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. A complex interaction occurs between inflammatory cells and airway epithelium. Mast cells, eosinophils and lymphocytes secrete mediators include histamine, tryptase, heparin, leukotrienes, platelet-activating factor, cytokines, interleukins, and tumor necrosis factor and create an environment toxic to respiratory epithelial cells by causing edema, mucous secretion, bronchospasm and increased work of breathing.

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. In 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.

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] Recently, it has been hypothesized that severe infection with Respiratory Syncytial Virus (RSV) may be a marker of a predisposing factor for asthma.[5]

There are several theories as to prevention of bronchospasm and asthma in children. The 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

Pediatric asthma is a chronic, multifactorial, lower airway disease that affects 5-15% of children (2.7 million children in the United States alone). In the United States, approximately one half of all ED and clinic visits for asthma are children younger than 18 years. ED visits peak in the fall while school holidays disrupt the spread of infections resulting in a subsequent decrease in ED visits and hospitalizations. 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.

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.[6] Homes in poverty areas were more likely to have high cockroach allergen levels. Asthma may develop in children from early exposure to cockroach allergen.[7] 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]

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.[9] 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.


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.


See the list below:


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. A correlation may exist between high levels of exposure to cockroach allergen and the frequency of asthma-related health problems in inner-city children.[6]

No correlation exists between education levels 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.


Childhood asthma and wheezy bronchitis persisting into adulthood could lead to chronic obstructive lung disease (COPD) in later decades of life.[11]   


The following information should be elicited:


See the list below:


See the list below:

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 evaluation of asthma.[14]

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

Other Tests

See the list below:


Procedures include the following:

Peak flow rates are described in the table below.

Table 1. Peak Flow Rates in Liters per Minute[15]

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.[16] 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.[18] 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.[19]

Recent experimental biological approaches targeting specific asthmatic inflammatory pathways based on immuno-inflammatory phenotypes. Mepolizumab and reslizumab, anti-IL5 antibodies, used in severe asthmatics with persistent sputum eosinophilia have shown to decrease exacerbations and oral corticosteroid use.[10]


See the list below:


PROSE (Preventative Omalizumab or Step-Up Therapy for Fall Exacerbations) Trial 

A 3-arm, randomized, double-blind, double placebo-controlled, multicenter clinical trial was conducted among inner-city asthmatic children aged 6 to 17 years with 1 or more recent exacerbations , comparing omalizumab or an inhaled steroid.

Study found that  asthma exacerbations, that are most frequent  during the fall season, can be reduced with a preventative strategy of treating high-risk group of allergic asthma subjects   with omalizumab (Xolair) four to six weeks before the start of school   and continuing it for the next four months.    Omalizumab   is thought to increase the release of an antiviral substance called interferon-alpha from certain immune cells thereby restoring  immune protection against common cold viruses.   Increasing inhaled steroid treatment levels above those determined to achieve control,  offered little to no additional benefit in preventing exacerbations.[20]


Intermittent use of inhaled corticosteroids at the start of asthma exacerbations can decrease the need for future oral corticosteroids. [21]

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 (LABA) 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.  LABA may not decrease the episodes of asthma exacerbations and may even lead to increased hospitalizations. [22]

Tiotropium (Spiriva HandiHaler, Spiriva Respimat)

Clinical Context:  long-acting, 24-hour, anticholinergic bronchodilator

Indicated for long-term, once-daily, maintenance treatment of asthma in patients aged ≥12 yr

Spiriva Respimat: 2.5 mcg (2 actuations; 1.25 mcg/actuation) inhaled PO qDay

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.

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.

Mepolizumab (Nucala)

Clinical Context:  Mepolizumab is a humanized IgG1 kappa monoclonal antibody specific for interleukin-5 (IL-5). Mepolizumab binds to IL-5, and therefore stops IL-5 from binding to its receptor on the surface of eosinophils. It is indicated for add-on maintenance treatment of patients with severe asthma aged ≥12 y, and with an eosinophilic phenotype.

Class Summary

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

Budesonide/formoterol (Symbicort)

Clinical Context:  Available as an MDI in 2 strengths; each actuation delivers formoterol 4.5-mcg with either 80-mcg or 160-mcg of budesonide.

Mometasone inhaled/formoterol (Dulera)

Clinical Context:  Available in 2 strengths; each actuation delivers mometasone/formoterol 100 mcg/5 mcg or 200 mcg/5 mcg.

Salmeterol/fluticasone inhaled (Advair HFA, Advair Diskus)

Clinical Context:  Two delivery mechanisms are available (ie, powder for inhalation [Diskus], metered-dose inhaler [MDI]). Diskus is available as a combination of salmeterol 50 mcg with fluticasone 100 mcg, 250 mcg, or 500 mcg. The MDI is available as 21 mcg salmeterol with fluticasone 45 mcg, 115 mcg, or 230 mcg.

Class Summary

The use of combination therapy with a long-acting beta2 agonist plus an inhaled corticosteroid as initial preventer treatment in children who are not already taking inhaled corticosteroids, is not supported by clinical trials. [23]

Budesonide inhaled (Pulmicort Flexhaler, Pulmicort Respules)

Clinical Context:  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.

Ciclesonide inhaled (Alvesco)

Clinical Context:  Aged 12 y and older

Receiving bronchodilators or inhaled corticosteroids: 80 mcg inhaled PO twice daily initially; may increase to 160 mcg twice daily Receiving Oral Corticosteroids: 80 mcg inhaled twice daily initially; may increase to 320 mcg twice daily

Beclomethasone, inhaled (Qvar)

Clinical Context:  <5 years: Safety and efficacy not established

5-12 years: 40 mcg inhaled PO BID for patients with/without prior history of inhaled corticosteroid use; do not exceed 80 mcg inhaled BID

>12 years

No prior history of inhaled corticosteroid use: 40-80 mcg inhaled PO BID; do not exceed 320 mcg BID Prior history of inhaled corticosteroid use: 40-160 mcg inhaled PO BID; do not exceed 320 mcg BID

Fluticasone inhaled (Flovent Diskus, Flovent HFA)

Clinical Context:  Inhaled aerosol

<4 years: Safety and efficacy not established 4-12 years: 88 mcg (2 actuations of 44 mcg) PO q12hr >12 years (prior inhaled corticosteroid use): 88-220 mcg PO q12hr; not to exceed 440 mcg q12hr >12 years (prior PO corticosteroid use): 440 mcg PO q12hr; not to exceed 880 mcg q12hr

Inhaled powder

<4 years: Safety and efficacy not established 4-12 years: 50-100 mcg PO q12hr >12 years (prior bronchodilator use): 100 mcg PO q12hr; not to exceed 500 mcg q12hr >12 years (prior inhaled corticosteroid use): 100-250 mcg PO q12hr; not to exceed 500 mcg q12hr >12 years (prior PO corticosteroid use): 500-1000 mcg PO q12hr; not to exceed 1000 mcg q12hr

Budesonide inhaled (Pulmicort Respules, Pulmicort Flexhaler)

Clinical Context:  Nebulized suspension

<1 years: Safety and efficacy not established 1-8 years (prior therapy with bronchodilators alone): 0.5 mg once daily or divided q12hr; not to exceed 0.5 mg/day 1-8 years (prior therapy with inhaled corticosteroids): 0.5 mg once daily or divided q12hr; not to exceed 1 mg/day 1-8 years (prior therapy with PO corticosteroids): 1 mg once daily or divided q12hr; not to exceed 1 mg/day Symptomatic children not responding to nonsteroidal therapy: May be initiated at 0.25 mg q12hr

Inhaled powder

<6 years: Safety and efficacy not established >6 years: 180 mcg PO q12hr; in some patients, may be initiated at 360 mcg q12hr; not to exceed 360 mcg q12hr

Mometasone inhaled (Asmanex HFA, Asmanex Twisthaler)

Clinical Context:  Asmanex Twisthaler

<4 years: Safety and efficacy not established 4-11 years: 110 mcg PO inhaled once daily in evening; not to exceed 110 mcg/day ≥12 years (received bronchodilators alone or inhaled corticosteroids): 220 mcg PO inhaled once daily in evening; may increase to 220 mcg q12hr if needed ≥12 years (received PO corticosteroids): 440 mcg PO inhaled q12hr; not to exceed 880 mcg/day

Asmanex HFA

<12 years: Safety and efficacy not established ≥12 years: 2 inhalations PO q12hr (ie, 200-400 mcg q12hr); starting dose based on prior asthma therapy -Received inhaled medium-dose corticosteroids: 200 mcg inhaled PO q12hr (as 2 actuations of 100 mcg/actuation) -Received inhaled high-dose corticosteroids: 400 mcg inhaled PO q12hr (as 2 actuations of 200 mcg/actuation) -Received oral corticosteroids: 400 mcg inhaled PO q12hr (as 2 actuations of 200 mcg/actuation)

Class Summary

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.

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)

See the list below:

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.[34] 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.


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.[35]

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

Pediatric Asthma Controller Trial (PACT)[36] 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.[37]

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.[38]

The trivalent inactive influenza vaccination administered intramuscularly is preferred over the live-attenuated vaccination administered intranasally.[39, 40]

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.[41]

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.[42]

FDA has approved tiotropium bromide Inhalation Spray for use in the treatment of asthma. It is approved by the FDA for the long-term, once-daily, maintenance treatment of asthma in patients 12 years of age and older. When used as an add-on treatment to inhaled corticosteroid maintenance therapy, a study has shown a significant reduction in severe asthma exacerbations. [43]


See the list below:


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

Fewer than 50% of patients "outgrow" asthma.

Predictors of mortality risk

Patient Education

Educate children and their families about asthma.

For excellent patient education resources, visit eMedicineHealth's Asthma Center. Also, see eMedicineHealth's patient education article Asthma.


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

Disclosure: Nothing to disclose.

Specialty Editors

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.

Chief Editor

Kirsten A Bechtel, MD, Associate Professor of Pediatrics, Section of Pediatric Emergency Medicine, Yale University School of Medicine; Co-Director, Injury Free Coalition for Kids, Yale-New Haven Children's Hospital

Disclosure: Nothing to disclose.

Additional Contributors

Debra Slapper, MD, Physician, Southwest Washington Free Clinic System-Urgent Care; Former FEMA Physician and Military Contractor; Former Associate Professor, University of Miami, Leonard M Miller School of Medicine and University of South Florida Morsani College of Medicine

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. 2009 Jul 1. 180(1):59-99. [View Abstract]
  3. Szefler SJ. Advances in pediatric asthma in 2007. J Allergy Clin Immunol. 2008 Mar. 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). 2009 Jul. 48(6):627-31. [View Abstract]
  5. Lotz MT, Moore ML, Peebles RS Jr. Respiratory syncytial virus and reactive airway disease. Curr Top Microbiol Immunol. 2013. 372:105-18. [View Abstract]
  6. 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. 1997 May 8. 336(19):1356-63. [View Abstract]
  7. 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. 2001 Jan. 107(1):41-7. [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. 2008 Sep. 19(6):535-40. [View Abstract]
  9. 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. 2000 Oct. 162(4 Pt 1):1403-6. [View Abstract]
  10. [Guideline] Kian Fan Chung, Sally E. Wenzel, Jan L. Brozek , Andrew Bush, Mario Castro. International ERS/ATS guidelines ondefinition, evaluation and treatment of severe asthma. Eur Respir J. April 2014. 43:343-373. [View Abstract]
  11. Tagiyeva N, Devereux G, Fielding S, Turner S, Douglas G. Outcomes of Childhood Asthma and Wheezy Bronchitis. A 50-Year Cohort Study. American journal of respiratory and critical care medicine. January 1, 2016. 193 (1):23-30. [View Abstract]
  12. 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. 2007 Jan. 119(1):50-6. [View Abstract]
  13. Stewart LJ. Pediatric asthma. Prim Care. 2008 Mar. 35(1):25-40, vi. [View Abstract]
  14. Hederos CA, Janson S, Andersson H, Hedlin G. Chest X-ray investigation in newly discovered asthma. Pediatr Allergy Immunol. 2004 Apr. 15(2):163-5. [View Abstract]
  15. 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. 1979 Aug. 95(2):192-6. [View Abstract]
  16. 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. 2011 Aug. 37(8):1338-43. [View Abstract]
  17. 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. 2010 Mar. 26(3):197-202. [View Abstract]
  18. 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. 2012 Nov. 161(5):903-7. [View Abstract]
  19. 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. 2012 Aug. 19(8):943-8. [View Abstract]
  20. SJ Teach et al. Preseasonal treatment with either omalizumab or an inhaled corticosteroid boost to prevent fall asthma exacerbations. Journal of Allergy and Clinical Immunology. December 2015. Volume 136, Issue 6:1476–1485.
  21. Chong J, Haran C, Chauhan BF, Asher I. Intermittent inhaled corticosteroid therapy versus placebo for persistent asthma in children and adults. The Cochrane database of systematic reviews. January 1, 2015. 7:[View Abstract]
  22. Chauhan BF, Chartrand C, Ni Chroinin M, Milan SJ, Ducharme FM. Addition of long-acting beta2-agonists to inhaled corticosteroids for chronic asthma in children. The Cochrane database of systematic reviews. January 1, 2015. 11:[View Abstract]
  23. Ducharme FM, Ni Chroinin M, Greenstone I, Lasserson TJ. Addition of long-acting beta2-agonists to inhaled steroids versus higher dose inhaled steroids in adults and children with persistent asthma. Cochrane Database Syst Rev. APR 2010. Issue 4:
  24. 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.
  25. Nino G, Grunstein MM. Current concepts on the use of glucocorticosteroids and beta-2-adrenoreceptor agonists to treat childhood asthma. Curr Opin Pediatr. 2010 Feb 15. [View Abstract]
  26. Childhood Asthma Treatment: Not One-Size-Fits-All. National Heart, Lung, and Blood Institute (NHLBI). March 2,2010. Available at
  27. 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). 2009 Oct. 48(8):859-65. [View Abstract]
  28. Sandstrom T. Omalizumab in the management of patients with allergic (IgE-mediated) asthma. Journal of Asthma and Allergy. May 2009. 2:49-62.
  29. 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. 2009 Dec. 124(6):1210-6. [View Abstract]
  30. Early Communication about an Ongoing Safety Review of Omalizumab (marketed as Xolair). US Department of Health and Human Services/FDA. July 2009. Available at
  31. Schramm CM, Carroll CL. Advances in treating acute asthma exacerbations in children. Curr Opin Pediatr. 2009 Jun. 21(3):326-32. [View Abstract]
  32. Blackhall K, Appleton S, Cates CJ. Ionisers for chronic asthma. Cochrane Database Syst Rev. 2003. CD002986. [View Abstract]
  33. 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. 2011 Nov 24. 365(21):1990-2001. [View Abstract]
  34. 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. 2011 Oct 5. 306(13):1454-60. [View Abstract]
  35. Mireku N, Wang Y, Ager J, Reddy RC, Baptist AP. Changes in weather and the effects on pediatric asthma exacerbations. Ann Allergy Asthma Immunol. 2009 Sep. 103(3):220-4. [View Abstract]
  36. 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. 2007 Jan. 119(1):64-72. [View Abstract]
  37. Li P, Guttmann A. Recent innovations to improve asthma outcomes in vulnerable children. Curr Opin Pediatr. 2009 Dec. 21(6):783-8. [View Abstract]
  38. 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. 2010 Dec 10. 59:1-18. [View Abstract]
  39. 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. 2010 Aug 6. 59:1-62. [View Abstract]
  40. Committee on Infectious Diseases, American Academy of Pediatrics. Recommendations for prevention and control of influenza in children, 2012-2013. Pediatrics. 2012 Oct. 130(4):780-92. [View Abstract]
  41. US Food and Drug Administration. Asthmatx, Inc. Alair Bronchial Thermoplasty System - P080032. 2010. Available at
  42. 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. 2012 Aug 18. 380(9842):651-9. [View Abstract]
  43. J. Bernstein et. al. Once-Daily Tiotropium Respimat Added-On to Inhaled Corticosteroids in a 1-Year Study in Adolescent Patients With Symptomatic Asthma Is Efficacious and Well Tolerated. Chest Journal. October 29, 2014. October 2014, Vol 146, No. 4_MeetingAbstracts:
  44. Amirav I, Newhouse MT. Metered-dose inhaler accessory devices in acute asthma: efficacy and comparison with nebulizers: a literature review. Arch Pediatr Adolesc Med. 1997 Sep. 151(9):876-82. [View Abstract]
  45. Apter AJ, Szefler SJ. Advances in adult and pediatric asthma. J Allergy Clin Immunol. 2004 Mar. 113(3):407-14. [View Abstract]
  46. Baren JM, Zorc JJ. Contemporary approach to the emergency department management of pediatric asthma. Emerg Med Clin North Am. 2002 Feb. 20(1):115-38. [View Abstract]
  47. Beasley R, Crane J, Lai CK, Pearce N. Prevalence and etiology of asthma. J Allergy Clin Immunol. 2000 Feb. 105(2 Pt 2):S466-72. [View Abstract]
  48. Becker A, Watson W, Ferguson A, et al. The Canadian asthma primary prevention study: outcomes at 2 years of age. J Allergy Clin Immunol. 2004 Apr. 113(4):650-6. [View Abstract]
  49. 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. 2000 Feb. 17(1 Pt 2):213-23. [View Abstract]
  50. Craig VL, Bigos D, Brilli RJ. Efficacy and safety of continuous albuterol nebulization in children with severe status asthmaticus. Pediatr Emerg Care. 1996 Feb. 12(1):1-5. [View Abstract]
  51. 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]
  52. Csonka P, Mertsola J, Klaukka T, et al. Corticosteroid therapy and need for hospital care in wheezing preschool children. Eur J Clin Pharmacol. 2000 Nov. 56(8):591-6. [View Abstract]
  53. Darr CD. Asthma and bronchiolitis. Emergency Medicine: Concepts and Clinical Practice. 4th ed. 1998. 1137-45.
  54. Eggleston PA, Wood RA, Rand C, et al. Removal of cockroach allergen from inner-city homes. J Allergy Clin Immunol. 1999 Oct. 104(4 Pt 1):842-6. [View Abstract]
  55. 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]
  56. Garde Garde Jf, Haro E, Sanchez-Lucas C, Garde Noguera J. Antileukotrienes. Their use in pediatrics [in Spanish]. Allergol Immunopathol (Madr). 2000 May-Jun. 28(3):136-43. [View Abstract]
  57. Gibbs MA, Camargo CA, Rowe BH, Silverman RA. State of the art: therapeutic controversies in severe acute asthma. Acad Emerg Med. 2000 Jul. 7(7):800-15. [View Abstract]
  58. 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. 2006 May 11. 354(19):1985-97. [View Abstract]
  59. Hondras MA, Linde K, Jones AP. Manual therapy for asthma. Cochrane Database Syst Rev. 2005 Apr 18. CD001002. [View Abstract]
  60. Kellner JD, Ohlsson A, Gadomski AM, Wang EE. Efficacy of bronchodilator therapy in bronchiolitis. A meta-analysis. Arch Pediatr Adolesc Med. 1996 Nov. 150(11):1166-72. [View Abstract]
  61. 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. 1998 Sep. 133(3):424-8. [View Abstract]
  62. Kitch BT, Chew G, Burge HA, et al. Socioeconomic predictors of high allergen levels in homes in the greater Boston area. Environ Health Perspect. 2000 Apr. 108(4):301-7. [View Abstract]
  63. Le Clainche L, Timsit S, Rigourd V, et al. Asthma in children below 5 years of age: diagnosis and treatment. Rev Mal Respir. 1999 Feb. 16(1):17-27. [View Abstract]
  64. Newson T, McKenzie S. Cough and asthma in children. Pediatr Ann. 1996 Mar. 25(3):156-8, 161. [View Abstract]
  65. Qureshi F, Zaritsky A, Lakkis H. Efficacy of nebulized ipratropium in severely asthmatic children. Ann Emerg Med. 1997 Feb. 29(2):205-11. [View Abstract]
  66. Roback MG, Dreitlein DA. Chest radiograph in the evaluation of first time wheezing episodes: review of current clinical practice and efficacy. Pediatr Emerg Care. 1998 Jun. 14(3):181-4. [View Abstract]
  67. Rubin BK, Albers GM. Use of anticholinergic bronchodilation in children. Am J Med. 1996 Jan 29. 100(1A):49S-53S. [View Abstract]
  68. Rudolph CD. Supraesophageal complications of gastroesophageal reflux in children: challenges in diagnosis and treatment. Am J Med. 2003 Aug 18. 115 Suppl 3A:150S-156S. [View Abstract]
  69. Schreck DM, Babin S. Comparison of racemic albuterol and levalbuterol in the treatment of acute asthma in the ED. Am J Emerg Med. 2005 Nov. 23(7):842-7. [View Abstract]
  70. 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. 2000 Sep 7. 343(10):689-94. [View Abstract]
  71. Spahn JD. Pharmacologic management of pediatric asthma. 1998. 18 (1):165-81.
  72. 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. 2001 Jan. 107(1):94-8. [View Abstract]
  73. Steyer TE, Mallin R, Blair M. Pediatric asthma. Clinics in Family Practice. 2003 Jun. 5:
  74. Suissa S, Ernst P, Benayoun S, et al. Low-dose inhaled corticosteroids and the prevention of death from asthma. N Engl J Med. 2000 Aug 3. 343(5):332-6. [View Abstract]
  75. 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. 2006 Oct. 24(6):709-13. [View Abstract]
  76. 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. 1996 Oct. 28(4):391-5. [View Abstract]
  77. Welliver RC. Immunologic mechanisms of virus-induced wheezing and asthma. J Pediatr. 1999 Aug. 135(2 Pt 2):14-20. [View Abstract]
  78. Werk LN, Steinbach S, Adams WG, Bauchner H. Beliefs about diagnosing asthma in young children. Pediatrics. 2000 Mar. 105(3 Pt 1):585-90. [View Abstract]
  79. Williams JR, Bothner JP, Swanton RD. Delivery of albuterol in a pediatric emergency department. Pediatr Emerg Care. 1996 Aug. 12(4):263-7. [View Abstract]
  80. Wohl ME, Majzoub JA. Asthma, steroids, and growth. N Engl J Med. 2000 Oct 12. 343(15):1113-4. [View Abstract]
  81. Wolfram RW. Asthma. The Clinical Practice of Emergency Medicine. 2nd ed. 1997. 1093-96.
  82. Zeffren BS, Windom HH, Bahna SL. Modern Treatment of Asthma in Children. Mosby Year Book; 1996. Vol 43: 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.