Acute asthma in adults


Published on

by Krit kuruchaiyapanich R3

1 Comment
No Downloads
Total views
On SlideShare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide

Acute asthma in adults

  1. 1. Acute Asthma inAdults Krit Kuruchaiyapanich, MD
  2. 2. Definition Asthma is a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role. ◦ This inflammation causes recurrent episodes of wheezing, breathlessness, chest tightness, and coughing, particularly at night or in the early morning. ◦ Associated with widespread but variable airflow obstruction that is often reversible either spontaneously or withProgram, EPR3: National Asthma Education and Prevention treatment. Guidelines for the
  3. 3. Definition Status asthmaticus ◦ severe bronchospasm that does not respond to aggressive therapies within 30 to 60 minutes. Near-fatal ◦ respiratory arrest or evidence of respiratory failure (Paco2 > 50 mm Hg).
  4. 4. Definition National Asthma Education and Prevention Program, EPR3: Guidelines for the
  5. 5. Severe/Refractory asthmaAmerican Thoracic Society workshop consensus for definition of severe/refractoryasthma (requires one or both major and two minor criteria and that other conditionshave been excluded, exacerbating factors have been treated, and patient is generallycompliant).
  6. 6. Pathophysiology Hallmark reduction in airway diameter caused by ◦ smooth muscle contraction ◦ vascular congestion ◦ bronchial wall edema ◦ thick secretions Bronchoconstriction occurs due to ◦ 1. allergic  mediators and metabolic products from inflammatory cells ◦ 2. nonallergic  exercise, aspirin- induced, and menstrual-related asthma
  7. 7. Pathophysiology
  8. 8. Pathophysiology National Asthma Education and Prevention Program, EPR3: Guidelines for the
  9. 9. Pathophysiology Early asthmatic response ◦ Release of preformed histamine from mast cell granules  bronchial smooth muscle and airway edema wheezing and airflow obstruction (resolves within an hour ) Late asthmatic response ◦ cytokines generated and released by mast cells and other local and recruited inflammatory cells prolonged airflow obstruction and bronchospasm
  10. 10. Pathophysiology Eosinophils are major effector cells in asthma Airway epithelial cells : produced Nitric oxide (NO) potent vasodilator and may reflect the presence of inflammation in asthma Airway remodeling : Inflammation, mucus hypersecretion , subepithelial fibrosis airway smooth muscle hypertrophy, angiogenesischronic irreversible airflow limitation
  11. 11. Aspirin-exacerbatedrespiratory disease (AERD) Triad ◦ aspirin sensitivity, asthma, and nasal polyps NSAIDs also precipitate AERD (but not reported after administration of COX-2 inhibitors ) common precipitant of life-threatening asthma Symptoms ◦ occur within 3 hoursprofuse rhinorrhea, conjunctival injection, periorbital edema, and occasionally a scarlet flushing of the head and neck Definitive diagnosis : provocation challenges
  12. 12. Aspirin-exacerbated respiratorydisease (AERD)
  13. 13. Exercise-induced asthma (EIA) Etiology is unclear Atopy is strongly associated with EIA, and up to 40% of patients with allergic rhinitis have EIA Symptom ◦ occur 3-8 min of exercise, peak 8-15 min after exercise, spontaneous recovery occurs within 60 min Prophylaxis : warm-up and a short- acting inhaled beta2-agonist
  14. 14. Menstruation-associatedasthma Perimenstrual reductions in PEFR of 35 to 80% Estradiol inhibits eosinophil degranulation and suppresses LT activity. Progesterone have bronchodilator and anti-inflammatory activity. Tx : LT antagonists, LABA , estradiol, progest erone, and gonadotropin-releasing
  15. 15. CLINICAL FEATURES  Classification ◦ 1. Type 1 (Slow onset> 6 hr) 80-90%  Female>male  Etiology: URI  Inflammation less severity than type 2  slower response to therapy ◦ 2. Type 2 (Sudden onset< 6 hr) 10-20%  Male>female  Etiology: respiratory allergen, exercise, stress  Bronchoconstriction more severe  faster response to therapyPicado C. Classification of severe asthma exacerbations: a proposal. Eur Respir J
  16. 16. CLINICAL FEATURES Symptom : Triad ◦ dyspnea, wheezing, and cough Early chest constriction and cough Exacerbation progresses wheezing, prolonged expiration and accessory muscle used(indicates diaphragmatic fatigue) Tachypnea and tachycardia >120 beats/min are associated with severe obstruction, but a lower rate does not R/O severe asthma. The "silent chest" reflects very severe
  17. 17. CLINICAL FEATURES bronchiolar smooth muscle tone airway resistance, pulponary infiltration, V/Q missmatch Dynamic hyperinflation auto-PEEP pulsus paradoxus, diastolic LV dysfn Acute hypercapnia+ intrathoracic pressure ICP Signs of impending respiratory failure (1) ◦ inability to speak, altered mental status, intercostal retraction, worsening fatigue, and a PCO2 of ≥42 mmHg (1) National Asthma Education and Prevention Program, EPR3: Guidelines for the
  18. 18. SEVERITY OF ASTHMAEXACERBATIONS National Asthma Education and Prevention Program, EPR3: Guidelines for the
  19. 19. Risk factors for death fromasthma
  20. 20. DIAGNOSTIC STRATEGIES Pulmonary Function Studies ◦ FEV1 or PEFR ◦ the best of 3 consecutive values should be recorded Arterial Blood Gas (mild to moderate hypoxemia with resp. alkalosis) ◦ 1. predicted PFTs of < 30% ◦ 2. clinical course is perplexing Indication ◦ 3. capnography is not available. ◦ acute ventilatory failure hypoventilation with CO2 retention and resp. acidosis
  21. 21. DIAGNOSTIC STRATEGIES CXR suspected… ◦ pneumonia, pneumothorax, ateltctasis, pn eumomediastinum, or CHF ECG should not be routinely obtained, except ◦ patients >40 yr, a separate complaint (e.g., chest pain), Hx of significant CVD ◦ severe asthma: a RV strain pattern Others ◦ LTE4 in the urine ◦ exhaled nitric oxide
  22. 22. Assessment Summary The severity of airflow obstruction cannot be accurately judged by patients’ symptoms, PE , and laboratory tests. Serial measurements of airflow obstruction (FEV1 or PEFR) are key components of disease assessment and response to therapy .
  23. 23. Peak Flow Meter
  24. 24. Management Emergency Treatment of Asthma, N ENGL J MED 363;8 august
  25. 25. Management Emergency Treatment of Asthma, N ENGL J MED 363;8 august
  26. 26. Management Emergency Treatment of Asthma, N ENGL J MED 363;8 august
  27. 27. Management Emergency Treatment of Asthma, N ENGL J MED 363;8 august
  28. 28. MedicationThe goal of treatment of acute asthma inthe ED is to reverse airflow obstructionrapidly by repetitive or continuousadministration of inhaled B 2-agonists, ensure adequate oxygenation, andrelieve inflammation
  29. 29. Medication1. Relievers - B2- adrenergic , Anticholinergics, Theophyli ne2. Controller - Glucocorticoids, Leukotriene modifiers, Cromones, Anti-IgE
  30. 30. β2-Adrenergic Agonists Relaxation of bronchial smooth muscle, inhibit mediator release and promote mucociliary clearance. Most common side effect: skeletal muscle tremor. ◦ others: nervousness, anxiety, insom nia, headache, hyperglycemia, palpitations, tachycardia, and hypertension.
  31. 31. β2-Adrenergic Agonists SABA (Solution=MDI) ◦ First line drug ◦ Nebulization = MDI + spacer (prefer nebulization) ◦ Salbutamol 2.5 – 5 * 3 time/hr ◦ MDI with spacer 4– 8 puffs q 20 min up to 4 h, then q 1–4 h as needed.
  32. 32. β2-Adrenergic Agonists IV form (not recommened in USA) ◦ severe nonresponsive acute asthma. ◦ albuterol loading dose 4 μg/kg for 2-5 min then infusion of 0.1 to 0.2 μg/kg/min ◦ Epinephrine IV titrated to effect (average 1.5 μg/min with a range of 0.5–13.3 μg/min) SC form ◦ may be used in pt who cannot adequately inhale albuterol or who experience severe bronchospasm. ◦ Epinephrine (1:1000 ) 0.2-0.5 mL q 20 -30 min ◦ Terbutaline 0.25 mg SC q 20 min * 3 dose
  33. 33. Corticosteroids Action in the airways ◦ inhibition of recruitment of inflammatory cells and inhibition of release of proinflammatory mediators and cytokines from activated inflammatory and epithelial cells, activate cytoplasmic glucocorticoid receptors to regulate directly or indirectly the transcription of certain target genes resulting in the synthesis of new proteins. Two forms ◦ 1. Systemic ◦ 2. Inhaled
  34. 34. Corticosteroids 1. Systemic (IV and oral) ◦ speeds the resolution of airflow obstruction, reduces the rate of relapse and may decrease admissions in severe, but not in mild to moderate attacks. ◦ Prednisone 40-60 mg oral loading ◦ Methylprednisolone 40–80 mg/day in one dose or two divided doses ◦ Demethasone 5 mg ◦ given q 6 hr until PEFR reaches 70% of predicted value or a personal best value
  35. 35. Corticosteroids IV = oral Side effects ◦ short-term (hours or days) reversible increases in glucose (important in diabetics) and decreases in potassium, fluid retention with wt gain, mood alterations including rare psychosis, hypertension, peptic ulcers, aseptic necrosis of the femur
  36. 36. Corticosteroids 2. Inhaled  ICS + SABA NB: reducing airway reactivity and edema more effectively  reduce rates of hospitalization  Side effect : Dysphonia, Reflex cough and bronchospasm, Oral candidiasis Discharged  Prednisone 40-60 mg oral for 7 day  ICS high-dose budesonide (400 μg, two puffs twice per day)
  37. 37. Anticholinergic AgentsAtropa BelladonnaLeave
  38. 38. Anticholinergic Agents Block smooth muscle constrictor and secretory consequences of the PNS, blocking reflex bronchoconstriction and reversing acute airway obstruction. affect large, central airways, but adrenergic drugs dilate smaller airways. Side effect ◦ dry mouth, thirst, and difficulty swallowing. Less commonly, tachycardia, restlessness, irritability, confusion, difficulty in micturition, ileus, blurring of vision, or an increase in IOP
  39. 39. Anticholinergic Agents Inhaled-ipratropium bromide ◦ Nebulizer solution (0.25 mg/ml) 0.5 mg q 20 min for 1 hr (three doses), then as needed; ◦ MDI (18 μg/puff) 8 puffs q 20 min as needed, for up to 3 hr ◦ not recommended as monotherapy in ED slow onset of action ◦ added to SABA for a greater and longer- lasting bronchodilator effect, reduce rates of hospitalization by approximately 25% in severe asthma Emergency Treatment of Asthma, N ENGL J MED 363;8 august
  40. 40. Magnesium Sulfate relaxes bronchial smooth muscle and dilates asthmatic airways. I/C (recommended IV > NB) ◦ severe asthma attacks (FEV1 < 25% predicted) improves airflow obstruction and decreases the need for hospital admission ◦ MgSO4 2 -3 g IV over 20 min or at rates of up to 1 g/min to patients with severe refractory asthma Side effect ◦ warmth, flushing, sweating, N/V, muscle weakness and loss of DTR, hypotension, and respiratory depression.
  41. 41. Treatments That Are NotRecommended 1. Methylxanthines ◦ lack of demonstrated efficacy and increases in adverse events 2. Antibiotics ◦ should be reserved for pt with bacterial infection (e.g., pneumonia or sinusitis) seems likely. 3. Aggressive hydration 4. Mucolytic agents ◦ worsen cough or airflow obstruction 5. Sedation Emergency Treatment of Asthma, N ENGL J MED 363;8 august
  42. 42. Leukotriene Modifiers non-beta-mediated bronchodilating effects Zafirlukast (20 mg twice a day) Montelukast (10 mg daily) Currently, there is no indication for the
  43. 43. Pregnancy The principles of managing acute asthma in pregnancy and during lactation are similar to those for the nonpregnant state. Early intervention during acute exacerbation is key to the prevention of impaired maternal and fetal oxygenation. PaO2 <70 mm Hg  severe hypoxemia PaCO2 >35 mm Hg  respiratory failure B2-agonist and ICS : safe during pregnancy and are recommended as a routine part of asthma management
  44. 44. NPPV BiPAP ◦ well tolerated by children , decrease the need for intubation and mechanical ventilation. ◦ Consider for pt. who decline intubation and pt. who cooperate with mask therapy ◦ but more data are needed to recommend this approach Patient must be alert mental status and intact airway reflexes Emergency Treatment of Asthma, N ENGL J MED 363;8 august
  45. 45. Ketamine potent bronchodilator effects no randomized trials have been conducted. not recommended for therapy of acute asthma in the nonintubated patient Ketamine 1–2 mg/kg IV Side effect ◦ increased airway secretions and emergence reactions
  46. 46. Intubation and VentilatorStrategy  Avoid nasotracheal route  Intubate before the crisis of respiratory arrest  Selected largest ET-tube as soon as possible.  Pretreatment ◦ Lidocaine 1.5 mg/kg IV  Induction ◦ Midazolam 1 mg IV q 2-3 min ◦ Ketamine 1–2 mg/kg IV  Neuromuscular blocking agent ◦ Preferred Rocuronium (1 mg/kg) > Rodrigo GJ, Rodrigo C, Hall JB. Acute asthma in adult: a review. Chest 2004; 125:
  47. 47. Intubation and VentilatorStrategy  Ventilator strategy ◦ adequate oxygenation and ventilation, minimizing high airway pressure, barotrauma, and systemic hypotension  Permissive hypercapnia technique ◦ TV 6–8 mL/kg, MV 6-8 LPM ◦ I:E > 1:3, RR 11-14 /min ◦ End-inspiratory pressure < 35 cmH2O ◦ pH maintained at 7.15–7.2 ◦ Paco2 <100 mm Hg
  48. 48. Intubation and VentilatorStrategy  Complications of mechanical ventilation ◦ Hypotension and barotrauma ◦ Pneumothorax !!!  sudden clinical deterioration  hypotension  significant rise in peak inspiratory ventilator pressures and falling oxygen saturation.  External lateral chest compression : patients cannot exhale esp; children
  49. 49. Cardiopulmonary arrest May result from unrecognized barotrauma. ◦ Empirical bilateral tube thoracostomy should be performed if unexplained cardiac arrest occurs, especially in the context of dramatic increases in peak inspiratory pressure. ◦ IV epinephrine has both cardiostimulatory and bronchodilatory properties.
  50. 50. DISPOSITION When should be discharged ◦ FEV or PEF after treatment is >= of the 11 personal best or predicted value ◦ Improvements in lung function and symptoms > 60 min Emergency Treatment of Asthma, N ENGL J MED 363;8 august
  51. 51. DISPOSITION Emergency Treatment of Asthma, N ENGL J MED 363;8 august
  52. 52. THANK YOU