Etiologic studies of acute bronchitis are difficult to interpret because the disease lacks a precise definition and the cause is undetermined in 31% to 84% of cases vigorously tested.16-23 Respiratory viruses are the most common causative agents, with confirmed cases in 9% to 63% of patients studied, depending on the criteria used to make the diagnosis and the population.16-23 Influenza A and B viruses are the most common cause, accounting for 6% to 35% of cases.16-23 Parainfluenza virus, respiratory syncytial virus, coronavirus, adenovirus, rhinovirus, and human metapneumovirus combined account for another third of cases.16-23 Bacterial causes of acute bronchitis range from less than 10%16 to as much as 44% of cases in studies of older populations with comorbidities and severe symptoms.21 Streptococcus pneumoniae (0% to 30% of cases), Haemophilus influenzae (0% to 9% of cases), and Moraxella catarrhalis (0% to 2% of cases) have been isolated in patients with acute bronchitis.16-23 Atypical bacterial species such as Bordetella pertussis (0% to 1%),24 Chlamydia pneumoniae (0% to 17%), and Mycoplasma pneumoniae (1% to 10%) also cause acute bronchitis.16-23
There are two overlapping sequential phases in the pathophysiology of acute bronchitis.25 The first phase results from the direct inoculation of the tracheobronchial epithelium, yielding variable constitutional symptoms of fever, myalgias, malaise, and organism-specific upper respiratory symptoms, lasting 1 to 5 days, the severity of which depends on the infectious agent. The second phase is characterized by hypersensitivity of the tracheobronchial epithelium and airway receptors resulting in persistent, productive cough and lasting 1 to 3 weeks, peaking at 7 to 14 days. It is this second phase that best characterizes the illness. Sloughed epithelial cells and increased mucus produce sputum in most patients; sputum is not an indication of ongoing bacterial infection as frequently suspected by clinicians.25 Inflammation and thickening of the bronchial and tracheal mucosa (Figure 1) result in airflow obstruction and decreased forced expiratory volume in 1 second, manifesting as wheezing and dyspnea in many patients.
The respiratory epithelial infection of acute bronchitis leads to inflammation, thickening, and increased mucus production in the airways.
The clinical manifestations of acute bronchitis depend on the infectious agent, especially in the first phase of the illness. Therefore, the initial symptoms are variable and may include fever, dyspnea, myalgias, malaise, sore throat, nasal congestion, and cough. The hallmark of acute bronchitis is cough (with or without phlegm production) persisting into the second phase of the illness lasing more than 5 days and up to 3 or 4 weeks.1,25 The mean duration of cough is 18 days.26 During this phase, the patient may or may not have dyspnea and/or chest discomfort. Physical exam may be completely normal, or the patient may have tachypnea, tachycardia, fever, wheezing, rhonchi, or rales. One important etiology of acute bronchitis to identify is Bordetella pertussis, because antibiotic treatment is recommended (see later discussion).25,27 Suspect pertussis in patients with posttussive emesis or inspiratory whoop27; consider pertussis in any patient with cough lasting greater than 2 weeks if exposed to a known case or presenting during an epidemic.1,25
The diagnosis of acute bronchitis is made using clinical findings and historical information: when acute cough (dry or productive) is present for more than 5 days and when evidence of pneumonia, acute asthma, or an alternative explanation for the symptoms is are absent. Patients with chronic obstructive pulmonary disease are excluded from the diagnosis (see chapter titled Chronic Obstructive Pulmonary Disease).
The primary objective in patient evaluation is carefully excluding pneumonia, either clinically or radiographically. Physicians are poor at differentiating patients with pneumonia from patients with bronchitis based on history and physical exam.28-31 The addition of C-reactive protein testing does not improve diagnostic accuracy.29,32 Identification of patients at low risk for pneumonia may be accomplished based on the absence of vital sign abnormalities and physical exam findings.30,31,33 See Table 1 for criteria suggesting pneumonia; patients meeting none of these criteria have a probability of pneumonia of 5% or less, and further testing is not required provided the patient has follow-up in the next 3 days and is able to return to the ED if symptoms worsen.30,31,33 Patients with hypoxia or unstable vital signs (in the setting of respiratory symptoms) are at high risk for pneumonia and require further testing and treatment (see chapter titled Community-Acquired Pneumonia, Aspiration Pneumonia, and Noninfectious Pulmonary Infiltrates). Obtain a chest radiograph in patients at intermediate risk for pneumonia. Although chest radiography remains the most common confirmatory test for pneumonia,34,35 the sensitivity of a standard two-view chest film ranges from 69% in symptomatic patients suspected of pneumonia in the community,36 to as low as 43.5% in patients being evaluated for pulmonary embolism in the ED37 (both studies using high-resolution CT scan as the criterion reference). Therefore, if pneumonia is suspected on clinical grounds, treat accordingly regardless of a negative chest radiograph (see chapter titled Community-Acquired Pneumonia, Aspiration Pneumonia, and Noninfectious Pulmonary Infiltrates) especially in the elderly, among whom distinctive signs and symptoms of pneumonia may be lacking.1 Laboratory tests should be obtained if treatment for B. pertussis is being planned; tests include a culture, using a Dacron swab specimen, collected from the posterior nasopharynx; performing direct fluorescent antibody staining; collecting a polymerase chain reaction test; or testing for serum antibodies by enzyme-linked immunosorbent assays or Western blot.27 Otherwise, further testing for acute bronchitis is not necessary unless alternative diagnoses require investigation. The differential diagnosis of cough is broad; see Table 5, Differential of Consequence: Cough, in chapter titled Respiratory Distress.
Table 1 Clinical Criteria Suggesting Possible Pneumonia |Favorite Table|Download (.pdf)
Table 1 Clinical Criteria Suggesting Possible Pneumonia
Heart rate >100 beats/min
Respiratory rate >24 breaths/min
Temperature of >38°C (100.4°F)
Chest examination findings of focal consolidation, egophony (increased resonance of voice sounds heard when auscultating the lungs), or fremitus (tactile vibrations felt over the chest when the patient repeats "boy oh boy")
Age > 64 y old
Case definitions of acute bronchitis that specify constitutional or respiratory symptoms including characteristics of sputum are used by research investigators and can define the spectrum of microbiologic causes but have not identified a patient subset that clearly benefits from antibiotics.
Despite the fact that some patients with acute bronchitis have evidence of a bacterial infection in epidemiologic studies, antibiotics are not beneficial and are not indicated except in isolated cases.1,5,38,39 A Cochrane analysis reviewed 15 randomized controlled trials, involving 2618 patients, including smokers and nonsmokers, comparing any antibiotic versus placebo or no treatment for acute bronchitis. At follow-up, patients receiving antibiotics were less likely to have cough (relative risk 0.64; 95% confidence interval 0.49 to 0.85), were less likely to have abnormal lung exam findings (relative risk 0.54; 95% confidence interval 0.41 to 0.70), experienced fewer days of feeling ill (mean difference –0.64; 95% confidence interval –1.16 to –0.13), and had fewer days with limited activity (mean difference –0.49; 95% CI –0.94 to –0.04).39 Although the differences between these outcome measures reached statistical significance, the benefits demonstrated were modest (less than 1-day benefit in an illness lasting 10 to 21 days). Consider potential medication side effects, cost, and the potential for microbial resistance when using antibiotics to achieve these modest benefits for an otherwise self-limiting illness. Despite the lack of evidence supporting their use, the majority of acute bronchitis patients receive antibiotics, especially elderly patients and smokers.1,5,38,40-42
To counter public perception and patients' prior experiences with antibiotics, offer patient education.43 Both printed and computer-assisted patient educational intervention reduce antibiotic prescriptions in the primary care setting.44 Give azithromycin (500 milligrams on day 1, 250 milligrams on days 2 to 5) or similar macrolide for patients with presumed or confirmed B. pertussis infection to prevent transmission to contacts.1,5,27 For influenza, if the patient presents very early in the course and influenza is suspected as the cause, consider influenza-specific antiviral therapy (see later section, Influenza).
There is little evidence to support the routine use of β2-agonists for acute bronchitis in the absence of wheezing on physical exam.1,5,39 A Cochrane Review reported no significant differences in daily cough scores or in duration of cough among adults with acute bronchitis who received β2-agonists versus placebo or no treatment. Adults treated with β2-agonists were more likely to report adverse effects such as tremor, shakiness, and nervousness (relative risk 7.94; 95% confidence interval 1.17 to 53.94).45 However, among patients with evidence of airflow obstruction, β2-agonists result in lower symptom scores and faster cough resolution.45 Therefore, consider bronchodilators in acute bronchitis patients with wheezing.46 Antihistamines do not reduce mean cough scores in acute bronchitis. Limited data are available on the efficacy of antitussives for acute bronchitis, and no data exist on the value of oral corticosteroids in nonasthmatics with acute bronchitis.47 Dextromethorphan and codeine preparations may be no more effective than placebo in improving symptoms or reducing cough severity in acute bronchitis.38 If used, limit antitussive therapy to those patients with a cough causing discomfort where inhibition of airway secretion clearance will not compromise breathing.46