Bronchitis 

  • Author: Jazeela Fayyaz, DO; Chief Editor: Zab Mosenifar, MD   more...
 
Updated: Mar 29, 2011
 

Background

Bronchitis is one of the top conditions for which patients seek medical care. It is characterized by inflammation of the bronchial tubes (or bronchi), the air passages that extend from the trachea into the small airways and alveoli. (See Clinical Presentation.)

Chronic bronchitis is defined clinically as cough with sputum expectoration for at least 3 months a year during a period of 2 consecutive years. Chronic bronchitis is associated with hypertrophy of the mucus-producing glands found in the mucosa of large cartilaginous airways. As the disease advances, progressive airflow limitation occurs, usually in association with pathologic changes of emphysema. This condition is called chronic obstructive pulmonary disease. (See Clinical Presentation.)

When a stable patient experiences sudden clinical deterioration with increased sputum volume, sputum purulence, and/or worsening of shortness of breath, this is referred to as an acute exacerbation of chronic bronchitis, as long as conditions other than acute tracheobronchitis are ruled out. (See Diagnosis.)

Triggers of bronchitis may be infectious agents, such as viruses or bacteria, or noninfectious agents, such as smoking or inhalation of chemical pollutants or dust. Bronchitis typically occurs in the setting of an upper respiratory illness; thus, it is observed more frequently in the winter months. (See Etiology.)

Allergens and irritants can produce a similar clinical picture. Asthma can be mistakenly diagnosed as acute bronchitis if the patient has no prior history of asthma. In one study, one third of patients who had been determined to have recurrent bouts of acute bronchitis were eventually identified as having asthma. Generally, bronchitis is a diagnosis made by exclusion of other conditions such as sinusitis, pharyngitis, tonsillitis, and pneumonia. (See Diagnosis.)

Acute bronchitis is manifested by cough and, occasionally, sputum production that last for no more than 3 weeks. Although bronchitis should not be treated with antimicrobials, it is frequently difficult to refrain from prescribing them. Accurate testing and decision-making protocols regarding who might benefit from antimicrobial therapy would be useful but are not currently available. (See Treatment and Management, as well as Medication.)

To see complete information on Pediatric Bronchitis, please go to the main article by clicking here.

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Pathophysiology

During an episode of acute bronchitis, the cells of the bronchial-lining tissue are irritated and the mucous membrane becomes hyperemic and edematous, diminishing bronchial mucociliary function. Consequently, the air passages become clogged by debris and irritation increases. In response, copious secretion of mucus develops, which causes the characteristic cough of bronchitis.

In the case of mycoplasmal pneumonia, bronchial irritation results from the attachment of the organism (Mycoplasma pneumoniae) to the respiratory mucosa, with eventual sloughing of affected cells. Acute bronchitis usually lasts approximately 10 days. If the inflammation extends downward to the ends of the bronchial tree, into the small bronchi (bronchioles), and then into the air sacs, bronchopneumonia results.

Chronic bronchitis is associated with excessive tracheobronchial mucus production sufficient to cause cough with expectoration for 3 or more months a year for at least 2 consecutive years. The alveolar epithelium is both the target and the initiator of inflammation in chronic bronchitis.

A predominance of neutrophils and the peribronchial distribution of fibrotic changes result from the action of interleukin 8, colony-stimulating factors, and other chemotactic and proinflammatory cytokines. Airway epithelial cells release these inflammatory mediators in response to toxic, infectious, and inflammatory stimuli, in addition to decreased release of regulatory products such as angiotensin-converting enzyme or neutral endopeptidase.

Chronic bronchitis can be categorized as simple chronic bronchitis, chronic mucopurulent bronchitis, or chronic bronchitis with obstruction. Mucoid sputum production characterizes simple chronic bronchitis. Persistent or recurrent purulent sputum production in the absence of localized suppurative disease, such as bronchiectasis, characterizes chronic mucopurulent bronchitis.

Chronic bronchitis with obstruction must be distinguished from chronic infective asthma. The differentiation is based mainly on the history of the clinical illness: patients who have chronic bronchitis with obstruction present with a long history of productive cough and a late onset of wheezing, whereas patients who have asthma with chronic obstruction have a long history of wheezing with a late onset of productive cough.

Chronic bronchitis may result from a series of attacks of acute bronchitis, or it may evolve gradually because of heavy smoking or inhalation of air contaminated with other pollutants in the environment. When so-called smoker's cough is continual rather than occasional, the mucus-producing layer of the bronchial lining has probably thickened, narrowing the airways to the point where breathing becomes increasingly difficult. With immobilization of the cilia that sweep the air clean of foreign irritants, the bronchial passages become more vulnerable to further infection and the spread of tissue damage.

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Etiology

Respiratory viruses are the most common causes of acute bronchitis, and cigarette smoking is indisputably the predominant cause of chronic bronchitis.

Viral and becterial infections in acute bronchitis

The most common viruses include influenza A and B, parainfluenza, respiratory syncytial virus, and coronavirus, although an etiologic agent is identified only in a minority of cases.[1]

Acute bronchitis is usually caused by infections, such as those caused by Mycoplasma species, Chlamydia pneumoniae, Streptococcus pneumoniae, Moraxella catarrhalis, and Haemophilus influenzae, and by viruses, such as influenza, parainfluenza, adenovirus, rhinovirus, and respiratory syncytial virus. Exposure to irritants, such as pollution, chemicals, and tobacco smoke, may also cause acute bronchial irritation.

Bordetella pertussis should be considered in children who are incompletely vaccinated, though studies increasingly report this bacterium as the causative agent in adults as well.[2]

Smoking and other causes of chronic bronchitis

Cigarette smoking is indisputably the predominant cause of chronic bronchitis. Common risk factors for acute exacerbations of chronic bronchitis are advanced age and low forced expiratory volume in one second (FEV1).[3] Most (70-80%) acute exacerbations of chronic bronchitis are estimated to be due to respiratory infections.[4]

Estimates suggest that cigarette smoking accounts for 85-90% of chronic bronchitis and chronic obstructive pulmonary disease. Studies indicate that smoking pipes, cigars, and marijuana causes similar damage. Smoking impairs ciliary movement, inhibits the function of alveolar macrophages, and leads to hypertrophy and hyperplasia of mucus-secreting glands.

Smoking can also increase airway resistance via vagally mediated smooth muscle constriction. Unless some other factor can be isolated as the irritant that produces the symptoms, the first step in dealing with chronic bronchitis is for the patient to stop smoking.

Air pollution levels have been associated with increased respiratory health problems among people living in affected areas. The Air Pollution and Respiratory Health Branch of the National Center for Environmental Health directs the fight of the US Centers for Disease Control and Prevention against respiratory illness associated with air pollution.

According to the Healthy People 2000 report, each year in the United States, health costs of human exposure to outdoor air pollutants range from $40 to $50 billion, and an estimated 50,000 to 120,000 premature deaths are associated with exposure to air pollutants. In addition, the report states that those with asthma experience more than 100 million days of restricted activity, costs related to asthma exceed $4 billion, and about 4,000 people die of the condition each year.

A growing body of literature has demonstrated that specific occupational exposures are associated with the symptoms of chronic bronchitis. The list of agents includes coal, manufactured vitreous fibers, oil mist, cement, silica, silicates, osmium, vanadium, welding fumes, organic dusts, engine exhausts, fire smoke, and secondhand cigarette smoke.

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Epidemiology

According to estimates from national interviews taken by the National Center for Health Statistics in 2006, approximately 9.5 million people, or 4% of the population, were diagnosed with chronic bronchitis. These statistics may underestimate the prevalence of chronic obstructive pulmonary disease by as much as 50%, because many patients underreport their symptoms, and their conditions remain undiagnosed.

An overdiagnosis of chronic bronchitis by patients and clinicians has also been suggested, however. The term bronchitis is often used as a common descriptor for a nonspecific and self-limited cough, thereby falsely increasing its incidence even though the patient does not meet the criteria for diagnosis.

In one study, acute bronchitis affected 44 of 1000 adults annually, and 82% of episodes occurred in fall or winter.[5] By way of comparison, 91 million cases of influenza, 66 million cases of the common cold, and 31 million cases of other acute upper respiratory tract infections occurred that year.

Acute bronchitis is common throughout the world and is one of the top 5 reasons for seeking medical care in countries that collect such data. No difference in racial distribution is reported, though bronchitis occurs more frequently in populations with a low socioeconomic status and in people who live in urban and highly industrialized areas.

In terms of gender-specific incidence, bronchitis affects males more than females. In the United States, up to two thirds of men and one fourth of women have emphysema at death. Although found in all age groups, acute bronchitis is most frequently diagnosed in children younger than 5 years, whereas chronic bronchitis is more prevalent in people older than 50 years.

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Prognosis

Patients with acute bronchitis have a good prognosis. Bronchitis is almost always self-limited in individuals who are otherwise healthy, although it may result in absenteeism from work and school. Severe cases occasionally produce deterioration in patients with significant underlying cardiopulmonary disease or other comorbidities.

Complications

Complications occur in approximately 10% of patients with acute bronchitis and include the following:

  • Bacterial superinfection
  • Pneumonia develops in about 5% of patients with bronchitis (incidence of subsequent pneumonia, unaffected by antibiotic treatment)
  • Chronic bronchitis may develop with repeated episodes of acute bronchitis
  • Reactive airway disease can occur as a result of acute bronchitis
  • Hemoptysis
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Patient Education

Patient education is essential in the prevention and treatment of acute bronchitis. Unfortunately, health care providers usually underemphasize education. Patients should be counseled to take the following measures:

  • Avoid smoking and secondhand smoke
  • Live in a clean environment
  • Receive the influenza vaccine yearly between October and December
  • Receive the pneumonia vaccine every 5-10 years if aged 65 years or older or with chronic disease

For excellent patient education resources, visit eMedicine's Asthma Center.

Additionally, see eMedicine's patient education article Asthma.

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Contributor Information and Disclosures
Author

Jazeela Fayyaz, DO  Senior Fellow, Department of Pulmonology, Lenox Hill Hospital

Jazeela Fayyaz, DO is a member of the following medical societies: American College of Physicians and American Thoracic Society

Disclosure: Nothing to disclose.

Coauthor(s)

Klaus-Dieter Lessnau, MD, FCCP  Clinical Associate Professor of Medicine, New York University School of Medicine; Medical Director, Pulmonary Physiology Laboratory; Director of Research in Pulmonary Medicine, Department of Medicine, Section of Pulmonary Medicine, Lenox Hill Hospital

Klaus-Dieter Lessnau, MD, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Medical Association, American Thoracic Society, and Society of Critical Care Medicine

Disclosure: Sepracor None None

Jeffrey Nascimento, DO, MS  Fellow, Department of Pulmonary Medicine, Lenox Hill Hospital

Jeffrey Nascimento, DO, MS is a member of the following medical societies: American College of Chest Physicians, American Medical Association, American Osteopathic Association, American Thoracic Society, New York County Medical Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Roger B Olade, MD, MPH  Medical Director, Providence Health Group

Roger B Olade, MD, MPH is a member of the following medical societies: American College of Occupational and Environmental Medicine and American College of Physicians

Disclosure: Nothing to disclose.

Samuel Ong, MD  Visiting Assistant Professor, Department of Emergency Medicine, Olive View-UCLA Medical Center

Disclosure: Nothing to disclose.

Specialty Editor Board

David FM Brown, MD  Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Paul Blackburn, DO, FACOEP, FACEP  Program Director, Department of Emergency Medicine, Maricopa Medical Center; Assistant Professor, Department of Surgery, University of Arizona College of Medicine

Paul Blackburn, DO, FACOEP, FACEP is a member of the following medical societies: American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, American Medical Association, and Arizona Medical Association

Disclosure: Nothing to disclose.

Robert E O'Connor, MD, MPH  Professor and Chair, Department of Emergency Medicine, University of Virginia Health System

Robert E O'Connor, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physician Executives, American Heart Association, American Medical Association, Medical Society of Delaware, National Association of EMS Physicians, Society for Academic Emergency Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD  Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild Pulmonary Disease Institute, Professor and Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine

Zab Mosenifar, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, and American Thoracic Society

Disclosure: Nothing to disclose.

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