3/6/2014 Pediatric Bronchitis

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Pediatric Bronchitis
Author: Patrick L Carolan, MD; Chief Editor: Michael R Bye, MD more...

Updated: Mar 18, 2014
Background
Acute bronchitis is a clinical syndrome produced by inflammation of the trachea, bronchi, and bronchioles. In
children, acute bronchitis usually occurs in association with viral respiratory tract infection. Acute bronchitis is
rarely a primary bacterial infection in otherwise healthy children. (See Pathophysiology, as well as Etiology.)
Examples of normal airway color and architecture and an airway in a patient with chronic bronchitis are shown
below. (See Anatomy.)
Normal airway color and architecture (in a child with mild tracheomalacia).
Airway of a child with chronic bronchitis shows erythema, loss of normal architecture, and swelling.
Symptoms of acute bronchitis usually include productive cough and sometimes retrosternal pain during deep
breathing or coughing. Generally, the clinical course of acute bronchitis is self-limited, with complete healing and
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full return to function typically seen within 10-14 days following symptom onset. (See Clinical Presentation.)
Chronic bronchitis is recurring inflammation and degeneration of the bronchial tubes that may be associated with
active infection. Patients with chronic bronchitis have more mucus than normal because of either increased
production or decreased clearance. Coughing is the mechanism by which excess secretion is cleared.
Chronic bronchitis is often associated with asthma, cystic fibrosis, dyskinetic cilia syndrome, foreign body
aspiration, or exposure to an airway irritant. Recurrent tracheobronchitis may occur with tracheostomies or
immunodeficiency states. (See Diagnosis.)
Defining chronic bronchitis and its prevalence in childhood has been complicated by the significant clinical overlap
with asthma and reactive airway disease states. In adults, chronic bronchitis is defined as daily production of
sputum for at least 3 months in 2 consecutive years. Some have applied this definition to childhood chronic
bronchitis. Others limit the definition to a productive cough that lasts more than 2 weeks despite medical therapy.
Chronic bronchitis has also been defined as a complex of symptoms that includes cough that lasts more than 1
month or recurrent productive cough that may be associated with wheezing or crackles on auscultation. Elements
of these descriptors are present in the working definitions of asthma, as well.
[1]
Treatment of chronic bronchitis in pediatric patients includes rest, use of antipyretics, adequate hydration, and
avoidance of smoke. (See Treatment and Management.)
Analgesics and antipyretics target the symptoms of pediatric bronchitis. In chronic cases, bronchodilator therapy
should be considered. Oral corticosteroids should be added if cough continues and the history and physical
examination findings suggest a wheezy form of bronchitis. (See Medication.)
Pathophysiology
Acute bronchitis leads to the hacking cough and phlegm production that often follows upper respiratory tract
infection. This occurs because of the inflammatory response of the mucous membranes within the lungs' bronchial
passages. Viruses, acting alone or together, account for most of these infections.
[2, 3]
In children, chronic bronchitis follows either an endogenous response (eg, excessive viral-induced inflammation) to
acute airway injury or continuous exposure to certain noxious environmental agents (eg, allergens or irritants). An
airway that undergoes such an insult responds quickly with bronchospasm and cough, followed by inflammation,
edema, and mucus production. This helps explain the fact that apparent chronic bronchitis in children is often
actually asthma.
Mucociliary clearance is an important primary innate defense mechanism that protects the lungs from the harmful
effects of inhaled pollutants, allergens, and pathogens.
[4]
Mucociliary dysfunction is a common feature of chronic
airway diseases.
The mucociliary apparatus consists of 3 functional compartments: the cilia, a protective mucus layer, and an
airway surface liquid (ASL) layer, which work together to remove inhaled particles from the lung. Animal study data
have identified a critical role for ASL dehydration in the pathogenesis of mucociliary dysfunction and chronic airway
disease.
[5]
ASL depletion resulted in reduced mucus clearance and histologic signs of chronic airway disease,
including mucous obstruction, goblet cell hyperplasia, and chronic inflammatory cell infiltration. Study animals
experienced reduced bacterial clearance and high pulmonary mortality as a result.
The role of irritant exposure, particularly cigarette smoke and airborne particulates, in recurrent (wheezy) bronchitis
and asthma is becoming clearer. Kreindler et al demonstrated that the ion transport phenotype of normal human
bronchial epithelial cells exposed to cigarette smoke extract is similar to that of cystic fibrosis epithelia, in which
sodium is absorbed out of proportion to chloride secretion in the setting of increased mucus production.
[6]
These
findings suggest that the negative effects of cigarette smoke on mucociliary clearance may be mediated through
alterations in ion transport.
McConnell et al noted that organic carbon and nitrogen dioxide airborne particulates were associated with the
chronic symptoms of bronchitis among children with asthma in southern California.
[7]
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A chronic or recurrent insult to the airway epithelium, such as recurrent aspiration or repeated viral infection, may
contribute to chronic bronchitis in childhood. Following damage to the airway lining, chronic infection with
commonly isolated airway organisms may occur. The most common bacterial pathogen that causes lower
respiratory tract infections in children of all age groups is Streptococcus pneumoniae. Nontypeable Haemophilus
influenzae and Moraxella catarrhalis may be significant pathogens in preschoolers (age < 5 y), whereas
Mycoplasma pneumoniae may be significant in school-aged children (ages 6-18 y).
Children with tracheostomies are often colonized with an array of flora, including alpha-hemolytic streptococci and
gamma-hemolytic streptococci. With acute exacerbations of tracheobronchitis in these patients, pathogenic flora
may include Pseudomonas aeruginosa and Staphylococcus aureus (including methicillin-resistant strains), among
other pathogens. Children predisposed to oropharyngeal aspiration, particularly those with compromised protective
airway mechanisms, may become infected with oral anaerobic strains of streptococci.
Etiology
Acute bronchitis is generally caused by respiratory infections; approximately 90% are viral in origin, and 10% are
bacterial. Chronic bronchitis may be caused by repeated attacks of acute bronchitis, which can weaken and
irritate bronchial airways over time, eventually resulting in chronic bronchitis. Industrial pollution is also a common
cause; however, the chief culprit is heavy long-term cigarette smoke exposure.
Viral infections include the following:
Adenovirus
Influenza
Parainfluenza
Respiratory syncytial virus
Rhinovirus
Human bocavirus
[8, 9, 10]
Coxsackievirus
Herpes simplex virus
Secondary bacterial infection as part of an acute upper respiratory tract infection is extremely rare in nonsmoke-
exposed patients without cystic fibrosis or immunodeficiency but may include the following:
S pneumoniae
M catarrhalis
H influenzae (nontypeable)
Chlamydia pneumoniae (Taiwan acute respiratory [TWAR] agent)
Mycoplasma species
Air pollutants, such as those that occur with smoking and from second-hand smoke, also cause incident
bronchiolitis.
[11]
Tsai et al demonstrated that in utero and postnatal household cigarette smoke exposure is
strongly linked to asthma and recurrent bronchitis in children.
[12]
Other causes include the following:
Allergies
Chronic aspiration or gastroesophageal reflux
Fungal infection
Plastic bronchitis
Plastic bronchitis is an unusual but potentially devastating form of obstructive bronchial disease. The disease is
characterized by the development of arborizing, thick, tenacious casts of the tracheobronchial tree that produce
airway obstruction (Brooks 2013).
Patients with congenital heart disease who have undergone a Fontan operation are a group at high risk for
development of this problem, for unknown reasons. In some cases, plastic bronchitis appears many years after the
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Fontan procedure is performed.
[13]
Zahorec et al describe cases occurring in the immediate postoperative period
following a Fontan procedure. These patients were successfully managed with short periods of high-frequency jet
ventilation and vigorous pulmonary toilet.
[14]
Therapies include endoscopic debridement of the airway, vigorous pulmonary toilet, and aerosolized tissue
plasminogen activator. Shah et al performed thoracic duct ligation, resulting in complete resolution of the formation
of casts in 2 patients with plastic bronchitis refractory to medical management.
[15]
These results suggest that high
intrathoracic lymphatic pressures are related to the development of the recurrent bronchial casts seen in this
disorder.
Epidemiology
Data collected from the National Ambulatory Care Survey 1991 Summary showed that 2,774,000 office visits by
children younger than 15 years resulted in a diagnosis of bronchitis.
[16]
Although the report did not separate
diagnoses into acute and chronic bronchitis, the frequency of visits made bronchitis just slightly less common
than otitis media and slightly more common than asthma. However, in children, asthma is often underdiagnosed
and is frequently misdiagnosed as chronic or recurrent bronchitis. Since 1996, 9-14 million Americans have been
diagnosed with chronic bronchitis annually.
Bronchitis, both acute and chronic, is prevalent throughout the world and is one of the top 5 reasons for childhood
physician visits in countries that track such data. The incidence of bronchitis in British schoolchildren is reported
to be 20.7%.
Weigl et al noted an overall increase in hospitalization for lower respiratory tract infection
(laryngotracheobronchitis, bronchitis, wheezing bronchitis, bronchiolitis, bronchopneumonia, pneumonia) among
German children from 1996 to 2000; this is consistent with observations among children from the United States,
United Kingdom, and Sweden.
[17]
The incidence rate of bronchitis in children in this German cohort was 28%.
Differences in population prevalences have been identified in patients with chronic bronchitis. For example,
because of the association of chronic bronchitis with asthma and the concentration of asthma risk factors among
inner-city populations, this population group is at higher risk.
The incidence of acute bronchitis is equal in males and females. The incidence of chronic bronchitis is difficult to
state precisely because of the lack of definitive diagnostic criteria and the considerable overlap with asthma.
However, in recent years, the prevalence of chronic bronchitis has been reported to be consistently higher in
females than in males.
Acute (typically wheezy) bronchitis occurs most commonly in children younger than 2 years, with another peak
seen in children aged 9-15 years. Chronic bronchitis affects people of all ages but is more prevalent in persons
older than 45 years.
Prognosis
Acute bronchitis is almost always a self-limited process in the otherwise healthy child. However, it frequently
results in absenteeism from school and, in older patients, work. Chronic bronchitis is manageable with proper
treatment and avoidance of known triggers (eg, tobacco smoke). Proper management of any underlying disease
process, such as asthma, cystic fibrosis, immunodeficiency, heart failure, bronchiectasis, or tuberculosis, is also
key. These patients need careful periodic monitoring to minimize further lung damage and progression to chronic
irreversible lung disease.
Patient Education
Instruct older patients regarding the need for immunization against pertussis, diphtheria, and influenza, which
reduces the risk of bronchitis due to the causative organisms. Instruct these patients to avoid passive
environmental tobacco smoke; to avoid air pollutants, such as wood smoke, solvents, and cleaners; and to obtain
medical attention for prolonged respiratory infections.
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Instruct parents that children may attend school or daycare without restrictions except during episodes of acute
bronchitis with fever. Also instruct parents that children may return to school or daycare when signs of infection
have decreased, appetite returns, and alertness, strength, and a feeling of well-being allow.
For excellent patient education resources, see eMedicineHealth's Asthma Center. Also, visit eMedicineHealth's
patient education articles Asthma and Bronchoscopy.

Contributor Information and Disclosures
Author
Patrick L Carolan, MD Adjunct Associate Professor, Departments of Pediatrics, Family Practice, and
Community Health, University of Minnesota Medical School; Medical Director of Minnesota Sudden Infant Death
Center; Attending Staff, Department of Emergency Services, Children's Hospitals and Clinics of Minnesota
Patrick L Carolan, MD is a member of the following medical societies: American Academy of Pediatrics and
International Society of SIDS Researchers
Disclosure: Nothing to disclose.
Chief Editor
Michael R Bye, MD Professor of Clinical Pediatrics, State University of New York at Buffalo School of
Medicine; Attending Physician, Pediatric Pulmonary Division, Women's and Children's Hospital of Buffalo
Michael R Bye, MD is a member of the following medical societies: American Academy of Pediatrics, American
College of Chest Physicians, and American Thoracic Society
Disclosure: Nothing to disclose.
Additional Contributors
Charles Callahan, DO Professor, Deputy Chief of Clinical Services, Walter Reed Army Medical Center
Charles Callahan, DO is a member of the following medical societies: American Academy of Pediatrics,
American College of Chest Physicians, American College of Osteopathic Pediatricians, American Thoracic
Society, Association of Military Surgeons of the US, and Christian Medical & Dental Society
Disclosure: Nothing to disclose.
Christine D Dittmer, MD Resident Physician, Department of Pediatrics, Tripler Army Medical Center
Disclosure: Nothing to disclose.
Thomas Scanlin, MD Chief, Division of Pulmonary Medicine and Cystic Fibrosis Center, Department of
Pediatrics, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School
Thomas Scanlin, MD is a member of the following medical societies: American Association for the
Advancement of Science, American Society for Biochemistry and Molecular Biology, American Thoracic
Society, Society for Pediatric Research, and Society for Pediatric Research
Disclosure: Nothing to disclose.
Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of
Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Nothing to disclose.
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