Chapter 388 – Wheezing, Bronchiolitis, and Bronchitis

DEFINITIONS AND GENERAL PATHOPHYSIOLOGY

A wheeze is a musical and continuous sound that originates from oscillations in narrowed
airways. Wheezing is heard mostly on expiration as a result of critical airway obstruction.
Wheezing is polyphonic when there is widespread narrowing of the airways causing various
pitches or levels of obstruction to airflow as seen in asthma. Monophonic wheezing refers
to a single-pitch sound that is produced in the larger airways during expiration as in distal
tracheomalacia or bronchomalacia. When obstruction occurs in the extrathoracic airways
during inspiration, the noise is referred to as stridor.

Infants are prone to wheeze due to a differing set of lung mechanics in comparison to older
children and adults. The obstruction to flow is affected by the airway caliber and compliance
of the infant lung. Resistance to airflow through a tube is inversely related to the radius of
the tube to the 4th power. In children <5 yr old, small caliber peripheral airways can
contribute up to 50% of the total airway resistance. Marginal additional narrowing can cause
further flow limitation and a subsequent wheeze.

With the very compliant newborn chest wall, the inward pressure produced in expiration
subjects the intrathoracic airways to collapse. Flow limitation is further affected in infants by
the differences in tracheal cartilage composition and airway smooth muscle tone causing
further increase in airway compliance in comparison to older children. All of these
mechanisms combine to make the infant more susceptible to airway collapse, increased
resistance, and subsequent wheezing. Many of these conditions are outgrown in the 1st year
of life.

Immunologic and molecular influences can contribute to the infant's propensity to wheeze.
In comparison to older children and adults, infants tend to have higher levels of lymphocytes
and neutrophils, rather than mast cells and eosinophils, in bronchoalveolar lavage fluid. A
variety of inflammatory mediators have also been implicated in the wheezing infant such as
histamine, leukotrienes, and interleukins. Fetal and/or early postnatal “programming” in
which the structure and function of the lung are affected by factors including fetal nutrition
and fetal and neonatal exposure to maternal smoking may also occur.

ETIOLOGY

Most wheezing in infants is caused by inflammation (generally bronchiolitis), but many other
entities can present with wheezing ( Table 388-1 ).

TABLE 388-1 -- Differential Diagnosis of Wheezing in Infancy

INFECTION
Viral
Respiratory syncytial virus (RSV)
Human metapneumovirus
Parainfluenza
Adenovirus
Influenza
Rhinovirus
Other
Chlamydia trachomatis
Tuberculosis
Histoplasmosis
Papillomatosis
ASTHMA
Transient wheezer
Initial risk factor is primarily diminished lung size
Persistent wheezers
Initial risk factors include passive smoke exposure, maternal asthma history, and an
elevated immunoglobulin E (IgE) level in the 1st year of life
At increased risk of developing clinical asthma
Late-onset wheezer
ANATOMIC ABNORMALITIES
Central airway abnormalities
Malacia of the larynx, trachea, and/or bronchi
Tracheoesophageal fistula (specifically H-type fistula)
Laryngeal cleft (resulting in aspiration)
Extrinsic airway anomalies resulting in airway compression
Vascular ring or sling
Mediastinal lymphadenopathy from infection or tumor
Mediastinal mass/tumor
Esophageal foreign body
Intrinsic airway anomalies
Airway hemangioma, other tumor
Cystic adenomatoid malformation
Bronchial/lung cyst
Congenital lobar emphysema
Aberrant tracheal bronchus
Sequestration
Congenital heart disease with left-to-right shunt (increased pulmonary edema)
Foreign body
IMMUNODEFICIENCY STATES
IgA deficiency
B-cell deficiencies
Primary ciliary dyskinesia
AIDS
Bronchiectasis
MUCOCILIARY CLEARANCE DISORDERS

Cystic fibrosis
Primary ciliary dyskinesias
Bronchiectasis
BRONCHOPULMONARY DYSPLASIA
ASPIRATION SYNDROMES

Gastroesophageal reflux disease

Pharyngeal/swallow
dysfunction
INTERSTITIAL LUNG DISEASE, INCLUDING BRONCHIOLITIS OBLITERANS
HEART FAILURE
ANAPHYLAXIS
INHALATION INJURY—BURNS

ACUTE BRONCHIOLITIS AND INFLAMMATION OF THE AIRWAY.

Infection can cause obstruction to flow by internal narrowing of the airways.

Acute bronchiolitis is predominantly a viral disease. Respiratory syncytial virus (RSV) is

responsible for >50% of cases (see Chapter 257 ). Other agents include parainfluenza (see
Chapter 256 ), adenovirus, Mycoplasma, and, occasionally, other viruses. Human
metapneumovirus (see Chapter 258 ) is an important primary cause of viral respiratory
infection or it can occur as a co-infection with RSV. There is no evidence of a bacterial cause
for bronchiolitis, although bacterial pneumonia is sometimes confused clinically with
bronchiolitis and bronchiolitis is rarely followed by bacterial superinfection.

Approximately 50,000–80,000 of hospitalizations annually among children <1 yr old are

attributable to RSV infection, with 200–500 deaths per yr in the United States. Increasing
rates of hospitalization may reflect increased attendance of infants in daycare centers,
changes in criteria for hospital admission, and/or improved survival of premature infants and
others at risk for severe RSV-associated disease.

Bronchiolitis is more common in males, in those who have not been breast-fed, and in those
who live in crowded conditions. Older family members are a common source of infection;
they may only experience minor respiratory symptoms. The clinical manifestations of lower
respiratory tract illness (LRTI) seen in young infants may be minimal in older patients, in
whom bronchiolar edema is better tolerated.
Not all infected infants develop LRTI. Host anatomic and immunologic factors seem to play a
significant role in the severity of the clinical syndrome. Infants with pre-existent smaller
airways and diminished lung function have a more severe course. In addition, RSV infection
incites a complex immune response. Eosinophils degranulate and release eosinophil cationic
protein, which is cytotoxic to airway epithelium. Immunoglobulin E (IgE) antibody release
may also be related to wheezing. Other mediators invoked in the pathogenesis of airway
inflammation include chemokines such as interleukin 8 (IL-8), macrophage inflammatory
protein (MIP) 1α, and RANTES (regulated on activation, normal Tcell expressed and
secreted). RSV-infected infants who wheeze express higher levels of interferon-γ in the
airway as well as leukotrienes. RSV co-infection with metapneumovirus can be more severe
than monoinfection.

Acute bronchiolitis is characterized by bronchiolar obstruction with edema, mucus, and

cellular debris. Even minor bronchiolar wall thickening significantly affects airflow because
resistance is inversely proportional to the 4th power of the radius of the bron chiolar
passage. Resistance in the small air passages is increased during both inspiration and
exhalation, but because the radius of an airway is smaller during expiration, the resultant
respiratory obstruction leads to early air trapping and overinflation. If obstruction becomes
complete, there will be resorption of trapped distal air, and the child will develop atelectasis.

Hypoxemia is a consequence of ventilation-perfusion mismatch early in the course. With

severe obstructive disease and tiring of respiratory effort, hypercapnia may develop.

Chronic infectious causes of wheezing should be considered in those infants who seem to
fall out of the range of a normal clinical course. Cystic fibrosis is one such entity; suspicion
increases in a patient with persistent respiratory symptoms, digital clubbing, malabsorption,
failure to thrive, electrolyte abnormalities, or a resistance to bronchodilator treatment (see
Chapter 400 ).

Allergy and asthma are important causes of wheezing and probably generate the most
questions by the parents of a wheezing infant. Asthma is characterized by airway
inflammation, bronchial hyperreactivity, and reversibility of obstruction (see Chapter 143 ).
Three identified patterns of infant wheezing are: the transient early wheezer, 19.9% of the
general population, had wheezing at least once with a lower respiratory infection before the
age of 3 yr but never wheezed again; the persistent wheezer, 13.7% of the general
population, had wheezing episodes before 3 yr and was still wheezing at 6 yr of age; and the
late onset wheezer, 15% of the general population, had no wheezing by 3 yr but was
wheezing by 6 yr. The other ½ of the children had never wheezed by 6 yr. Of all the infants
who wheezed before 3 yr old, almost 60% stopped wheezing by 6 yr. Risk factors for
persistent wheezing included maternal asthma, maternal smoking, persistent rhinitis (apart
from acute upper respiratory tract infections), and eczema at <1 yr of age.

OTHER CAUSES.

Congenital malformations of the respiratory tract cause wheezing in early infancy. These
findings can be diffuse or focal and can be from an external compression or an intrinsic
abnormality. External vascular compression includes a vascular ring, in which the trachea
and esophagus are surrounded completely by vascular structures, or a vascular sling, in
which the trachea and esophagus are not completely encircled (see Chapter 432 ).
Cardiovascular causes of wheezing include dilated chambers of the heart including massive
cardiomegaly, left atrial enlargement, and dilated pulmonary arteries. Pulmonary edema
caused by heart failure can also cause wheezing by lymphatic and bronchial vessel
engorgement that leads to obstruction and edema of the bronchioles and further obstruction
(see Chapter 442 ).
Foreign body aspiration (see Chapter 384 ) can cause acute or chronic wheezing. It is
estimated that 78% of those who die from foreign body aspiration are between 2 mo and 4
yr old. Even in young infants, a foreign body can be ingested if given to the infant by
another person such as an older sibling. Infants who have atypical histories or misleading
clinical and radiologic findings may be misdiagnosed with asthma or another obstructive
disorder as inflammation and granulation develop around the foreign body. Esophageal
foreign body can transmit pressure to the membranous trachea, causing compromise of the
airway lumen.

Gastroesophageal reflux (see Chapter 320.1 ) can cause wheezing with or without direct
aspiration into the tracheobronchial tree. Without aspiration, the reflux is thought to trigger
a vagal or neural reflex, causing increased airway resistance and airway reactivity.
Aspiration from gastroesophageal reflux or from the direct aspiration from oral liquids can
also cause wheezing.Trauma and tumors are much more rare causes of wheezing in
infants. Trauma of any type to the tracheobronchial tree can cause an obstruction to airflow.
Accidental or nonaccidental aspirations, burns, or scalds of the tracheobronchial tree can
cause inflammation of the airways and subsequent wheezing. Any space-occupying lesion
either in the lung itself or extrinsic to the lung can cause tracheobronchial compression and
obstruction to airflow.

CLINICAL MANIFESTATIONS
HISTORY AND PHYSICAL EXAMINATION.

Initial history of a wheezing infant should include accounts of the recent event including
onset, duration, and associated factors ( Table 388-2 ). Birth history includes weeks of
gestation, neonatal intensive care unit admission, history of intubation or oxygen
requirement, maternal complications including infection, herpes simplex virus (HSV) status,
HIV status, and prenatal smoke exposure. Past medical history includes any co-morbid
conditions including syndromes or associations. Family history of cystic fibrosis,
immunodeficiencies, asthma in a 1st-degree relative, or any other recurrent respiratory
conditions in children should be obtained. Social history should include an environmental
history including any smokers at home, inside or out, daycare exposure, number of siblings,
occupation of inhabitants of the home, pets, tuberculosis exposure, and concerns regarding
home environment (i.e. dust mites, construction dust, heating and cooling techniques, mold,
cockroaches).

TABLE 388-2 -- Pertinent Medical History in the Wheezing Infant

Did the onset of symptoms begin at birth or thereafter?
Is the infant a noisy breather and when is it most prominent?
Is there a history of cough apart from wheezing?
Was there an earlier lower respiratory tract infection?
Have there been any emergency department visits, hospitalizations, or intensive care
unit admissions for respiratory distress?
Is there a history of eczema?
Does the infant cough after crying or cough at night?
How is the infant growing and developing?
Is there associated failure to thrive?
Is there failure to thrive without feeding difficulties?
 Is there a history of electrolyte abnormalities?
Are there signs of intestinal malabsorption including frequent, greasy, or oily stools?
Is there a maternal history of genital herpes simplex virus (HSV) infection?
What was the gestational age at delivery?
Was the patient intubated as a neonate?
Does the infant bottle-feed in the bed or the crib, especially in a propped position?
Are there any feeding difficulties including choking, gagging, arching, or vomiting with
feeds?
Any new food exposure?
Is there a toddler in the home or lapse in supervision in which foreign body aspiration
could have occurred?
Change in caregivers or chance of nonaccidental trauma?

On physical examination, evaluation of the patient's vital signs with special attention to
the respiratory rate and the pulse oximetry reading for oxygen saturation is an important
initial step. There should also be a thorough review of the patient's growth chart for signs of
failure to thrive. Wheezing produces an expiratory whistling sound that can be polyphonic or
monophonic in nature. Prolonged expiratory time may be present. Biphasic wheezing can
occur if there is a central, large airway obstruction. The lack of audible wheezing is not
reassuring if the infant shows other signs of respiratory distress because complete
obstruction to airflow can eliminate the turbulence, which causes the sound to resonate.
Aeration should be noted and a trial of a bronchodilator may be warranted to evaluate for
any change in wheezing after treatment. Listening to breath sounds over the neck will help
differentiate upper airway from lower airway sounds. The absence or presence of stridor
should be noted and appreciated on inspiration. Signs of respiratory distress include
tachypnea, increased respiratory effort, nasal flaring, tracheal tugging, subcostal and
intercostal retractions, and excess use of accessory muscles. In the upper airway, signs of
atopy, including boggy turbinates and posterior oropharynx cobblestoning, can be evaluated
in older infants. It is also useful to evaluate the skin of the patient for eczema and any
significant hemangiomas; midline lesions may be associated with an intrathoracic lesion.
Digital clubbing should be noted (see Chapter 371 ).

Acute bronchiolitis is usually preceded by exposure to an older contact with a minor

respiratory syndrome within the previous wk. The infant 1st develops a mild upper
respiratory tract infection with sneezing and clear rhinorrhea. This may be accompanied by
diminished appetite and fever of 38.5–39°C (101–102°F), although the temperature may
range from subnormal to markedly elevated. Gradually, respiratory distress ensues, with
paroxysmal wheezy cough, dyspnea, and irritability. The infant is often tachypneic, which
may interfere with feeding. The child does not usually have other systemic complaints, such
as diarrhea or vomiting. Apnea may be more prominent than wheezing early in the course of
the disease, particularly with very young infants (<2 mo old) or former premature infants.

The physical examination is characterized most prominently by wheezing. The degree of

tachypnea does not always correlate with the degree of hypoxemia or hypercarbia, so the
use of pulse oximetry and noninvasive carbon dioxide determination is essential. Work of
breathing may be markedly increased, with nasal flaring and retractions. Auscultation may
reveal fine crackles or overt wheezes, with prolongation of the expiratory phase of
breathing. Barely audible breath sounds suggest very severe disease with nearly complete
bronchiolar obstruction. Hyperinflation of the lungs may permit palpation of the liver and
spleen.

DIAGNOSTIC EVALUATION.

Initial evaluation is dependent on likely etiology; a baseline chest radiograph, including

posteroanterior and lateral films, is warranted in many cases and for any infant in acute
respiratory distress. Focal infiltrates are most often found in wheezing infants who have a
pulse oximetry reading <93%, grunting, decreased breath sounds, prolonged inspiratory to
expiratory ratio, and crackles. The chest radiograph may also be useful for evaluation of
hyperinflation (common in bronchiolitis and viral pneumonia), signs of chronic disease such
as bronchiectasis, or a space-occupying lesion causing airway compression. A trial of
bronchodilator may be diagnostic as well as therapeutic because these medications can
reverse conditions such as bronchiolitis (occasionally) and asthma but will not affect a fixed
obstruction. Bronchodilators may potentially worsen a case of wheezing caused by tracheal
or bronchial malacia. A sweat test to evaluate for cystic fibrosis and evaluation of baseline
immune status are reasonable in infants with recurrent wheezing or complicated courses.
Further evaluation such as upper gastrointestinal (GI) contrast x-rays, chest CT,
bronchoscopy, infant pulmonary function testing, video swallow study, and pH probe can be
considered second-tier diagnostic procedures in complicated patients.

In acute bronchiolitis, chest radiography reveals hyperinflated lungs with patchy

atelectasis. The white blood cell and differential counts are usually normal. Viral testing
(usually rapid immunofluorescence, polymerase chain reaction, or viral culture) is helpful if
the diagnosis is uncertain or for epidemiologic purposes. The diagnosis is clinical,
particularly in a previously healthy infant presenting with a first-time wheezing episode
during a community outbreak. Because concurrent bacterial infection (sepsis, pneumonia,
meningitis) is highly unlikely, confirmation of viral bronchiolitis may obviate the need for a
sepsis evaluation in a febrile infant and assist with respiratory precautions and isolation if
the patient requires hospitalization.

TREATMENT

Treatment of an infant with wheezing depends on the underlying etiology. Response to

bronchodilators is unpredictable, regardless of cause, but suggests a component of
bronchial hyperreactivity. It is appropriate to administer albuterol aerosol and objectively
observe the response. For infants <3 yr of age, it is acceptable to continue to administer
inhaled medications through an MDI with mask and spacer if a therapeutic benefit is
demonstrated. Therapy should be continued in all patients with asthma exacerbations from
a viral illness.

The use of ipratropium bromide in this population is controversial, but it appears to be

somewhat effective as an adjunct therapy. It is also useful in infants with significant tracheal
and bronchial malacia who may be made worse by β-2 agonists such as albuterol because of
the subsequent decrease in smooth muscle tone.

A trial of inhaled steroids may be warranted in a patient who has responded to multiple
courses of oral steroids, has moderate to severe wheezing, or a significant history of atopy
including food allergy or eczema. Inhaled steroids are appropriate for maintenance therapy
in patients with known reactive airways but are controversial when used for episodic or
acute illnesses.
Oral steroids are generally reserved for atopic wheezing infants thought to have asthma that
is refractory to other medications. Their use in first-time wheezing infants or those infants
that do not warrant hospitalization is controversial.

Infants with acute bronchiolitis who are experiencing respiratory distress should be
hospitalized; the mainstay of treatment is supportive. If hypoxemic, the child should receive
cool humidified oxygen. Sedatives are to be avoided because they may depress respiratory
drive. The infant is sometimes more comfortable if sitting with head and chest elevated at a
30-degree angle with neck extended. The risk of aspiration of oral feedings may be high in
infants with bronchiolitis, owing to tachypnea and the increased work of breathing. The
infant may be fed through a nasogastric tube. If there is any risk for further respiratory
decompensation potentially necessitating tracheal intubation, however, the infant should
not be fed orally but be maintained with parenteral fluids. Frequent suctioning of nasal and
oral secretions often provides relief of distress or cyanosis. Oxygen is indicated in all infants
with hypoxia.

A number of agents have been proposed as adjunctive therapies for bronchiolitis.

Bronchodilators produce modest short-term improvement in clinical features, but the
statistical improvement in clinical scoring systems seen with them is not always clinically
significant. Several studies have included both infants with 1st-time wheezing and those
with recurrent wheezing, complicating interpretation of the data. Nebulized epinephrine may
be more effective than β-agonists. A trial dose of inhaled bronchodilator may be reasonable,
with further therapy predicated on response in the individual patient. Corticosteroids,
whether parenteral, oral, or inhaled, have been used for bronchiolitis despite conflicting and
often negative studies. Differences of diagnostic criteria, measures of effect, timing and
route of administration, and severity of illness complicate these studies. Corticosteroids are
not recommended in previously healthy infants with RSV. Ribavirin, an antiviral agent
administered by aerosol, has been used for infants with congenital heart disease or chronic
lung disease. There is no convincing evidence of a positive impact on clinically important
outcomes such as mortality and duration of hospitalization. Antibiotics have no value unless
there is secondary bacterial pneumonia. Likewise, there is no support for RSV
immunoglobulin administration during acute episodes of RSV bronchiolitis.

PROGNOSIS

Infants with acute bronchiolitis are at highest risk for further respiratory compromise in
the 1st 48–72 hr after onset of cough and dyspnea; the child may be desperately ill with air
hunger, apnea, and respiratory acidosis. The case fatality rate is <1%, with death
attributable to apnea, uncompensated respiratory acidosis, or severe dehydration. After this
critical period, symptoms may persist. The median duration of symptoms in ambulatory
patients is ≈12 days. Infants with conditions such as congenital heart disease,
bronchopulmonary dysplasia, and immunodeficiency often have more severe disease, with
higher morbidity and mortality. There is a higher incidence of wheezing and asthma in
children with a history of bronchiolitis unexplained by family history or other atopic
syndromes. It is unclear whether bronchiolitis incites an immune response that manifests as
asthma later or whether those infants have an inherent predilection for asthma that is
merely unmasked by their episode of RSV. Approximately 60% of infants who wheeze will
stop wheezing.

PREVENTION

Reduction in the severity and incidence of acute bronchiolitis due to RSV is possible
through the administration of pooled hyperimmune RSV intravenous immunoglobulin (RSV-
IVIG, RespiGam) and palivizumab (Synagis), an intramuscular monoclonal antibody to the
RSV F protein, before and during RSV season. Palivizumab is recommended for infants <2 yr
of age with chronic lung disease (bronchopulmonary dysplasia) or prematurity. Meticulous
handwashing is the best measure to prevent nosocomial transmission.

388.2 Bronchitis

Denise M. Goodman

Bronchitis refers to nonspecific bronchial inflammation and is associated with a number of

childhood conditions. Acute bronchitis is a syndrome, usually viral in origin, with cough as a
prominent feature.

Acute tracheobronchitis is a term used when the trachea is prominently involved.

Nasopharyngitis may also be present, and a variety of viral and bacterial agents, such as
those causing influenza, pertussis, and diphtheria, may be responsible. Isolation of common
bacteria such as pneumococcus, Staphylococcus aureus, and Streptococcus pneumoniae
from the sputum may not imply a bacterial cause requiring antibiotic therapy.

ACUTE BRONCHITIS
CLINICAL MANIFESTATIONS.

Acute bronchitis is commonly preceded by a viral upper respiratory tract infection. It is more
common in the winter when respiratory viral syndromes predominate. The tracheobronchial
epithelium is invaded by the infectious agent, leading to activation of inflammatory cells and
release of cytokines. Constitutional symptoms, such as fever and malaise, follow. The
tracheobronchial epithelium may become significantly damaged or hypersensitized, leading
to a protracted cough lasting 1–3 wk.

The child 1st presents with nonspecific upper respiratory infectious symptoms, such as
rhinitis. Three to 4 days later, a frequent, dry, hacking cough develops, which may or may
not be productive. After several days, the sputum may become purulent, indicating
leukocyte migration but not necessarily bacterial infection. Many children swallow their
sputum, and this may produce emesis. Chest pain may be a prominent complaint in older
children, exacerbated by coughing. The mucus gradually thins, usually within 5–10 days, and
then the cough gradually abates. The entire episode usually lasts about 2 wk and seldom
longer than 3 wk.

Findings on physical examination vary with age of the patient and stage of the disease. Early
findings are absent or are low-grade fever and upper respiratory signs such as
nasopharyngitis, conjunctivitis, and rhinitis. Auscultation of the chest may be unremarkable
at this early phase. As the syndrome progresses and cough worsens, breath sounds become
coarse, with coarse and fine crackles and scattered high-pitched wheezing. Chest
radiographs are normal or may have increased bronchial markings.

The principal objective of the clinician is to exclude pneumonia, which is more likely caused
by bacterial agents requiring antibiotic therapy. In adults, absence of abnormality of vital
signs (tachycardia, tachypnea, fever) and a normal physical examination of the chest reduce
the likelihood of pneumonia.

DIFFERENTIAL DIAGNOSIS.
Persistent or recurrent symptoms should lead the clinician to consider entities other than
acute bronchitis. Many entities manifest with cough as a prominent symptom ( Table 388-
3 ).

TABLE 388-3 -- Disorders with Cough as a Prominent Finding

CATEGORY DIAGNOSES
Inflammatory Asthma
Chronic pulmonary processes Bronchopulmonary dysplasia/chronic lung disease
Postinfectious bronchiectasis
Cystic fibrosis
Tracheo- or bronchomalacia
Ciliary abnormalities
Other chronic disease/congenital Laryngeal cleft
disorders
Swallowing disorders
Gastroesophageal reflux
Airway compression (such as a vascular ring or
hemangioma)
Congenital heart disease
Infectious/immune disorders Immunodeficiency
Tuberculosis
Allergy
Sinusitis
Tonsillitis or adenoiditis
Chlamydia, Ureaplasma (infants)
Bordetella pertussis
Mycoplasma pneumoniae
Acquired Foreign body aspiration, tracheal or esophageal

TREATMENT.

There is no specific therapy for acute bronchitis. The disease is self-limited, and antibiotics,
although frequently prescribed, do not hasten improvement. Frequent shifts in position may
facilitate pulmonary drainage in infants. Older children are sometimes more comfortable
with humidity, but this does not shorten the disease course. Cough suppressants may
produce symptomatic relief but may also increase the risk of suppuration and inspissated
secretions and, therefore, should be used judiciously. Antihistamines dry secretions and are
not helpful; expectorants are likewise not indicated.
CHRONIC BRONCHITIS

Chronic bronchitis is well recognized in adults, formally defined as ≥3 mo of productive

cough each year for ≥2 yr. The disease may develop insidiously, with episodes of acute
obstruction alternating with quiescent periods. A number of predisposing conditions can lead
to progression of airflow obstruction or chronic obstructive pulmonary disease (COPD), with
smoking as the major factor (up to 80% of patients have a smoking history). Other
conditions include air pollution, occupational exposures, and repeated infections. In children,
cystic fibrosis, bronchopulmonary dysplasia, and bronchiectasis must be ruled out.

The applicability of this definition to children is unclear. The existence of chronic bronchitis
as a distinct entity in children is controversial. Like adults, however, children with chronic
inflammatory diseases or those with toxic exposures can develop damaged pulmonary
epithelium. Thus, chronic or recurring cough in children should lead the clinician to search
for underlying pulmonary or systemic disorders (see Table 388-3 ).