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Bronchial asthma and anaesthesia
This document discusses the definition, diagnosis, treatment and management of asthma. It begins by defining asthma as a chronic inflammatory airway disease characterized by variable and recurring symptoms. It then discusses the diagnosis of asthma based on symptoms and evidence of variable airflow limitation. The document outlines treatment for acute severe asthma which focuses on relieving airflow limitation through bronchodilators and treating inflammation with corticosteroids. Key medications discussed include nebulized beta-agonists, ipratropium, systemic corticosteroids, and magnesium sulfate. Perioperative management and considerations are also reviewed.
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Bronchial asthma and anaesthesia
- 1. Dr.Malaka Munasinghe Registrar inAnaesthesia 2017-01-20
- 2. Definition of asthma Aheterogeneous 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 ofthe 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 presenceof 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 Initiativefor 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
- 8.
- 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 -ClinicalDefinition 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 Acutesevere 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 Clinicaland 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 bronchospasmin asthmatic patients undergoing routine surgery <2% complications increased in Poorly controlled asthmatics patients over 50 years major surgery
- 15. Preop assessment History frequencyof 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 butindicated 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 mildasthma - 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
- 21. Preop anxiolytics -midazolam- effective no effect on bronchial tone
- 22. Antibiotics Not routinelyindicated 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 bronchodilatoryproperties decrease the possibility of bronchospasm with induction increases bronchial secretions (an anticholinergic drug such as glycopyrrolate or atropine is useful)
- 25. IV lignocaine increasesthe 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 potentbronchodilators via β-adrenergic stimulation decrease airway responsiveness ease histamine induced bronchospasm
- 27. Desflurane pungent irritableto 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 ofany 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 inhalationalagents A method to administer another bronchodilatory agent Observe for bronchospasms How? Exclude other causes of airway obstruction
- 32. Severe bronchospasms duringanaesthesia 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 agonistinhaler 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 - inextremis (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- deepextubation 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 anaesthesiaor plexus/nerve blocks - safe provided the patient is able to lie flat comfortably
- 37. Analgesic requirementpost 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 AcuteSevere 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 Notto 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 ofβ2-agonists Cardiovascular system Tachycardia Increased QTc interval Dysarrhythmia Hypertension
- 46. Adverse effects ofβ2-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 aspossible- 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: Systemicallyreduce 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 Xanthinederivative 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 Therapeuticrange -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 - Notresponding to above measures
- 56. Fluid Restoration ofeuvolemia 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 Poorresponse 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 andMuscle 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 Maintainadequate 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 Volumecontrolled 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 FORCO2 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 ofmechanical ventilation cardiac stunning Arrhythmia rhabdomyolysis lactic acidosis Myopathy CNS injury
- 68. Maintenance Ketamine 0.5–1 mg/kgIV bolus Continuous infusion 1-2 mg/kg/hr
- 69. Heliox Mechanism: Low-densitygas 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 Analternative 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 Usefulin patients with segmental or lobar atelectasis. In others no therapeutic benefit in the critically ill patient with severe asthma.
- 73. Leukotriene Modifiers Littledata 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 Controlledthermal 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 oxygentitrated 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 Guidelineon 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 IIAnaesthesiology 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?
- 79.