Bronchitis

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Practice Essentials

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

Signs and symptoms

A complete history must be obtained, including information on exposure to toxic substances and smoking. Symptoms of bronchitis include the following:

Physical examination findings in acute bronchitis are variable and may include the following:

See Presentation for more detail.

Diagnosis

Bronchitis may be suspected in patients with an acute respiratory infection with cough; yet, because many more serious diseases of the lower respiratory tract cause cough, bronchitis must be considered a diagnosis of exclusion.

Studies that may be helpful include the following:

See Workup for more detail.

Management

Therapy is generally focused on alleviation of symptoms. Care for acute bronchitis is primarily supportive. Care for chronic bronchitis includes avoidance of environmental irritants.

Agents employed for symptomatic treatment include the following:

Among otherwise healthy individuals, antibiotics have not demonstrated any consistent benefit in acute bronchitis. The following recommendations have been made with respect to treatment of acute bronchitis with antibiotics:

In stable patients with chronic bronchitis, long-term prophylactic therapy with antibiotics is not indicated.

Influenza vaccination may reduce the incidence of upper respiratory tract infections and, subsequently, reduce the incidence of acute bacterial bronchitis. It may be less effective in preventing illness than in preventing serious complications and death.

See Treatment and Medication for more detail.

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.

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.

Etiology

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

Viral and bacterial 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 1 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.[5] 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.

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.[6] 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.

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.

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:

For patient education resources, see the Asthma Center, as well as Asthma.

History

Obtain a complete history, including information on exposure to toxic substances and smoking. Patients with chronic bronchitis are often overweight and cyanotic. Initially, cough is present in the winter months. Over the years, the cough progresses from hibernal to perennial, and mucopurulent relapses increase in frequency, the duration and severity of which increase to the point of exertional dyspnea.

Cough is the most commonly observed symptom. It begins early in the course of many acute respiratory tract infections and becomes more prominent as the disease progresses. Acute bronchitis may be indistinguishable from an upper respiratory tract infection during the first few days, though cough lasting greater than 5 days may suggest acute bronchitis.[7]

In patients with acute bronchitis, cough generally lasts from 10-20 days. Sputum production is reported in approximately half the patients in whom cough occurred. Sputum may be clear, yellow, green, or even blood-tinged. Purulent sputum is reported in 50% of persons with acute bronchitis. Changes in sputum color are due to peroxidase released by leukocytes in sputum; therefore, color alone cannot be considered indicative of bacterial infection.

Fever is a relatively unusual sign and, when accompanied by cough, suggests either influenza or pneumonia. Nausea, vomiting, and diarrhea are rare. Severe cases may cause general malaise and chest pain. With severe tracheal involvement, symptoms include burning, substernal chest pain associated with respiration, and coughing.

Dyspnea and cyanosis are not observed in adults unless the patient has underlying chronic obstructive pulmonary disease or another condition that impairs lung function.

Other symptoms of acute bronchitis include the following:

Physical Examination

The physical examination findings in acute bronchitis can vary from normal-to-pharyngeal erythema, localized lymphadenopathy, and rhinorrhea to coarse rhonchi and wheezes that change in location and intensity after a deep and productive cough.

Diffuse wheezes, high-pitched continuous sounds, and the use of accessory muscles can be observed in severe cases. Occasionally, diffuse diminution of air intake or inspiratory stridor occurs; these findings indicate obstruction of a major bronchi or the trachea, which requires sequentially vigorous coughing, suctioning, and, possibly, intubation or even tracheostomy.

Sustained heave along the left sternal border indicates right ventricular hypertrophy secondary to chronic bronchitis. Clubbing on the digits and peripheral cyanosis indicate cystic fibrosis. Bullous myringitis may suggest mycoplasmal pneumonia. Conjunctivitis, adenopathy, and rhinorrhea suggest adenovirus infection.

Complications

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

Approach Considerations

Bronchitis may be suspected in patients with an acute respiratory infection with cough; yet, because many more serious diseases of the lower respiratory tract cause cough, bronchitis must be considered a diagnosis of exclusion. A complete blood count with differential may be obtained.

Procalcitonin levels may be useful to distinguish bacterial infections from nonbacterial infections. Trials from 2008 and 2009 have shown that they may help guide therapy and reduce antibiotic use.[8, 9]

Sputum cytology may be helpful if the cough is persistent.

Chest radiography should be performed in those patients whose physical examination findings suggest pneumonia. Elderly patients may have no signs of pneumonia; therefore, chest radiography may be warranted in these patients, even without other clinical signs of infection.

Bronchoscopy may be needed to exclude foreign body aspiration, tuberculosis, tumors, and other chronic diseases of the tracheobronchial tree and lungs.

Influenza tests may be useful. Additional serologic tests, such as that for atypical pneumonia, are not indicated.

Spirometry may be useful because patients with acute bronchitis often have significant bronchospasm, with a large reduction in forced expiratory volume in one second (FEV1). This generally resolves over 4-6 weeks.

Laryngoscopy can exclude epiglottitis.

Goblet cell hyperplasia, mucosal and submucosal inflammatory cells, edema, peribronchial fibrosis, intraluminal mucous plugs, and increased smooth muscle are characteristic findings in small airways in chronic obstructive lung disease.

Cultures and Staining

Obtain cultures of respiratory secretions for influenza virus, Mycoplasmapneumoniae, and Bordetella pertussis when these organisms are suspected. Culture methods and immunofluorescence tests have been developed for laboratory diagnosis of C pneumoniaeinfection.

Obtain a throat swab. Culture and gram stain of sputum is often performed, though these tests usually show no growth or only normal respiratory florae.[1]

Blood culture may be helpful if bacterial superinfection is suspected.

Procalcitonin Levels

Procalcitonin is a prohormone of calcitonin and part of a inflammatory cascade in the immune system. Levels have been shown to be elevated in bacterial infections and not in viral or other inflammatory conditions. Studies suggest values of greater than or equal to 0.25 mcg/L in non-ICU patients and levels greater than 0.5 mcg/L in ICU patients may be appropriate to use as cutoffs for initiation of antibiotic therapy.[10] A subsequent drop of at least 80% in levels may be appropriate to use as a guide for discontinuing antibiotics. Additional data suggest using a procalcitonin algorithm reduces antibiotic usage without increasing the risk of complications.[11]

Approach Considerations

Therapy is generally focused on alleviation of symptoms.Toward this goal, a doctor may prescribe a combination of medications that open obstructed bronchial airways and thin obstructive mucus so that it can be coughed up more easily. Care for acute bronchitis is primarily supportive and should ensure that the patient is oxygenating adequately. Bed rest is recommended.

The most effective means for controlling cough and sputum production in patients with chronic bronchitis is the avoidance of environmental irritants, especially cigarette smoke.

Also see Pediatric Bronchitis.

Symptomatic Treatment

Based on 2006 American College of Chest Physicians (ACCP) guidelines,[12, 13] central cough suppressants such as codeine and dextromethorphan are recommended for short-term symptomatic relief of coughing in patients with acute and chronic bronchitis.[14]

Also based on 2006 ACCP guidelines, therapy with short-acting beta-agonists ipratropium bromide and theophylline can be used to control symptoms such as bronchospasm, dyspnea, and chronic cough in stable patients with chronic bronchitis. For this group, treatment with a long-acting beta-agonist, when coupled with an inhaled corticosteroid, can be offered to control chronic cough.

For patients with an acute exacerbation of chronic bronchitis, therapy with short-acting agonists or anticholinergic bronchodilators should be administered during the acute exacerbation. In addition, a short course of systemic corticosteroid therapy may be given and has been proven to be effective.

In acute bronchitis, treatment with beta2-agonist bronchodilators may be useful in patients who have associated wheezing with cough and underlying lung disease. Little evidence indicates that the routine use of beta2-agonists is otherwise helpful in adults with acute cough.[15]

Nonsteroidal anti-inflammatory drugs are helpful in treating constitutional symptoms of acute bronchitis, including mild-to-moderate pain. Albuterol and guaifenesin products treat cough, dyspnea, and wheezing.

In patients with chronic bronchitis or chronic obstructive pulmonary disease (COPD), treatment with mucolytics has been associated with a small reduction in acute exacerbations and a reduction in the total number of days of disability. This benefit may be greater in individuals who have frequent or prolonged exacerbations.[16] Mucolytics should be considered in patients with moderate-to-severe COPD, especially in the winter months.[3]

Antibiotic Therapy

Among otherwise healthy individuals, antibiotics have not demonstrated any consistent benefit in the symptomatology or natural history of acute bronchitis.[17, 18] Most reports have shown that 65-80% of patients with acute bronchitis receive an antibiotic despite evidence indicating that, with few exceptions, they are ineffective.[19, 20] An exception is with cases of acute bronchitis caused by suspected or confirmed pertussis infection.

The most recent recommendations on whether to treat patients with acute bronchitis with antibiotics are from the National Institute for Health and Clinical Excellence in the United Kingdom. They recommend not treating acute bronchitis with antibiotics unless a risk of serious complications exists because of comorbid conditions. Antibiotics, however, are recommended in patients older than 65 years with acute cough if they have had a hospitalization in the past year, have diabetes mellitus or congestive heart failure, or are on steroids.[21]

In patients with acute exacerbations of chronic bronchitis, the use of antibiotics is recommended. Trials have shown that antibiotics improve clinical outcomes in such cases, including a reduction in mortality.[22, 23]

A meta-analysis found no difference in treatment success for acute exacerbations of chronic bronchitis with macrolides, quinolones, or amoxicillin/clavulanate.[24] Another meta-analysis comparing the effectiveness of semisynthetic penicillins to trimethoprim-based regimens found no difference in treatment success or toxicity.[25] These findings support earlier studies that have shown antibiotics to be useful in exacerbations of chronic bronchitis, regardless of the agent used.

In addition, a short course of antibiotics (5 d) is as effective as the traditional longer treatments (>5 d) in these patients.[26] Patients with severe exacerbations and those with more severe airflow obstruction at baseline are the most likely to benefit. In stable patients with chronic bronchitis, long-term prophylactic therapy with antibiotics is not indicated.

Influenza Vaccinations

The influenza vaccine may reduce the incidence of upper respiratory tract infections and, subsequently, reduce the incidence of acute bacterial bronchitis. The influenza vaccine may be less effective in preventing illness than it is in preventing serious complications and death.[27]

Influenza vaccine provides reasonable protection against immunized strains. The vaccination becomes effective 10-14 days after administration. Specific recommendations for individuals who should be immunized can be obtained from the CDC, which publishes regular updates of this information (see Seasonal Influenza Vaccination Resources for Health Professionals).

Zinc

Several studies have shown conflicting results on the use of zinc as an adjunct treatment against influenza A. Most studies demonstrated favorable results, but participants complained of a bad taste and significant nausea.

On June 16, 2009, the US Food and Drug Administration (FDA) issued a public health advisory and notified consumers and health care providers to discontinue use of intranasal zinc products. The intranasal zinc products (Zicam Nasal Gel/Nasal Swab products by Matrixx Initiatives) are herbal cold remedies that claim to reduce the duration and severity of cold symptoms and are sold without a prescription. The FDA received more than 130 reports of anosmia (inability to detect odors) associated with intranasal zinc. Many of the reports described the loss of the sense of smell with the first dose.[28]

Consultations

Primary care providers can usually treat acute bronchitis unless severe complications occur or the patient has underlying pulmonary disease or immunodeficiency. Pulmonary medicine specialists and infectious disease specialists also may need to be consulted.

Long-Term Monitoring

Routine follow-up care is usually not necessary. If symptoms worsen (eg, shortness of breath, high fever, vomiting, persistent cough), consider an alternative diagnosis. If symptoms recur (> 3 episodes/y), further investigation is recommended. If symptoms persist beyond 1 month, reassess patient for other causes of cough.

Medication Summary

Therapy for patients with acute bronchitis is generally aimed toward alleviation of symptoms and includes the use of analgesics, antipyretics, antitussives, and expectorants.

Among otherwise healthy individuals, antibiotics have not demonstrated consistent benefit in the symptomatology or natural history of acute bronchitis.[12, 29] Nonetheless, surveys from Europe, Australia, and the United States show that 80% of patients with acute bronchitis receive antibiotics.

Antibiotic overuse contributes to the emergence of drug-resistant organisms. Cognizant of this, the Centers for Disease Control and Prevention recently collaborated with numerous medical societies to publish a series of articles on the judicious use of antibiotics for several common conditions, including bronchitis, and have recommended against routine antibiotic use in uncomplicated bronchitis.

Patients are up to 4 times more likely to expect antibiotics for the diagnosis of bronchitis than for a chest cold. Therefore, limiting use of the diagnosis of bronchitis may make reduction of antibiotic use more acceptable to patients.

Reviews have also noted that antibiotic use in smokers without chronic obstructive pulmonary disease is no more effective than use in nonsmokers.[30]

Amoxicillin and clavulanate (Augmentin)

Clinical Context:  This agent inhibits bacterial cell wall synthesis by binding to penicillin-binding proteins. The addition of clavulanate inhibits beta-lactamase–producing bacteria.

It is a good alternative antibiotic for patients allergic to or intolerant of the macrolide class. It is usually well tolerated and provides good coverage of most infectious agents, but it is not effective against Mycoplasma and Legionella species. The half-life of the oral dosage is 1-1.3 hours. It has good tissue penetration but does not enter the cerebrospinal fluid.

For children older than 3 months, base the dosing protocol on amoxicillin content. Because of different amoxicillin/clavulanic acid ratios in the 250-mg tab (250/125) vs the 250-mg chewable tab (250/62.5), do not use the 250-mg tab until the child weighs more than 40 kg.

Erythromycin (E.E.S., E-Mycin, Ery-Tab)

Clinical Context:  Erythromycin inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. It is indicated for staphylococcal, streptococcal, chlamydial, and mycoplasmal infections.

Azithromycin (Zithromax)

Clinical Context:  Azithromycin acts by binding to the 50S ribosomal subunit of susceptible microorganisms and blocks dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Nucleic acid synthesis is not affected.

It concentrates in phagocytes and fibroblasts, as demonstrated by in vitro incubation techniques. In vivo studies suggest that the concentration in phagocytes may contribute to drug distribution to inflamed tissues. Azithromycin treats mild-to-moderate microbial infections.

Tetracycline (Sumycin)

Clinical Context:  Tetracycline may be an option outside the United States. It treats gram-positive and gram-negative organisms, as well as mycoplasmal, chlamydial, and rickettsial infections. This agent inhibits bacterial protein synthesis by binding with the 30S and, possibly, the 50S ribosomal subunit(s). It is less effective than erythromycin.

Cefditoren (Spectracef)

Clinical Context:  Cefditoren is a semisynthetic cephalosporin administered as a prodrug. It is hydrolyzed by esterases during absorption and is distributed in circulating blood as active cefditoren.

Bactericidal activity results from inhibition of cell wall synthesis via an affinity for penicillin-binding proteins. No dose adjustment is necessary for mild renal impairment (CrCl 50-80 mL/min/1.73 m2) or mild-to-moderate hepatic impairment. It is indicated for acute exacerbation of chronic bronchitis caused by susceptible strains of S pyogenes.

The 400-mg dose is indicated for AECB caused by susceptible strains of H influenzae, H parainfluenzae, S pneumoniae (penicillin-susceptible strains only), or M catarrhalis.

Trimethoprim-sulfamethoxazole (Bactrim DS, Septra)

Clinical Context:  Trimethoprim-sulfamethoxazole inhibits bacterial synthesis of dihydrofolic acid by competing with para-aminobenzoic acid, resulting in inhibition of bacterial growth. Antibacterial activity of trimethoprim-sulfamethoxazole includes common urinary tract pathogens, except Pseudomonas aeruginosa. As with tetracycline, it has in vitro activity against B pertussis. It is not useful in mycoplasmal infections.

Amoxicillin (Biomox, Trimox, Amoxil)

Clinical Context:  Amoxicillin interferes with synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria.

Levofloxacin (Levaquin)

Clinical Context:  Levofloxacin has a bacteriocidal property by inhibiting the DNA gyrase and, consequently, cell growth.

Clarithromycin (Biaxin)

Clinical Context:  Clarithromycin is a semisynthetic macrolide antibiotic that reversibly binds to the P site of the 50S ribosomal subunit of susceptible organisms and may inhibit RNA-dependent protein synthesis by stimulating dissociation of peptidyl t-RNA from ribosomes, causing bacterial growth inhibition.

Doxycycline (Bio-Tab, Doryx, Vibramycin)

Clinical Context:  Doxycycline is a broad-spectrum, synthetically derived bacteriostatic antibiotic in the tetracycline class. It is almost completely absorbed, concentrates in bile, and is excreted in urine and feces as a biologically active metabolite in high concentrations.

It inhibits protein synthesis and, thus, bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria. It may block dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Class Summary

Studies have focused on healthy individuals (patients with asthma excluded) or patients with chronic obstructive pulmonary disease (COPD). Antimicrobials appear to offer a small benefit when treating patients with COPD, and trimethoprim-sulfamethoxazole remains a good and inexpensive choice. Amoxicillin and doxycycline are also good alternatives. Therefore, extending antimicrobial use to patients with asthma and others with limited cardiopulmonary reserve may be reasonable.

Dextromethorphan/guaifenesin (Children's Delsym Cough + Chest Congestion, Coricidin HBP Chest Congestion & Cough, Delsym Cough + Chest Congestion)

Clinical Context:  This agent treats minor cough resulting from bronchial and throat irritation.

Codeine/guaifenesin (Robitussin AC)

Clinical Context:  The prototype antitussive, codeine, has been used successfully in some chronic cough and induced-cough models, but scant clinical data exist for upper respiratory tract infections.

Class Summary

Sparse data attest to the efficacy of expectorants outside the test tube.

Albuterol (Proventil, Ventolin)

Clinical Context:  Albuterol relaxes bronchial smooth muscle by action on beta2-receptors with little effect on cardiac muscle contractility.

Metaproterenol

Clinical Context:  Metaproterenol is a beta agonist for bronchospasms that relaxes bronchial smooth muscle by action on beta2 receptors with little effect on cardiac muscle contractility.

Theophylline (Theo-24, Uniphyl)

Clinical Context:  Theophylline is used to control symptoms such as bronchospasm, dyspnea, and chronic cough in stable patients with chronic bronchitis. It potentiates exogenous catecholamines and stimulates endogenous catecholamine release and diaphragmatic muscular relaxation, which, in turn, stimulates bronchodilation.

Ipratropium

Clinical Context:  Ipratropium is an anticholinergic bronchodilator that is often used to control symptoms such as bronchospasm, dyspnea, and chronic cough in stable patients with chronic bronchitis.

Class Summary

Studies (although limited) have shown an advantage to using bronchodilators and possible superiority to antibiotics for relieving bronchitis symptoms.

Prednisolone (Pediapred, Orapred)

Clinical Context:  Prednisolone works by decreasing inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability.

Prednisone (Sterapred)

Clinical Context:  Prednisone may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear leukocyte activity. Prednisone stabilizes lysosomal membranes and suppresses lymphocytes and antibody production.

Class Summary

For patients with an acute exacerbation of chronic bronchitis, a short course of systemic corticosteroid therapy may be given and has been proven to be effective.

Beclomethasone (Qvar)

Clinical Context:  Beclomethasone inhibits bronchoconstriction mechanisms, causes direct smooth muscle relaxation, and may decrease the number and activity of inflammatory cells, which, in turn, decrease airway hyperresponsiveness. It is available in a metered-dose inhaler (MDI) that delivers 40 or 80 mcg/actuation.

Fluticasone (Flovent HFA, Flovent Diskus)

Clinical Context:  Fluticasone has extremely potent vasoconstrictive and anti-inflammatory activity. It is available in an MDI (44-mcg, 110-mcg, or 220-mcg per actuation) and Diskus powder for inhalation (50-mcg, 100-mcg, or 250-mcg per actuation).

Budesonide (Pulmicort Flexhaler, Pulmicort Respules)

Clinical Context:  Budesonide reduces inflammation in airways by inhibiting multiple types of inflammatory cells and decreasing production of cytokines and other mediators involved in the asthmatic response. It is available as Flexhaler powder for inhalation (90 mcg/actuation [delivers approximately 80 mcg/actuation]) and Respules suspension for inhalation.

Class Summary

Corticosteroids are the most potent anti-inflammatory agents. Inhaled forms are topically active, poorly absorbed, and least likely to cause adverse effects. In patients who are stable with chronic bronchitis, treatment with a long-acting beta-agonist coupled with an inhaled corticosteroid may offer relief of chronic cough.

Zanamivir (Relenza)

Clinical Context:  Zanamivir is an inhibitor of neuraminidase, which is a glycoprotein on the surface of the influenza virus that destroys the infected cell's receptor for viral hemagglutinin. By inhibiting viral neuraminidase, release of viruses from infected cells and viral spread are decreased. It is effective against both influenza A and B and is inhaled through Diskhaler oral inhalation device. Circular foil disks containing 5-mg blisters of drug are inserted into the supplied inhalation device.

Rimantadine (Flumadine)

Clinical Context:  Rimantadine inhibits viral replication of influenza A virus H1N1, H2N2, and H3N2 and prevents viral penetration into a host by inhibiting uncoating of influenza A. NOTE: Because of resistance, it is not recommended by the CDC as of the 2005-2006 influenza season. Laboratory testing by the CDC on the predominant strain of influenza (H3N2) currently circulating in the United States shows that it is resistant to these drugs.

Oseltamivir (Tamiflu)

Clinical Context:  Oseltamivir inhibits neuraminidase, which is a glycoprotein on the surface of influenza virus that destroys an infected cell's receptor for viral hemagglutinin. By inhibiting viral neuraminidase, this agent decreases release of viruses from infected cells and thus viral spread. It is effective in treating influenza A or B. Start within 40 hours of symptom onset. It is available as a capsule and oral suspension.

Peramivir (Rapiacta)

Clinical Context:  Peramivir is an investigational neuraminidase inhibitor. Emergency-use authorization has been issued by the FDA for use of peramivir in hospitalized adult and pediatric patients with suspected or laboratory-confirmed 2009 H1N1 influenza unresponsive to oseltamivir or zanamivir, in patients unable to take PO or inhaled drugs (or delivery route not dependable or feasible), or in other patients determined by clinician. To request peramivir, see the information at www.cdc.gov/h1n1flu/eua or call (800) CDC-INFO (232-4636).

Class Summary

Influenza vaccinations offer greater protection for the appropriate populations because they offer coverage for influenza A and B. Influenza vaccine provides reasonable protection against immunized strains. The vaccination becomes effective 10-14 days after administration. Specific recommendations for individuals who should be immunized can be obtained from the CDC, which publishes regular updates of this information (see Seasonal Influenza Vaccination Resources for Health Professionals).

Influenza A viruses, including the 2 subtypes H1N1 and H3N2, and influenza B viruses currently circulate worldwide, but the prevalence of each can vary among communities and within a single community over the course of an influenza season.

In the 2009-2010 flu season, approximately 99% of typed influenza viruses were H1N1. In the United States, 4 prescription antiviral medications (ie, oseltamivir, zanamivir, amantadine, rimantadine) are approved for treatment and chemoprophylaxis of influenza.

The vast majority of the 2009-2010 influenza was susceptible to oseltamivir and zanamivir but resistant to the adamantanes (amantadine, rimantadine). In addition, the FDA issued an emergency use authorization for a third neuraminidase inhibitor, peramivir, for the treatment of hospitalized patients with H1N1 influenza who have potentially life-threatening suspected or laboratory-confirmed infection. Peramivir IV is available through the CDC upon request of a licensed physician.

Complete recommendations are available in a CDC Health Advisory.

Ibuprofen (Ibuprin, Advil, Motrin)

Clinical Context:  Ibuprofen is usually the drug of choice for the treatment of mild to moderate pain, if no contraindications exist.

Acetaminophen (Tylenol, Panadol, Aspirin-Free Anacin)

Clinical Context:  Acetaminophen is the drug of choice for the treatment of pain in patients who have documented hypersensitivity to aspirin or NSAIDs, who have upper gastrointestinal disease, or who are taking oral anticoagulants.

Class Summary

Analgesics and antipyretics are often helpful in relieving the associated lethargy, malaise, and fever associated with illness.

How is bronchitis characterized?What are the signs and symptoms of bronchitis?What physical findings suggest acute bronchitis?When should bronchitis be suspected?Which lab studies may be helpful in the diagnosis of bronchitis?What is the focus of therapy for bronchitis?Which agents are used in the treatment of bronchitis?What is the role of antibiotic therapy in the treatment of acute bronchitis?Is long-term antibiotic prophylaxis indicated in the management of chronic bronchitis?How is influenza vaccination beneficial in the prevention of bronchitis?How is bronchitis characterized?How is chronic bronchitis defined?How is an acute exacerbation of chronic bronchitis characterized?What triggers bronchitis?Which condition is frequently misdiagnosed as acute bronchitis?What are the signs and symptoms of acute bronchitis?What is pediatric bronchitis?What is the pathophysiology of acute bronchitis?What is the role of mycoplasmal pneumonia in the pathophysiology of bronchitis?What is the pathophysiology of chronic bronchitis?How is chronic bronchitis categorized?How is chronic bronchitis with obstruction distinguished from chronic infective asthma?What causes chronic bronchitis?What are the most common causes of acute and chronic bronchitis?Which viruses cause bronchitis?Which infections cause acute bronchitis?What is the predominant cause of chronic bronchitis and what are the risk factors for acute exacerbations of chronic bronchitis?What is the role of cigarette smoking in the etiology of chronic bronchitis?What is the role of air pollutants in the etiology of bronchitis?Which occupational exposures increase the risk of developing chronic bronchitis?What is the incidence of chronic bronchitis in the US?What is the global incidence of acute bronchitis?How does the incidence of bronchitis vary among male and females and different age groups?What is the prognosis of acute bronchitis?What education should be given to patients with bronchitis?What is the focus of the history of patients with suspected bronchitis?What is the most common symptom of bronchitis?How long does cough usually last in patients with acute bronchitis?What are less common signs and symptoms of bronchitis?What is the likelihood of dyspnea and cyanosis in patients with bronchitis?What are other symptoms of acute bronchitis?How do physical findings in acute bronchitis vary?What is the presentation in severe cases of bronchitis?Which physical findings suggest bronchitis?What are the possible complications of acute bronchitis?Which co-infections may occur with bronchitis?What are concerns regarding diagnosing streptococcal pharyngitis in patients with bronchitis?Which conditions should be included in the differential diagnoses of bronchitis?What are the differential diagnoses for Bronchitis?In which patients may bronchitis be suspected?Which test may be useful to distinguish bacterial infections from nonbacterial infections in bronchitis?If the cough is persistent, which test may be helpful in the workup of bronchitis?What is the role of imaging studies in the workup of bronchitis?What is the role of bronchoscopy in the workup of bronchitis?What is the role of influenza tests in the workup of bronchitis?What is the role of spirometry in the workup of bronchitis?What is role of laryngoscopy in the workup of bronchitis?Which findings suggest chronic obstructive lung disease in the workup of bronchitis?What is the role of cultures and staining in the workup of bronchitis?When are blood cultures indicated in the workup of bronchitis?What is the role of procalcitonin level measurement in the workup of bronchitis?What is the goal of therapy for bronchitis?What is the most effective approach to control cough and sputum production in patients with chronic bronchitis?What are the ACCP recommendations for short-term symptomatic relief in patients with acute and chronic bronchitis?What are the treatment options for acute exacerbation of chronic bronchitis?What are the treatment options for acute bronchitis?What is the role of mucolytics in the treatment of chronic bronchitis or COPD?What is the role of antibiotic therapy in the treatment of bronchitis?What are the NICE recommendations for antibiotic treatment of acute bronchitis?When are antibiotics indicated in the treatment of bronchitis?What is the efficacy of antibiotic treatment in patients with bronchitis?What is the role of influenza vaccines in the treatment of bronchitis?What is the role of zinc in the treatment of bronchitis?Which specialist consultations may be indicated in the treatment of bronchitis?What monitoring is needed for patients with bronchitis?What is the goal of therapy for acute bronchitis?What is the role of antibiotic treatment for bronchitis?Which medications in the drug class Antimicrobials are used in the treatment of Bronchitis?Which medications in the drug class Antitussives/expectorants are used in the treatment of Bronchitis?Which medications in the drug class Bronchodilators are used in the treatment of Bronchitis?Which medications in the drug class Corticosteroids, Systemic are used in the treatment of Bronchitis?Which medications in the drug class Corticosteroids, Inhaled are used in the treatment of Bronchitis?Which medications in the drug class Antiviral Agents are used in the treatment of Bronchitis?Which medications in the drug class Analgesics/antipyretics are used in the treatment of Bronchitis?

Author

Jazeela Fayyaz, DO, Attending Physician, Department of Pulmonary and Sleep Medicine, Medical Director of Sleep Lab, Unity Hospital

Disclosure: Nothing to disclose.

Coauthor(s)

Klaus-Dieter Lessnau, MD, FCCP, Former 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

Disclosure: Nothing to disclose.

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

Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD, FACP, FCCP, Geri and Richard Brawerman Chair in Pulmonary and Critical Care Medicine, Professor and Executive Vice Chairman, Department of Medicine, Medical Director, Women's Guild Lung Institute, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine

Disclosure: Nothing to disclose.

Acknowledgements

Paul Blackburn, DO, FACOEP, FACEP Attending Physician, Department of Emergency Medicine, Maricopa Medical Center

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.

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: Lippincott textbook royalty; Wiley textbook royalty

Ali Hmidi, MD Resident Physician, Department of Internal Medicine, Brooklyn Hospital Center, Weill Cornell Medical College

Disclosure: Nothing to disclose.

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.

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.

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

Disclosure: Nothing to disclose.

Samer Qarah, MD Pulmonary Critical Care Consultant, Department of Internal Medicine, Division of Pulmonary and Critical Care, The Brooklyn Hospital Center and Cornell University

Samer Qarah, MD, is a member of the following medical societies: American College of Critical Care Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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