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Bronchial Asthma Dr. Nooreldin Mohamed Elkosh PGY1 Family Medicine Residency Program, Hamad Medical Corporation
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Page 1: Asthma

Bronchial Asthma

Dr. Nooreldin Mohamed Elkosh PGY1 Family Medicine Residency

Program, Hamad Medical Corporation

Page 2: Asthma

DEFENITION

• Asthma is a common chronic inflammatory disease of the airways characterized by recurent and reversible episodes of airflow obstruction and bronchospasm.

• Common symptoms include wheezing, coughing, chest tightness, and shortness of breath.

Page 3: Asthma

EPIDEMIOLOGY

• As of 2004, it was estimated that as many as 300 million people of all ages suffer from asthma. By 2025, it is expected that this number will rise to 400 million worldwide.

• The rate of asthma increases as communities adopt western lifestyles .

Page 4: Asthma

• The increase in the prevalence of asthma has been associated with an increase in atopic sensitization and other allergic disorders such as eczema and rhinitis

• It is estimated that asthma accounts for about 1 in every 250 deaths worldwide. Many of these could be prevented with optimal access to medical care

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• Asthma in the Gulf countries:Saudi Arabia took the lead, with a rate of 24%

of the population suffering. Qatar and Kuwait came next, with a rate of

19.8% and 16.8% respectively, followed by 13% in the United Arab Emirates

Oman had the lowest prevalence among the Gulf Cooperation

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• Prevalence of asthma among Qatari schoolchildren aged 6-14 years according to International Study of Asthma and Allergies in Childhood, Qatar:

A cross-sectional study of 3,283 school children living in both urban and rural areas was conducted between February 2003-February 2004:

Page 7: Asthma

• The population sample had a high prevalence of diagnosed asthma (19.8%), allergic rhinitis (30.5%), eczema (22.5%), and chest infection (11.9%).

• The frequency of asthma, allergic rhinitis, and eczema among parents reflected the same pattern as seen in their children

Page 8: Asthma

• Overall, males had more asthma, allergic rhinitis, and chest infections than females

• In general, the prevalence rate of asthma and allergic rhinitis decreased with age

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• Genetic factors related to the high rates of consanguinity may play an important role in the high prevalence rates noted in the Qatari population, but changes in lifestyle and environmental factors cannot be discounted as possible causes of the high prevalence noted in this study.

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The Impact of Asthma and Allergic Diseases on Schoolchildren: Are they at Increased Risk of Absenteeism and Poor School Performance?Dept. of Epidemiology and Medical Statistics, Hamad Medical Corporation Dept. of Public Health, Weill Cornell Medical College State of Qatar

Page 11: Asthma

• Asthma is the most common chronic illness among school children and an important cause of school absenteeism and reduced participation in sports and other activities

• Asthma is the principal cause of school absences due to chronic disease in childhood accounting for 20% of school days lost among elementary and high school students

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Page 13: Asthma

RISK FACTORS

• GENDER — There are clear-cut gender differences in the

prevalence of asthma. Childhood asthma tends to be a predominantly male disease, with the relative male predominance being maximal at puberty.

After age 20, the prevalence remains approximately equal until age 40, when the disease becomes more common in females.

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• Airway hyperreactivity — Abnormal and exaggerated airway

responsiveness to noxious stimuli is a central feature in the pathophysiology of asthma, and all patients with asthma have airway hyperresponsiveness

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• FAMILIAL HISTORY OF ASTHMA —

Page 16: Asthma

• ATOPY AND ALLERGENS — Atopy may be defined as the state of having IgE antibodies

to specific allergens, which is a prerequisite for developing allergic disease.

The association between asthma and other atopic conditions is well-documented.

The "atopic march" is a term used to describe the pattern of onset of different allergic diseases that is observed in some atopic individuals.

This pattern begins with atopic dermatitis in infancy and childhood, followed by the onset of allergic rhinitis and then asthma during later childhood and adolescence.

Page 17: Asthma

• Allergen exposure — Sources of indoor allergens include: house dust mites, animal proteins (particularly

cat and dog allergens), cockroaches, and fungi• RHINITIS — Adults with rhinitis are at greater risk than

those without rhinitis for developing adult-onset asthma

Page 18: Asthma

• OCCUPATIONAL EXPOSURES — The European Community Respiratory Health

Surveys (ECRHS and ECRHS-II) identified several occupations that are associated with an increased risk of new onset asthma; nursing and cleaning were responsible for the most cases .Inhalational accidents (eg, fires, mixing cleaning agents, industrial spills) were also associated with an increased risk of new onset asthma.

Page 19: Asthma

In the Agricultural Health Study of 25,814 adult farm women, growing up on a farm was protective against asthma, but use of certain pesticides (eg, organophosphates) was associated with an increased risk of adult-onset atopic asthma

Page 20: Asthma

• Outdoor pollution — There is a known correlation between levels of air pollution and lung disease, but the association between air pollution and asthma is less clear

• Indoor pollution— Gas stoves are the primary source of indoor NO2 which is responsible for increasing wheeze ,shortness of breath and chest tightness

Page 21: Asthma

• RESPIRATORY INFECTIONS —Viral and bacterial respiratory infections are

well-known triggers that can cause exacerbations in children and adults with asthma

There are no conclusive epidemiologic data linking infections to causation of asthma in previously normal adults

Page 22: Asthma

• SMOKING AND EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE —

1- Active smoking — Several studies have demonstrated that active smoking increases the risk for developing asthma

Secondhand smoke — There is a growing evidence that secondhand smoke exposure is associated with the development of asthma in early life

Page 23: Asthma

• Maternal smoking is the most important cause of secondhand smoke exposure, because of the greater exposure of the child to the mother than the father

Page 24: Asthma

• OBESITY — There is a linear relationship between BMI and

the risk of developing asthma• EARLY MENARCHE —asthma symptoms and bronchial hyperreactivity

are more common among adult women with menarche before the age of 11 years compared with menarche at age 13 or later based on a large multinational study

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• MEDICATION USE — Epidemiologic studies have found associations

between the development of asthma and both the regular use of acetaminophen and exposure to antibiotics during infancy.

However, these studies have inadequately accounted for confounding bias. Both of these associations warrant further study.

Page 26: Asthma

• Asprin induced asthma (Samter's triad ):is a medical condition consisting of asthma,

aspirin and NSAID sensitivity, and nasal/ethmoidal polyposis.

Page 27: Asthma

• Mode of delivery — Delivery by Cesarean section may increase the

risk of childhood asthma compared with vaginal delivery

• Exercise, Cold exposure, Excessive laughing

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Page 29: Asthma

PATHOGENESIS• 1- Allergic Asthma (Extrensic Asthma )• 2-Non allergic Asthma (Intrensic Astma )

Page 30: Asthma

EXTRENSIC ASTHMA

Page 31: Asthma
Page 32: Asthma

• Allergic (Extrinsic) Asthma : Bronchoconstriction Airway edemaAirway hyperresponsivenessAirway remodeling

Page 33: Asthma

• Non allergic (Intrinsic) Asthma: triggered by factors not related to allergies Many of the symptoms of allergic and non-allergic

asthma are the same (coughing, wheezing, shortness of breath or rapid breathing, and chest tightness), but non-allergic asthma is triggered by other factors such as anxiety, stress, exercise, cold air, dry air, hyperventilation, smoke, viruses or other irritants

the immune system is not involved in the reaction.

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Page 36: Asthma

THANK YOU

Page 37: Asthma

Drugs used in Bronchial Asthma

Dr. Sherif Adel Saleh, PGY-1 Family Medicine Residency Program,

Hamad Medical Corporation

Page 38: Asthma

Pathophysiology of asthma

Page 39: Asthma

Classification• Bronchodilators

– β Sympathomimetics: Salbutamol, Terbutaline, Bambuterol, Salmeterol, Formoterol, Ephedrine.

– Methylxanthines: Theophylline (anhydrous), Aminophylline, Choline theophyllinate, Hydroxyethyl theophylline, Theophylline ethanolate of piperazine, Doxophylline.

– Anticholinergics (muscarnic receptor antagonist): Ipratropium bromide, Tiotropium bromide.

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Classification

• Leukotriene antagonists: Montelukast, Zafirlukast.

• Mast cell stabilizers: Sodium cromoglycate, Ketotifen.

• Corticosteroids– Systemic: Hydrocortisone, Prednisolone and others.– Inhalational: Beclomethasone dipropionate, Budesonide, Fluticasone

propionate, Flunisolide, Ciclesonide.

• Anti-lgE antibody: Omalizumab

Page 41: Asthma

Bronchial Asthma: Treatment approaches• Prevention of antigen antibody reaction: Avoidance of antigen,

hyposensitization

• Neutralization of IgE: Omalizumab

• Suppression of inflammation and bronchial hyper reactivity: Cotricosteroids

• Prevention of release of mediators: Mast cell stabilizers

• Antagonism of released mediators: Leukotriene antagonists, antihistamines, platelet aggravating factor (PAF) antagonist

• Blockade of constrictor neurotransmitter: Sympathomimetics

• Directly acting bronchodilators: Methylxanthines

Page 42: Asthma

Bronchodilators

Stimulates

2-adrenergic

receptors of bronchi

2-agonists Anticholinergic drugs

Smooth muscle

relaxation

reduce tonus

of vagus

Methylxanthinesinhibit phosphodiesterase

2-agonists: treatment of acute asthmatic attacks

Muscarinic antagonist: Less useful in asthma, may be given in refractory cases

Methylxanthines: Long-term/ prevent bronchoconstriction

2-agonists: treatment of acute asthmatic attacks

Muscarinic antagonist: Less useful in asthma, may be given in refractory cases

Methylxanthines: Long-term/ prevent bronchoconstriction

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Sympathomimetics

• The selective β2 agonist is the primary bronchodilators used in acute asthmatic attacks.

• β2 adrenergic receptor agonists increase the cAMP concentration in smooth muscles causing bronchodilatation.

• Types: – Long-acting β2 adrenergic receptor agonists (Salmeterol; formoterol)

– Short-acting β2 adrenergic receptor agonists (salbutamol, levalbuterol, metaproterenol, terbutaline, and pirbuterol )

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Sympathomimetics• Salbutamol:

– Selective β2 agonists with less cardiac side effects

– Inhaled salbutamol produce bronchodililation within 5-min and the action lasts for 2-4 h.

– Used for acute asthmatic attack. Not suitable for prophylaxis– Side effect: Palpitation, restlessness, nervousness, throat irritation and ankle

edema.– Metabolism: metabolized in gut; oral bioavailability is 50%.– Duration of action: oral salbutamol acts 4-6 h.– Dose: 2-4 mg/ oral; 0.25- 0.5 mg/ i,.p., or s.c.,; 100-200 μg/ inhalation

• Terbutaline:– Similar to salbutamol; regular use dose not reduce bronchial hyper-reactivity– Dose: 5 mg/ oral; 0.25 mg/ i,.p., or s.c.,; 250 μg/ inhalation

Cont.,

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Sympathomimetics• Bambuterol:

– prodrug of terbutaline– Slowly hydrolyzed in plasma and lung by pseudocholinesterase to release the

active drug over 24 h. It also reversely inhibits pseudocholinesterase in a dose dependent manner.

– Used in chronic bronchial asthma in a singe evening dose of 10-20 mg/ oral.

• Salmeterol:– First long acting selective β2 agonists with slow onset of action

– Twice daily for maintain the therapy/ nocturnal asthma, but not for acute asthma– Concurrent use of inhaled glucocorticoid with salmeterol is advised for patient

with persistent asthma. – COPD: equivalent to inhaled anticholinergics in COPD. Reduce breathlessness by

abolishing the reversible component of airway obstruction.

• Formoterol:– Long acting selective β2 agonists which acts 12 h when inhaled.

– Compare to salmeterol it has a faster onset of action (with in 10 min)

Cont.,

Page 46: Asthma

Methylxanthines• Caffeine (from coffee) , theophylline (from tea) and theobromine

(from cocoa) are naturally occurring xanthine alkaloids which have qualitatively similar actions.

• Mechanism of action:

– Methylxanthines inhibits cyclic nucleotide phosphodiesterase (PDEs), thereby lead to an accumulation of intracellular cAMP and cGMP causing bronchodilation.

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Methylxanthines

• Mechanism of action:

BronchodilationBronchodilation

Bronchial tone

Muscarinic antagonistMuscarinic antagonist

AcetylcholineAdenosine

Theophylline

cAMP

ATP

AMP

Adenylyl cyclaseAdenylyl cyclase

Phosphodiesterase (PDE)Phosphodiesterase (PDE)TheophyllineTheophylline

Beta agonistBeta agonist

Page 48: Asthma

Pharmacological actions of Methyl xanthines

CNSStimulationIncrease motor activityImprove the performance

CVSStimulate the heartIncrease the force of contractionHigh dose: cardiac arrhythmiasBP: effect is variable Stimulation of Vegas stimulation: ↓ BP Vasomotor center : ↑ BP

Smooth muscle

RelaxationLungs vital capacity- increasedBiliary spasm: relieved

Kidney

Mild diuretics (Inhibiting reabsorption of Na+ & H2O)

Increase the renal blood flowIncrease the g.f.r.

Mast cellInhibit the release of histamine

StomachEnhance the secretion of acid, Pepsin

MetabolismIncrease BMR

It has variable physiological actions

Page 49: Asthma

Methylxanthines- Theophylline Cont.,

• Adverse effects:– Narrow margin safety, – Multiple drug interactions (Erythromycin, ciprofloxacin, cimetidine, oral

contraceptives, allopurinol, phenytoin, rifampicin, phenobarbital)– CVS and CNS stimulant; ADRs not dependent to dose; GIT distress– Children are more liable to developed CNS toxicity– Rapid IV injection cause- precordial pain, syncope and sudden death

Page 50: Asthma

AnticholinergicsIpratropium (derivative of atropine)

• Parasympathetic activation causes bronchoconstriction and increases mucus secretion.

• Blocking the action of ACh by anticholinergic drugs produce bronchodilation and also reduce the volume of respiratory secretion.

• Less effective bronchodilator than sympathomimetic.

• ADR: Dry mouth, respiratory tract discomfort

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Leukotriene antagonistsMontelukast, Zafirlukast

• Block the cys-leukotrienes C4, D4 and E4 (LTC4, LTD4, LTE4)

• Alternative for inhaled glucocorticoids• Prophylactic therapy for mild, moderate asthma; not used for

terminating asthma.• Both are very safe drugs and ADRs are few (headache, rashes);

eosinophilia and neuropathy are infrequent. Few cases Churg-Strauss syndrome (vasculitis with eosinophilia) have been reported.

• Dose: Montelukast 10 mg OD, Zafirlukast 20 mg BD

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Leukotriene antagonists• Mechanism of action of leukotriene antagonist, antiinflammatory drugs

Cont.,

Bronchoconstriction, Inflammation, increased mucus

Bronchoconstriction, Inflammation, increased mucus

Bronchoconstriction, Inflammation, PainBronchoconstriction, Inflammation, Pain

Block by steroidal antiinflammatory drugs

Block by steroidal antiinflammatory drugs

Block by nonsteroidal antiinflammatory drugs

Block by nonsteroidal antiinflammatory drugs

Block by Leukotriene antagonists

Block by Leukotriene antagonists

Page 53: Asthma

Corticosteroids

• Corticosteroids are not bronchodilators; benefit by reducing bronchial hyperreactivity/mucosal edema and by suppressing inflammation.

• Inhaled glucocorticoids are partially absorbed and because of their systemic AEs systemic glucocorticoids are usually reserved for patients with severe refractory asthma.

• Systemic steroid therapy– Severe chronic asthma: Not contorted by bronchodilator and inhaled steroids. – Status asthmaticus/ acute asthma exacerbation

Page 54: Asthma

Mast cell stabilizersSodium cromoglycate, Ketotifen

• Inhibits degranulation of mast cell by trigger stimuli by blocking calcium channels

• Once degranulation has occurred, mast cell stabilizers are ineffective (in the acute setting)

• Long time therapy reduce cellular inflammatory response.

• Pharmacokinetic: – Not absorbed orally. It is administered as an aerosol through metered dose

inhaler delivering 1 mg per dose; 2 puffs 4 times a day– Not popular- production of cough and bronchospasm because of particulate

nature of the inhalation.– Small fraction of the inhaled drug is absorbed systemically and excreted

unchanged form in urine and bile.

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Mast cell stabilizers

• Use:– Bronchial asthma: Sodium. Cromoglycate is used as a long term prophylactic in

patients not adequately controlled by inhaled bronchodilators. Alternative for inhaled steroids in mild to moderate asthma but not severe cases.

– Allergic rhinitis: Cromoglycate is not nasal decongestant, regular prophylactic use as a nasal spray produces symptomatic improvement in many patients.

– Allergic conjunctivitis: Regular use as eye drops is benificial in some chronic cases

Cont.,

Adverse effect (cromoglycate):BronchospasmThroat irritationCough, headacheArthralgia, rashes and dysuriaRarely nasal congestion

Adverse effect (Ketotifen):Generally well toleratedSedation and dry mouth Dizziness, nausea and weight gain

Page 56: Asthma

Anti-lgE antibody: Omalizumab (Xolair)

• recombinant DNA-derived monoclonal antibody

• Selectively binds to human immunoglobulin E (IgE) and decrease binding affinity of IgE to the high-affinity IgE receptor on the surface of mast cells and basophils, reduce allergic response.

• Omalizumab may be particularly useful for treatment of moderate to severe allergic asthma in patients who are poorly controlled with conventional therapy.

• Due to the high cost of the drug, limitations on dosage, and limited clinical trial data, it is not currently used as firstline therapy.

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Page 58: Asthma

Acute Management of Acute Management of AsthmaAsthma

Dr. Mohamed Suliman Abdelhamid, Dr. Mohamed Suliman Abdelhamid, PGY-1 PGY-1

Family Medicine Residency Program, Family Medicine Residency Program,

Hamad Medical CorporationHamad Medical Corporation

Page 59: Asthma

Status AsthmaticusStatus Asthmaticus

Treatment Treatment – AlbuterolAlbuterol– AtroventAtrovent– SteroidSteroid– TerbutalineTerbutaline– EpinephrineEpinephrine– HelioxHeliox– BIPAPBIPAP– IntubationIntubation– KetamineKetamine– Inhalational anestheticsInhalational anesthetics

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Status AsthmaticusStatus Asthmaticus

Severe bronchospasm that does not respond to Severe bronchospasm that does not respond to aggressive therapies within 30-60 minutesaggressive therapies within 30-60 minutes

Severe asthmatic attack with one or more of the Severe asthmatic attack with one or more of the following:following:– Dyspnea (precluding speech), accessory muscle use, Dyspnea (precluding speech), accessory muscle use,

RR 35/minRR 35/min– Hr > 140/minHr > 140/min– Peak expiratory flow < 100 l/min Peak expiratory flow < 100 l/min

– Hypercapnea ( >= 50 mmHg)Hypercapnea ( >= 50 mmHg)

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Acute Severe AsthmaAcute Severe Asthma

Critical limitation of expiratory flowCritical limitation of expiratory flow

Increased airway resistanceIncreased airway resistance

Premature airway closurePremature airway closure

Lung and chest wall dynamic Lung and chest wall dynamic hyperinflationhyperinflation

High intrinsic PEEPHigh intrinsic PEEP

Respiratory muscle fatigueRespiratory muscle fatigue

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Near-Fatal AsthmaNear-Fatal Asthma

Respiratory arrest or respiratory failure Respiratory arrest or respiratory failure (PCO2 > 50 mmHg)(PCO2 > 50 mmHg)

Page 63: Asthma

Fatal AsthmaFatal Asthma

Slow-onsetSlow-onset– Gradual deterioration of asthma symptoms over Gradual deterioration of asthma symptoms over

several days several days – Usually associated with chronic poorly controlled Usually associated with chronic poorly controlled

asthmaasthma– EosinophilicEosinophilic predominance and mucus in predominance and mucus in

submucosasubmucosa

Rapid-onsetRapid-onset– Symptom onset and progression to life-threatening Symptom onset and progression to life-threatening

status within 3 hoursstatus within 3 hours– ““Greater” hypercapneaGreater” hypercapnea– NeutrophilicNeutrophilic predominance in airway submucosa predominance in airway submucosa

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The Four Compartments The Four Compartments o o

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Respiratory MechanicsRespiratory Mechanics

The lung is not homogenous during acute The lung is not homogenous during acute severe asthmasevere asthmaDriving force for expiratory flow is Driving force for expiratory flow is decreaseddecreasedPersistent activation of inspiratory Persistent activation of inspiratory muscles during expirationmuscles during expiration------– Abnormal low pulmonary elastic recoil Abnormal low pulmonary elastic recoil – High outward recoil of chest wall High outward recoil of chest wall

Resistance to airflow strongly increasedResistance to airflow strongly increased

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Respiratory MechanicsRespiratory Mechanics

Markedly prolonged expirationMarkedly prolonged expiration

Inspiration starts before static equilibrium Inspiration starts before static equilibrium is reachedis reached

Positive End-Expiratory alveolar Positive End-Expiratory alveolar PressurePressure– Auto-PEEP (intrinsic PEEP, PEEPi)Auto-PEEP (intrinsic PEEP, PEEPi)

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Dynamic HyperinflationDynamic Hyperinflation

Incomplete alveolar emptying at Incomplete alveolar emptying at

the end of expirationthe end of expiration– Intrinsic PEEPIntrinsic PEEP

Measure end-expiratory flow orMeasure end-expiratory flow or

End-expiratory pressureEnd-expiratory pressure

Increased ventilatory requirementIncreased ventilatory requirement

Prolonged expiratory timeProlonged expiratory time

Increased inspiratory threshold loadIncreased inspiratory threshold load

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Dynamic HyperinflationDynamic Hyperinflation

Shortening of:Shortening of:– DiaphragmDiaphragm– Inspiratory intercostalsInspiratory intercostals– Accessory musclesAccessory muscles

Decreased mechanical efficiencyDecreased mechanical efficiency– Increased risk of fatigueIncreased risk of fatigue

With increased obstruction:With increased obstruction:– CO2 production > Elimination by alveolar ventilationCO2 production > Elimination by alveolar ventilation

CO2 increasesCO2 increases

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Dynamic HyperinflationDynamic Hyperinflation

Mean pleural pressure becomes more Mean pleural pressure becomes more negativenegative– Interstitial pressures are also loweredInterstitial pressures are also lowered– Vascular pressure is maintainedVascular pressure is maintained

The result:The result:– Interstitial edema and further increase in Interstitial edema and further increase in

airway resistanceairway resistance

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Asthmatic PatientsAsthmatic Patients

Who do we worry about?Who do we worry about?– Previously intubatedPreviously intubated– Noncompliant or poorly controlledNoncompliant or poorly controlled– Psychosocial or emotional problemsPsychosocial or emotional problems– Frequent flyersFrequent flyers– Environmental triggersEnvironmental triggers

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What do we look for on exam?What do we look for on exam?

Severe respiratory distressSevere respiratory distressAccessory muscle useAccessory muscle useMay be hypoxemicMay be hypoxemicTachypneicTachypneicTachycardicTachycardicDiaphoreticDiaphoreticAnxiousAnxious1-2 word dyspnea1-2 word dyspnea

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What do we do?What do we do?

Rapid assessmentRapid assessment

Manage the airwayManage the airway

Aggressive treatmentAggressive treatment

Respiratory therapist at bedsideRespiratory therapist at bedside

Have all the needed equipment at the bedsideHave all the needed equipment at the bedside– Intubation…Intubation…

Team approachTeam approach

2 IVs2 IVs

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TreatmentTreatment

Albuterol nebAlbuterol neb

Atrovent nebAtrovent neb

Methylprednisolone 125 mg IVMethylprednisolone 125 mg IV

Terbutaline Terbutaline – 0.25 mg SQ q20 minutes x 3 doses0.25 mg SQ q20 minutes x 3 doses

EpinephrineEpinephrine– 1:1000, 0.3 mg SQ or IM q20 minutes x 3 doses1:1000, 0.3 mg SQ or IM q20 minutes x 3 doses

Magnesium sulfateMagnesium sulfate

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MgSO4MgSO4

Possible inhibition of calcium influx into Possible inhibition of calcium influx into airway smooth muscleairway smooth muscle

Inhibits cholinergic neuromuscular Inhibits cholinergic neuromuscular transmissiontransmission

Stabilization of mast cells and T Stabilization of mast cells and T lymphocyteslymphocytes

Stimulation of nitric oxide and prostacyclinStimulation of nitric oxide and prostacyclin

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PregnancyPregnancy

EpinephrineEpinephrine– Concern re: alpha effect and vasoconstriction in Concern re: alpha effect and vasoconstriction in

uteroplacental circulationuteroplacental circulation– Avoid during pregnancy except in anaphylaxisAvoid during pregnancy except in anaphylaxis

TerbutalineTerbutaline– Preterm laborPreterm labor

High dose steroids in animal studies:High dose steroids in animal studies:– ??? cleft palate??? cleft palate

Palatal closure usually by 12Palatal closure usually by 12thth week week

Albuterol, Atrovent safeAlbuterol, Atrovent safe

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PedsPedsAcute severe asthmaAcute severe asthma

Albuterol Albuterol – 0.15mg/kg/hr 0.15mg/kg/hr

Albuterol continuous: Albuterol continuous: – 20 mg/hr if > 20 kg20 mg/hr if > 20 kg

Atrovent Atrovent – 0.5 mg/dose if > 20 kg or > 6y.o.0.5 mg/dose if > 20 kg or > 6y.o.

MgSO4 MgSO4 – 25-75 mg/kg IV25-75 mg/kg IV

Terbutaline Terbutaline – 10 mcg/kg IV over 10 minutes10 mcg/kg IV over 10 minutes – Infusion of 0.1-10 mcg/kg/minInfusion of 0.1-10 mcg/kg/min

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HelioxHeliox

Usually 70% Helium: 30% oxygenUsually 70% Helium: 30% oxygen– Inert gasInert gas– 3X reduction in density compared to air3X reduction in density compared to air

Reduces resistance in airways with nonlaminar flow Reduces resistance in airways with nonlaminar flow – Upper and ProximalUpper and Proximal

Reduces respiratory muscle workReduces respiratory muscle workMay improve gas exchangeMay improve gas exchangeMay increase the mass ofalbuterol delivered May increase the mass ofalbuterol delivered – Allows smaller particles to better penetrate the lung peripheryAllows smaller particles to better penetrate the lung periphery

May use with:May use with:– Face maskFace mask– BIPAPBIPAP– Mechanical ventilationMechanical ventilation

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CPAPCPAP

Seems to increase Functional residual Seems to increase Functional residual capacity and lung compliancecapacity and lung compliance

May decrease fatigue of respiratory May decrease fatigue of respiratory musclesmuscles

Decreases the adverse hemodynamic Decreases the adverse hemodynamic effects of large negative inspiratory swings effects of large negative inspiratory swings in pleural pressure which compromise RV in pleural pressure which compromise RV and LV performanceand LV performance

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BIPAPBIPAP

Provides CPAPProvides CPAP

Delivers higher pressure in inspiration than Delivers higher pressure in inspiration than expirationexpiration

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When to IntubateWhen to Intubate

When do you intubate an asthmatic When do you intubate an asthmatic patient?patient?

Persistent hypercarbiaPersistent hypercarbia

Hemodynamic instabilityHemodynamic instability

Inability to tolerate the face mask, BIPAP..Inability to tolerate the face mask, BIPAP..

ExhaustionExhaustion

Altered mental status….Altered mental status….

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SummarySummary

Look for the “sick” asthmaticsLook for the “sick” asthmaticsBe aggressive in their treatmentBe aggressive in their treatmentDo not forget about Do not forget about – Terbutaline ( SQ)Terbutaline ( SQ)– Epi ( SQ or IM)Epi ( SQ or IM)

If they are young and “fighting”, consider:If they are young and “fighting”, consider:– BIPAPBIPAP– HelioxHeliox– IV EpinephrineIV Epinephrine

Intubate if the patient is:Intubate if the patient is:– FatiguedFatigued– Unable to cooperate with interventionsUnable to cooperate with interventions

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Thank YouThank You

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Dr. Mostafa Hamdy Rashed, PGY-1 Family Medicine Residency Program, Hamad Medical

Corporation

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Levels of Asthma Control

CharacteristicControlled

(All of the following)

Partly controlled(Any present in any

week)Uncontrolled

Daytime symptomsNone (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

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Goals of Long-term Management

Achieve and maintain control of symptoms

Maintain normal activity levels, including exercise

Maintain pulmonary function as close to normal levels as possible

Prevent asthma exacerbations Avoid adverse effects from asthma

medications Prevent asthma mortality

Achieve and maintain control of symptoms

Maintain normal activity levels, including exercise

Maintain pulmonary function as close to normal levels as possible

Prevent asthma exacerbations Avoid adverse effects from asthma

medications Prevent asthma mortality

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1. Develop Patient/Doctor Partnership

2. Identify and Reduce Exposure to Risk Factors

3. Assess, Treat and Monitor Asthma

4. Manage Asthma Exacerbations

5. Special Considerations

1. Develop Patient/Doctor Partnership

2. Identify and Reduce Exposure to Risk Factors

3. Assess, Treat and Monitor Asthma

4. Manage Asthma Exacerbations

5. Special Considerations

Asthma Management and PreventionAsthma Management and PreventionProgram: Five ComponentsProgram: Five ComponentsAsthma Management and PreventionAsthma Management and PreventionProgram: Five ComponentsProgram: Five Components

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Asthma Management and Prevention Program

Asthma can be effectively controlled in most patients by intervening to suppress and reverse inflammation as well as treating bronchoconstriction and related symptoms

Early intervention to stop exposure to the risk factors that sensitized the airway may help improve the control of asthma and reduce medication needs.

Asthma can be effectively controlled in most patients by intervening to suppress and reverse inflammation as well as treating bronchoconstriction and related symptoms

Early intervention to stop exposure to the risk factors that sensitized the airway may help improve the control of asthma and reduce medication needs.

.

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Asthma Management and Prevention Program

Although there is no cure for asthma, appropriate management that includes a partnership between the physician and the patient/family most often results in the achievement of control

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Clear communication between health care professionals and asthma patients is key to enhancing compliance

Clear communication between health care professionals and asthma patients is key to enhancing compliance

Component 1: Develop Patient/Doctor Partnership Component 1: Develop Patient/Doctor Partnership

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Component 1: Develop Patient/Doctor Partnership Component 1: Develop Patient/Doctor Partnership

Educate continually

Include the family

Provide information about asthma

Provide training on self-management skills

Emphasize a partnership among health care providers, the patient, and the patient’s family

Educate continually

Include the family

Provide information about asthma

Provide training on self-management skills

Emphasize a partnership among health care providers, the patient, and the patient’s family

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Component 1: Develop Patient/Doctor PartnershipComponent 1: Develop Patient/Doctor Partnership

Key factors to facilitate communication:

Friendly demeanor

Interactive dialogue

Encouragement and praise

Provide appropriate information

Feedback and review

Key factors to facilitate communication:

Friendly demeanor

Interactive dialogue

Encouragement and praise

Provide appropriate information

Feedback and review

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Example Of Contents Of An Action Plan To Maintain Asthma Control

Your Regular Treatment: 1. Each day take ___________________________ 2. Before exercise, take _____________________

WHEN TO INCREASE TREATMENTAssess your level of Asthma ControlIn the past week have you had: Daytime asthma symptoms more than 2 times ? No Yes Activity or exercise limited by asthma? No Yes Waking at night because of asthma? No Yes The need to use your [rescue medication] more than 2 times? No Yes If you are monitoring peak flow, peak flow less than________? No YesIf you answered YES to three or more of these questions, your asthma is uncontrolled and you may need to step up your treatment.

HOW TO INCREASE TREATMENTSTEP-UP your treatment as follows and assess improvement every day:____________________________________________ [Write in next treatment step here] Maintain this treatment for _____________ days [specify number]

WHEN TO CALL THE DOCTOR/CLINIC.Call your doctor/clinic: _______________ [provide phone numbers]If you don’t respond in _________ days [specify number]______________________________ [optional lines for additional instruction]

EMERGENCY/SEVERE LOSS OF CONTROLIf you have severe shortness of breath, and can only speak in short sentences,If you are having a severe attack of asthma and are frightened,If you need your reliever medication more than every 4 hours and are not improving.1. Take 2 to 4 puffs ___________ [reliever medication] 2. Take ____mg of ____________ [oral glucocorticosteroid]3. Seek medical help: Go to _____________________; Address___________________ Phone: _______________________4. Continue to use your _________[reliever medication] until you are able to get medical help.

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Factors Involved in Non-AdherenceFactors Involved in Non-Adherence

Medication Usage Difficulties associated

with inhalers

Complicated regimens

Fears about, or actual side effects

Cost

Distance to pharmacies

Medication Usage Difficulties associated

with inhalers

Complicated regimens

Fears about, or actual side effects

Cost

Distance to pharmacies

Non-Medication Factors

Misunderstanding/lack of information

Fears about side-effects

Inappropriate expectations

Underestimation of severity

Attitudes toward ill health

Cultural factors

Poor communication

Non-Medication Factors

Misunderstanding/lack of information

Fears about side-effects

Inappropriate expectations

Underestimation of severity

Attitudes toward ill health

Cultural factors

Poor communication

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Component 2: Identify and Reduce Exposure to Risk FactorsComponent 2: Identify and Reduce Exposure to Risk Factors

Measures to prevent the development of asthma, and asthma exacerbations by avoiding or reducing exposure to risk factors should be implemented wherever possible.

Asthma exacerbations may be caused by a variety of risk factors – allergens, viral infections, pollutants and drugs.

Reducing exposure to some categories of risk factors improves the control of asthma and reduces medications needs.

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Reduce exposure to indoor allergens Avoid tobacco smoke Avoid vehicle emission Identify irritants in the workplace Explore role of infections on asthma

development, especially in children and young infants

Component 2: Identify and Reduce Exposure to Risk FactorsComponent 2: Identify and Reduce Exposure to Risk Factors

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Influenza VaccinationInfluenza Vaccination

Influenza vaccination should be provided to patients with asthma when vaccination of the general population is advised.

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Component 3: Assess, Treat and Monitor AsthmaComponent 3: Assess, Treat and Monitor Asthma

The goal of asthma treatment, to achieve and maintain clinical control, can be achieved in a majority of patients with a pharmacologic intervention strategy developed in partnership between the patient/family and the health care professional

The goal of asthma treatment, to achieve and maintain clinical control, can be achieved in a majority of patients with a pharmacologic intervention strategy developed in partnership between the patient/family and the health care professional

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Component 3: Assess, Treat and Monitor AsthmaComponent 3: Assess, Treat and Monitor Asthma

Depending on level of asthma control, the patient is assigned to one of five treatment steps

Treatment is adjusted in a continuous cycle driven by changes in asthma control status. The cycle involves:

- Assessing Asthma Control

- Treating to Achieve Control

- Monitoring to Maintain Control

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A stepwise approach to pharmacological therapy is recommended

The aim is to accomplish the goals of therapy with the least possible medication

A stepwise approach to pharmacological therapy is recommended

The aim is to accomplish the goals of therapy with the least possible medication

Component 3: Assess, Treat and Monitor AsthmaComponent 3: Assess, Treat and Monitor Asthma

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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

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

Component 3: Assess, Treat and Monitor AsthmaComponent 3: Assess, Treat and Monitor Asthma

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Controller MedicationsController Medications

Inhaled glucocorticosteroids Leukotriene modifiers Long-acting inhaled β2-agonists Systemic glucocorticosteroids Theophylline Cromones Long-acting oral β2-agonists Anti-IgE Systemic glucocorticosteroids

Inhaled glucocorticosteroids Leukotriene modifiers Long-acting inhaled β2-agonists Systemic glucocorticosteroids Theophylline Cromones Long-acting oral β2-agonists Anti-IgE Systemic glucocorticosteroids

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Reliever MedicationsReliever Medications

Rapid-acting inhaled β2-agonists

Systemic glucocorticosteroids

Anticholinergics

Theophylline

Short-acting oral β2-agonists

Rapid-acting inhaled β2-agonists

Systemic glucocorticosteroids

Anticholinergics

Theophylline

Short-acting oral β2-agonists

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controlled

partly controlled

uncontrolled

exacerbation

LEVEL OF CONTROLLEVEL OF CONTROL

maintain and find lowest controlling step

consider stepping up to gain control

step up until controlled

treat as exacerbation

TREATMENT OF ACTIONTREATMENT OF ACTION

TREATMENT STEPSREDUCE INCREASE

STEP

1STEP

2STEP

3STEP

4STEP

5

RE

DU

CE

INC

RE

AS

E

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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)

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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

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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)

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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)

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Step 4 – Reliever medication plus two or more controllers

Selection of treatment at Step 4 depends on prior selections at Steps 2 and 3

Where possible, patients not controlled on Step 3 treatments should be referred to a health professional with expertise in the management of asthma

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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)

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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)

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When control as been achieved, ongoing monitoring is essential to:

- maintain control

- establish lowest step/dose treatment

Asthma control should be monitored by the health care professional and by the patient

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Levels of Asthma Control

CharacteristicControlled

(All of the following)

Partly controlled(Any present in any

week)Uncontrolled

Daytime symptomsNone (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

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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)

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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)

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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

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Stepping up treatment in response to loss of control

Use of a combination rapid and long-acting inhaled β2-agonist (e.g., formoterol) and an inhaled glucocorticosteroid (e.g., budesonide) in a single inhaler both as a controller and reliever is effecting in maintaining a high level of asthma control and reduces exacerbations (Evidence A)

Doubling the dose of inhaled glucocortico-steroids is not effective, and is not recommended (Evidence A)

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Childhood and adult asthma share the same underlying mechanisms. However, because of processes of growth and development, effects of asthma treatments in children differ from those in adults.

Childhood and adult asthma share the same underlying mechanisms. However, because of processes of growth and development, effects of asthma treatments in children differ from those in adults.

Children 5 Years and YoungerChildren 5 Years and Younger

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Many asthma medications (e.g. glucocorticosteroids, β2- agonists, theophylline) are metabolized faster in children than in adults, and younger children tend to metabolize medications faster than older children

Many asthma medications (e.g. glucocorticosteroids, β2- agonists, theophylline) are metabolized faster in children than in adults, and younger children tend to metabolize medications faster than older children

Children 5 Years and YoungerChildren 5 Years and Younger

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Rapid-acting inhaled β2-agonists are the most effective reliever therapy for children

These medications are the most effective bronchodilators available and are the treatment of choice for acute asthma symptoms

Rapid-acting inhaled β2-agonists are the most effective reliever therapy for children

These medications are the most effective bronchodilators available and are the treatment of choice for acute asthma symptoms

Children 5 Years and YoungerChildren 5 Years and Younger

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Special ConsiderationsSpecial Considerations

Special considerations are required tomanage asthma in relation to: Pregnancy Surgery Rhinitis, sinusitis, and nasal polyps Occupational asthma Respiratory infections Gastroesophageal reflux Aspirin-induced asthma Anaphylaxis and Asthma

Special considerations are required tomanage asthma in relation to: Pregnancy Surgery Rhinitis, sinusitis, and nasal polyps Occupational asthma Respiratory infections Gastroesophageal reflux Aspirin-induced asthma Anaphylaxis and Asthma

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