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Bronchial asthma

DR SHYAM SUDHIR PROF YMC. Bronchial asthma. Epidemiology Pathophysiology Diagnosis. asthma. Childhood bronchial asthma is characterized by Airway obstruction – due to muscle spasm associated with mucosal oedema and stagnation of the mucus - which is reversible

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Bronchial asthma

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  1. DR SHYAM SUDHIR PROF YMC Bronchial asthma

  2. Epidemiology Pathophysiology Diagnosis asthma

  3. Childhood bronchial asthma is characterized by • Airway obstruction – due to muscle spasm associated with mucosal oedema and stagnation of the mucus - which is reversible • Airway inflammation • Airway hyper responsiveness- virus and irritants • Airway remodeling in uncontrolled asthma. CHILDHOOD ASTHMA

  4. > 9% 6 to < 9% 3 to 6% < 3% Worldwide Asthma prevalence (adolescents outside Europe) ISAAC Steering Committee, Lancet 1998

  5. Worldwide variation in prevalence Variation within countries ISAAC study – prevalence up to 25% More than 180,000 people die of asthma each year 5,000 deaths in the United States Prevalence of Bronchial Asthma

  6. Asthma components Asthmatic Airway Healthy Airway Mucus and plasma exudation Inflammation and oedema Alveolar septum Smooth muscle Epithelium Smooth muscle contraction Epithelial shedding / damage

  7. ASTHMA – AN INFLAMMATORY DISEASE Asthma Normal

  8. INFLAMMATION INDUCERS Allergens, Chemical sensitisers, Air pollutants, Virus infections Airway Hyperresponsiveness Airflow Limitation SYMPTOMS Cough Wheeze Chest tightness Dyspnoea TRIGGERS Allergens, Exercise Cold Air, SO2 Particulates

  9. Modern view of Asthma Allergen Macrophage/ dendritic cell Mast cell Th2 cell Neutrophil Eosinophil Mucus plug Epithelial shedding Nerve activation Subepithelial fibrosis Plasma leak Oedema Sensory nerve activation Vasodilatation New vessels Cholinergic reflex Mucus hypersecretion Hyperplasia Bronchoconstriction Hypertrophy / hyperplasia

  10. Inflammation in Asthma Acute inflammation Steroid response Chronic inflammation Airway remodeling Structural changes Time

  11. Bronchial asthma is an iceberg disease Classical features Persistent cough, wheezing and dyspnoea are seen in 30% Atypical features Cough-variant asthma Nocturnal asthma Activity-induced asthma Persistent cough after an URI Recurrent pneumonia at different sites/ same site (middle lobe) Diagnosis

  12. Diagnosis is mainly clinical Episodic symptoms of airflow obstruction, more than 3 episodes are present Airway obstruction is reversible Alternative diagnoses are excluded Guidelines for diagnosis

  13. ALLERGENS animal dander dust mites pollen fungi Ask about Triggers Symptoms can occur or worsen in the presence of: • OTHERS • exercise • viral infection • smoke • changes in temperature • strong emotional expression • aerosol chemicals • drugs (NSAIDs, ß-blockers)

  14. Routine blood counts may not help Peripheral smear may show eosinophilia X–ray chest to rule out tuberculosis Sputum examination for eosinophils and Curschmanns spiral bodies – rarely needed Pulmonary function tests – Gold Standard Spirometry Peak Expiratory flow rate Investigations

  15. Simple, Cheap and convenient It is the fastest rate at which air can move through the airways during a forced expiration starting with fully inflated lungs PEFR correlates well with FEV1 Used in children above 6 years Useful for monitoring the patient both at home and office Peak expiratory flow rate (PEFR)

  16. Peak Flow Meter

  17. For diagnosis and monitoring of asthma. PEFR taken regularly can give a warning of an impending attack of bronchospasm before it starts. One can prevent it by stepping up the preventive therapies. Long term follow up: Personal-best PEFR persistently below 20–30% would indicate worsening of control of the disease. Uses of PEFR

  18. Gold standard for diagnosis Smaller children cannot perform adequately Spirometry FEV1 – The amount of air forcefully expired in the first second of an FVC manoeuvre FVC – The maximum amount of air forcefully expired after maximum inspiration. FEV1/FVC ratio less than 80% indicates airflow obstruction

  19. Volume FEV1 Normal Subject Asthmatic (After Bronchodilator) Asthmatic (Before Bronchodilator) 1 2 3 4 5 Time (sec) Typical Spirometric (FEV1) Tracings Note: Each FEV1 curve represents the highest of t hree repeat measurements

  20. Differential Diagnosis of wheezing

  21. Treatment of Bronchial Asthma

  22. Freedom from • Acute asthma attacks • Symptoms including nocturnal cough • Emergency doctor/hospital visits • Minimal need for quick relief (as needed) ß2-agonist • Minimal (or no) adverse effects from medicine • Normal • Physical activity including participation in sports • Maintain lung function as close to normal as possible • Growth Charts Treatment objectives

  23. Identify and avoid triggers that make asthma worse Achieve control by selecting appropriate medication Treat asthma attacks promptly and effectively Educate patients to manage their condition Monitor and modify asthma care to maintain effective long-term control Treatment strategy

  24. Classify Asthma severity at the start of treatment

  25. Drugs Relievers • To treat bronchospasm and relieve acute attacks Controllers • For prevention of further attacks

  26. RelieversCONTROLLERS • Selectiveshort-acting 2-agonistsSalbutamolTerbutaline • Non selective-agonistAdrenaline • Inhaled steroidsBeclomethasonedipropionateBudesonideFluticasone propionate • Mast cell stabilisers Sodium cromoglycateNedocromil Sodium

  27. Relievers Controllers • AnticholinergicsIpratropium bromide • Oral steroids • Theophylline • Long acting 2-agonist Salmeterol, Formoterol • Methyl XanthinesSustained-release theophylline • Oral Prednisolone • Leukotriene antagonistsMontelukast, Zafirlukast, Pranlukast

  28. Omalizumab—a recombinant humanised monoclonal anti-IgE antibody • Soft steroids– Ciclesonide ) • Phosphodiesterase 4 inhibitor-cilomilast. • Anti IL-5 therapy. • Vaccine.. NEW DRUGS

  29. Soluble cytokine receptors as thearapeutic agents. NuvanceNebulisation • Single Isomer -agonists Levalbuterol (S-albuterol) Dose required is less than that of R-albuterol • Respirable antisense oligonucleotides eg: EPI- 2010

  30. Step 1: Intermittent asthma • Reliever • Inhaled 2-agonist prn (not more than 3 times a week) • Inhaled 2-agonist or cromone prior to exercise or allergen exposure Controller None required Avoid or control triggers Grade 1

  31. Management of Persistent Asthma

  32. Beclomethasone Propionate (BDP) Budesonide (BUD) Fluticasone (FP) Dose Low dose < 400 mcg Medium dose < 400–800 mcg High dose > 800 mcg. Inhaled steroids – First line treatment

  33. Step 2: Mild persistent asthma • Reliever • Inhaled 2-agonist prn (but less than 3-4 times per day) • Controller • Daily low dose inhaled corticosteroid (<400 g) OR • Inhaled sodium cromoglycate Avoid or control triggers Grade 2 • Nedocromil or leukotriene ↑ use may indicate need for modifier, sustained release long term control therapy theophylline

  34. Step 3: Moderate persistent asthma • Reliever • Inhaled 2-agonist prn • ↑use may indicate need for long term control therapy • Preventer • Daily low dose inhaled steroid + a) inhaled long-acting ß2 agonist (may provide better control of symptoms) OR + • b) LTM, SR Theophylline and long acting ß agonist OR Avoid or control triggers Grade 3 • Daily medium dose corticosteroid • 400-800 g LTM:Leukotriene modifier

  35. Step 4: Severe persistent asthma • Reliever • Inhaled 2-agonist prn (but less than 3-4 times per day) • ↑use may indicate need for long term control therapy • Controller • Daily high dose inhaled corticosteroid > 800g OR • Daily medium dose ICS + • Daily long-acting bronchodilator +theophylline or LTM • Daily oral corticosteroid tablets or syrup • during acute exacerbation of asthma Avoid or control triggers Grade 4

  36. The only drug recommended in children is Montelukast – for children > 1 year Dose – 4-5 mg once daily Indications – Mild persistent Asthma – Exercise induced Asthma – Aspirin induced Asthma -- As an add-on agent at steps 2,3,and 4 when inhaled steroids are not enough Disadvantage – Poor efficacy (compared to inhaled steroids) – Few responders (unpredictable) – Expensive – Headaches (in 10%) – Weak anti–inflammatory effect Role of Leukotriene antagonists

  37. STEP 4: SEVERE PERSISTENT • PREVENTER: daily multiple medications • Inhaled high dose steroid • Long-acting bronchodilator • Oral steroid, theophylline,LTM • RELIEVER • Inhaled ß2-agonist p.r.n. Step down when controlled Avoid or control triggers STEP 3: MODERATE PERSISTENT • PREVENTER: daily medications • Inhaled low dose steroid and long-acting bronchodilator OR • Inhaled medium dose steroid • LTM,Theophylline • RELIEVER • Inhaled ß2-agonist p.r.n. • Patient education essential at every step • Reduce therapy if controlled for at least3 months • Continue monitoring Avoid or control triggers STEP 2: MILD PERSISTENT • PREVENTERr: daily • medications • Inhaled low dose steroid • Or possibly cromone • LTM,Theophylline • RELIEVER • Inhaled ß2-agonist p.r.n. Avoid or control triggers STEP 1: INTERMITTENT • RELIEVER • Inhaled ß2-agonist p.r.n. PRENVENTER:None Step upif not controlled (after check on inhaler technique and compliance) Avoid or control triggers TREATMENT

  38. Management of Acute Severe Asthma

  39. Too breathless to feed Respiratory rate > 50 min Heart rate > 140 / min PEFR < 50% of the best Poor or only transient (<2hr) response to bronchodilator Worsening despite 2–3 doses of recent dose of bronchodilator at 15 minutes interval Severe acute attack

  40. Unable to talk or cry Cyanosis Feeble chest movements Absent breath sounds Fatigue or exhausted Agitated Altered sensorium Oxygen saturation < 91% in pulse oximeter Life-Threatening Asthma is characterized by

  41. Assessment of severity of an acute attack of bronchial asthma can be done by a simple scoring system called pulmonary score Index (PSI)–(PCNA December ‘99)

  42. Pulmonary score index Respiratory Rate Wheezing Accessory muscle 6years > 6 yearsSternomastoid activity SCORE 0 < 30 < 20 None No apparent activity 1 31–45 21–35 Terminal Questionable expiration with stethoscope 2 46–60 36–50 Entire expiration Increase apparent with stethoscope 3 > 60 > 50 During inspiration Maximal activity and expiration without stethoscope Score0–3 Mild If no wheezing due to minimal air exchange, score-3 4–6 Moderate > 6 Severe Those children whose score is > 6 should be admitted to a paediatric ICU

  43. Oxygen Adequate hydration Nebulised2-agonist, Intravenous beta agonist Electrolyte balance (hypokalemia due to repeated salbutamolnebulisations) Anticholinergic drugs Steroids S.C.inj of Epinephrine or S.C.inj agonists in severe cases Magnesium sulphate Ketamine IV Aminophylline Heliox Mechanical Ventilation Management

  44. Hypoxia is due to ventilation perfusion mismatch. –agonists may increase hypoxia by attenuating the hypoxic pulmonary vasoconstriction, hence oxygen should always be administered along with nebulised-agonist. Maintain oxygen saturation between 90–95%. Oxygen

  45. –agonists are the drug of choice in asthma. Patients with acute severe asthma will require and tolerate higher doses Dose of salbutamol - 0.15 mg/kg, minimum 0.25 ml for < 6 months, 0.5 ml for > 6 months, 0.5 – 1 ml for older children and adults. Dilute in normal saline only, never distilled water. Nebulised2-Agonists

  46. Steroids reduce inflammation in this predominantly inflammatory illness Should be used early in all patients with acute severe asthma Hydrocortisone or methylprednisolone (MPS) may be administered IV if patient is unable to take oral steroids Steroids

  47. Dose: MPS 2mg/kg stat followed by 1mg/kg q 6 hr OR Hydrocortisone 10mg/kg stat followed by 5mg/kg q 6 hr IV steroids may be stopped after 48 hours or after improvement commences to thrice daily dosages Oral or IV steroids are of more therapeutic value in the treatment of acute severe asthma Inhaled or nebulised steroids are generally used as preventive therapy. However, some reports show benefits even in acute asthma Rescue steroids

  48. Useful as an adjunct with salbutamol in the treatment of acute severe asthma Dose: < 1year – 0.5ml , > 1year – 1ml Has longer duration of action and less systemic side effects compared to atropine Smaller children with spasmodic cough respond well to Ipratropium as compared to Salbutamol Anticholinergic agents: Ipratropium

  49. Useful in severe asthmatics Mechanism: Calcium channel modulation results in decreased acetylcholine and histamine release Efficacy, dose and frequency have not been clearly worked out To be reserved for use in severe resistant asthma not responding to routine therapy Magnesium Sulphate

  50. Suggested dose 25–50mg/kg to be diluted in normal saline and administered as an infusion over ½ hour Side effects Tachycardia/bradycardia, hypotension, muscle weakness at higher serum level

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