Bronchial Asthma in Children

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Group didactics regarding Bronchial Asthma in Children. …

Group didactics regarding Bronchial Asthma in Children.
Source: GINA guidelines, Nelson's Textbook of Pediatrics 19th ed.

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  • Host factors predispose individuals to, or protect them from, developing asthmaEnvironmental factors influence susceptibility to development of asthma in predisposed individuals, precipitate asthma exacerbations, and/or cause symptoms to persist
  • In the predisposed host, immune responses to these common exposures can be a stimulus for prolonged, pathogenic inflammation and aberrant repair of injured airways tissues. Lung dysfunction (i.e., AHR and reduced airflow) develops. These pathogenic processes in the growing lung during early life adversely affect airways growth and differentiation, leading to altered airways at mature ages. Once asthma has developed, ongoing exposures appear to worsen it, driving disease persistence and increasing the risk of severe exacerbations.
  • We identified high risk children based on a modified asthma predictive index developed by Castro-Rodriguez using data from the Tucson CRS study.
  • Asthma can be diagnosed on the basis of a patient’s symptoms and medical history


  • 1. Jackie Lou C. Acha Clinical Clerk Department of Pediatrics- OPD
  • 2. Asthma  A chronic inflammatory condition of the lung airways resulting in episodic airflow obstruction  Chronic inflammation => heightened twitchiness of airways => Airways hyperresponsiveness (AHR) to provocative exposures
  • 3. Asthma  AHR leads to recurrent episodes of  Wheezing  breathlessness  Chest tightness  Coughing, at night or in early morning  symptoms are usually associated with widespread but variable airflow obstruction that is generally reversible either spontaneously or with treatment
  • 4. Epidemiology  One of the most common chronic diseases  ~300 M individuals affected worldwide  Prevalence increasing in many countries  Major cause of school/work absence
  • 5. Risk Factors for Asthma Environment -Allergens -Infections -Microbes -Pollutants -Stress Biological and Genetic Risk -Immune -Lung -Repair Age
  • 6. Host factors + Environmental factors ASTHMA
  • 7. Asthma Predictive Index  Identify high risk children (2 and 3 years of age):  ≥4 wheezing episodes in the past year (at least one must be MD diagnosed) PLUS OR One major criterion • Parent with asthma • Atopic dermatitis • Aero-allergen sensitivity  Two minor criteria • Food sensitivity • Peripheral eosinophilia (≥4%) • Wheezing not related to infection Modified from: Castro-Rodriguez JA, Holberg CJ, Wright AL, et al. A clinical index to define risk of asthma in young children with recurrent wheezing. Am J Respir Crit Care Med. 2000;162(4 Pt 1):1403–1406
  • 8. Pathophysiology
  • 9. Clinical Manifestations  Dry coughing  Expiratory wheezing  Chest tightness  Dyspnea commonly provoked by physical exertion and airways irritants (e.g., cold and dry air, environmental tobacco smoke)
  • 10. Diagnosis  History and patterns of symptoms  Physical examination  Measurements of lung functions  Measurements of allergic status to identify risk factors
  • 11. History and Patterns of Symptoms  Wheezing – high pitched whistling sounds when breathing out  History of any of the following  Cough, worse particularly at night  Recurrent wheeze  Recurrent difficult breathing  Recurrent chest tightness
  • 12. History and Patterns of Symptoms  Symptoms occur or worsen at night, awakening the patient  Symptoms occur or worsen in a seasonal pattern  Patient has eczema, hay fever, or a family history of asthma or atopic diseases
  • 13. History and Patterns of Symptoms  Symptoms occur or worsen in the presence of  Animals with fur  Aerosol chemicals  Changes in temperature  Domestic dust mites  Drugs (aspirin, beta blockers)  Exercise  Pollen  Respiratory infections  Smoke  Strong emotional expression
  • 14.  Symptoms respond to anti-asthma therapy  Patient’s cold go to the chest or take more than 10 days to clear up
  • 15. Physical Examination  During routine clinic visits  No abnormal signs  Normal chest examination  Deeper breaths can sometimes elicit otherwise undetectable wheezing  During asthma exacerbations  Expiratory wheezing  Prolonged expiratory phase  Decreased breath sounds in some of the lung fields  Crackles and rhonchi (excess mucous production)  Labored breathing and respiratory distress (retractions, nasal flaring
  • 16. Common viral infections of the respiratory tract Aeroallergens in sensitized asthmatics Animal dander Indoor allergens Dust mites Cockroaches Molds Seasonal aeroallergens Pollens (trees, grasses, weeds) Seasonal molds Environmental tobacco smoke Air pollutants Ozone Sulfur dioxide Particulate matter Wood- or coal-burning smoke Endotoxin, mycotoxins Dust Asthma Triggers Strong or noxious odors or fumes Perfumes, hairsprays Cleaning agents Occupational exposures Farm and barn exposures Formaldehydes, cedar, paint fumes Cold air, dry air Exercise Crying, laughter, hyperventilation Co-morbid conditions Rhinitis Sinusitis Gastroesophageal reflux
  • 17. UPPER RESPIRATORY TRACT CONDITIONS Allergic rhinitis[*] Chronic rhinitis[*] Sinusitis[*] Adenoidal or tonsillar hypertrophy Nasal foreign body MIDDLE RESPIRATORY TRACT CONDITIONS Laryngotracheobronchomalacia[*] Laryngotracheobronchitis (e.g., pertussis)[*] Laryngeal web, cyst, or stenosis Vocal cord dysfunction[*] Vocal cord paralysis Tracheoesophageal fistula Vascular ring, sling, or external mass compressing on the airway (e.g., tumor) Foreign body aspiration[*] Chronic bronchitis from environmental tobacco smoke exposure[*] Toxic inhalations Differential Diagnosis of Childhood Asthma LOWER RESPIRATORY TRACT CONDITIONS Bronchopulmonary dysplasia (chronic lung disease of preterm infants) Viral bronchiolitis[*] Gastroesophageal reflux[*] Causes of bronchiectasis: Cystic fibrosis Immune deficiency Allergic bronchopulmonary mycoses (e.g., aspergillosis) Chronic aspiration Immotile cilia syndrome, primary ciliary dyskinesia Bronchiolitis obliterans Interstitial lung diseases Hypersensitivity pneumonitis Pulmonary eosinophilia, Churg-Strauss vasculitis Pulmonary hemosiderosis Tuberculosis Pneumonia Pulmonary edema (e.g., congestive heart failure) Medications associated with chronic cough Acetylcholinesterase inhibitors β-adrenergic antagonists
  • 18. Asthma Severity Classification
  • 19. Levels of Asthma Control Characteristic Controlled Partly controlled (Any present in any week) Uncontrolled Daytime symptoms None (2 or less / week) More than twice / week 3 or more features of partly controlled asthma present in any week Limitations of activities None Any Nocturnal symptoms / awakening None Any Need for rescue / “reliever” treatment None (2 or less / week) More than twice / week Lung function (PEF or FEV1) Normal < 80% predicted or personal best (if known) on any day Exacerbation None One or more / year 1 in any week
  • 20. Classification of Severity of Asthma Exacerbation
  • 21. Treatment  The choice of treatment should be guided by:  Level of asthma control  Current treatment  Pharmacological properties and availability of the various forms of asthma treatment  Economic considerations Cultural preferences and differing health care systems need to be considered
  • 22. Controller Medications  Inhaled glucocorticosteroids  Leukotriene modifiers  Long-acting inhaled β2-agonists  Systemic glucocorticosteroids  Theophylline  Cromones  Long-acting oral β2-agonists  Anti-IgE  Systemic glucocorticosteroids
  • 23. Estimate Comparative Daily Dosages for Inhaled Glucocorticosteroids by Age Drug Low Daily Dose ( g) Medium Daily Dose ( g) High Daily Dose ( g) > 5 y Age < 5 y > 5 y Age < 5 y > 5 y Age < 5 y Beclomethasone 200-500 100-200 >500-1000 >200-400 >1000 >400 Budesonide 200-600 100-200 600-1000 >200-400 >1000 >400 Budesonide-Neb Inhalation Suspension 250-500 >500-1000 >1000 Ciclesonide 80 – 160 80-160 >160-320 >160-320 >320-1280 >320 Flunisolide 500-1000 500-750 >1000-2000 >750-1250 >2000 >1250 Fluticasone 100-250 100-200 >250-500 >200-500 >500 >500 Mometasone furoate 200-400 100-200 > 400-800 >200-400 >800-1200 >400 Triamcinolone acetonide 400-1000 400-800 >1000-2000 >800-1200 >2000 >1200
  • 24. Reliever Medications  Rapid-acting inhaled β2-agonists  Systemic glucocorticosteroids  Anticholinergics  Theophylline  Short-acting oral β2-agonists
  • 25. Component 4: Asthma Management and Prevention Program Allergen-specific Immunotherapy  Greatest benefit of specific immunotherapy using allergen extracts has been obtained in the treatment of allergic rhinitis  The role of specific immunotherapy in asthma is limited  Specific immunotherapy should be considered only after strict environmental avoidance and pharmacologic intervention, including inhaled glucocorticosteroids, have failed to control asthma  Perform only by trained physician
  • 26. controlled partly controlled uncontrolled exacerbation LEVEL OF CONTROL maintain and find lowest controlling step consider stepping up to gain control step up until controlled treat as exacerbation TREATMENT OF ACTION TREATMENT STEPS REDUCE INCREASE STEP 1 STEP 2 STEP 3 STEP 4 STEP 5 REDUCEINCREASE
  • 27. Step 1 – As-needed reliever medication  Patients with occasional daytime symptoms of short duration  A rapid-acting inhaled β2-agonist is the recommended reliever treatment (Evidence A)  When symptoms are more frequent, and/or worsen periodically, patients require regular controller treatment (step 2 or higher) Treating to Achieve Asthma Control
  • 28. Step 2 – Reliever medication plus a single controller  A low-dose inhaled glucocorticosteroid is recommended as the initial controller treatment for patients of all ages (Evidence A)  Alternative controller medications include leukotriene modifiers (Evidence A) appropriate for patients unable/unwilling to use inhaled glucocorticosteroids Treating to Achieve Asthma Control
  • 29. Step 3 – Reliever medication plus one or two controllers  For adults and adolescents, combine a low-dose inhaled glucocorticosteroid with an inhaled long- acting β2-agonist either in a combination inhaler device or as separate components (Evidence A)  Inhaled long-acting β2-agonist must not be used as monotherapy  For children, increase to a medium-dose inhaled glucocorticosteroid (Evidence A) Treating to Achieve Asthma Control
  • 30. Additional Step 3 Options for Adolescents and Adults  Increase to medium-dose inhaled glucocorticosteroid (Evidence A)  Low-dose inhaled glucocorticosteroid combined with leukotriene modifiers (Evidence A)  Low-dose sustained-release theophylline (Evidence B) Treating to Achieve Asthma Control
  • 31. Step 4 – Reliever medication plus two or more controllers  Medium- or high-dose inhaled glucocorticosteroid combined with a long-acting inhaled β2-agonist (Evidence A)  Medium- or high-dose inhaled glucocorticosteroid combined with leukotriene modifiers (Evidence A)  Low-dose sustained-release theophylline added to medium- or high-dose inhaled glucocorticosteroid combined with a long-acting inhaled β2-agonist (Evidence B) Treating to Achieve Asthma Control
  • 32. Treating to Achieve Asthma Control Step 5 – Reliever medication plus additional controller options  Addition of oral glucocorticosteroids to other controller medications may be effective (Evidence D) but is associated with severe side effects (Evidence A)  Addition of anti-IgE treatment to other controller medications improves control of allergic asthma when control has not been achieved on other medications (Evidence A)
  • 33. Treating to Maintain Asthma Control  When control as been achieved, ongoing monitoring is essential to: - maintain control - establish lowest step/dose treatment
  • 34. Treating to Maintain Asthma Control Stepping down treatment when asthma is controlled  When controlled on medium- to high-dose inhaled glucocorticosteroids: 50% dose reduction at 3 month intervals (Evidence B)  When controlled on low-dose inhaled glucocorticosteroids: switch to once-daily dosing (Evidence A)
  • 35. Treating to Maintain Asthma Control Stepping down treatment when asthma is controlled  When controlled on combination inhaled glucocorticosteroids and long-acting inhaled β2- agonist, reduce dose of inhaled glucocorticosteroid by 50% while continuing the long-acting β2-agonist (Evidence B)  If control is maintained, reduce to low-dose inhaled glucocorticosteroids and stop long-acting β2-agonist (Evidence D)
  • 36. Treating to Maintain Asthma Control Stepping up treatment in response to loss of control  Rapid-onset, short-acting or long- acting inhaled β2-agonist bronchodilators provide temporary relief.  Need for repeated dosing over more than one/two days signals need for possible increase in controller therapy
  • 37. Prevention  hygiene hypothesis  naturally occurring microbial exposures in early life might drive early immune development away from allergen sensitization, persistent airways inflammation, and remodeling Other measures: avoidance of environmental tobacco smoke (beginning prenatally) prolonged breastfeeding (>4 mo) an active lifestyle and a healthy diet
  • 38. Thank you..