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Bronchospasm during induction


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Bronchospasm during induction

  1. 1. Pascale Dewachter, Claudie Mouton-Faivre, Charles W. Emala,Sadek Beloucif Anesthesiology 2011; 114:1200 –10 DR. RISHABH MITTALMODERATOR – DR. AVNISH BHARADWAJ
  2. 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. 3. Case Report – Anaesthetic coursePremedication – Tab. Hydroxyzine (100 mg) the day before and 1 h before inductionInduction - 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. 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. 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.VBlood sample 40 and 90 min after the clinical reaction- to measure serum tryptase concentrations
  6. 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. 7. 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.
  8. 8. 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 )
  9. 9. 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.
  10. 10. 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
  11. 11. 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
  12. 12. 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
  13. 13. 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
  14. 14. 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
  15. 15. Etiology in the Current CaseIn 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
  16. 16. 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)
  17. 17. 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)
  18. 18. 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
  19. 19. 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
  20. 20. 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
  21. 21. Perioperative Bronchospasm & AsthmaWesthorpe RN, Ludbrook GL, Helps SC: Crisis management during anaesthesia: Bronchospasm. Qual Saf Health Care 2005; 14:e7In 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%)
  22. 22. 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)
  23. 23. Mechanisms of Reflex-induced Bronchoconstriction Irritation of the upper airway by a foreign body Afferent sensory pathwaysStimulatory - Glutamate++ Nucleus of solitary Tract Inhibitory- γ aminobutyric acid - -Glutamate++ Airway-related Vagal Pre- ganglionic Neurons Airways via Vagus nerve Acetylcholine release ++ Bronchoconstriction (M3 muscarinic receptor)
  24. 24. 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.
  25. 25. 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
  26. 26. 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.
  27. 27. 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
  28. 28. 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
  29. 29. 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.
  30. 30. Prevention of Perioperative BronchospasmHISTORY 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
  31. 31. Prevention of Perioperative BronchospasmPreoperative 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 postponedSmetana GW: Preoperative pulmonary evaluation. N Engl J Med 1999; 340:937– 44
  32. 32. Prevention of Perioperative BronchospasmMeasurement 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
  33. 33. 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)
  34. 34. Stepwise Approach for Asthma Treatment / optimization of TreatmentPrevention of Perioperative BronchospasmLevel of Asthma Control Step Levels Treatment At each step, short-acting β2-agonist isGlobal Initiative for Asthma Five recommended as needed Intermittent treatment 1 — Daily medication 2 Low-dose inhaled corticosteroid Low-dose inhaled corticosteroid + inhaled long- — 3 acting β 2-agonist Medium- or high-dose inhaled Steroid + inhaled — 4 long-acting β 2-agonist — 5 Addition of oral steroid to other controllers At each step, short-acting β 2-agonist is Expert Panel Report six recommended as needed Intermittent treatment 1 — Daily medication 2 Low-dose inhaled corticosteroid — 3 Medium-dose inhaled corticosteroid Medium-dose inhaled corticosteroid + inhaled — 4 long-acting β 2-agonist High-dose inhaled corticosteroid + inhaled long- — 5 acting β2-agonist — 6 Step 5 + oral corticosteroids
  35. 35. 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
  36. 36. 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
  37. 37. Perioperative Bronchospasm - TreatmentAIM- 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)
  38. 38. Perioperative Bronchospasm - TreatmentInhaled 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
  39. 39. 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
  40. 40. 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
  41. 41. Perioperative Bronchospasm - Treatment AMINOPHYLLINE  Intravenous aminophylline has no role  Not result in additional bronchodilatation  Adverse effects - arrhythmia and vomiting have been reportedBateman 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
  42. 42. 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
  43. 43. 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.
  44. 44. Thanks for Your attention!
  45. 45. 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..
  46. 46. 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.....
  47. 47. 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)?