Department of Health

Vicente Sotto Memorial Medical Center

Training & Research Division
Department of Anesthesia

Bronchospasm During General Anesthesia Induction

A Case Report By:

Joann Melody M. Molleno

2nd Year Resident

September 2013
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 Abstract

Bronchospasm is an anaesthetic emergency that can lead to a fatal outcome

unless an appropriate treatment is administered. An anaesthesiologist must
immediately initiate treatment if bronchspasm is suspected in order to avoid negative
sequelae especially during general anaesthesia which can present in isolation or as
a component of a more serious underlying pathology. Bronchospasm occurs most
commonly and approximately equally during the induction and maintenance stages
of anaesthesia. The key to an uncomplicated perioperative course are to be detailed
in preoperative assessment, and maintenance of the anti-inflammatory and
bronchodilatory regimens. Potential trigger agents should be identified and avoided.
The ultimate goals of preoperative medical assessment are to reduce the patient’s
surgical and anesthetic perioperative morbidity or mortality, and to return him/her to
desirable functioning as quickly as possible. It is imperative to realize that
“perioperative” risk is multifactorial and a function of the preoperative medical
condition of the patient, the invasiveness of the surgical procedure and the type of
anesthetic administered. A history and physical examination, focusing on risk factors
for cardiac and pulmonary complications and a determination of the patient’s
functional capacity, are essential to any preoperative evaluation. Accordingly, prompt
recognition and appropriate treatment are crucial for an uneventful patient outcome.
Whatever the clinical circumstances, different triggers are identified in the
occurrence of perioperative bronchospasm with asthma, a chronic inflammatory
disorder of the airways frequently involved.

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 Table of Contents

Title Page ……………………………………………………………………………1

Abstract ……………………………………………………………………………....2

Introduction ………………………………………………………………………….4

Objectives ……………………………………………………………………………5

Case Overview ………………………………………………………………………5

Discussion …………………………………………………………………………...8

Conclusion …………………………………………………………………………..13

Recommendations ………………………………………………………………….14

References …………………………………………………………………………..15

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I.Introduction:

Bronchospasm is a clinical feature of exacerbated underlying airway

hyperreactivity which has the potential to become an anesthetic disaster. During the
perioperative period, bronchospasm usually arises during induction of anesthesia but
may also be detected at any stage of the anesthetic course.

The incidence of bronchospasm in intra- and postoperative period was not

associated with age, sex, duration of bronchial asthma, severity of disease, duration
of the anesthesia and operation. During induction of anesthesia, bronchospasm was
mainly related to airway irritation, whereas others were due to tube misplacement,
aspiration, and other pulmonary edema or unknown causes.

The occurrence of perioperative bronchospasm has been reported in up to

9% of asthmatic patients given general anesthesia, mainly after endotracheal tube
insertion. Smoking also represents a major risk compared with that of nonsmokers,
the relative risk of perioperative bronchospasm in smokers appears higher in
females and in young smokers (16–39 yrs old) and is higher in patients with chronic
bronchitis than in asymptomatic patients. Thus, uncontrolled asthma/chronic
obstructive pulmonary disease is frequently involved with either pathophysiologic
mechanisms (allergic vs. nonallergic), regardless of the stage of anesthesia
(induction or maintenance).

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II. Objectives:

The purpose of this case report is to discuss the diagnosis and differential
diagnosis during perioperative bronchospasm. Determination of the pathophysiologic
mechanism. The prevention and therapeutic management. How to deal with the
emergence and postoperative care after incidence of bronchospasm.

III.Case Overview:

A case of 59 year old, female, Roman Catholic from Talisay City, Cebu was
admitted for the first time last September 8, 2012 due to Breast mass, left for elective
Total Mastectomy.

Patient’s history of present illness started 3 years PTA, patient noted a slowly
growing lump on her left breast which was round, movable, firm and non-tender. No
consult was done. Condition persisted until few months PTA, it developed into a firm,
large fixed mass on lower outer quadrant of the left breast. 2 weeks PTA, the mass
progressed into an erythematous and tender with an open ulcer which prompted
consult at VSMMC. Patient underwent biopsy and laboratory work-up and thus
admission for further management.

Patient is a non-hypertensive, non-diabetic, non-asthmatic. No previous

hospitalization nor surgeries. Diagnosed PTB last 1995 and treatment completed for
6 months. She claimed of having a non-productive cough for 3 days.

Patient is a G3P3 (3003), all were delivered via NSVD. Had her menarche at
the age of 12 years old, regular monthly intervals, 3 days duration and consumes 4-6
napkins per day. Menopausal at the age of 51 years old.

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 A Housewife, non-alcoholic beverage drinker, a 4 pack year smoker, no food
and drug allergies, No history of other drugs intake. No heredofamilial disease.

Patient was seen and examined a day prior to surgery, awake, ambulatory,
conscious and coherent, weighs 55kg and height is 165 cm with BMI 20.20 kg/m2
which is classified as normal. Vitals signs were: BP of 140/70 mmHg, heart rate of
92bpm, respiratory rate of 20cpm, temperature of 36.2 C. Physical Examinations
were pale palpebral conjunctivae, ulcerating mass (6x6cm) on lower outer quadrant
left breast, and other sysyems were unremarkable. Airway examination showed a
Mallampati class I, thyromental distance of 6-7 centimeter, mouth opening of >four
finger breaths, atlanto-occipital extension >35 degrees rotation, and no restricttion in
the temporomandibular joint mobility.

Laboratory tests were done. CBC showed slight anemia of 115g/L

hemoglobin, hematocrit of 36 vol% and with adequate platelet of 201,000cummm.
FBS, creatinine, and prothrombin time were normal. Non-reactive HBsAg. A Chest
X-Ray showed fibrosis both upper lungs, pleurodiaphragmatic adhesion left,
atherosclerosis of thoracic aorta. Electrocardiogram was sinus rhythm with non
specific ST wave changes. Cardio-pulmonary evaluation was done and cleared by
internal medicine department as intermediate risk.

Patient was categorized in American Society of Anesthesiology (ASA) as

class II. The anaesthetic plan was general endotracheal anesthesia under direct
laryngoscopy. Patient was appraised regarding her condition, the anesthesia plan of
management, the possible risks and complications.

Patient was put to NPO for eight hours. Venoclysis started with Plain Lactated
Ringers 1 liter at 30 drops per minute. she was premedicated with Ranitidine 50 mg
IVTT, Diphenhydramine 50mg IVTT, and Metoclopramide 10 mg IVTT, nebulize with
Salbutamol 1 nebule every 15minutes for 2 doses an hour prior to operation, and
Hydoxyzine 25mg 1tab at bedtime.

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 Intra-operative course, patient received at operating room awake, conscious,
coherent, not in respiratory distress, patient was attached to ASA standard monitors,
her baseline oxygen saturation was 94-95% in room air. Other baseline parameters
were normal. Intravenous fluids was checked for patency, medications and materials
were prepared. Preoxygenation with 100% oxygen was administered for 5 minutes.
Induction started with the following anesthetic agents: Midazolam 1mg IVTT,
Fentanyl 50mcg IVTT, Propofol 100mg IVTT, Isoflurane at 3%, Atracurium 40mg
IVTT. Vital signs upon induction were normal with oxygen saturation of 97%. About
10minutes, patient was intubated under direct laryngoscopy using macintosh blade
#3 with ETT size 7.0 mmID cuffed and fixed at 20cm, and was hooked to semi-
closed rebreathing circuit. However, patient could not be ventilated and evaluation of
chest examination was done and noted no breath sounds upon auscultation, and
then noticed the oxygen saturation was dropped to 92-84%, and other parameters
also were decreasing like blood pressure and heart rate. And so, the author’s senior
anesthesia resident thought that the tube had been inserted into the esophagus and
re-intubation was performed. Patient was then rapidly using hyperventilation with
100% oxygen, given vasoconstrictors for 3 doses, deepened the volatile anesthetic
agent to 5-8% of Isoflurane, anti-inflammatory agent, nebulize with beta2 agonists,
and one dose of loop diuretics. At about 15-30minutes, oxygen saturation was
increasing to 92-94% and other parameters were in normal limits. After stabilizing
the patient, the author and her senior discussed the situation with the surgery
resident to defer and re-schedule the case, to reassess more of the case and further
evaluate the management of the patient for lowering the risks and complications for
the next proposed surgery. An hour after, the patient was reversed and extubated
after a spontaneous regular breathing. Patient was observed in the recovery room
for 2 hours, O2 saturation was 97-98% and auscultation of the patient’s chest noted
a clear breath sounds bilaterally.

At the ward, patient was stable, fully awake, not in respiratory distress. She
was re-scheduled 5days after further investigation and management of the case with
the same proposed surgery.

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 Patient’s chart were reviewed for the next day after the second surgery since
it was already in-charged with other anesthesia resident, the entire surgery was
uneventful and ended about 3 hours with no complications.

IV.Discussion:

Bronchospasm is an abnormal contraction of the smooth muscle of the

bronchi resulting in an acute narrowing and obstruction of the respiratory airway.
It is encountered during the perioperative period and especially after
induction/intubation may involve an immediate hypersensitivity reaction including
IgE-mediated anaphylaxis caused by the release (degranulation) of substances
from mast cells/ basophils or a nonallergic mechanism triggered by factors such as
mechanical (intubation-induced bronchospasm) or pharmacologic-induced
(histamine-releasing drugs such as atracurium or mivacurium) bronchoconstriction
in patients with uncontrolled underlying airway hyperreactivity. Bronchospasm
during anaesthesia usually manifests as prolonged expiration. An associated
expiratory wheeze may be auscultated in the chest or heard in the breathing circuit.
Breath sounds may be reduced or absent. With IPPV, peak airway pressures are
increased, tidal volumes reduced, or both. The differential diagnoses and
contributing factors are to be considered: Mechanical obstruction: a kinked,
blocked (mucous plug, cuff herniation) or misplaced (endobronchial, oesophageal)
tracheal tube or occlusion in the breathing circuit can mimic severe bronchospasm.
Laryngospasm: This should be considered and excluded. In non-intubated patients,
acute laryngospasm can produce upper airway noise (usually inspiratory), reduced
breath sounds and difficulty in ventilation. Laryngospasm can present with signs of
airway obstruction including increased respiratory effort and paradoxical movement
of the chest and abdomen (‘see-saw’ respiration). Bronchial hyperreactivity: If the
patient is known to be at increased risk of bronchial hyperreactivity, the suspicion of
bronchospasm is increased. The main patient groups are those with reactive airways
disease, especially poorly controlled asthma and COPD. Bronchial hyperreactivity is

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also associated with preoperative exposure to tobacco smoke, upper respiratory
tract infection (URTI) and a history of atopy. Inadequate depth of anaesthesia:
Manipulation of the airway or surgical stimulation under light anaesthesia increases
the risk of bronchospasm. Certain surgical procedures have highly stimulating stages
that can trigger bronchospasm (and laryngospasm). Examples of these include anal
or cervical dilatation, stripping of the long saphenous vein during varicose vein
surgery and traction on the peritoneum. Pharmacological: Certain volatile
anaesthetic agents (isoflurane, desflurane) if introduced quickly can trigger
bronchospasm. IV agents including beta-blockers, prostaglandin inhibitors (NSAIDs)
and cholinesterase inhibitors (neostigmine) are implicated. Histamine release
(thiopental, atracurium, mivacurium, morphine, d-tubocurarine) can also precipitate
bronchospasm; care should be taken with these drugs in higher risk patients.

The chronology of evolving clinical features is crucial to understand the

pathophysiologic mechanism of an immediate hypersensitivity reaction.
Cardiovascular disturbance is the hallmark of severe IgE-mediated anaphylaxis. In
patients with neuromuscular blocking agent-induced perioperative anaphylaxis,
cardiovascular signs are usually the clinical event and occur within minutes after the
drug challenge. These cardiovascular signs may be associated with or followed by
bronchospasm in 19–40% of patients, more likely in those with underlying asthma or
chronic obstructive pulmonary disease. Drug-induced anaphylactic bronchospasm
may occur either before or after instrumentation of the airway. Four clinical variables
were identified as independent predictors of allergic compared with nonallergic
perioperative bronchospasm: the presence of any cutaneous symptoms; shock;
episodes of desaturation; and the prolonged duration of clinical features (longer than
60 min). Compared with that of patients who did not present with these “predictive”
signs as part of the clinical syndrome, the occurrence of hypotension or episodes of
oxygen desaturation are higher, respectively, more likely to be associated with IgE-
mediated anaphylaxis. In the current case, inaugural severe bronchospasm triggered
by endotracheal tube insertion and followed by cardiovascular collapse, likely related
to subsequent hypoxemia after the patient's extubation, yields clinical insight into the

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pathophysiologic mechanism of the reaction and suggests nonallergic
bronchospasm.

The prevention of bronchospasm in patients with asthma and COPD should

be thoroughly assessed to ensure they are optimised for surgery. Wheezing,
cough, increased sputum production, shortness of breath and diurnal variability in
peak expiratory flow rate (PEFR) indicate poor control. Recent or frequent
exacerbations or admission to hospital may be an indication to postpone non-
essential surgery. Patients should be encouraged to continue their medication until
the time of surgery. Preoperative bronchodilators, inhaled or oral corticosteroids,
chest physiotherapy and referral to a respiratory physician may all be appropriate. A
careful medication history should be taken with particular reference to drug
sensitivities. All patients should be counselled and encouraged to stop smoking
preoperatively. Six to eight weeks of abstinence before surgery significantly reduces
the risk of respiratory complications including bronchospasm. URTI in children
increases the risk of bronchospasm and so it may be necessary to postpone surgery.
The complete resolution of symptoms(approximately 2 weeks) correlates well with a
decreased incidence of airway hyperreactivity. Pretreatment with an
inhaled/nebulized beta agonist, 30 minutes prior to surgery, induction of anaesthesia
with propofol and adequate depth of anaesthesia before airway instrumentation
reduces the risk of bronchospasm. The use of an LMA (in suitable patients) has
been shown to reduce the incidence of bronchospasm compared to tracheal
intubation. Regional techniques where appropriate can also avoid the need for
general anaesthesia and intubation.

Therapeutic considerations:
Quick-acting β2-selective adrenergic agonists provided by metered-dose
inhalers (MDIs) are the mainstay for fast relief of bronchoconstriction. Examples of
this class of drugs are albuterol (salbutamol), levalbuterol (levosalbutamol), and
pirbuterol. Their onset of action occurs within 5 min, peak effect is within 1 h, and
their duration of action is 4–6 h. Patients with poor inhalation technique should use a
valved holding chamber (spacer). These drugs are recommended only for short-term

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relief of symptoms or before known triggers such as exercise; β 2-agonists are not
contraindicated in patients taking β-blockers for cardiac disease. Side-effects such
as tremor, anxiety, palpitations, and tachycardia occur but are not common at
standard doses. Long-acting β2-selective agonists, such as arformoterol, formoterol,
and salmeterol, provide bronchodilation for >12 h and are largely free of side-effects.
Unfortunately, some of the bronchoprotective effect of the long-acting β 2-selective
agonists decreases with time; short-acting β2-selective agonist effect is not blunted
by this phenomenon. The long-acting agents do not suppress inflammation and
should not be used without anti-inflammatory treatment for the control of asthma.
Parenteral steroids remain a mainstay of the treatment, however, their beneficial
effect on airway mechanics can take 4–6 h in acute bronchospasm. Adrenal
suppression, infection, delayed healing, hyperglycaemia, and fluid retention are
common complications of prolonged therapy. Patients who have been taking
systemic corticosteroids for >2 weeks during the prior 6 months should be
considered at risk for adrenal suppression in the setting of severe acute disease,
trauma, or major surgery. Anticholinergic bronchodilators such as ipratropium have
a more limited role in the therapy of acute bronchospasm than β 2-selective agonists.
They act by inhibiting cyclic guanosine monophosphate formation and block vagus
nerve-mediated bronchoconstriction, which is an important component of
bronchospasm in patients with COPD. Indications for their use include, as implied,
patients with COPD, but also patients who are intolerant of β 2-selective agonists, or
who are severely asthmatic, or have β-blocker-induced bronchospasm. Inhaled
glycopyrrolate can be bronchoprotective in asthma and COPD. Anticholinergic
agents dry airway secretions. Although controversy exists as to whether this
improves inflammation or worsens inspissation, it certainly decreases airway
hyperresponsiveness, an important consideration for the anaesthetist. Signs of
airway obstruction consistent with bronchospasm include elevation of the peak
inspiratory pressure, prolonged expiratory phase, and visible slowing or lack of chest
fall. The patient should be turned to 100% inspired oxygen and manual bag
ventilation should immediately be instituted to directly assess compliance; the bag
will not fill on exhalation if the bronchospasm is severe. The chest (and, if not
accessible, the expiratory limb of the anaesthetic circuit) should be auscultated to
confirm wheezing. Diminished or absent breath sounds can be an ominous sign

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suggesting critically low airflow. If none of these conditions exists, or if
bronchospasm persists after they have been corrected, a treatment algorithm for
acute intraoperative bronchospasm should be instituted. This should include frequent
monitoring of ABGs to evaluate hypoxaemia and hypercarbia. The adverse effects
on the circulation can add a metabolic component to the respiratory acidosis.
Hypercarbia, hypoxaemia, and acidaemia promote arrhythmias and impair the
response to bronchodilator therapy.

The advantage of hand-ventilation in assessing lung compliance and

exhalation has already been mentioned. It can be impossible for a conventional
ventilator to achieve the rapid inspiratory flows needed to facilitate a prolonged
expiratory time. Increased concentrations of a volatile anaesthetic (sevoflurane and
isoflurane) are often helpful. If this is not effective, a rapid-acting β 2-selective agonist
should be administered via a nebulizer or, if an MDI is available, via an airway
adaptor. Consideration should be given to high-dose steroids, a 125 mg i.v.
methylprednisolone, with the understanding that it will take 4–6 h before they exert
their beneficial effect. If bronchospasm remains refractory, epinephrine 5–10 mg can
be administered i.v., although this has a high risk of exacerbating tachycardia and
tachyarrhythmias. Alternatively, a continuous epinephrine infusion of 0.5–2 µg min −1
in adults can provide maintenance bronchodilation with less adverse effect.
Magnesium sulphate (1.2–2 g i.v.) can be helpful in difficult cases; it is cheap,
available, and can suppress tachyarrhythmias. However, high doses induce muscle
weakness and central nervous system depression. Nitroglycerin has been reported
anecdotally to reverse acute bronchospasm, probably through direct smooth muscle
relaxation.

Airway obstruction, laryngospasm, bronchospasm, poor ventilation, and

hypoxaemia are major hazards of the emergence phase. Suctioning of the airways
must be rendered cautiously. Aspiration can not only cause injury in its own right but
also trigger severe bronchospasm. Prophylactic use of anti-emetic agents, gastric
motility agents, antacids, and gastric suctioning before emergence should be
considered. Respiratory mechanics must be fully assessed before extubation and

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emergence. If acute bronchospasm persists at the end of the case or if it has been
severe, or if the patient has a difficult airway, trauma, or a full stomach,
consideration should be given to a period of postoperative mechanical ventilation to
avoid having to reverse neuromuscular block and to allow time for airway recovery.
Repeat administration of a β2-agonist such as albuterol before emergence is
advised. When emergence does occur, it should be with adequate analgesia in
place, whether i.v. or neuraxial. Reversal of neuromuscular block has a number of
hazards. Neostigmine increases bronchospasm risk because of its muscarinic and
pro-secretory effects. These can be blunted by co-administration of atropine or
glycopyrrolate, but the duration of action of neostigmine can outlast that of the
vagolytic agent, especially in the presence of renal insufficiency. ‘Deep extubation’
(tracheal extubation while still deeply anaesthetized) has been practiced for many
years, especially in children, but it has its own inherent hazards. It mandates full
reversal of neuromuscular block. Even if tracheal extubation is smooth, emergence
through the arousal stage can initiate severe bronchospasm with an unprotected
airway. The risk of regurgitation and aspiration is ever-present. The keys to
minimizing postoperative pulmonary complications are vigilance for bronchospasm
and its causes; good pain control, be it by the neuraxial route or patient-controlled
analgesia; bronchodilator therapy; incentive spirometry, deep breathing exercises,
and early mobilization.

V.Conclusion:

Bronchospasm remains a serious life-threatening perioperative event. Its

dramatic consequences involving brain damage or death may be partly explained by
substandard care and/or inadequate practice and system failures. Optimal
management of perioperative bronchospasm should therefore be encouraged and
have further investigation. The incidence of asthma and COPD are increasing
worldwide, but morbidity and mortality are decreasing because of improvements in
medical care.

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 Several guidelines on the management of asthma and COPD are available.
Although they focus largely on assessment and management in the chronic
outpatient setting, much of their advice also applies to the preoperative holding area,
operating theatre, and post-anaesthetic care unit or intensive care unit. Given its
prevalence and often subclinical nature, a routine and standard approach to acute
bronchospasm enables quick response and good outcome.

V.Recommendations:

Most types of therapy intended to treat and prevent bronchospasms involve

medications, but these troublesome occurrences can be made much simply by
following basic recommendations. These simple yet essential steps may help you
avoid aggravating your symptoms by distancing yourself from certain substances,
actions and activities that may worsen your condition. Directions that may aid in
prevention of bronchospasms which includes: Avoid allergy triggers and irritant
which often associate with the management of your environment and your diet,
reducing the amount of irritants in your direct environment will greatly benefit your
condition as well as help to prevent bronchospasms. Manage physical exercise.
Reduce anxiety and emotional stress which is more common in children. Promptly
treat infections in any type of upper respiratory tract which poses a risk of worsening
the symptoms and possibly causing bronchospasms. Lastly, is to commit your
designated treatment and it is imperative to follow the directions and
recommendations provided by your physician.

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References:

1. Barash, P., Cullen, B., Stoelting, R., et al. 2009. Clinical Anesthesia 6th
Edition. Philadelphia. Lippincolt Williams and Wilkins.

2. Ronald D. Miller, MD, Lars I. Eriksson, Lee A. Fleisher, MD, Jeanine P.

Wiener-Kronish, MD and William L. Young. 2010. Miller's Anesthesia, 7th
Edition. Churchill Living Stone Elsevier.

3. G. Edward Morgan, Jr., Maged S. Mikhail, Michael J. Murray. Clinical

Anesthesiology, 4th edition. Anesthetic Complications.

4. B. D. Woods and R. N. Sladen. Oxford Journals, BJA, Volume 103, Issue

suppl 1, Pp. i57-i65. Perioperative considerations for the patient with
asthma and bronchospasm.

5. Fisher MM, Ramakrishnan N, Doig G, Rose M, Baldo B. The investigation of

bronchospasm during induction of anesthesia. Intensive Care Unit, Royal
North Shore Hospital, Sydney. University of Sydney, Australia.

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