Chronic bronchitis: primary care management - Cover Story

Author: John M. Heath, Rupa Mongia
Date: May 15, 1998

Chronic bronchitis is one of the principal manifestations of chronic obstructive pulmonary disease (COPD), the fourth leading cause of death in the United States. About 10 million Americans are affected by some degree of COPD; it causes 40,000 deaths annually.[1]

Chronic bronchitis is a clinical diagnosis characterized by a cough productive of sputum for over three months' duration during two consecutive years and airflow obstruction. These requisites exclude more transient causes of cough associated with sputum production, such as acute bronchitis. The airflow obstruction in chronic bronchitis is caused by excessive tracheobronchial mucus production and is distinct from the anatomic findings of distal air space distention and alveolar septa destruction, which define emphysema.[2]

Cigarette smoking is the most important risk factor for the development of chronic bronchitis. Over 90 percent of patients with chronic bronchitis have a smoking history, although only 15 percent of all cigarette smokers are ultimately diagnosed with some form of obstructive airway disease.[1] Studies have demonstrated persistent markers of active airway inflammation in bronchial biopsy specimens from symptomatic ex-smokers, even after they had been smoke-free for 13 years.[2]

The overall 10-year mortality rate following the diagnosis of chronic bronchitis is 50 percent,[3] with respiratory failure following an acute exacerbation being the most frequent terminal event. Such acute exacerbations are often precipitated by bacterial infection, manifested by purulent sputum, fever and a worsening of the symptoms of poor ventilation. Other known precipitants include viral upper respiratory infections, seasonal changes in the weather, medications and exposure to irritant inhalants.


Streptococcus pneumoniae, Haemophilus influenzae and Moraxella catarrhalis are the three leading bacterial pathogens isolated from the lower bronchi of patients with chronic bronchitis, in contrast to the causative organisms of acute bronchitis, which include Mycoplasma pneumoniae and Chlamydia trachomatis. However, studies of acutely symptomatic patients with COPD have failed to reveal definite organisms in over 50 percent of patients.[4] Nonbacterial pathogens (such as viruses) and Chlamydia and Mycoplasma species are also, rarely, isolated in patients with chronic bronchitis, although their role in either causing symptoms directly or triggering the characteristic inflammatory response is poorly understood.

One speculative explanation of the interaction between infection and chronic bronchitis is that low-intensity colonization of the lower respiratory tract by infectious agents can set up an inflammatory reaction that itself triggers subsequent acute exacerbations.[5] Documentation supporting this concept comes from studies in which patients with chronic bronchitis were found to have circulating bacteria-specific IgE that triggered release of histamine following exposure to the same bacteria cultured from their lower respiratory tracts.[6,7] Additional mechanisms, such as neurogenic inflammation, may then develop, and the symptomatic flare-up of chronic bronchitis may continue by means of sustained inflammatory mediators.[8,9] These and similar studies are the reason for greater therapeutic emphasis on reducing airway inflammation in chronic bronchitis.

Diagnostic Testing

Documentation of airflow obstruction by pulmonary function testing is critical for the diagnosis of chronic bronchitis and provides valuable therapeutic information about the patient's responsiveness to inhaled bronchodilator therapy. A measured forced expiratory volume in one second ([FEV.sub.1]) of less than 70 percent of the total forced vital capacity (FVC)--the [FEV.sub.1]/FVC ratio--defines obstructive airway disease. An [FEV.sub.1]/FVC ratio of less than 50 percent indicates endstage obstructive airway disease.

In most adults beyond the mid-life years, age-related physiologic changes in the elasticity of the lungs cause a 30 mL per year decline in the [FEV.sub.1], so that progressive rates of decline in the [FEV.sub.1] that exceed this amount represent true disease progression. Airflow obstruction in the presence of chronic sputum production confirms the clinical diagnosis of chronic bronchitis.

Evidence of obstructive airflow changes on pulmonary function tests in patients without the characteristic symptom of sputum production is often accompanied by radiographic findings consistent with emphysema. Younger patients with emphysematous obstructive pulmonary findings, especially those without a smoking history, should be evaluated for alpha, antitrypsin deficiency. The median survival for patients with an [FEV.sub.1] of less than 1 L is four years.[1]

Blood Tests

Hypoxemia is a common finding on arterial blood gas sampling in patients with advanced chronic bronchitis and ventilatory failure secondary to bronchospasm and inflammation. Concomitant hypercapnia is associated with worsening ventilatory gas exchange as the illness progresses. Blood tests may reveal mild polycythemia secondary to the hypoxia.

Chest Radiograph

Radiographic findings correlate poorly with symptoms in most patients with chronic bronchitis. Common, but nonspecific, findings include hyperinflation, bullae, blebs, diaphragmatic flattening and peribronchial markings.


Electrocardiographic findings can sometimes include supraventricular rhythm disturbances, such as multifocal atrial tachycardia, atrial fibrillation or atrial flutter with "P" pulmonale. Findings on airway biopsy include goblet cell hyperplasia, mucosal and submucosal inflammation, and increased smooth muscle at the level of the small non-cartilaginous airways.[2] These changes can be quantitated pathologically as the Reid index.

Sputum Cultures

The role of sputum cultures remains limited in nonhospitalized patients who present with acute exacerbation of chronic bronchitis, since cultures of expectorated samples do not reflect the organism(s) present at distal bronchial levels. Gram stain of sputum is often suggested as a means of directing initial antibiotic therapy. But because of the likelihood of multiple organisms, the role of Gram stain in acute decision-making is de-emphasized.[10] For expectorated sputum samples to be considered valid, conventional wisdom is that there should be fewer than 10 squamous cells and more than 25 white blood cells per high-power microscopic field.

Patients with a history of chronic bronchitis and the onset of new symptoms while hospitalized may have acquired a nosocomial infection. For these patients and for others in whom atypical organisms are suspected as the cause of an exacerbation, "protected-tip" cultures of samples obtained from the airway level that appears the most inflamed on bronchoscopy offer the best chance of identifying causative infectious agents.

Overall Management

Figure 1 provides an overview of the management of chronic bronchitis.[1]


Smoking Cessation

Smoking cessation is the single most effective way to reduce the risk of future morbidity from chronic bronchitis. The documentation of an accelerated rate of decline in the [FEV.sub.1]--greater than the normal decline of 30 mL per year--may provide an important motivation for smokers who continue to deny that their persistent smoking will cause future symptoms.

Once the patient makes a commitment to stop smoking, use of various smoking cessation tools, such as nicotine replacement systems, behavior modification training and support groups, can be helpful. Such tools are most effective when a supportive primary care physician sees the patient regularly throughout the smoking cessation period. Primary care physicians should enlist and educate available family members to aid in the patient's smoking cessation efforts, which may require repeated commitments before the patient ultimately succeeds.

Other Management Considerations

Reduction or elimination of exposure to environmental inhaled irritants, such as aerosolized hair and deodorant products in the home and organic dusts or noxious gases in the workplace, and of prolonged exposure to outside air pollution with high sulfur dioxide levels is also a prudent management suggestion.[2]

[PaO.sub.2] [is less than or equal to] 55 mm Hg or [SaO.sub.2] [is less than or equal to] 88%

[PaO.sub.2] of 56 to 59 mm Hg or [SaO.sub.2] [is less than or equal to] [is less than or equal to] 89% if [there is] evidence of cor pulmonale ("P" pulmonale, polycythemia or congestive heart failure)

COPD = chronic obstructive pulmonary disease, [PaO.sub.2] = partial pressure of arterial oxygen; [SaO.sub.2] = arterial oxygen saturation.

Reprinted with permission from Ferguson GT, Cherniack RM. Management of chronic obstructive pulmonary disease, N Engl J Med 1993;328:1017-22.

Oxygen can be provided in a variety of forms, including economic oxygen concentrators for patients who require only low flow rates. Because the monthly expense of oxygen therapy is substantial, selected patients may benefit from oxygen-conserving devices, which are triggered by respiration to deliver a fixed dose of oxygen only during inhalation.

Expectorant mucolytic therapy is generally regarded as unhelpful in most patients with chronic bronchitis. Cough suppressants and sedatives should be avoided as routine measures. Increased mobilization of secretions may be accomplished through adequate systemic hydration and the use of effective cough methods and postural drainage. One effective method of coughing up retained secretions is to lean forward and "huff" repeatedly; the huffing is interspersed with relaxed breaths. Forceful paroxysms of coughing are to be discouraged. Opiates may increase exercise tolerance, although they are not considered standard treatment in most patients.

Surgical approaches for the treatment of chronic bronchitis are limited to use in those rare patients with coexisting bullous emphysema, in whom a bullectomy may allow greater respiratory expansion, or in those patients who might tolerate reduction pneumoplasty, in which bilateral resection of 20 to 30 percent of the lung volume is performed. Lung transplantation remains an expensive ($300,000 the first year) and extraordinary consideration for only highly selected patients with emphysema and very limited functional status despite exhaustive medical management. Patients being considered for lung transplantation should have an established social support network to cope with the emotional and functional stresses of this surgery.

Optimizing Functional Capacity

Pulmonary rehabilitative efforts for patients with chronic bronchitis can improve airway function and allow greater mobility. In addition to exercise conditioning of the respiratory and associated muscles, nutrition and hydration support and psychologic and vocational services are necessary.

Common strategies for attaining respiratory muscle conditioning include graded aerobic exercise such as walking or bicycling over progressively longer durations three times a week, with oxygen supplementation as needed. Instruction regarding pursed--lip breathing--taking deep breaths and breathing out slowly through pursed lips--can help patients reduce the exhausting rapid respiratory rate that many develop. Training the inspiratory muscles to inhale against progressively larger resistance loads can improve exercise tolerance, especially when this conditioning technique is accompanied by abdominal breathing exercises to relieve thoracic respiratory muscle fatigue. The increased respiratory muscle work associated with these pulmonary rehabilitative efforts often requires enhanced nutritional support. Improved hydration through greater fluid intake and provision of airway humidity can also facilitate sputum mobilization, more so than pharmacologic expectorants or mucolytic agents.

Figure 1 reprinted with permission from American Thoracic Society Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease.

Am J Respir Crit Care Med 1995;152(5 Pt 2):S77-121. Figure 2 reprinted with permission from Ferguson GT, Cherniack RM. Management of chronic obstructive pulmonary disease. N Engl J Med 1993;328:1017-22.


[1.] American Thoracic Society. Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1995;152(5 Pt 2):S77-121.

[2.] Ingram RH. Chronic bronchitis, emphysema, and airways obstruction. In: Wilson JD, Braunwald E, Isselbacher KJ et al., eds. Harrison's Principles of internal medicine. 13th ed. New York: McGraw-Hill, 1994:1197-205.

[3.] Turato G, Di Stefano A, Maestrelli P, Mapp CE, Ruggieri MP, Roggeri A, et al. Effect of smoking cessation on airway inflammation in chronic bronchitis. Am J Respir Crit Care Med 1995;152(4 Pt 1): 1262-7.

[4.] Murphy TF, Sethi S. Bacterial infection in chronic obstructive pulmonary disease. Am Rev Respir Dis 1992;146:1067-83.

[5.] Woolcock AJ. How does inflammation cause symptoms? Am J Respir Crit Care Med 1996;153(6 Pt 2):S21-2.

[6.] Kjaergard LL, Larsen FO, Norn S, Clementsen P, Skov PS, Permin H. Basophil-bound IgE and serum IgE directed against Haemophilus influenzae and Streptococcus pneumoniae in patients with chronic bronchitis during acute exacerbations. APMIS 1996; 104:61-7.

[7.] Clementsen P, Larsen FO, Milman N, Skov PS, Norn S. Haemophilus influenzae release histamine and enhance histamine release from human bronchoalveolar cells. Examination of patients with chronic bronchitis and controls. APMIS 1995; 103:806-12.

[8.] Tomaki M, Ichinose M, Miura M, Hirayama Y, Yamauchi H, Nakajima N, et al. Elevated substance P content in induced sputum from patients with asthma and patients with chronic bronchitis. Am J Respir Crit Care Med 1995;151(3 Pt 1):613-7.

[9.] Riise GC, Ahlstedt S, Larsson S, Enander I, Jones I, Larsson P, et al. Bronchial inflammation in chronic bronchitis assessed by measurement of cell products in bronchial lavage fluid. Thorax 1995;50:360-5.

[10.] McCue JD. Oral antibiotic transition therapy for elderly patients with acute exacerbations of chronic obstructive pulmonary disease. Intern Med World Rep 1996; 11(18):14-5.

[11.] Ferguson GT, Cherniack RM. Management of chronic obstructive pulmonary disease. N Engl J Med 1993;328:1017-22.

[12.] Saint S, Bent S, Vittinghoff E, Grady D. Antibiotics in chronic obstructive pulmonary disease exacerbations. A meta-analysis. JAMA 1995;273:957-60.

[13.] Aboussouan LS. Acute exacerbations of chronic bronchitis: focusing management for optimum results. Postgrad Med 1996;99(4):89-90,95-8,101-2.

JOHN M. HEATH, M.D., is associate professor and co-director of the geriatric medicine fellowship program in the Department of Family Medicine at the University of Medicine and Dentistry of New Jersey--Robert Wood Johnson Medical School, New Brunswick. A graduate of Hahnemann University School of Medicine, Philadelphia, he completed a family medicine residency at St. Vincent Health Center, Erie, Pa., and a geriatric medicine fellowship at the University of Cincinnati College of Medicine.

RUPA MONGIA, M.D., is associate program director for the combined medicine-primary care psychiatry residency training program at the UMDNJ--Robert Wood Johnson Medical School, where she serves as a clinical instructor. A graduate of T.N. Medical College, Bombay, India, she completed a residency in internal medicine and a fellowship in geriatric medicine at UMDNJ--Robert Wood Johnson Medical School, based at St. Peters Medical Center, New Brunswick, N.J.

Address correspondence to John M. Heath, M.D., Department of Family Medicine, 1 Robert Wood Johnson Place, MEB 288, New Brunswick, NJ 08903. Reprints are not available from the authors.

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