Childhood Asthma

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Chapter 138 Childhood Asthma

Asthma is a chronic inflammatory condition of the lung airways resulting in episodic airflow obstruction. This chronic inflammation heightens the twitchiness of the airways—airways hyperresponsiveness (AHR)—to provocative exposures. Asthma management is aimed at reducing airways inflammation by minimizing proinflammatory environmental exposures, using daily controller anti-inflammatory medications, and controlling co-morbid conditions that can worsen asthma. Less inflammation typically leads to better asthma control, with fewer exacerbations and decreased need for quick-reliever asthma medications. Nevertheless, exacerbations can still occur. Early intervention with systemic corticosteroids greatly reduces the severity of such episodes. Advances in asthma management and, especially, pharmacotherapy enable all but the uncommon child with severe asthma to live normally.


Although the cause of childhood asthma has not been determined, contemporary research implicates a combination of environmental exposures and inherent biologic and genetic vulnerabilities (Fig. 138-1). Respiratory exposures in this causal environment include inhaled allergens, respiratory viral infections, and chemical and biologic air pollutants such as environmental tobacco smoke. In the predisposed host, immune responses to these common exposures can be a stimulus for prolonged, pathogenic inflammation and aberrant repair of injured airways tissues. Lung dysfunction (i.e., AHR and reduced airflow) develops. These pathogenic processes in the growing lung during early life adversely affect airways growth and differentiation, leading to altered airways at mature ages. Once asthma has developed, ongoing exposures appear to worsen it, driving disease persistence and increasing the risk of severe exacerbations.


Asthma is a common chronic disease, causing considerable morbidity. In 2007, 9.6 million children (13.1%) had been diagnosed with asthma in their lifetimes. Of this group, 70% had asthma currently, and 3.8 million children (5.2%), nearly 60% of those with current asthma, had experienced at least one asthma attack in the prior year. Boys (14% vs 10% girls) and children in poor families (16% vs 10% not poor) are more likely to have asthma.

In the USA, childhood asthma is among the most common causes of childhood emergency department visits, hospitalizations, and missed school days, accounting in 2004 for 12.8 million missed school days, 750,000 emergency department visits, 198,000 hospitalizations, and 186 childhood deaths. A disparity in asthma outcomes links high rates of asthma hospitalization and death with poverty, ethnic minorities, and urban living. In the past 2 decades, African-American children had 2 to 4 times more emergency department visits, hospitalizations, and deaths due to asthma than white children. For ethnic minority asthmatic patients living in U.S. inner-city low-income communities, a combination of biologic, environmental, economic, and psychosocial risk factors is believed to increase the likelihood of severe asthma exacerbations. Although current asthma prevalence is higher in black than in non-black U.S. children (12.8%, in 2003-2005, vs 7.9% for white and 7.8% for Latino children), prevalence differences cannot fully account for this disparity in asthma outcomes.

Worldwide, childhood asthma appears to be increasing in prevalence, despite considerable improvements in our management and pharmacopeia to treat asthma. Numerous studies conducted in different countries have reported an increase in asthma prevalence of about 50% per decade. Globally, childhood asthma prevalence varies widely in different locales. A large international survey study of childhood asthma prevalence in 97 countries (International Study of Asthma and Allergies in Childhood) found a wide range in the prevalence of current wheeze, 0.8-37.6%. Asthma prevalence correlated well with reported allergic rhinoconjunctivitis and atopic eczema prevalence. Childhood asthma seems more prevalent in modern metropolitan locales and more affluent nations, and it is strongly linked with other allergic conditions. In contrast, children living in rural areas of developing countries and farming communities are less likely to experience asthma and allergy, although childhood asthma in less affluent nations seems more severe.

Approximately 80% of all asthmatic patients report disease onset prior to 6 yr of age. However, of all young children who experience recurrent wheezing, only a minority go on to have persistent asthma in later childhood. Early childhood risk factors for persistent asthma have been identified (Table 138-1). Prediction of asthma includes major (parent asthma, eczema, inhalant allergen sensitization) and minor (allergic rhinitis, wheezing apart from colds, ≥4% eosinophils, food allergen sensitization) risk factors. Allergy in young children has emerged as a major risk factor for the persistence of childhood asthma.

Types of Childhood Asthma

Asthma is considered to be a common clinical presentation of intermittent, recurrent wheezing and/or coughing, resulting from different airways pathologic processes underlying different types of asthma. There are 2 main types of childhood asthma: (1) recurrent wheezing in early childhood, primarily triggered by common viral infections of the respiratory tract, and (2) chronic asthma associated with allergy that persists into later childhood and often adulthood. A 3rd type of childhood asthma typically emerges in females who experience obesity and early-onset puberty (by 11 yr of age). Some children may be hypersensitive to common air pollutants (environmental tobacco smoke, ozone, endotoxin) such that exposures to these pollutants might not only make existing asthma worse but may also have a causal role in the susceptible. The most common persistent form of childhood asthma is associated with allergy and susceptibility to common respiratory virus–induced exacerbations (Table 138-2).








Children with asthma associated with occupational-type exposures known to trigger asthma in adults in occupational settings (e.g., endotoxin exposure in children raised on farms)

From Taussig LM, Landau LI, et al, editors: Pediatric respiratory medicine, ed 2, Philadelphia, 2008, Mosby/Elsevier, p 822.


Airflow obstruction in asthma is the result of numerous pathologic processes. In the small airways, airflow is regulated by smooth muscle encircling the airways lumens; bronchoconstriction of these bronchiolar muscular bands restricts or blocks airflow. A cellular inflammatory infiltrate and exudates distinguished by eosinophils, but also including other inflammatory cell types (neutrophils, monocytes, lymphocytes, mast cells, basophils), can fill and obstruct the airways and induce epithelial damage and desquamation into the airways lumen. Helper T lymphocytes and other immune cells that produce proallergic, proinflammatory cytokines (IL-4, IL-5, IL-13), and chemokines (eotaxin) mediate this inflammatory process. Pathogenic immune responses and inflammation may also result from a breach in normal immune regulatory processes (such as regulatory T lymphocytes that produce IL-10 and transforming growth factor [TGF]-β) that dampen effector immunity and inflammation when they are no longer needed. Hypersensitivity or susceptibility to a variety of provocative exposures or triggers (Table 138-3) can lead to airways inflammation, AHR, edema, basement membrane thickening, subepithelial collagen deposition, smooth muscle and mucous gland hypertrophy, and mucus hypersecretion—all processes that contribute to airflow obstruction (Chapter 134).

Clinical Manifestations and Diagnosis

Intermittent dry coughing and expiratory wheezing are the most common chronic symptoms of asthma. Older children and adults report associated shortness of breath and chest tightness; younger children are more likely to report intermittent, nonfocal chest pain. Respiratory symptoms can be worse at night, especially during prolonged exacerbations triggered by respiratory infections or inhalant allergens. Daytime symptoms, often linked with physical activities or play, are reported with greatest frequency in children. Other asthma symptoms in children can be subtle and nonspecific, including self-imposed limitation of physical activities, general fatigue (possibly due to sleep disturbance), and difficulty keeping up with peers in physical activities. Asking about previous experience with asthma medications (bronchodilators) may provide a history of symptomatic improvement with treatment that supports the diagnosis of asthma. Lack of improvement with bronchodilator and corticosteroid therapy is inconsistent with underlying asthma and should prompt more vigorous consideration of asthma-masquerading conditions.

Asthma symptoms can be triggered by numerous common events or exposures: physical exertion and hyperventilation (laughing), cold or dry air, and airways irritants (see Table 138-3). Exposures that induce airways inflammation, such as infections (rhinovirus, respiratory syncytial virus, metapneumovirus, torque teno virus, parainfluenza virus, influenza virus, adenovirus, Mycoplasma pneumonia, Chlamydia pneumoniae), and inhaled allergens, also increase AHR to irritant exposures. An environmental history is essential for optimal asthma management (Chapter 135).

The presence of risk factors, such as a history of other allergic conditions (allergic rhinitis, allergic conjunctivitis, atopic dermatitis, food allergies), parental asthma, and/or symptoms apart from colds, supports the diagnosis of asthma. During routine clinic visits, children with asthma commonly present without abnormal signs, emphasizing the importance of the medical history in diagnosing asthma. Some may exhibit a dry, persistent cough. The chest findings are often normal. Deeper breaths can sometimes elicit otherwise undetectable wheezing. In clinic, quick resolution (within 10 min) or convincing improvement in symptoms and signs of asthma with administration of a short-acting inhaled β-agonist (SABA; e.g., albuterol) is supportive of the diagnosis of asthma.

During asthma exacerbations, expiratory wheezing and a prolonged expiratory phase can usually be appreciated by auscultation. Decreased breath sounds in some of the lung fields, commonly the right lower posterior lobe, are consistent with regional hypoventilation owing to airways obstruction. Crackles (or rales) and rhonchi can sometimes be heard, resulting from excess mucus production and inflammatory exudate in the airways. The combination of segmental crackles and poor breath sounds can indicate lung segmental atelectasis that is difficult to distinguish from bronchial pneumonia and can complicate acute asthma management. In severe exacerbations, the greater extent of airways obstruction causes labored breathing and respiratory distress, which manifests as inspiratory and expiratory wheezing, increased prolongation of exhalation, poor air entry, suprasternal and intercostal retractions, nasal flaring, and accessory respiratory muscle use. In extremis, airflow may be so limited that wheezing cannot be heard (Table 138-4).

Differential Diagnosis

Many childhood respiratory conditions can present with symptoms and signs similar to those of asthma (Table 138-5). Besides asthma, other common causes of chronic, intermittent coughing include gastroesophageal reflux (GER) and rhinosinusitis. Both GER and chronic sinusitis can be challenging to diagnose in children. Often, GER is clinically silent in children, and children with chronic sinusitis do not report sinusitis-specific symptoms, such as localized sinus pressure and tenderness. In addition, both GER and rhinosinusitis are often co-morbid with childhood asthma and, if not specifically treated, may make asthma difficult to manage.

In early life, chronic coughing and wheezing can indicate recurrent aspiration, tracheobronchomalacia, a congenital anatomic abnormality of the airways, foreign body aspiration, cystic fibrosis, or bronchopulmonary dysplasia.

In older children and adolescents, vocal cord dysfunction (VCD) can manifest as intermittent daytime wheezing. In this condition, the vocal cords involuntarily close inappropriately during inspiration and sometimes exhalation, producing shortness of breath, coughing, throat tightness, and often audible laryngeal wheezing and/or stridor. In most cases of VCD, spirometric lung function testing reveals “truncated” and inconsistent inspiratory and expiratory flow-volume loops, a pattern that differs from the reproducible pattern of airflow limitation in asthma that improves with bronchodilators. VCD can coexist with asthma. Flexible rhinolaryngoscopy in the patient with symptomatic VCD can reveal paradoxical vocal cord movements with anatomically normal vocal cords. This condition can be well managed with specialized speech therapy training in the relaxation and control of vocal cord movement. Furthermore, treatment of underlying causes of vocal cord irritability (e.g., high gastroesophageal reflux/aspiration, allergic rhinitis, rhinosinusitis, asthma) can improve VCD. During acute VCD exacerbations, in addition to relaxation breathing techniques in conjunction with inhalation of heliox (a mixture of 70% helium and 30% oxygen) can relieve vocal cord spasm and VCD symptoms.

In some locales, hypersensitivity pneumonitis (farming communities, homes of bird owners), pulmonary parasitic infestations (rural areas of developing countries), or tuberculosis may be common causes of chronic coughing and/or wheezing. Rare asthma-masquerading conditions in childhood include bronchiolitis obliterans, interstitial lung diseases, primary ciliary dyskinesias, humoral immune deficiencies, allergic bronchopulmonary mycoses, congestive heart failure, mass lesions in or compressing the larynx, trachea, or bronchi, and coughing and/or wheezing that is an adverse effect of medication. Chronic pulmonary diseases often produce clubbing, but clubbing is a very unusual finding in childhood asthma.

Laboratory Findings

Lung function tests can help to confirm the diagnosis of asthma and to determine disease severity.

Pulmonary Function Testing

Forced expiratory airflow measures are helpful in diagnosing and monitoring asthma and in assessing efficacy of therapy. Lung function testing is particularly helpful in children with asthma who are poor perceivers of airflow obstruction or when physical signs of asthma do not occur until airflow obstruction is severe.

Many asthma guidelines promote spirometric measures of airflow and lung volumes during forced expiratory maneuvers as standard for asthma assessment. Spirometry is helpful as an objective measure of airflow limitation (Fig. 138-2). Knowledgeable personnel are needed to perform and interpret findings of spirometry tests. Valid spirometric measures depend on a patient’s ability to properly perform a full, forceful, and prolonged expiratory maneuver, usually feasible in children > 6 yr of age (with some younger exceptions). Reproducible spirometric efforts are an indicator of test validity; if the FEV1 (forced expiratory volume in 1 sec) is within 5% on 3 attempts, then the highest FEV1 effort of the 3 is used. This standard utilization of the highest of 3 reproducible efforts is indicative of the effort dependence of reliable spirometric testing.

In asthma, airways blockage results in reduced airflow with forced exhalation and smaller partial-expiratory lung volumes (see Fig. 138-2). Because asthmatic patients typically have hyperinflated lungs, FEV1 can be simply adjusted for full expiratory lung volume—the forced vital capacity (FVC)—with an FEV1/FVC ratio. Generally, an FEV1/FVC ratio <0.80 indicates significant airflow obstruction (Table 138-6). Normative values for FEV1 have been determined for children on the basis of height, gender, and ethnicity. Abnormally low FEV1 as a percentage of predicted norms is 1 of 6 criteria used to determine asthma severity in the National Institutes of Health (NIH)–sponsored asthma guidelines.

Such measures of airflow alone are not diagnostic of asthma, because numerous other conditions can cause airflow reduction. Bronchodilator response to an inhaled β-agonist (e.g., albuterol) is greater in asthmatic patients than nonasthmatic persons; an improvement in FEV1 ≥12% or >200 mL is consistent with asthma. Bronchoprovocation challenges can be helpful in diagnosing asthma and optimizing asthma management. Asthmatic airways are hyperresponsive and therefore more sensitive to inhaled methacholine, histamine, and cold or dry air. The degree of AHR to these exposures correlates to some extent with asthma severity and airways inflammation. Although bronchoprovocation challenges are carefully dosed and monitored in an investigational setting, their use is rarely practical in a general practice setting. Exercise challenges (aerobic exertion or “running” for 6-8 min) can help to identify children with exercise-induced bronchospasm. Although the airflow response of non-asthmatic persons to exercise is to increase functional lung volumes and improve FEV1 slightly (5-10%), exercise often provokes airflow obstruction in persons with inadequately treated asthma. Accordingly, in asthmatic patients, FEV1 typically decreases during or after exercise by >15% (see Table 138-6). The onset of exercise-induced bronchospasm is usually within 15 min after a vigorous exercise challenge and can spontaneously resolve within 30-60 min. Studies of exercise challenges in school-aged children typically identify an additional 5-10% with exercise-induced bronchospasm and previously unrecognized asthma. There are two caveats regarding exercise challenges: first, treadmill challenges in the clinic are not completely reliable and can miss exertional asthma that can be demonstrated on the playing field; and second, treadmill challenges can induce severe exacerbations in at-risk patients. Careful patient selection for exercise challenges and preparedness for severe asthma exacerbations are required.

Measuring exhaled nitric oxide (FENO), a marker of airway inflammation in allergy-associated asthma, has been thought to help with anti-inflammatory management and in confirming the diagnosis of asthma.

Peak expiratory flow (PEF) monitoring devices provide simple and inexpensive home-use tools to measure airflow and can be helpful in a number of circumstances (Fig. 138-3). “Poor perceivers” of airflow obstruction due to asthma can benefit by monitoring PEFs daily to assess objectively airflow as an indicator of asthma control or problems that would be more sensitive than their symptom perception. PEF devices vary in the ability to detect airflow obstruction: they are generally less sensitive than spirometry to airflow obstruction such that, in some patients, PEF values decline only when airflow obstruction is severe. Therefore, PEF monitoring should be started by measuring morning and evening PEFs (best of 3 attempts) for several weeks for patients to practice the technique, to determine a “personal best,” and to correlate PEF values with symptoms (and ideally spirometry). PEF variation >20% is consistent with asthma (see Fig. 138-3 and Table 138-6).


The findings of chest radiographs (posteroanterior and lateral views) in children with asthma often appear to be normal, aside from subtle and nonspecific findings of hyperinflation (flattening of the diaphragms) and peribronchial thickening (Fig. 138-4). Chest radiographs can be helpful in identifying abnormalities that are hallmarks of asthma masqueraders (aspiration pneumonitis, hyperlucent lung fields in bronchiolitis obliterans), and complications during asthma exacerbations (atelectasis, pneumomediastinum, pneumothorax). Some lung abnormalities can be better appreciated with high-resolution, thin-section chest CT scans. Bronchiectasis, which is sometimes difficult to appreciate on chest radiograph but is clearly seen on CT scan, implicates an asthma masquerader, such as cystic fibrosis, allergic bronchopulmonary mycoses (aspergillosis), ciliary dyskinesias, or immune deficiencies.

Other tests, such as allergy testing to assess sensitization to inhalant allergens, help with the management and prognosis of asthma. In a comprehensive U.S. study of 5-12 yr old asthmatic children (Childhood Asthma Management Program [CAMP]), 88% of the subjects had inhalant allergen sensitization according to results of allergy prick skin testing.


The National Asthma Education and Prevention Program’s Expert Panel Report 3 (EPR3): Guidelines for the Diagnosis and Management of Asthma 2007 is available online (, and the highlights of significant changes from the previous version of the guidelines have been published. The key components to optimal asthma management are specified (Fig. 138-5). Management of asthma should have the following components: (1) assessment and monitoring of disease activity; (2) provision of education to enhance the patient’s and family’s knowledge and skills for self-management; (3) identification and management of precipitating factors and co-morbid conditions that may worsen asthma; and (4) appropriate selection of medications to address the patient’s needs. The long-term goal of asthma management is attainment of optimal asthma control.

Component 1: Regular Assessment and Monitoring

Regular assessment and monitoring are based on the concepts of asthma severity, asthma control, and responsiveness to therapy. Asthma severity is the intrinsic intensity of disease, and assessment is generally most accurate in patients not receiving controller therapy. Hence, assessing asthma severity directs the initial level of therapy. The 2 general categories are intermittent asthma and persistent asthma, the latter further subdivided into mild, moderate, and severe. Asthma severity is to be assessed only once, during a patient’s initial evaluation, and only in patients who are not yet using a daily controller agent. In contrast, asthma control refers to the degree to which symptoms, ongoing functional impairments, and risk of adverse events are minimized and goals of therapy are met. In children receiving controller therapy, asthma control is to be assessed. Assessment of asthma control is important in adjusting therapy and is categorized in 3 levels: well-controlled, not well-controlled, and very poorly controlled. Responsiveness to therapy is the ease with which asthma control is attained by treatment. It can also encompass monitoring for adverse effects related to medication use.

Classification of asthma severity and control is based on the domains of Impairment and Risk. These domains may not correlate with each other and may respond differently to treatment. The NIH guidelines have criteria for 3 age groups—0-4 yr, 5-11 yr, and ≥12 yr—for the evaluation of both severity (Table 138-7) and control (Table 138-8). The level of asthma severity or control is based on the most severe impairment or risk category. In assessing asthma severity, impairment consists of an assessment of the patient’s recent symptom frequency (daytime and nighttime with subtle differences in numeric cutoffs between the 3 age groups), need for short-acting β2-agonists for quick relief, ability to engage in normal or desired activities, and airflow compromise, which is evaluated with spirometry in children 5 yr and older. Risk refers to an evaluation of the likelihood of developing asthma exacerbations for the individual patient. Of note, in the absence of frequent symptoms, persistent asthma should be considered, and therefore long-term controller therapy should be initiated for infants or children who have risk factors for asthma (see earlier) and 4 or more episodes of wheezing over the past year that lasted longer than 1 day and affected sleep, or 2 or more exacerbations in 6 months requiring systemic corticosteroids.

Asthma management can be optimized through regular clinic visits every 2-6 wk until good asthma control is achieved. For children already on controller medication therapy, management is tailored to the child’s level of control. The NIH guidelines provide tables for evaluating asthma control for the 3 age groups (see Table 138-8). In evaluation of asthma control, as in severity assessment, impairment includes an assessment of the patient’s symptom frequency (daytime and nighttime), need for short-acting β2-agonists for quick relief, ability to engage in normal or desired activities, and, for older children, airflow measurements. In addition, determination of quality of life measures for older children is included. Furthermore, with respect to risk assessment, besides considering severity and frequency of exacerbations requiring systemic corticosteroids, tracking of lung growth in older children and monitoring of untoward effects of medications are also warranted. As already mentioned, the degree of impairment and risk are used to determine the patient’s level of asthma control as well-controlled, not well-controlled, or very poorly controlled. Children with well-controlled asthma have: daytime symptoms ≤2 days/week and need a rescue bronchodilator ≤2 days/week; an FEV1 of >80% of predicted (and FEV1/FVC ratio >80% for children 5-11 yr of age); no interference with normal activity; and <2 exacerbations in the past year. The impairment criteria vary slightly depending on age group: there are different thresholds in the frequency of nighttime awakenings; addition of FEV1/FVC ratio criteria for children 5-11 yr old, and addition of validated questionnaires in evaluating quality of life for older children. Children whose status does not meet all of the criteria defining well-controlled asthma are determined to have either not well-controlled or very poorly controlled asthma, which is determined by the single criterion with the lowest rating.

Two to four asthma checkups per year are recommended for reassessing and maintaining good asthma control. During these visits, asthma control can be assessed by determining the: (1) frequency of asthma symptoms during the day, at night, and with physical exercise; (2) frequency of “rescue” SABA medication use and refills; (3) quality of life for youths with an assessment tool; (4) lung function measurements for older children and youths; (5) number and severity of asthma exacerbations; and (6) presence of medication adverse effects since the last visit (see Fig. 138-5). Lung function testing (spirometry) is recommended at least annually and more often if asthma is inadequately controlled or lung function is abnormally low. PEF monitoring at home can be helpful in the assessment of asthmatic children with poor symptom perception, other causes of chronic coughing in addition to asthma, moderate to severe asthma, or a history of severe asthma exacerbations. PEF monitoring is feasible in children as young as 4 yr who are able to master this skill. Use of a stoplight zone system tailored to each child’s “personal best” PEF values can optimize effectiveness and interest (see Fig 138-3

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