description & case study of bronchospasm

1. Pascale Dewachter, Claudie Mouton-Faivre, Charles W. Emala,Sadek Beloucif
Anesthesiology 2011; 114:1200 –10
DR. RISHABH MITTAL
MODERATOR – DR. AVNISH BHARADWAJ

2. Case Report
 A 25-yr-old woman
 Body mass index: 54 kg/m2 ( morbidly obese)
 Noninsulin-dependent diabetes
 Scheduled for cochlear implant surgery.
 h/o 2 previous surgeries without incident during childhood.
 NO history of atopy or drug allergy
 Normal Chest auscultation before anaesthesia.

3. Case Report – Anaesthetic course
Premedication – Tab. Hydroxyzine (100 mg) the day before
and 1 h before induction
Induction - Inj. sufentanil (20 µg I.V) + Inj. propofol (350 mg
I.V)
Tracheal Intubation (Cormack and Lehane grade I) -
Inj. succinylcholine (130 mg I.V).
Chest auscultation -complete absence of bilateral breath
sounds.
End-tidal carbon dioxide (ETCO2) - Low. initially

4. What had happened??
SUSPECTED -Esophageal intubation ??
Patient immediately extubated
Mask ventilation attempted - difficult to perform
Dramatically decreased lung compliance
ETCO2 - marked prolonged expiratory upstroke of the capnogram
Bronchospasm !!!!!!!!

5. What was DONE??
WITHIN FIVE MINUTES –
SpO2 – 55%, Arterial hypotension ( From 130/75 to 50/20 mmHg),
Moderate tachycardia (100 beats/min)
Titrated epinephrine (two I.V boluses of 100 µg each) ,
Ringer lactate- 1000 ml
Blood pressure, 110/50 mmHg; heart rate, 110 beats/min),
Ventilation became easier to perform
Audible wheezing over both lung fields.
A localized (face and upper thorax) erythema -
Hydrocortisone(200 mg) I.V
Blood sample 40 and 90 min after the clinical reaction- to measure
serum tryptase concentrations

6. And then…..
 Surgery was postponed
 Patient was transferred to the intensive care unit.
 Inhaled β 2-agonist (salbutamol)
 I.V corticoids (hydrocortisone, cumulative dose: 800 mg
over24 h)
 Respiratory symptoms resolved within 2 h
 h/o wheezing induced by cold and exercise was elicited
 No additional supportive vasopressor therapy was
required
 Patient discharged home the following day
 Allergologic assessment - after 6 wk

8. Bronchospasm??
 Is defined as constriction of bronchi and bronchioles
 Clinical feature of exacerbated underlying airway hyper-
reactivity
 symptoms include difficulty in breathing, wheezing,
coughing, and dyspnea.
 Chest auscultation –
 wheezing
 decreased or absent breath sounds - critically low airflow.

9. Peri-operative bronchospasm..
 Usually arises during induction of anesthesia
 May be detected at any stage of the anaesthetic course.
 Bronchoconstriction due to -
 Immediate hypersensitivity reaction – EVOKING
ALLERGY
I. IgE-mediated anaphylaxis
II. Anaphylactoid reaction – Non immune Mechanism
 Non-allergic mechanism triggered by
I. Mechanical factors ( intubation-induced bronchospasm)
II. Pharmacologic factors (via histamine-releasing drugs such as
atracurium or mivacurium )

10. D/D of Intra-operative Bronchospasm
 Esophageal intubation
 Inadequate anaesthesia
 Mucous plugging of the airway
 Kinked or obstructed tube/circuit,
 Pulmonary aspiration.
Unilateral wheezing suggests endobronchial intubation or
an obstructed tube by a foreign body (such as a tooth).
If the clinical symptoms fail to resolve despite appropriate
therapy, pulmonary edema or pneumothorax should be
considered.

11. Periop. Immediate Hypersenstivity Reaction
 Clinical entity evoking allergy that varies in severity
 Occurs within 60 min after the injection/introduction of the
culprit agent
 Diagnosis is linked to a triad including -
1. Clinical features ( Graded acc. to Ring and Messmer clinical
severity scale)
2. Blood tests (Tryptase level measurements, serum-specific IgEs)
3. Postoperative skin tests with the suspected drugs or agents

12. Ring and Messmer clinical severity scale
 Grade I: Erythema, urticaria with or without angioedema
 Grade II: Cutaneous-mucous signs ± hypotension ±
tachycardia ± dyspnea ± gastrointestinal disturbances
 Grade III: Cardiovascular collapse ± tachycardia or
bradycardia ± cardiac dysrythmia ± bronchospasm ±
cutaneous-mucous signs ± gastrointestinal disturbances;
 Grade IV: Cardiac arrest

13. Etiology in the Current Case
 Clinical diagnosis initially suggested drug-induced
anaphylactic reaction (allergic bronchospasm)
 Sudden occurrence of bronchospasm after induction
 Cardiovascular disturbances
 Cutaneous signs
 Succinylcholine-induced anaphylaxis was suggested as the
most likely etiology at first sight.
 Neuromuscular blocking agents are the most frequent
agents involved in perioperative anaphylaxis in adults

14. Etiology in the Current Case
 How can we differentiate between allergic and non-
allergic bronchospasm clinically??
 Clinical variables predicting IgE mediated anaphylaxis
 Presence of any cutaneous symptoms ( 7times)
 Shock (cardiovascular collapse) – HALLMARK (27 t1mes)
 Episodes of desaturation (22 times)
 Prolonged duration of clinical features (longer than 60
min)
 Cardiovascular collapse -usually the inaugural clinical
event , occur within minutes after the drug challenge
 May occur either before or after instrumentation of the
airway

15. Etiology in the Current Case
 Non-allergic bronchospasm
 Immediately follows nonspecific stimuli (irritation by ETT,
suction catheter)
 Usually not associated with cardiovascular symptoms but..
 PEEP with severe bronchospasm may lead to a decrease in venous
return & hence cardiac output.
 Hypoxia and respiratory failure from inadequate ventilation may
lead to cardiovascular collapse (occurs late after bronchospasm)
 Cutaneous signs may be observed

17. Etiology in the Current Case
In the current case
 Skin testing remained negative in response to propofol,
sufentanil, succinylcholine, and latex solutions.
 Tryptase level were unchanged (N less than 13.5 µg/l.) -
specific for mast cell activation
 Serum-specific IgEs against succinylcholine and latex were not
detectable.
 Basophil activation test- Succinylcholine induced neither
CD63 nor CD203c up-regulation.
 Succinylcholine-induced anaphylaxis was ruled out

18. Etiology in the Current Case
 Bronchospasm triggered by endotracheal tube insertion and
followed by cardiovascular collapse (hypoxemia) suggests
non-allergic bronchospasm
 Erythema may also be observed during non-allergic
bronchospasm.
 Morbid obesity of the patient -precipitating factor of rapid
arterial desaturation
 Uncontrolled Asthma -main trigger of this non-allergic
bronchospasm (h/o wheezing induced by cold and exercise
elicited from patient in post-op period)

19. What is ASTHMA??
“Asthma is a chronic disorder of the airway in which many cells and
cellular elements play a role. The chronic inflammation is
associated with airway responsiveness that leads to recurrent
episodes of wheezing, breathlessness, chest tightness and
coughing, particularly at night or in the early morning. These
episodes are usually associated with widespread, but variable
airflow obstruction within the lung, that is often reversible
either spontaneously or with treatment.” (2008)

22. ASTHMA
 Two main phenotypes:-
 Allergic
 Non-allergic
Overlap may occur within these groups
Allergic Rhinitis and Allergic Asthma Belong to the
Same Airway Disease -More than 80% of asthmatic individuals
have rhinitis, and 10–40% of patients with rhinitis have asthma

23. Allergic Asthma
 Onset occurs primarily in early childhood
 Results from immunologic reactions, mostly initiated by IgE
antibodies
 Atopy - (Genetic predisposition for the development of an IgE-
mediated response to common aeroallergens) - strongest
identifiable predisposing factor
 Triggers-
 Environmental factors - tobacco smoke, air pollutants,
and exposure to allergens
 Obesity, diet, and hygiene hypothesis
 ATOPY + TRIGGERS ALLERGIC ASTHMA

24. Non-allergic Asthma: Aspirin-induced Asthma
 Widely under diagnosed condition
 Not seen in childhood
 Inhibition of cyclooxygenase enzymes by aspirin-like drugs in
the airway of sensitive patients
 Characterized by eosinophilic rhinosinusitis, nasal polyposis,
senstivity to aspirin or NSAID’s and asthma
 Rhinorrhea, nasal congestion, and anosmia are the first clinical
features
 Asthma and sensitivity to aspirin appear approximately 1–5 yr after
the onset of rhinitis

25. Perioperative Bronchospasm & Asthma
Westhorpe RN, Ludbrook GL, Helps SC: Crisis management during anaesthesia: Bronchospasm. Qual Saf Health Care 2005; 14:e7
In a study conducted by Westhorpe RN et al (103 cases)
PERIOPERATIVE BRONCHOSPASM
Allergic (21%) / Non-allergic mechanism(79%)
 Of Non-allergic cases, 44% during induction, 36% during
maintenance phase, and 20% during emergence/recovery stage.
 Major causes during -
 Induction - airway irritation (64%), tube misplacement (17%),
aspiration (11%), and other pulmonary edema or unknown causes (8%).
 Maintenance -allergy (34%), endotracheal tube malposition (23%),
airway irritation (11%), aspiration with a laryngeal mask airway(9%)

26. Perioperative Bronchospasm & Asthma
 Bronchospasm induced by airway irritability occurred more
frequently in patients who had one or more predisposing
factors such as asthma, heavy smoking, or bronchitis.
 Previous history of asthma was present in
 50% cases of Non-allergic Bronchospasm
 60% patients with allergic bronchospasm
 Uncontrolled asthma/chronic obstructive pulmonary disease is
frequently involved with both allergic and non-allergic
bronchospasm, regardless of the stage of anesthesia (induction
or maintenance)

27. Mechanisms of Reflex-induced Bronchoconstriction
Irritation of the upper airway by a foreign body
Afferent sensory pathways
Nucleus of solitary Tract
Airway-related Vagal Pre- ganglionic Neurons
Airways via Vagus nerve
Bronchoconstriction
Stimulatory - Glutamate++
Glutamate++
Inhibitory- γ aminobutyric acid - -
Acetylcholine
release ++
(M3 muscarinic receptor)

28. Reflex-induced Bronchoconstriction
 Non-adrenergic non-cholinergic nerves (releasing tachykinins,
vasoactive intestinal peptide, and calcitonin gene-related peptide) may
participate in this reflex arc and/or locally release the pro-
contractile neurotransmitters via activation of inter-neurons in
the airway.
 Since Acetylcholine acting on M3 muscarinic receptors on
airway smooth muscle is a key component in mechanism, use of
antimuscarinic - inhaled medications (e.g., ipratropium or
tiotropium) should be advantageous to prevent /treat it.

29. Reflex-induced Bronchoconstriction
 Propofol and volatile inhalational anaesthetics (except
desflurane) are clinically effective
 Have activity at inhibitory GABA-A chloride channels
 Have direct bronchodilatory effects at the level of airway smooth muscle
(via GABA-A channels/ modulating calcium sensitivity of the
contractile proteins)
 Propofol preferentially relaxes tachykinin- induced airway constriction
 Deepening anesthesia
 Prevents /relieves reflex-induced bronchoconstriction
 Modulation of GABA input to the airway-related vagal preganglionic
neurons from the nTS/ higher centers

31. BUT….
 Despite these protective effects of intravenous
propofol and the adequate induction dose used in the
current case, reflex-induced bronchoconstriction
developed in this patient who had previously
unrecognized and untreated asthma.

32. Obesity and Asthma: Is There Any Relationship?
 Obesity- body mass index of at least 30 kg/m2
 Both are systemic inflammatory states
 Chromosomal regions with loci common to obesity and asthma
phenotypes have been identified
Obesity
FRC & TV
contractile responses of airway smooth muscle
airway reactivity

33. Obesity and Asthma: Is There Any Relationship?
 Gastroesophageal reflux resulting from obesity may potentially trigger a
latent asthmatic condition
 Hormonal influences-
 hormone leptin produced by adipocytes has effects on immune cell
function and inflammation
 Recent changes in lifestyle and diet are associated with both
 Asthma remains under diagnosed in obese patients - respiratory
symptoms are frequently attributed to being overweight (current case)
 Sleep-disordered breathing is more prevalent in asthmatic as well as obese
individuals

34. Prevention of Perioperative Bronchospasm
 Acc. To Global Initiative for Asthma guidelines -
Perioperative and postoperative complications rely on
 Severity of asthma at the time of surgery
 Type of surgery (thoracic /upper abdominal surg risk)
 Modalities of anesthesia (GA with intubation risk)
Uncontrolled asthma is considered to be the main risk
factor for bronchoconstriction during surgery.

35. Prevention of Perioperative Bronchospasm
HISTORY
 Poorly controlled Asthma may be assessed through
 Degree of asthma control (inc. Use of medications, recent
exacerbations of symptoms, hospital visit within the last months)
 Potential risks or complication factors (recent respiratory
tract inf., previous bronchospasm / pulmonary complications
during/after previous surg, long-term use of a systemic corticosteroids,
assso. gastroesophageal reflux or smoking).
 Abstinence from smoking before surgery reduces
perioperative pulmonary complications

36. Prevention of Perioperative Bronchospasm
Preoperative Clinical and Physical Examination
 Acc. To Smetana et al perioperative pulmonary
complications occur if preoperative examination reveals
-
 Decreased breath sounds
 Dullness to percussion
 Wheezing
 Rhonchi
 Prolonged expiratory phase
 In the presence of active bronchospasm, elective surgery
should be postponed
Smetana GW: Preoperative pulmonary evaluation. N Engl J Med 1999; 340:937– 44

37. Prevention of Perioperative Bronchospasm
Measurement of lung function (PFT)
 FEV1 /PEFR -better indicators of the severity of asthma
exacerbation than clinical symptoms.
 FEV1/ FVC (normal > 75%) - sensitive measure of severity
and control
 Reversibility with the use of a bronchodilator –defined as
increase in FEV1 of at least 12% or 200 ml.
 Before surgery
 PEF or FEV1 >> 80% of the predicted or personal best is
recommended.
 If PEF or FEV1 is << 80%, a brief course of oral
corticosteroids should be considered

38. Prevention of Perioperative Bronchospasm
REVIEW OF MEDICATION
 Rapid-acting inhaledβ 2-agonists are used for quick relief of
acute asthma exacerbations
 Inhaled glucocorticosteroids are currently the most effective
anti-inflammatory drug for the treatment of persistent
asthma.( reduce asthma symptoms, improve lung function, decrease airway hyper-
reactivity, modulate airway inflammation, and reduce asthma exacerbations & asthma
mortality)
 Inhaled long-acting β 2-agonists (formoterol, salmeterol)
should never be used as single therapy.
 efficient when combined with glucocorticosteroids (synergistic)

39. Prevention of Perioperative BronchospasmStepwise Approach for Asthma Treatment / optimization of Treatment
Level of Asthma Control Step Levels Treatment
Global Initiative for Asthma Five
At each step, short-acting β2-agonist is
recommended as needed
Intermittent treatment 1 —
Daily medication 2 Low-dose inhaled corticosteroid
— 3
Low-dose inhaled corticosteroid + inhaled long-
acting β 2-agonist
— 4
Medium- or high-dose inhaled Steroid + inhaled
long-acting β 2-agonist
— 5 Addition of oral steroid to other controllers
Expert Panel Report six
At each step, short-acting β 2-agonist is
recommended as needed
Intermittent treatment 1 —
Daily medication 2 Low-dose inhaled corticosteroid
— 3 Medium-dose inhaled corticosteroid
— 4
Medium-dose inhaled corticosteroid + inhaled
long-acting β 2-agonist
— 5
High-dose inhaled corticosteroid + inhaled long-
acting β2-agonist
— 6 Step 5 + oral corticosteroids

40. Follow Up of Current Case
 Initial Spirometric evaluation
 FEV1 - 67%
 PEFR - 70%
 FEV1/forced vitality capacity - 83% of predicted.
 Treatment started –
 High doses of inhaled therapy with fluticasone and salmeterol
(1,000 μg BD)
 Educative measures
 Second Spirometric evaluation (after 3 months)
 Reversibility of nearly - 15%,
 FEV1 -80%
 PEFR - 82%,
 FEV1/forced vitality capacity - 97% of predicted values
 Reduction of clinical signs noted by the patient
 Wheezing disappeared

41. Follow Up of Current Case
 Surgery was performed 6 months after the initial
perioperative event.
 Anesthesia was conducted with propofol, sufentanil, and
sevoflurane
 Anesthesia and surgery as well as the postoperative course
remained uneventful

42. Perioperative Bronchospasm - Treatment
AIM- to relieve airflow obstruction and subsequent
hypoxemia as quickly as possible.
 FiO2 – 100%
 Switch to Manual Bag Ventilation - Bains circuit (to evaluate
pulmonary and circuit complaince)
 conc. of volatile anaesthetic (except desflurane)
 Deepening anaesthesia with an intravenous anaesthetic
(if bronchospasm related to inadequate depth)

43. Perioperative Bronchospasm - Treatment
Inhaled Short-acting β2-Selective Agents - immediately
 Terbutaline and Salbutamol
 onset of action - 5 min
 peak effect - 60 min
 duration of action - 4–6 h.
 VIA
 Nebulizer (8–10 puffs repeated at 15- to 30-min intervals)
 Metered-dose inhaler (5–10 mg/h) connected to the
inspiratory limb of the ventilator circuit.
 Continuous administration - greater improvement in PEFR
 Nebulised epinephrine has no beneficial effect

44. Perioperative Bronchospasm - Treatment
 Systemic Glucocorticosteroids
 Methylprednisone (1 mg/kg) - preferred over cortisone
 Benefit - not immediate
 Combined Nebulized ipratropium bromide with a β2-
agonist
 0.5 mg 4–6 times/hour
 greater bronchodilatation when used in combination
 to treat life-threatening bronchospasm
 those with a poor initial response

45. Perioperative Bronchospasm - Treatment
 Magnesium
 Causes bronchial smooth muscle relaxation
 Intravenous(single dose: 2 g over 20 min) or
 Inhaled (110 mg to 1,100 mg)
 In patients with severe bronchospasm that fails to be
relieved with β2-agonists
Salbutamol administered in isotonic magnesium sulfate
provides greater benefit (compared with that diluted with saline)
Bateman ED, Hurd SS, Barnes PJ, Bousquet J, Drazen JM,FitzGerald M, Gibson P, Ohta K, O’Byrne P, Pedersen SE,Pizzichini E,
Sullivan SD, Wenzel SE, Zar HJ: Global strategy for asthma management and prevention: GINA executive summary. Eur
Respir J 2008; 31:143–78

46. Perioperative Bronchospasm - Treatment
 AMINOPHYLLINE
 Intravenous aminophylline has no role
 Not result in additional bronchodilatation
 Adverse effects - arrhythmia and vomiting have been
reported
Bateman ED, Hurd SS, Barnes PJ, Bousquet J, Drazen JM,FitzGerald M, Gibson P, Ohta K, O’Byrne P,
Pedersen SE,Pizzichini E, Sullivan SD, Wenzel SE, Zar HJ: Global strategy for asthma management
and prevention: GINA executive summary. Eur Respir J 2008; 31:143–78

47. Perioperative Bronchospasm - Treatment
 Epinephrine
 In cases of associated cardiovascular collapse suggestive
of IgE-mediated anaphylaxis
 In case of Isolated bronchospasm - its inhaled/systemic use
is not recommended
 Currently recommended as a rescue therapy in patients with
severe asthma complicated by hypotension that is not
secondary to dynamic hyperinflation.
 Elective Surgery should be postponed - bronchospasm
persists at baseline despite maximal medical optimization
of the patient

49. THE CURRENT CASE
 Extubation was performed because of suspected
Oesophageal intubation - Resulting in arterial
desaturation and subsequent hemodynamic
disturbances.
 Instead- Verification of correct endotracheal tube
position would have been the appropriate procedure
before extubation.

50. Thanks for Your
attention！

52. KNOWLEDGE GAP
 Whether perioperative bronchospasm is a clinical entity of
its own occurring in predisposed patients and triggered
either by mechanical, pharmacologic, or inflammatory (i.e.,
anaphylaxis) factors??
 Basic assumptions regarding the management of general
anesthesia in patients at risk for bronchoconstriction have
not been rigorously studied..

53. KNOWLEDGE GAP
 Interaction between anesthetics, airway irritation, and the
role of tachykinins and other C fiber neurotransmitters in
the control of airway tone......
 Mechanisms by which intravenous and inhaled anesthetics
affect airway nerves and directly modulate airway smooth
muscle tone likely involve modulation of plasma membrane
ion channels, membrane potential, and intracellular calcium
sensitivity but remain poorly understood.....

54. Example of Targeting Questions to Identify Patients at
Risk with Undiagnosed Airway Hyperreactivity..
 Do you smoke?
 Do you have gastroesophageal reflux disease?
 Have you ever felt chest tightness or difficulty catching your breath? If
so, at rest or with physical effort?
 Have you ever been told that you have wheezing or asthma?
 Have you ever used an inhaled medication for your breathing?
 Have you ever visited an emergency department for breathing
problems?
 Have you ever had frequent bronchitis?
 Have you ever had rhinitis?
 Do you frequently cough?
 Do you have allergies to latex or tropical fruits (kiwi,
 banana, papaya, avocado)?