Bronchospasm During Anaesthesia Update 2011

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Clinical Overview Articles

Update in
Anaesthesia
Management of bronchospasm during general
anaesthesia
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INTRODUCTION pressures during anaesthesia (Boxes 1 and 2). With


Bronchospasm during general anaesthesia can present capnography, narrowed airways and prolonged
in isolation or as a component of a more serious expiration result in a delayed rise in end-tidal
underlying pathology such as anaphylaxis. It is carbon dioxide, producing a characteristic ‘shark-
characterised by prolonged expiration, wheeze and ëO BQQFBSBODF 'JHVSF 
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increased peak airway pressures during Intermittent diagnostic, representing an obstruction at some stage
Positive Pressure Ventilation (IPPV). Untreated it can in the expiratory pathway. With limitation in air flow,
Summary
cause hypoxia, hypotension and increased morbidity a prolonged period of exhalation is needed for alveolar
pressure to normalise. Positive pressure ventilation Bronchospasm is a relatively
and mortality. Suspected bronchospasm during common event during
anaesthesia should be assessed and treated promptly. delivered before exhalation is complete can result in
general anaesthesia.
Ongoing management should address the underlying ‘breath-stacking’ and the development of an intrinsic Management begins
cause. (or auto) positive end-expiratory pressure (iPEEP or XJUITXJUDIJOHUP
autoPEEP). Intrinsic PEEP can increase intrathoracic PYZHFOBOEDBMMJOH
BRONCHOSPASM pressure, decrease venous return and impair cardiac for help early. Stop all
Bronchospasm and wheeze are common features output.2 potential precipitants
of reactive airways disease. Patients with bronchial and deepen anaesthesia.
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asthma and some with chronic obstructive
obstruction or occlusion
pulmonary disease (COPD) show hyperreactive of the breathing circuit.
airway responses to mechanical and chemical Figure 1. The characteristic ‘shark-fin’ capnograph
suggestive of airway obstruction "JNUPQSFWFOUDPSSFDU
irritants. In these groups there is a combination of IZQPYBFNJBBOESFWFSTF
constriction of bronchial smooth muscle, mucosal Box 1. Causes of wheeze during general anaesthesia bronchoconstriction.
oedema and mucous hypersecretion with plugging. Partial obstruction of tracheal tube (including ETT Consider a wide range
Perioperative bronchospasm in patients with reactive abutting the carina or endobronchial intubation) of differential diagnoses
airways disease is however relatively uncommon. In JODMVEJOHBOBQIZMBYJT 
Bronchospasm
patients with well-controlled asthma and COPD the aspiration or acute
Pulmonary oedema pulmonary oedema.
incidence is approximately 2%. The overall incidence Aspiration of gastric contents
of bronchospasm during general anaesthesia is Pulmonary embolism
approximately 0.2%.1 5FOTJPOQOFVNPUIPSBY
Exposure to tobacco smoke, history of atopy and viral Foreign body in the tracheobronchial tree
upper respiratory tract infection (URTI) all increase
the risk of bronchospasm during anaesthesia. In many Box 2. Causes of increased peak airway pressure during
patients with bronchospasm during anaesthesia there IPPV
is no history of reactive airways disease. Anaesthetic equipment
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RECOGNITION OF BRONCHOSPASM )JHIJOTQJSBUPSZóPXSBUFT
Bronchospasm during anaesthesia usually manifests Airway device
as prolonged expiration. An associated expiratory Small diameter tracheal tube
wheeze may be auscultated in the chest or heard in Endobronchial intubation
the breathing circuit. Wheezing requires movement Tube kinked or blocked Alex Looseley
of gas through narrowed airways and so in severe Core Trainee
Patient Department of Anaesthesia
bronchospasm wheeze may be quiet or absent. Obesity 3PZBM%FWPOBOE&YFUFS/)4
Similarly, breath sounds may be reduced or absent. Head down position Foundation Trust
With IPPV, peak airway pressures are increased, tidal Pneumoperitoneum Barrack Road
volumes reduced, or both. Bronchospasm is not 5FOTJPOQOFVNPUIPSBY &YFUFS&9+5
the only cause of wheeze or increased peak airway Bronchospasm UK

Update in Anaesthesia | www.anaesthesiologists.org page 17


DIFFERENTIAL DIAGNOSIS predictable and can be prevented or countered by an intravenous
Bronchospasm occurs most commonly and approximately equally bolus of opioid and/or anaesthetic agent such as propofol.
during the induction and maintenance stages of anaesthesia and
is less often encountered in the emergence and recovery stages.3 Pharmacological
Bronchospasm during the induction stage is most commonly caused Certain volatile anaesthetic agents (isoflurane, desflurane) if
by airway irritation, often related to intubation. introduced quickly can trigger bronchospasm. IV agents including
beta-blockers, prostaglandin inhibitors (NSAIDs) and cholinesterase
During the maintenance stage of anaesthesia, bronchospasm may inhibitors (neostigmine) are implicated. Histamine release
result from an anaphylactic or serious allergic reaction. Drugs (thiopentone, atracurium, mivacurium, morphine, d-tubocurarine)
(antibiotics, neuromuscular blockers), blood products (red blood DBOBMTPQSFDJQJUBUFCSPODIPTQBTNDBSFTIPVMECFUBLFOXJUIUIFTF
cells, fresh frozen plasma) and other allergens (latex) are the agents drugs in higher risk patients.
commonly responsible. Other features of allergic or anaphylactic
reaction include cutaneous signs (rash, urticaria, angioedema) and Airway soiling
cardiovascular signs (tachy/bradycardia, hypotension, circulatory Unexplained bronchospasm, especially in patients without increased
collapse). risk of airway hyperreactivity, should prompt consideration of
When assessing bronchospasm there are other important differential airway soiling due to secretions, regurgitation or aspiration. This is
diagnoses and contributing factors to consider: particularly true with the use of the laryngeal mask airway (LMA)
but may also occur with an uncuffed endotracheal tube (ETT) or an
Mechanical obstruction inadequately inflated/punctured cuff. A history of gastro-oesophageal
reflux or sudden coughing in a patient breathing spontaneously with
A kinked (see case report in this edition), blocked (mucous plug, cuff
an LMA should increase the suspicion of airway soiling.
herniation) or misplaced (endobronchial, oesophageal) tracheal tube
or occlusion in the breathing circuit can mimic severe bronchospasm.
Unless rapidly recognised and corrected this can have disastrous PREVENTION OF BRONCHOSPASM
consequences. A recent death in the UK (initially treated as severe Patients with asthma and COPD should be thoroughly assessed
bronchospasm) was found to be due to blockage of the breathing and care taken to ensure they are optimised for surgery. Wheezing,
circuit with the protective cap from an IV giving set. The subsequent cough, increased sputum production, shortness of breath and diurnal
Department of Health report ‘Protecting the Breathing Circuit variability in peak expiratory flow rate (PEFR) indicate poor control.
in Anaesthesia’ (2004) reiterated the importance of checking the Recent or frequent exacerbations or admission to hospital may be
breathing circuit prior to each patient and ensuring the availability an indication to postpone non-essential surgery. Patients should be
of another means of ventilation (i.e. a self-inflating bag).4 encouraged to continue their medication until the time of surgery.
Preoperative bronchodilators, inhaled or oral corticosteroids, chest
Laryngospasm physiotherapy and referral to a respiratory physician may all be
This should be considered and excluded. In non-intubated patients appropriate.
acute laryngospasm can produce upper airway noise (usually A careful medication history should be taken with particular
inspiratory), reduced breath sounds and difficulty in ventilation. reference to drug sensitivities. NSAID-induced bronchospasm in
Laryngospasm can present with signs of airway obstruction including adult asthmatics may be as high as 15% and so a thorough history
increased respiratory effort, tracheal tug and paradoxical movement is vital.5
of the chest and abdomen (‘see-saw’ respiration).
All patients should be counselled and encouraged to stop smoking
Bronchial hyperreactivity preoperatively. Six to eight weeks of abstinence before surgery
TJHOJëDBOUMZSFEVDFTUIFSJTLPGSFTQJSBUPSZDPNQMJDBUJPOTJODMVEJOH
If the patient is known to be at increased risk of bronchial
bronchospasm.6
hyperreactivity the suspicion of bronchospasm is increased. The
main patient groups are those with reactive airways disease, especially URTI in children increases the risk of bronchospasm and so it may be
poorly controlled asthma and COPD. Bronchial hyperreactivity is necessary to postpone surgery. The complete resolution of symptoms
also associated with preoperative exposure to tobacco smoke, upper (approximately 2 weeks) correlates well with a decreased incidence of
respiratory tract infection (URTI) and a history of atopy. Many of airway hyperreactivity.7
these factors also predispose to laryngospasm.
Pretreatment with an inhaled/nebulised beta agonist, 30 minutes
prior to surgery, induction of anaesthesia with propofol and adequate
Inadequate depth of anaesthesia
depth of anaesthesia before airway instrumentation reduces the risk
Manipulation of the airway or surgical stimulation under light of bronchospasm.
anaesthesia increases the risk of bronchospasm. Certain surgical
procedures have highly stimulating stages that can trigger The use of an LMA (in suitable patients) has been shown to reduce
bronchospasm (and laryngospasm). Examples of these include anal the incidence of bronchospasm compared to tracheal intubation.8
or cervical dilatation, stripping of the long saphenous vein during Regional techniques where appropriate can also avoid the need for
varicose vein surgery and traction on the peritoneum. These are often general anaesthesia and intubation.

page 18 Update in Anaesthesia | www.anaesthesiologists.org


Figure 2. Algorithm to guide management of intraoperative bronchospasm. Red numbers refer to notes over leaf.

Management of patient with suspected bronchospasm


during general anaesthesia
On suspecting bronchospasm A
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Difficulty with ventilation/falling SpO2 CALL FOR HELP

Immediate management; prevent hypoxia & reverse bronchoconstriction B


• Deepen anaesthesia 1
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 CMPDLFENJTQMBDFEUVCF 2
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Consider transfer to HDU / ICU

Secondary management, provide ongoing therapy and address underlying cause


C
• Optimise mechanical ventilation
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• Consider transfer to a critical care area for ongoing investigations and therapy

1st Line Drug Therapy 2nd Line Drug Therapy


D
Salbutamol Ipratropium bromide: 0.5mg nebulised 6 hourly
• Metered Dose Inhaler: 6-8 puffs repeated as Magnesium sulphate: 50mg.kg-1*7PWFSNJO
 OFDFTTBSZ VTJOHJOMJOFBEBQUPSCBSSFMPGNM NBYH

syringe with tubing or down ETT directly) HydrocortisoneNH*7IPVSMZ


• /FCVMJTFENH NM
SFQFBUFEBT Ketamine: Bolus 10-20mg. Infusion 1-3mg.kg-1.h-1
necessary IN EXTREMIS: Epinephrine (Adrenaline)
• *OUSBWFOPVTNDHTMPX*7UIFONDHNJO-1 Nebulised: 5mls 1:1000
up to 20mcg.min-1
Intravenous: 10mcg (0.1ml 1:10,000) to 100mcg
(1ml 1:10,000) tirtrated to response
Follow up*GBTFSJPVTBMMFSHJDBOBQIZMBDUJDSFBDUJPOXBTTVTQFDUFEPSJEFOUJñFEUIFBOBFTUIFUJTUNVTUFOTVSFUIFQBUJFOUJTSFGFSSFEUPB
TQFDJBMJTUBMMFSHZJNNVOPMPHZDFOUSFGPSGVSUIFSJOWFTUJHBUJPO5IFQBUJFOU TVSHFPOBOEHFOFSBMQSBDUJUJPOFSTIPVMEBMTPCFJOGPSNFE

Update in Anaesthesia | www.anaesthesiologists.org page 19


MANAGEMENT OF BRONCHOSPASM - Figure 2 emergency, the MDI can be discharged directly down the ETT
although much of the aerosol will not reach the patient’s
Notes on the algorithm airways.
1. Increasing the inspired concentration of all volatile anaesthetic
Salbutamol can also be given intravenously. Anticholinergic
agents will produce bronchodilatation (the exception is
drugs such as inhaled ipratropium bromide block
desflurane, which at higher alveolar concentrations has
parasympathetic constriction of bronchial smooth muscle.
been shown to increase airway resistance9). If bronchospasm
In unresponsive bronchospasm, consider the use of epinephrine
is severe, the effective delivery of volatile anaesthetic agents will
(adrenaline), magnesium sulphate, aminophylline, or ketamine.
be difficult. An intravenous agent may be necessary and
propofol is desirable as it obtunds airway reflexes to a greater
degree than thiopentone. If propofol is not available, ketamine
is widely available and produces bronchodilatation.

2. Exclude oesophageal/endobronchial intubation. Consider a


kinked tube or obstruction caused by secretions, mucous, cuff
herniation, or the tube abutting the carina. A suction catheter
may be passed down the tracheal tube to assess patency and
clear secretions.

3. Box D covers in more detail the main agents used to treat acute
 CSPODIPTQBTN*OUIFëSTUJOTUBODFUSFBUNFOUJTXJUIBOJOIBMFE
beta agonist such as salbutamol. This can be repeated several
times or given ‘back-to-back’. Administration must be
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and can be with an in-line adaptor (Figure 3), nebuliser, or
if these are not available, the metered dose inhaler (MDI) can
be placed in the barrel of a 60ml syringe, the plunger replaced
and a 15cm length of IV tubing attached to the end by Luer Figure 3. A metered dose inhaler (MDI) adaptor fitted in the breathing
lock (Figure 4). This tubing is then fed down the ETT and circuit, on the patient side of the heat and moisture exchanger. Depress
reduces the deposition of aerosol on the tracheal tube. As an the canister by hand during inspiration to administer the drug

Table 1. Drug doses for use in bronchospasm

Drug Adult dose Paediatric dose

Salbutamol MDI (metered dose inhaler) 6-8 puffs MDI 6-8 puffs
NebulisedNM NH
   NebulisedZSTNH ZSTNH
IVNDHTMPX*7UIFONDHNJO-1 IV – 4mcg.kg-1TMPX*7UIFONDHLH-1.min-1
up to 20mcg.min -1

Epinephrine IV - 10mcg-100mcg (0.1-1.0 ml 1:10,000) IV – 0.1-1.0mcg.kg-1 (0.01- 0.1ml.kg-1 of 1:100,000)


(Adrenaline) titrated to response
IMmNHJGOP*7BDDFTT  IMNPOUITNDH NUITZSTNDH ZST
         NDH ZSTNDH
Nebulised 5ml 1:1000 Nebulised 0.5ml.kg-1 NBYNMT

Ipratropium bromide Nebulised 0.5mg 6 hourly Nebulised (2-12yrs) 0.25mg 6 hourly


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  NHLH-1*7PWFSNJO NBYH VOMJDFOTFE

Ketamine Infusion: 1-3mg.kg-1.h-1 Bolus dose: 10-20mg Infusion: 1-3mg.kg-1.h-1


Aminophylline 5mg.kg-1*7PWFSNJOUIFONHLH-1.h -1 5mg.kg-1*7PWFSNJOUIFONHLH-1.h-1 ZST

infusion 0.8mg.kg-1.h-1 (9-16yrs) infusion
Omit loading dose if taking theophylline Omit loading dose if taking theophylline
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$IMPSQIFOBNJOF   NHTMPX*7    NPOUITNDHLH-1 *7 NPOUITZSTNH*7 
         ZSTZSTNH*7

page 20 Update in Anaesthesia | www.anaesthesiologists.org


Ventilation should incorporate a long expiratory time to allow
complete exhalation and reduce ‘breath-stacking’ and intrinsic
PEEP. Intrinsic PEEP can increase intra-thoracic pressure, decrease
venous return and cause hypotension. Minimising intrinsic PEEP is
best achieved with a slow respiratory rate, an inspiratory:expiratory
ratio of at least 1:2. If bronchospasm is severe, only 3-4 breaths per
minute may be possible if you allow full expiration - it is useful to
either auscultate or listen at the end of the disconnected endotracheal
UVCFUPDPOëSNUIBUFYQJSBUJPOIBTëOJTIFE CFGPSFDPNNFODJOHUIF
next breath. Rarely, to facilitate this, it is necessary to apply manual
external pressure to the chest. There is no consensus on application
of (external) PEEP, but many advocate trying to match the applied
PEEP to the estimated iPEEP.

POSTOPERATIVE CARE
With ongoing symptoms a chest radiograph should be requested
Figure 4. An MDI canister can be placed in the barrel of a 60ml syringe
and a 15cm length of IV tubing attached via the Luer lock. Feed the and reviewed to exclude pulmonary oedema and pneumothorax. If
tubing down the ETT and press the plunger to administer the drug, then appropriate, regular therapy (bronchodilators, corticosteroids, chest
reconnect the breathing circuit and ventilate physiotherapy) should be arranged. With ongoing bronchospasm,
arrangements should be made for the patient to go to a high
SECONDARY MANAGEMENT dependency or intensive care unit.
The secondary management of acute bronchospasm should provide In the event that a serious allergic or anaphylactic reaction was
ongoing therapy and address the underlying cause. Corticosteroids JEFOUJëFE PS TVTQFDUFE  SFNFNCFS UP UBLF TBNQMFT GPS NBTU DFMM
and antihistamines (Box D) have a role in the secondary treatment of tryptase. It is the responsibility of the anaesthetist to ensure the
bronchospasm and should be given early if the problem is not settling patient is referred to a specialist allergy/immunology centre for further
with initial measures. investigation. The patient, surgeon and general practitioner should
also be informed.
Further consideration should be given to allergy/anaphylaxis and a
thorough examination made for cutaneous and cardiovascular signs. REFERENCES
Review the medication history and consider all drugs given in the 1. Olsson GL. Bronchospasm during anaesthesia. A computer-aided
perioperative period. Examine the patient and reconsider alternative incidence study of 136,929 patients. Acta Anaesthesiol Scand 1987;
diagnoses such as acute pulmonary oedema, tension pneumothorax, 31: 244-52.
pulmonary embolism or foreign body.  1FQF 1&  .BSJOJ ++ 0DDVMU QPTJUJWF FOEFYQJSBUPSZ QSFTTVSF JO
 NFDIBOJDBMMZ WFOUJMBUFE QBUJFOUT XJUI BJSóPX PCTUSVDUJPO UIF BVUP
If the indication for surgery is not life-threatening, consider abandoning PEEP effect. Rev Respir Dis 1982; 126: 166-70.
surgery, especially if there is ongoing difficulty with ventilation, falling
3. Westhorpe RN, Ludbrook GL, Helps SC. Crisis management during
oxygen saturations or haemodynamic compromise. In a non-intubated anaesthesia: bronchospasm. Qual Saf Health Care 2005; 14: e7.
patient with severe bronchospasm, it may be necessary to intubate the
4. Department of Health 2004. Protecting the Breathing Circuit in
trachea and mechanically ventilate the lungs while therapy is initiated.
 "OBFTUIFTJB3FQPSU UP UIF $IJFG .FEJDBM 0îDFS PG BO &YQFSU (SPVQ
If this is the case then avoidance of histamine release is important and on Blocked Anaesthetic Tubing Available from: www.dh.gov.uk
an appropriate muscle relaxant should be used (e.g. rocuronium or
 4[D[FLMJL "  4UFWFOTPO % "TQJSJOJOEVDFE BTUINB "EWBODFT JO
vecuronium if available). pathogenesis, diagnosis, and management. J Allergy Clin Immunol
If the bronchospasm has resolved or improved with initial 2003; 111: 913–21.
management, so that there is no ongoing compromise of the respiratory  %VE[JǤTLB ,  .BZ[OFS;BXBE[LB & 5PCBDDP TNPLJOH BOE UIF
or cardiovascular systems, it may be appropriate to wake the patient perioperative period. Anestezjol Intens Ter 2008; 40: 108-13.
and provide any subsequent therapy on the recovery ward. 7. Nandwani N, Raphael JH, Langton JA. Effects of an upper respiratory
tract infection on upper airway reactivity. Br J Anaesth 1997; 78: 352-
5.
Mechanical ventilation
8. Kim ES, Bishop MJ. Endotracheal intubation, but not laryngeal mask
The primary aim of mechanical ventilation in acute bronchospasm
airway insertion, produces reversible bronchoconstriction.
is to prevent or correct hypoxaemia. Tidal volumes may need to be Anesthesiology 1999; 90: 391-4.
reduced to avoid high peak airway pressures and barotrauma.
9. Dikmen Y, Eminoglu E, Salihoglu Z, Demiroluk S. Pulmonary
Hypercapnia is tolerated if oxygenation is adequate, as long as severe  NFDIBOJDT EVSJOH JTPóVSBOF  TFWPóVSBOF BOE EFTóVSBOF
acidosis does not develop (pH<7.15). anaesthesia. Anaesthesia 2003; 58: 745–48.

Update in Anaesthesia | www.anaesthesiologists.org page 21

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