Clinical Evidence Concise
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Am Fam Physician. 2004 Aug 1;70(3):557-558.
This clinical content conforms to AAFP criteria for evidence-based continuing medical education (EB CME). EB CME is clinical content presented with practice recommendations supported by evidence that has been systematically reviewed by an AAFP-approved source. The practice recommendations in this activity are available at http://www.clinicalevidence.com/ceweb/conditions/rda/1508/1508.jsp.
What are the effects of treatment in people without chronic respiratory disease?
TRADE OFF BETWEEN BENEFITS AND HARMS
One systematic review and one subsequent randomized controlled trial (RCT) have found that antibiotics modestly reduced cough at one to two weeks compared with placebo. However, they found no significant difference in quality of life or impairment in normal activity compared with placebo. We found no systematic review or RCTs comparing amoxicillin versus placebo. RCTs found no significant difference in clinical improvement or cure between amoxicillin (amoxycillin) and roxithromycin or cefuroxime. One RCT found that erythromycin reduced the mean number of days of impaired activities compared with placebo. However, RCTs comparing erythromycin versus placebo found no significant difference in other outcomes. RCTs found no significant difference between azithromycin and clarithromycin, among different cephalosporins, or between cefuroxime and amoxicillin plus clavulanic acid. RCTs found that doxycycline significantly reduced the number of people with cough at follow-up or the mean number of days of cough compared with placebo. Antibiotics increased risk of adverse events such as nausea, vomiting, rash, headache, and vaginitis compared with placebo. Two RCTs found that adverse effects were less common with cefuroxime than with amoxicillin plus clavulanic acid. Widespread antibiotic use may lead to bacterial resistance to antibiotics.
We found insufficient evidence about the effects of antihistamines compared with placebo in people with acute bronchitis.
RCTs found no significant difference in cough severity between codeine or dextromethorphan and placebo in children or adults with acute bronchitis. We found limited evidence from one RCT that moguisteine modestly reduced cough severity compared with placebo in adults, but it was associated with more adverse gastrointestinal effects.
One systematic review found no significant difference in cough or ability to return to work between inhaled or oral beta2 agonists and placebo in people with acute bronchitis. It found limited evidence from one small RCT that beta2 agonists reduce cough compared with erythromycin. The review found that beta2 agonists are more frequently associated with shaking and tremor in adults compared with placebo.
We found insufficient evidence about the effects of expectorants in people with acute bronchitis.
Acute bronchitis is transient inflammation of the trachea and major bronchi. Clinically, it is diagnosed on the basis of cough and occasionally sputum, dyspnea, and wheeze. This review is limited to episodes of acute bronchitis in people (smokers and nonsmokers) with no preexisting respiratory disease such as a pre-existing diagnosis of asthma or chronic bronchitis, or evidence of fixed airflow obstruction, and excluding those with clinical or radio-graphic evidence of pneumonia. However, using a clinical definition for acute bronchitis implies that people with transient or mild asthma or mild chronic obstructive pulmonary disease may have been recruited to some of the reported studies.
Acute bronchitis affects 44 out of 1,000 adults (older than 16 years) annually, with 82 percent of episodes occurring in fall or winter.1 Acute bronchitis was the fifth most common reason to present to a general practitioner in Australia.2
Infection is believed to be the trigger for acute bronchitis. However, pathogens have been identified in fewer than 55 percent of people.1 Community studies that attempted to isolate pathogens from the sputum of people with acute bronchitis found viruses in 8 to 23 percent, typical bacteria (i.e., Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis) in 45 percent, and atypical bacteria (i.e., Mycobacterium pneumoniae, Chlamydia pneumoniae, Bordetella pertussis) in zero to 25 percent.1,3,4 It is unclear whether smoking affects the risk for developing acute bronchitis.
Acute bronchitis is regarded as a mild self-limiting illness, but there are few data on prognosis and rates of complications such as chronic cough or progression to chronic bronchitis or pneumonia. One prospective longitudinal study reviewed 653 previously well adults who presented to suburban general practices during a 12-month period with symptoms of acute lower respiratory tract infection.1 The results found that within the first month of the illness, 20 percent of people represent to their general practitioner with persistent or recurrent symptoms. One prospective study of 138 previously well adults found that 34 percent had symptoms consistent with chronic bronchitis or asthma three years after initial presentation with acute bronchitis.5 It also is unclear whether acute bronchitis plays a causal role in the progression to chronic bronchitis or is simply a marker of predisposition to chronic lung disease. Although smoking has been identified as the most important risk factor for chronic bronchitis,6,7 it is unclear whether the inflammatory effects of cigarette smoke and infection causing acute bronchitis have additive effects in leading to chronic inflammatory airway changes.
EDITOR’S NOTE: Roxithromycin and moguisteine are not available in the United States.
SEARCH DATE: September 2003
Adapted with permission from Wark PA. Bronchitis (acute). Clin Evid Concise 2004;11:362-3.
1. Macfarlane J, Holmes W, Gard P, et al. Prospective study of the incidence, aetiology and outcome of adult lower respiratory tract illness in the community. Thorax. 2001;56:109-14.
2. Meza RA, Bridges-Webb C, Sayer GP, et al. The management of acute bronchitis in general practice: results from the Australian morbidity and treatment survey. Aust Fam Physician. 1994;23:1550-3.
3. Boldy DA, Skidmore SJ, Ayres JG. Acute bronchitis in the community: clinical features, infective factors, changes in pulmonary function and bronchial reactivity to histamine. Respir Med. 1990;84:377-85.
4. Grayston JT, Aldous MB, Easton A, et al. Evidence that Chlamydia pneumoniae causes pneumonia and bronchitis. J Infect Dis. 1993;168:1231-5.
5. Jonsson JS, Gislason T, Gislason D, et al. Acute bronchitis and clinical outcome three years later: prospective cohort study. BMJ. 1998;317:1433-
6. Whittemore AS, Perlin SA, DiCiccio Y. Chronic obstructive pulmonary disease in lifelong nonsmokers: results from NHANES. Am J Public health. 1995;85:702-6.
7. Brunekreef B, Fischer P, Remijn B, et al. Indoor air pollution and its effects on pulmonary function of adult non-smoking women: III. Passive smoking and pulmonary function. Int J Epidemiol. 1985;14:227-30.
This is one in a series of chapters excerpted from Clinical Evidence Concise, published by the BMJ Publishing Group, Tavistock Square, London, United Kingdom. Clinical Evidence Concise is published in print twice a year and is updated monthly online. Each topic is revised every eight months, and subscribers should view the most up-to-date version at http://www.clinicalevidence.com. If you are interested in contributing to Clinical Evidence, please contact Claire Folkes (firstname.lastname@example.org). This series is part of the AFP ’s CME. See “Clinical Quiz” on page 437.
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