British Journal of Anaesthesia 83 (1): 42–9 (1999)
New inhalation agents in paediatric anaesthesia
D. J. Hatch
Institute of Child Health, University of London, London, UK and Portex Department of Paediatric
Anaesthesia, Great Ormond Street Children’s Hospital NHS Trust, Great Ormond Street, London
WC1N 3JH, UK
Br J Anaesth 1999; 83: 42–9
Keywords: anaesthesia, paediatric; anaesthetics volatile, sevoflurane; anaesthetics volatile,
desflurane
A survey in August 1995 showed that, despite the introduction of topical analgesic creams, approximately 30% of
anaesthetists responding used inhalation induction of
anaesthesia more frequently than i.v. induction, especially
in children less than 3–5 yr of age.9 In this age group,
uptake of inhaled agents is particularly rapid. In children
therefore, the induction characteristics of the ideal
inhalation agent are particularly important although clearly
the recovery profile, cardiovascular stability, minimal
metabolism, stability in soda lime, lack of central nervous
system excitation and antiemetic effect during recovery are
as important as they are in adults (Table 1). Although
cyclopropane provided rapid smooth induction, the risk of
explosions led to its withdrawal from anaesthetic practice.
In recent years, halothane has been accepted widely as the
least pungent of the inhalation agents available, giving the
smoothest induction with minimal risk of laryngospasm and
hypoxaemia. Its disadvantages are well known and include
myocardial irritability, especially in the presence of
epinephrine, depression of myocardial and respiratory function, cerebral vasodilatation, biotransformation and rarely
hepatotoxicity. Lack of familiarity with its use in adult
practice by younger anaesthetists must now be added to
this list of disadvantages.
Two new inhalation agents have recently become available in this country: sevoflurane and desflurane. Both are
fluorinated ethers, and as fluorine has 0.001% of the ozonedepleting activity of chlorine, both of these new drugs
should be more environmentally friendly than halothane.
Sevoflurane is relatively non-pungent, so that the vaporizer
may be set to its maximum setting from the start of
induction.77 Desflurane, however, is extremely pungent and
causes severe irritation of the upper respiratory tract if
used for induction of anaesthesia. Although desflurane is
therefore not recommended for inhalation induction, there
has been some recent interest in its use as a maintenance
agent in infants, because of its shorter recovery time.65
Sevoflurane
Physical characteristics
Sevoflurane is a fluorinated methyl isopropyl ether (Fig. 1)
with a blood:gas partition coefficient of 0.68, giving it the
potential for rapid induction and recovery. It is relatively
non-pungent and non-irritant with a high potency, and is
very useful for induction in children. It has a boiling point
of 58.5°C and a saturated vapour pressure of 160 mm Hg
at 20°C, so that it can be given from a standard vaporizer
(Table 2). Although unlike other potent inhalation agents,
the solubility of sevoflurane in blood is not related to age,
the minimum alveolar concentration (MAC) decreases from
approximately 3.3 in infancy to 2.5 in older children, and
to 1.7 in adults (Table 3). Interestingly, data from Lerman’s
group in Toronto suggest that the MAC of sevoflurane does
not increase over the first few months of life in the way
that it does with most other agents.48 Lerman and colleagues
also found that the MAC-sparing effect of nitrous oxide is
significantly less for sevoflurane and desflurane than it is
for the more soluble agents (Table 4).
Metabolism and toxicity
Although as much as 5% of sevoflurane may be metabolized,
trifluoroacetic acid, one of the main hepatotoxic breakdown
products of halothane metabolism, is not produced during
hepatic metabolism of this agent. Metabolism occurs by
defluorination via cytochrome P450-2E1 to hexafluoroisopropanol and inorganic fluoride which is then conjugated
with glucuronic acid and excreted in urine. Peak fluoride
concentrations in adults and children are greater than those
reported for isoflurane or enflurane, but are usually less
than 50% of the widely accepted nephrotoxic level of
50 mmol litre–1, and elimination is rapid.42 49 56 Although
higher peak concentrations have been reported,47 there have
been no clinical reports of renal toxicity even in renally
impaired patients or after long anaesthetics. Renal function
did not deteriorate in adult patients with stable renal
© British Journal of Anaesthesia
New inhalation agents in paediatric anaesthesia
Table 1 Ideal inhalation anaesthetic for children
d
d
d
d
d
d
d
Non-pungent
Rapid induction and recovery
Cardiovascular stability
Minimal metabolism
Stable in soda lime
CNS stability
Antiemetic
Fig 1 Chemical structure of sevoflurane (a fluorinated methyl isopropyl
ether).
of compound A in a child than in an adult. However, this
may be offset by the increased MAC in children and the
fact that many paediatric anaesthetists may rely more
heavily on inhaled anaesthetics alone rather than a balance
with i.v. agents.
Even though no renal toxicity has been reported in
humans which can be attributed directly to compound A,
even after prolonged administration, the American FDA
currently does not recommend the use of sevoflurane with
flow rates less than 2 litre min–1. The Committee on Safety
of Medicines in the UK has not issued a similar restriction.
Further research is clearly needed to justify or challenge
the FDA’s restriction. Some feel that even this flow rate
may not be safe,17 while experience in several million
anaesthetics suggests to others that the hazards of compound
A toxicity are more theoretical than real.
Fang and co-workers in 1995 pointed out that dry soda
lime or baralyme can degrade some anaesthetic agents to
produce carbon monoxide, particularly if the absorber is
not flushed after standing overnight.20 This problem is
greatest with desflurane and least with halothane and
sevoflurane.
Malignant hyperthermia has been reported with sevoflurane.15 70
Table 2 Physical and chemical properties of sevoflurane
Molecular weight
Boiling point
Saturated vapour pressure
Blood:gas ratio
Fat:blood ratio
200
58.5°C
160 mm Hg
0.68
48
Table 3 Minimum alveolar concentration of sevoflurane
Age
Sevoflurane (%)
Less than 1 month
1–6 months
6–12 months
3–5 yr
Adult
3.3
3.2
2.5
2.5
2.0
Table 4 MAC-sparing effect of nitrous oxide
Halothane
Isoflurane
Sevoflurane
Desflurane
60%
40%
24%
20%
insufficiency after sevoflurane anaesthesia.11 The area under
the curve was significantly less than that with known
nephrotoxic agents, such as methoxyflurane, which is
metabolized by P450-311P450-2E1. Kharasch, Hankins
and Thummel have suggested that intra-renal metabolism
of fluoride ions, which appears not to occur to any significant
degree with sevoflurane, may be more important than
hepatic metabolism in producing nephrotoxicity and it is
interesting to note that the cytochrome P450 enzyme
required for metabolism is not found in the human kidney.40
Sevoflurane is partially degraded by carbon dioxide
absorbents to produce small amounts of compound A
(fluoromethyl-2,2-difluoro-1-(trifluoromethyl)vinyl ether)
which causes mild renal changes in rats at concentrations above those found clinically. However, these
changes depend on a beta lyase of which rats possess more
than humans. The LC50 of compound A in rats is 1 h at
1000 ppm and 3 h at 400 ppm. In humans, the maximum
reported concentration (peaking after 9 h) is 37 ppm, apart
from one report of 60 ppm with baralyme. The maximum
reported in children at 2 litre min–1 is 15 ppm.23 Concentrations of compound A are increased with increase in
temperature and with decrease in flow rate, and are higher
in the presence of baralyme and fresh soda lime.19 58
Paediatric patients produce less carbon dioxide so that a
given fresh gas flow rate produces a lower concentration
Sevoflurane in clinical practice
Induction and recovery characteristics
Although opinions vary about the smell, there is no doubt
that sevoflurane lacks pungency, even at high inspired
concentrations. This allows as much as 8% to be delivered
from the outset without significant breath-holding, coughing
or laryngospasm, and clinical experience shows this concentration to be well tolerated.6 77 This can be particularly
valuable in older, needle-phobic children, who will often
agree to have a clear plastic mask closely applied to the
face, leading to very rapid induction, either during tidal
breathing or using the single-breath technique. Younger
children may have to be approached more subtly. As an
increased incidence of involuntary seizure-like movements
has been demonstrated in the lighter planes of anaesthesia
with sevoflurane,1 the use of 8% from the start with
consequently rapid deepening may minimize this problem.
A recent case report described the onset of complete heart
block during slow induction in a child with impaired cardiac
conduction.53
The results of early studies comparing the speed of induction of sevoflurane with halothane in children were inconclusive, some finding sevoflurane to be more rapid than halothane
43
Hatch
halothane.62 72 76 Sevoflurane may have an antiemetic
effect.33 37 73 However, pain scores are significantly higher
in the earlier recovery period with sevoflurane, suggesting
that when this drug is used even more care must be taken
to provide children with adequate analgesia.78 There may
also be a higher incidence of delirium during recovery after
sevoflurane, particularly if it has been used for maintenance
of anaesthesia.2
and others finding no difference when inhaled concentrations were increased incrementally.3 8 18 37 48 62 65 72 A study
comparing approximately equi-MAC concentrations of
halothane (5%) and sevoflurane (8%) found no statistically
significant difference in the time to loss of eyelash reflex
or end of induction between the two agents.77 Lerman has
suggested that using an overpressure technique, induction
with sevoflurane should theoretically not be more rapid than
with halothane, although 5% halothane may not be as well
tolerated as 8% sevoflurane,47 an observation which was
confirmed in the study referred to above.77 Significantly more
children in this study resisted induction with halothane, and
most of the parents whose children had received halothane
on a previous occasion preferred the experience with sevoflurane. Taivainen and colleagues also found that sevoflurane
gave improved quality of induction compared with halothane.81 Thus it would seem that the difference in speed of
induction between sevoflurane and halothane may not be
as important as the quality of induction. The incidence of
complications during induction with sevoflurane and halothane is similar, with serious complications or significant
desaturation being reported rarely.
The time required for satisfactory intubating conditions
without neuromuscular blocking agents has been shown
by several authors to be lower for sevoflurane than for
halothane.31 64 Sevoflurane has been suggested as an
alternative to succinylcholine for intubation in elective cases
where return to spontaneous breathing is required, such as
some elective ENT and dental anaesthesia.32 End-tidal
concentrations of at least 30% above MAC are required for
intubation,30 31 while laryngeal mask insertion is possible
at 1 MAC.79
The cost of new agents such as sevoflurane and desflurane
has revived interest in the use of low-flow breathing systems
in children. Despite the theoretical concerns described
above, sevoflurane is used widely in such systems and there
have been no reports of toxicity from compound A. The
low solubility of these agents compared with isoflurane
should allow more rapid equilibration within circle systems
and more precise control over anaesthetic depth.
The low blood:gas solubility of sevoflurane should lead
to rapid recovery, and similar elimination kinetics to nitrous
oxide have been demonstrated in children.45 Fredman and
colleagues, in adults, could not detect significant differences
in early or intermediate recovery times between patients
anaesthetized with sevoflurane or propofol.22 Recovery
scores using a modified Aldrete scoring system in unpremedicated children have been shown to be significantly
lower after sevoflurane than after halothane.37 62 78 The time
to tracheal extubation and times taken to open eyes in
response to verbal command after the end of surgery,
to demonstrate purposeful movement such as squeezing
the hands, to discharge from the recovery unit and to
spontaneous interaction with a nurse or parent have
been shown to be statistically significantly less in
children receiving sevoflurane than in those receiving
Pharmacodynamics of sevoflurane
Cardiovascular system
Sevoflurane is relatively cardiostable in children, any
decrease in arterial pressure being less than that with
desflurane. Its use for producing controlled hypotension
during spinal surgery has been described.83 Sevoflurane
produces less tachycardia than isoflurane24 and less
myocardial depression than halothane.28 A recent study in
infants found that halothane caused a greater decrease in
heart rate, myocardial contractility and cardiac output than
sevoflurane at all concentrations.87
Although increases in arterial pressure and heart rate
have been described during induction of anaesthesia,38
adult data suggest that sevoflurane does not activate the
sympathetic system,16 does not cause coronary steal39 and
produces less myocardial sensitization to epinephrine than
halothane.63
Arrhythmias are uncommon with sevoflurane.
Johannesson, Floren and Lindahl reported an incidence
of 61% in ENT surgery with halothane, compared with
5% with sevoflurane.33 There have been similar reports in
dental anaesthesia.71
Respiratory system
Specific aspects of the respiratory physiology of infants and
young children contribute to their susceptibility to the
respiratory complications of infectious diseases, and to the
depressant effects of anaesthetic agents.26 The horizontal
rib cage prevents much increase in tidal volume in response
to increased respiratory demand, as opposed to the adult
with the downward sloping rib configuration.69 In addition,
reduced functional residual capacity (FRC) relative to the
size of the child, caused largely by the very compliant chest
wall with low outward recoil allowing the inwardly directed
recoil forces of the lung to be relatively unopposed,4
together with a tendency to airway closure within the
tidal volume range because of the relatively less negative
intrathoracic pressure in absolute terms,27 and an oxygen
consumption which is approximately double that of the
adult, contribute to the speed with which infants can
become hypoxic.
Anaesthesia worsens these already limited reserves,
affecting tidal volume, frequency of breathing, control of
carbon dioxide, lung mechanics and oxygenation. All of
the commonly used inhalation anaesthetic agents cause dosedependent depression of tidal volume, with no significant
differences in depression of the slope of carbon dioxide
44
New inhalation agents in paediatric anaesthesia
response curves.51 59 67 84 Within the clinical range of
anaesthetic depth, tidal volumes as low as 4–5 ml kg–1 have
been described, compared with approximately 7 ml kg–1 in
the awake state and 10 ml kg–1 or more during controlled
ventilation of the lungs. In one study of 39 unpremedicated
infants aged 15–300 days, end-tidal carbon dioxide partial
pressure ranged from 3.7 to 8 kPa when infants were
breathing nitrous oxide, oxygen and halothane via a Rendell
Baker low deadspace face mask for minor surgery.46 The
highest values were seen in neonates, and the authors
recommended the use of controlled ventilation in this
age group. Depression of tidal volume seems to occur
irrespective of the use of preoperative opioid or sedative
premedication,50 and nitrous oxide has a slight ‘sparing
effect’, with less reduction in tidal volume than with an
equal MAC of the inhalation agent alone.61
Several investigators have compared the effects of the
older inhalation agents, halothane, enflurane and isoflurane,
on respiratory frequency in children.34 59 66 89 The effect of
anaesthesia on the frequency of breathing varies from one
agent to another. Halothane increases respiratory frequency,
with enflurane there is a marked decrease, and isoflurane
and nitrous oxide cause no significant change.
In a study in 13 unpremedicated children aged 2–4 yr
receiving isoflurane, with surgical stimulus blocked by
continuous epidural, Murat and colleagues found dosedependent increases in end-tidal carbon dioxide partial
pressure.59 In a separate study in children of a similar age,
also unpremedicated, Murat and colleagues found that the
increase in end-tidal carbon dioxide concentration when
breathing 1.5% halothane did not recover immediately on
reducing the concentration to 0.5%.60 This might be because
of a prolonged direct effect of halothane on inspiratory
muscle activity or it may be more centrally mediated.
Since much of the early work on sevoflurane was carried
out in countries where spontaneous breathing is less
frequently used during anaesthesia, there is naturally concern in the UK about the respiratory effects of this new
anaesthetic agent. An early article from Japan in 1987
suggested that it might have a greater depressant effect on
respiration than halothane, although this study was poorly
controlled.14 More recently, Yamakage and co-workers,
using a respiratory inductive plethysmograph, demonstrated
a dose-dependent increase in end-tidal carbon dioxide partial
pressure with both halothane and sevoflurane, the latter
producing more profound respiratory depression than halothane at 1.5 MAC.90 However, there was no mention of
any attempt to validate the plethysmograph for quantitative
measurements.
A recently published study by Brown and colleagues
showed that minute ventilation and respiratory frequency
were lower in infants and young children less than 2 yr
breathing 1 MAC of sevoflurane in nitrous oxide via a
laryngeal mask airway (LMA) than during equi-MAC
halothane anaesthesia, which may reflect different effects
of these anaesthetic agents on ventilatory control.10 If
Lerman and colleagues’ suggestion is correct that the MACsparing effect of nitrous oxide is greater for halothane than
for sevoflurane,48 the differences between the two agents
observed in this study may have been an underestimate.
However, tidal volumes are maintained at a higher level
during the lighter plane of anaesthesia needed when using
the LMA than tracheal intubation, and the adverse effects
of anaesthesia on ventilation may be minimized by the
effect of nitrous oxide61 or surgical stimulation. In the study
of Brown and colleagues,10 flow, airway pressure and endtidal carbon dioxide tension (PE9CO2) were measured during
spontaneous ventilation together with airway pressure
change during transient occlusions, reflecting respiratory
drive. Respiratory inductive plethysmography was also used
to assess chest wall motion. Mild respiratory depression,
evidenced by a PE9CO2 of 6 kPa, was present in both groups.
However, despite the fact that respiratory frequency and
minute ventilation were reduced in the sevoflurane group,
end-tidal carbon dioxide concentrations in both groups were
similar. Ventilation may therefore be more efficient during
sevoflurane anaesthesia. The greater thoraco-abdominal
asynchrony during halothane anaesthesia is consistent with
the loss of intercostal tone which has been shown to occur
with this agent.84 The differences in asynchrony between
the groups may also reflect more efficient ventilation with
sevoflurane, although the significance of these findings is
not yet fully understood. Early studies in dogs also suggest
that sevoflurane and halothane affect the muscles of the
diaphragm and ribcage differently.29 There was no difference
in respiratory drive between the two anaesthetics in Brown’s
study, but the shape of the flow waveform differed according
to anaesthetic agent, with peak inspiratory flow being
reached later, and peak expiratory flow earlier, in the
sevoflurane group. These skewed waveforms contrast with
the symmetrical patterns reported in a previous study
of children recovering from halothane anaesthesia.74 The
clinical relevance of the skewed inspiratory waveform
during sevoflurane anaesthesia is as yet unknown but may
reflect the recruitment pattern of the inspiratory motor
neurone pool which may differ significantly with different
agents.
In clinical practice, respiratory variables during spontaneous breathing of up to 1.3 MAC in children are similar
for sevoflurane and isoflurane.43 Although sevoflurane
appears to be effective in reversing bronchoconstriction,
the mechanism is unclear.25 54 There have been relatively
few studies on the effects of sevoflurane in children with
asthma and these tend to confirm adult findings.57
Nervous system
Sevoflurane has a similar effect to isoflurane on intracranial
pressure and minimal effects on cerebral blood flow, cerebral
metabolic oxygen consumption and autoregulation of the
cerebral blood supply. In adults, cerebrovascular changes
appear similar to those seen with isoflurane.35 41 Cerebrovascular changes during induction of anaesthesia in children
45
Hatch
are similar to those of halothane.7 Seizure-like movements have been described during induction in adults
and children,1 13 and electroencephalographic evidence of
seizure activity has been reported in two epileptic children,
without clinical seizures developing.44
Sevoflurane potentiates the duration of neuromuscular
block with mivacurium and vecuronium compared with
halothane, although onset time is not altered.36 80 Recovery
of neuromuscular function from block with vecuronium
is slower during anaesthesia with sevoflurane than with
halothane or balanced anaesthesia with propofol and
alfentanil.80
Fig 2 Chemical structure of desflurane (a fluorinated methyl ethyl ether).
Table 5 Physical and chemical properties of desflurane
Molecular weight
Boiling point
Saturated vapour pressure
Blood:gas ratio
Fat:blood ratio
168
22.8°C
669 mm Hg
0.42
27
Table 6 Minimum alveolar concentration of desflurane
Is sevoflurane replacing halothane?
The superiority of sevoflurane over halothane in so many
areas raises the question of whether there remains a role
for halothane in paediatric anaesthetic practice. A motion
proposing that there is not was overwhelmingly defeated
at the 1998 annual meeting of the Association of
Paediatric Anaesthetists of Great Britain and Ireland,
partly on the grounds of cost. In many countries, halothane
is the only affordable potent inhalation anaesthetic, and
for the manufacturers to discontinue its production would
be a disaster. However, there are also serious concerns
among some paediatric anaesthetists about sevoflurane
being used for laryngoscopy or bronchoscopy in children
with upper airway obstruction, for acute epiglottitis or
for difficult tracheal intubation. They feel that a drug
such as halothane with a more prolonged action might
be safer, because with sevoflurane children tend to lighten
too quickly during the laryngoscopy phase. In some parts
of Australia, methoxyflurane is still being used for these
procedures. Others feel that sevoflurane is quicker and
safer, having a benign haemodynamic side effect profile
more in common with isoflurane than halothane and even
fewer airway complications than halothane. The fact that
patients spend less time in stage two is seen as an
advantage. A more rapid return of consciousness and
airway reflexes is not only safer if things go awry, but
allows less intense postoperative monitoring sooner. The
perceived problems with sevoflurane are not only its
insolubility, but the fact that the maximum inhaled
concentration achievable with the vaporizer is only
33MAC, as opposed to more than 53MAC with
halothane, and the smoother recovery profile of halothane.
Barker has described recently the satisfactory use of
sevoflurane for induction followed by isoflurane for
maintenance in 30 such children.5 However, Meretoja
and colleagues found a lower incidence of cardiac
arrhythmias during bronchoscopy and gastroscopy with
sevoflurane than with halothane and concluded that it
was a superior agent for these procedures.55 Other workers
suggest that sevoflurane may also have antiemetic
properties after short administrations.33 73
Age
Desflurane (%)
Less than 1 month
1–6 months
6–12 months
3–5 yr
Adult
9.16
9.42
9.92
8.62
6.0
Desflurane
Physical characteristics
Desflurane, a fluorinated methyl ethyl ether, differs from
isoflurane in the substitution of the chlorine atom by fluorine
(Fig. 2). It has a molecular weight of 168, blood:gas
solubility coefficient of 0.42 and lower tissue solubility
than any other agent (Table 5). It is less potent than
isoflurane, with a MAC in infants of 8–10%, decreasing to
6% in adults (Table 6)21 so that closed circuit use is
recommended. It has a boiling point of 22.8°C and a
saturated vapour pressure approaching 1 atmosphere at
room temperature, making it unsuitable for use from a
conventional vaporizer.
Metabolism and toxicity
Desflurane is a remarkably stable molecule which does not
liberate fluoride ions, is stable in the presence of soda lime
and is minimally metabolized. The clinical significance
of this stability in children may be small, however, as
hepatotoxicity is rare in children even after halothane.
Unlike sevoflurane, desflurane is not degraded by soda
lime, but dry soda lime or baralyme can cause degradation
to produce carbon monoxide.20
Malignant hyperthermia has not been reported with
desflurane, although evidence from animal studies suggests
it could occur.85
Desflurane in clinical practice
Induction and recovery characteristics
The irritant effects of desflurane on the upper airway are
well known and it is not recommended for inhalation
induction of anaesthesia in children. In one study of
unpremedicated patients, approximately 50% of children in
46
New inhalation agents in paediatric anaesthesia
6 Baum VC, Yemen TA, Baum LD. Immediate 8% sevoflurane
induction in children: a comparison with incremental sevoflurane
and incremental halothane. Anesth Analg 1997; 85: 313–16
7 Berkowitz RA, Hoffman WE, Cunningham F, McDonald T. Changes
in cerebral blood flow velocity in children during sevoflurane and
halothane anesthesia. J Neurosurg Anesthesiol 1996; 8: 194–8
8 Black A, Sury MRJ, Hemington L, Howard R, Mackersie A, Hatch
DJ. A comparison of the induction characteristics of sevoflurane
and halothane in children. Anaesthesia 1996; 51: 539–42
9 Bowhay A, Harmer M, Jones R, et al. Current Anaesthetic Practice–
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10 Brown K, Aun C, Stocks J, Jackson E, Mackersie A, Hatch D. A
comparison of the respiratory effects of sevoflurane and halothane
in infants and young children. Anesthesiology 1998; 89: 86–92
11 Conzen PF, Nuscheler M, Melotte A, et al. Renal function
and serum fluoride concentrations in patients with stable renal
insufficiency after anesthesia with sevoflurane or enflurane. Anesth
Analg 1995; 81: 569–75
12 Davis PJ, Cohen IT, McGowan FX, Latta K. Recovery
characteristics of desflurane versus halothane for maintenance of
anesthesia in pediatric ambulatory patients. Anesthesiology 1994;
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13 Derbyshire SW. Do fetuses feel pain? Analgesic and anaesthetic
procedures are being introduced because of shoddy sentimental
argument. BMJ 1997; 314: 1201
14 Doi M, Takahashi T, Ikeda K. Respiratory effects of sevoflurane
used in combination with nitrous oxide and surgical stimulation.
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15 Ducart A, Adnet P, Renaud B, Riou B, Krivosic-Horber R.
Malignant hyperthermia during sevoflurane administration. Anesth
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and emergence. J Clin Anesth 1995; 7: 237–44
19 Fang ZX, Eger EI II. Factors affecting the concentration of
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20 Fang ZX, Eger EI, Laster MJ, Chortkoff BS, Kandel L, Ionescu P.
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whom anaesthesia was induced with desflurane experienced
breath-holding, and one-third developed severe episodes of
coughing or laryngospasm. In 18% of children, oxygen
saturation decreased to less than 90%.82 In another study,
premedication did not reduce the incidence of complications
during induction.91
Although desflurane is not suitable for induction, it has
many desirable qualities for maintenance. It is minimally
metabolized and cardiovascular variables are stable.82 Time
to recovery appears to be quicker with desflurane than with
sevoflurane.52 75 82 88 91 Emergence has been reported by
most authors as smooth, although Davis and colleagues
found a higher incidence of emergence delirium than with
halothane12 and Olsson reported a case of emergence
laryngospasm in a child with pre-existing upper airway
infection.68 Welborn and colleagues found recovery from
desflurane associated with more agitation than from sevoflurane.86 Wolf and colleagues found that postoperative
apnoea, seen in infants after isoflurane anaesthesia, was
not seen after desflurane, and suggested that it might be
particularly useful in the ex-premature infant.88 A recent
study by O’Brien, Robinson and Morton also suggested that
its recovery profile makes desflurane particularly suitable for
neonatal anaesthesia.65 As with sevoflurane, pain management in the immediate recovery period becomes more
critical.
Pharmacodynamics of desflurane
The pharmacodynamics of desflurane are similar to those
of isoflurane. Its respiratory effects have been investigated
almost exclusively in adults. It appears to cause similar
effects to isoflurane (dose-dependent depression of tidal
and minute volume, and increase in respiratory frequency
and carbon dioxide concentration). Studies in animals
have demonstrated that desflurane causes a dose-dependent
reduction in myocardial contractility, although in the dog
it produces less negative inotropy and less peripheral
vasodilatation than isoflurane. Sympathetic tone appears to
be increased, but desflurane has not been shown to sensitize
the myocardium to epinephrine.
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