Pediatric Reactive Airway Disease



Not all children who wheeze have asthma. Most children younger than 3 years who wheeze are not predisposed to asthma. Only 30% of infants who wheeze go on to develop asthma. Reactive airway disease has a large differential diagnosis and must not be confused with asthma.

To establish the diagnosis of asthma, certain criteria should be met:[1]

  1. At least 5 years of age
  2. Episodic symptoms of airflow obstruction or airway hyperresponsiveness
  3. Reversible airflow obstruction of at least 10% of predicted forced expiratory volume in one second (FEV1) after use of short-acting beta2-agonist
  4. Alternative diagnoses have been excluded

On June 25, 2009, The American Thoracic Society and the European Respiratory Society jointly released new official standards on asthma evaluation for clinical trials and practice.[2] The Medscape Medical News article, New Guidelines Issued for Asthma Assessment, has a more detailed discussion.


Numerous environmental stimuli induce an allergen-antibody interaction, causing a release of mediators that create airway inflammation. Airway inflammation is the primary factor responsible for smooth muscle hyperresponsiveness, edema, and increased mucous production, resulting in increased work of breathing. A complex interaction occurs between inflammatory cells and airway epithelium. Mediators released from mast cells induce edema, mucous secretion, and bronchospasm. These mediators include histamine, tryptase, heparin, leukotrienes, platelet-activating factor, cytokines, interleukins, and tumor necrosis factor. The other inflammatory cells (ie, eosinophils, lymphocytes) also release mediators and create a toxic environment to respiratory epithelial cells.

In infants and children younger than 3 years, the intrapulmonary airways are so small that any lower airway infection results in diminished airway function. Other anatomical factors, such as poor collateral ventilation, decreased elastic recoil pressure, and a partially developed diaphragm, may predispose the very young child to respiratory compromise.

Speculation exists that all infants are born with highly responsive airways. Increased immunoglobulin E (IgE) levels have been found in those younger than 2 years. A decrease in airway responsiveness may be associated with environmental allergens, viral respiratory diseases, and hereditary factors.

Rhinovirus infections are an important contributor to asthma exacerbations in children. Hence, therapies against rhinovirus might reduce the risk of severe exacerbations.[3]

Fever and bronchospasm are not associated with a more severe clinical course. In fact, fever as a response to infection may have a beneficial effect and can be seen as a good prognostic indicator.[4]

Hygiene hypothesis suggests that early exposure to infections and allergens might protect children from developing asthma later in life because of improved immune system.[4]

Breastfeeding might protect children younger than 24 months of age against recurrent wheezing. The cytokine, TGF-B1, in human milk may have both suppression and enhancement functions in the immune reaction.

Exposure to maternal environmental tobacco smoke during pregnancy or the first year appears to predispose children to reactive airway disease.

Current research on the genetic basis for the pathogenesis of asthma may lead to new diagnostic and preventive treatments. The ADAM33 gene on the short arm of chromosome 20 is hypothesized as being important in the development and pathogenesis of asthma.



United States

Risk of developing asthma is 7% if neither parent has asthma, 20% if one parent has asthma, and 64% if both parents have asthma. In the United States, approximately one half of all ED and clinic visits for asthma are children younger than 18 years. Pediatric asthma is a chronic, multifactorial, lower airway disease that affects 5-15% of children (2.7 million children in the United States alone). ED visits peak in the fall. School holidays disrupt the spread of infections with a subsequent decrease in hospitalization. Asthma prevalence appears to be increasing worldwide. Air pollutants may play a role in the prevalence increase. Higher prevalence occurs in poverty stricken urban areas where children are less likely to have routine doctor visits and access to the availability of medications.

A correlation may exist between high levels of exposure to cockroach allergen and the frequency of asthma-related health problems in inner-city children.[5] Homes in poverty areas were more likely to have high cockroach allergen levels. Asthma may develop in children from early exposure to cockroach allergen.[6]

Status asthmaticus appears to be on the rise; several retrospective studies reflect an increase in hospital admissions, particularly in those younger than 4 years. Fewer hospital and ED visits occur in children using inhaled corticosteroid therapy.

An algorithm has been developed to determine the risk factors for developing persistent asthma symptoms among children younger than 3 years of age who had 4 or more episodes of wheezing during the previous year.[7] The Asthma Predictive Index included either (1) one of the following: parental history of asthma, a physician diagnosis of atopic dermatitis, or evidence of sensitization to aeroallergens; or (2) two of the following: evidence of sensitization to foods, ≥4% peripheral blood eosinophilia, or wheezing apart from colds.

An association may exist between obesity and childhood asthma. Increased resistin, an adipokine produced by adipose tissue, may play a negative predictive role in asthma.[8]


Worldwide, the prevalence of asthma is increasing. Asthma is found to be more common in Western countries than in developing countries. Asthma is more prevalent in English-speaking countries. Prevalence increases as a developing country becomes more Westernized and urbanized.



Reactive airway disease is more common in black and Hispanic children; hospitalization rates in African Americans are 4 times greater than in the white population.

No correlation exists with income or education level from a retrospective review.


The male-to-female ratio is 1.5:1.


The peak prevalence of asthma is in those aged 6-11 years.


The following information should be elicited:



Laboratory Studies

A complete blood count (CBC) may be indicated for a suspected viral infection (lymphocytosis, leukopenia), parasitic infection (eosinophilia), or hemosiderosis.

An arterial blood gas (ABG) determination should be performed for any patient in status asthmaticus to check for hypoxia, hypercarbia, or acidosis; alternatively, a venous blood gas measurement can be used to assess for hypercarbia and acidosis and combined with pulse oximetry monitoring.

An assessment of electrolyte levels may reveal hypokalemia in patients who are using albuterol.

Although theophylline is prescribed less frequently, a theophylline level is useful for those on the drug.

Imaging Studies

Routine radiography does not need to be part of the initial routine workup of asthma.[11]

Consider chest radiography if increased temperature, absence of family history of asthma, and the presence of localized wheezes or rales.

Other Tests


Procedures include the following:

Peak flow rates are described in the table below.

Table 1. Peak Flow Rates in Liters per Minute[12]

View Table

See Table

Prehospital Care

Provide oxygen during transport, cardiorespiratory monitoring and pulse oximetry, beta-agonist nebulization, and intravenous access if the patient is in moderate-to-severe respiratory distress. Subcutaneous terbutaline or epinephrine may be considered if severe distress and very poor air movement are present.

Emergency Department Care

Mild-to-moderate exacerbations (PEF >50% and/or oxygen saturation >92% on room air)

Albuterol is recommended for the initial treatment of mild-to-moderate acute exacerbations of asthma, administered either by a metered-dose inhaler with spacer (with or without mask) or by a hand-held nebulizer.

Two to six puffs of albuterol via metered-dose inhaler with spacer or 0.15 mg/kg (2.5 mg minimum dose, 5 mg maximum dose) via hand-held nebulizer every 20 minutes for up to 3 doses is recommended.

Oral dexamethasone 0.6 mg/kg/dose (first-line treatment) or oral prednisolone 2 mg/kg/dose (second-line treatment).

Severe exacerbations (PEF < 50% and/or oxygen saturation < 92% on room air) or exacerbations refractory to first-line treatment

Nebulized ipratropium bromide and short-acting beta-agonists, every 20 minutes for up to 3 treatments, are recommended for the treatment of children (250 mcg/dose) and adolescents (500 mcg/dose) with severe exacerbations.

Supplemental oxygen (by nasal cannula or mask, whichever is better tolerated) to maintain an oxygen saturation >92% is recommended during the delivery of short-acting beta-agonists and anticholinergics in patients with severe exacerbations.

Oral dexamethasone 0.6 mg/kg/dose (first-line treatment) or oral prednisolone 2 mg/kg/dose (second-line treatment) may be administered if early response to bronchodilators, otherwise parenteral steroids (dexamethasone or methylprednisolone) should be given.

Management of status asthmaticus

Management of status asthmaticus includes continuous inhaled beta-agonist of 0.5 mg/kg/h, nebulized ipratropium, IV dexamethasone 0.6 mg/kg, and intravenous magnesium 25-40 mg/kg (given over 20 min as a single dose up to a maximum of 2 g) concurrently for the child in severe respiratory distress. Consideration for IM or SC epinephrine or terbutaline. IV hydration is recommended in severe asthmatic requiring admission. Patient should be kept NPO in case of respiratory failure and need for intubation.

Frequent evaluation of the patient's cardiorespiratory status is imperative. Pulse oximetry and noninvasive end-tidal CO2 monitoring are ideal. Serial blood gas measurements may be necessary if the patient remains critically ill. If a child fails to improve with these interventions, admission to an ED observation area, inpatient unit, or pediatric critical care unit should be initiated. Continued failure to respond with mental status changes is an ominous finding and suggests rising pCO2. Consider noninvasive positive pressure ventilation (PPV) (eg, continuous positive airway pressure [CPAP] 3-5 cm H2 O, intermittent positive airway pressure [IPAP] 10-18 cm H2 O) prior to rapid sequence intubation. BiPAP utilization in acute pediatric asthma exacerbations for patients 20 kg or less is safe and may improve clinical outcomes.[13] Consider the increased risk of pneumothorax if intubated. Optimize ventilator settings.

Asthma management is shown in the illustration below.

View Image

Stepwise approach for managing asthma in children 0 to 4 years of age. National Institutes of Health. National Heart, Lung, and Blood Institute. Natio....

One study showed that the rate of return to the emergency department or admission to the hospital was decreased if the patient was discharged home with an inhaled corticosteroid.[15] Another study showed that 2 days of dexamethasone instead of 5 days of prednisone at the time of emergency department visit for asthma leads to a decreased number of emergency department visits and hospital admissions.[16]


Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Salmeterol (Serevent Diskus)

Clinical Context:  Long-acting beta2-agonist. Not for emergent use since onset is 30 min or more. By relaxing the smooth muscles of the bronchioles in conditions associated with bronchitis, emphysema, asthma, or bronchiectasis, can relieve bronchospasms. Effect may also facilitate expectoration.

Adverse effects are more likely to occur when administered at high or more frequent doses than recommended. Available as a dry powder for inhalation in 50 mcg blister packs.

Albuterol (Ventolin HFA, Proventil HFA)

Clinical Context:  Beta-agonist for bronchospasm refractory to epinephrine. Relaxes bronchial smooth muscle by action on beta2-receptors with little effect on cardiac muscle contractility. May decrease mediator release from mast cells and basophils and inhibit airway microvascular leakage. MDI delivers 90 mcg/actuation.

Continuous therapy may reduce need for mechanical ventilation.

Levalbuterol (Xopenex)

Clinical Context:  Used for treatment or prevention of bronchospasm. A selective beta2-agonist agent. Albuterol is a racemic mixture, while levalbuterol contains only the active R-enantiomer of albuterol. The S-enantiomer does not bind to beta2-receptors but may be responsible for some adverse effects of racemic albuterol, including bronchial hyperreactivity and reduced pulmonary function during prolonged use.

Class Summary

These agents relieve reversible bronchospasm by relaxing smooth muscles of the bronchi. Systemic beta-agonists allow systemic delivery of medication to the pulmonary system in medical conditions where bronchoconstriction may inhibit delivery of medication to desired site because of little to no air movement. Oral administration is less effective than inhaled beta-adrenergic agonists, and has therefore fallen into disfavor. Does not appear to alter admission.

Salmeterol is a highly selective, long-acting beta2-adrenergic agonist with bronchodilatory activity. Salmeterol's benzene moiety resembles the structure of catecholamines, and occupies the active site of beta2-adrenergic receptor, while the long, lipophilic side chain of salmeterol, binds to the so-called exosite near the beta2-receptors. The binding at the exosite allows the active portion of the molecule to remain at the receptor site and continually engage and disengage with the receptor, therefore providing a long duration of action. This agent stimulates intracellular adenyl cyclase to catalyze the conversion of adenosine triphosphate to cyclic-3',5'-adenosine monophosphate (cAMP). Increased cAMP levels result in relaxation of bronchiolar smooth muscle, bronchodilation, and increased bronchial airflow.

Ipratropium (Atrovent)

Clinical Context:  A quaternary ammonium anticholinergic bronchodilator acting at muscarinic receptors of the parasympathetic nervous system. Chemically related to atropine. Has antisecretory properties and, when applied locally, inhibits secretions from serous and seromucous glands lining the nasal mucosa.

Synergistic with beta2-agonists. Each actuation delivers 17 mcg. Solution for nebulization available as 0.02% (500 mcg/vial).

Class Summary

These agents decrease muscle tone in the small and large pulmonary airways.

Epinephrine (Adrenalin)

Clinical Context:  Elicits alpha-agonist effects that include increased peripheral vascular resistance, reversed peripheral vasodilatation, systemic hypotension, and vascular permeability. Beta2-agonist effects include bronchodilatation, chronotropic cardiac activity, and positive inotropic effects.

Terbutaline (Brethine)

Clinical Context:  Acts directly on beta2-receptors to relax bronchial smooth muscle, relieving bronchospasm and reducing airway resistance.

Class Summary

These agents act to decrease the muscle tone in the small and large pulmonary airways.

Theophylline, 85% (Aminophylline)

Clinical Context:  Potentiates exogenous catecholamines, stimulates endogenous catecholamine release and diaphragmatic muscular relaxation, which, in turn, stimulates bronchodilation.

For bronchodilation, near toxic (>20 mg/dL) levels are usually required.

No role in acute asthma exacerbation.

Considered in children who are responding poorly on maximal therapy.

Class Summary

These agents provide bronchodilation at the cellular level. The exact mechanism is unknown (eg, alteration of intracellular calcium, inhibition of phosphodiesterase, and/or antagonism of prostaglandins). Routine addition to beta-agonist provides benefit in ED management. May be of benefit in impending respiratory failure.

Magnesium sulfate

Clinical Context:  Thought to produce bronchodilation through counteraction of calcium-mediated smooth muscle constriction.

Class Summary

These agents decrease acetylcholine release at the neuromuscular junction and may decrease resting tone of smooth muscle.

Helium and oxygen (Heliox)

Clinical Context:  Reduces airway resistance in bronchi with turbulent flow because of low density. Decreases the work of breathing, hence, delaying the onset of respiratory muscle fatigue, allowing other therapies to work.

Available in mixtures of 80:20 (helium:oxygen), 70:30, and 60:40.

Class Summary

This agent is a blend of oxygen and helium that is less dense than air.

Ketamine (Ketalar)

Clinical Context:  Acts on the cortex and limbic system, decreasing bronchospasm.

Class Summary

Nonbarbiturate anesthetic/analgesic agent. An induction agent for airway management in patients with status asthmaticus and has a brief bronchodilatory effect.

Cromolyn (Intal)

Clinical Context:  Inhibits histamine release and slow-reacting substance of anaphylaxis from mast cell. MDI delivers 800 mcg/actuation. Solution for nebulization available as 20 mg/2 mL

Class Summary

These agents inhibit degranulation of sensitized mast cells following exposure to specific antigens.

Zileuton (Zyflo)

Clinical Context:  Effective in aspirin-induced, cold air, and exercise-induced asthma. Not for use in acute episodes of asthma. Prophylactic use only.

Hepatic transaminase levels should be evaluated before initiation. Contraindicated in patients with active liver disease.

Zafirlukast (Accolate)

Clinical Context:  Cysteinyl leukotriene-receptor antagonist. Inhibits aspirin-induced, cold air, and exercise-induced asthma.

Not for use in acute episodes of asthma.

Montelukast (Singulair)

Clinical Context:  Cysteinyl leukotriene-receptor antagonist. Inhibits aspirin-induced, cold air, and exercise-induced asthma. Not for use in acute episodes of asthma.

Class Summary

These agents inhibit the synthesis of leukotriene.

Dexamethasone (Decadron)

Clinical Context:  Has many pharmacologic benefits but significant adverse effects. Stabilizes cell and lysosomal membranes, increases surfactant synthesis, increases serum vitamin A concentration, inhibits prostaglandin and proinflammatory cytokines (eg, TNF-alpha, IL-6, IL-2, and IFN-gamma). The inhibition of chemotactic factors and factors that increase capillary permeability inhibits recruitment of inflammatory cells into affected areas. Suppresses lymphocyte proliferation through direct cytolysis and inhibits mitosis. Breaks down granulocyte aggregates, and improves pulmonary microcirculation. Has multiple glucocorticoid and mineralocorticoid effects.

Readily absorbed via the GI tract and metabolized in the liver. Inactive metabolites are excreted via the kidneys. Lacks salt-retaining property of hydrocortisone.

Patients can be switched from an IV to PO regimen in a 1:1 ratio.

Prednisolone (Orapred, Prelone, Pediapred)

Clinical Context:  Glucocorticosteroid that occurs naturally and synthetically. Used for both acute and chronic asthma. May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.

Loading or initial dose should be taken all at once in the am; may suppress natural cortisone production; hence, requires tapering the dose upon discontinuation.

As soon as the dose for relief is found, a maintenance dose may be established until the nonsteroidal drugs are effective; must always use a decreasing dose to avoid serious renal suppression.

In seasonal allergy a "booster" of prednisone may speed resolution of symptoms. Quite effective in "exhaustion" stage of seasonal allergy.

Prednisone (Sterapred)

Clinical Context:  May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.

Methylprednisolone (Medrol, Solu-Medrol)

Clinical Context:  For treatment of inflammatory and allergic reactions. By reversing increased capillary permeability and suppressing PMN activity, may decrease inflammation. Allows reduction of ongoing airway inflammation. May increase responsiveness to beta2-agonists by increasing the number of beta2-adrenergic receptors. Prophylactic inhaled steroids in those diagnosed with asthma may impede airway remodeling, bronchial hyperreactivity, and future airway damage.

Systemic adverse effects rarely occur with inhaled corticosteroids. Systemic response time is the same in IV and PO.

Steroid use is recommended if minimal improvement occurs after first beta2-agonist treatment, the patient was recently discontinued from steroids, the patient reports a history of asthma symptoms for a few days before presentation, or URI-associated symptoms are present.

Budesonide inhaled (Pulmicort Flexhaler, Pulmicort Respules)

Clinical Context:  Inhibits bronchoconstriction mechanisms, produces direct smooth muscle relaxation, may decrease number and activity of inflammatory cells, in turn decreasing airway hyperresponsiveness. Has extremely potent vasoconstrictive and anti-inflammatory activity. Alters level of inflammation in airways by inhibiting multiple types of inflammatory cells and decreasing production of cytokines and other mediators. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability.

Available as powder for inhalation in 90 mcg/actuation (actuation delivers ~80 mcg) or 180 mcg/actuation (actuation delivers ~160 mcg). Also available as suspension for nebulized inhalation in 0.25-mg/2 mL, 0.5-mg/2 mL, and 1-mg/2 mL. Indicated for maintenance treatment of asthma and prophylactic therapy.

Class Summary

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. They modify the body's immune response to diverse stimuli. Oral prednisone should never be substituted for an inhaled corticosteroid in children with a severe acute asthma exacerbation.

Frequent use of inhaled corticosteroid therapy is associated with less ED visits and less hospitalizations. Current research has not proven any long-term adverse effects with children receiving long-term inhaled corticosteroid.

Cimetidine (Tagamet)

Clinical Context:  If no response to H1 antagonist alone, coadministration with this H2 antagonist treats itching and flushing in anaphylaxis, pruritus, urticaria, and contact dermatitis.

Class Summary

The combination of H1 and H2 antagonists may be useful in anaphylaxis not responding to H1 antagonists alone.

Omalizumab (Xolair)

Clinical Context:  Recombinant, DNA-derived, humanized IgG monoclonal antibody that binds selectively to human IgE on surface of mast cells and basophils. Reduces mediator release, which promotes allergic response. Indicated for moderate-to-severe persistent asthma in patients who react to perennial allergens in whom symptoms are not controlled by inhaled corticosteroids.

Class Summary

May be considered in patients with severe asthma caused by allergens and unresponsive to other treatments.

Further Inpatient Care

Consider admission if the initial peak expiratory flow rate (PEFR) is less than 20-25% of predicted and posttreatment is less than 70% of predicted or if no improvement occurs after 4 hours.

If a child fails to improve within the first 2-3 hours of ED management, admission to an ED observation area, inpatient unit, or pediatric critical care unit is warranted.

If the patient is able to ambulate and tolerate fluids in the ED without distress, discharge may be considered.

Arrange for follow-up with the primary care provider within 24 hours.

The Children’s Asthma Care (CAC) measure set assesses whether pediatric patients admitted to hospitals with asthma exacerbation receive relievers (CAC-1) and systemic corticosteroids (CAC-2) during admission and whether they are discharged with a complete home management plan of care (CAC-3). A cross-sectional study using data for 30 US children’s hospitals found that CAC-1 and CAC-2 hospital compliance was high and that CAC-3 hospital compliance was moderate.[17] There was no significant association between CAC-3 hospital compliance and subsequent ED visits and asthma-related readmissions, suggesting that the CAC-3 measure needs further refinement to ensure evidence-based home management plans are being developed and conveyed to families in an effective manner.

Further Outpatient Care


Follow-up of pediatric asthma patients may be conducted by phone or in person; may include physical examination and/or spirometry; and may be performed by a case manager, registered nurse, nurse practitioner, or physician. Follow-up is recommended:

Assessment of severity and treatment plan

Assess the severity of the symptoms and effectiveness of treatment.[1]

Maintenance treatment (a recommended approach)


Parents of asthmatic children should have at least 2 sets of inhalers (eg, one for school and one for home).

After an asthma exacerbation, the child may return to school when asymptomatic and the PEFR is within 20% of normal.

Reduction in allergen exposure results in reduction of asthma and rhinitis symptoms and medications needed.

Avoid outdoor exposure and/or physical activity during periods of high smog alerts in community.

Change home furnace filters, remove dust, change linen, and vacuum regularly to reduce potential triggers.

In humid climates, keep humidity below 50% by using a dehumidifier to keep mold from growing.

Fluctuations in humidity and temperature can cause exacerbation of asthma attacks up to 2 days later.[28]

Avoid second-hand tobacco smoke, a well-known trigger of asthma attacks in infants and children.

Pediatric Asthma Controller Trial (PACT)[29] compared the effectiveness of 3 regimens in achieving asthma control:

Volunteers in the community can help as educators by providing home visits or in-school visits. Internet and MP3 players may help to engage adolescents in acquiring asthma knowledge.[30]

Annual influenza vaccination is recommended to prevent the complications from infection. The CDC's Advisory Committee on Immunization Practices (ACIP) and the American Academy of Pediatrics (AAP) recommend annual influenza vaccination for all persons aged at least 6 months.

In addition to the pneumococcal conjugate vaccine (PCV13) that is administered per schedule for healthy children, asthmatics should receive the 23-valent pneumonococcal polysaccharide vaccine (PPSV23) at least 8 weeks after they have completed immunization with PCV13.[31]

The trivalent inactive influenza vaccination administered intramuscularly is preferred over the live-attenuated vaccination administered intranasally.[32, 33]

Bronchial thermoplasty is a novel procedure approved by the FDA in 2010 for severe asthmatics (aged at least 18 years) who are not well controlled with medications. Ablation or radiofrequency is used to destroy the overgrowth of smooth muscle in the airway. The concept behind the treatment is that with less muscle, there is a decrease of the ability of the airways to constrict and narrow during a bronchospasm. The procedure is not without risk and does not cure asthma, but rather decreases the severity of asthmatic episodes.[34]

A new drug being tested is mepolizumab—a monoclonal antibody against interleukin 5—and is thought to inhibit eosinophilic airway inflammation. A multicenter, double-blind, placebo-controlled trial found mepolizumab to be effective and well-tolerated treatment that reduces the risk of asthma exacerbations in patients with eosinophilic asthma.[35]



The prognosis is excellent with attention to general health and appropriate use of medications.

Fewer than 50% of patients "out grow" asthma.

Predictors of mortality risk


Eric S Chin, MD, Consulting Staff, Department of Emergency Medicine, Kaiser Permanente Hospital, South San Francisco

Disclosure: Nothing to disclose.

Specialty Editors

Debra Slapper, MD, Consulting Staff, Department of Emergency Medicine, St Anthony's Hospital

Disclosure: Nothing to disclose.

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

Disclosure: Nothing to disclose.

Grace M Young, MD, Associate Professor, Department of Pediatrics, University of Maryland Medical Center

Disclosure: Nothing to disclose.

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

Disclosure: Nothing to disclose.

Chief Editor

Richard G Bachur, MD, Associate Professor of Pediatrics, Harvard Medical School; Associate Chief and Fellowship Director, Attending Physician, Division of Emergency Medicine, Children's Hospital of Boston

Disclosure: Nothing to disclose.


  1. [Guideline] Expert panel commissioned by the National Asthma Education and Prevention Program (NAEPP) Coordinating Committee(CC), coordinated by the National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health. The Expert Panel Report 3 (EPR-3) Full Report 2007: Guidelines for the Diagnosis and Management of Asthma. August 28, 2007;
  2. [Guideline] Reddel HK, Taylor DR, Bateman ED, et al. An official American Thoracic Society/european Respiratory Society statement: asthma control and exacerbations: standardizing endpoints for clinical asthma trials and clinical practice. Am J Respir Crit Care Med. Jul 1 2009;180(1):59-99. [View Abstract]
  3. Szefler SJ. Advances in pediatric asthma in 2007. J Allergy Clin Immunol. Mar 2008;121(3):614-9. [View Abstract]
  4. Sahib El-Radhi A, Patel S. The clinical course of childhood asthma in association with fever. Clin Pediatr (Phila). Jul 2009;48(6):627-31. [View Abstract]
  5. Rosenstreich DL, Eggleston P, Kattan M, et al. The role of cockroach allergy and exposure to cockroach allergen in causing morbidity among inner-city children with asthma. N Engl J Med. May 8 1997;336(19):1356-63. [View Abstract]
  6. Litonjua AA, Carey VJ, Burge HA, et al. Exposure to cockroach allergen in the home is associated with incident doctor-diagnosed asthma and recurrent wheezing. J Allergy Clin Immunol. Jan 2001;107(1):41-7. [View Abstract]
  7. Castro-Rodriguez JA, Holberg CJ, Wright AL, Martinez FD. A clinical index to define risk of asthma in young children with recurrent wheezing. Am J Respir Crit Care Med. Oct 2000;162(4 Pt 1):1403-6. [View Abstract]
  8. Kim KW, Shin YH, Lee KE, Kim ES, Sohn MH, Kim KE. Relationship between adipokines and manifestations of childhood asthma. Pediatr Allergy Immunol. Sep 2008;19(6):535-40. [View Abstract]
  9. Federico MJ, Wamboldt FS, Carter R, Mansell A, Wamboldt MZ. History of serious asthma exacerbations should be included in guidelines of asthma severity. J Allergy Clin Immunol. Jan 2007;119(1):50-6. [View Abstract]
  10. Stewart LJ. Pediatric asthma. Prim Care. Mar 2008;35(1):25-40, vi. [View Abstract]
  11. Hederos CA, Janson S, Andersson H, Hedlin G. Chest X-ray investigation in newly discovered asthma. Pediatr Allergy Immunol. Apr 2004;15(2):163-5. [View Abstract]
  12. Hsu KH, Jenkins DE, Hsi BP, et al. Ventilatory functions of normal children and young adults--Mexican- American, white, and black. II. Wright peak flowmeter. J Pediatr. Aug 1979;95(2):192-6. [View Abstract]
  13. Williams AM, Abramo TJ, Shah MV, et al. Safety and clinical findings of BiPAP utilization in children 20 kg or less for asthma exacerbations. Intensive Care Med. Aug 2011;37(8):1338-43. [View Abstract]
  14. Kaashmiri M, Shepard J, Goodman B, Lincourt WR, Trivedi R, Ellsworth A, et al. Repeat dosing of albuterol via metered-dose inhaler in infants with acute obstructive airway disease: a randomized controlled safety trial. Pediatr Emerg Care. Mar 2010;26(3):197-202. [View Abstract]
  15. Andrews AL, Teufel RJ 2nd, Basco WT Jr, Simpson KN. A cost-effectiveness analysis of inhaled corticosteroid delivery for children with asthma in the emergency department. J Pediatr. Nov 2012;161(5):903-7. [View Abstract]
  16. Andrews AL, Wong KA, Heine D, Scott Russell W. A cost-effectiveness analysis of dexamethasone versus prednisone in pediatric acute asthma exacerbations. Acad Emerg Med. Aug 2012;19(8):943-8. [View Abstract]
  17. Morse RB, Hall M, Fieldston ES, McGwire G, Anspacher M, Sills MR, et al. Hospital-level compliance with asthma care quality measures at children's hospitals and subsequent asthma-related outcomes. JAMA. Oct 5 2011;306(13):1454-60. [View Abstract]
  18. Stanford R, et al. Comparative clinical and economic outcomes in children with asthma initiating eitherfluticasone propionate plus salmeterol or inhaled corticosteroids plus montelukast. Ann Allergy Asthma Immunol. Nov 2009;103(5):62.
  19. Nino G, Grunstein MM. Current concepts on the use of glucocorticosteroids and beta-2-adrenoreceptor agonists to treat childhood asthma. Curr Opin Pediatr. Feb 15 2010;[View Abstract]
  20. Childhood Asthma Treatment: Not One-Size-Fits-All. National Heart, Lung, and Blood Institute (NHLBI); March 2,2010.
  21. Massanari M, Milgrom H, Pollard S, Maykut RJ, Kianifard F, Fowler-Taylor A, et al. Adding omalizumab to the therapy of adolescents with persistent uncontrolled moderate--severe allergic asthma. Clin Pediatr (Phila). Oct 2009;48(8):859-65. [View Abstract]
  22. Sandstrom T. Omalizumab in the management of patients with allergic (IgE-mediated) asthma. Journal of Asthma and Allergy. May 2009;2:49-62.
  23. Lanier B, Bridges T, Kulus M, Taylor AF, Berhane I, Vidaurre CF. Omalizumab for the treatment of exacerbations in children with inadequately controlled allergic (IgE-mediated) asthma. J Allergy Clin Immunol. Dec 2009;124(6):1210-6. [View Abstract]
  24. Early Communication about an Ongoing Safety Review of Omalizumab (marketed as Xolair). US Department of Health and Human Services/FDA; July 2009.
  25. Schramm CM, Carroll CL. Advances in treating acute asthma exacerbations in children. Curr Opin Pediatr. Jun 2009;21(3):326-32. [View Abstract]
  26. Blackhall K, Appleton S, Cates CJ. Ionisers for chronic asthma. Cochrane Database Syst Rev. 2003;CD002986. [View Abstract]
  27. Zeiger RS, Mauger D, Bacharier LB, Guilbert TW, Martinez FD, Lemanske RF Jr, et al. Daily or intermittent budesonide in preschool children with recurrent wheezing. N Engl J Med. Nov 24 2011;365(21):1990-2001. [View Abstract]
  28. Mireku N, Wang Y, Ager J, Reddy RC, Baptist AP. Changes in weather and the effects on pediatric asthma exacerbations. Ann Allergy Asthma Immunol. Sep 2009;103(3):220-4. [View Abstract]
  29. [Best Evidence] Sorkness CA, Lemanske RF Jr, Mauger DT, Boehmer SJ, Chinchilli VM, Martinez FD, et al. Long-term comparison of 3 controller regimens for mild-moderate persistent childhood asthma: the Pediatric Asthma Controller Trial. J Allergy Clin Immunol. Jan 2007;119(1):64-72. [View Abstract]
  30. Li P, Guttmann A. Recent innovations to improve asthma outcomes in vulnerable children. Curr Opin Pediatr. Dec 2009;21(6):783-8. [View Abstract]
  31. Nuorti JP, Whitney CG. Prevention of pneumococcal disease among infants and children - use of 13-valent pneumococcal conjugate vaccine and 23-valent pneumococcal polysaccharide vaccine - recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep. Dec 10 2010;59:1-18. [View Abstract]
  32. Fiore AE, Uyeki TM, Broder K, et al. Prevention and control of influenza with vaccines: recommendations of the Advisory Committee on Immunization Practices (ACIP), 2010. MMWR Recomm Rep. Aug 6 2010;59:1-62. [View Abstract]
  33. Committee on Infectious Diseases, American Academy of Pediatrics. Recommendations for prevention and control of influenza in children, 2012-2013. Pediatrics. Oct 2012;130(4):780-92. [View Abstract]
  34. US Food and Drug Administration. Asthmatx, Inc. Alair Bronchial Thermoplasty System - P080032. 2010.
  35. Pavord ID, Korn S, Howarth P, Bleecker ER, Buhl R, Keene ON, et al. Mepolizumab for severe eosinophilic asthma (DREAM): a multicentre, double-blind, placebo-controlled trial. Lancet. Aug 18 2012;380(9842):651-9. [View Abstract]
  36. Amirav I, Newhouse MT. Metered-dose inhaler accessory devices in acute asthma: efficacy and comparison with nebulizers: a literature review. Arch Pediatr Adolesc Med. Sep 1997;151(9):876-82. [View Abstract]
  37. Apter AJ, Szefler SJ. Advances in adult and pediatric asthma. J Allergy Clin Immunol. Mar 2004;113(3):407-14. [View Abstract]
  38. Baren JM, Zorc JJ. Contemporary approach to the emergency department management of pediatric asthma. Emerg Med Clin North Am. Feb 2002;20(1):115-38. [View Abstract]
  39. Beasley R, Crane J, Lai CK, Pearce N. Prevalence and etiology of asthma. J Allergy Clin Immunol. Feb 2000;105(2 Pt 2):S466-72. [View Abstract]
  40. Becker A, Watson W, Ferguson A, et al. The Canadian asthma primary prevention study: outcomes at 2 years of age. J Allergy Clin Immunol. Apr 2004;113(4):650-6. [View Abstract]
  41. Clainche LL, Timsit S, Rigourd V, et al. Asthma and the child below 5 years of age: diagnosis and treatment [in French]. Rev Mal Respir. Feb 2000;17(1 Pt 2):213-23. [View Abstract]
  42. Craig VL, Bigos D, Brilli RJ. Efficacy and safety of continuous albuterol nebulization in children with severe status asthmaticus. Pediatr Emerg Care. Feb 1996;12(1):1-5. [View Abstract]
  43. Crain EF, Mortimer KM, Bauman LJ, et al. Pediatric asthma care in the emergency department: measuring the quality of history-taking and discharge planning. J Asthma. 1999;36(1):129-38. [View Abstract]
  44. Csonka P, Mertsola J, Klaukka T, et al. Corticosteroid therapy and need for hospital care in wheezing preschool children. Eur J Clin Pharmacol. Nov 2000;56(8):591-6. [View Abstract]
  45. Darr CD. Asthma and bronchiolitis. In: Emergency Medicine: Concepts and Clinical Practice. 4th ed. 1998:1137-45.
  46. Eggleston PA, Wood RA, Rand C, et al. Removal of cockroach allergen from inner-city homes. J Allergy Clin Immunol. Oct 1999;104(4 Pt 1):842-6. [View Abstract]
  47. Farber HJ, Johnson C, Beckerman RC. Young inner-city children visiting the emergency room (ER) for asthma: risk factors and chronic care behaviors. J Asthma. 1998;35(7):547-52. [View Abstract]
  48. Garde Garde Jf, Haro E, Sanchez-Lucas C, Garde Noguera J. Antileukotrienes. Their use in pediatrics [in Spanish]. Allergol Immunopathol (Madr). May-Jun 2000;28(3):136-43. [View Abstract]
  49. Gibbs MA, Camargo CA, Rowe BH, Silverman RA. State of the art: therapeutic controversies in severe acute asthma. Acad Emerg Med. Jul 2000;7(7):800-15. [View Abstract]
  50. [Best Evidence] Guilbert TW, Morgan WJ, Zeiger RS, Mauger DT, Boehmer SJ, Szefler SJ, et al. Long-term inhaled corticosteroids in preschool children at high risk for asthma. N Engl J Med. May 11 2006;354(19):1985-97. [View Abstract]
  51. [Best Evidence] Hondras MA, Linde K, Jones AP. Manual therapy for asthma. Cochrane Database Syst Rev. Apr 18 2005;CD001002. [View Abstract]
  52. Kellner JD, Ohlsson A, Gadomski AM, Wang EE. Efficacy of bronchodilator therapy in bronchiolitis. A meta-analysis. Arch Pediatr Adolesc Med. Nov 1996;150(11):1166-72. [View Abstract]
  53. Kemp JP, Dockhorn RJ, Shapiro GG, et al. Montelukast once daily inhibits exercise-induced bronchoconstriction in 6- to 14-year-old children with asthma. J Pediatr. Sep 1998;133(3):424-8. [View Abstract]
  54. Kitch BT, Chew G, Burge HA, et al. Socioeconomic predictors of high allergen levels in homes in the greater Boston area. Environ Health Perspect. Apr 2000;108(4):301-7. [View Abstract]
  55. Le Clainche L, Timsit S, Rigourd V, et al. Asthma in children below 5 years of age: diagnosis and treatment. Rev Mal Respir. Feb 1999;16(1):17-27. [View Abstract]
  56. Newson T, McKenzie S. Cough and asthma in children. Pediatr Ann. Mar 1996;25(3):156-8, 161. [View Abstract]
  57. Qureshi F, Zaritsky A, Lakkis H. Efficacy of nebulized ipratropium in severely asthmatic children. Ann Emerg Med. Feb 1997;29(2):205-11. [View Abstract]
  58. Roback MG, Dreitlein DA. Chest radiograph in the evaluation of first time wheezing episodes: review of current clinical practice and efficacy. Pediatr Emerg Care. Jun 1998;14(3):181-4. [View Abstract]
  59. Rubin BK, Albers GM. Use of anticholinergic bronchodilation in children. Am J Med. Jan 29 1996;100(1A):49S-53S. [View Abstract]
  60. Rudolph CD. Supraesophageal complications of gastroesophageal reflux in children: challenges in diagnosis and treatment. Am J Med. Aug 18 2003;115 Suppl 3A:150S-156S. [View Abstract]
  61. Schreck DM, Babin S. Comparison of racemic albuterol and levalbuterol in the treatment of acute asthma in the ED. Am J Emerg Med. Nov 2005;23(7):842-7. [View Abstract]
  62. Schuh S, Reisman J, Alshehri M, et al. A comparison of inhaled fluticasone and oral prednisone for children with severe acute asthma. N Engl J Med. Sep 7 2000;343(10):689-94. [View Abstract]
  63. Spahn JD. Pharmacologic management of pediatric asthma. 1998;18 (1):165-81.
  64. Stempel DA, Meyer JW, Stanford RH, Yancey SW. One-year claims analysis comparing inhaled fluticasone propionate with zafirlukast for the treatment of asthma. J Allergy Clin Immunol. Jan 2001;107(1):94-8. [View Abstract]
  65. Steyer TE, Mallin R, Blair M. Pediatric asthma. Clinics in Family Practice. Jun 2003;5.
  66. Suissa S, Ernst P, Benayoun S, et al. Low-dose inhaled corticosteroids and the prevention of death from asthma. N Engl J Med. Aug 3 2000;343(5):332-6. [View Abstract]
  67. Sun HL, Chou MC, Lue KH, et al. The relationship of air pollution to ED visits for asthma differ between children and adults. Am J Emerg Med. Oct 2006;24(6):709-13. [View Abstract]
  68. Walsh-Kelly CM, Kim MK, Hennes HM. Chest radiography in the initial episode of bronchospasm in children: can clinical variables predict pathologic findings?. Ann Emerg Med. Oct 1996;28(4):391-5. [View Abstract]
  69. Welliver RC. Immunologic mechanisms of virus-induced wheezing and asthma. J Pediatr. Aug 1999;135(2 Pt 2):14-20. [View Abstract]
  70. Werk LN, Steinbach S, Adams WG, Bauchner H. Beliefs about diagnosing asthma in young children. Pediatrics. Mar 2000;105(3 Pt 1):585-90. [View Abstract]
  71. Williams JR, Bothner JP, Swanton RD. Delivery of albuterol in a pediatric emergency department. Pediatr Emerg Care. Aug 1996;12(4):263-7. [View Abstract]
  72. Wohl ME, Majzoub JA. Asthma, steroids, and growth. N Engl J Med. Oct 12 2000;343(15):1113-4. [View Abstract]
  73. Wolfram RW. Asthma. In: The Clinical Practice of Emergency Medicine. 2nd ed. 1997:1093-96.
  74. Zeffren BS, Windom HH, Bahna SL. Modern Treatment of Asthma in Children. Vol 43. Mosby Year Book; 1996:423-68.

Stepwise approach for managing asthma in children 0 to 4 years of age. National Institutes of Health. National Heart, Lung, and Blood Institute. National Asthma Education and Prevention Program. Expert Panel Report 3: Guidelines for the diagnosis and management of asthma. August 2007. NIH publication no. 07-4051. Available at: 3 Accessed December 30, 2007. PRN, As necessary.

Patient peak flow record.

This nomogram results from tests carried out by S. Godfrey, MD, and his colleagues on a sample of 382 healthy boys and girls aged 5-18 years. Each child blew 5 times into a standard Wright Peak Flow Meter, and the highest reading was accepted in each case. All measurements were completed within a 6-week period. The outer lines of the graph indicated that the results of 95% of the children fell within these boundaries.

Stepwise approach for managing asthma in children 0 to 4 years of age. National Institutes of Health. National Heart, Lung, and Blood Institute. National Asthma Education and Prevention Program. Expert Panel Report 3: Guidelines for the diagnosis and management of asthma. August 2007. NIH publication no. 07-4051. Available at: 3 Accessed December 30, 2007. PRN, As necessary.

Height in




Range*Height in




*Includes 95% of white males aged 7-20 years.

Derived and adapted from J Pediatr 1979;95:192-6.