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 hadhappened??
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
7.
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.
11. D/DofIntra-operativeBronchospasm
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.
12. Periop.ImmediateHypersenstivityReaction
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
14. Etiology intheCurrentCase
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
15. Etiology intheCurrentCase
How can we differentiate between allergic and non- allergic bronchospasm
clinically??
Clinical variables predicting IgE mediated anaphylaxis
Presence of any cutaneous symptoms ( 7 times more likely allergic)
Shock (cardiovascular collapse) – HALLMARK (27 times)
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
16. Etiology intheCurrentCase
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.
18. Etiology intheCurrentCase
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
19. Etiology intheCurrentCase
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)
20.
21. 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
22. 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
23. Non-allergicAsthma:Aspirin-inducedAsthma
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
24. PerioperativeBronchospasm&Asthma
WesthorpeRN,LudbrookGL,HelpsSC:Crisismanagementduringanaesthesia:Bronchospasm.QualSafHealthCare2005;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%)
25. PerioperativeBronchospasm&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)
26. MechanismsofReflex-inducedBronchoconstriction
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)
27. A Case Report recently notified an event of bronchospasm during inguinal
hernioplasty under spinal anesthesia.
Pt. started having bronchospasm at the time the surgeons were handling the
loops of intestine.
After ruling out all other causes they concluded that the parasympathetic
stimulation due to bowel manipulation was the cause of bronchospasm.
It is also likely that anxiety in the patient, after bronchospasm, aggravated
the symptoms.
H. PRABHAKAR & G. P. RATH M.E.J. ANESTH 19 (1), 2007
28. Reflex-inducedBronchoconstriction
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-inducedBronchoconstriction
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
30.
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. ObesityandAsthma:IsThereAnyRelationship?
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. ObesityandAsthma:IsThereAnyRelationship?
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. PreventionofPerioperativeBronchospasm
Acc. To Global Initiative for Asthma guidelines - Perioperative and
postoperative complications rely on
o Severity of asthma at the time of surgery
o Type of surgery (thoracic /upper abdominal surg risk)
o Modalities of anesthesia (GA with intubation risk)
Uncontrolled asthma is considered to be the main risk factor for
bronchoconstriction during surgery.
35. PreventionofPerioperativeBronchospasm
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. 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)?
37. PreventionofPerioperativeBronchospasm
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
38. Preoperative Clinical and Physical Examination
active lung infection (which should defer elective surgery),
chronic lung disease,
and right heart failure.
39. PreventionofPerioperativeBronchospasm
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
40. PreventionofPerioperativeBronchospasm
Measurement of lung function (PFT)
A simple screening test for prolonged exhalation is the forced
expiratory time (FET).
It can be assessed by listening over the trachea while the patient
exhales forcibly and fully.
An FET >6 s correlates with a substantially lowered FEV1/FVC ratio
and should initiate further investigation.
41. Useful Investigations
Formal pulmonary function tests
Arterial blood gas (ABG) (during asthmatic attacks)
ECG (right atrial or ventricular hypertrophy, acute strain, right axis deviation, and
right bundle branch block.)
Chest radiographs (flattened diaphragms if the lungs are hyperinflated, and
are useful to evaluate for pulmonary congestion, oedema, or infiltrate.)
42. The anaesthetic plan
Goals of patient safety, comfort, and a quiet surgical field.
Choice of anaesthetic method must be tailored to the patient, the
procedure, clinical assessment, and the preferences of all involved.
It seems prudent to avoid direct instrumentation of the airway if at all
possible,
But anxiety or pain during regional anaesthesia (peripheral nerve or
neuraxial block) could themselves precipitate an attack of bronchospasm.
43. Preoperative preparation
Stop smoking at least 2 months before surgery
Lung function should be improved by optimizing medications and
compliance, or considering a short course of oral corticosteroids.
Oral methylprednisolone 40 mg for 5 days before surgery post-intubation
wheezing
A short-acting steroid such as hydrocortisone (e.g. 100 mg i.v. every 8 h)
during the perioperative period
44. Preoperative preparation
Short-acting bronchodilator therapy given prophylactically
An optimal premedication allays anxiety, improves work of breathing
Dexmedetomidine has a favourable profile, including anxiolysis,
sympatholysis, and drying of secretions without respiratory depression.
46. Medications:
Neuromuscular blocking agents
most common
Mivacurium and atracurium,Rapacuronium, -- culprits
Cisatracurium, rocuronium -- safe
Non-synthetic opioids such as morphine
I.V. induction agents
Propofol appears to be superior to thiopental and etomidate in constraining
increases in airway resistance
Inhalational:isoflurane or sevoflurane confers protective bronchodilation.
desflurane provokes bronchoconstriction in smokers.
47. Ester local anaesthetics : allergic reactions
Vancomycin can induce hypotension, erythema, and bronchospasm through
histamine release, the so-called ‘red-man syndrome’.
Beta lactams
Protamine sulphate can induce type I anaphylaxis. Risk is greater in patients
receiving protamine–insulin who develop IgE and IgG antibodies.
Polymethylmethacrylate and i.v. contrast agents :Anaphylactic reactions
Beta blockers
48. Acuteintraoperative bronchospasm
Signs of airway obstruction consistent with bronchospasm
include
Sweating
Diminished or absent breath sounds
visible slowing or lack of chest fall.
elevation of the peak inspiratory pressure.
prolonged expiratory phase.
49. Cardio pulmonary impact
increased work of breathing (WOB),
decreased airflow,
air trapping,
dynamic hyperinflation,
ventilation–perfusion (V/Q) mismatch,
increased pulmonary vascular resistance (PVR),
and right ventricular overload.
50. PerioperativeBronchospasm- 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)
51.
52. PerioperativeBronchospasm- 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
53. PerioperativeBronchospasm- Treatment
Systemic Glucocorticosteroids
Methylprednisone (1 mg/kg) - preferred over cortisone
Benefit - not immediate (4–6 hrs )
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
54. PerioperativeBronchospasm- 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
High doses induce muscle weakness and central nervous system depression
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
55. PerioperativeBronchospasm- 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
56. PerioperativeBronchospasm- 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.
57. 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.
58. Helium–oxygen mixtures (heliox) :
Used to maintain laminar flow in acute bronchospasm.
A major limitation is that heliox mixtures can provide only 21–30% oxygen.
Helium facilitates ventilation but does not reverse the underlying
bronchospasm
Nitroglycerin :
reverse acute bronchospasm, probably through direct smooth muscle
relaxation.
59. Elective Surgery should be postponed - bronchospasm persists
at baseline despite maximal medical optimization of the patient
60.
61. 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
Editor's Notes
The upper airway is well innervated by afferent sensory pathways synapsing in the nucleus of the solitary tract (nTS), which projects excitatory glutaminergic and inhibitory -aminobutyric acid-A (GABA)-ergic neurons to the airway-related vagal preganglionic neurons
(AVPN). Parasympathetic preganglionic efferents travel in the vagus nerve to release acetylcholine onto M3 muscarinic receptors on airway smooth muscle inducing bronchoconstriction.
Stepwise approach to treatment of perioperative bronchospasm according to the clinical scenario. * May be used in
life-threatening bronchospasm or those with a poor initial response to 2-agonist; † may be used in cases of severe
bronchospasm that fails to relieve with 2-agonist; ‡ for further details, see Reference 1.