Bronchitis and Pneumonia
Andrew J. Grimone
Virginia P. Arcangelo
Eric T. Wittbrodt
ACUTE BRONCHITIS
In the United States, acute bronchitis is diagnosed in 5% of adults and accounts for over 10 million outpatient office visits annually (Liapikou & Torres, 2014). The disease is a reversible inflammatory condition of the tracheobronchial tree that occurs in all age groups and is usually self-limiting. Typically, acute bronchitis occurs during the winter months. Predisposing factors for acute bronchitis include cold air, damp climates, fatigue, malnutrition, and inhalation of irritating substances, such as polluted air and cigarette smoke.
CAUSES
Viral infections cause over 90% of acute bronchitis episodes; the most common respiratory viruses associated with acute bronchitis are rhinovirus, coronavirus, influenza virus A and B, parainfluenza virus, adenovirus, and respiratory syncytial virus (RSV). Bacterial infections cause less than 10% of acute bronchitis (Liapikou & Torres, 2014). The only bacterial microorganisms implicated in the pathogenesis of uncomplicated acute bronchitis are Bordetella pertussis, Chlamydophila pneumoniae, and Mycoplasma pneumoniae. Limited evidence indicates that other common respiratory tract pathogens such as Streptococcus pneumoniae can contribute to acute bronchitis.
PATHOPHYSIOLOGY
Acute bronchitis is characterized by infection of the tracheobronchial tree. This infection results in hyperemic and edematous mucous membranes, yielding an increase in bronchial secretions. Destruction of the respiratory epithelial lining and reduced mucociliary function result from these changes. This process is usually transient and resolves after the infection clears.
DIAGNOSTIC CRITERIA
Signs and symptoms of acute bronchitis are preceded by manifestations of an upper respiratory tract infection such as coryza, malaise, chills, back and muscle pain, headache, and sore throat. If fever is present, it rarely exceeds 102.2°F (39°C) and lasts for 3 to 5 days. Fever is more commonly seen with adenovirus, influenza virus, and M. pneumoniae infection. The hallmark of acute bronchitis is a cough that is initially dry and nonproductive; however, as the production of bronchial secretions increases, the cough becomes more abundant and mucoid. The cough usually lasts for 7 to 10 days, although in some patients, it can persist for weeks to months. Patients also present with phlegm, hoarseness, and wheezing.
Pulmonary examination may reveal signs of coarse, moist bilateral crackles, rhonchi, and wheezing. The chest x-ray typically reveals no active disease; thus, a chest x-ray is not indicated unless pneumonia is suspected. The usefulness of cultures to identify the causative microorganisms is limited because most cases of acute bronchitis are viral in origin, and cultures usually are negative or grow normal nasopharyngeal flora. Laboratory tests may reveal a normal or slightly elevated white blood cell (WBC) count.
The high reported incidence of acute bronchitis can be correlated with the absence of definitive diagnostic signs or laboratory tests. Thus, the diagnosis is based purely on the patient’s
risk factors and signs and symptoms. In many patients, an upper respiratory tract infection (sinusitis or allergic rhinitis) may be misdiagnosed as acute bronchitis.
risk factors and signs and symptoms. In many patients, an upper respiratory tract infection (sinusitis or allergic rhinitis) may be misdiagnosed as acute bronchitis.
INITIATING DRUG THERAPY
The general treatment for acute bronchitis is symptomatic and supportive care (Figure 27.1). Patients should be encouraged to drink plenty of fluids to prevent dehydration and decrease the viscosity of bronchial secretions. Bed rest is indicated until fever subsides. Mild analgesic/antipyretic therapy is effective for relief of fever and musculoskeletal pains. Aspirin or acetaminophen (Tylenol; 650 mg in adults or 10 to 15 mg/kg per dose in children) or ibuprofen (Advil, others; 200 to 400 mg in adults or 5 to 10 mg/kg per dose in children) administered every 4 to 6 hours can be used as analgesic/antipyretic therapy. Acetaminophen is the agent of choice because aspirin should be avoided in children, given the correlation of aspirin and the development of Reye syndrome in this age group. Aspirin and ibuprofen should also be used cautiously in the elderly, patients with a history of peptic ulcer disease or recent gastrointestinal (GI) bleeding, and patients with renal insufficiency.
 FIGURE 27.1 Treatment algorithm for acute bronchitis. |
Nonprescription cough and cold medications (see Chapter 24) often are used to help reduce the signs and symptoms of acute bronchitis. The use of nonprescription medications that contain various combinations of antihistamines, sympathomimetic agents, and antitussives can result in dehydration of bronchial secretions. This could lead to further aggravation of symptoms, which prolongs the recovery process. Cough that is associated with acute bronchitis can become bothersome. Dextromethorphan, an antitussive
agent, is recommended to help treat mild, persistent cough. Severe cough may require a more potent cough medication that contains codeine or hydrocodone.
agent, is recommended to help treat mild, persistent cough. Severe cough may require a more potent cough medication that contains codeine or hydrocodone.
In patients with fever and a productive cough persisting beyond 4 to 6 days, treatment with antibiotics may be indicated to treat bacterial coinfection, especially in patients with underlying pulmonary disease.
Goals of Drug Therapy
The goals of pharmacotherapy include providing the patient with comfort and, in severe cases, treating associated dehydration and respiratory compromise. If antibiotics are administered, minimizing side effects is also a goal.
Antibiotics
Antibiotics are often prescribed for patients with acute bronchitis; however, in otherwise healthy patients, they offer little relief from the respiratory symptoms of the disease and do not shorten the course of the illness. Therefore, routine use of antibiotics for acute bronchitis is discouraged. Despite this, studies have shown that approximately two thirds of patients diagnosed with acute bronchitis in the United States are prescribed antibiotic therapy. Part of the reason for antibiotic overprescribing is lack of patient and caregiver education on the causes of acute bronchitis. Surveys suggest that over 50% of patients believe that antibiotics are effective in treating viral upper respiratory tract infections. Patient education on appropriate treatment is crucial to prevent inappropriate antibiotic use. One educational method useful in teaching patients and caregivers about this illness is selection of descriptive words such as “chest cold” or “viral upper respiratory tract infection” instead of using the term “acute bronchitis.”
Antibiotics are indicated if the patient has concomitant chronic obstructive pulmonary disease (COPD), high fevers, purulent sputum, or respiratory symptoms for more than 4 to 6 days. Additionally, antibiotics may be considered in patients over 65 years of age or those with chronic diseases such as heart failure, diabetes mellitus, or serious neurological disorders. Empiric antibiotic therapy should be directed against the microorganisms commonly suspected to cause acute bronchitis.
Selecting the Most Appropriate Agent
Table 27.1 lists the antibiotics that are commonly used to treat acute bronchitis caused by bacteria. Aminopenicillins such as amoxicillin (Amoxil) are effective against infections caused by S. pneumoniae and Haemophilus influenzae.
For microorganisms that produce beta-lactamase, such as Moraxella catarrhalis and H. influenzae, aminopenicillins given in combination with a beta-lactamase inhibitor, such as amoxicillin-clavulanate (Augmentin), or a second- or third-generation cephalosporin should be administered.
For acute bronchitis due to atypical bacteria such as M. pneumoniae and Chlamydophila species, macrolides (e.g., erythromycin [Eryc], clarithromycin [Biaxin], or azithromycin [Zithromax]) or doxycycline (Vibramycin) are effective. Doxycycline should not be used in children younger than age 8. In this population, the agent of choice is a macrolide. If B. pertussis is the likely microorganism, erythromycin or another macrolide is the drug of choice.
TABLE 27.1 Acute Bronchitis: Drug Therapy for Selected Microorganisms | ||||||||||||||
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During epidemics caused by influenza A or B virus, oseltamivir (Tamiflu) and zanamivir (Relenza Diskhaler) may be administered early in the course of the illness to minimize symptoms of influenza in adults and pediatrics who have been symptomatic for no longer than 2 days. For more information about antibiotic/antimicrobial therapy, refer to Chapter 8.
CHRONIC BRONCHITIS
Chronic bronchitis is a component of COPD, which is one of the five leading causes of death in the United States. (See Chapter 26 for a discussion of COPD.) The standard description/definition of chronic bronchitis is productive cough and sputum production for 3 months per year for at least two consecutive years. An acute exacerbation of chronic bronchitis is defined as worsening of respiratory symptoms such as increased cough, sputum, and dyspnea that warrants a change in medications. Chronic bronchitis primarily affects adults and occurs more commonly in men than in women. Over 10% of the adult population in the United States aged 40 or older is afflicted with chronic bronchitis, which accounts for a large amount of health care expenditures and lost wages (Kim & Criner, 2013). Patients with chronic bronchitis are more likely to have frequent and severe episodes of acute bacterial bronchitis. Exacerbations of COPD account for more than 50% of the overall cost related to the treatment of COPD (Qureshi et al., 2014). Because many infections are untreated, the exact morbidity of acute exacerbations of chronic bronchitis is unknown.
CAUSES
Several factors are implicated in the pathogenesis of chronic bronchitis, leading to chronic inflammation and sputum production. The predominant factor in chronic bronchitis is
cigarette smoke, a well-known respiratory irritant, and most patients with chronic bronchitis have a history of cigarette smoking. However, chronic bronchitis has been noted in 4% to 22% of patients who never smoked (Kim & Criner, 2013), suggesting other causative factors. Occupational dust, fumes, and environmental pollution are some additional risk factors that contribute to the etiology of the disease. The presence of gastroesophageal reflux and hypersecretion of mucus in patients with asthma has also been shown to yield symptoms of chronic bronchitis. Evidence suggests that recurrent respiratory infections may predispose a person to development of chronic bronchitis, although the exact reason for this is unclear.
cigarette smoke, a well-known respiratory irritant, and most patients with chronic bronchitis have a history of cigarette smoking. However, chronic bronchitis has been noted in 4% to 22% of patients who never smoked (Kim & Criner, 2013), suggesting other causative factors. Occupational dust, fumes, and environmental pollution are some additional risk factors that contribute to the etiology of the disease. The presence of gastroesophageal reflux and hypersecretion of mucus in patients with asthma has also been shown to yield symptoms of chronic bronchitis. Evidence suggests that recurrent respiratory infections may predispose a person to development of chronic bronchitis, although the exact reason for this is unclear.
Colonization of the lower airways with bacteria such as H. influenzae, M. catarrhalis, and S. pneumoniae has been frequently detected in patients with chronic bronchitis. Up to 25% of patients with stable COPD have been found to be colonized with these bacteria. These and other microorganisms harbored in the bronchial epithelium act as reservoirs for infection when patient host defenses become compromised. In patients with acute exacerbations of COPD, 70% to 80% of cases are triggered by bacterial or viral infections (Liapikou & Torres, 2014). Viral infections account for nearly one third of acute exacerbations. Other bacteria such as Pseudomonas aeruginosa and Enterobacteriaceae are more likely to be associated with acute exacerbations in patients with frequent exacerbations and advanced stages of COPD. Exposures to environmental pollution or unknown factors contribute to the remainder of acute exacerbations. The frequency and severity of exacerbations of chronic bronchitis are more frequent and severe with increasing stages of COPD.
PATHOPHYSIOLOGY
Several physiologic abnormalities of the bronchial mucosa may lead to chronic bronchitis. It has been suggested that patients with chronic bronchitis are predisposed to respiratory infections because of overproduction and hypersecretion of mucus from goblet cells and impaired mucociliary clearance due to chronic inhalation of irritating substances. A factor leading to impaired mucociliary clearance is the replacement of ciliated epithelium with nonciliated metaplastic cells. This leads to the inability of the bronchi to clear the profuse, thick, sticky secretions present in patients with chronic bronchitis. In addition, inhalation of toxic irritants results in bronchial obstruction because of stimulation of cholinergic activity and increased bronchomotor tone.
DIAGNOSTIC CRITERIA
As with acute bronchitis, cough is the hallmark of chronic bronchitis. Cough, with sputum production, can be mild or severe and may be stimulated by simple conversation. Many patients with chronic bronchitis expectorate a large quantity of white to yellow tenacious sputum in the morning. Because of the characteristics of sputum, many patients complain of a foul taste in the mouth.
Clinical assessment and the patient’s medical history contribute to the diagnosis of chronic bronchitis. Other diseases such as bronchiectasis, cardiac failure, cystic fibrosis, tuberculosis, pulmonary emboli, and lung carcinoma must be excluded before diagnosing a patient with chronic bronchitis or an acute exacerbation of chronic bronchitis. Patients with chronic bronchitis must have a cough with sputum production for at least 3 consecutive months for 2 consecutive years.
Physical examination of patients with chronic bronchitis is usually unremarkable except that chest auscultation reveals inspiratory and expiratory rales, rhonchi, and mild wheezing; normal breath sounds are diminished. As the severity of the disease progresses, an increase in the anteroposterior diameter of the thoracic cage (barrel chest appearance), hyperresonance on percussion, and limited mobility of the diaphragm are observed. Pulmonary function tests demonstrate a decrease in vital capacity and prolongation of expiratory flow. Other features of disease progression include clubbing of the fingers, cor pulmonale, hepatomegaly, and edema of the lower extremities.
The diagnosis of an acute exacerbation of chronic bronchitis relies on the clinical presentation of an acute change in symptoms. Since an acute exacerbation of chronic bronchitis is defined as worsening of respiratory symptoms that warrants a change in medications, diagnosis focuses on early changes in symptoms such as an increase in frequency and severity of cough. Other symptoms include increased sputum production, purulent sputum, hemoptysis, chest congestion and discomfort, increased dyspnea, and wheezing. Malaise, loss of appetite, and fever may also be present. True chills (rigors) and high-grade fever suggest pneumonia rather than an acute exacerbation of chronic bronchitis. This finding requires a chest x-ray for diagnosis. The duration of worsening or new symptoms, number and frequency of previous exacerbations, severity of underlying disease, comorbidities, and current treatment regimen for COPD are helpful in assessing a patient who presents with an acute exacerbation of chronic bronchitis. In these patients, pulse oximetry is useful for tracking and/or adjusting supplemental oxygen therapy. An electrocardiogram (ECG) may help in the diagnosis of or to rule out cardiac problems. A complete blood count (CBC) will help to identify leukocytosis.
To determine the need for hospitalization during an acute exacerbation of chronic bronchitis, the presence of severe symptoms including use of accessory muscles, worsening or new cyanosis, development of peripheral edema, hemodynamic instability, or deterioration in mental status needs to be assessed. A sputum gram stain can assist in empiric antibiotic prescribing. Sputum culture and susceptibility testing may guide the clinician in choosing appropriate antibiotic therapy. In outpatients, sputum cultures are not often feasible or practical, as they take too long to return and frequently do not provide reliable results (i.e., more than 4 hours often elapses between expectoration of sputum and analysis in the laboratory). However, a sputum culture should be considered, especially in patients with frequent exacerbations requiring
antibiotic use, failing current antibiotic therapy, known or suspected resistant pathogens, severe airflow limitation, and/or exacerbations requiring mechanical ventilation. Additionally, procalcitonin, a biomarker specific for bacterial infections, can be obtained to help in determining the presence of active infection. However, this test is currently reserved for patients in acute care settings, given the cost, lack of widespread availability, and delayed turnaround time for results.
antibiotic use, failing current antibiotic therapy, known or suspected resistant pathogens, severe airflow limitation, and/or exacerbations requiring mechanical ventilation. Additionally, procalcitonin, a biomarker specific for bacterial infections, can be obtained to help in determining the presence of active infection. However, this test is currently reserved for patients in acute care settings, given the cost, lack of widespread availability, and delayed turnaround time for results.
TABLE 27.2 Classification of Chronic Bronchitis and Treatment Options for Acute Exacerbations | ||||||||||||||||||||
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A classification system for patients with chronic bronchitis is frequently used to identify high-risk patients and select the appropriate antimicrobial therapy for acute exacerbations according to the suspected microorganism. Table 27.2 outlines the classification system and treatment options, taking into consideration the baseline clinical status, risk factors, and common pathogens.
Patients with uncomplicated chronic bronchitis have little or no lung impairment and no major risk factors for antibiotic resistance. The most common pathogens include H. influenzae, M. catarrhalis, and S. pneumoniae. Viral infections should be considered before bacterial infections in this patient category. Although antibiotic resistance is less common in this group, over 50% of H. influenza and M. catarrhalis produce beta-lactamase, making amoxicillin ineffective. This should be considered especially in patients who fail amoxicillin therapy.
Patients with complicated chronic bronchitis include those with moderate to severe (FEV1 50% less than predicted) lung impairment, those who are elderly (over 65 years of age), those who have frequent exacerbations, and those who have comorbid illnesses such as congestive heart failure, diabetes mellitus, chronic renal failure, or chronic liver disease. The most common pathogens isolated in severe chronic bronchitis are H. influenzae, S. pneumoniae, and M. catarrhalis. Frequent exacerbations in this population increase the likelihood of antibiotic use and the risk for antibiotic resistance, including penicillin-resistant S. pneumoniae.
Patients with severe complicated chronic bronchitis have characteristics similar to those in the previous group, but they have severe airflow obstruction and often have constant purulent sputum production. The same microorganisms found in the other groups should be considered in these patients; however, gram-negative microorganisms such as P. aeruginosa and Enterobacteriaceae should also be suspected.
INITIATING DRUG THERAPY
A complete assessment of the patient’s occupational and environmental history should be performed to treat chronic bronchitis properly. Patients should reduce or eliminate cigarette smoking and their exposure to second-hand smoke. This can be accomplished by counseling sessions and the use of nicotine replacement therapy. Also, exposure to inhaled irritants at work or home should be reduced or eliminated. Pharmacologic treatment should be optimized to prevent or control symptoms, reduce the frequency of exacerbations, and improve quality of life. (See Chapter 26 for a discussion of COPD.)
 FIGURE 27.2 Treatment algorithm for chronic bronchitis. |
The approach to treatment of acute exacerbations of chronic bronchitis is multifactorial (Figure 27.2). The therapies listed in Box 27.1 should be initiated. Antibiotics should be initiated in patients with the three “cardinal symptoms” (Box 27.2) (or at least two cardinal symptoms if increased purulence of sputum is one of the two symptoms) or in hospitalized patients who require mechanical ventilation. Fever alone is not an indication for antibiotic therapy.
BOX 27.1
Nonantibiotic Therapy for Acute Exacerbations of Chronic Bronchitis
Nonantibiotic Therapy for Acute Exacerbations of Chronic Bronchitis
Stop smoking
Avoid inhalation of polluted air
Increase ingestion of fluids (nonalcoholic)
Humidify atmosphere
Use short-acting bronchodilators
Treat any associated asthma
Data from Global Initiative for Chronic Obstructive Lung Disease (GOLD). (2015). Retrieved from www.goldcopd on July 10, 2015.
Goals of Drug Therapy
There are two goals for the treatment of exacerbations of chronic bronchitis: to minimize the impact of the current exacerbation and to prevent the development of subsequent exacerbations with prolonged infection-free intervals. Depending on the severity of the exacerbation and the underlying disease, exacerbations can be managed in the outpatient or inpatient setting. More than 80% of exacerbations can be managed on an outpatient basis (Global Initiative for Chronic Obstructive Lung Disease [GOLD], 2015).
Antimicrobial Therapy
Among the antimicrobial agents used to treat acute exacerbations of chronic bronchitis are the aminopenicillins (amoxicillin) with or without clavulanic acid, cephalosporins, tetracyclines, macrolides, and fluoroquinolones. Table 27.3 reviews antibiotic agents used for patients with chronic bronchitis and pneumonia.
Aminopenicillins
Aminopenicillins, such as amoxicillin, inhibit the final step of bacterial cell wall synthesis by binding to one or more of the penicillin-binding proteins. They are safe for use in children, adults, and pregnant women. Table 27.3 reviews the dose of amoxicillin for acute exacerbations of chronic bronchitis.
BOX 27.2
Cardinal Symptoms Associated with Exacerbations of COPD
Cardinal Symptoms Associated with Exacerbations of COPD
Increase in dyspnea (shortness of breath)
Increase in sputum volume
Increase in or presence of sputum purulence
Contraindications
Aminopenicillins should not be administered to patients with severe hypersensitivity reactions to these agents.
Adverse Events
Hypersensitivity reactions to aminopenicillins manifest as eosinophilia or rash (urticarial, erythematous, morbilliform). Angioedema, exfoliative dermatitis, and erythema multiforme have also been reported as hypersensitivity reactions to aminopenicillins. These reactions occur less frequently than does eosinophilia or rash. Rarely, Stevens-Johnson syndrome has been reported as a hypersensitivity reaction to aminopenicillins.
Nausea, vomiting, and diarrhea, however, are the most common adverse effects that occur with aminopenicillins. Diarrhea is more common with amoxicillin-clavulanate. Pseudomembranous colitis may occur during or after the antibiotic treatment.
Interactions
Aminopenicillins may interrupt the enterohepatic circulation of estrogen by reducing the bacterial hydrolysis of conjugated estrogen in the GI tract. Therefore, the efficacy of oral contraceptives is decreased. Probenecid may increase the effects of aminopenicillins by competing with renal tubular secretion. An increased risk for rash occurs with the coadministration of allopurinol (Zyloprim) and aminopenicillins; the exact mechanism of this interaction has not been established.
Cephalosporins
Cephalosporins consist of several agents, including cephalexin (Keflex), cefaclor (Ceclor), cefuroxime axetil (Ceftin), cefpodoxime (Vantin), cefdinir (Omnicef), and others that are frequently used for the treatment of acute exacerbations of chronic bronchitis. Like penicillins, cephalosporins inhibit bacterial cell wall synthesis by binding to one or more of the penicillin-binding proteins. These drugs are safe for use by children and adults. The dosages of cephalosporins are listed in Table 27.3.
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