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Asthma in children younger than 12 years: Initial


evaluation and diagnosis
AUTHORS: Gregory Sawicki, MD, MPH, Kenan Haver, MD
SECTION EDITORS: Robert A Wood, MD, Gregory Redding, MD
DEPUTY EDITOR: Elizabeth TePas, MD, MS

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Aug 2023.


This topic last updated: Feb 15, 2022.

INTRODUCTION

Asthma is a significant health problem worldwide, and it is one of the most common chronic
diseases of childhood in many countries [1,2]. The prevalence in different countries ranges
from 1 to 18 percent. In the United States, for example, over nine million children have been
ever told they had asthma, and 5.5 million still have asthma [3]. Establishing a diagnosis of
asthma involves a careful process of history taking, physical examination, and diagnostic
studies. The differential diagnosis of wheezing must be carefully considered, particularly in
infants and very young children, for whom testing for reversible airflow obstruction is not
done routinely.

The epidemiology, initial evaluation, and diagnosis of childhood asthma are reviewed here.
The assessment of severity/control and monitoring, and treatment of childhood asthma are
discussed separately. (See "Asthma in children younger than 12 years: Overview of initiating
therapy and monitoring control" and "Asthma in children younger than 12 years:
Management of persistent asthma with controller therapies" and "Asthma in children
younger than 12 years: Quick-relief (rescue) treatment for acute symptoms".)

The pathogenesis, genetics, risk factors, and natural history of asthma are also reviewed
separately. (See "Pathogenesis of asthma" and "Genetics of asthma" and "Risk factors for
asthma" and "Wheezing phenotypes and prediction of asthma in young children" and
"Natural history of asthma".)
EPIDEMIOLOGY

A wide global variation exists in the prevalence of asthma, with higher rates typically seen in
higher-income countries [4]. Asthma is the most common chronic disease in childhood in
resource-rich countries. A significant increase in the estimated prevalence of asthma was
seen in resource-rich countries in the 1980s and 1990s, with slower rates of increase in the
2000s and a plateau thereafter [5]. Approximately 7.5 percent of US children had asthma in
2018, down from 9.4 percent in 2010 and 8.7 percent in 2001. However, asthma prevalence
continues to increase in other countries such as China [6]. Possible causes for the increase in
asthma prevalence are reviewed in detail separately. (See "Increasing prevalence of asthma
and allergic rhinitis and the role of environmental factors".)

Prevalence rates for current asthma in children under age 18 years increased in the United
States from 2001 to 2009 (8.7 to 9.7 percent), then decreased, with a prevalence of 7.5
percent in 2018 [7,8]. Disparities in prevalence remained, with increasing prevalence seen in
poor children and those living in the Southern US and the highest prevalence still seen in
Puerto Rican and non-Hispanic Black American children, particularly for those living in urban
environments. Before the onset of puberty, boys have a higher current prevalence of asthma
than girls (9.2 versus 7.4 percent) [3,9]. This trend reverses in adolescence. Lifetime asthma
prevalence for children was 12.7 percent in 2013 and 2016. The prevalence of asthma
appears to have plateaued in other countries as well [10-14].

Asthma exacerbation rates among children with current asthma in the United States
decreased from a rate of 62 percent among children <18 years old in 2001 to 48 percent in
2014 but increased in 2016 to 54 percent [3,8].

HISTORY

The history in a child with suspected asthma should focus on the presence of symptoms,
typical symptom patterns, precipitating factors or conditions (ie, atopy), and known asthma
risk factors ( table 1).

Additional history that should be obtained in a child with established asthma who presents
for disease monitoring includes previous and current therapy (controller and quick-relief
medication use), exposure to triggers, utilization of health care services (emergency
department [ED], hospital, unscheduled clinic visits), school attendance and performance,
and participation in physical activity. Review of an asthma questionnaire such as the Asthma
Control Test may provide additional useful information. (See "Asthma in children younger
than 12 years: Overview of initiating therapy and monitoring control", section on
'Assessment of control'.)
The evaluation of a child who presents with an acute asthma exacerbation is discussed
separately. (See "Acute asthma exacerbations in children younger than 12 years: Emergency
department management".)

Symptoms — Approximately 80 percent of children with asthma develop symptoms before


five years of age, but the disease is frequently misdiagnosed or not suspected, particularly in
infants and toddlers [15]. Evaluating the presence of asthma symptoms is an important first
step in establishing a proper diagnosis.

Coughing and wheezing are the most common symptoms of childhood asthma.
Breathlessness, chest tightness or pressure, and chest pain also are reported. Poor school
performance and fatigue may indicate sleep deprivation from nocturnal symptoms.

Cough — The presence of a nocturnal cough, a cough that recurs seasonally, a cough in
response to specific exposures (eg, cold air, exercise, laughing, allergen exposure, or crying),
or a cough that lasts more than three weeks should raise the suspicion for asthma [16].
Although wheezing is considered the hallmark of childhood asthma, cough is frequently the
sole presenting complaint [17]. The most common cause of chronic cough in children older
than three years is asthma, even if it is not accompanied by wheezing. The cough is typically
dry and hacking but may be productive; when the cough is productive, clear or whitish
sputum may be expectorated (which often contains eosinophils). It is not unusual for chronic
cough lasting more than three weeks to be labeled "bronchitis" and to be treated with
medications, such as cough suppressants, decongestants, or antibiotics. However, these
types of cough may be manifestations of asthma and are likely to respond to asthma
therapy. (See "Approach to chronic cough in children".)

Wheeze — Wheezing is a high-pitched, musical sound produced when air is forced through
narrow airways. The wheezing of asthma tends to be polyphonic (varied in pitch), reflecting
the heterogeneous distribution of affected airways. When airflow obstruction becomes
severe, wheezing can be heard on both inspiration and expiration. In contrast to asthma,
central airway obstruction may cause a harsh expiratory monophonic wheeze, as occurs with
tracheomalacia. Upper airway obstruction (eg, vocal cord dysfunction) should be suspected if
an inspiratory monophonic (of single pitch) wheeze (typically called stridor) is the only
audible sound during an exacerbation. (See "Assessment of stridor in children".)

A silent chest in the context of an asthma exacerbation implies airflow limitation of such
severity that audible wheezes cannot be produced; this represents a medical emergency.
(See "Acute asthma exacerbations in children younger than 12 years: Emergency department
management".)

Seasonal symptoms — Symptoms that are worse in certain pollen seasons are
characteristic of atopic asthma. Trees in temperate climates pollinate in early spring, grasses
in summer, and weeds in the fall. Children who are sensitive to molds tend to wheeze or
cough during rainy seasons or if they are exposed to flooding or indoor dampness. Other
allergic symptoms, such as rhinitis, conjunctivitis, or eczema, may flare concurrently with the
chest complaints. (See "Chronic rhinosinusitis: Clinical manifestations, pathophysiology, and
diagnosis" and "Allergic conjunctivitis: Clinical manifestations and diagnosis" and "Atopic
dermatitis (eczema): Pathogenesis, clinical manifestations, and diagnosis".)

Symptom patterns — Chronic asthma symptoms assume several typical patterns:

● Intermittent exacerbations superimposed upon an asymptomatic baseline

● Chronic symptoms punctuated by periods of worsening symptoms

● Morning "dipping" (an accentuation of the physiologic cycle of pulmonary function in


normal individuals, characterized by worsening of symptoms and decreased peak flow
in the early morning, with improvement as the day progresses)

Precipitating factors — Wheezing or cough may occur at any time, but certain patterns and
precipitating factors ( table 2) are typical. Depending upon the type and intensity of the
provocative agent, most acute asthma exacerbations have a slow onset over several days.
Uncommonly, severe attacks may occur suddenly and with minimal warning, resulting in life-
threatening exacerbations [18-22]. (See "Acute asthma exacerbations in children younger
than 12 years: Emergency department management" and "Trigger control to enhance
asthma management".)

Respiratory tract infections — Viral upper respiratory infections (URIs) are the most
important triggering factor for patients with asthma of all ages, including infants and young
children [23]. Clustering of asthma attacks between fall and spring suggests viral illness-
induced phenomena [24,25]. Among children who are hospitalized for wheezing, respiratory
syncytial virus, influenza virus, and rhinovirus are most common in those younger than three
years (depending upon the season); rhinovirus is most common among older children [24].
(See "Role of viruses in wheezing and asthma: An overview".)

One study found that clusters of asthma hospitalizations in school-aged children in Canada
occurred predictably after they returned to school following summer vacation and other
breaks [26]. Specifically, there was a "September asthma epidemic" approximately 18 days
after Labor Day (the first Monday of September), with a lesser increase in attacks two days
later in preschool children and six days later in adults. Viral infections were the presumed
cause, although a reduction in daily asthma medication use (eg, therapeutic holiday) during
the summer months has also been implicated.

Chronic sinusitis (which is often bacterial) and respiratory infections due to Mycoplasma
pneumoniae and Chlamydia pneumoniae may precipitate worsening of asthma [27-31]. (See
"Pneumonia caused by Chlamydia pneumoniae in children" and "Mycoplasma pneumoniae
infection in children", section on 'Other respiratory manifestations'.)

Exercise — Exercise-induced bronchospasm (EIB) may be the only manifestation of asthma


in children [32]. It occurs in up to 90 percent of children with asthma [33].

Typical symptoms are shortness of breath, chest tightness, and cough. Exercise-triggered
symptoms typically develop several minutes into prolonged exercise. Symptoms usually
resolve with rest over 30 to 60 minutes. Lung function changes little or may even improve
somewhat during most of the actual period of exercise. Lung function may begin to
deteriorate towards the end of the exercise period and can fall quite markedly in some
patients. The major fall in lung function normally occurs 5 to 10 minutes after stopping the
exercise. Lung function then normally returns spontaneously to baseline over 30 to 45
minutes. A late-phase reaction occurs in a small proportion of patients with asthma [34], and
some patients have both an immediate and a late-phase response to exercise [35]. (See
"Exercise-induced bronchoconstriction".)

Certain types of exertion (eg, swimming) appear to be less provocative of asthma than
others (eg, running, skating), probably because they produce less airway cooling and drying,
which are thought to be provocative of EIB [32]. In a systematic review, patients with stable
asthma who participated in swimming training had improved lung function and physical
fitness, with no change in asthma symptoms or exacerbations [36]. However, there is an
ongoing debate about potential lung damage caused by repeated respiratory exposure to
chlorine byproducts in recreational swimmers [37-40]. We allow our patients to swim and
only advise against it if chlorine appears to be an irritant trigger in a particular patient.

Short bursts of activity tend to be better tolerated than prolonged exercise. Repeated short
periods of exercise tend to result in diminishing EIB with each episode. Nonetheless, children
with asthma do not need to be steered toward particular sports, since they can participate in
sports at any level (including the Olympics) with proper treatment, and improved exercise
conditioning leads to lower respiratory rates with the same level of activity.

If untreated, longstanding EIB may result in poor overall fitness, decreased exercise stamina,
a preference for a sedentary lifestyle, and exercise avoidance due to the distress brought on
by physical activity. EIB that is difficult to control often indicates inadequately controlled
underlying asthma.

Weather — Cold air; hot, humid air; changes in barometric pressure; rain; thunderstorms;
or wind may be provocative factors for asthma in individual patients. (See "Trigger control to
enhance asthma management", section on 'Atmospheric conditions'.)
Tobacco smoke — Exposure to secondhand cigarette smoke is the single, most common,
external risk factor for the development and progression of asthma symptoms in children
[41-43]. (See "Secondhand smoke exposure: Effects in children".)

Allergens — Indoor and outdoor allergens are an important trigger of childhood asthma
for the 80 percent of children with asthma and allergies, particularly those older than three
years of age (see "Allergen avoidance in the treatment of asthma and allergic rhinitis"). These
include [44]:

● House dust mites, cockroaches, and rodents [45-48]

● Pet exposures; cats and dogs are especially provocative, but other furry animals
(gerbils, rabbits, hamsters, etc) may be suspect, especially if symptoms only occur in
settings where these animals reside [49]

● Pollens [50]

● Molds

Irritant exposures — Asthma symptoms that occur after prolonged time indoors (eg,
winter months or during periods of inclement weather) should raise a suspicion of sensitivity
to indoor exposures to allergens (see 'Allergens' above) or inhaled airway irritants, such as
[44,51]:

● Nitrogen dioxide (from gas stoves) [52]


● Particulates and smoke from wood fires, pellet stoves, or kerosene space heaters
● Exposure to chemicals via vaping
● Propellant cleaning sprays
● Perfumes, hair sprays
● Paint
● Room deodorizers
● Cleaning products with strong odors

Stress — Various types of stress can trigger or exacerbate asthma [53], although asthma
can also cause stress. However, asthma symptoms and exacerbations should not be
attributed to stress unless all other exacerbating factors have been excluded. In addition,
asthma should be sufficiently well controlled to allow patients to tolerate stressful situations
and other unavoidable triggers without asthma exacerbations.

Additional history — Additional history that should be obtained in children with suspected
asthma includes a personal history of other atopic diseases, family history of asthma or
other atopic diseases (eg, allergic rhinitis, atopic dermatitis, and food allergy), environmental
history, past medical history, medication use, medical utilization, school attendance, and
psychosocial factors.

Allergic history — Allergic disease is associated with the development, severity, and
persistence of asthma. As an example, up to 80 percent of children with atopic dermatitis
develop asthma and/or allergic rhinitis later in childhood [54]. Approximately 30 percent of
children with food allergy have asthma and respiratory allergy compared with 10 percent of
children without food allergy [55]. Food allergy is also a risk factor for life-threatening
asthma, as evidenced by a substantially higher rate of food allergy in children requiring
intubation for asthma compared with a control group of asthmatic children [56]. Sensitivity
to many mold allergens is associated with increased asthma severity and persistence [57,58].
(See "Role of allergy in atopic dermatitis (eczema)" and "Allergen avoidance in the treatment
of asthma and allergic rhinitis" and "Risk factors for asthma", section on 'Atopy and
allergens'.)

In a study of children who were hospitalized for wheezing (cases), total serum
immunoglobulin E (IgE) concentrations in the subgroup <3 years of age were similar to
hospitalized children without wheezing (controls) but were significantly elevated among the
cases in the subgroup >3 years old [24]. In addition, a higher percentage of cases were
sensitized to at least one inhaled allergen (84 versus 33 percent).

In atopic infants, sensitization to common foods, such as egg white and cow's milk, may
occur and peaks at approximately eight months of age [59]. IgE antibodies to inhalant
allergens generally appear beginning at two years of age and increase throughout childhood
[59]. Food allergy and eczema are the most common manifestations of atopy in early life,
whereas asthma and allergic rhinitis are more common in older children. (See "Atopic
dermatitis (eczema): Pathogenesis, clinical manifestations, and diagnosis" and "Clinical
manifestations of food allergy: An overview" and "Food allergy in children: Prevalence,
natural history, and monitoring for resolution".)

Sensitization to foods and the presence of atopic dermatitis represent an atopic diathesis,
whereas sensitization to airborne allergens also represents a trigger for asthma
exacerbations.

Family history — The influence of genetics in the development of asthma has not been
fully defined [43,60-66]. Because families also share environments, determining the
influence of the genetic contribution to asthma is complicated. Nonetheless, a family history
of asthma or other atopic disease (ie, allergic rhinitis, atopic dermatitis, or food allergy)
certainly strengthens the likelihood that a child with a compatible history has asthma.

Children with one asthmatic parent are 2.6 times more likely to have asthma; with two
asthmatic parents, the odds ratio rises to 5.2 [60]. Maternal asthma appears to make a
bigger contribution than paternal asthma to asthma in offspring, although this finding is
inconsistent [62-64].

Environment — A thorough review of all regular environments, including home, school,


daycare, and relatives' homes, is essential to evaluate possible provocative situations in the
child with asthma. The table outlines some questions that may be helpful in obtaining this
history ( table 3). A strategy to avoid asthma triggers is one of the essential elements for
managing the disease. (See "Trigger control to enhance asthma management" and "Allergen
avoidance in the treatment of asthma and allergic rhinitis".)

Past medical history — A careful survey of all aspects of the child's medical history is
critical to formulate a differential diagnosis of the child's complaint. Questions about the
neonatal course, early respiratory symptoms, and the coexistence of systemic symptoms
(failure to thrive, fever, developmental delay, recurrent infections) may point toward other
diagnoses. Additional questioning may reveal evidence of comorbid conditions, such as
obstructive sleep apnea (OSA), gastroesophageal reflux, or chronic rhinosinusitis.

Sleep disordered breathing, for example, was associated with a 3.6-fold increased risk of
severe asthma in one study [67]. Another large, observational study found an improvement
in asthma control (eg, decreased exacerbations, hospitalizations, and medication use)
following adenotonsillectomy [68]. The latter results did not show, however, that
adenotonsillectomy caused a reduction in the severity of childhood asthma. It is possible
that the children who underwent adenotonsillectomy shared another unknown factor that
led to improvements in their asthma over time, such as a reduction in upper respiratory tract
infections. (See 'Differential diagnosis' below and "Evaluation of severe asthma in
adolescents and adults", section on 'Assessing comorbid conditions'.)

Medications — A careful review of prior and present medications (including over-the-


counter and alternative remedies) provides information on adherence to therapy, drug
efficacy, drug delivery systems in use, accuracy of diagnosis, and control of asthma.
Response to treatment with albuterol, as demonstrated by a decreased respiratory rate,
diminished retractions, increased aeration, and/or decreased cough or wheezing, can be
helpful in making the diagnosis of asthma, particularly in children unable to perform
spirometry. The onset of action is within 20 minutes, and the benefits should last four to six
hours.

Common reasons for poor response to asthma medications include:

● Nonadherence to the prescribed regimen. Caregivers and children often over-report


adherence with controller medications; objective measures (eg, an inhaler with a dose
counter) may be necessary to verify adherence [69]. Overuse of quick-relief medications
(eg, short-acting beta agonists) with resultant tolerance can also be an issue. (See
"Enhancing patient adherence to asthma therapy" and "Beta agonists in asthma: Acute
administration and prophylactic use", section on 'Tolerance'.)

● Improper inhaler technique. Since the efficacy of many asthma medications depends
upon their deposition in the lung, inhalation technique figures strongly in the success
or failure of inhaled therapies. Metered dose inhalers (MDIs) require a significant
degree of coordination for optimal drug delivery, and there is considerable evidence
that many patients and health care professionals do not regularly perform or teach
proper inhalation technique [70,71]. Errors also can be made with dry powder inhalers
(DPIs). Patient education materials, use of spacers (with MDIs), and frequent
reappraisal of technique contribute to greater success with this form of therapy.
Spacers with masks are especially helpful to the very young child. (See "Delivery of
inhaled medication in children" and "The use of inhaler devices in children".)

● Ineffective drug dose or dosing interval. (See "Asthma in children younger than 12
years: Management of persistent asthma with controller therapies".)

● Complicating medical problems (eg, chronic sinusitis, vocal cord dysfunction,


gastroesophageal reflux, environmental allergies) [72,73]. (See "Chronic rhinosinusitis:
Clinical manifestations, pathophysiology, and diagnosis" and "Inducible laryngeal
obstruction (paradoxical vocal fold motion)" and "Clinical manifestations and diagnosis
of gastroesophageal reflux disease in children and adolescents" and "Relationships
between rhinosinusitis and asthma".)

● Complicating psychosocial factors (which can interfere with regularly obtaining and
properly using medications).

● Inappropriate treatment (eg, antibiotics, antitussives, over-the-counter or alternative


medications).

● Different response to controller medications depending upon the child's intrinsic


characteristics [74-77].

Health care utilization — The degree of asthma control is usually linked to health care
utilization, such that more severe or poorly controlled patients with asthma tend to be
treated more often in EDs, urgent care centers, or doctors' offices. A history of more than a
few such interventions is often indicative of poorly controlled asthma, regardless of the level
of chronic symptoms [78]. In addition, a history of prior hospitalizations, ED visits, or
exacerbations requiring oral glucocorticoids confers an increased risk for future asthma
exacerbations.

School attendance — One-third of children with asthma suffer noticeable disability [79].
Interference with regular school attendance or achievement is a good measure of disability
from childhood asthma. A pattern of significant numbers of lost days from school and a
deteriorating academic performance should prompt more aggressive asthma management.

Nearly 14 million school days are missed each year due to asthma, although the percent of
children with asthma who reported one or more missed school days declined significantly
from 2003 to 2013 (61.4 versus 49 percent) [3] and held steady at 49 percent in 2016 [8].
Childhood asthma is also a major cause of parent/caregiver work absenteeism [80,81].

Physical activity — Most children with asthma can have symptoms brought on by intensive
activity; therefore, many children limit their level of exertion. In one study, children with
newly diagnosed, untreated asthma were less fit and spent less time in vigorous activity than
their healthy peers [82]. However, physical activities need not be restricted. Rather,
appropriate treatment should allow full participation, which should be encouraged. With
appropriate therapy, children with asthma can participate in all activities, including sports at
every level up to and including participation in the Olympics [83], without restriction.

Psychosocial profile — Chronic asthma may create or exacerbate psychosocial problems


for patients and their caregivers. Conversely, psychosocial factors can affect asthma
symptoms and health behaviors [84]. Stressors surrounding asthma can include:

● Anxiety about the often sudden, life-threatening nature of attacks

● Fear of dying

● Fear of peer rejection because of being "different"

● Concern regarding the adverse effects of asthma drugs (particularly glucocorticoids,


also called corticosteroids)

● Sleep deprivation due to nocturnal symptoms

● Poor school performance

● Financial consequences

● Disruption in family routines

● Siblings' resentment of the patient's special status within the family

● Limitation of social or geographic venues because of potential triggering of asthma (eg,


cannot visit places where environmental tobacco smoke or allergen exposure is likely)

● Family discord over asthma treatment


Predictive tools — Parents/caregivers often ask if their young children with recurrent cough
or wheeze have asthma and if they might outgrow it. Various predictive models or clinical
indicators of risk have been studied to help the clinician identify young children who will
continue wheezing later in childhood, although these tools were primarily designed to enrich
study populations rather than actually predict asthma. These models have employed various
risk factors associated with the development of asthma in longitudinal epidemiologic
studies, such as baseline forced expiratory volume in one second (FEV1)/forced vital capacity
(FVC), parental history of allergic sensitization and asthma, wheezing history, atopic disease
in the child, IgE levels, and cytokine secretion profiles. However, none of these clinical tools
have been validated in populations different from the study group. These tools and risk
factors are discussed in greater detail separately. (See "Wheezing phenotypes and prediction
of asthma in young children", section on 'Predictive tools in children with wheezing' and
"Natural history of asthma", section on 'Infants and children'.)

PHYSICAL EXAMINATION

Examination findings during an acute exacerbation include tachypnea, hypoxia, wheezing,


accessory muscle use, retractions, and prolonged expiratory phase. These findings are
discussed in detail separately. (See "Acute asthma exacerbations in children younger than 12
years: Emergency department management".)

Physical examination of a child with asthma is generally normal if performed when the
patient does not have an acute exacerbation. Abnormal findings in the absence of an acute
exacerbation may suggest severe disease, suboptimal control, or associated atopic
conditions. Abnormalities that may be observed include [78]:

● Decreased air entry or wheezing on auscultation

● A prolonged expiratory phase on auscultation

● Dry cough

● Signs of rhinitis, conjunctivitis, and sinusitis (nasal discharge, inflamed nasal mucosa,
sinus tenderness, dark circles under the eyes) (see "Chronic rhinosinusitis: Clinical
manifestations, pathophysiology, and diagnosis")

● Signs of an acute respiratory infection

● A transverse nasal crease due to frequent itching (allergic salute)

● Halitosis due to chronic rhinitis, sinusitis, and mouth breathing

● Eczema/atopic dermatitis
● Nasal polyps ( picture 1 and picture 2) (glistening, gray, mucoid masses within the
nasal cavities, which may be associated with asthma and aspirin sensitivity in
adolescents and adults, but should prompt evaluation for cystic fibrosis in children of
any age) (see "Cystic fibrosis: Clinical manifestations and diagnosis")

● An increased anterior-posterior diameter of the chest due to air trapping

Obesity — Results are conflicting regarding the relationship between obesity and asthma
severity [67,85-88]. Obesity and higher percent body fat are associated with an increased
incidence of asthma [89] and are more commonly seen in children with newly diagnosed,
untreated asthma than their healthy peers [82]. Higher body mass index (BMI) is also
associated with greater asthma severity [85,89]. However, biologic causality has not been
proven, and reverse causation may also occur (ie, asthma limiting physical activity leading to
obesity). (See "Risk factors for asthma" and "Evaluation of severe asthma in adolescents and
adults", section on 'Assessing comorbid conditions'.)

DIAGNOSIS

A history of intermittent or chronic symptoms typical of asthma plus the finding on physical
examination of characteristic musical wheezing (present in association with symptoms and
absent when symptoms resolve) strongly point to a diagnosis of asthma (see 'History' above
and 'Physical examination' above). Confirmation of the diagnosis of asthma is based on three
key additional elements [78,90,91]:

● The demonstration of variable expiratory airflow limitation, preferably by spirometry,


when possible
● Documentation of reversible obstruction
● Exclusion of alternative diagnoses (see 'Differential diagnosis' below)

Evidence of airway obstruction on spirometry, especially if acutely reversible with a


bronchodilator, strongly supports the diagnosis of asthma. However, normal spirometry, or
the lack of reversibility of obstruction in the setting of an acute exacerbation, does not
exclude the diagnosis. A trial of asthma medication is warranted in patients with symptoms
suggestive of asthma who have normal or near-normal spirometry or who are unable to
perform spirometry due to age or other factors. Improvement on medications is sufficient to
make the diagnosis in these patients. If a trial of asthma medication fails to improve
symptoms, bronchoprovocation testing with methacholine, cold air, or exercise may be
warranted. (See 'Spirometry' below and 'Medications' above and 'Ancillary studies' below.)

Spirometry — Demonstration of reversible airflow obstruction establishes the diagnosis of


asthma and facilitates the assessment of severity ( figure 1) [78]. Spirometry is the
preferred method of diagnosis of airflow obstruction. The National Asthma Education and
Prevention Program (NAEPP) expert panel recommends performing spirometry in patients
five years of age and older if a diagnosis of asthma is suspected [78]. (See "Overview of
pulmonary function testing in children".)

Spirometry measurements include forced vital capacity (FVC) and the forced expiratory
volume in one second (FEV1). Airflow obstruction is defined as FEV1 reduced to less than 80
percent predicted and an FEV1/FVC ratio of less than 0.85 (85 percent) ( table 4A).
Reference values are based on age, height, sex, and race [92]. FEV1/FVC appears to be a
more sensitive measure of impairment than FEV1, whereas FEV1 may be a more useful
measure of risk for future exacerbations [78,93-96] (see "Asthma in children younger than 12
years: Overview of initiating therapy and monitoring control", section on 'Assessment of
control'). Forced expiratory flow between 25 and 75 percent of vital capacity (FEF25-75) less
than 65 percent correlates with reversible airflow obstruction in children with normal FEV1
and may be a useful measure in this subgroup, although further studies are needed [97].

Spirometry should be performed before and after administration of a bronchodilator to


assess for reversibility (bronchodilator response [BDR]) even in children with a normal
baseline FEV1 because many of these children will still have a BDR (both within the normal
range and sometimes also supranormal) after treatment. Significant reversibility is indicated
by an increase in FEV1 of ≥12 percent from baseline after administration of a short-acting
bronchodilator. This definition for BDR positivity was established primarily in adults. An
increase in FEV1 of ≥8 percent may be a better definition for BDR in children [98-100]. (See
"Overview of pulmonary function testing in children".)

There is some evidence from cross-sectional studies to suggest that the NAEPP criteria for
percent predicted FEV1 ( table 4A-B) do not accurately categorize asthma severity in
children and that symptom frequency and rescue medication use may be more sensitive
measures [93,94,101-103]. In the Childhood Asthma Management Program (CAMP) study, for
example, the mean FEV1 of all children studied was 94 percent predicted [94], although this
study included only children with mild-to-moderate asthma based upon symptoms, use of
medications, and response to methacholine [104]. Nonetheless, percent predicted FEV1
remains a useful measure because it is strongly associated with the risk of asthma
exacerbation in the 12 months after measurement [95,96].

Another potential spirometric measure of risk for asthma severity and poor control (asthma
instability) is the air-trapping obstruction phenotype, defined as a FVC Z-score of <-1.64
(equivalent to fifth percentile in a healthy population) or a ≥10 percent change in the
predicted value of FVC after bronchodilation. In a study of 560 children aged 6 to 17 years
from low-income, urban areas who had physician-diagnosed asthma, the risk of ≥2 asthma
exacerbations during the 12-month study period was more than fourfold higher (odds ratio
4.41, 95% CI 2.37-8.21) in those with this phenotype compared with those without any
evidence of obstruction on spirometry [105]. Children with the air-trapping obstruction
phenotype also had higher Composite Asthma Severity Index scores and asthma treatment
steps, as well as greater sensitivity to methacholine challenge and variability in FEV1 over
time.

Measurements of peak expiratory flow using a peak flow meter are more variable and effort
dependent. In addition, there is wide variability in the published predicted peak expiratory
flow reference values and in the reference values from brand to brand [78]. Thus, peak flow
measurements alone should not be used to diagnose asthma. Peak flow measurements may
be more useful in monitoring a patient's symptoms and response to therapy over time,
although serial spirometry is preferred ( table 4B) [78]. (See "Peak expiratory flow
monitoring in asthma".)

Children <5 years — In infants and children younger than five years of age, the diagnostic
steps should remain the same as described above, except that spirometry often cannot be
performed in this age group. A trial of asthma medications may help to establish the
diagnosis in these children. Reversal of symptoms and signs in the time expected for
albuterol to work is suggestive of the diagnosis of asthma. Impulse oscillometry (IOS) is an
alternative to spirometry in younger children since it only requires passive cooperation [106-
108]. However, it is not readily available to most clinicians treating children with asthma,
limiting its clinical utility [109]. IOS measurements at baseline and postbronchodilator
differed significantly between children aged three to six years with and without asthma,
whereas no significant differences were seen with traditional spirometry [110-112]. IOS may
detect alterations in respiratory mechanics not seen with spirometry even in older children
[113-115]. (See 'Diagnosis' above and 'Medications' above.)

Debate is ongoing regarding how to best classify infants and young children with recurrent
wheezing. The terms asthma, reactive airway disease, wheezy bronchitis, bronchiolitis,
asthmatic bronchitis, wheezing-associated respiratory illness, and postinfectious bronchial
hyperreactivity have all been employed. This jargon reflects an attempt to describe and
define a subgroup of wheezing children with a more benign prognosis than is implied by
"asthma," which is, by definition, chronic. "Wheezy bronchitis" usually defines nonatopic
babies or toddlers with recurrent, virus-induced wheezing (the majority of this group of
wheezing young children) that tends to disappear by five years of age [116,117]. Asthma, on
the other hand, has been taken to mean a chronic condition, frequently associated with
atopy, provoked by a number of triggers in addition to viruses, and carrying a poorer
prognosis for spontaneous resolution. (See "Asthma in adolescents and adults: Evaluation
and diagnosis", section on 'Definition' and "Natural history of asthma", section on 'Infants
and children' and "Wheezing phenotypes and prediction of asthma in young children" and
"Role of viruses in wheezing and asthma: An overview" and "Evaluation of wheezing in
infants and children" and "Approach to chronic cough in children".)

Ancillary studies — The history and physical examination, in conjunction with spirometry,
are usually adequate to establish the diagnosis of asthma. Ancillary studies are most helpful
to exclude competing diagnoses or to identify comorbid conditions.

Allergy testing — Allergy testing, done either by skin or in vitro testing, is helpful even in
the very young child when used selectively. Specifically, when the environmental history
uncovers exposure to furry animals (pets or pests), molds, cockroaches, or dust mites, it is
worthwhile to test for these or other limited allergens to formulate proper avoidance
strategies. Outdoor aeroallergens are unusual triggers in infants and very young children
but may be triggers in older children. Food allergy testing is not helpful unless there is a
sound history of gastrointestinal complaints, worsening eczema, urticaria, shortness of
breath, throat tightness, cough, hoarse voice, or asthma that is temporally associated with
the ingestion of certain foods. Children with this type of history should be evaluated by a
clinician familiar with food allergies and prescribed epinephrine since ingestion of a food
allergen can be life threating in a patient with food allergies, particularly in a patient with
concomitant asthma. In addition, when indicated testing reveals the presence of IgE
antibody to any allergen, an atopic diathesis is demonstrated, increasing the likelihood that
chest symptoms are due to asthma. (See "Overview of skin testing for IgE-mediated allergic
disease".)

Bronchoprovocation testing — We advise performing bronchoprovocation testing (with


methacholine, cold air, or exercise) when the clinical features are suggestive of asthma but
spirometry is normal and there is no significant response to asthma medications. An exercise
challenge of sufficient magnitude may provoke symptoms in children with asthma [118-120].
A negative bronchoprovocation study may also be useful in reducing the likelihood that a
child has asthma, although it cannot be used to exclude the diagnosis. For safety reasons,
these tests should be conducted in a specialized facility with trained technicians and should
not be performed if a patient has severe airflow limitation (FEV1 <50 percent predicted) [121].
Exercise challenge has a high specificity, whereas methacholine challenge had a high
sensitivity. Bronchial challenge tests are discussed in greater detail separately. (See
"Overview of pulmonary function testing in children" and "Bronchoprovocation testing".)

Chest radiograph — We advise performing a chest radiograph (chest x-ray [CXR]) only in
children who do not respond to initial therapy. In those children, the chest radiograph may
display findings suggestive of causes for wheezing other than asthma including congenital
malformations (eg, a right aortic arch suggestive of a vascular ring); evidence of airspace
disease consistent with aspiration or cystic fibrosis; or findings consistent with asthma, such
as hyperinflation, peribronchial thickening, and mucoid impaction with atelectasis.
Sweat chloride test — A sweat chloride test below established cut-off values reduces the
likelihood of the diagnosis of cystic fibrosis in children with respiratory complaints often in
association with frequent foul-smelling stools or other evidence of malabsorption (eg,
undigested food or oil), recurrent pneumonia, edema, and/or failure to thrive. There should
be a low threshold to perform this test in children with this clinical picture, even if prenatal
maternal screening or newborn screening was negative, since identifying a patient with
cystic fibrosis has major implications for the patient, the family, and future reproductive
decisions. Mutation analysis should be performed even if the sweat chloride is below
established cut-off values if the suspicion for cystic fibrosis remains high. (See "Cystic
fibrosis: Clinical manifestations and diagnosis".)

Barium swallow — A modified barium swallow should be included in the diagnostic


evaluation if swallowing dysfunction with aspiration is a consideration. (See "Clinical
manifestations and diagnosis of gastroesophageal reflux disease in children and
adolescents" and "Evaluation of wheezing in infants and children".)

Exhaled nitric oxide — Measurement of the fraction of exhaled nitric oxide (FENO) may be
used as an adjunct to other assessments when the diagnosis of asthma is uncertain [122].
The use of this test in diagnosing asthma is discussed in greater detail separately. (See
"Exhaled nitric oxide analysis and applications", section on 'Clinical use of FENO in asthma'.)

DIFFERENTIAL DIAGNOSIS

Although wheezing is most commonly caused by asthma, it is not a pathognomonic finding.


The lack of objective measures of pulmonary function in very young children and the
relatively high prevalence of congenital infections and inherited disorders that present with
wheezing make it imperative to consider the differential diagnosis of wheezing illnesses
before making a diagnosis of asthma solely on the basis of wheezing ( table 5 and
table 6). In particular, other causes of wheezing in children must be excluded if there is a
failure to respond to asthma therapy or if the history and/or physical examination suggest
alternative diagnoses. Cough is the primary manifestation in some children with asthma;
therefore, the differential diagnosis for chronic cough in children should also be considered
( table 7 and algorithm 1). Clinical features suggestive of a diagnosis other than asthma
are seen in the table ( table 8) and are discussed in detail separately. (See "Evaluation of
wheezing in infants and children" and "Approach to chronic cough in children" and "Causes
of chronic cough in children".)

INDICATIONS FOR REFERRAL


Consultation with an asthma specialist, either a pulmonologist or an allergist, is warranted
when the diagnosis of asthma is uncertain, the asthma is difficult to control, medication side
effects are problematic, or a patient has frequent exacerbations. Pulmonologists may be
most helpful if alternative pulmonary diseases are suspected or if further pulmonary testing
or bronchoscopy may be needed. Referral to an allergist may be most helpful if allergic
triggers need further evaluation if food allergy is suspected or if concomitant nasal and
ocular allergy symptoms are difficult to control.

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Asthma in children".)

INFORMATION FOR PATIENTS

UpToDate offers two types of patient education materials, "The Basics" and "Beyond the
Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th
grade reading level, and they answer the four or five key questions a patient might have
about a given condition. These articles are best for patients who want a general overview
and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are
longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th
grade reading level and are best for patients who want in-depth information and are
comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to
print or e-mail these topics to your patients. (You can also locate patient education articles
on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

● Basics topic (see "Patient education: Cough in children (The Basics)")

● Beyond the Basics topics (see "Patient education: Asthma symptoms and diagnosis in
children (Beyond the Basics)" and "Patient education: Asthma treatment in children
(Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

● Overview of approach to diagnosis – Establishing a diagnosis of asthma involves a


careful process of history taking, physical examination, and diagnostic studies; other
causes of wheezing must be excluded. (See 'Introduction' above.)
● History – The history in a child with suspected asthma centers on the presence of
symptoms (cough and wheeze are the most common), precipitating factors or
conditions ( table 1 and table 2), typical symptom patterns, and response to
asthma therapy. (See 'History' above.)

Additional history that should be obtained in children with suspected asthma includes a
history of atopy, family history of asthma, environmental history, and past medical
history. (See 'Additional history' above.)

Important aspects of the history in a child with asthma who presents for monitoring
include previous and current therapy, exposure to triggers, medical utilization, school
attendance and performance, comorbidities, and psychosocial stressors. (See
'Additional history' above.)

● Physical examination – The physical examination of a child with asthma is generally


normal if performed in the absence of an acute exacerbation. Abnormal findings may
suggest severe disease, suboptimal control, or associated atopic conditions. (See
'Physical examination' above.)

● Diagnosis – The diagnosis of asthma requires a history of episodic symptoms of airflow


obstruction or bronchial hyperresponsiveness ( table 1), demonstration (with
spirometry if possible) that airflow obstruction is reversible ( figure 1), and exclusion
of alternate diagnoses. If spirometry cannot be performed, a trial of medications may
help to establish reversibility. (See 'Diagnosis' above.)

● Differential diagnosis – Other causes of wheezing in children must be excluded if


there is a failure to respond to asthma therapy or if the history and/or physical
examination suggest alternative diagnoses ( table 5 and table 6 and table 7 and
algorithm 1 and table 8). (See 'Differential diagnosis' above and "Evaluation of
wheezing in infants and children".)

Use of UpToDate is subject to the Terms of Use.

Topic 5742 Version 40.0


GRAPHICS

Sample questions* for the diagnosis and initial assessment of asthma

A "yes" answer to any question suggests that an asthma diagnosis is likely.

In the past 12 months, have you ¶ ...

Had a sudden severe episode or recurrent episodes of coughing, wheezing (high-pitched


whistling sounds when breathing out), chest tightness, or shortness of breath?

Had colds that "go to the chest" or take more than 10 days to get over?

Had coughing, wheezing, or shortness of breath during a particular season or time of the year?

Had coughing, wheezing, or shortness of breath in certain places or when exposed to certain
things (eg, animals, tobacco smoke, perfumes)?

Used any medications that help you breathe better? How often?

Had symptoms relieved when the medications are used?

In the past four weeks, have you ¶ had coughing, wheezing, or shortness of breath...

At night that has awakened you?

Upon awakening?

After running, moderate exercise, or other physical activity?

* These questions are examples and do not represent a standardized assessment or diagnostic
instrument. The validity and reliability of these questions have not been assessed.

¶ Or "your child," if a parent/caregiver is answering the questions for a child.

Reproduced from: National Heart, Blood, and Lung Institute Expert Panel Report 3 (EPR 3): Guidelines for the Diagnosis
and Management of Asthma. NIH Publication no. 08-4051, 2007.

Graphic 79182 Version 7.0


Questions to help identify asthma triggers*

Allergen exposures
Do you have asthma symptoms year-round or only certain times of year?

Do you have pets? Or birds? Are they indoors or outdoors most of the time?

Have you seen cockroaches at home/school/work in the past month? How about rodents?

Is there moisture, dampness, moldy odor, or visible mold in your home? ¶

For patients who live in dry climates, do you use an evaporative cooler (also known as a swamp
cooler)? These coolers are associated with increased humidity and increased mold/dust mites.

Do your asthma symptoms get worse during pollen seasons (eg, tree pollen in early spring in
New England) or more humid times of year (suggests molds and dust mites)?

Have you ever had allergy skin or IgE testing? If so, do you have the results?

Irritant exposures
Do you smoke cigarettes? If so, how many/day and how long have you smoked?

Does anyone at home/work/daycare smoke?

Do you smoke cannabis (marijuana), use electronic cigarettes, or vape?

Do you use a wood-burning stove or fireplace at home?

Do you have any unvented/open fire stoves or heaters at home?

Are you exposed regularly to smells or fumes from perfumes, cleaning agents, or sprays?
Work and school
Do you cough, wheeze or need your inhaler more during the week at work/school than on
weekends or times away from work/school?

Do your eyes or nose itch or feel irritated at work/school?

Do coworkers or other students have similar symptoms?

Are you exposed to fumes, dusts, or vapors at work? If so, what?

Nasal problems
Do you have seasonal or persistent nasal congestion, runny nose, postnasal drip, or decreased
sense of smell?

Are your nasal symptoms worse at home/school/work?

Gastroesophageal reflux
Do you have heartburn (burning sensation in the chest); does food come back up into your
mouth; or do you sense/taste sour stomach acid coming up into your throat?

Medications that can worsen asthma


Do you use eye drops? If so, which? Do your asthma symptoms worsen after taking them?

Do you use any medications that contain beta-blockers or ACE inhibitors? Has your asthma
worsened since you started taking this medication?

Do you take aspirin or other NSAIDs? Do your asthma symptoms flare when you take them?

Possible sulfite sensitivity Δ


Do you have wheezing, coughing, or shortness of breath after eating shrimp, dried fruit, or
processed potatoes or after drinking beer or wine?
IgE: immunoglobulin E; ACE: angiotensin-converting enzyme; NSAID: nonsteroidal anti-
inflammatory drug.

* These questions are examples and do not represent a standardized assessment or diagnostic
instrument. The validity and reliability of these questions have not been assessed.

¶ Higher humidity makes mold and mite exposure more likely. Visible mold suggests significant
mold exposure.

Δ Rare issue in children.

Adapted from: National Heart, Blood, and Lung Institute Expert Panel Report 3 (EPR 3): Guidelines for the Diagnosis and
Management of Asthma. NIH Publication no. 08-4051, 2007.

Graphic 80507 Version 12.0


Environmental history for the child with asthma

Passive tobacco smoke exposure (house, car, daycare)

Siblings and ages

Wood-burning stoves and ventilation system

Animals (dogs, cats, birds, furry pets); where animals reside and how often they are in the house
or in the patient's bedroom

Leaky plumbing, recent flooding, obvious mold, mildew in any part of the house

Method of heating, cooling; is there an evaporative cooler? window air conditioner?

Patient's bedroom: type and age of mattress, bedding, window-coverings, flooring, dust-collecting
items, stuffed animals and how often laundered

Graphic 59599 Version 2.0


Nasal polyps in nostril

Nasal polyps appear as glistening, gray or white, mucoid masses in


the nasal cavities.

Courtesy of Glenis Scadding, MD and Peter Andrews, BSc, FRCS.

Graphic 50105 Version 4.0


Nasal polyposis

Graphic 73419 Version 1.0


Obstructive defect on spirometry in a nine-year-old child

Note the reduced FEV1/FVC and FEV1 (red boxes) and the scooped curve
shape of the green expiratory flow loop (red arrow, above x-axis),
consistent with an obstructive defect. The airflow obstruction is reversible.

After treatment with a bronchodilator, there is significant improvement


(>10%) in FEV1 and the FEV1/FVC ratio also increases (orange boxes). The
expiratory flow volume loop (above x-axis) shown in blue is now nearly
normal.

Rx: treatment (with bronchodilator); FEV1: forced expiratory volume in the


first second; FVC: forced vital capacity; % Pred: percent predicted.

* Prebronchodilator.

¶ Postbronchodilator.

Graphic 73165 Version 5.0


Classifying asthma severity in children 5 to 11 years of age

Classification of asthma severity (children 5 to 11


years of age)
Components of severity
Persistent
Intermittent
Mild Moderate Severe

Impairment Symptoms ≤2 days/week >2 Daily Throughout


days/week, the day
but not daily

Nighttime ≤2 times/month 3 to 4 >1 Often 7


awakenings times/month time/week, times/week
but not
nightly

Short-acting ≤2 days/week >2 Daily Several


beta2-agonist days/week, times per
use for but not daily day
symptom
control (not
prevention of
EIB)

Interference None Minor Some Extremely


with normal limitation limitation limited
activity

Lung function Normal FEV1 FEV1 = FEV1 = 60 FEV1


between >80% to 80% <60%
exacerbations predicted predicted predicted
FEV1 >80% FEV1/FVC FEV1/FVC FEV1/FVC
predicted >80% = 75 to <75%
FEV1/FVC 80%
>85%

Risk Exacerbations 0 to 1/year (see ≥2 in 1 year (see footnote)


requiring oral footnote)
systemic
Consider severity and interval since last exacerbation
glucocorticoids
Frequency and severity may fluctuate over time for patients
in any severity category

Relative annual risk of exacerbations may be related to FEV1

Classifying severity in children who are not currently taking long-term control medication.
Level of severity is determined by both impairment and risk. Assess impairment domain by
patient's/caregiver's recall of the previous 2 to 4 weeks and spirometry. Assign severity to the
most severe category in which any feature occurs. At present, there are inadequate data to
correspond frequencies of exacerbations with different levels of asthma severity. In general,
more frequent and intense exacerbations (eg, requiring urgent, unscheduled care,
hospitalization, or ICU admission) indicate greater underlying disease severity. For treatment
purposes, patients who had ≥2 exacerbations requiring oral systemic glucocorticoids in the past
year may be considered the same as patients who have persistent asthma, even in the absence
of impairment levels consistent with persistent asthma.

EIB: exercise-induced bronchoconstriction; FEV1: forced expiratory volume in 1 second; ICU:


intensive care unit.

Reproduced from: National Heart, Blood, and Lung Institute Expert Panel Report 3 (EPR 3): Guidelines for the Diagnosis
and Management of Asthma. NIH Publication no. 08-4051, 2007.

Graphic 51579 Version 10.0


Assessing asthma control in children 5 to 11 years of age

Classification of asthma control (children 5 to 11


years of age)
Components of control
Not well Very poorly
Well controlled
controlled controlled

Impairment Symptoms ≤2 days/week, but >2 days/week or Throughout the


not more than once multiple times on day
on each day ≤2 days/week

Nighttime ≤1 time/month ≥2 times/month ≥2 times/week


awakenings

Interference None Some limitation Extremely limited


with normal
activity

Short-acting ≤2 days/week >2 days/week Several times per


beta2-agonist day
use for
symptom
control (not
prevention of
EIB)

Lung function

FEV1 or peak >80% 60 to 80% <60%


flow predicted/personal predicted/personal predicted/personal
best best best

FEV1/FVC >80% 75 to 80% <75%

Risk Exacerbations 0 to 1/year ≥2/year (see footnote)


requiring oral
systemic Consider severity and interval since last exacerbation
glucocorticoids

Treatment- Medication side effects can vary in intensity from none to very
related adverse troublesome and worrisome. The level of intensity does not
effects correlate to specific levels of control but should be considered in
the overall assessment of risk.

The level of control is based on the most severe impairment or risk category. Assess impairment
domain by patient's/caregiver's recall of previous two to four weeks and by spirometry/or peak
flow measures. Symptom assessment for longer periods should reflect a global assessment, such
as inquiring whether the patient's asthma is better or worse since the last visit. At present, there
are inadequate data to correspond frequencies of exacerbations with different levels of asthma
control. In general, more frequent and intense exacerbations (eg, requiring urgent, unscheduled
care, hospitalization, or ICU admission) indicate poorer disease control. For treatment purposes,
patients who had ≥2 exacerbations requiring oral systemic glucocorticoids in the past year may
be considered the same as patients who have not well-controlled asthma, even in the absence of
impairment levels consistent with not well-controlled asthma.

EIB: exercise-induced bronchospasm; FEV1: forced expiratory volume in 1 second; FVC: forced
vital capacity; ICU: intensive care unit.

Reproduced from: National Heart, Blood, and Lung Institute Expert Panel Report 3 (EPR 3): Guidelines for the Diagnosis
and Management of Asthma. NIH Publication no. 08-4051, 2007.

Graphic 73634 Version 3.0


Causes of wheezing in children

Acute Chronic or recurrent


Asthma Structural abnormalities
Bronchiolitis* Tracheo-bronchomalacia*
Laryngotracheobronchitis ¶ Vascular compression/rings*

Atypical infection (Mycoplasma Tracheal stenosis/webs*


pneumonia) Δ
Cystic lesions/masses
Bacterial tracheitis
Tumors/lymphadenopathy
Foreign body aspiration ¶
Cardiomegaly
Esophageal foreign body
Functional abnormalities

Asthma

Gastroesophageal reflux

Recurrent aspiration

Cystic fibrosis

Immunodeficiency

Primary ciliary dyskinesia

Bronchopulmonary dysplasia

Retained foreign body (trachea or


esophagus)

Bronchiolitis obliterans

Pulmonary edema

Inducible laryngeal obstruction (vocal cord


dysfunction) Δ

Interstitial lung disease

* These disorders tend to present in infancy.

¶ These disorders are more commonly seen in young children (toddlers and preschoolers).

Δ These disorders are more commonly seen in teenagers.

Graphic 67370 Version 6.0


Approach to evaluation of wheezing in children based upon suspected
diagnosis

Suspected diagnosis Signs and symptoms Diagnostic evaluation


Acute

Asthma History of recurrent wheeze, History, PFT with


cough, at least partial bronchodilators, empiric trial
response to bronchodilator of bronchodilators, exercise or
methacholine challenge
testing, chest radiography only
if atypical, skin (or in vitro)
testing for aeroallergen
sensitization if history
suggests inhalant allergen
triggers

Viral bronchiolitis Prodrome with rhinitis, occurs History, age, season


in infancy and early childhood,
In selected cases: Rapid
seasonal pattern
antigen testing (RSV,
influenza), viral cultures, chest
radiography

Foreign body Sudden onset of coughing and History, physical examination,


wheezing chest radiography, rigid
bronchoscopy

Chronic

Asthma As above As above

Tracheomalacia Persistent wheeze, starts early History, fluoroscopy, flexible


in life, poor response to bronchoscopy or dynamic CT
bronchodilators, varies with with airway protocol
position and activity

Cystic fibrosis Chronic productive cough, Sweat chloride test, genetic


crackles, with or without testing
clubbing, failure to thrive,
recurrent respiratory
infections

Swallowing dysfunction Neurologic abnormality Videofluoroscopic swallowing


(nonuniversal), choking with study (modified barium
eating, symptoms swallow)
exaggerated by feeding

Gastroesophageal reflux Symptoms sometimes related 24-hour esophageal pH


to eating, vomiting, refusal to monitoring, multichannel
eat, failure to thrive intraluminal impedance
monitoring

Vascular ring or sling Persistent symptoms, starts Chest radiograph, MRI, or CT


early in infancy, may be angiogram
exaggerated by position,
Barium swallow
homophonous wheeze
Tracheal stenosis Persistent symptoms, with or Chest radiograph, CT scan,
without stridor, homophonous bronchoscopy
wheeze

Mediastinal nodes or mass Persistent symptoms, localized Chest radiograph, CT scan


wheezing, no response to
bronchodilator, systemic
symptoms of underlying
disease

Immunodeficiency Recurrent sinopulmonary Immunoglobulins, vaccine


infections, crackles, FTT, responses
clubbing

Primary ciliary dyskinesia Persistent sinusitis and otitis Ciliary biopsy, genetic testing,
media with draining ears, exhaled nasal nitric oxide
recurrent respiratory infection, (ENO)
wet cough with sputum
production, crackles, clubbing,
FTT

Inducible laryngeal Inspiratory stridor, poor Exercise testing, pulmonary


obstruction (vocal cord response to bronchodilators, function tests, laryngoscopy
dysfunction) absent symptoms during while symptomatic
sleep, teenage, exercise
related

Bronchiolitis obliterans History of predisposing Chest CT scan


disease, ie, viral infection or
In rare cases: Lung biopsy is
transplantation, dyspnea,
needed
persistent wheezing

PFT: pulmonary function test; RSV: respiratory syncytial virus; CT: computed tomography; MRI:
magnetic resonance imaging; FTT: failure to thrive.

Data from: Dorkin HL. Noisy breathing. In: Respiratory Disease in Children: Diagnosis and Management, Loughlin GM,
Eigen H (Eds), Williams and Wilkins 1994. p.171.

Graphic 62889 Version 11.0


Approach to a child with chronic specific cough*

Condition Underlying causes Evaluation

Asthma Bronchospasm Spirometry

Environmental triggers Chest radiography

Allergy testing

Trial of antiasthma
medications

Protracted bacterial bronchitis Haemophilus influenzae Empiric treatment with


antibiotics (two-week course
Streptococcus
or more)
pneumoniae
Bronchoscopy with cultures
Moraxella catarrhalis

Chronic suppurative lung Cystic fibrosis Sweat test


disease/bronchiectasis, or recurrent
Ciliary dyskinesia Bronchoscopy
pneumonia
Previous severe Cilia biopsy
pneumonia
Immune workup
Immunodeficiency
HRCT chest
Structural airway lesions
Barium swallow
Congenital lung lesions
Sputum cultures
Missed foreign body

TEF/H-fistula

Airway abnormality Foreign body Chest radiography

Tracheo-bronchomalacia Bronchoscopy and lavage

Other intraluminal CT chest


lesions (eg, tumors)
MRI chest
Extrinsic compressive
lesions

Aspiration Neurologic Barium swallow


abnormalities
Bronchoscopy and lavage
Weak cough reflex
Video fluoroscopy
Neuromuscular disease
pH monitor
Laryngeal abnormalities
Lung milk scan/salivagram
Adenotonsillar
hypertrophy

TEF/H-fistula

Severe GERD
Chronic or less common infections Tuberculosis Mantoux test

Nontuberculous Bronchoscopy and lavage


mycobacteria
HRCT chest
Mycoses
Sputum cultures
Parasites

Interstitial lung disease Rheumatic diseases Autoimmune markers

Cytotoxic drugs HRCT chest

Drugs Lung biopsy

External beam radiation

Cardiac Pulmonary Pediatric cardiology


hypertension consultation

Cardiac edema Echocardiogram

Cardiac catheterization

Other Upper airway cough Evaluate for sinusitis and


syndrome chronic rhinitis

Post-pertussis cough PCR, culture and serology for


Bordetella pertussis

TEF: tracheoesophageal fistula; HRCT: high-resolution chest computerized tomography; GERD:


gastroesophageal reflux disease; CT: computerized tomography; MRI: magnetic resonance
imaging; PCR: polymerase chain reaction.

* "Specific cough" refers to a cough that is caused by an underlying abnormality or disease.

Adapted from guidelines in: Chang AB, Glomb WB. Guidelines for evaluating chronic cough in pediatrics: ACCP evidence-
based clinical practice guidelines. Chest 2006; 129(1) Supplement: 260S-283S.

Graphic 75873 Version 6.0


Algorithm for the evaluation of chronic cough in children

FeNO: exhaled nitric oxide fraction; PBB: protracted bacterial bronchitis; TB: tuberculosis; CF: cystic fibrosi

* Specific cough pointers include [1] :


Symptoms – Chronic wet/productive cough, chest pain, history suggestive of inhaled foreign body
difficulties (including choking/vomiting), cardiac or neurodevelopmental abnormalities, recurrent
exposure to TB
Signs – Respiratory distress, digital clubbing, chest wall deformity, or auscultatory crackles
Tests – Chest radiographic changes (other than perihilar changes) or lung function abnormalities

Refer to UpToDate content on chronic cough in children.

¶ Habit cough (also known as tic cough) is typically absent at night or when distracted and may be honki

Δ FeNO value ≥25 ppb with asthma symptoms supports a diagnosis of asthma [3] .

◊ For diagnostic evaluation, refer to UpToDate content on pertussis and tracheomalacia. Tic (habit) cough

References:
1. Kantar A, Chang AB, Shields MD, et al. ERS statement on protracted bacterial bronchitis in children. Eur Respir J 2017; 50: 1
2. Weinberger M, Hoegger M. The cough without a cause: Habit cough syndrome. J Allergy Clin Immunol 2016; 137:930.
3. Gaillard EA, Kuehni CE, Turner S, et al. European Respiratory Society clinical practice guidelines for the diagnosis of asthma

Graphic 113691 Version 4.0


Features suggestive of a diagnosis other than asthma in children

History
Onset of symptoms in early infancy

Neonatal respiratory distress +/- ventilatory support

Neonatal neurologic dysfunction

Intractable wheezing unresponsive to bronchodilators

Wheezing associated with feeding or vomiting

Difficulty swallowing +/- recurrent vomiting

Diarrhea

Poor weight gain

Stridor

Oxygen requirement >1 week after acute attack

Physical examination
Failure to thrive

Clubbing

Cardiac murmur

Stridor

Focal lung signs

Nasal polyps

Crackles on auscultation

Cyanosis

Laboratory features
Focal or persistent chest radiograph abnormalities

Anemia

Irreversible airflow obstruction

Hypoxemia

Adapted from: Canny GJ, Levison H. Childhood asthma: A rational approach to treatment. Ann Allergy 1990; 64:406.

Graphic 70442 Version 4.0

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