Anaesthetic management in asthma

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Anaesthetic management in asthma
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                                                                                           MINERVA ANESTESIOL 2007;73:357-65

                                               R EV I EW A RT I C L E

                    Anaesthetic management in asthma
                            S. M. BURBURAN 1, 2, D. G. XISTO 2, P. R. M. ROCCO 2
1Division of Anaesthesiology, Department of Surgery, Faculty of Medicine, Federal University of Rio de Janeiro, Rio de Janeiro,
Brazil; 2Laboratory of Pulmonary Investigation Carlos Chagas Filho Biophysics Institute, Federal University of Rio de
Janeiro, Rio de Janeiro, Brazil

                                                     ABSTRACT
    Anaesthetic management in asthmatic patients has been focused on avoiding bronchoconstriction and inducing bron-
    chodilation. However, the definition of asthma has changed over the past decade. Asthma has been defined as a clin-
    ical syndrome characterized by an inflammatory process that extends beyond the central airways to the distal airways
    and lung parenchyma. With this concept in mind, and knowing that asthma is a common disorder with increasing preva-
    lence rates and severity worldwide, a rational choice of anaesthetic agents and procedures is mandatory. Thus, we pur-
    sued an update on the pharmacologic and technical anaesthetic approach for the asthmatic patient. When feasible, region-
    al anaesthesia should be preferred because it reduces airway irritation and postoperative complications. If general
    anaesthesia is unavoidable, a laryngeal mask airway is safer than endotracheal intubation. Lidocaine inhalation, alone
    or combined with albuterol, minimizes histamine-induced bronchoconstriction. Propofol and ketamine inhibit bron-
    choconstriction, decreasing the risk of bronchospasm during anaesthesia induction. Propofol yields central airway
    dilation and is more reliable than etomidate or thiopental. Halothane, enflurane, and isoflurane are potent bron-
    chodilators and can be helpful even in status asthmaticus. Sevoflurane has shown controversial results in asthmatic
    patients. Vecuronium, rocuronium, cisatracurium, and pancuronium do not induce bronchospasm, while atracurium
    and mivacurium can dose-dependently release histamine and should be cautiously administered in those patients.
    Further knowledge about the sites of action of anaesthetic agents in the lung, allied with our understanding of asth-
    ma pathophysiology, will establish the best anaesthetic approach for people with asthma.
    Key words: Asthma - Anaesthesia - Anaesthetics - Bronchial spasm - Bronchial hypereactivity.

A    sthma is a major public health issue with high
     and increasing prevalence rates 1 and a con-
comitant increase in morbidity and mortality.2
                                                                     The pathophysiological hallmark of asthma is a
                                                                  reduction in airway diameter due to the contrac-
                                                                  tion of smooth muscle, vascular congestion, oede-
Studies have shown that the lifetime prevalence of                ma of the bronchial wall, and tenacious secretions.5
asthma among adults is 11%,3 and it is even high-                 The chronic inflammatory process leads to tissue
er among children.4 These data contribute to make                 injury and subsequent reorganization. The term
challenging adverse events due to asthma a wide-                  “airway remodelling” is widely used to refer to the
spread situation in anaesthesiological practice.                  development of those structural changes,6, 7 such
   Therefore, in order to avoid increasing the risk               as: epithelial shedding, subepithelial fibrosis,
of perioperative complications, a good understand-                increased numbers and volume of mucous cells in
ing of asthma pathophysiology, an adequate pre-                   the epithelium, airway smooth muscle hyperpla-
operative evaluation, and optimisation of the                     sia and hypertrophy, and increased vascularization
patient’s condition, allied with the best pharmaco-               of the airway wall.8 These changes in the extracel-
logical and technical approach, are imperative.                   lular matrix, smooth muscle, and mucous glands

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BURBURAN                                                                 ANAESTHETIC MANAGEMENT IN ASTHMA

have the capacity to influence airway function and       patient’s pulmonary function. Warner et al.15
reactivity in asthmatic patients manifested by a         observed that the frequency of perioperative bron-
decline in forced expiratory volume in 1 s (FEV1)        chospasm and laryngospasm was surprisingly low
and bronchial hyper-responsiveness.9                     in asthmatic patients. They identified 3 factors
   Bronchospasm and mucous plugging obstruct             correlated with perioperative bronchospasm: the
both inspiratory and expiratory airflow. Resistance      use of antibronchospastic medications; recent
to expiratory airflow results in positive alveolar       symptomatic exacerbation; and recent visit to a
pressures at the end of expiration, which causes         medical facility for treatment of asthma. Therefore,
air-trapping and hyperinflation of the lungs and         they reached the following conclusions: 1) per-
thorax, increased work of breathing, and alter-          sons with asthma but no symptoms are at low risk
ations in respiratory muscle function. Airflow           for severe morbidity from anaesthesia; 2) persons
obstruction is not uniform, and the mismatching          with asthma are, however, at a low but increased
of ventilation to perfusion occurs, leading to           risk for severe morbidity; and 3) adverse outcomes
changes in arterial blood gases.10, 11                   from bronchospasm occur in patients with no pre-
   The definition of asthma has changed over the         vious history of asthma.16
past decade. Asthma has been defined as a clinical          In view of this, the approach to the asthmatic
syndrome characterized by an inflammatory process        patient should include a detailed history of the
that extends beyond the central airways to the dis-      patient’s experience with reactive airway disease,
tal airways and the lung parenchyma. Small airways       searching for the following: 1) a recent upper res-
have recently been recognized as a site of airflow       piratory infection; 2) allergies; 3) possible precip-
obstruction and hyper-responsiveness.12-14               itating factors for asthma; 4) use of medications,
   In view of these new pathophysiological find-         including drugs that could precipitate the attack,
ings, we attempted this review to outline available      as well as those used to prevent an attack; and 5)
data and the criteria for the anaesthetic manage-        the occurrence of dyspnoea at night or in the ear-
ment in asthmatic patients.                              ly morning hours. Furthermore, to better under-
                                                         stand a patient’s bronchial reactivity, it is impor-
                     Methods                             tant to know whether he or she can tolerate cold
                                                         air, dust, or smoke and if he or she has ever under-
   A computerized search of the English-language         gone tracheal intubation under general anaesthe-
literature of PUBMED between 1995 and 2005               sia.17 Documentation of an episode of status asth-
was conducted using the terms airway obstruction,        maticus requiring intubation portends of a diffi-
asthma, bronchial hyper-reactivity, anaesthesia, and     cult perioperative course.10
anaesthetics. Various combinations of the terms             Drugs are commonly associated with the induc-
were used to maximize the results. Bibliographies of     tion of acute episodes of asthma, and it is impor-
original research, commentaries, textbooks, and          tant to recognize drug-induced bronchial narrow-
symposia were reviewed for additional relevant ref-      ing because its presence is often associated with
erences. These publications were abstracted and          great morbidity. Even the selective β1-adrenergic
compiled into tabular form under types of study          antagonists regularly obstruct the airways in indi-
design. Two-hundred twenty-two articles were select-     viduals with asthma and should be avoided.5
ed for critical review. Of the articles excluded, most
                                                            The triad of bronchial asthma, nasal polyposis,
were reports that described anaphylactic reactions,
                                                         and intolerance to aspirin or aspirin-like chemicals
bronchial hyper-responsiveness, and bronchospasm
                                                         is designated aspirin-induced asthma (AIA) or
in nonasthmatic patients.
                                                         Samter’s syndrome. In these patients, marked cross-
                                                         sensitivity with nonsteroidal anti-inflammatory
       Anaesthetic management strategy                   drugs may precipitate severe bronchospasm and
                                                         adverse reactions. Hence, it is important to refer
Preoperative evaluation                                  these patients to allergy clinics to evaluate possible
  The anaesthesiologist’s responsibility starts at       analgesic cross reactivity and intolerance to anaes-
the preoperative phase with the evaluation of the        thetic agents.18

358                                        MINERVA ANESTESIOLOGICA                                     June 2007
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ANAESTHETIC MANAGEMENT IN ASTHMA                                                                     BURBURAN

   Physical examination of the lungs may be nor-          ment in asthmatics should include the following
mal or reveal wheezing and/or other adventitial           measures:
sounds. Preoperative wheezing is predictive of a             1. bronchospasm should be treated with inhaled
difficult perioperative course. Indeed, if a severe       β2-agonists;
asthmatic history and auscultatory wheezing are              2. if a patient is at risk for complications, pre-
encountered during the initial screening, a con-          operative treatment with 40-60 mg of pred-
sultation with the pulmonologist may be recom-            nisone/day or hydrocortisone 100 mg every 8 h
mended. In severe cases of asthma, laboratory stud-       intravenously is suggested. Anyone with a preop-
ies such as arterial blood gases and pulmonary            erative FEV1
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vascular permeability, bronchial smooth muscle          and do not alter bronchial tone.17 In this context,
constriction, and local vasodilatation.27 The anaes-    Kil et al.31 noticed that oral midazolam (0.5 mg/kg)
thesiologists’ goal should be to minimize the risk      did not change oxygen saturation, respiratory rate,
of inciting bronchospasm and to avoid triggering        and pulse rate in children with mild to moderate
stimuli.                                                asthma undergoing dental treatment. Hence, mida-
   The effect of endotracheal intubation, even in       zolam at a dose of 0.5 mg/kg is a safe and effective
symptom-free asthmatics, was demonstrated by            means for sedation of patients with mild to mod-
Groeben et al.28 in a randomized double-blind           erate asthma.
fashion study of 10 volunteers with mild asthma
who underwent endotracheal intubation under             INHALATIONAL ANAESTHETICS
local anaesthesia. They performed lung function
tests before and after intubation and observed over        Inhalational agents possess bronchodilatory
a 50% reduction in FEV1 after the procedure.            effects, decrease airway responsiveness, and atten-
However, after prophylactic administration of a         uate histamine-induced bronchospasm.10 The
β2-adrenergic agonist and topical lidocaine, the        mechanism is thought to be β-adrenergic receptor
reduction in FEV1 was lower (20%).                      stimulation leading to increased intracellular cyclic-
   In summary, it is preferable to avoid airway         AMP. This has a direct bronchial muscle relaxing
instrumentation in asthmatic patients, and region-      effect. Increased cAMP may bind free calcium
al anaesthesia should always be considered for this     within bronchial myoplasm and cause relaxation
purpose, as well as for reducing postoperative com-     by negative feedback. It may impede antigen-anti-
plications.17                                           body mediated enzyme production and the release
   Pregnancy can adversely affect the course of         of histamine from leukocytes as well.11
asthma, increasing perioperative risk in these             For all these reasons, volatile agents such as
patients. For this reason, regional anaesthesia is      halothane and isoflurane have been recommend-
the technique of choice for pregnant asthmatics         ed for general anaesthetic techniques in patients
and parturients, especially if prostaglandins and       with obstructive airway diseases for many years,
their derivates are administered for abortion or        and they are even helpful to treat status asthmati-
operative delivery.20, 29                               cus. An exception should be made for desflurane,
   When regional anaesthesia is not feasible and        which can lead to increased secretions, coughing,
general anaesthesia is required, prophylactic antiob-   laryngospasm, and bronchospasm.32
structive treatment, volatile anaesthetics, propofol,      Thus far, studies using sevoflurane have shown
opioids, and an adequate choice of muscle relax-        controversial results. Rooke et al.33 compared the
ants minimize the anaesthetic risk.17 In addition to    bronchodilating efficacy of sevoflurane, isoflu-
this, the use of face masks and laryngeal mask air-     rane, and halothane after tracheal intubation in
ways have been reported to cause less airway irri-      patients without asthma. In their study, halothane
tation. Kim and Bishop 30 randomized 52 nonasth-        was not significantly better than isoflurane at
matic patients to receive an endotracheal tube or       reducing Rrs. Nonetheless, sevoflurane decreased
a laryngeal mask airway under general anaesthesia;      Rrs more than either halothane or isoflurane.
they observed that respiratory system resistance           Habre et al.34 studied lung function in children
(Rrs) was lower in patients receiving laryngeal         with and without asthma receiving anaesthesia
mask airways than in those submitted to endotra-        with sevoflurane and concluded that, in children
cheal intubation. This result supports the idea that    with mild to moderate asthma, endotracheal intu-
use of a laryngeal mask might be a more reliable        bation during sevoflurane anaesthesia was associ-
alternative than endotracheal intubation.               ated with an increase in Rrs that was not seen in
                                                        nonasthmatic children. In spite of this, no appar-
                                                        ent clinical adverse event was observed, and accord-
PREMEDICATION
                                                        ing to the Scalfaro et al. study,35 a pre-anaesthet-
   Adequate sedation of the patient should be           ic treatment with inhaled salbutamol adminis-
achieved in order to avoid perioperative complica-      tered before sevoflurane anaesthesia can prevent
tions. For this purpose, benzodiazepines are safe       that increase of Rrs.

360                                       MINERVA ANESTESIOLOGICA                                     June 2007
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ANAESTHETIC MANAGEMENT IN ASTHMA                                                                   BURBURAN

   Correa et al.36 analysed the respiratory mechan-      mined by an inhibition of neurally-induced bron-
ics and lung histology in normal rats anaesthetised      choconstriction.
with sevoflurane. They observed that sevoflurane            Propofol, a widely used short-acting i.v. anaes-
anaesthesia did not act at the airway level but at the   thetic, has been associated with less bronchocon-
lung periphery, stiffening lung tissues and increas-     striction during anaesthetic induction than other
ing mechanical inhomogeneities. In addition,             anaesthetic agents.42 In vitro data suggest that
Takala et al.37 evaluated pulmonary inflammato-          propofol has a direct airway smooth muscle relax-
ry mediators in bronchoalveolar lavage fluid after       ant action.43 Pizov et al.44 in a randomized con-
sevoflurane anaesthesia in pigs and reported that        trolled clinical trial evaluated the incidence of
sevoflurane increased pulmonary leukotriene C4,          wheezing in asymptomatic asthmatic and nonasth-
NO3-, and NO2- production, suggesting an                 matic patients receiving i.v. anaesthetic agents for
inflammatory response.                                   induction of anaesthesia. They observed that both
                                                         asthmatic and nonasthmatic patients who received
INTRAVENOUS ANAESTHETICS                                 a thiobarbiturate for induction had a greater inci-
                                                         dence of wheezing than did patients receiving
   Ketamine is an i.v. general anaesthetic that is
considered an attractive choice because of its sym-      propofol. Similarly, Eames et al.45 assessed Rrs in
pathomimetic bronchodilatory properties and its          a nonasthmatic patient population with a high
effectiveness at preventing and reversing wheezing       incidence of smoking and compared thiopental,
in patients with asthma who require anaesthesia          etomidate, and propofol. They observed that tra-
and intubation.38 Ketamine relaxes the bronchi-          cheal intubation with propofol anaesthesia pro-
olar musculature and prevents the bronchocon-            duced a lower Rrs than when thiopental or a rel-
striction induced by histamine, decreasing the           atively high dose of etomidate was used. To com-
risk of bronchospasm during the induction of             pare the effects of propofol anaesthesia in children
anaesthesia. These effects derive from a direct          with and without asthma, Habre et al.46 induced
action on bronchial muscle as well as a potentia-        anaesthesia with propofol, fentanyl, and atracuri-
tion of catecholamines. Nonetheless, ketamine            um and maintained with an infusion of propofol
increases bronchial secretions and it is usual to        and 50% nitrous oxide in oxygen. Final results
administer an anticholinergic agent such as              showed that respiratory mechanics were not altered
atropine or glycopyrrolate in conjunction.               by propofol anaesthesia in children both with and
Hallucinations are the most unpleasant side effect       without asthma. In this context, Peratoner et al.47
of ketamine and can be minimized with concomi-           analysed the effects of propofol on respiratory
tant sedation with benzodiazepines.10 However, its       mechanics in normal rats and correlated these
effectiveness has not been demonstrated in a con-        parameters with lung histology, to define the sites
trolled trial.39, 40 Although previous studies           of action of propofol. They observed that propo-
analysed the effects of ketamine on central air-         fol acts at the airway level, decreasing respiratory
ways, Alves-Neto et al.41 observed in rats without       system and lung impedances as a result of central
pre-existing airway constriction that ketamine           airway dilation.
acted not at the airway level but at the lung periph-       On the basis of the aforementioned, propofol
ery, increasing mechanical inhomogeneities, which        is considered safe for patients with asthma who
may result from dilation of distal airways and           require timely intubation. Nevertheless,
alveolar collapse.                                       Nishiyama and Hanaoka 48 reported 2 cases of
   Brown and Wagner 38 examined the local air-           bronchoconstriction following propofol induc-
way effects of ketamine and propofol on attenuat-        tion. Both patients had allergic problems, and it
ing direct and reflex-induced airway constriction.       was postulated that it was the particular formula-
They developed a nonasthmatic animal model in            tion of propofol which contained yolk lecithin
which they administered ketamine and propofol            and soybean oil that caused the problem.
directly to the airways via the bronchial artery and     Accordingly, propofol should be used with caution
concluded that the major mechanism of bron-              in patients with allergic disease or drug-induced
choprotection of ketamine and propofol is deter-         asthma.

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OPIOIDS                                                 choconstriction and can be used to attenuate the
                                                        response to airway irritations like endotracheal suc-
   Although opioids could release histamine, they
are considered safe for patients with increased         tion or intubation. Groeben et al.51 demonstrated
bronchial reactivity. Fentanyl and its analogues        that, in awake humans, both i.v. lidocaine and
are frequently used in the induction of anaesthe-       inhaled albuterol significantly increased the hista-
sia, and they can lead to thorax rigidity that can be   mine threshold when given alone. They recom-
misinterpreted as bronchospasm. With slow injec-        mended preoperative treatment with inhaled
tion, this effect is hardly observed.                   albuterol and i.v. lidocaine to prevent reflex bron-
   Moreover, the suppression of the cough reflex        chospasm with tracheal intubation. Alternatively,
and the deepening of anaesthesia level achieved         Maslow et al.22 studied 60 asthmatic patients and
after opioid administration can be helpful in asth-     found that inhaled albuterol attenuated the airway
matic patients.17                                       response to tracheal intubation in asthmatic
                                                        patients, while i.v. lidocaine did not.
                                                           Inhalation of lidocaine can attenuate the
MUSCLE RELAXANTS
                                                        response to airway irritation with plasma concen-
    Depending on which type of muscarinic receptor      trations lower than those following systemic
is stimulated, increased or decreased bronchial tone    administration.17 Nevertheless, the attenuation of
and reactivity can be expected. It has been shown       bronchial reactivity is preceded by a mild airway
that muscle relaxants which affect M2 receptors more    irritation 52, 53 that can be avoided with pretreat-
than M3 receptors (gallamin, pipecuronium,              ment with a β2-adrenergic agonist or minimized by
rapacuronium) can cause and enhance bronchocon-         using lidocaine inhalation in a dose of 2 mg/kg as
striction.49 Otherwise, muscle relaxants which seem     a 4% solution for topical anaesthesia.50 This is the
to bind M3 receptors more or at least the same way      regimen that attenuates bronchial hyper-reactivi-
as M2 receptors do not induce bronchospasm.             ty with the least airway irritation.54 In addition,
Among those, vecuronium, rocuronium, cisatracuri-       Hunt et al.55 recruited 50 subjects with mild to
um, and pancuronium are considered safe.11              moderate asthma to receive either an inhaled place-
    In addition to these direct effects on muscarinic   bo or inhaled lidocaine 4% for 8 weeks. Their
receptors, atracurium and mivacurium dose-              results showed that nebulized lidocaine was an
dependently release histamine and have been iden-       effective therapy in those patients.
tified as triggers of bronchoconstriction and should       Moreover, local anaesthetics, absorbed from the
be used carefully in asthmatic patients.17              epidural space to the blood, attenuate bronchial
    Furthermore, the reversal of muscle relaxation      hyper-reactivity to chemical stimuli. Shono et al.56
at the end of surgery should be avoided since           reported a case of a man with bronchial asthma
neostigmine and physostigmine cause bradycar-           under continuous epidural anaesthesia with 2%
dia, increased secretion, and bronchial hyper-reac-     lidocaine in which wheezing gradually diminished
tivity. For this purpose, doses of muscle relaxants     after the epidural injection and completely disap-
should be timed so as to be worn off at the end of      peared over 155 min during continuous epidural
surgery.11                                              injection of lidocaine. Wheezing reappeared 55
                                                        min after termination of the continuous epidural
LOCAL ANAESTHETICS                                      injection of lidocaine. This corroborates the
   Local anaesthetics of the amide type that atten-     hypothesis that regional anaesthesia in asthmatic
uate and even block afferent and efferent nerve         patients, alone or in combination with general
conduction of autonomic nerve fibres and auto-          anaesthesia, is advantageous.
nomic reflexes, such as the coughing or bron-
choconstriction reflex, can be suppressed with plas-     Treatment of intraoperative bronchospasm
ma concentrations of lidocaine below the toxic
threshold of 5 mg/mL.50 In asthmatic volunteers,          If intraoperative wheezing should develop, non-
i.v. lidocaine doses of 1-2 mg/kg of body weight        bronchospastic causes of wheezing (mechanical
significantly attenuated histamine-induced bron-        obstruction of the endotracheal tube, endo-

362                                       MINERVA ANESTESIOLOGICA                                    June 2007
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ANAESTHETIC MANAGEMENT IN ASTHMA                                                                      BURBURAN

bronchial intubation, pulmonary aspiration, pul-          relieved by usual therapy in 30 to 60 min. The
monary embolism, pulmonary oedema, tension                term refractory status asthmaticus describes those
pneumothorax, and negative pressure inspiration)          cases in which the patient’s condition continues
must be ruled out.19 The first step is to deepen the      to deteriorate despite aggressive pharmacologic
level of anaesthesia via the i.v. or inhalational route   interventions and persists for more than 24 h.10
or both. Administration of 100% oxygen should                 When conventional bronchodilators fail, the
be instituted to prevent hypoxemia.                       intensivist may resort to the use of drugs such as
   β2-agonists via metered dose inhaler should be         ketamine and inhalation anaesthesia. In this con-
administered through the airway. It is important          text, deep sedation is important not only to
to consider the fact that delivery of aerosolized         improve oxygenation but also to reduce cerebral
agents during mechanical ventilation is not ade-          metabolic requirements.57
quate, being estimated that as little as 1% to 3% of          Therapy with inhalational anaesthetic agents
a dose of nebulized medication actually reaches the       such as halothane, enflurane, isoflurane, and
lungs of a patient on positive pressure ventilation.      diethyl ether has been successfully used in the
The amount of aerosol reaching the lungs could            management of refractory status asthmaticus.10, 58
be improved by means of an increase in respirato-         Iwaku et al.59 treated patients with status asthmati-
ry time, a reduction of respiratory rate, an increase     cus with isoflurane inhalation and observed that
in the volume of nebulizer fill, and positioning of       tidal volume, pH, and PaCO2 improved after
the nebulizer between the Y-piece and catheter            anaesthesia and that these patients stayed in the
mount or on the inspiratory limb of the ventila-          Intensive Care Unit (ICU) and underwent
tor circuit Y-piece when jet nebulizers are used.27       mechanical ventilation for a shorter period than
   Epinephrine, either subcutaneously or intra-           those who were not treated with isoflurane.
venously, can help in severely bronchospastic                 Que and Lusaya 60 successfully used sevoflu-
patients. Corticosteroids can be utilized, but their      rane inhalation in a parturient in status asthmati-
onset of action takes place within 4 to 8 h of            cus for caesarean section. Schultz 61 reported the use
administration.27                                         of sevoflurane in a 26-year-old woman who pre-
   Leukotriene receptor antagonists and mast cell         sented to a rural critical access hospital emergency
inhibitors have no use in acute bronchospasm.             department in status asthmaticus and subsequent-
Intravenous aminophylline can be started, but side        ly failed conventional therapy. Sevoflurane was
effects such as tachycardia and hypertension may          administered for approximately 150 min, stabi-
limit its usefulness. As a result, methylxantines are     lizing the patient’s condition enough to allow fixed-
no longer recommended for acute exacerbations.            wing air transport to a tertiary facility. Likewise,
   A smooth, slow emergence minimizes the risk            Mazzeo et al.57 reported an 8-year-old boy treated
of bronchospasm. Deep extubation can be attempt-          with ketamine and sevoflurane and observed no
ed if no airway difficulties were encountered dur-        episode of haemodynamic instability despite severe
ing induction. If deep extubation is contraindi-          prolonged hypercapnia. Oxygenation was main-
cated, the patient may be taken to the postanesthe-       tained and successful recovery followed without
sia care unit intubated and opioids administered          sequelae.
to facilitate tolerance to the endotracheal tube.
When the patient is awake and possesses appro-
priate airway reflexes, extubation can occur.                                Conclusions
Intravenous lidocaine may be of use in prevent-              Some anaesthetics have been used even for
ing bronchospasm with extubation.19                       intractable status asthmaticus. Despite this, and
                                                          the fact that the understanding of the pathophys-
 Inhalation anaesthesia in status asthmaticus             iology of asthma has changed, there are only a few
                                                          studies describing the sites and mechanisms of
   Status asthmaticus refers to acute asthma attacks      action of our frequently used anaesthetic agents
in which the degree of bronchial obstruction is           in a chronically inflamed, hyper-responsive, and
either severe from the onset or worsens and is not        remodelled lung, as seen in asthmatic patients.

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Knowledge of these mechanisms will stimulate a                          17. Groeben H. Strategies in the patient with compromised res-
                                                                            piratory function. Best Pract Res Clin Anaesthesiol
great revolution in anaesthetic management, allow-                          2004;18:579-94.
ing anaesthesiologists and intensivists to optimise                     18. Celiker V, Basgul E. Anaesthesia in aspirin-induced asthma.
                                                                            Allergol Immunopathol 2003;31:338-41.
the use of anaesthetic drugs and techniques in                          19. Stasic AF. Perioperative implications of common respiratory
those patients, and it will direct researchers to                           problems. Semin Pediatr Surg 2004;13:174-80.
                                                                        20. Bremerich DH. Anesthesia in bronchial asthma. Anasthesiol
develop new drugs effective not only on inhibiting                          Intensivmed Notfallmed Schmerzther 2000;35:545-58.
hyper-responsiveness and producing bronchodila-                         21. Silvanus MT, Groeben H, Peters J. Corticosteroids and inhaled
tion, but also on reducing or even suppressing the                          salbutamol in patients with reversible airway obstruction
                                                                            markedly decrease the incidence of bronchospasm after tra-
underlying inflammation process and remodel-                                cheal intubation. Anesthesiology 2004;100:1052-7.
ling. Therefore, the incidence of anaesthetic com-                      22. Maslow AD, Regan MM, Israel E, Darvish A, Mehrez M,
                                                                            Boughton R et al. Inhaled albuterol, but not intravenous lido-
plications and adverse events will be strongly min-                         caine, protects against intubation-induced bronchoconstric-
imized, which will be very beneficial to patients                           tion in asthma. Anesthesiology 2000;93:1198-204.
                                                                        23. Barnes PJ. Mechanisms of action of glucocorticoids in asth-
and physicians.                                                             ma. Am J Respir Crit Care Med 1996;154:S21-6; discussion
                                                                            S6-7.
                                                                        24. Kabalin CS, Yarnold PR, Grammer LC. Low complication rate
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ANAESTHETIC MANAGEMENT IN ASTHMA                                                                                              BURBURAN

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Supported by The Centres of Excellence Program (PRONEX-FAPERJ), Brazilian Council for Scientific and Technological Development (CNPq),
Carlos Chagas Filho Rio de Janeiro State Research Supporting Foundation (FAPERJ).
Acknowledgments.—The authors would like to express their gratitude to A. Benedito da Silva and S. Cezar da Silva Junior for their techni-
cal assistance.
Received January 26. 2006 - Accepted for publication October 24, 2006.
Address reprint requests to: P. R. M. Rocco, MD, PhD, Laboratório de Investigação Pulmonar, Instituto de Biofísica Carlos Chagas Filho,
C.C.S., Universidade Federal do Rio de Janeiro, Ilha do Fundão. CEP. 21.949-900 – Rio de Janeiro, RJ, Brazil. E-mail: prmrocco@biof.ufrj.br

Vol. 73 - No. 6                                        MINERVA ANESTESIOLOGICA                                                         365
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