Outpatient management of chronic bronchitis in the elderly

Author: John M. Health
Date: Oct, 1993

Chronic bronchitis as a manifestation of obstructive pulmonary disease is a significant cause of morbidity, especially in the elderly. Functional impairments of mobility and communication may result from the associated breathlessness and copious respiratory secretions that are produced in chronic bronchitis. Frequent hospitalizations for respiratory failure are not uncommon. This article reviews the pathophysiologic aspects of chronic bronchitis and discusses outpatient management strategies for patients with this illness.


Chronic obstructive lung disease causes 8 percent of all deaths in the United States and is second only to arthritis as the leading cause of long-term disability and functional impairment.[1,2] The three principal manifestations of chronic obstructive lung disease are chronic bronchitis, emphysema and asthma. Because these conditions have a number of overlapping features, both the epidemiologic classification and the clinical picture of adult-onset chronic airway disease can become quite complicated. The salient features of emphysema and chronic bronchitis are compared in Table 1.[3]


The diagnosis of chronic bronchitis requires the occurrence during the preceding two years of at least two separate three-month episodes of daily coughing in association with the significant production of tracheobronchial secretions.[4] The minimum three-month duration of daily coughing episodes over two years distinguishes chronic bronchitis from other acute, isolated episodes of upper or lower airway infection.

The vast majority of patients with chronic bronchitis are men. However, the incidence of this disease is rapidly increasing in women.[1]


The characteristic pathologic features of chronic bronchitis are hyperplasia and hypertrophy of the mucus-secreting goblet cell glands and the upper- and mid-level bronchi. These anatomic airway changes can be quantified pathologically by measurement of goblet cell density, and they are distinct from the smooth muscle changes that occur in asthma and the alveolar changes that occur in emphysema.[5]

Exposure to tobacco smoke is a common causal factor in most forms of obstructive lung disease, including chronic bronchitis. The relative risk for chronic bronchitis in smokers versus nonsmokers is 8.8 for men and 5.9 for women.[2] In a British study of respiratory symptoms,[6] 80 percent of the male subjects who reported symptoms of chronic bronchitis were tobacco smokers.

The association between chronic bronchitis and tobacco smoke exposure, either directly or by secondhand smoke inhalation, is so strong that it has been difficult to study associations with other inhaled irritants. However, occupational silica exposure and the inhalation of sulfur dioxide and other respiratory irritant components of urban air pollution can certainly worsen the symptoms of chronic bronchitis.[7]

Physiologic Basis of Clinical Symptoms

Airway mucus hypersecretion in chronic bronchitis occurs as a result of a variety of physiologic mechanisms. Among these are decreased levels of lymphocyte-derived salivary immunoglobulin A, glycoprotein and salivary lysoenzyme. At reduced levels, these substances are less able to inhibit the attachment of bacteria to respiratory epithelial cells.[8] Chronic exposure of respiratory tract cilia to tobacco smoke has consistently been found to produce impaired frequency and strength of respiratory clearing; consequently, the airway defenses against infection are decreased.[9]

For the older patient with chronic bronchitis, these changes compound the physiologic decreases in the reserve capacity of the aging lung. Forcefulness of cough declines with aging, as does the viscosity of upper respiratory secretions, although these age-related changes rarely cause symptoms by themselves.[10] Because of the reduction in reserve capacity, symptoms are likely to be more severe in older patients with chronic bronchitis than in younger patients with the same condition.

Patients with chronic bronchitis also demonstrate systemic changes, such as a hypermetabolic rate with higher circulating norepinephrine levels and reduced visceral protein levels.[11] Circulatory changes include elevated right-sided heard pressures due to increased pulmonary vascular resistance. The chronic state of relative hypoxia, which worsens during periods of respiratory failure or acute infection, may also contribute to pulmonary hypertension and secondary cardiac dysfunction.

The clinical picture resulting from these cumulative changes is that of the "blue bloater" - a sedentary, cyanotic, edematous, breathless patient. This situation is often a result of the coexistence of chronic bronchitis and one or more other smoking-related illnesses, such as coronary artery disease, cerebrovascular disease or peripheral vascular occlusive disease. Secondary muscular and cardiovascular deconditioning can lead to additional functional impairment.


The infectious agents commonly isolated in chronic bronchitis are listed in Table 2,[12] along with their primary and alternative treatments. However, the role of active infection versus airway colonization by these organisms in the clinical course of chronic bronchitis is not clear.


Although bacterial colonization has been generally thought to be asymptomatic, it may increase the production of airway secretions. The bacterial agents most consistently isolated from patients with chronic bronchitis during highly symptomatic periods are Haemophilus influenzae, Streptococcus pneumoniae, Moraxella catarrhalis and Haemophilus parainfluenzae. However, these organisms are also commonly found as colonization flora during asymptomatic periods.

One British study[13] examined acute episodes of bronchitis that were treated with antibiotics selected on the basis of the results of initial sputum culture sensitivities. The study found that while patients did improve with antimicrobial therapy, the incidence of colonization with gram-negative bacteria, such as Klebsiella, Pseudomonas and Enterobacteriaceae species, was higher following treatment.

In one rigorous microbiologic study[14] of severely ill intubated patients with chronic bronchitis, cultures were obtained by bronchoscopy, using a protected tip to avoid contamination. The investigators found that in one half of the patients, no single respiratory pathogen was present where the most acute airway inflammation was seen. This finding suggests that pathogenic bacteria may not always be present at the level of acute airway inflammation during acute, severe exacerbations of chronic bronchitis.


Outpatient management of chronic bronchitis patients requires that attention be given in five areas: preventive care, antimicrobial therapy, airway management, supplemental oxygen delivery and supportive measures.


Cessation of smoking is perhaps the most important aspect of preventive care in patients with chronic bronchitis. After patients have quit smoking, an improvement in disabling airway symptoms will become apparent over time. Since it can be especially difficult to persuade older patients with chronic bronchitis to stop smoking, the physician may need to schedule appointments to deal specifically with this issue.

Preventive efforts should also be include immunization with the pneumococcal vaccine and annual administration of influenza vaccine. The tuberculosis exposure status of patients should be clarified, using a two-step intradermal skin testing procedure, early in their care because of the potential reactivation of old tuberculosis by future corticosteroid therapy.

Patients with chronic bronchitis should be advised to avoid known sources of respiratory infection and unnecessary exposure to high concentrations of indoor smoke or outdoor air pollution. They also need be aware of the benefits of prompt amantadine (Symmetrel) therapy after influenza exposure.

Chronically ill patients often feel increasingly helpless because of their progressive breathlessness. A frank discussion of their wishes regarding future care, such as the use of mechanical ventilation, enteral feeding systems and cardiopulmonary resuscitation, can help affirm their sense of control and involvement. As part of the discussion, these patients should be encouraged to appoint a health care proxy or durable power of attorney for health care, depending on the applicable state laws for such advance directives.


[1.] Higgins M. Risk factors associated with chronic obstructive lung disease. Ann NY Acad Sci 1991; 624:7-17. [2.] Lee PN, Fry JS, Forey BA. Trends in lung cancer, chronic obstructive lung disease, and emphysema death rates for England and Wales 1941-85 and their relation to trends in cigarette smoking. Thorax 1990;45:657-65. [3.] Wilson JD, et al., eds. Harrison's Principles of internal medicine. 12th ed. New York: McGraw-Hill, Health Professions Division, 1991:1077. [4.] Irwin RS, Curley FJ, French CL. Chronic cough. The spectrum and frequency of causes, key components of the diagnostic evaluation, and outcome of specific therapy. Am Rev Respir Dis 1990;141:640-7. [5.] Lange, P, Nyboe J, Appleyard M, Jensen G, Schnohr P. Relation of ventilatory impairment and of chronic mucus hypersecretion to mortality from obstructive lung disease and from all causes. Thorax 1990; 45:579-85. [6.] Horsley JR, Sterling IJ, Waters WE, Howell JB. Respiratory symptoms among elderly people in the New Forest area as assessed by postal questionnaire. Age Ageing 1991;20:325-31. [7.] Cowie RL, Mabena SK. Silicosis, chronic airflow limitation, and chronic bronchitis in South African gold miners. Am Rev Respir Dis 1990;143:80-4. [8.] Venge P, Rak S, Steinholtz L, Hakansson L, Lindblad G. Neutrophil function in chronic bronchitis Eur Respir J 1991;4:536-43. [9.] Cazzola M, Franco C, Gioia V, Legnani D, Mancini V, Polverino M, et al. Cefaclor in the treatment of infective exacerbations of chronic bronchitis in cigarette smokers. J Chemother 1991;3:245-9. [10.] Rubenstein E, Federman DD, eds. Scientific American medicine. New York: Scientific American, 1978:2-18. [11.] Hofford JM, Milakofsky L, Vogel WH, Sacher RS, Savage GJ, Pell S. The nutritional status in advanced emphysema associated with chronic bronchitis. Am Rev Respir Dis 1990;141(4 Pt 1):902-8. [12.] The choice of antibacterial drugs. Med Lett Drugs Ther 1992;34(871):49-56 [Published errata appear in Med Lett Drugs Ther 1992;34(875):72 and 1992;34 (884):110]. [13.] Trigg CJ, Wilks M, Herdman MJ, Clague JE, Tabaqchali S, Davies RJ. A double-blind comparison of the effects of cefaclor and amoxicillin on respiratory tract and oropharyngeal flora and clinical response in acute exacerbations or bronchitis. Respir Med 1991;85:301-8. [14.] Fagon JY, Chastre J, Trouillet JL, Domart Y, Dombret MC, Bornet M, et al. Characterization of distal bronchial microflora during acute exacerbation of chronic bronchitis. Use of the protected specimen brush technique in 54 mechanically ventilated patients. Am Rev Respir Dis 1990;142:1004-8. [15.] Ruben FL. The prevention of severe lower respiratory infections in chronic bronchitis. Semin Respir Infect 1989;4:261-5. [16.] Weinberger SE. Recent advances in pulmonary medicine. I.N Engl J Med 1993;328:1389-96. [17.] Rock RC. Monitoring therapeutic drug levels in older patients. Geriatrics 1985;40:75-7,80-3,86. [18.] van Schayck CP, Dompeling E, van Herwaarden CL, Folgering H, Verbeek AL, van der Hoogen HJ, et al. Bronchodilator treatment in moderate asthma or chronic bronchitis: continuous or on demand? A randomised controlled study. BMJ 1991;303:1426-31. [19.] Braun SR, McKenzie WN, Copeland C, Knight L, Ellersieck M. A comparison of the effect of ipratropium and albuterol in the treatment of chronic obstructive airway disease. Arch Intern Med 1989;149:544-7 [Published erratum appears in Arch Intern Med 1990;150:1242]. [20.] Ferguson GT, Cherniack RM. Management of chronic obstructive pulmonary disease. N Engl J Med 1993;328:1017-22. [21.] Tamaoki J, Chiyotani A, Kobayashi K, Sakai N, Kanemura T, Takizawa T. Effect of indomethacin on bronchorrhea in patients with chronic bronchitis, diffuse panbronchiolitis, or bronchiectasis. Am Rev Respir Dis 1992;145:548-52. [22.] Pelty TL. Chronic obstructive pulmonary disease. In: Kelley WN, DeVita VT Jr, et al., eds. Textbook of internal medicine. Philadelphia: Lippincott, 1992:1717-22. [23.] Pierson DJ. Respiratory therapy techniques. In: Kelley WN, DeVita VT Jr, et al., eds. Textbook of internal medicine. Philadelphia: Lippincott, 1989: 2009-12. [24.] Tiep BL, Nicotra MB, Carter R, Phillips R, Otsap B. Low-concentration oxygen therapy via a demand oxygen delivery system. Chest 1985;87:636-8.

JOHN H. HEATH, M.D. is an assistant professor in the Department of Family Medicine and the Program in Geriatrics at the State University of New York Health Science Center at Syracuse. He also maintains an active clinical primary care practice, teaches at the Saint Joseph's Hospital Health Center family practice residency program in Syracuse and serves as medical director for an urban nursing home and two home care agencies in the Central New York region. A graduate of the Hahnemann University School of Medicine, Philadelphia, Dr. Health completed a family practice residency at Saint Vincent Health Center in Erie, Pa., and a two-year fellowship in geriatric medicine at the University of Cincinnati.

COPYRIGHT 1993 American Academy of Family PhysiciansCOPYRIGHT 2004 Gale Group

© 2006, DrPlace.com, All Rights Reserved.