incidence of esophageal strictures and esophagitis after general anesthesia. Proceedings of the 8th World Congress of Veterinary Anesthesia, Knoxville, Tennessee USA. p. 184.

15. Ljungqvist 0 and Soreide E (2003) Preoperative fasting. Br J Surg 90, 400-406.

16. Miller M, Wishart HY, Nimmo WS (1983) Gastric contents at induction of anaesthesia. Is a 4-hour fast necessary? Br J Anaesth 55, 1185-1188.

17. Morgan M (1984) Control of intragastric pH and volume. Br J Anaesth 56, 47-57.

18. Muir WW, Hubbell JAE, Skarda RT, Bednarski RM (2000) Handbook of Veterinary Anesthesia (3rd ed). Mosby Inc., St. Louis.

19. Ng A and Smith G (2001) GastroesophageaI reflux and aspiration of gastric contents in anesthetic practice. Anesth Analg 93, 494-513.

20. Pandit SK, Loberg KW, Pandit UA (2000) Toast and tea before elective surgery? A national survey on current practice. Anesth Analg 90, 1348-1351.

21. Phillips S, Daborn AK, Hatch DJ (1994) Preoperative fasting for paediatric anaesthesia. Br J Anaesth 73,529-536.

22. Roberts RB and Shirley MA (1974) Reducing the risk of acid aspiration during cesarean section. Anesth Analg 53, 859-868.

23. Savvas I (2000) The effect of pre-operative fasting and food composition on the incidence of gastrooesophageal ref lux during anaesthesia in the dog. PhD Thessis. Aristotle University of Thessaloniki.

24. Savvas I and Raptopoulos D (2000) Incidence of gastro-oesophageal reflux during anaesthesia, following fasting of different duration in dogs. Association of Veterinary Anaesthetists, Autumn Meeting, Madrid, 22nd-24th September 1999, Proceedings. Vet Anaesth Analg 1, 59.

25. Soreide E, Hausken T, Soreide JA, Steen PA (1996) Gastric emptying of a light hospital breakfast. A study using real time ultrasonography. Acta Anaesthesiol Scand 40, 549-553.

26. Spence AA (1989) Postoperative pulmonary complications. In: General Anaesthesia (5th ed). Nunn JF, Utting JE, Brown BR (eds). Butterworths, London, pp. 1149-1159.

27. Strunin L (1993) How long should patients fast before surgery? Time for new guidelines. Br J Anaesth 70,1-3.

28. Turner DAB (1996) Emergency anaesthesia. In: Textbook of Anaesthesia (3rd ed). Aitkenhead AR, Smith G (eds). Churchill Livingstone, Edinburgh, pp. 519-532.

29. Warner MA, Caplan RA, Epstein BS, Keller CE, Leak JA, Maltby R, Nickinivich DG, Schreiner MS, Weinlander CM (1999) Practice guidelines for preoperative fasting and the use of pharmacologic agents to reduce the risk of pulmonary aspiration: application to healthy patients undergoing elective procedures. A report by the American Society of Anesthesiologists Task Force on preoperative fasting. Anesthesiology 90, 896-905.

30. Warner MA, Warner ME, Weber JG (1993) Clinical significance of pulmonary aspiration during the perioperative period. Anesthesiology 78, 56-62.

31. Watson K and Rinomhota S (2002) Preoperative fasting: we need a new consensus. Nurs Times 98, 36-37.

Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)
Dimitris Raptopoulos, DVM, PhD, DVA, DECVA
Clinic of Surgery, Faculty of Veterinary Medicine, Aristotle University of Thessaloniki
Thessaloniki, Greece

Speaker Information:
Dimitris Raptopoulos is Professor of Veterinary Anesthesiology at the Faculty of Veterinary Medicine, University of Thessaloniki, Greece, since 1995 Graduated from the same Faculty in 1969. For about 3.5 years he did postgraduate studies and postdoctoral research in Bristol, England, where he obtained the Diploma in Veterinary Anaesthesia (DVA) in 1978. In 1985 he spent 6 months as Visiting Assistant Professor of Anaesthesiology in the Veterinary School of the University of Florida, USA. In 1995 he was nominated Invited Specialist (de facto Diplomate) and member of the Interim Board of the European College of Veterinary Anaesthesia (ECVA), of which he was Honorary Secretary until 2002. Since then, he is the President of the College. From 2000 to 2002 he was President of the Association of Veterinary Anaesthetists (AVA). He is currently Dean of the Faculty of Veterinary Medicine, University of Thessaloniki, Greece. His main research interests are in gastro-oesophageal reflux during anaesthesia and pre-operative fasting.

Ioannis Savvas, DVM, PhD
Clinic of Surgery, Faculty of Veterinary Medicine, Aristotle University of Thessaloniki
Thessaloniki, Greece

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In: Recent Advances in Veterinary Anesthesia and Analgesia: Companion Animals, Gleed R.D. and Ludders J.W. (Eds.). International Veterinary Information Service, Ithaca NY (www.ivis.org), Last updated: 14-Nov-2005; A1413.1105

Inhalants Used in Veterinary Anesthesia
R. D. Keegan

College of Veterinary Medicine, Washington State University, Pullman, Washington, USA.

Introduction
Inhalant anesthetics in use in veterinary anesthesia include nitrous oxide, halothane, isoflurane, sevoflurane, and desflurane. The latter four agents are commonly referred to as "the potent inhalants" as their MAC values (minimal alveolar concentration) are such that they may be used as the sole anesthetic agents during a surgical procedure. Nitrous oxide lacks sufficient potency to be used as a sole anesthetic in healthy, young veterinary patients. It must be pointed out that the clinical use of nitrous oxide is, if not controversial, at least contentious among veterinary anesthesiologists. Many specialists feel that the lack of potency of nitrous oxide renders the drug undesirable as an adjunct to inhalation anesthesia. Halothane

Introduced into veterinary anesthesia practice in 1956, halothane is still a widely used inhalant anesthetic. Synthesized in an effort to produce a non-flammable inhalant anesthetic, the drug was an attractive alternative to diethyl ether and cyclopropane. Although the fluorinated hydrocarbons are not flammable, significant arrhythmogenic properties limited their future development as inhalant anesthetics. Halothane is a potent drug, having a MAC value in dogs of 0.87% and 1.14% in cats. The vapor pressure of halothane (243 mm Hg at 20°C) is such that it must be administered using a precision vaporizer if precise, predictable concentrations are desired. Clinically useful settings in small animals are 2 - 3% for induction of anesthesia, and 1 - 1.5% for maintenance of anesthesia. The moderate blood solubility of halothane (blood/gas PC = 2.4) translates to a more rapid induction of anesthesia compared with more soluble agents such as methoxyflurane or diethyl ether.

Cardiovascular Effects
The cardiovascular effects of halothane may be significant. In a dose dependent manner, halothane decreases blood pressure by decreasing myocardial contractility via direct depression of the myocardium which results in a reduction of cardiac output [4]. As mentioned previously, halothane has arrhythmogenic properties. Studies investigating inhalant anesthetic arrhythmogenicity using the arrhythmogenic dose of epinephrine (ADE) test have shown decreased arrhythmogenic thresholds during administration of halothane. Cardiac arrhythmias during clinical use of halothane are frequently encountered. Most are fairly benign and do not require administration of anti-arrhythmogenic drugs. If halothane associated arrhythmias are worrisome, switching to a less arrhythmogenic inhalant anesthetic such as isoflurane will often reduce or eliminate the arrhythmias. Switching inhalant anesthetics mid-anesthesia may be performed safely provided the anesthetist is mindful of both the solubilities and the potencies of the two inhalant anesthetics. Inhalants having low blood solubility (low PC values) will result in a more rapid induction into and recovery from anesthesia compared with inhalants having high blood solubility (high PC values). Inhalant anesthetics having high potency (low MAC values) require lower alveolar concentrations to induce general anesthesia. These two physical properties of halothane and isoflurane indicate that isoflurane, having lower solubility, will be taken up more rapidly than halothane will be eliminated. Isoflurane is also less potent (higher MAC) than is halothane, thus it might appear that the more rapid effect seen with isoflurane would be counterbalanced by the higher concentrations needed for anesthesia. Clinically it appears that the lower solubility of isoflurane more than compensates for the higher alveolar concentrations necessary, therefore, if a patient is immediately switched from halothane to isoflurane, a deepening of the anesthetic plane is frequently seen. Thus when switching from halothane to isoflurane it is recommended that the administration of halothane be discontinued or at least reduced until the patient displays signs consistent with a lighter anesthetic plane before administering isoflurane.
A similar line of reasoning applies when switching from halothane or isoflurane to the less soluble sevoflurane or desflurane. Always decrease administration of the more soluble inhalant before switching to the less soluble agent.

Respiratory Effects
Administration of halothane is associated with a dose-dependent respiratory depression that is initially manifested as a decrease in tidal volume; as anesthetic depth increases a decrease in respiratory rate also is seen. Common to all inhalant anesthetics, the respiratory depressing effects of halothane may be at least partially offset by surgical stimulation [5].

CNS Effects
Inhalation of halothane results in global depression of the central nervous system. Increasing depth of anesthesia results in reduced EEG activity but unlike with isoflurane a burst suppression pattern is not frequently observed [6]. Halothane decreases cerebral metabolic rate of oxygen utilization and is a potent cerebrovasodilator that results in increased cerebral blood flow (CBF) and intracranial pressure (ICP) [7]. The dilating effect of halothane on the cerebral vasculature may be greatly modified by the patient’s arterial PCO2 tension [8].
Hypoventilation and associated elevations in PaCO2 will greatly exacerbate the increases in ICP while mild hyperventilation (controlled manually or mechanically) - PaCO2 ~ 30 mm Hg - will diminish halothane-induced increases in ICP. Since other inhalant anesthetics do not result in the same magnitude of increase in CBF and ICP at similar MAC levels [9], halothane is usually not recommended for patients presenting with or suspected of having raised ICP.

Other Effects
Of all inhalant anesthetics in veterinary use today, halothane is the least inert and most highly metabolized with 20 - 25% of the anesthetic recovered as metabolites. Although all inhalant anesthetics have the potential to be associated with a hepatocellular injury that is usually manifested as centrilobular necrosis, halothane has been the drug most frequently implicated [10]. While the precise mechanism of hepatic injury remains unknown, a likely cause is the production of reactive metabolites from hepatic biotransformation, especially during periods of regional hepatic hypoxemia or hypoperfusion, together with an autoimmune reaction.

Isoflurane
An isomer of the inhalant anesthetic enflurane, isoflurane was introduced into veterinary practice in the 1980's. Similar to the fluorinated hydrocarbon halothane, isoflurane is nonflammable and non-explosive in clinically useful concentrations, but its fluorinated ether structure seems to markedly reduce the potential for cardiac dysrhythmias. Isoflurane is slightly less potent than halothane with a MAC value of 1.31 in dogs and 1.61% in cats. The solubility of isoflurane (Blood:Gas PC = 1.3) is lower than that of halothane and inductions into and recoveries from anesthesia occur more rapidly than with halothane. Isoflurane has a vapor pressure similar to that of halothane (238 mmHg at 20°C) and as such it is recommended that it be administered in a precision vaporizer. Clinically useful settings in small animals are 2 - 4% for induction of anesthesia, and 1 - 2% for maintenance of anesthesia. The current popularity of isoflurane in veterinary practice reflects the drug’s cardiovascular stability, low blood solubility, resistance to hepatic metabolism and attractive price.

Cardiovascular Effects
Isoflurane appears to be among the best of the inhalant anesthetics in preserving cardiovascular function. The drug is less likely than is halothane to sensitize the myocardium to the dysrhythmogenic effects of catecholamines. As a consequence, isoflurane is preferred over halothane in patients presenting with pre-existing dysrhythmias. Indeed, in our clinical experience many patients presenting with ventricular premature contractions prior to anesthesia are actually improved under isoflurane anesthesia, that is, the incidence of the ventricular premature contractions is often markedly reduced or eliminated. The exact mechanism of this effect is unknown but may be a result of a decrease in sympathetic nervous system activity and/or a reduction in painful stimuli. Isoflurane is associated with a dose dependant reduction in cardiac output and blood pressure. The effect on cardiac output is less than that seen with halothane although the reduction in blood pressure may be more significant. Reduction of cardiac output appears to be due to a decrease in myocardial contractility and a concomitant but mild decrease in stroke volume. However, isoflurane is associated with an increase in heart rate which compensates for the mild depression of stroke volume and the net result is a slight decrease or no change in cardiac output. Isoflurane is a potent vasodilator and as such reduces systemic vascular resistance which results in depression of mean arterial pressure despite the fact that cardiac output remains essentially unchanged. The mechanism whereby isoflurane causes vasodilation may be related to its ability to activate peripheral opioid receptors by an endogenous opioid peptide possibly related to methionine enkephalin [11].

Respiratory Effects
Similar to other inhalant anesthetics, isoflurane depresses ventilation in a dose dependant manner. In anesthetized animals not experiencing surgical stimulation, tidal volume decreases and arterial CO2 tension increases as depth of anesthesia is increased. As the administered dose of isoflurane approaches 2.0 MAC, respiratory frequency decreases and arterial CO2 tension increases [12]. As with all inhalant anesthetics, the effect of surgical stimulation mitigates the respiratory depression caused by isoflurane [5]. This effect is most pronounced during light planes of anesthesia and may be clinically insignificant at very deep levels.

CNS Effects
Similar to halothane, administration of isoflurane results in global central nervous system depression. Whereas increasing depth of halothane anesthesia is characterized by an isoelectric EEG pattern, increasing depth of isoflurane anesthesia is associated with a "burst suppression" pattern on the EEG. The burst suppression pattern is commonly seen in dogs at concentrations of 1.8 - 2.0% (1.4 - 1.5 MAC) and is characterized by a period of electrical quiescence interrupted by bursts of activity [13]. Administration of isoflurane is associated with an increase in CBF and therefore in ICP, however the magnitude of increase is much less than for halothane at equi-MAC concentrations. Hyperventilation and the associated reduction in arterial CO2 may be used to limit the isoflurane-associated increase in CBF since the cerebral circulation remains responsive to changes in PaCO2 [14,15]. As the increase in CBF is less for isoflurane compared with halothane and a lowering of the patient’s PaCO2 through the use of judicious hyperventilation is usually quite easily accomplished, isoflurane is generally preferred over halothane for maintenance of inhalant anesthesia in a patient presenting with raised intracranial pressure.

Other Effects
Isoflurane is an extremely inert and stable compound. Less than 0.2% of the administered dose is metabolized. As with halothane, hepatic blood flow is decreased in a dose dependant manner. Despite the potential reduction in hepatic blood flow, post anesthetic serum biochemical tests show minimal changes in hepatocyte integrity or function, presumably reflecting the inertness and lack of metabolism of the drug [16]. The lack of significant effect on hepatic function and the extremely small amount of the drug that undergoes hepatic metabolism has made isoflurane a popular inhalant anesthetic for use in patients presenting with compromised hepatic function.

Sevoflurane
Sevoflurane is the newest inhalant anesthetic that has been approved for use in veterinary anesthesia. The drug was initially described in 1975 but not released until the 1990s. Sevoflurane is nonflammable and non-explosive in concentrations used clinically. It has a MAC value of 2.36% in dogs and 2.58% in cats, and a blood:gas partition coefficient of 0.69 making it both less potent and less soluble in blood than either halothane or isoflurane. Typical vaporizer settings are 4 - 5% for induction and 2.5 - 4.0% for maintenance. The lower blood solubility of sevoflurane compared with isoflurane results in more rapid inductions and recoveries, and a more rapid change in anesthetic depth in response to a change in inspired concentration.

Cardiovascular Effects
The cardiovascular effects of sevoflurane are comparable to those of isoflurane. Sevoflurane does not markedly increase the sensitivity of the myocardium to circulating catecholamines and thus the potential for developing intraoperative arrhythmias is less for sevoflurane than for halothane [17]. As with all inhalants, sevoflurane depresses cardiac output and blood pressure in a dose dependent manner.

Respiratory Effects
The respiratory depressant effects of sevoflurane are similar to those of isoflurane.

CNS Effects
The effect of sevoflurane on intracranial hemodynamics appears to be similar to that of isoflurane. In a rabbit model, sevoflurane was associated with changes in ICP, CBF and EEG pattern that were indistinguishable from those seen with isoflurane [18].

Other Effects
Approximately 3% of administered sevoflurane may be recovered as sevoflurane metabolites [19]. Sevoflurane is susceptible to degradation both by the patient and within the breathing circuit. Hepatic metabolism of sevoflurane results in the production of free fluoride ions. This discovery caused initial concern, since the older inhalant anesthetic methoxyflurane, had been withdrawn from human anesthesia practice due to documented nephrotoxicity associated with release of fluoride ions during its metabolism. The rate of production of fluoride ions is much less than with methoxyflurane, however, and no reports of nephrotoxicity in humans or animals have been reported. Sevoflurane will decompose in the presence of CO2 absorbants such as soda lime and Baralyme® and produce vinyl ether having nephrotoxic properties. The toxic ether, known as Compound A, is produced when sevoflurane contacts alkaline compounds. Featuring prominently amongst the factors influencing the production of Compound A is the use of dry carbon dioxide absorbant [20,21]. Desiccation of carbon dioxide absorbent can be minimized by disconnecting anesthesia machines from the oxygen source to ensure that gas flow and consequent drying of absorbent does not occur when the equipment is not in use.

Desflurane
Desflurane is the newest of the inhalant anesthetics introduced into human anesthesia practice. The chemical structure of desflurane is very similar to that of isoflurane, differing only in the substitution of a fluoride ion for a chloride ion on one of the carbon atoms. This seemingly trivial substitution results in an inhalant anesthetic that is much more inert and much less soluble in blood than its parent, isoflurane. At a blood:gas partition coefficient of 0.42, desflurane is the least soluble of all inhalant anesthetics including nitrous oxide. The low blood solubility means that inductions and recoveries are extremely rapid. In addition, changes in anesthetic depth occur much more rapidly with desflurane than with isoflurane. Desflurane is the least potent of the so called potent inhalant anesthetics (all inhalant anesthetics except nitrous oxide) having a MAC value in dogs of 7.2% and 9.79% in cats. Typical vaporizer settings range from 12 - 18% for induction and 8 - 10% for maintenance.

Desflurane is highly volatile as evidenced by its vapor pressure of 664 mm Hg at 20°C. Since the boiling point of a liquid is defined as the temperature at which the liquid’s vapor pressure equals atmospheric pressure, desflurane begins to boil when the temperature rises above 20°C at sea level; at a lower barometric pressure such as at an altitude of 1000 meters, desflurane boils at 20°C. Its high vapor pressure required developing a vaporizer designed to accurately meter anesthetic at such high vapor pressures. The Ohmeda Tec 6 vaporizer is electrically heated to a constant temperature of 37°C. At this temperature, desflurane is converted to the gaseous phase enabling an electronically controlled pressure regulating valve to provide precise and controllable output from the vaporizer.

Cardiovascular Effects
The cardiovascular effects associated with desflurane are similar to those produced by isoflurane. In contrast to halothane and similar to isoflurane, the myocardium is not sensitized to the arrhythmogenic effects of catecholamines [22]. Similar to all potent inhalant anesthetics, desflurane is a cardiac depressant. It decreases myocardial contractility, cardiac output and blood pressure in a dose related manner while increasing heart rate at all levels of anesthesia [23], effects that are quite similar to those associated with administration of an equipotent concentration of isoflurane. In a dog model of myocardial failure, desflurane was reported to preserve diastolic function to a greater degree than did sevoflurane [24].

Respiratory Effects
The respiratory depression associated with administration of desflurane appears to be comparable to that produced by isoflurane. In children, concentrations of desflurane greater than 1 MAC are associated with an increase in respiratory depression that is due mostly to a reduction in tidal volume [25].

CNS Effects
Desflurane appears to induce effects on EEG, cerebral vascular resistance (CVR), and CBF that are similar to those associated with isoflurane. In dogs, increasing concentrations of desflurane were associated with decreases in CVR and concomitant increases in CBF [26].

Other Effects
Desflurane is the most stable and inert of any potent inhalant anesthetic in use. Replacement of the sole chloride atom on isoflurane with a fluoride ion results in an inhalant anesthetic that is more stable and more resistant to biodegradation; indeed only approximately 0.2% of the drug may be recovered as metabolites [19].

References
1. Imai A, Ilkiw JE, Pypendop BH, et al. Nitrous Oxide does not Consistently Reduce Isoflurane Requirement in Cats. Vet Anaesth Analg 2002; 29(2):98.
2. Cahill FJ, Ellenberger EA, Mueller JL, et al. Antagonism of nitrous oxide antinociception in mice by intrathecally administered antisera to endogenous opioid peptides. J Biomed Sci 2000;7:299-303. - Pubmed -
3. Eger EI. Anesthetic Uptake and Action. Baltimore: Williams & Wilkins, 1974; 171-183.
4. Brown BR, Crout JR. A comparative study of the effects of five general anesthetics on myocardial contractility: I. Isometric conditions. Anesthesiology 1971; 34:236-245.
5. France CJ, Plumer MH, Eger EI 2nd, et al. Ventilatory effects of isoflurane (Forane) or halothane when combined with morphine, nitrous oxide and surgery. Br J Anaesth 1974; 46:117-120.
6. Eger EI, Stevens WC, Cromwell TH. The electroencephalogram in man anesthetized with forane. Anesthesiology 1971; 35:504-508.
7. Artru AA. Relationship between cerebral blood volume and CSF pressure during anesthesia with halothane or enflurane in dogs. Anesthesiology 1983; 58:533-539. - Pubmed -
8. Smith RB, Aass AA, Nemoto EM. Intraocular and intracranial pressure during respiratory alkalosis and acidosis. Br J Anaesth 1981; 53:967-972. - Pubmed -
9. Adams RW, Cucchiara RF, Gronert GA, et al. Isoflurane and cerebrospinal fluid pressure in neurosurgical patients. Anesthesiology 1981; 54:97-99. - Pubmed -
10. Brown BR Jr, Gandolfi AJ. Adverse effects of volatile anaesthetics. Br J Anaesth 1987; 59:14-23. - Pubmed -
11. Ellenberger EA, Lucas HL, Russo JM, et al. An opioid basis for early-phase isoflurane-induced hypotension in rats. Life Sci 2003; 73:2591-2602. - Pubmed -
12. Hodgson DS, Dunlop CI, Chapman PL, et al. Cardiopulmonary effects of anesthesia induced and maintained with isoflurane in cats. Am J Vet Res 1998; 59:182-185. - Pubmed -
13. Moore MP, Greene SA, Keegan RD, et al. Quantitative electroencephalography in dogs anesthetized with 2.0% end-tidal concentration of isoflurane anesthesia. Am J Vet Res 1991; 52:551-560. - Pubmed -
14. Aladj LJ, Croughwell N, Smith LR, et al. Cerebral blood flow autoregulation is preserved during cardiopulmonary bypass in isoflurane-anesthetized patients. Anesth Analg 1991; 72:48-52. - Pubmed -
15. Eger EI. The pharmacology of isoflurane. Br J Anaesth 1984; 56 Suppl 1:71S-99S. - Pubmed -
16. Topal A, Gul N, Ilcol Y, et al. Hepatic effects of halothane, isoflurane or sevoflurane anaesthesia in dogs. J Vet Med A Physiol Pathol Clin Med 2003; 50:530-533. - Pubmed -
17. Navarro R, Weiskopf RB, Moore MA, et al. Humans anesthetized with sevoflurane or isoflurane have similar arrhythmic response to epinephrine. Anesthesiology 1994; 80:545-549. - Pubmed -
18. Scheller MS, Tateishi A, Drummond JC, Z et al. The effects of sevoflurane on cerebral blood flow, cerebral metabolic rate for oxygen, intracranial pressure, and the electroencephalogram are similar to those of isoflurane in the rabbit. Anesthesiology 1988; 68:548-551. - Pubmed -
19. Eger EI. New inhaled anesthetics. Anesthesiology 1994; 80:906-922. - Pubmed -
20. Fang ZX, Kandel L, Laster MJ, et al. Factors affecting production of compound A from the interaction of sevoflurane with Baralyme and soda lime. Anesth Analg 1996; 82:775-781. - Pubmed -
21. Steffey EP, Laster MJ, Ionescu P, et al. Dehydration of Baralyme increases compound A resulting from sevoflurane degradation in a standard anesthetic circuit used to anesthetize swine. Anesth Analg 1997; 85:1382-1386. - Pubmed -
22. Weiskopf RB, Eger EI , Holmes MA, et al. Epinephrine-induced premature ventricular contractions and changes in arterial blood pressure and heart rate during I-653, isoflurane, and halothane anesthesia in swine. Anesthesiology 1989; 70:293-298. - Pubmed -
23. Weiskopf RB, Holmes MA, Eger EI II, et al. Cardiovascular effects of I-653 in swine. Anesthesiology 1988; 69:303-309. - Pubmed -
24. Preckel B, Mullenheim J, Hoff J, et al. Haemodynamic changes during halothane, sevoflurane and desflurane anaesthesia in dogs before and after the induction of severe heart failure. Eur J Anaesthesiol 2004; 21:797-806. - Pubmed -
25. Behforouz N, Dubousset AM, Jamali S, et al. Respiratory effects of desflurane anesthesia on spontaneous ventilation in infants and children. Anesth Analg 1998; 87:1052-1055. - Pubmed -
26. Lutz LJ, Milde JH, Milde LN. The cerebral functional, metabolic, and hemodynamic effects of desflurane in dogs. Anesthesiology 1990; 73:125-131. - Pubmed -
Click on the author's name to view a list of his/her publications: R. D. Keegan

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Veterinary anaesthesia and analgesia
Volume 33 | Issue 4 (July 2006)
Evaluation of the clinical efficacy and safety of dexmedetomidine or medetomidine in cats and their reversal with atipamezoleVet Anaesth Analg. July 2006;33(4):214-23.

Mikael Granholm, Brett C McKusick, Fia C Westerholm, John C Aspegrén
Orion Corporation, Orion Pharma Animal Health, Turku, Finland.
Abstract

Objective To evaluate and compare the clinical effects of dexmedetomidine (DEX) and medetomidine (MED) in cats, and their reversal with atipamezole (ATI). Study design Prospective blinded randomized multi-centre clinical trial. Animals One hundred and twenty client-owned cats. Methods Cats were randomly allocated to receive a single intramuscular (IM) injection of either DEX (0.04 mg kg(-1), n = 62) or MED (0.08 mg kg(-1), n = 58) for minor procedures requiring sedation and analgesia. Afterwards, ATI (0.2 mg kg(-1)) was administered IM to half the cats, randomly assigned. Prior to, during and after the procedure the sedative, analgesic and cardiorespiratory effects and body temperature were assessed. Results Dexmedetomidine and MED produced clinically and statistically comparable effects. The intended procedure(s) could be performed in over 90% of cats. Sedation and analgesia were apparent within 5 minutes, peak effects were observed at approximately 30 minutes and spontaneous recovery occurred by 180 minutes of injection. Heart and respiratory rate and body temperature decreased significantly over time and had not returned to baseline values 180 minutes after administration. ATI administration completely reversed the sedative and analgesic effects, returned the heart rate to normal and prevented any further reductions in respiratory rate and body temperature in both DEX- and MED-treated cats. The reporting of adverse events was low and the most commonly observed event was vomiting (7%). No serious adverse events or concerns regarding safety were reported. Conclusions and clinical relevance Dexmedetomidine (0.04 mg kg(-1)) produced comparable sedative and analgesic effects to MED (0.08 mg kg(-1)) in cats. DEX produced adequate sedation and analgesia for radiography, grooming, dental care and lancing of abscesses. ATI fully reversed the clinical effects of DEX.
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