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Dr.Malaka Munasinghe
Registrar in Anaesthesia
2017-01-20
Definition of asthma
A heterogeneous disease with
chronic airway inflammation
Defined by
- history of respiratory symptoms
(wheeze, SOB, chest tightness and
cough)
-that vary over time and in intensity
-variable expiratory airflow
limitation
GINA-2015
Airway inflammation
obstruction
 one of the most common chronic diseases worldwide
(estimated 300 million affected)
 Prevalence increasing especially in children
 Mean age of onset- 4 years
 a major cause of school and work absence
 very high health care expenditure
Epidemiology
Aetiology
 Gender
 Atopy
 Allergens
 Infections
 Lifestyle-Obesity/ Tobacco smoke
 Perinatal factors
 based on:
 A history of characteristic symptom patterns
 Evidence of variable airflow limitation,
( from bronchodilator reversibility testing or other tests )
Diagnosis of asthma
GINA 2015
 Confirm presence of airflow limitation
 reduced FEV1/FVC
 healthy adults >0.75 – 0.80/ >0.90 in children
 Confirm variation in lung function
 greater the variation/ frequency of variation - greater
probability of diagnosis
 Excessive bronchodilator reversibility (adults: FEV1>12%
and >200mL; children: >12% predicted)
 Excessive diurnal variability from 1-2 weeks’ twice-daily
PEF monitoring
 Significant increase in FEV1 or PEF after 4 weeks of controller
treatment
Diagnosis of asthma – variable
airflow limitation
GINA 2015, Box 1-2
© Global Initiative for Asthma
Time (seconds)
Volume
Note: Each FEV1represents the highest of
three reproducible measurements
Typical spirometric tracings
FEV1
1 2 3 4 5
Normal
Asthma
(after BD)
Asthma
(before BD)
Flow
Volume
Normal
Asthma
(after BD)
Asthma
(before BD)
GINA 2015
British thoracic society- 2014
Assessment of severity
 Becker Asthma score
 A score >4 is moderate acute severe asthma
 score 7 and above is severe and needs ICU admission
Assessment of severity
 Clinical Asthma score
 A score >4 is impending Resp failure
 Score 7 and above is Resp failure
Acute severe asthma
-Clinical Definition
 Severe asthma that fails to respond to
 inhaled β2 agonists
 oral or IV steroids and O2
 requires admission to the hospital for treatment
Pathophysiology in Acute severe
asthma
 Pathologic changes in the airway  airflow
obstruction  premature airway closure on expiration
 dynamic hyperinflation  hypercarbia
 Dynamic hyperinflation or “air-trapping” also leads to
ventilation / perfusion (V/Q) mismatching causing
hypoxemia
 Prolonged respiratory acidosis- pulmonary
hypertension
Acute Asthma Management
Clinical and Laboratory Assessment
 Assess clinically – accessory muscle use,
tachypnea, tachycardia, diaphoresis, pulsus
paradoxus, exhaustion.
 Assess airflow limitation – peak flow
measurement.
 Assess oxygenation – pulse oximetry.
 Assess for hypercapnia –somnolent, fatigued,
difficulty with speech, elderly, concomitant use of
sedatives.
 Imaging – chest X ray
 Blood work – CBC, glucose
Anaesthetic considerations
perioperative bronchospasm in asthmatic patients
undergoing routine surgery <2%
complications increased in
Poorly controlled asthmatics
patients over 50 years
major surgery
Preop assessment
History
 frequency of symptoms/ sputum production
 asthma triggers/Allergies
 recent URTI
 activity level/ exercise tolerance
 previous history of surgery and anaesthesia
 hospitalizations and emergency department
attendance
 drug history-use and effectiveness of medication
NSAID/aspirin induced asthma
Examination
 wheezing
 Cough
 Respiratory rate
 use of accessory muscles
 cyanosis
 changes in mental status
 Spo2 value as baseline
CXR
Limited role but indicated in-
 First time wheezers
 Clinical evidence of parenchymal disease
 Suspected pneumothorax or pneumonia
 underlying cause in doubt
 suspected pulmonary hypertension ( + ECG)
ABG
Not routnely indicated
 severe asthma (poorly controlled, frequent hospital
admissions, previous ICU admission)
 major surgery
 PaO2< 60 mmHg or PaCO2> 45mmHg- impending
respiratory failure
Preop optimization
 mild asthma
- nebulized β2-adrenergic agonist 30 mnts prior to
surgery
 moderate asthma
- additional optimization with any inhaled anti-
inflammatory agent and consistent use of nebulized
β2 agonists 1 week prior to surgery
 severe persistent asthma
- optimize treatment with consultation with physician
- short-term oral corticosteroid therapy
 Preop chest physiotherapy in major thoracic and
abdominal surgeries
 Preop anxiolytics
- midazolam- effective
no effect on bronchial tone
Antibiotics
 Not routinely indicated
 Reserved for patients with evidence of bacterial
infection
 High fever
 Purulent secretions
 Consolidation on X ray film
 Very high leucocyte counts
Intraop management
Induction
 Propofol
- inhibits bronchoconstriction
- increases central airway dilation by directly relaxing
the airway smooth muscle
- decrease the possibility of bronchospasm during
induction.
( may not be suitable for haemodynamically unstable
patients)
 TPS ???
Ketamine
 Direct bronchodilatory properties
 decrease the possibility of bronchospasm with
induction
 increases bronchial secretions
(an anticholinergic drug such as glycopyrrolate or
atropine is useful)
IV lignocaine
 increases the histamine threshold
 blocks the cough reflex
 may be given to decrease the airway responses
associated with intubation(local spray as well)
Halothane /enflurane/isoflurane
 potent bronchodilators via β-adrenergic stimulation
 decrease airway responsiveness
 ease histamine induced bronchospasm
Desflurane
 pungent
 irritable to the airway
 increase secretions, coughing, and laryngospasm
Sevoflurane???
Nitrous oxide/ Ether- OK
Analgesia
Morphine
 histamine release – bronchospasms
Fentanyl
 if rapidly administered in large doses - chest rigidity
mistaken for bronchospasm
Muscle relaxation
Vecuronium, Rocuronium, Cisatracurium and
Pancuronium
stimulate the M2 and M3 muscarinic receptors
evenly
 do not cause bronchoconstriction
Atracurium and mivacurium
 dose-dependently release histamine
 trigger bronchoconstriction
 Well controlled asthmatics –routine doses -OK
Intubation
 avoidance of any stimulation of the airway
 avoidance of tracheal intubation preferred unless
airway protection needed
 LMA - less stimulating
 ET insertion in a deep plane of anaesthesia
 Avoiding carinal stimulation
Maintenance
 Bronchodilatory inhalational agents
 A method to administer another bronchodilatory
agent
 Observe for bronchospasms
 How?
 Exclude other causes of airway obstruction
Severe bronchospasms during anaesthesia
 Common following intubation
 Exclude blocked tubes/circuits
 100% O2
 Deepen anaesthesia ( inhalational/ IV- ketamine preferred)
 Higher inflation pressures may be needed
 minimise build up of auto PEEP
( gas trapping and positive pressure build up in obstructed
alveoli in expiration)
- slower respiratory rates
( 6-8/min in adults)
 Hypercarbia tolerated
 B2 agonist inhaler 6-8 puffs with a special adaptor in to
ETT
 IV salbutamol if not responding (250 mcg slow bolus
then 5–20 mcg/min)
 Hydrocortisone 100 mg IV 6 hourly or prednisolone
orally 40–50 mg/day.
 Magnesium 2g IV over 20 minutes
 Aminophylline 5mg/kg IV followed by infusion
Adrenaline - in extremis (decreasing conscious level or
exhaustion)
 nebuliser 5 ml of 1 in 1,000
 IV 10 mcg (0.1 ml 1 : 10,000) increasing to 100 mcg (1
ml 1 : 10,000) depending on response
 S/C or IM administration (0.5–1 mg) if IV access not
available
 risk of arrhythmias in the presence of hypoxia and
hypercapnia
Extubation
Elective cases- deep extubation unless contraindicated
Emergency/ full stomach situations
- fully awake extubation with prior redosing of inhaled
β2-agonists
Avoid reversal agents
( Neostigmine/pyridostigmine- increased secretions and
air way hyperactivity)
 Spinal anaesthesia or plexus/nerve blocks - safe
provided the patient is able to lie flat comfortably
 Analgesic requirement post op similar to a normal
patient
 NOT in a higher risk of respiratory depression with
oipiods
 NSAIDS’s avoided with patients who are sensitive
Post op management
 Patients with severe disease/ major thoracic and
abdominal surgeries- POST OP HDU/ICU care
 Adequate analgesia- epidurals preferred( avoid dense
intercostal blockade)
- regular opioids/ pethidine
- NSAID’s if previously tolerated
 Supplemental O2
 Regular nebulisation/ b2 agonists sos/ Ipratropium?
 Continue steroids
 Worsening dyspnoea/ wheezing post op
- Exclude heart failure/ pul. Embolism/ pneumothorax
Treatment of Acute Severe Asthma
Principles and Primary Goals of care
 Relieve airflow limitation: bronchodilator therapy
 Treat airway inflammation: steroids
 Treat hypoxemia or hypercapnia if present
Life threatening asthma
Life threatening asthma
 ABC assessment
 Increased FiO2- deescalate to maintain Spo2> 92%
Nebulized b2 agonists
 Mainstay of therapy
 Salbutamol and terbutaline have relative β2-selectivity.
 Short-acting b2-agonists (e.g. salbutamol) - given repeatedly in 5 mg
doses or by continuous nebulization at 10 mg/ h driven by oxygen
 No difference in clinical response to treatment with racemic salbutamol
vs lev-salbutamol in acute severe asthma in children
Qureshi F. et al. Ann Emerg Med. 2005;46:29–36.
 MDI
 4-8 puffs (100 mcg each) per dose
 MDI with a holding chamber is at least as effective as nebulized
salbutamol in young children with moderate to severe asthma
exacerbations
 Continued until a clinical response seen or side effects occur
 Oral/s/c / IV routes
Intravenous β2-agonists
 Not to give routinely in acute exacerbations
Travers A. et al. Cochrane Database Syst Rev. 2001; (2): CD002988.
 Use in patients unresponsive to inhaled β2-agonists
 Those in whom nebulization is not feasible
 Intubated patients
 patients with poor air entry
 IV Salbutamol 5-20mcg/min
 IV Terbutaline
 Loading 10 mcg/kg IV over 10 min, followed by continuous infusion at
0.1–10 mcg/kg/min.
70% develop lactic acidosis 2-4hrs after IV therapy
Subcutaneous β2 agonist
 Primarily used for children with no IV access
 As a rapidly available adjunct to inhaled β2 agonist.
 Subcutaneous terbutaline 0.01 mg/kg/dose (max of 0.3
mg)
 May be repeated every 15–20 min for up to three doses
 Not recommended for acute severe asthma!
Adverse effects of β2-agonists
 Cardiovascular system
 Tachycardia
 Increased QTc interval
 Dysarrhythmia
 Hypertension
Adverse effects of β2-agonists
 Excessive CNS stimulation
 Hyperactivity
 Tremors
 Nausea with vomiting
 Hypokalemia
 Hyperglycemia
 Long acting B2 agonists- NO PLACE in acute severe
asthma ( associated with increased mortality)
Nebulized ipratropium bromide
 for all patients with life-threatening asthma
 added to nebulized b2 agonists treatment (500 mcg 4
hourly)
 Mechanism:
 Muscarinic agonist (anticholinergic)
 M1 receptor  decrease cGMP  decreases intracellular Ca2+
 Synergistic effects with beta agonists
 Minimal side effects
( Dry mouth, bitter taste, flushing, tachycardia, and
dizziness, unilateral pupillary dilation (local effect)
Corticosteroids
 Early as possible- improve survival
 Parenteral: preferred for critically ill
 Oral: equal efficacy if it can be given
 Aerosolized: limited role in severe asthma
 Effect starts in 1–3 h and reach at max in 4–8 h
Corticosteroids
 Mechanism:
 Systemically reduce inflammation, decrease mucus production, and
enhance the effects of B2-agonists
 Prevents the sustained inflammatory phase which occurs 6-8 hours
after allergen exposure
 Dosing:
 Hydrocortisone: 10 mg/kg followed by 5 mg/kg 6hrly
 Methylprednisone: 0.5–1 mg/kg IV 6h (2-4 mg/kg/day)
 Dexamethasone: 0.15 mg/kg/dose 4-6 hrly
 Prednisolone: 1-2 mg/kg/day
 Duration 5-7 days
 In severe asthma, steroids should be administered IV to assure
adequate drug delivery in a timely manner
Corticosteroids: Side effects
 Short-term use of high-dose steroids
 Hyperglycemia
 Hypertension
 Acute psychosis
 Prolonged steroid
 Immunosuppression
 Hypothalamic-pituitary-adrenal axis suppression,
 Osteoporosis
 Myopathy
 Weakness
Magnesium Sulfate
 Mechanism:
 Inhibits Ca2+ influx into cytosol  smooth muscle
relaxant
 Increases B2 agonist affinity for its receptor, thereby
potentiating its effect
 Inhibits histamine release from mast cells
 40 mg/kg IV over 20-30 min with max of 2 g
 Repeat once or twice after 4–6 h
 Nebulised form- no benefit
Magnesium -Side effects
 Hypotension
 CNS depression
 Muscle weakness
 Flushing
 Very high serum magnesium levels (usually >10–12 mg/dL).
 Cardiac arrhythmia/ complete heart block
 Respiratory failure due to severe muscle weakness
 Sudden cardiopulmonary arrest
 Treatment: IV Calcium Gluconate
Aminophylline
 Mechanism
 Xanthine derivative
 Decreases intracellular Ca2+
 Inhibits TNF-alpha and leukotriene synthesis
 Loading dose: 5 mg/kg over 20 min IV
 Continuous infusion: 0.5–0.75mg/kg/min IV
 Limited role in unresponsive to steroids, inhaled and IV β2
agonist, and O2 with severe asthma
Ream RS et al. Chest 2001;119:1480–8.
Aminophylline Toxicity
-Narrow Therapeutic range -10 – 20 mcg/ml
 Nausea and vomiting
 Tachycardia
 Agitation
 Severe toxicity (high serum concentrations)
 Cardiac arrhythmias
 Hypotension
 Seizures
 Death
 Monitor drug level in blood:
 8hr after drug initiation and then every morning
 Adrenaline
- Not responding to above measures
Fluid
 Restoration of euvolemia
 Isotonic fluid like normal saline or Ringer’s lactate
 Fluid balance
 Avoid overhydration; Risk of pulm edema
 Serum potassium monitoring
Mechanical Ventilation
Absolute indications
 Severe refractory hypoxaemia
 coma
 Respiratory or cardiac arrest
Relative indications
 Poor response to initial management
 fatigue and somnolence
 cardiovascular compromise
 development of a pneumothorax
 Hypercapnia???
Intubation Tips
 50% of life threatening complications occur during induction
 Carried out via the most senior member of anaesthetic team
 Preoxygenate with 100% oxygen
 RSI
 Anticipate hypotension – preload/ vasopressors ready at hand
 If profound hypotension- disconnect from circuit and allow
passive expiration
 Cuffed ET tube with the largest appropriate diameter
 Avoid histamine-producing agents like morphine or atracurium
 Ketamine: preferred induction agent due to its bronchodilatory
action
 Avoid overenthusiastic hand ventilation
Sedation, Analgesia and Muscle
Relaxants
Is sedation needed at all?
 Propofol+fentanyl
 Ketamine+midazolam
 Morphine???
Initial muscle relaxation needed
 Rocuronium or pancuronium preferred
 Vecuronium /atracurium
( Neuromyopathy with vecuronium
Histamine release with atracurium)
- should discontinue as early as possible
Ventilation Principles
 Maintain adequate oxygenation
 permissive hypercarbia with arterial pH of >7.2
 Adjust minute ventilation
 Slow ventilator rates
 Avoid air trapping
 Prolonged expiratory phase, short inspiratory time
 Minimal PEEP< 5cmH2o
Stewart TE, Slutsky AS. Crit Care Med. 1996;24:379–80
 Attempt extubation as soon as possible
 In Volume controlled ventilation
- P plat< 35cmH2o and pH>7.2
- P plat > 30cmH2 o – reduce minute ventilation( Vt or Rate)
-pH < 7.2 / P plat < 35cmH2O- increase MV
- pH<7.2/ Pplat > 35cmH2O- no change
 minute ventilation is the most important determinant
of hyperinflation
 the risk of barotrauma is proportional to end inspiratory
lung volume
Management of hypercarbia
 hypercapnia -well tolerated
 BUT- cerebral hypoxia secondary to a respiratory
arrest
ICP management of hypercarbia
extra corporeal CO2 removal
Extra-corporeal support FOR CO2 elimination
 extra-corporeal membrane oxygenation
 Novalung
 Buffering- Bicarbonate/ Tromethamine (THAM)
 Measures to limit CO2 production-anti-pyretics /
active cooling
Dynamic hyperinflation (gas-trapping) due to
excessive ventilation — especially in the patient with
bronchospasm.
Hypovolemia exacerbated by decreased venous
return due to positive intrathoracic pressure.
Vasodilation and myocardial depression due to the
induction drugs used for rapid sequence intubation
(e.g. thiopentone, propofol).
Tension pneumothorax due to positive-pressure
ventilation.
Hypotension following intubation !
Typical Ventilator Setting
 VT of 6–8 mL/kg,
 RR approximately half of the normal for age
 I: E ratio of 1:3 /1:4
 PEEP of 2–3 cm of H2O
 In infants, pressure controlled ventilation: adjust PIP
to achieve adequate ventilation
Other complications of mechanical ventilation
 cardiac stunning
 Arrhythmia
 rhabdomyolysis
 lactic acidosis
 Myopathy
 CNS injury
Maintenance
Ketamine
 0.5–1 mg/kg IV bolus
 Continuous infusion 1-2 mg/kg/hr
Heliox
 Mechanism:
 Low-density gas that increases laminar flow of oxygen and
decreases turbulent flow.
 Reduce work of breathing in spontaneously breathing patients
 Adjunct therapy
 For patients unresponsive to conventional therapy
 Children on high-pressure mechanical ventilatory support
 Dosing: 60%/40% or 80%/20% helium/O2
 No systemic side effects
-Colebourn CL et al. Anaesthesia 2007;62:34–42.
Noninvasive Mechanical
Ventilation
 An alternative to conventional mechanical ventilation
in early phase
 While weaning off conventional ventilator
 Only found to be effective in mild to moderate asthma
 No place in life threatening asthma
-Carroll CL, Schramm CM. Ann Allergy Asthma Immunol. 2006;96:454–9.
Issues with heliox
 Max FiO2- 0.4
 Need recalibration of ventilators
Chest Physiotherapy
 Useful in patients with segmental or lobar atelectasis.
 In others no therapeutic benefit in the critically ill
patient with severe asthma.
Leukotriene Modifiers
 Little data to suggest a role for leukotriene modifiers in
acute asthma
 It is not part of standard management of severe
asthma
Silverman RA et al. Chest 2004;126:1480–9.
TodiVK, Lodha R, Kabra SK. Arch Dis Child. 2010;95:540–3.
Bronchial thermoplasty
 Controlled thermal energy to airway wall
 Aim to reduce hyperresponsiveness and smooth
muscle mass
 Found to be effective in long-term (5-year) and
relatively safe in severe asthma¶
¶ J Allergy Clin Immunol. 2013 Aug 30.
Anti-IgE therapy
 Omalizumab
 monoclonal antibody that blocks IgE
 used in treatment of selected patients with moderate to
severe allergic asthma.
 No place in life threatening asthma
 More potent anti-IgE antibodies - in development
§ J Allergy Clin Immunol. 2003 Sep;112(3):563-70.
 Humidified oxygen titrated to SpO2 90-92%
 Nebulised beta-agonist bronchodilators
 Nebulised anticholinergic drugs
 Steroids: IV hydrocortisone or oral prednisone
First-tier therapies with strong supporting evidence
Second-tier therapies with weak supporting evidence
Intravenous beta-agonist bronchodilators for refractory bronchospasm
Methylxanthines
Nebulised adrenaline
Magnesium sulfate
Helium-oxygen mixture
Third-tier therapies without any supporting evidence
Ketamine
Volatile anaesthetics
ECMO in asthma
References
 British Guideline on the Management of Asthma
-A national clinical guideline revised in 2012
 GINA Guidelines for asthma management- revised in 2015
 The ICU BOOK- 6TH EDITION 2012
 Kumar & Clerk- 7th edition
 Anaesthesia tutorial of the week –asthma and anaesthesia-
2005.05.16
 Preoperative considerations for the patient with asthma
and bronchospasm:woods B.D Sladen R.N BJA103 I 57-65
Questions-
MD part II Anaesthesiology
 1991-– Long essay
- Describe the assessment and preoperative preparation of a
severly asthmatic patient for elective abdominal surgery
 2006- SAQ
- How would you asess a patient presenting with acute severe
asthma?
 2011- SAQ
- A 19 year old patient with acute severe asthma is admitted
with severe respiratory distress to ICU
a) Describe your immediate management
b) What are the indications for mechanical ventilation?
c) How would you intubate and ventilate this patient?
THANK YOU!

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Bronchial asthma and anaesthesia

  • 1. Dr.Malaka Munasinghe Registrar in Anaesthesia 2017-01-20
  • 2. Definition of asthma A heterogeneous disease with chronic airway inflammation Defined by - history of respiratory symptoms (wheeze, SOB, chest tightness and cough) -that vary over time and in intensity -variable expiratory airflow limitation GINA-2015 Airway inflammation obstruction
  • 3.  one of the most common chronic diseases worldwide (estimated 300 million affected)  Prevalence increasing especially in children  Mean age of onset- 4 years  a major cause of school and work absence  very high health care expenditure Epidemiology
  • 4. Aetiology  Gender  Atopy  Allergens  Infections  Lifestyle-Obesity/ Tobacco smoke  Perinatal factors
  • 5.  based on:  A history of characteristic symptom patterns  Evidence of variable airflow limitation, ( from bronchodilator reversibility testing or other tests ) Diagnosis of asthma GINA 2015
  • 6.  Confirm presence of airflow limitation  reduced FEV1/FVC  healthy adults >0.75 – 0.80/ >0.90 in children  Confirm variation in lung function  greater the variation/ frequency of variation - greater probability of diagnosis  Excessive bronchodilator reversibility (adults: FEV1>12% and >200mL; children: >12% predicted)  Excessive diurnal variability from 1-2 weeks’ twice-daily PEF monitoring  Significant increase in FEV1 or PEF after 4 weeks of controller treatment Diagnosis of asthma – variable airflow limitation GINA 2015, Box 1-2
  • 7. © Global Initiative for Asthma Time (seconds) Volume Note: Each FEV1represents the highest of three reproducible measurements Typical spirometric tracings FEV1 1 2 3 4 5 Normal Asthma (after BD) Asthma (before BD) Flow Volume Normal Asthma (after BD) Asthma (before BD) GINA 2015
  • 9. Assessment of severity  Becker Asthma score  A score >4 is moderate acute severe asthma  score 7 and above is severe and needs ICU admission
  • 10. Assessment of severity  Clinical Asthma score  A score >4 is impending Resp failure  Score 7 and above is Resp failure
  • 11. Acute severe asthma -Clinical Definition  Severe asthma that fails to respond to  inhaled β2 agonists  oral or IV steroids and O2  requires admission to the hospital for treatment
  • 12. Pathophysiology in Acute severe asthma  Pathologic changes in the airway  airflow obstruction  premature airway closure on expiration  dynamic hyperinflation  hypercarbia  Dynamic hyperinflation or “air-trapping” also leads to ventilation / perfusion (V/Q) mismatching causing hypoxemia  Prolonged respiratory acidosis- pulmonary hypertension
  • 13. Acute Asthma Management Clinical and Laboratory Assessment  Assess clinically – accessory muscle use, tachypnea, tachycardia, diaphoresis, pulsus paradoxus, exhaustion.  Assess airflow limitation – peak flow measurement.  Assess oxygenation – pulse oximetry.  Assess for hypercapnia –somnolent, fatigued, difficulty with speech, elderly, concomitant use of sedatives.  Imaging – chest X ray  Blood work – CBC, glucose
  • 14. Anaesthetic considerations perioperative bronchospasm in asthmatic patients undergoing routine surgery <2% complications increased in Poorly controlled asthmatics patients over 50 years major surgery
  • 15. Preop assessment History  frequency of symptoms/ sputum production  asthma triggers/Allergies  recent URTI  activity level/ exercise tolerance  previous history of surgery and anaesthesia  hospitalizations and emergency department attendance  drug history-use and effectiveness of medication NSAID/aspirin induced asthma
  • 16. Examination  wheezing  Cough  Respiratory rate  use of accessory muscles  cyanosis  changes in mental status  Spo2 value as baseline
  • 17. CXR Limited role but indicated in-  First time wheezers  Clinical evidence of parenchymal disease  Suspected pneumothorax or pneumonia  underlying cause in doubt  suspected pulmonary hypertension ( + ECG)
  • 18. ABG Not routnely indicated  severe asthma (poorly controlled, frequent hospital admissions, previous ICU admission)  major surgery  PaO2< 60 mmHg or PaCO2> 45mmHg- impending respiratory failure
  • 19. Preop optimization  mild asthma - nebulized β2-adrenergic agonist 30 mnts prior to surgery  moderate asthma - additional optimization with any inhaled anti- inflammatory agent and consistent use of nebulized β2 agonists 1 week prior to surgery  severe persistent asthma - optimize treatment with consultation with physician - short-term oral corticosteroid therapy  Preop chest physiotherapy in major thoracic and abdominal surgeries
  • 20.
  • 21.  Preop anxiolytics - midazolam- effective no effect on bronchial tone
  • 22. Antibiotics  Not routinely indicated  Reserved for patients with evidence of bacterial infection  High fever  Purulent secretions  Consolidation on X ray film  Very high leucocyte counts
  • 23. Intraop management Induction  Propofol - inhibits bronchoconstriction - increases central airway dilation by directly relaxing the airway smooth muscle - decrease the possibility of bronchospasm during induction. ( may not be suitable for haemodynamically unstable patients)  TPS ???
  • 24. Ketamine  Direct bronchodilatory properties  decrease the possibility of bronchospasm with induction  increases bronchial secretions (an anticholinergic drug such as glycopyrrolate or atropine is useful)
  • 25. IV lignocaine  increases the histamine threshold  blocks the cough reflex  may be given to decrease the airway responses associated with intubation(local spray as well)
  • 26. Halothane /enflurane/isoflurane  potent bronchodilators via β-adrenergic stimulation  decrease airway responsiveness  ease histamine induced bronchospasm
  • 27. Desflurane  pungent  irritable to the airway  increase secretions, coughing, and laryngospasm Sevoflurane??? Nitrous oxide/ Ether- OK
  • 28. Analgesia Morphine  histamine release – bronchospasms Fentanyl  if rapidly administered in large doses - chest rigidity mistaken for bronchospasm
  • 29. Muscle relaxation Vecuronium, Rocuronium, Cisatracurium and Pancuronium stimulate the M2 and M3 muscarinic receptors evenly  do not cause bronchoconstriction Atracurium and mivacurium  dose-dependently release histamine  trigger bronchoconstriction  Well controlled asthmatics –routine doses -OK
  • 30. Intubation  avoidance of any stimulation of the airway  avoidance of tracheal intubation preferred unless airway protection needed  LMA - less stimulating  ET insertion in a deep plane of anaesthesia  Avoiding carinal stimulation
  • 31. Maintenance  Bronchodilatory inhalational agents  A method to administer another bronchodilatory agent  Observe for bronchospasms  How?  Exclude other causes of airway obstruction
  • 32. Severe bronchospasms during anaesthesia  Common following intubation  Exclude blocked tubes/circuits  100% O2  Deepen anaesthesia ( inhalational/ IV- ketamine preferred)  Higher inflation pressures may be needed  minimise build up of auto PEEP ( gas trapping and positive pressure build up in obstructed alveoli in expiration) - slower respiratory rates ( 6-8/min in adults)  Hypercarbia tolerated
  • 33.  B2 agonist inhaler 6-8 puffs with a special adaptor in to ETT  IV salbutamol if not responding (250 mcg slow bolus then 5–20 mcg/min)  Hydrocortisone 100 mg IV 6 hourly or prednisolone orally 40–50 mg/day.  Magnesium 2g IV over 20 minutes  Aminophylline 5mg/kg IV followed by infusion
  • 34. Adrenaline - in extremis (decreasing conscious level or exhaustion)  nebuliser 5 ml of 1 in 1,000  IV 10 mcg (0.1 ml 1 : 10,000) increasing to 100 mcg (1 ml 1 : 10,000) depending on response  S/C or IM administration (0.5–1 mg) if IV access not available  risk of arrhythmias in the presence of hypoxia and hypercapnia
  • 35. Extubation Elective cases- deep extubation unless contraindicated Emergency/ full stomach situations - fully awake extubation with prior redosing of inhaled β2-agonists Avoid reversal agents ( Neostigmine/pyridostigmine- increased secretions and air way hyperactivity)
  • 36.  Spinal anaesthesia or plexus/nerve blocks - safe provided the patient is able to lie flat comfortably
  • 37.  Analgesic requirement post op similar to a normal patient  NOT in a higher risk of respiratory depression with oipiods  NSAIDS’s avoided with patients who are sensitive
  • 38. Post op management  Patients with severe disease/ major thoracic and abdominal surgeries- POST OP HDU/ICU care  Adequate analgesia- epidurals preferred( avoid dense intercostal blockade) - regular opioids/ pethidine - NSAID’s if previously tolerated  Supplemental O2  Regular nebulisation/ b2 agonists sos/ Ipratropium?  Continue steroids
  • 39.  Worsening dyspnoea/ wheezing post op - Exclude heart failure/ pul. Embolism/ pneumothorax
  • 40. Treatment of Acute Severe Asthma Principles and Primary Goals of care  Relieve airflow limitation: bronchodilator therapy  Treat airway inflammation: steroids  Treat hypoxemia or hypercapnia if present Life threatening asthma
  • 41. Life threatening asthma  ABC assessment  Increased FiO2- deescalate to maintain Spo2> 92%
  • 42. Nebulized b2 agonists  Mainstay of therapy  Salbutamol and terbutaline have relative β2-selectivity.  Short-acting b2-agonists (e.g. salbutamol) - given repeatedly in 5 mg doses or by continuous nebulization at 10 mg/ h driven by oxygen  No difference in clinical response to treatment with racemic salbutamol vs lev-salbutamol in acute severe asthma in children Qureshi F. et al. Ann Emerg Med. 2005;46:29–36.  MDI  4-8 puffs (100 mcg each) per dose  MDI with a holding chamber is at least as effective as nebulized salbutamol in young children with moderate to severe asthma exacerbations  Continued until a clinical response seen or side effects occur  Oral/s/c / IV routes
  • 43. Intravenous β2-agonists  Not to give routinely in acute exacerbations Travers A. et al. Cochrane Database Syst Rev. 2001; (2): CD002988.  Use in patients unresponsive to inhaled β2-agonists  Those in whom nebulization is not feasible  Intubated patients  patients with poor air entry  IV Salbutamol 5-20mcg/min  IV Terbutaline  Loading 10 mcg/kg IV over 10 min, followed by continuous infusion at 0.1–10 mcg/kg/min. 70% develop lactic acidosis 2-4hrs after IV therapy
  • 44. Subcutaneous β2 agonist  Primarily used for children with no IV access  As a rapidly available adjunct to inhaled β2 agonist.  Subcutaneous terbutaline 0.01 mg/kg/dose (max of 0.3 mg)  May be repeated every 15–20 min for up to three doses  Not recommended for acute severe asthma!
  • 45. Adverse effects of β2-agonists  Cardiovascular system  Tachycardia  Increased QTc interval  Dysarrhythmia  Hypertension
  • 46. Adverse effects of β2-agonists  Excessive CNS stimulation  Hyperactivity  Tremors  Nausea with vomiting  Hypokalemia  Hyperglycemia  Long acting B2 agonists- NO PLACE in acute severe asthma ( associated with increased mortality)
  • 47. Nebulized ipratropium bromide  for all patients with life-threatening asthma  added to nebulized b2 agonists treatment (500 mcg 4 hourly)  Mechanism:  Muscarinic agonist (anticholinergic)  M1 receptor  decrease cGMP  decreases intracellular Ca2+  Synergistic effects with beta agonists  Minimal side effects ( Dry mouth, bitter taste, flushing, tachycardia, and dizziness, unilateral pupillary dilation (local effect)
  • 48. Corticosteroids  Early as possible- improve survival  Parenteral: preferred for critically ill  Oral: equal efficacy if it can be given  Aerosolized: limited role in severe asthma  Effect starts in 1–3 h and reach at max in 4–8 h
  • 49. Corticosteroids  Mechanism:  Systemically reduce inflammation, decrease mucus production, and enhance the effects of B2-agonists  Prevents the sustained inflammatory phase which occurs 6-8 hours after allergen exposure  Dosing:  Hydrocortisone: 10 mg/kg followed by 5 mg/kg 6hrly  Methylprednisone: 0.5–1 mg/kg IV 6h (2-4 mg/kg/day)  Dexamethasone: 0.15 mg/kg/dose 4-6 hrly  Prednisolone: 1-2 mg/kg/day  Duration 5-7 days  In severe asthma, steroids should be administered IV to assure adequate drug delivery in a timely manner
  • 50. Corticosteroids: Side effects  Short-term use of high-dose steroids  Hyperglycemia  Hypertension  Acute psychosis  Prolonged steroid  Immunosuppression  Hypothalamic-pituitary-adrenal axis suppression,  Osteoporosis  Myopathy  Weakness
  • 51. Magnesium Sulfate  Mechanism:  Inhibits Ca2+ influx into cytosol  smooth muscle relaxant  Increases B2 agonist affinity for its receptor, thereby potentiating its effect  Inhibits histamine release from mast cells  40 mg/kg IV over 20-30 min with max of 2 g  Repeat once or twice after 4–6 h  Nebulised form- no benefit
  • 52. Magnesium -Side effects  Hypotension  CNS depression  Muscle weakness  Flushing  Very high serum magnesium levels (usually >10–12 mg/dL).  Cardiac arrhythmia/ complete heart block  Respiratory failure due to severe muscle weakness  Sudden cardiopulmonary arrest  Treatment: IV Calcium Gluconate
  • 53. Aminophylline  Mechanism  Xanthine derivative  Decreases intracellular Ca2+  Inhibits TNF-alpha and leukotriene synthesis  Loading dose: 5 mg/kg over 20 min IV  Continuous infusion: 0.5–0.75mg/kg/min IV  Limited role in unresponsive to steroids, inhaled and IV β2 agonist, and O2 with severe asthma Ream RS et al. Chest 2001;119:1480–8.
  • 54. Aminophylline Toxicity -Narrow Therapeutic range -10 – 20 mcg/ml  Nausea and vomiting  Tachycardia  Agitation  Severe toxicity (high serum concentrations)  Cardiac arrhythmias  Hypotension  Seizures  Death  Monitor drug level in blood:  8hr after drug initiation and then every morning
  • 55.  Adrenaline - Not responding to above measures
  • 56. Fluid  Restoration of euvolemia  Isotonic fluid like normal saline or Ringer’s lactate  Fluid balance  Avoid overhydration; Risk of pulm edema  Serum potassium monitoring
  • 57. Mechanical Ventilation Absolute indications  Severe refractory hypoxaemia  coma  Respiratory or cardiac arrest
  • 58. Relative indications  Poor response to initial management  fatigue and somnolence  cardiovascular compromise  development of a pneumothorax  Hypercapnia???
  • 59. Intubation Tips  50% of life threatening complications occur during induction  Carried out via the most senior member of anaesthetic team  Preoxygenate with 100% oxygen  RSI  Anticipate hypotension – preload/ vasopressors ready at hand  If profound hypotension- disconnect from circuit and allow passive expiration  Cuffed ET tube with the largest appropriate diameter  Avoid histamine-producing agents like morphine or atracurium  Ketamine: preferred induction agent due to its bronchodilatory action  Avoid overenthusiastic hand ventilation
  • 60. Sedation, Analgesia and Muscle Relaxants Is sedation needed at all?  Propofol+fentanyl  Ketamine+midazolam  Morphine??? Initial muscle relaxation needed  Rocuronium or pancuronium preferred  Vecuronium /atracurium ( Neuromyopathy with vecuronium Histamine release with atracurium) - should discontinue as early as possible
  • 61. Ventilation Principles  Maintain adequate oxygenation  permissive hypercarbia with arterial pH of >7.2  Adjust minute ventilation  Slow ventilator rates  Avoid air trapping  Prolonged expiratory phase, short inspiratory time  Minimal PEEP< 5cmH2o Stewart TE, Slutsky AS. Crit Care Med. 1996;24:379–80  Attempt extubation as soon as possible
  • 62.  In Volume controlled ventilation - P plat< 35cmH2o and pH>7.2 - P plat > 30cmH2 o – reduce minute ventilation( Vt or Rate) -pH < 7.2 / P plat < 35cmH2O- increase MV - pH<7.2/ Pplat > 35cmH2O- no change  minute ventilation is the most important determinant of hyperinflation  the risk of barotrauma is proportional to end inspiratory lung volume
  • 63. Management of hypercarbia  hypercapnia -well tolerated  BUT- cerebral hypoxia secondary to a respiratory arrest ICP management of hypercarbia extra corporeal CO2 removal
  • 64. Extra-corporeal support FOR CO2 elimination  extra-corporeal membrane oxygenation  Novalung  Buffering- Bicarbonate/ Tromethamine (THAM)  Measures to limit CO2 production-anti-pyretics / active cooling
  • 65. Dynamic hyperinflation (gas-trapping) due to excessive ventilation — especially in the patient with bronchospasm. Hypovolemia exacerbated by decreased venous return due to positive intrathoracic pressure. Vasodilation and myocardial depression due to the induction drugs used for rapid sequence intubation (e.g. thiopentone, propofol). Tension pneumothorax due to positive-pressure ventilation. Hypotension following intubation !
  • 66. Typical Ventilator Setting  VT of 6–8 mL/kg,  RR approximately half of the normal for age  I: E ratio of 1:3 /1:4  PEEP of 2–3 cm of H2O  In infants, pressure controlled ventilation: adjust PIP to achieve adequate ventilation
  • 67. Other complications of mechanical ventilation  cardiac stunning  Arrhythmia  rhabdomyolysis  lactic acidosis  Myopathy  CNS injury
  • 68. Maintenance Ketamine  0.5–1 mg/kg IV bolus  Continuous infusion 1-2 mg/kg/hr
  • 69. Heliox  Mechanism:  Low-density gas that increases laminar flow of oxygen and decreases turbulent flow.  Reduce work of breathing in spontaneously breathing patients  Adjunct therapy  For patients unresponsive to conventional therapy  Children on high-pressure mechanical ventilatory support  Dosing: 60%/40% or 80%/20% helium/O2  No systemic side effects -Colebourn CL et al. Anaesthesia 2007;62:34–42.
  • 70. Noninvasive Mechanical Ventilation  An alternative to conventional mechanical ventilation in early phase  While weaning off conventional ventilator  Only found to be effective in mild to moderate asthma  No place in life threatening asthma -Carroll CL, Schramm CM. Ann Allergy Asthma Immunol. 2006;96:454–9.
  • 71. Issues with heliox  Max FiO2- 0.4  Need recalibration of ventilators
  • 72. Chest Physiotherapy  Useful in patients with segmental or lobar atelectasis.  In others no therapeutic benefit in the critically ill patient with severe asthma.
  • 73. Leukotriene Modifiers  Little data to suggest a role for leukotriene modifiers in acute asthma  It is not part of standard management of severe asthma Silverman RA et al. Chest 2004;126:1480–9. TodiVK, Lodha R, Kabra SK. Arch Dis Child. 2010;95:540–3.
  • 74. Bronchial thermoplasty  Controlled thermal energy to airway wall  Aim to reduce hyperresponsiveness and smooth muscle mass  Found to be effective in long-term (5-year) and relatively safe in severe asthma¶ ¶ J Allergy Clin Immunol. 2013 Aug 30.
  • 75. Anti-IgE therapy  Omalizumab  monoclonal antibody that blocks IgE  used in treatment of selected patients with moderate to severe allergic asthma.  No place in life threatening asthma  More potent anti-IgE antibodies - in development § J Allergy Clin Immunol. 2003 Sep;112(3):563-70.
  • 76.  Humidified oxygen titrated to SpO2 90-92%  Nebulised beta-agonist bronchodilators  Nebulised anticholinergic drugs  Steroids: IV hydrocortisone or oral prednisone First-tier therapies with strong supporting evidence Second-tier therapies with weak supporting evidence Intravenous beta-agonist bronchodilators for refractory bronchospasm Methylxanthines Nebulised adrenaline Magnesium sulfate Helium-oxygen mixture Third-tier therapies without any supporting evidence Ketamine Volatile anaesthetics ECMO in asthma
  • 77. References  British Guideline on the Management of Asthma -A national clinical guideline revised in 2012  GINA Guidelines for asthma management- revised in 2015  The ICU BOOK- 6TH EDITION 2012  Kumar & Clerk- 7th edition  Anaesthesia tutorial of the week –asthma and anaesthesia- 2005.05.16  Preoperative considerations for the patient with asthma and bronchospasm:woods B.D Sladen R.N BJA103 I 57-65
  • 78. Questions- MD part II Anaesthesiology  1991-– Long essay - Describe the assessment and preoperative preparation of a severly asthmatic patient for elective abdominal surgery  2006- SAQ - How would you asess a patient presenting with acute severe asthma?  2011- SAQ - A 19 year old patient with acute severe asthma is admitted with severe respiratory distress to ICU a) Describe your immediate management b) What are the indications for mechanical ventilation? c) How would you intubate and ventilate this patient?