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ASTHMA MANAGEMENT and EDUCATION INITIATIVE

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  1. ASTHMA MANAGEMENT andEDUCATION INITIATIVE JOB CORPS 2005 National Health and Wellness Conference Orlando, Florida June 7, 2005 Gary Strokosch, MD Region V Medical Consultant

  2. Guidelines for the Diagnosis and Management of Asthma--------------------------------------Update on Selected Topics - 2002 - • Expert Panel Report (EPR) – Update 2002 • National Asthma Education and Prevention Program (NAEPP) • NIH Publication No. 02-5074 • June 2003

  3. PREVIOUS REPORTS • 1997 Guidelines for the Diagnosis and Management of Asthma (EPR-2) • 1991 National Asthma Education and Prevention Program’s (NAEPP) first report

  4. AVAILABLE NAEPP PUBLICATIONS http://www.nhlbi.gov.nhlbi/nhlbi.htm (National Heart, Lung and Blood Institute)

  5. OBJECTIVE To give participants the tools to develop up-to-date individual management plans for JC students with asthma

  6. SCOPE OF ASTHMA - I • 11 million people reported having an asthma attack in 2000 • More than 5% of all children under 19 report asthma attacks in 2000 • In 2003 14.7% of teens 12-17 years of age have had asthma diagnosed

  7. SCOPE OF ASTHMA - II • 1999: 2 million ER visits • 1999: 478,000 hospitalizations for asthma • 1999: 4426 deaths from asthma • Mortality is 3 times higher in Black males than white males • Mortality is 2 ½ times higher in Black females than while females

  8. 2002 UPDATE OUTLINE • Overview of asthma • Medication Updates • Steroids Efficacy & Safety • Combination Therapy • Antibiotics • Monitoring Issues • Written Plans for Management • Peak Flow Vs. Symptom Monitoring • Management

  9. DEFINITION Asthma is a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role. ----------------------note---------------------- The ability to synthesize IgE antibody to environmental allergens (i.e., atopy) remains a major risk factor in asthma pathogenesis.

  10. NATURAL HISTORY OF PERSISTENT ASTHMA • The majority of children who wheeze before 3 years of age do not experience any more symptoms after 6 years of age. • A smaller group of children wheezing before 3 years of age go on to have persistent asthma. • A predictive index identified the following risk factors for developing persistent asthma

  11. PREDICTIVE INDEXMajor and Minor Risk Factors • Physician diagnosis of atopic dermatitis/eczema - OR - • Parental history of asthma --------- OR --------- • Two out of three of the following asthma-associated phenotypes: • Peripheral blood eosinophilia (>4%) • Wheezing apart from colds • Physician-diagnosed allergic rhinitis

  12. BIRTH COHORTFOLLOWED FOR 13 YEARS • 76% of those diagnosed with asthma after 6 years of age had a positive predictive index • 97% of those without a diagnosis of asthma after 6 years of age had a negative predictive index (Castro-Rodriguez, et.al. 2000)

  13. SPIROMETRYRecommends tests be done: • At the time of the initial assessment • After treatment is initiated and symptoms and PEF have stabilized • At least every 1-2 years

  14. SYMPTOM CLASSIFICATION • Severe Persistent • Moderate Persistent • Mild Persistent • Mild Intermittent

  15. SYMPTOM CLASSIFICATION • Severe Persistent • Day: continual • Night: frequent • Moderate Persistent • Day: daily • Night: >1/week • Mild Persistent • Day: >2/week (<1/day) [3-6/week] • Night: >2/month • Mild Intermittent • Day: 2/week • Night: 2/month

  16. TARGET OF THERAPY - I 1) Acute symptoms of asthma usually arise from BRONCHOSPASM and require and respond to bronchodilator therapy.

  17. TARGET OF THERAPY - II 2) Acute and chronic INFLAMMATION affects the airway caliber and airflow and also causes bronchial hyper responsiveness, resulting in susceptibility to bronchospasm. Therapy is with anti inflammatory drugs but may require weeks to achieve a successful response.

  18. TARGET OF THERAPY - III 3) Some patients experience persistent airflow limitations and this REMODELING has NO current therapy.

  19. INFLAMMATION This inflammation causes recurrent episodes of wheezing, breathlessness, chest tightness and cough, particularly at night and in the early morning.

  20. INFLAMMATION - I Airway inflammation in asthma is found in patients with mild, moderate and severe disease.

  21. INFLAMMATION – IIMild / Moderate Persistent Asthma • Inflammation of airway by inflammatory cells such as activated lymphocytes & eosinophils • Denudation of the epithelium • Deposition of collagen in the subbasement membrane area • Mast cell degranulation

  22. INFLAMMATION – IIISevere Persistent & Deaths from Asthma • Occlusion of bronchial lumen by mucous • Hyperplasia & hypertrophy of bronchial smooth muscle • Goblet cell hyperplasia

  23. IgE PATHOGENESIS • IgE antibodies are synthesized to environmental allergens (atopy) • Synthesized IgE binds to mast cells and basophils via high-affinity IgE receptors • These cells are signaled to release preformed and newly generated mediators, including histamine & cysteinyl leukotrienes to rapidly contract airway smooth muscle • Mast cells also produce a variety of cytokines (pro-inflammatory proteins) including interleukin (IL 1,2,3,4 &5), granulocyte-macrophage colony-stimulating factor, interferon and tumor necrosis factor-α

  24. ATOPY • Atopy is the genetic susceptibility to produce IgE ABs directed toward common environmental allergens, including house-dust mites, animal proteins, and fungi. • With the production of IgE ABs, mast cells and possibly other airway cells (e.g., lymphocytes) are sensitized and become activated when they encounter specific antigens. • Atopy has been found in 30 to 50% of the general population, therefore frequently found in the absence of asthma. • Atopy is one of the strongest predisposing factors in the development of asthma.

  25. EOSINOPHIL PATHOGENESIS • Infiltration seen in all acute inflammation & many patients with chronic persistent asthma • The granules are the source of inflammatory mediators • Injure airway epithelium • Enhance bronchial responsiveness • Affect acetylcholine release • Release cysteinyl leukotrienes to contract airway smooth muscle • Eosinophils are produced & released from bone marrow via IL-5, migrate to airway via a number of factors

  26. EOSINOPHIL PATHOGENESIS Although its role in pathophysiology is less clear, it is affected by anti-inflammatory therapy.

  27. ASTHMA MEDICATIONS • Beta2-Agonists • Corticosteroids • Leukotriene Modifiers • Methyl Xanthines • Cromolyn and Nedocromil • Anticholinergics

  28. ASTHMA MEDICATIONS • Beta2-Agonists • Injected • Short-acting inhaled • Long-acting inhaled • Corticosteroids • Inhaled • Systemic (oral) • Leukotriene Modifiers • Methyl Xanthines • Cromolyn and Nedocromil • Anticholinergics

  29. COMBINATIONASTHMA MEDICATIONS • Beta2-Agonists • Long-acting inhaled • Corticosteroids • Inhaled

  30. ADVAIR100/50, 250/50 & 500/50 • Fluticasone DPI 100/250/500 mcg • Salmererol DPI 50 mcg

  31. ASTHMA MEDICATIONS • Beta2-Agonists • Injected • Short-acting inhaled • Long-acting inhaled • Corticosteroids • Inhaled • Systemic (oral) • Leukotriene Modifiers • Methyl Xanthines • Cromolyn and Nedocromil • Anticholinergics

  32. ASTHMA MEDICATIONS • Beta2-Agonists • Short-acting inhaled • Anticholinergics

  33. COMBIVENTFor Use In COPD • Ipratropium 18 mcg/puff MDI • Albuterol 90 mcg/puff MDI • Ipratropium 0.5 mg/3ml Nebulizer Solution • Albuterol 2.5 mg/3ml Nebulizer Solution

  34. CORTICOSTEROID EFFICACY

  35. Does chronic use of inhaled corticosteroids improve long-term outcomes with mild or moderate persistent asthma, in comparison to the following treatment? • PRN beta2-agonists? • Long-acting beta2-agonists? • Theophylline? • Cromolyn/Nedocromil? • Combinations of above drugs?

  36. RESULT Inhaled corticosteroids improve long-term outcomes with mild or moderate persistent asthma, compared to previously outlined treatments.

  37. RECOMMENDATION Inhaled corticosteroids are the preferred treatment for initiating therapy for persistent asthma.

  38. CORTICOSTEROID SAFETY

  39. What are the long term adverse effects of chronic inhaled corticosteroid use on the following outcomes? • Vertical Growth? • Bone Mineral Density? • Ocular Toxicity (posterior subcapsular cataract and glaucoma)? • Suppression of adrenal/pituitary axis?

  40. RESULT The use of corticosteroids at recommended doses does not have long-term, clinically significant, or irreversible effects on any of the outcomes reviewed.

  41. LINEAR GROWTH • Growth reduction my occur from inadequate control of any chronic disease. • Although low/medium doses may have the potential of decreased growth velocity, the effects are small, nonprogressive and may be reversible. • When high doses are needed, the use of adjunctive therapy should be initiated in order to reduce the steroid dose. • Children and adolescents taking steroids by any route should be monitored for growth interference.

  42. BONE MINERAL DENSITY A small, dose-dependent reduction in BMD may be associated with inhaled corticosteroid use in patients older than 18 years of age, but the clinical significance of these findings is not clear.

  43. CATARACTS / GLAUCOMA In children, no significant effects are seen with low-to-medium doses. However, high (>2000 mg) cumulative lifetime doses of inhaled corticosteroids may increase slightly the prevalence of cataracts in two studies of adult and elderly patients.

  44. HPA AXIS FUNCTION Available evidence indicates that, on average, children may experience only clinically insignificant, if any, effects of low-to-medium dose of inhaled corticosteroids. Rare individuals may be more susceptible to their effects even at conventional doses.

  45. OVERALLRECOMMENDATION Inhaled corticosteroids are the preferred treatment for initiating therapy for persistent asthma.

  46. COMBINATION THERAPY:ADDITION OF OTHER LONG-TERM-CONTROL MEDICATIONS TO INHALED CORTICOSTEROIDS

  47. QUESTION In patients with moderate persistent asthma who are receiving inhaled corticosteroids, does addition of another long-term-control agent improve outcomes?

  48. ANSWER • Strong evidence consistently indicates that long-acting inhaled beta2-agonists added to low-to-medium inhaled corticosteroids improve outcomes. • Adding a leukotriene modifier or theophylline to inhaled corticosteroids also improves outcomes, but the evidence is not as substantial.

  49. RECOMMENDATION The preferred treatment for adults and children older than 5 years of age is the addition of long-acting inhaled beta2-agonists to low-to-medium doses of inhaled corticosteroids (not as a substitute).

  50. “JUST DOUBLE THE DOSE” Studies of adults in which the dose of inhaled corticosteroids was at least doubled consistently demonstrate improved outcomes when their asthma was not controlled with low-to-medium-doses of inhaled steroids, but these results are consistently less effective than adding a long-acting inhaled beta2-agonist.