KENYA MEDICAL ASSOCIATION

CME: SAROVA PANAFRIC HOTEL

ASTHMA UPDATE

DR. JOSEPH A ALUOCH F.R.C.P., E.B.S.,

2nd JUNE 2011

Epidemiology/pathology

Between 100 - 150 million people suffer from asthma worldwide 1

Worldwide prevalence rates are increasing, on average, by 50% per decade 1

Worldwide, costs of asthma greater than Tuberculosis and HIV / AIDS 1

Major factors contributing to asthma morbidity and mortality are underdiagnosis and inappropriate treatment 2

1. WHO Bronchial Asthma Fact Sheet 20002. GINA Guidelines 1998

Facts and Figures

ASTHMA

Less understanding of Aetiology/Pathogenesis Genetics complex Control of Airway Tone? Reversible AWO: variability BHR Asthma no single aetiology Chronic Inflammation Dynamic Process Healing and Repair (Remodelling)

ASTHMA THE DISEASE

No clear concept of normality Disease variation Lack of correlation between disease and

outcome Patient understanding the severity. Lack of correlation between FEV and other

outcome.

Defining asthma can be difficult !

Defining Asthma

Bronchial hyperresponsiveness Airway inflammation

Central features, but not defining for individual characteristics of phenotypes

DEFINITION

Asthma is a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role

The ability to synthesize IgE antibody to environmental allergens (i.e., atopy) remains a major risk factor in asthma pathogenesis.

INFLAMMATION IN ASTHMA

MECHANISM: CHANGES PROCESS

ASSESSMENT

HISTOLOGICAL CHANGES

INFLAMMATORY CELLS

LOCAL FACTOR FACTORS

:STILL LARGELY UNCLEAR: PRIMARY OR SECONDARY: INITIATION:PERSISTENCE PROGRESSE.C.P, N.O, PEFR;RELATION TO SEVERITY: NON-ALLERGIC:ATOPY:EXERCISE INDUCED:PRIMARY:SECONDARY:LUNG TRANSPLANT:ATOPY:ENVIRONMENT

INDUCERSAllergens,Chemical sensitisers,Air pollutants, Virus infections

INFLAMMATION

TRIGGERSAllergens, Exercise

Cold Air, SO2 Particulates

SYMPTOMSCough WheezeChest tightness

Dyspnoea

AirwayHyper-responsiveness Airflow Limitation

ASTHMA UPDATE

OTHER FACTORS LIMITING AIRFLOW Airway edema secondary to eosinophilic

inflammation Mucus hypersecretion Structural changes i.e. hypertrophy and

hyperplasia of smooth muscular tissue; tissue fibrosis as part of remodeling.

Inflammatary Cells

Mast Cells

Eosinophils

Th2 Cells

Basophils

Platelets

Structural Cells

Epithelial Cells

Smooth Muscles Cells

Fibroblast

Nerves

Mediators

Histamine

Leukotrienes

Prostanoids

PAF

Kinins

Adenosine

Endothelins

Nitric Oxide

Cytokines

Chemokines

Growth Factors

Effects

Bronchospasm

Plasma exudation

Mucus secretion

AHR

Structural Changes

IgE PATHOGENESIS

1. IgE antibodies are synthesized to environmental allergens (atopy)

2. Synthesized IgE binds to mast cells and basophils via high-affinity IgE receptors

3. These cells are signaled to release preformed and newly generated mediators, including histamine & cysteinyl leukotrienes to rapidly contract airway smooth muscle

4. 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

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.

EOSINOPHIL PATHOGENESIS

1. Infiltration seen in all acute inflammation & many patients with chronic persistent asthma

2. The granules are the source of inflammatory mediators

Injure airway epithelium Enhance bronchial responsiveness Affect acetylcholine release

3. Release cysteinyl leukotrienes to contract airway smooth muscle

4. Eosinophils are produced & released from bone marrow via IL-5, migrate to airway via a number of factors

EOSINOPHIL PATHOGENESIS

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

Reversibility of airways’ obstruction Increased PEF >15% 15-20 minutes after inhaling ß2-agonist

Variability of airways’ obstruction PEF varies between morning and evening

>20% in patients taking bronchodilator>10% in patients not taking bronchodilator

Exercise-induced airways’ obstruction Decreased PEF >15% after 6 minutes of exercise

GINA Guidelines 1998

Reversible and variable airflow limitation

ASTHMA UPDATE

AIRFLOW LIMITATION Bronchoconstriction occurs secondary to release of multi-mediators (histamine, leukotrienes, prostaglandins, PAF etc.

Aeroallergen sensitivity Aspirin ( Non-IgE) Multi-factorial (exercise and cold air-osmotic;

airborne irritants, laughing, GERD & sinusitis via neurogenic reflex; infections)

GOAL OF MANAGEMENT

Minimal (ideally no) chronic (inc. nocturnal) symptoms

Minimal (infrequent ) exacerbations No emergency visits Minimal need for prn Beta2-agonists No limitations on activities (inc. exercise) Near normal PEFR & variability <20% Minimal (or no ) adverse effects from medicine

Control

Day time symptoms Limitation of activities Nocturnal symptoms Nocturnal awakenings Use of rescue medications Objective Ass. Lung F.Test

ASTHMA UPDATE NEW DIRECTIONS

CHANGES IN GUIDELINES CONTROL VS. SEVERITY

HETEROGENEITY REGARDING ETIOLOGY DIFFERENT PHENOTYPES

DIFFERENTIAL DIAGNOSIS- MASQUERADERS BETTER MONITORING

ASTHMA EDUCATION BETTER SELF MONITORING MEDICAL MONITORING:SPIROMETRY

NEW THERAPIES INHALED STEROIDS WITH NO OR MINIMAL BIOVAILABILITY OTHER NEW MOLECULES IMPROVED IMMUNOTHERAPIES IMPROVED EMPHASIS ON SELF-IMPROVEMENT: NUTRITION;

PERSONAL HABITS; HOME ENVIRONMENT

ASTHMA UPDATE

EARLY IDENTIFICATION OF HIGH RISK PATIENTS: IMMEDIATE CONCERNS:

Improve quality of life Reduce risk for hospitalizations and death.

LONG TERM CONCERNS: Prevent irreversible changes in airway structure i.e.

remodeling with sub-basement fibrosis, mucus hypersecretion, s.m hypertrophy, & injury of lining (epithelium).

SYMPTOM CLASSIFICATION

Severe Persistent

Moderate Persistent

Mild Persistent

Mild Intermittent

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

ASTHMA UPDATE

AIRWAY HYPER-RESPONSIVENESS (TWITCHY LUNGS) Exaggerated bronchoconstrictor response to

stimuli- triggers such as exercise, cold air, laughing, stress.

Defined by methacholine/adenosine/mannitol responsiveness

Rx directed towards reducing inflammation can reduce airway hyper-responsiveness.

ASTHMA UPDATE

HETEROGENOUS PHENOTYPES OF ASTHMA:

Different patterns of inflammation-targets for eventual treatment

Many patients have overlapping phenotypes. Intermittent; Persistent Atopic (extrinsic) vs. Intrinsic Exercise induced Aspirin sensitive Late Onset Infection induced (RSV; parainfluenza; adenovirus,

rhinovirus) Cough variant asthma Steroid resistant

ASTHMA UPDATE

ESTABLISH DIAGNOSIS OF ASTHMA: History, physical and PFT to establish there are

symptoms of airflow obstruction and/or airway hyperresponsiveness;

At least evidence for reversibility Value of history

What are the triggers in the home? Outdoor triggers?-pollens, time of year What else triggers asthma- aspirin, NSAIDs, URI’s cold air

exercise, forest fires, smoking; positioning, foods, Family history

ASTHMA UPDATE

Differential diagnosis:co-morbidities GERD; vocal cord dysfunction; foreign body; anatomical abn; hypersensitivity bronchopulmonary aspergillosis; Chronic sinusitis

Churg’s syndrome; Samter’s syndrome; Cystic Fibrosis bronchiectasis; sleep apnea with aspiration; occupation and hobbies (birds); wheezing” with COPD

ASTHMA UPDATE

PHYSICAL EXAM: Nasal exam- polyps Level of wheezing (high, low)

High level over trachea: consider vocal cord dysfunction Hyperexpansion of chest

Signs of chronicity i.e.(clubbing); consider bronchiectasis, COPD, C.F.

Signs of hypoxemia (cyanotic nail beds) Lymphadenopathy or lack of with history of recurring

respiratory infections (consider ID workup) Keep in mind undiagnosed adult CF (sweat test is not

useful in adults)

ASTHMA UPDATELABORATORY EVALUATION:

r/o Atopy: skin tests properly applied and interpreted; Properly performed PFT pre and post BD

PEF > FEV1; Expiration plateau for at least 6 seconds Reproducibility with BD- at least 2 measurements with FEV1

within 0.15 L. Reversibility in adults: >250 ml; FEV1> 12% or

> 10% increase of pred FEV1% for adults. Later may separate COPD from asthma. May need oral steroids for reversibility.

FEV1/FVC% should be included for children .

ASTHMA UPDATE

Laboratory evaluation: Other PFT:

Inspiratory loop for VCD Methacholine challenge

Nasal exam/endoscopy- polyps; sinusitis;VCD Chest Xray/ CT of chest on rare occasion Sinus CT Trial with protonics as a diagnostic tool (pH

studies) Consider bronchoscopy and lung biopsy for

difficult to diagnose and/or treat.

ASTHMA UPDATE

NIH Guidelines: asthma classification Initially severity assessment:

Based on medication usage; history of recent exacerbations, PFT; night time awakenings; persistent or intermittent.

Initial Rx based on classification of severity Manage based on control of symptoms i.e. more

functional emphasis: Use of rescue meds Night time awakenings Exacerbation rate Objective parameters –PFT; NO measurements

ASTHMA UPDATE

Goals of Therapy Reduce impairment (current)

Prevent troublesome symptoms (cough, breathlessness with exertion and at night)

Reduce frequent use of SABA to < 2 days a week Maintain near normal PFT Maintain normal activity

Reduce risk (future) Exacerbations Prevent ER visits and hospitalizations Prevent loss of lung function; children-prevent reduced lung

growth

Managing asthma needs brains !

UPDATE ON ASTHMA

Therapeutic Strategies to Improve Control: Education: preferably by experienced or

certified asthma educator: Peak flows- setting parameters of when to call. Awareness of questions to ask: nocturnal

awakenings, use of rescue meds. Asthma treatment plan: what to do when sx develop. How to use medications and when- very important Compliance checks

ASTHMA UPDATE

Environmental & Personal Health Strategies Eliminate tobacco smoke ( in utero and passive)

Associated with severity and dec. response to steroid Rx.

Air pollution- forest fires Wood burning stoves Use of air purifier (HEPA) especially near open

windows during pollen seasons

UPDATE ON ASTHMA

Environmental & Personal Health Strategies Encourage breast feeding up to 6 months to

minimize food allergy induction Home environmental control Individualize recommendations for aerobics in cold

weather and during peak pollen counts. Speculative HYGIENE THEORY but worth noting:

early exposure to daycare; rural environment; early exposure to animals- Favor immune responses away from allergy development;

antibiotic use; Western lifestyle- Favor immune responses towards allergy responses.

UPDATE ON ASTHMA

Environmental & Personal Health Strategies Control co-morbidities that can increase asthma:

Allergic rhinitis/sinusitis –studies demonstrate that regular use of nasal steroids and/or AH reduce asthma flares and ER visits

GERD- use of protonics decreases asthma. Obesity-dieting is important

Leptin increases in obesity: inc. IgE sensitization Adiponectin decreases in obesity: enhancing remodeling and

increased inflammation. CPAP for sleep apnea can help control obesity, aspiration New concerns: overuse of vitamins, folic acid in pregnancy may

be increase incidence of asthma: based on mice studies.

ASTHMA UPDATE

MONITORING ASTHMA TO ASSESS CONTROL: Symptom retrieval- ACT Spirometrics- frequency Other Monitoring Parameters

Peak flow measurements Sputum Eosinophils Nitric Oxide and pH Measurements on Exhaled Air

ASTHMA UPDATE

Sputum eosinophils : correlates with inflammatory response but impractical

NO produced by epithelial and alveoli cells. Correlates with eosinophil bronchial lavage studies

Many convincing studies that suggest NO can be used to reflect status of eosinophilic inflammation in asthma.

May be best used as a compliance check with inhaled steroids.

ASTHMA UPDATE

Medications: Rescue medications and long term beta agonists:

Controversy re’ LABA. New data supports use with ICS. Xopenex® vs. albuterol

Inhaled corticosteroids- reduced decline in lung function (FEV1)

Mometasone and ciclesonide –both have minimal or no bioavailability (absorption)

Dynamic dosing- use of ICS as a burst to treat exacerbations in well controlled asthma patients and normal lung function

ASTHMA UPDATE

TARGETED THERAPY:

IgE- anti-IgE (Xolair) Leukotrienes (anti-leukotrienes – Singulair;

Zyflo Trials with Anti-IL-5- reduce eosinophils Anti- IL-4 trials-reduce IgE

ASTHMA UPDATE

Monoclonal anti-IgE (Xolair) Must be used for difficult to manage severe and persistent asthmatics

Resistant to high dose inhaled steroids Require oral steroids

Must have IgE levels in a certain range Expensive Does it work –in some cases, noticeable reduction in exacerbations Side effects-anaphylaxis-very rare but requires close observation for 2

hours after dose. Leukotriene modifiers:

Montelukast ( prevents exercise induction up to 24 hrs- single dose) Zyflo ( aspirin sensitive asthmatics)

ASTHMA UPDATE

Approaches Based on Hygiene Theory Shifting Th2 to Th1 to modify asthma. The shift to Th1

induces IL-2 and IFN critical in defense against infection

Alter balance between Th1 and Th2- towards Th1 by immunotherapies

SLIT vs. SCIT Factors favoring Th1:

Older siblings; early exposure to daycare; rural environment; certain infections (TB, measles, hep A); early exposure to animals;

Factors favoring Th2: Antibiotic use; Western lifestyle; urban environment; diet;

house dust mite and cockroach sensitization; RSV

Potential Treatments for Acute Asthma

B-agonists Corticosteroids Oxygen Intubation &

Mechanical Ventilation

Methylxanthines Ipratropium

Bromide BiPAP Heliox MgSO4 Infusion

Mucolytics Chest Physical

Therapy Aggressive

Hydration Antibiotics Inhalational

Anesthetics ECMO Inhalational

Furosemide Inhalational

MgSO4

Methylxanthines (Theophylline)

Used for over 50 years to treat asthma Poorly understood mechanism of action Physiologic effects thought to include

bronchodilation, stimulation of diaphragmatic contractility, mucocilliary clearance, and possibly some anti-inflammatory effect.

Dose related toxicities include nausea, vomiting, headache, CNS stimulation, seizure, hematemasis, hyperglycemia, and hypokalemia

Bottom Line on Methylxanthines

"theophylline/aminophylline is not recommended because it appears to provide no additional benefit to optimal inhaled B2-agonist therapy and may increase adverse effects.”

Use after admission remains controversial

Ipratropium Bromide A synthetic anticholinergic compound Anticholinergic compounds are known to

cause bronchodilation Atropine has been used, but often limited

due to side effects such as tachycardia, dry mouth, disturbances of visual accommodation, etc.

Ipratropium thought to be relatively free of side effects, but with preservation of bronchodilatory properties

Ipratropium Bromide Bottom Line

Small, early studies tend to favor its use More recent, larger studies fail to find benefit Given ipratropium’s relative lack of toxicity,

one “safely” can use it

Noninvasive Positive-Pressure Ventilation (BiPAP)

Literature is extensive in treatment of COPD, but sparse in treatment of acute asthma

Studies using CPAP in asthma have shown it to improve symptoms, but not gas exchange

BiPAP BiPAP theoretical benefits:

Decreased work of breathing (and CO2 production)

Ameliorating large negative intrapleural pressures and accompanying potential for hemodynamic compromise

Bronchodilation with decreased airway resistance (due to “splinting” airways open with air pressure)

Improved delivery of inhalational medication Problems include:

Discomfort with facemask and pressure apparatus

Requires very close observation by trained personnel

BiPAP Bottom Line

Little evidence to guide us Existing evidence seems to support its use Given few known risks with an attempt, would

consider BiPAP in patients refractory to conventional therapy (B-agonists and corticosteroids), or facing impending intubation

Magnesium Sulfate (Infused) Mechanism of action not

well understood but may inhibit bronchial smooth muscle contraction by inhibiting intracellular influx of calcium

Side effects are dose and rate related: facial warmth, flushing,

decrease in BP, sweating, nausea, emesis, CNS effects (including coma)

Bottom Line on MgSO4

Lower doses (2g in 20 min) well tolerated but probably only helpful in severe asthma if at all

Weak evidence that higher doses (2g in 2 min or 10-20 g in 1 hour) more effective, but side effects may be more of a problem Doses on the order of 2g in 2 min shown to be safe

in obstetrical literature

Heliox

As described by Gluck: “Helium-oxygen mixtures improve ventilation by reducing the Reynolds number and reducing density dependent resistance. Helium’s beneficial effects are due to its high kinematic viscosity, high binary diffusion coefficient for CO2, and high diffusivity.”

In English: Helium flows through airways more “easily” that nitrogen, decreasing work of breathing

Not thought to directly promote bronchodilation

Heliox: an Ethereal Treatment

Few clinical trials mostly consisting of case series, uncontrolled studies, and some pediatric literature

No “definitive” study, but seems to be a consensus in the literature supporting its use in some cases - particularly severe asthma

Heliox Bottom Line

Little available evidence May be helpful (at least in very severe asthma)

in “buying time” until other treatments become effective

Use unlikely to cause harm unless it delays other necessary treatment such as B-agonists or necessary intubation

The Bottom, Bottom Line B-agonists and corticosteroids remain the

mainstay treatments for asthma exacerbation

Methylxanthines not helpful acutely, but may play a role subacutely and/or in chronic management

Ipratropium Bromide not harmful, may help BiPAP and Heliox may spare a patient from

more morbid treatments such as intubation MgSO4 is without good evidence of

benefit, but high doses may be helpful in severe asthma

ASTHMA MEDICATIONS

1. Beta2-Agonists Injected Short-acting inhaled Long-acting inhaled

2. Corticosteroids Inhaled Systemic (oral)

3. Leukotriene Modifiers4. Methyl Xanthines5. Cromolyn and Nedocromil6. Anticholinergics

COMORBID INFECTIONS

Most asthma exacerbations are associated with infection by a respiratory virus, especially rhinovirus.

Only a small percentage of exacerbations are associated with infection by an atypical bacterium, like Mycoplasma pneumoniae or Chlamydia pneumoniae.

It is widely believed that coincident bacterial sinusitis contributes to asthma exacerbations.

Airway obstruction due to mucus plugging possibly predisposes patients to bacterial infection of non-draining regions of the lungs.

Viral and bacterial infections are both associated with neutrophilic inflammation of the upper and lower airways.

RECOMMENDATION

Antibiotics are not recommended for the treatment of acute asthma exacerbations except as needed for comorbid conditions – e.g., for the patients with fever and purulent sputum, evidence of pneumonia, or suspected bacterial sinusitis.

PROPELLENTS

CFC: chlorofluorocarbons Safe to inhale but damaging to the earth’s

ozone layer MDIs with CFC are being phased out

HFA: hydrofluoroalkane Safe for the environment and the patient Delivers nearly twice as much medication to

the patient

ORAL CORTICOSTEROIDS

Only prednisone needed for PO use Once per day about equivalent to BID May stop med abruptly after ~5 days Used almost exclusively for quick relief, not for

supplementing (long term) inhaled steroids or long acting beta2-agonists in step 4

INHALED STEROIDSCOMMON PRACTICES

Beclomethasone (Beclovent) not in common use in some medical centers

Budesonide (Pulmicort) ~20% absorbed, but used mostly in nebulizer for children

Flunisolide (Aerobid) not used much Fluticasone (Flovent) ~1% absorbed,

commonly used & available in 3 strengths

Triamcinolone acetonide (Azmacort) not in common use in some medical centers

Keep asthma medicine cool !

Ciclesonide

Newest ICS (About 5 years in use)

1. Small airways effect

2. High level of efficacy of available ICS

3. Safety profile

4. Does not affect circadian rhythm

5. High degree of serum protein binding

6. Rapid clearance rate; reduced systemic effect

CIC

• OPTIMAL EFFICACY• MINIMAL SYTEMIC ABSORPTION• LOW SIDE EFFECTS• RETENTION IN LUNG • DISTRIBUTION IN LYPOPHILLIC TISSUE

OF THE LUNG, SLOW ABSORPTION , PROLONGED HALF LIFE

LONG ACTINGBETA2-AGONISTS

Salmeterol (Serevent) off market (CFC) Fixed dose of salmeterol now only available

in combination with 3 strengths of fluticasone as Advair (100/50, 250/50 & 500/50)

Formoterol (Foradil) available

FORMOTEROL

Available as Foradil It is both short acting and long acting 12 mcg of Foradil is equivalent to 50 mcg

of salmeterol (Serevent) Provided as 12 mcg capsules to be used in

aerolizer (not PO) every 12 hours

CROMOLYN & NEDOCROMIL

Cromolyn is available as Intal Nedocromil is available as Tilade

Not commonly used

LEUKOTRIENE MODIFIERS

Used as adjunctive therapy for asthma Oral treatment available Simultaneously treats allergic rhinits

LEUKOTRIENE MODIFIERS

Leukotriene Receptor Antagonists (LTRAs) Montelukast is available as Singulair prescribed as one 10 mg

tablet per day Zafirlukast is available as Accolate prescribed as 20 mg tablet

BID

5-Lipoxygenase Inhibitors Zileuton is available as Zyflo prescribed as 600 mg QID

Children and allergy in asthma

METHYLXANTHINES

Theophylline used very little now and requires blood level monitoring

OTHERS

Pulse oximetry – most useful in emergency rooms

Spirometry – useful to detect degree of obstruction and if it can clear with bronchodilators and or steroids

Asthma specialists – useful for step 3 and/or step 4 patients or difficulty with management

Other Drugs

Surfactant Replacement Therapy New anti-inflammatory Agents Inhaled antibiotics Anticytokine Agents Protease inhibitors immunomodulators

Anti-IgE

Recombinant humanized monoclonal antibody to treat persons over 12 years with moderate to severe asthma-Omalizumab - Xolair-Inhibits binding of IgE to receptors on mast cells and basophils-Prevents the release of mediators of allergic response that cause bronchospasm-Given subcutaneously q 2-4 weeks, very expensive but effective in reducing hospital visits and steroids use.

Special AdministrationTechniques

Devices used to deliver aerosol medication

-MDI

-Jet Nebulizer

-UItrasonic Nebulizer

-Dry powder inhaler

-Spacer

Inhalation devices

CONSEQUENCES OF POOR ASTHMA CONTROL

Social economic waste that is preventable Loss in school/job absenteeism High morbidity Marginalization of Asthmatics in life Family life disruption (divorces and single

mother hood) All ADDS up to poor quality of life and early

demise

Barriers to asthma medication

BARRIERS IN ASTHMA

Patient Healthcare system Health care provider environmental

BARRIERS IN ASTHMA

Patient Varying cultural issues Complex treatment regimen Fear of medication Poor adherence – side effects of mediation – poor

coping Embarrassment over asthma Low – income – lack of resources Lack of appreciation of severity of asthma

BARRIERS IN ASTHMA

Health care provider Busy with other respiratory disease Attitude: misdiagnosis and under diagnosis Training and knowledge Managing acute attacks rather than long term

control Limited time to give asthma education Lack of awareness of existence of clinical

guidelines

BARRIERS IN ASTHMA CONT’

Health care system Geographical Poor infrastructure Availability of drugs Low public health Priorities (TB/HIV malaria Private versus public Cost of hospital visits

BARRIERS IN ASTHMA CONT’D

Environmental factors School Home Workplace Tobacco – smoke Urbanization - pollution

BARRIERS IN ASTHMA CONT’D

Effects of barriers Socio-economic Frequent symptoms Severe symptoms More emergency room visits More absenteeism Frequent hospitalization Higher mortality

The challenges of asthma management

Over-reliance on rescue medication1 Suboptimal control1

Poor adherence to maintenance therapy1

Complexity of current treatments1

Lack of education and understanding among patients1

1FitzGerald JM, et al. Can Resp J 2006;13:253–259; 2Harrison TW, et al. Lancet 2004;363:271–275.

THANK YOU FOR YOUR KIND ATTENTION