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Pediatric Asthma

Author: Girish D Sharma, MD, FCCP, FAAP; Chief Editor: Michael R Bye, MD more...

Updated: Nov 25, 2013

Practice Essentials

Asthma, which occurs in adult and pediatric patients, is a chronic inflammatory disorder of the airwayscharacterized by an obstruction of airflow. Among children and adolescents aged 5-17 years, asthma accounts fora loss of 10 million school days annually and costs caretakers $726.1 million per year because of work absence.[1]

Essential update: Asthma Symptom Tracker effective for self-monitoring

In a 6-month longitudinal cohort study of 210 children (aged 2-18 years) with asthma, Nkoy and colleagues foundthat the Asthma Symptom Tracker (AST), which combines weekly use of the Asthma Control Test questionnairewith a graph displaying trends over time, was useful in monitoring asthma symptoms. Each 1-point decrease(worsening) in the 25-point AST score was associated with a 13% increase in patient use of oral corticosteroids

and a 23% increase in the likelihood of an unscheduled acute care visit for asthma.[2, 3]

In children with scores lower than 15, indicating poor asthma control, the rate of oral steroid use and the likelihoodof an unscheduled hospital visit were sharply higher. Moreover, for each 1-point increase in the Asthma ControlQuestionnaire score, indicating worsening, there was a 2.65-point decrease in the AST score at baseline and a

3.11-point decrease in the AST score during follow-up.[2, 3]

Signs and symptoms

History

The clinician should establish whether the patient has any of the following symptoms:

Wheezing: A musical, high-pitched whistling sound produced by airflow turbulence is one of the mostcommon symptoms of asthmaCough: Usually, the cough is nonproductive and nonparoxysmal; coughing may be present with wheezingCough at night or with exercise: Coughing may be the only symptom of asthma, especially in cases ofexercise-induced or nocturnal asthma; children with nocturnal asthma tend to cough after midnight, duringthe early hours of morningShortness of breathChest tightness: A history of tightness or pain in the chest may be present with or without other symptomsof asthma, especially in exercise-induced or nocturnal asthma

Sputum production

In an acute episode of asthma, symptoms vary according to the episode’s severity. Infants and young childrensuffering a severe episode display the following characteristics:

Breathless during restNot interested in feedingSit upright

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Talk in words (not sentences)Usually agitated

With imminent respiratory arrest, the child displays the aforementioned symptoms and is also drowsy andconfused. However, adolescents may not have these symptoms until they are in frank respiratory failure.

Physical examination

Findings during a severe episode include the following:

Respiratory rate is often greater than 30 breaths per minuteAccessory muscles of respiration are usually usedSuprasternal retractions are commonly presentThe heart rate is greater than 120 beats per minuteLoud biphasic (expiratory and inspiratory) wheezing can be heardPulsus paradoxus is often present (20-40 mm Hg)Oxyhemoglobin saturation with room air is less than 91%

Findings in status asthmaticus with imminent respiratory arrest include the following:

Paradoxical thoracoabdominal movement occursWheezing may be absent (in patients with the most severe airway obstruction)Severe hypoxemia may manifest as bradycardiaPulsus paradoxus may disappear: This finding suggests respiratory muscle fatigue

See Clinical Presentation for more detail.

Diagnosis

Tests used in the diagnosis of asthma include the following:

Pulmonary function tests: Spirometry and plethysmographyExercise challenge: Involves baseline spirometry followed by exercise on a treadmill or bicycle to a heartrate greater than 60% of the predicted maximum, with monitoring of the electrocardiogram andoxyhemoglobin saturationFraction of exhaled nitric oxide (FeNO) testing: Noninvasive marker of airway inflammationRadiography: Reveals hyperinflation and increased bronchial markings; radiography may also showevidence of parenchymal disease, atelectasis, pneumonia, congenital anomaly, or a foreign bodyAllergy testing: Can identify allergic factors that may significantly contribute to asthmaHistologic evaluation of the airways: Typically reveal infiltration with inflammatory cells, narrowing of airwaylumina, bronchial and bronchiolar epithelial denudation, and mucus plugs

See Workup for more detail.

Management

Guidelines from the National Asthma Education and Prevention Program emphasize the following components of

asthma care[4] :

Assessment and monitoring: In order to assess asthma control and adjust therapy, impairment and riskmust be assessed; because asthma varies over time, follow-up every 2-6 weeks is initially necessary (whengaining control of the disease), and then every 1-6 months thereafterEducation: Self-management education should focus on teaching patients the importance of recognizingtheir own level of control and signs of progressively worsening asthma symptoms; educational strategiesshould also focus on environmental control and avoidance strategies, as well as on medication use andadherence (eg, correct inhaler techniques and use of other devices)Control of environmental factors and comorbid conditionsPharmacologic treatmentPharmacologic treatment

Pharmacologic asthma management includes the use of agents for control and agents for relief. Control agentsinclude the following:

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Inhaled corticosteroidsInhaled cromolyn or nedocromilLong-acting bronchodilatorsTheophyllineLeukotriene modifiersAnti-immunoglobulin E (IgE) antibodies (omalizumab)

Relief medications include the following:

Short-acting bronchodilatorsSystemic corticosteroidsIpratropium

See Treatment and Medication for more detail.

Image library

Pediatric asthma. Classification of asthma control (PDF)

Background

Asthma is a chronic inflammatory disorder of the airways characterized by an obstruction of airflow, which may becompletely or partially reversed with or without specific therapy. Airway inflammation is the result of interactionsbetween various cells, cellular elements, and cytokines. In susceptible individuals, airway inflammation may causerecurrent or persistent bronchospasm, which causes symptoms that include wheezing, breathlessness, chesttightness, and cough, particularly at night (early morning hours) or after exercise.

Airway inflammation is associated with airway hyperreactivity or bronchial hyperresponsiveness (BHR), which isdefined as the inherent tendency of the airways to narrow in response to various stimuli (eg, environmental

allergens and irritants).[5]

Asthma affects an estimated 300 million individuals worldwide (see Epidemiology). The prevalence of asthma isincreasing, especially in children. Annually, the World Health Organization (WHO) has estimated that 15 million

disability-adjusted life-years are lost and 250,000 asthma deaths are reported worldwide.[6] Approximately 500,000annual hospitalizations (34.6% in individuals aged 18 y or younger) are due to asthma. In the United States,asthma prevalence, having increased from 1980 to 1996, showed a plateau at 9.1% of children (6.7 million) in

2007.[7]

The cost of illness related to asthma is around $6.2 billion. Each year, an estimated 1.81 million people (47.8% inindividuals aged 18 y or younger) require treatment in the emergency department. Among children andadolescents aged 5-17 years, asthma accounts for a loss of 10 million school days and costs caretakers $726.1

million because of work absence.[1]

Guidelines from the National Asthma Education and Prevention Program provide recommendations on thediagnosis and treatment of pediatric asthma (see Clinical Presentation, Workup, and Treatment andManagement).

For more information, see the Medscape Reference topic Asthma.

Pathophysiology

Interactions between environmental and genetic factors result in airway inflammation, which limits airflow and leadsto functional and structural changes in the airways in the form of bronchospasm, mucosal edema, and mucusplugs.

Airway obstruction causes increased resistance to airflow and decreased expiratory flow rates. These changeslead to a decreased ability to expel air and may result in hyperinflation. The resulting overdistention helps maintainairway patency, thereby improving expiratory flow; however, it also alters pulmonary mechanics and increases thework of breathing.

Hyperinflation compensates for the airflow obstruction, but this compensation is limited when the tidal volumeapproaches the volume of the pulmonary dead space; the result is alveolar hypoventilation. Uneven changes in

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airflow resistance, the resulting uneven distribution of air, and alterations in circulation from increased intra-alveolarpressure due to hyperinflation all lead to ventilation-perfusion mismatch.

Vasoconstriction due to alveolar hypoxia also contributes to this mismatch. Vasoconstriction is also consideredan adaptive response to ventilation/perfusion mismatch.

In the early stages, when ventilation-perfusion mismatch results in hypoxia, hypercarbia is prevented by the readydiffusion of carbon dioxide across alveolar capillary membranes. Thus, patients with asthma who are in the earlystages of an acute episode have hypoxemia in the absence of carbon dioxide retention. Hyperventilation triggeredby the hypoxic drive also causes a decrease in PaCO2. An increase in alveolar ventilation in the early stages of an

acute exacerbation prevents hypercarbia.

With worsening obstruction and increasing ventilation-perfusion mismatch, carbon dioxide retention occurs. In theearly stages of an acute episode, respiratory alkalosis results from hyperventilation. Later, the increased work ofbreathing, increased oxygen consumption, and increased cardiac output result in metabolic acidosis. Respiratoryfailure leads to respiratory acidosis.

Role of inflammation

Chronic inflammation of the airways is associated with increased BHR, which leads to bronchospasm and typicalsymptoms of wheezing, shortness of breath, and coughing after exposure to allergens, environmental irritants,viruses, cold air, or exercise. In some patients with chronic asthma, airflow limitation may be only partiallyreversible because of airway remodeling (hypertrophy and hyperplasia of smooth muscle, angiogenesis, andsubepithelial fibrosis) that occurs with chronic untreated disease.

New insights in the pathogenesis of asthma suggest that lymphocytes play a role. Airway inflammation in asthmamay represent a loss of normal balance between two "opposing" populations of T helper (Th) lymphocytes. Twotypes of Th lymphocytes have been characterized: Th1 and Th2. Th1 cells produce interleukin (IL)-2 and interferon-α (IFN-α), which are critical in cellular defense mechanisms in response to infection. Th2, in contrast, generates afamily of cytokines (interleukin-4 [IL-4], IL-5, IL-6, IL-9, and IL-13) that can mediate allergic inflammation.

The hygiene hypothesis

The current "hygiene hypothesis" of asthma illustrates how this cytokine imbalance may explain some of the

dramatic increases in asthma prevalence in Westernized countries.[8] This hypothesis is based on the conceptthat the immune system of the newborn is skewed toward Th2 cytokine generation (mediators of allergicinflammation). Over time, environmental stimuli such as infections activate Th1 responses and bring the Th1/Th2relationship to an appropriate balance.

Evidence suggests that the prevalence of asthma is reduced in children who experience the following events:

Certain infections (Mycobacterium tuberculosis, measles, or hepatitis A)Rural livingExposure to other children (eg, presence of older siblings and early enrollment in childcare

Less frequent use of antibiotics, including in the first week of life[9]

Early introduction of fish in the diet[9]

Furthermore, the absence of these lifestyle events is associated with the persistence of a Th2 cytokine pattern.

Under these conditions, the genetic background of the child, with a cytokine imbalance toward Th2, sets the stageto promote the production of immunoglobulin E (IgE) antibody to key environmental antigens (eg, dust mites,cockroaches, Alternaria, and possibly cats). Therefore, a gene-by-environment interaction occurs in which thesusceptible host is exposed to environmental factors that are capable of generating IgE, and sensitization occurs.

A reciprocal interaction is apparent between the two subpopulations, in which Th1 cytokines can inhibit Th2generation and vice versa. Allergic inflammation may be the result of an excessive expression of Th2 cytokines.Alternatively, recent studies have suggested the possibility that the loss of normal immune balance arises from a

cytokine dysregulation in which Th1 activity in asthma is diminished.[10]

Results of two recently reported cross sectional studies of children growing up on farms in Central Europe whowere exposed to greater variety of environmental microorganisms showed an inverse relationship between

microbial exposure and the probability of asthma.[11]

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Genetic factors

Some studies highlight the importance of genotypes in contributing to asthma susceptibility and allergic

sensitization, as well as response to specific asthma treatments.[12, 13, 14, 15]

Through the use of cluster analysis, the Severe Asthma Research Program of the National Heart, Lung, and Blood

Institute identified 5 phenotypes of asthma.[16] Cluster 1 patients have early-onset atopic asthma with normal lungfunction treated with two or fewer controller medications and minimal health care utilization. Cluster 2 patientshave early-onset atopic asthma and preserved lung function but increased medication requirements (29% on threeor more medications) and health care utilization.

Cluster 3 comprises mostly older obese women with late-onset nonatopic asthma, moderate reductions inpulmonary function, and frequent oral corticosteroid use to manage exacerbations. Cluster 4 and cluster 5 patientshave severe airflow obstruction with bronchodilator responsiveness but differ in to their ability to attain normal lung

function, age of asthma onset, atopic status, and use of oral corticosteroids.[16]

A recently reported meta-analysis of genome-wide association studies of asthma in ethnically diverse NorthAmerican populations identified 5 susceptibility loci. Four were on previously reported loci on 17q21 and a new

asthma susceptibility locus at PYHIN1, which is specific to the African American population.[17]

An Australian study identified 2 new loci with genome-wide significant association with asthma risk: rs4129267 inIL6R and rs7130588 on band 11q13.5. The IL6R association supports the hypothesis that cytokine dysregulationaffects asthma risk, hence a specific antagonist to IL6R may help. The results for the 11q13.5 locus suggest its

association with allergic sensitization and subsequent development of asthma.[18]

Other factors

A 2012 study reported a significant association between lung function deficit and bronchial responsiveness in the

neonatal period with development of asthma by age seven years.[19]

Lemanske et al reported that wheezing illnesses caused by rhinovirus infection during infancy were the strongest

predictor of wheezing in the third year of life.[20]

In a study of preschool children with asthma, Guilbert et al found that 2 years of inhaled corticosteroid therapy didnot change the asthma symptoms or lung function during a third, treatment-free year. This suggests that no

disease-modifying effect of inhaled corticosteroids is present after the treatment is discontinued.[21]

In a study of children in the Cincinnati area, Reponen et al found that a high Environmental Relative Moldiness

Index (ERMI)[22] at age 1 year made asthma at age 7 years more likely. The ERMI did not predict specific moldallergies at age 7 years. Air conditioning made asthma less likely. An elevated ERMI at age 7 years had nocorrelation with current asthma. Seeing or smelling mold in a home inspection at age 1 year did not correlate withthe ERMI or with the development of asthma. They also found that black race, having a parent with asthma, and

house dust allergy was predictive of a greater likelihood of asthma.[23]

A recent study from Australia reported that obesity is a determinant of asthma control independent of

inflammation, lung function, and airway hyperresponsiveness.[24] A similar association between increased risk ofworse asthma control and obesity was reported in a recent retrospective study of 32,321 children aged 5-17 years.[25]

A significant inverse relationship between serum vitamin D levels and patient IgE levels, steroid requirements, and

in vitro responsiveness to corticosteroids in children has been reported.[26]

Parental cigarette smoking has been shown to increase the likelihood of asthma. This is more true for maternalsmoking, though the authors of one study did not correct for primary caretakers. The more cigarettes the mother

smoked, the greater the risk of asthma.[27]

A 2012 publication reported a weak correlation between maternal use of margarines during lactation and increased

asthma risk in offspring by the age of five years.[28]

Etiology

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In most cases of asthma in children, multiple triggers or precipitants are recognized, and the patterns of reactivitymay change with age. Treatment can also change the pattern. Certain viral infections, such as respiratorysyncytial virus (RSV) bronchiolitis in infancy, predispose the child to asthma.

Respiratory infections

Most commonly, these are viral infections. In some patients, fungi (eg, allergic bronchopulmonary aspergillosis),bacteria (eg, Mycoplasma, pertussis), or parasites may be responsible. Most infants and young children whocontinue to have a persistent wheeze and asthma have high immunoglobulin E (IgE) production and eosinophilicimmune responses (in the airways and in circulation) at the time of the first viral upper respiratory tract infection(URTI). They also have early IgE-mediated responses to local aeroallergens.

Allergens and irritants

In patients with asthma, 2 types of bronchoconstrictor responses to allergens are recognized: early and late. Earlyasthmatic responses occur via IgE-induced mediator release from mast cells within minutes of exposure and lastfor 20-30 minutes.

Late asthmatic responses occur 4-12 hours after antigen exposure and result in more severe symptoms that canlast for hours and contribute to the duration and severity of the disease. Inflammatory cell infiltration andinflammatory mediators play a role in the late asthmatic response. Allergens can be foods, household inhalants(eg, animal allergens, molds, fungi, roach allergens, dust mites), or seasonal outdoor allergens (eg, mold spores,pollens, grass, trees).

Tobacco smoke, cold air, chemicals, perfumes, paint odors, hair sprays, air pollutants, and ozone can initiateBHR by inducing inflammation.

Other factors

Asthma attacks can be related to changes in atmospheric temperature, barometric pressure, and the quality of air(eg, humidity, allergen and irritant content). In some individuals, emotional upsets clearly aggravate asthma.

Exercise can trigger an early asthmatic response. Mechanisms underlying exercise-induced asthmatic responseremain somewhat uncertain. Heat and water loss from the airways can increase the osmolarity of the fluid liningthe airways and result in mediator release. Cooling of the airways results in congestion and dilatation of bronchialvessels. During the rewarming phase after exercise, the changes are magnified because the ambient air breathedduring recovery is warm rather than cool.

The presence of acid in the distal esophagus, mediated via vagal or other neural reflexes, can significantlyincrease airway resistance and airway reactivity. Inflammatory conditions of the upper airways (eg, allergic rhinitis,sinusitis, or chronic and persistent infections) must be treated before asthmatic symptoms can be completelycontrolled.

Multiple factors have been proposed to explain nocturnal asthma. Circadian variation in lung function andinflammatory mediator release in the circulation and airways (including parenchyma) have been demonstrated.Other factors, such as allergen exposure and posture-related irritation of airways (eg, gastroesophageal reflux,sinusitis), can also play a role. In some cases, abnormalities in CNS control of the respiratory drive may bepresent, particularly in patients with a defective hypoxic drive and obstructive sleep apnea.

Children exposed to higher maternal stress during the pre- and postnatal period were reported to be at higher risk

for wheeze. This was only true in non-atopic mothers.[29]

A 2012 Danish study reported an association between maternal obesity (BMI ≥35 and gestational weight gain ≥25

kg) during pregnancy with increased risk of asthma and wheezing in the offspring.[30]

Results of a prospective birth cohort study of 568 pregnant women and their offspring showed that postnatalbisphenol A (BPA) exposure in the first years of a child's life is associated with significantly increased risk forwheeze and asthma. The study also found, however, that fetal exposure to BPA during the third trimester of

pregnancy was inversely associated with risk for wheeze in offspring at age 5 years.[31, 32]

Epidemiology

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Approximately 34.1 million people in the United States have been diagnosed with asthma in their lifetime.According to the most recent US Centers for Disease Control and Prevention (CDC) Asthma Surveillance Survey,the prevalence of current asthma during 2001-2003 prevalence is estimated at 6.7% in adults and 8.5% in children,

and the burden of asthma increased more than 75% from 1980-1999.[33, 34]

Asthma accounts for more school absences and more hospitalizations than any other chronic illness. In mostchildren's hospitals in the United States, it is the most common diagnosis at admission.

Worldwide, 130 million people have asthma. The prevalence is 8-10 times higher in developed countries (eg, UnitedStates, Great Britain, Australia, New Zealand) than in the developing countries. In developed countries, theprevalence is higher in low-income groups in urban areas and inner cities than in other groups.

A long-term study of a birth cohort on the Isle of Wight showed that maternal asthma and eczema wereassociated with asthma and eczema in their daughters, but not in their sons. Similarly, paternal asthma and

eczema were associated with asthma and eczema in their sons, but not in their daughters.[35]

Race-, sex-, and age-related demographics

The prevalence of asthma is higher in minority groups (eg, blacks, Hispanics) than in other groups; however,findings from one study suggest that much of the recent increase in the prevalence is attributed to asthma in whitechildren. Approximately 5-8% of all black children have asthma at some time. The prevalence in Hispanic childrenis reported to be as high as 15%. In blacks, the death rate is consistently higher than in whites.

Before puberty, the prevalence of asthma is 3 times higher in boys than in girls. During adolescence, theprevalence is equal among males and females. Adult-onset asthma is more common in women than in men.

In most children, asthma develops before age 5 years, and, in more than half, asthma develops before age 3years.

Among infants, 20% have wheezing with only upper respiratory tract infections (URTIs), and 60% no longer havewheezing by age 6 years. As Martinez et al have pointed out, however, many of these children are "transient

wheezers" whose symptoms subside during the preschool or early school years.[36, 37] They tend to have noallergies, although their lung function is often abnormal. These findings have led to the idea that they have smalllungs.

Children in whom wheezing begins early in conjunction with allergies are more likely to have wheezing when theyare aged 6-11 years. Similarly, children in whom wheezing begins after age 6 years often have allergies, and the

wheezing is more likely to continue when they are aged 11 years.[20]

Prognosis

Of infants who wheeze with URTIs, 60% are asymptomatic by age 6 years. However, children who have asthma(recurrent symptoms continuing at age 6 y) have airway reactivity later in childhood. Some findings suggest a poorprognosis if asthma develops in children younger than 3 years, unless it occurs solely in association with viralinfections.

Individuals who have asthma during childhood have significantly lower forced expiratory volume in 1 second (FEV1),

higher airway reactivity, and more persistent bronchospastic symptoms than those with infection-associatedwheezing.

Children with mild asthma who are asymptomatic between attacks are likely to improve and be symptom-free laterin life.

Children with asthma appear to have less severe symptoms as they enter adolescence, but half of these childrencontinue to have asthma. Asthma has a tendency to remit during puberty, with a somewhat earlier remission ingirls. However, compared with men, women have more BHR.

Mortality and morbidity associated with asthma

Globally, morbidity and mortality associated with asthma have increased over the last 2 decades. This increase isattributed to increasing urbanization. Despite advancements in the understanding of asthma and the developmentof new therapeutic strategies, the morbidity and mortality rates due to asthma definitely increased from 1980-1995.

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In the United States, the mortality rate due to asthma has increased in all age, race, and sex strata. In the UnitedStates, the mortality rate due to asthma is more than 17 deaths per 1 million population (ie, 5000 deaths peryear).

From 1975-1993, the number of deaths nearly doubled in people aged 5-14 years. In the northeastern andmidwestern United States, the highest mortality rate has been among persons aged 5-34 years. According to themost recent report from the CDC and the National Center for Health Statistics, 187 children aged 0-17 years diedfrom asthma, or 0.3 deaths per 100,000 children compared with 1.9 deaths per 100,000 adults aged 18 or older in

the year 2002.[33]

Non-Hispanic blacks were the most likely to die from asthma and had an asthma death rate more than 200%higher than non-Hispanic whites and 160% higher than Hispanics.

Patient Education

Patient and parent education should include instructions on how to use medications and devices (eg, spacers,nebulizers, metered-dose inhalers [MDIs]). The patient's MDI technique should be assessed on every visit.Discuss the management plan, which includes instructions about the use of medications, precautions with drugand/or device usage, monitoring symptoms and their severity (peak flow meter reading), and identifying potentialadverse effects and necessary actions.

Write and discuss in detail a rescue plan for an acute episode. This plan should include instructions for identifyingsigns of an acute attack, using rescue medications, monitoring, and contacting the asthma care team. Parentsshould understand that asthma is a chronic disorder with acute exacerbations; hence, continuity of managementwith active participation by the patient and/or parents and interaction with asthma care medical personnel isimportant. Emphasize the importance of adherence to treatment.

Incorporate the concept of expecting full control of symptoms, including nocturnal and exercise-inducedsymptoms, in the management plans and goals (for all but the most severely affected patients). Avoidunnecessary restrictions in the lifestyle of the child or family. Expect the child to participate in recreationalactivities and sports and to attend school as usual.

A systematic review by Coffman and colleagues suggested a benefit school-based asthma education. Their review

included 25 studies in children aged 4-17 years.[38] In most of those studies, compared with usual care, school-based asthma education improved knowledge of asthma (7 of 10 studies), self-efficacy (6 of 8 studies), and self-management behaviors (7 of 8 studies). Fewer studies reported favorable effects on quality of life (4 of 8 studies),days of symptoms (5 of 11 studies), nights with symptoms (2 of 4 studies), and school absences (5 of 17

studies).[38]

For patient education information, see the Asthma Center, as well as Asthma, Asthma FAQs, UnderstandingAsthma Medications, Asthma in Children, and Asthma in School Children: Educational Slides.

Contributor Information and DisclosuresAuthorGirish D Sharma, MD, FCCP, FAAP Professor of Pediatrics, Director, Section of Pediatric Pulmonology andRush Cystic Fibrosis Center, Rush Medical College; Senior Attending, Department of Pediatrics, RushUniversity Medical Center

Girish D Sharma, MD, FCCP, FAAP is a member of the following medical societies: American Academy ofPediatrics, American College of Chest Physicians, American Thoracic Society, and Royal College ofPhysicians of Ireland

Disclosure: Nothing to disclose.

Coauthor(s)Payel Gupta, MD Department of Allergy and Immunology, ENT Faculty Practice

Payel Gupta, MD is a member of the following medical societies: American College of Physicians

Disclosure: Nothing to disclose.

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Specialty Editor BoardThomas Scanlin, MD Chief, Division of Pulmonary Medicine and Cystic Fibrosis Center, Department ofPediatrics, Rutgers Robert Wood Johnson Medical School

Thomas Scanlin, MD is a member of the following medical societies: American Association for theAdvancement of Science, American Society for Biochemistry and Molecular Biology, American ThoracicSociety, Society for Pediatric Research, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College ofPharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Charles Callahan, DO Professor, Deputy Chief of Clinical Services, Walter Reed Army Medical Center

Charles Callahan, DO is a member of the following medical societies: American Academy of Pediatrics,American College of Chest Physicians, American College of Osteopathic Pediatricians, American ThoracicSociety, Association of Military Surgeons of the US, and Christian Medical & Dental Society

Disclosure: Nothing to disclose.

Chief EditorMichael R Bye, MD Professor of Clinical Pediatrics, State University of New York at Buffalo School ofMedicine; Attending Physician, Pediatric Pulmonary Division, Women's and Children's Hospital of Buffalo

Michael R Bye, MD is a member of the following medical societies: American Academy of Pediatrics, AmericanCollege of Chest Physicians, and American Thoracic Society

Disclosure: Nothing to disclose.

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