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

Updated: Mar 18, 2014

Ba ckground

Acut e bronchitis is a clinical syndrome produced by inflammation of the trachea, bronchi, and br onchioles. In

child ren, acute bronchitis usually occurs in association with viral respiratory tract infection. Acute bronchitis israrel y a primary bacterial infection in otherwise healthy children. (See Pathophysiology, as well a s Etiology.)

Exa mples of normal airway color and architecture and an airway in a patient with chronic bronchi tis are shownbelo w. (See Anatomy.)

Normal airw ay c olor and architecture (in a child w ith mild tracheomalacia).

Airw ay of a child w ith chronic bronchitis show s ery thema, loss of normal architecture, and sw elling.

Symptoms of acute bronchitis usually include productive cough and sometimes retrosternal pain during deepbreathing 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 withactive infection. Patients with chronic bronchitis have more mucus than normal because of either increasedproduction 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 bodyaspiration, 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 overlapwith 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 chronicbronchitis. 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 1month or recurrent productive cough that may be associated with wheezing or crackles on auscultation. Elementsof 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, andavoidance of smoke. (See Treatment and Management.)

Analgesics and antipyretics target the symptoms of pediatric bronchitis. In chronic cases, bronchodilator therapyshould be considered. Oral corticosteroids should be added if cough continues and the history and physicalexamination 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 tractinfection. This occurs because of the inflammatory response of the mucous membranes within the lungs' bronchialpassages. 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) toacute 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 oftenactually asthma.

Mucociliary clearance is an important primary innate defense mechanism that protects the lungs from the harmfuleffects of inhaled pollutants, allergens, and pathogens. [4] Mucociliary dysfunction is a common feature of chronicairway diseases.

The mucociliary apparatus consists of 3 functional compartments: the cilia, a protective mucus layer, and anairway surface liquid (ASL) layer, which work together to remove inhaled particles from the lung. Animal study datahave identified a critical role for ASL dehydration in the pathogenesis of mucociliary dysfunction and chronic airwaydisease. [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 animalsexperienced reduced bacterial clearance and high pulmonary mortality as a result.

The role of irritant exposure, particularly cigarette smoke and airborne particulates, in recurrent (wheezy) bronchitisand asthma is becoming clearer. Kreindler et al demonstrated that the ion transport phenotype of normal humanbronchial epithelial cells exposed to cigarette smoke extract is similar to that of cystic fibrosis epithelia, in whichsodium is absorbed out of proportion to chloride secretion in the setting of increased mucus production. [6] Thesefindings suggest that the negative effects of cigarette smoke on mucociliary clearance may be mediated throughalterations in ion transport.

McConnell et al noted that organic carbon and nitrogen dioxide airborne particulates were associated with thechronic 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, maycontribute to chronic bronchitis in childhood. Following damage to the airway lining, chronic infection withcommonly 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 Haemophilusinfluenzae and Moraxella catarrhalis may be significant pathogens in preschoolers (age < 5 y), whereasMycoplasma 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 andgamma-hemolytic streptococci. With acute exacerbations of tracheobronchitis in these patients, pathogenic flora

may include Pseudomonas aeruginosa and Staphylococcus aureus (including methicillin-resistant strains), amongother pathogens. Children predisposed to oropharyngeal aspiration, particularly those with compromised protectiveairway 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% arebacterial. Chronic bronchitis may be caused by repeated attacks of acute bronchitis, which can weaken andirritate bronchial airways over time, eventually resulting in chronic bronchitis. Industrial pollution is also a commoncause; however, the chief culprit is heavy long-term cigarette smoke exposure.

Viral infections include the following:

AdenovirusInfluenzaParainfluenzaRespiratory syncytial virusRhinovirusHuman bocavirus [8, 9, 10]

CoxsackievirusHerpes 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 pneumoniaeM catarrhalisH 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 incidentbronchiolitis. [11] Tsai et al demonstrated that in utero and postnatal household cigarette smoke exposure isstrongly linked to asthma and recurrent bronchitis in children. [12]

Other causes include the following:

AllergiesChronic aspiration or gastroesophageal refluxFungal infection

Plastic bronchitis

Plastic bronchitis is an unusual but potentially devastating form of obstructive bronchial disease. The disease ischaracterized by the development of arborizing, thick, tenacious casts of the tracheobronchial tree that produceairway 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 periodfollowing a Fontan procedure. These patients were successfully managed with short periods of high-frequency jetventilation and vigorous pulmonary toilet. [14]

Therapies include endoscopic debridement of the airway, vigorous pulmonary toilet, and aerosolized tissueplasminogen activator. Shah et al performed thoracic duct ligation, resulting in complete resolution of the formationof casts in 2 patients with plastic bronchitis refractory to medical management. [15] These results suggest that highintrathoracic lymphatic pressures are related to the development of the recurrent bronchial casts seen in thisdisorder.

Epidemiology

Data collected from the National Ambulatory Care Survey 1991 Summary showed that 2,774,000 office visits bychildren younger than 15 years resulted in a diagnosis of bronchitis. [16] Although the report did not separatediagnoses into acute and chronic bronchitis, the frequency of visits made bronchitis just slightly less commonthan otitis media and slightly more common than asthma. However, in children, asthma is often underdiagnosedand is frequently misdiagnosed as chronic or recurrent bronchitis. Since 1996, 9-14 million Americans have beendiagnosed with chronic bronchitis annually.

Bronchitis, both acute and chronic, is prevalent throughout the world and is one of the top 5 reasons for childhoodphysician visits in countries that track such data. The incidence of bronchitis in British schoolchildren is reportedto be 20.7%.

Weigl et al noted an overall increase in hospitalization for lower respiratory tract infection(laryngotracheobronchitis, bronchitis, wheezing bronchitis, bronchiolitis, bronchopneumonia, pneumonia) amongGerman 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 amonginner-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 infemales than in males.

Acute (typically wheezy) bronchitis occurs most commonly in children younger than 2 years, with another peakseen in children aged 9-15 years. Chronic bronchitis affects people of all ages but is more prevalent in personsolder than 45 years.

Prognosis

Acute bronchitis is almost always a self-limited process in the otherwise healthy child. However, it frequentlyresults 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 diseaseprocess, such as asthma, cystic fibrosis, immunodeficiency, heart failure, bronchiectasis, or tuberculosis, is alsokey. These patients need careful periodic monitoring to minimize further lung damage and progression to chronicirreversible lung disease.

Patient Education

Instruct older patients regarding the need for immunization against pertussis, diphtheria, and influenza, whichreduces the risk of bronchitis due to the causative organisms. Instruct these patients to avoid passiveenvironmental tobacco smoke; to avoid air pollutants, such as wood smoke, solvents, and cleaners; and to obtainmedical attention for prolonged respiratory infections.

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Instruct parents that children may attend school or daycare without restrictions except during episodes of acutebronchitis with fever. Also instruct parents that children may return to school or daycare when signs of infectionhave 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'spatient education articles Asthma and Bronchoscopy .

Contributor Information and Disclosures Author Patrick L Carolan, MD Adjunct Associate Professor, Departments of Pediatrics, Family Practice, andCommunity Health, University of Minnesota Medical School; Medical Director of Minnesota Sudden Infant DeathCenter; 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 andInternational 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 , AmericanCollege of Chest Physicians , and American Thoracic Society

Disclosure: Nothing to disclose.

Additional ContributorsCharles 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 ThoracicSociety , 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 ThoracicSociety , 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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