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3. INTRODUCTION
• Bronchospam usually caused by underlying AIRWAY
HYPERSENSITIVITY and it had the potential to become an
anesthetic disaster
• Prompt recognition and appropriate treatment are crucial for
an uneventful patient outcome
4. INCIDENCE
• Perioperative bronchospam = 0.5 to 2%
• Higher incidence in asthamatic and in patients prone for allergy
• Airway surgery and cardiac surgery also have higher incidence
• Allergic mechanism was less frequently involved i.e, 27% than a non-
allergic mechanism i.e, 79%
• 44 % = occurred during the induction of anesthesia
• 36 % = During the maintenance phase
• 20% = During the emergency/ recovery stage
9. Time of onset of
bronchospasm
Pathophysiology
Immediate
cardiovascular
features
Mucocutaneous
features like rash
• Before ET tube
insertion
• Allergic bronchospasm
• YES
• Associated with OR
followed by
bronchospasm
• Yes
• After
• Non – allergic
• Usually none
• If present delayed when
compared to
bronchospam onset
• Usually none
10. NON-ALLERGIC BRONCHOSPAM
• Mechanical = Intubation induced bronchospam
• Pharmcological = via histamine releasing drugs like Mevacurium
• Other causes of Non-allergic brobronchospam
Inadequate anesthesia
Mucous plugging of the airway
Esophageal intubation
Kinked / obstructed tube / circuit
Pulmonary aspiration
11. NOTE:
1. Unilateral wheezing suggests endobronchial intubation OR an
obstructed tube by a foreign body such as tooth
1. If the clinical symptoms fail to resolve despite appropriate therapy,
other etiologies such ad pulmonary edema OR pneumothorax
should be considered
12. ALLERGIC BRONCHOSPASM
• Immediate hypersensitivity is divided into
1. Non-allergic hypersensitivity
Called anaphylactoid reaction where an immune mechanism is
excluded i.e, no immune mediated reaction in non-allergic
hypersensitivity
2. Allergic hypersensitivity
Called IgE mediated anaphylaxis
13. • By definition immediate hypersensitivity occurs with in 1 to 10min
after the injection OR induction of the culprit agent
• The initial diagnosis remains presumptive where as the etiologic
diagnosis is linked to a TRIAD
1. Tryptase level measurements
2. Serum specific IgE’s
3. Postoperative skin tests with the suspected drugs OR agents apart
from clinical features
14. • Clinically four clinical variables were identified as independent
predictors for allergic perioprative bronchospasm
1. Presence of any mucocutaneous symptoms like rash
2. Hemodynamic disturbances along with bronchospam
3. Episodes of bronchospam
4. Prolonged durtion of clinical features i.e, more than 60mins
20. • Upper airway is well innervated by afferent sensory pathways
synapsing in nucleus tractus solitorious(Recent findings suggest that
the neurons of the nucleus of the solitary tract (NTS), in the dorsal
medulla, are essential for the processing and coordination of
respiratory and sympathetic responses to hypoxia)
• We have to interupt this tract to prevent broncho constriction by
spraying of local anesthetics OR regional blocks to prevent this reflex
broncho constriction
21.
22. • Parasympathetic preganglionic efferents travels via vagus nerve to
release acetylcholine to M3 muscarnic receptors
• This can be protected by anticholinergics as well as volatile anestheics
and beta agonists
23. Central mechanism causing bronchospasm : By
anesthetizing the patient deeply we can prevent this
centrally induced bronchospasm
24. • Apart from CNS depression both propofol and inhalational
anesthetics have direct brochodilatory effects at the level of airway
smooth muscle itself by acting on aminobutyric acid A channels OR by
modulating calcium sensitivity to contractile proteins
MECHANISM
• Non-adrenergic & non-cholinergic nerves releasing
tachykinins,vasoactive intestinal peptide(VIP),calcitonin gene related
peptide(CGRP) may precipitate in this reflex arc and locally releases
the procontractile neurotransmitters via activation of interneurons in
the airway
• Propofol preferentially relaxes tachykinin induced airway constriction
in airway smooth muscle
25.
26. Causes of wheeze & increased peak airway pressures
during IPPV ( DD of intraoperative bronchospasm)
ANESTHETIC
EQUIPMENTS
• Excessive
tidal
volume
• High
inspiratory
flow rates
PATIENT
• Obesity
• Head down position
• Tension penumothorax
• Bronchospasm( unknown
cause)
• Aspiration of gastric
contents
• Pulmonary edema &
embolism
• Tracheobronchial foreign
body
AIRWAY DEVICES
•Small diameter
Ettube
•Endobronchial
intubation
•Tube
kinked/blocked
30. Factors related to surgery
1. Reduction of tone in
palatine/pharyngeal muscles
2. Reduction of lung volume
3. Alteration of diaphragmatic
function with anesthesia
4. Reduction in the ability to
cough
5. Reduction in mucociliary
function
Baseline uncontrolled clinical
functional conditions
1. Inadequate control of asthma
symptoms
2. High degree of bronchial
hypersensitivity
3. Marked functional instability
of airway caliber like in
tracheomalacia
31. Factors related to anesthesia
1. Inadequate pain relief
2. Light plane
3. Histamine releasing drugs
4. Multiple attempts of
intubation
Various factors
1. Site of surgery(airway,cardiac
surgery)
2. Stress,obesity
3. GERD
4. Occurrence of organic material
aspiration
32.
33. RISK FACTORS
Film theatre – Smoking is injurious to health
Opeartion theatre – Smoking causes bronchospasm
36. PREOPERATIVE CLINICAL & PHYSICAL
EXAMINATION
• Recent and OR frequent exacerbation of respiratory symptoms,
cough,exercise intolerance ,unexplained dyspnea & GERD
• Decreased breath sounds as seen in
- Decreased expiratory airflow
- Rhonchi
- Dullness to percussion
- Prolonged expiratory phase
37. PREOPERATIVE VISIT
1. Do you smoke ?
2. Do you have GERD ?
3. Have ever felt chest tightness OR difficulty catching ypur breath ? If
so, at rest OR with physical efforts ?
4. Have ever been told that you have wheezing OR asthma ?
5. Have ever used an inhaled medication for your breathing ?
6. Have you ever visited an emergency department for breathing
problems?
38. 7. Have you ever had frquent bronchitis ?
8. Have you ever had rhinitis ?
9. Do ypu frequently cough ?
10. Do you have allergies to latex ?
39. MONITORING
• Increase in peak & plataeu pressures
• Decrease in slop of expired Co2
• Hypoxia , hypercarbia & hypotension
• Development of auto PEEP
• Extensive rhonchi
40.
41.
42. PREVENTION OF BRONCHOSPASM
• Preoperative symptoms optimization
• Adequate preoperative anxiolysis
• Regional over general anesthesia if feasible
• Minimal airway instrumentation
• INDUCTION with
1. Ketamine = Sympathomimetic agent
2. Propofol = Central action + relaxes tachykinin induced airway
constriction
3. Sevoflurane = Good bronchodilating property
43. NOTE
• Try to avoid desflurane – it is irritant and it might precipitate
bronchospam
- Maintaine adequate depth of anesthesia ( lighter plane =
stimulating factor for bronchospam
- Inhaled Beta agonists OR anticholinergics before induction
44. TREATMENT
SUSPICION OF BRONCHOSPASM
• Switch to 100% oxygen
• Look at the compliance of bag and assess whether
the patient has bronchospam and ventilate by hand
• Stop administration of suspected agents like
1. Beta blockers
2. NSAIDS,Neostigmine
3. Antibiotics , neuromuscular blockers
45. FIRST LINE THERAPY
• Beta agonist = SALBUTAMOL
• Metered dose inhaler =6-8 puffs repated as necessary
• Nebulization = 5mg repeated as necessary
• Intravenous = 250mcg slow i.v , followed by 5mcg/min
upto 20mcg/min
NOTE
• Usually i.v is avoided but given in refractory cases becz
this i.v treatment causes dangerous arrhythmias
46. SECOND LINE OF THERAPY
1. Anticholinergics = Ipratropium bromide i.e, 4-8
puffs , 0.5mg nebulization 6 hourly
2. Magnesium sulphate = 50mg/kg over 20mins ( max
2grams)
3. Steriods = Hydrocortisone 200mg i.v 6 hourly
long acting – 1.Methylprednisolone 125mg i.v
2.Dexamethasone 8mg i.v
47. 4. Bronchodilating anesthetics
- Ketamine = Bolus 10-20mg ; Infusion 1-3mg/kg/hour
5. Epinephrine ( used in allergic bronchospasm )
- Nebulization = 5ml 1:1000 dilution
- Intravenous = 10 mcg to 100mcg,tritated to response
IMMEDIATE MANAGEMENT
• Reverse bronchoconstriction and prevent hypoxia
1. Deepens the plane : Volatiles > Ketamine > Propofol
2. Consider alternative causes of high airway pressure
like
48. • Endobronchial intubation
• Kinked circuit
• Excessive TV
• Small diameter tracheal tube
• Obseity etc
3. Check the tube position and exclude blocked / misplaced tube
4. Exclude laryngospasm and consider aspiration in non-intubated
patients
49. 5. Avoid dynamic hyperinflation ( becz already there is going to be
hyperinflation ) with appropriate ventilation by doing
- Longer expiratory time
- Low OR normal respiratory rate
- Permissive hypercapnia
SECONDARY MANAGEMENT
• Provide on going therapy & address underlying causes
1. Optimize mechanical ventilation
50. 2. Consider aborting the surgery
3. Request and review chest X-ray
4. Transfer patient to ICU
5. Apply ECMO with severe bronchospam and refractory to all others
treatment