Address for
Correspondence: Dr. MC Rajesh MD, MBA, Senior Consultant
Anaesthesiologist, Baby Memorial Hospital, Kozhikode, Kerala,
India. PIN: 673004. E- mail: rithraj2@yahoo.co.in
Introduction
Intraoperative bronchospasm caused by the spasmodic
contraction of bronchial smooth muscle is a rare but
potentially lethal challenge for anaesthesiologists.
Retrospective analysis shows an incidence of 1.7 per 1000
patients with a confirmed higher possibility in the presence
of irritable airway pathology [1] and accounts for almost
similar percentage of ASA closed claims study [2]. It can
happen in isolation or as a part of more serious pathology
such as type E immunoglobulin mediated anaphylaxis.
Bronchospasm results in decreased airway calibre and altered
distribution of gases within the lungs leading to ventilation
perfusion mismatch. Patients with reactive airway diseases
should be considered a potentially at risk candidates for peri
operative bronchospasm with increased chance of peri-operative
mortality and morbidity if not adequately controlled.
The goal of anaesthesiologist for at risk patients should be
to administer safe and sufficient anaesthesia without
precipitating bronchospasm. The anaesthesiologist should be
wise in choosing proper techniques and avoiding drugs which
can precipitate an intraoperative bronchospasm. Judicious use
of anti-inflammatory and bronchodilatory medications should be
instituted as part of preoperative preparation so that
patients are asymptomatic while taking up for procedure in an
elective case [3]. It is important to extend the care to the
post operative settings also. Good analgesia, post operative
respiratory monitoring and educating patients with proper
breathing exercises are important to prevent peri-operataive
respiratory morbidities.
Who are the patients at risk?
A definite history of obstructive pulmonary disease may not be
evident in all patients with bronchospasm. Also most patients
with obstructive pulmonary disease may not develop
bronchospasm under anaesthesia. Though the incidence of severe
peri operative bronchospasm is rare in severe asthmatics, when
it does occur, it can be life threatening [3]. There are
certain situations considered to be at risk for intra
operative bronchospasm due to underlying bronchial
hyperactivity. This include recent viral upper respiratory
tract infections, exposure to tobacco smoke, history of atopy
and recent hospital admission for exacerbations of bronchial
asthma [5]. Of course airway instrumentation is a potential
stimulus which can trigger bronchoconstriction in patients
with irritable airways [4]. Kim ES et al has shown that unlike
laryngeal mask airway insertion, endobroncheal intubation
produces reversible bronchoconstriction [6]. Manipulation of
the airway or surgical stimulation under light anaesthesia
increases the risk of bronchospasm. Airway soiling due to
secretions, regurgitation or aspiration in a patient with
irritable airway state is a potential stimulus for
bronchospasm. An analysis of incidence reported showed the
principal causes of bronchospasm as airway irritation (35%)
followed by problems with endotracheal tube (23%) and
aspiration of gastric contents (14%) [8].
Rule out mechanical causes of increased peak airway
pressure
Obstruction of natural or artificial air passages like kinked
endotracheal tube, breathing circuit or air filters, smaller
endotracheal tubes, overinflation of the tracheal tube cuff,
patients active respiratory efforts and fighting with
ventilator, endo bronchial intubation are commonly missed
causes for increased peak airway pressure. These possibilities
should be ruled out and corrected first. An excessive tidal
volume or high inspiratory flow rates set in the anaesthesia
machine, opioid induced muscle rigidity, also will results in
a high peak airway pressures in the monitor suspecting a
bronchospasm. Steep head down position, excessive
pneumoperitonium, morbidly obese patients are conditions
contributing to excessive peak airway pressures during IPPV.
Other than as a separate entity, bronchospasm could be
associated with life threatening conditions which requires
immediate action like anaphylaxis, pulmonary aspiration,
pneumothorax, pulmonary edema and pulmonary embolus.
How to diagnose?
Suspicion is the key to early detection. Under anaesthesia,
common presenting signs are expiratory wheeze on auscultation
over the chest or heard in the breathing circuit, decreased
pulmonary compliance and falling oxygen saturation.
Spontaneously breathing patient will show prolonged
exhalation. To demonstrate a wheeze, it requires some movement
of air. So in severe cases can expect even a silent chest on
auscultation and correct diagnosis in such circumstances is
made by the increased inflation pressures. Similarly breath
sounds may be uniformly reduced also. On positive pressure
ventilation, peak airway pressure is increased, tidal volume
reduced or both. Narrowed airways and prolonged expiration
results in a characteristic shark fin appearance in the
capnography wave form (Slowly increasing wave on the
capnography) and decreasing tidal volume. Positive pressures
when delivered before the expiratory phase can result in the
development of intrinsic positive end expiratory pressure.
This auto/intrinsic PEEP can result in an increase of intra
thoracic pressure, decrease venous return and impair cardiac
output.
When bronchospasm is associated with anaphylaxis or allergy,
the signs exhibited by the patient include rashes and
hypotension in addition to increased inflation pressure, fall
in saturation and capnography changes.
Implication of Pharmacological agents
Pharmacological agents which can potentially precipitate a
bronchospasm has to be kept in mind while anaesthetising a
high risk patient. These include beta adrenergic antagonists,
acetylcholinesterase inhibitors, NSAIDs. Non specific beta
blockers should be best avoided. But ultra short acting highly
selective beta-1 antagonists like esmolol and landiolol are
used peri operatively without much problem. Use of
acetylcholinesterase inhibitors for neuromuscular blockade
reversal should be combined with adequate doses of
anticholinergic agents. The concern with acetylcholinesterase
inhibitors is because of its muscarinic side effects. But in
practice this is not a major problem. Sugammadex which
encapsulates steroidal neuromuscular blocking agents without
muscarinic side effects is proposed as an alternative to
regular anticholinesterase inhibitors. There are some who
advocate avoiding reversal altogether allowing adequate time
for the recovery of neuromuscular function. Certain volatile
anaesthetic agents like Isoflurane and Desflurane when
introduced quickly can trigger bronchospasm. Drugs with the
potential for histamine release like thiopentone, atracurium,
morphine, mivacurium, protamine can also precipitate
bronchospasm. Sometimes Fentanyl induced muscle rigidity can
grossly reduce the chest wall compliance increasing peak
airway pressure to mimic bronchospasm.
Perioperative care in high risk patients
Whenever possible, regional anaesthesia should be preferred if
the site of surgery is suitable since it reduces airway
manipulations. If a general anaesthesia is perceived to be
mandatory, supraglottic airways to be preferred over routine
endotracheal intubations. In the event of emergency surgery in
asthmatic patients, anaesthesiologists have to balance the
risk between protecting the airway from risk of aspiration and
the risk of triggering bronchospasm. Scaltaro P et al has
shown that the increase in airway resistance that can occur
after tracheal intubation can be reduced by prophylactic
administration of bronchodilators [7]. In fact, airway
irritation at the time of intubation is a known potential
cause for bronchospasm. According to Westhorpe RN et al,
bronchospasm is most commonly encountered during induction and
maintenance than at the time of emergence and recovery phase
[8]. So it is important to make the patient at a deeper plane
prior to instrumentation of airway. Use of intravenous
Lidocaine because of its membrane stabilizing effect is found
to be useful to blunt the airway irritability during airway
instrumentation [9]. It has to be administered intravenously
60 to 90 seconds before intubation (1 to 1.5 mg/kg body
weight). Similarly extubation can also be performed under deep
planes.
Asthmatic patient with wheeze, irritable cough,recent
respiratory infections, shortness of breath, recent
exacerbations or hospital admission indicate poor control.
Patients should be asked to continue their medications with
which they are having symptom control. Children with active
upper respiratory obstruction may necessitate postponing
surgery till resolution of symptoms [3]. Asthmatic children
requires pre operative optimisation before any elective
procedure. For a well controlled asthmatic, use of inhaled
beta-2 adrenergic agonists 1 to 2 hours before surgery may be
enough [10]. An asymptomatic or moderately controlled
asthmatic requires additional optimisation with inhaled anti
inflammatory agents along with regular use of nebulised
adrenergic beta-2 agonists [10]. Whereas a poorly controlled
asthma requires in addition to beta-2 agonists and inhaled
steroids systemic steroids. Either oral prednisolone
(1mg/kg/day maximum of 60 mg) 3 to 5 days before surgery or
dexamethasone ( 0.6 mg/kg maximum of 16 mg) can also be used
[11].
Smokers should be encouraged to stop smoking preoperatively.
It was observed that those who quit smoking more than four
weeks before surgery have lower risk of pulmonary
complications compared to those who continued to smoke [12].
Adequate pain relief, hydration, correction of electrolyte
imbalance, anxiolysis, humidification of inspired gases,
airway suctioning under deep planes of anaesthesia are some of
the general measures to be given importance to prevent a
peri operative event.
Propofol is an ideal agent for induction in an
haemodynamically stable patient because of its ability to
attenuate bronchospastic response to airway instrumentation
[13]. For maintanence of anaesthesia, Sevoflurane is preferred
because of its bronchodilatory effects [14].
Ventilator strategies should be altered to limit the peak
inspiratory pressure, tidal volume and lengthening the I:E
ratio to avoid auto PEEP.
Intra operative crisis
Suspected bronchospasm should be assessed and treated
promptly. Management starts with ventilating the patient with
100% oxygen and calling for help early. Manual bag ventilation
should be started immediately to assess the compliance.
It is important to rule out mechanical causes of airway
obstruction and inadequate plane of anaesthesia before
initiating treatment. The asthma related bronchospasm usually
respond to deepening of anaesthesia with volatile anaesthetic
agents if haemodynamic status permits. But in severe cases
effective delivery of inhalational agents will be difficult.
Intravenous agents like Propofol are an ideal alternative in
such situations to deepen the plane. Ketamine on the other
hand produces bronchodilatation and is a widely available
agent. If bronchospasm still persists, then institution of
beta-2 agonist therapy should be considered [15]. Short acting
metered dose inhaler is the corner stone of management of
intra operative bronchospasm. With the advent of more specific
agents (Salbutamol, Terbutaline) the problem related to
tachyarrythmias of older agents never come to the picture.
Only a small fraction of the inhaled agent is absorbed
systemically. Metered dose inhaler (MDI) delivery should
synchronize with the onset of inspiratory flow and heat and
moisture exchanger (HME) should be removed during delivery of
the drug. MDI should be delivered to the inspiratory limb of
the circuit. Delivering drugs through endotracheal tube is a
challenge because majority of drug is lost in the endotracheal
tube. So a relatively large dose like 8 to 10 puffs should be
given. If in spite of beta-2 agonist therapy and deep general
anaesthesia, bronchospasm is not relieved, steroid
administration may be necessary (methyl prednisolone 125
milligram I/V). But for the therapeutic benefits of
corticosteroids to become apparent, it will take several hours
(4-6 hours). Anticholinergics is an accepted bronchodilating
agent. There is evidence for the addition of Magnesium
Sulphate for asthma [16] (50 mg/kg IV over 20 minutes, maximum
2 gram). Ipratopium bromide 0.5 mg nebulised 6 hourly in
combination with beta-2 agonists produce maximum
bronchodilatation. Ketamine bolus 10 to 20 mg or infusion
1-3mg/kg/hr and in extreme cases Epinephrine (Adrenaline)
nebulised 5 ml 1:1000, intravenous 10 microgram (0.1ml
1:10000) to 100 microgram (1ml 1:10000) titrated to response
have been tried. Use of Epinephrine is best reserved in
intractable cases especially in the presence of hypotension.
Nitroglycerin because of its direct smooth muscle relaxation
is found to have a positive effect in severe bronchospasm
[17]. Helium oxygen mixture (Heliox) have been used to provide
laminar flow during bronchospasm. The theoretical advantage
with Heliox is the ability to provide ventilation till
corticosteroids take effect. But to what extend this can be
incorporated in the protocol can't be commented at present
because of insufficient data [18].
Recently an analogue of Lidocaine, known as Lidocaine JM25-1
was pharmacologically evaluated [19]. It was found to have
less of local anaesthetic action because of limited impact on
the sodium channels but more effective as a bronchodilator and
anti-inflammatory agent [19, 20].
Management algorithm should also include frequent blood gas
assessment to know the extent of hypoxaemia and
hypercarbia.
Conclusion
Intraoperative bronchospasm is usually triggered by mechanical
or pharmacological causes or as a part of a systemic reason
like anaphylaxis. For asymptomatic asthmatics the incidence is
very low. It is important to identify patients at risk of
perioperative bronchospasm and avoid any intra operative
insult. Rational use of techniques and agents is the key.
Inhaled and parentral beta-2 agonist is the key element in
pharmacological therapy along with the judicious use of
steroids. Agents like Nitroglycerin, Heliox, and JM25-1
requires more evaluation and research before acceptance in
standard treatment protocols.
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