eMedicine Specialties > Pediatrics: General Medicine > Pulmonology

Bronchitis, Acute and Chronic

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
Coauthor(s): Charles Callahan, DO, Professor, Deputy Chief of Clinical Services, Walter Reed Army Medical Center
Contributor Information and Disclosures

Updated: Mar 19, 2009

Introduction

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. Symptoms of acute bronchitis usually include cough that produces phlegm and may be associated with retrosternal pain during deep breathing or coughing. Generally, the clinical course of acute bronchitis is self-limited, with complete healing and full return to function typically seen within 10-14 days following symptom onset.

Chronic bronchitis is recurring inflammation and degeneration of the bronchial tubes that may be associated with active infection. Chronic bronchitis is often part of an underlying disease process, such as asthma, cystic fibrosis, dyskinetic cilia syndrome, foreign body aspiration, or exposure to an airway irritant. Recurrent tracheobronchitis may also be seen in patients with tracheostomy or with certain forms of immunodeficiency. In all of these patient groups, chronic bronchitis should not be the primary diagnosis because it does not describe the pathology of the underlying disorder. 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.

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

Pathophysiology

Acute bronchitis leads to the hacking cough and phlegm production that often follows upper respiratory tract symptoms. This occurs because of the inflammatory response of the mucous membranes within the lungs' bronchial passages. If the patient is in otherwise good health, the mucous membrane returns to normal, heralding recovery from the initial active infection.  Symptoms typically resolve within 10-14 days.  

In adults, chronic bronchitis results from hypersecretion of mucus in the bronchi due to hypertrophy of submucosal mucus-producing glands and increased numbers of goblet cells within the epithelium. In most patients, this results from exposure to cigarette smoke. Mucociliary clearance is delayed because of excess mucus production and loss of ciliated cells, leading to a productive cough.

In children, chronic bronchitis follows either an endogenous response (eg, excessive 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 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.² Mucociliary dysfunction is a common feature of chronic airway disease states in humans. 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.³ ASL depletion resulted in reduced mucus clearance and histologic signs of chronic airway disease, including mucus 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.⁴ 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.⁵

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 by 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 (aged <5 y), whereas Mycoplasma pneumoniae may be significant in school-aged children (aged >5-18 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.

Frequency

United States

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.⁶ Although the report did not separate diagnoses into acute or 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.

International

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; this is consistent with observations among children from the United States, United Kingdom, and Sweden.⁷ The incidence rate of bronchitis in children in this German cohort was 28%.

Mortality/Morbidity

Acute bronchitis is almost always a self-limited process in the otherwise healthy child. However, it frequently results in absenteeism from school and 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, congestive heart failure, bronchiectasis, or tuberculosis, is also key.

Race

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.

Sex

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 rate of chronic bronchitis has been reported to be consistently higher in females than in males.

Age

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.

Clinical

History

• Acute bronchitis begins as a respiratory tract infection that manifests as the common cold. Symptoms often include coryza, malaise, chills, slight fever, sore throat, and back and muscle pain. The cough in these children is usually accompanied by an initial watery nasal discharge. After several days, the nasal discharge becomes thicker and colored or opaque. It then becomes clear again and has a mucoid watery consistency before it spontaneously resolves within 7-10 days. Purulent nasal discharge is common with viral respiratory pathogens and, by itself, does not imply a bacterial etiology to the infection.
  • Initially, the cough is dry and may be harsh or raspy sounding. The cough then loosens and becomes productive. Children younger than 5 years rarely expectorate. In this age group, sputum is usually seen in vomitus (ie, posttussive emesis). Parents frequently note a rattling sound in the chest.
  • Hemoptysis, a burning discomfort in the chest, and dyspnea may be present.
• Brunton et al notes that adult patients with chronic bronchitis have a history of persistent cough that produces yellow, white, or greenish sputum on most days for at least 3 months of the year and for more than 2 consecutive years.⁸ Wheezing and reports of breathlessness are also common. Pulmonary function testing in these adult patients reveals irreversible reduction in maximal airflow velocity.
• Recurrent episodes of acute or chronic bronchitis are unusual in children and should alert the clinician to the likelihood of asthma. Bronchitis is often repeatedly diagnosed in children in whom asthma has remained undiagnosed for many years. Similarly, a family history of asthma in parents or siblings may be masked within a history of “recurrent bronchitis.” The diagnosis of "asthmatic bronchitis" or "wheezy bronchitis" is simply asthma. For more detail on taking the history of pediatric patients with recurrent cough, wheezing, and shortness of breath, see Asthma.
• Recurrent episodes of acute or chronic bronchitis may be associated with immunodeficiency.
  • Stiehm identifies the 4 most common immunodeficiencies in pediatric patients: transient hypogammaglobulinemia of infancy (THI), immunoglobulin G (IgG) subclass deficiency, impaired polysaccharide responsiveness (partial antibody deficiency), and selective IgA deficiency (IgAD).⁹  A summary of immunodeficiency registries in 4 countries listed IgAD in 27.5% of the patients, IgG subclass deficiency in 4.8%, and THI in 2.3%. Patients typically have normal cellular immune systems, phagocyte function, and complement levels. All 4 immunodeficiency states are characterized by recurrent bacterial respiratory infections, such as purulent rhinitis, sinusitis, otitis, and bronchitis. Only a few cases require the use of intravenous IgG (IVIG) and the long-term prognosis is generally excellent.
  • Ozkan studied immunoglobulin A (IgA) and IgG deficiency in children who presented with recurrent sinopulmonary infection.¹⁰ The overall frequency of antibody defects was found to be 19.1%. IgA deficiency was observed in 9.3%, IgG subclass deficiency was observed in 8.4%, and both IgA and IgG subclass deficiencies were observed in 1.4%. The prevalence of IgA and/or IgG subclass deficiency was 25% in patients with recurrent upper respiratory tract infections, 22% in patients with recurrent pulmonary infections, and 12.3% in patients with recurrent bronchiolitis.
• Common variable immunodeficiency
  • Common variable immunodeficiency is the most frequent of the primary hypogammaglobulinemias. Kainulainen et al (2001) conducted a nationwide survey of all patients with common variable immunodeficiency who were receiving immunoglobulin replacement therapy in Finland.¹¹ Sinopulmonary infections were the most common clinical presentation; 66% had recurrent pneumonia, 60% had recurrent maxillary sinusitis, and 45% had recurrent bronchitis. The mean interval from the time of onset of symptoms to diagnosis was 8 years. Evidence of chronic lung damage was noted in 17% of patients at the time of diagnosis, highlighting the importance of early recognition in the prevention of chronic pulmonary sequelae.
  • To improve the recognition of common variable immunodeficiency, the authors suggest consideration of this condition in patients with recurrent sinopulmonary infection. In addition to a low serum IgG concentration, measurement of specific antibody production is recommended to establish the diagnosis.

Physical

• Lungs may sound normal. Crackles, rhonchi, or large airway wheezing, if any, tends to be scattered and bilateral.
• The pharynx may be injected.

Causes

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.

The most common causes of both acute and chronic bronchitis in the pediatric population are as follows:

• Viral infection
  • Adenovirus
  • Influenza
  • Parainfluenza
  • Respiratory syncytial virus
  • Rhinovirus
  • Human bocavirus^12,13,14
  • Coxsackievirus
  • Herpes simplex virus
• Secondary bacterial infection as part of an acute upper respiratory infection (extremely rare in nonsmokers without cystic fibrosis)
  • S pneumoniae
  • M catarrhalis
  • H influenzae (nontypeable)
  • Chlamydia pneumoniae (Taiwan acute respiratory [TWAR] agent)
  • Mycoplasma species
• Air pollutants, such as occur with smoking and from second-hand smoke (also causes incident bronchiolitis¹⁵ )
• 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.
  • Patients with congenital heart disease who have undergone a Fontan operation are a group at high risk for development of this problem for presently unknown reasons. In some cases, it appears many years after the Fontan procedure is performed.¹⁶
  • 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 two patients with plastic bronchitis refractory to medical management.¹⁷ These results suggest that high intrathoracic lymphatic pressures are related to the development of the recurrent bronchial casts seen in this disorder.

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