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Epitomes Important Advances in Clinical Medicine
Chest Diseases The Council on Scientific Affairs of the California Medical Association presents the following inventory of items ofprogress in chest diseases. Each item, in the judgment of a panel of knowledgeable physicians, has recently become reasonably firmly established, both as to scientific fact and important clinical significance. The items are presented in simple epitome, and an authoritative reference, both to the item itself and to the subject as a whole, is generally given for those who may be unfamiliar with a particular item. The purpose is to assist busy practitioners, students, researchers, or scholars to stay abreast of these items ofprogress in chest diseases that have recently achieved a substantial degree ofauthoritative acceptance, whether in their own field of special interest or another. The items ofprogress listed below were selected by the Advisory Panel to the Section on Chest Diseases of the California Medical Association, and the summaries were prepared under its direction. Reprint requests to Division of Scientific and Educational Activities, California Medical Association, PO Box 7690, San Francisco, CA 94120-7690
Occupational Asthma WHILE THE OVERALL prevalence of occupational asthma is unknown, it is estimated that from 5% to 15% of all cases of asthma in workers is attributable to workplace exposures. Occupational asthma can be defined as a variable airflow limitation caused by a specific agent in the workplace. Variable and sometimes chronic airflow limitation can result from sensitization to, pharmacologic effects of, recurrent inflammation from, or direct irritation by agents in the workplace. The treatment of occupational asthma may differ depending on its cause. The cornerstone of management is early diagnosis and identification of the offending agent, but diagnosis is not easy and often involves the investigation of exposure conditions at the workplace combined with an objective confirmation of exposure-related changes in lung function. It is a common misconception that occupational asthma caused by a worker's sensitivity to a specific agent-for example, toluene diisocyanate or laboratory animal proteinresolves after the worker is removed from further exposure to that agent. Although occupational asthma often resolves with this intervention, the results of several longitudinal studies indicate that most persons continue to have some degree of persistent asthma years after removal from exposure. Factors associated with a more favorable result are a short duration of symptoms before diagnosis and relatively normal lung function and mild, nonspecific airway hyperresponsiveness at diagnosis. Early diagnosis and removal from exposure may prevent or lessen persistent asthma and the resulting impairment or disability. Workers who continue in jobs that expose them to an agent to which they are sensitized tend to have increased respiratory symptoms, a progressive loss of ventilatory function, and increased airway responsiveness. This deterioration may occur despite suppressing symptoms with medication or reducing the intensity of exposure by using respiratory protective gear. Several deaths have been reported among workers with isocyanate-induced asthma who continued to work in jobs that involved exposure to that agent. Some patients with occupational asthma cannot change jobs because of financial constraints. In such cases, vigorous
efforts to reduce exposure to the lowest possible level are required. Product substitution, enclosure of specific work processes, and improved ventilation are preferable to the use of respirators, which are cumbersome, uncomfortable, and may leak. If respirators are to be used, however, patients must be medically certified, fit-tested, and properly trained to wear them. Careful monitoring can help assess the eff ctiveness of interventions to reduce exposure. Serial meas rements of peak expiratory flow rates can document a y recurrent subclinical bronchospasm, and serial methacl oline challenge can assess whether the level of airway re sponsiveness is increasing. Patients with evidence of bronc] iospasm or an accelerated annual rate of decline in ventilatc ry function should be strongly encouraged to change jobs. Drug therapy for occupational asthma is the same as that f r persons with nonoccupational asthma, but treatment with d gs cannot substitute for eliminating exposure. JOHN R. BALMES, MD San Francisco, California
REFERENCES Balmes JR: Surveillance for occupational asthma. Occup Med 1991; 6:101-1 10 Chan-Yeung M: Occupational asthma. Chest 1990; 98(suppl): 148S- 161S Fabbri LM, Danieli D, Crescioli S, et al: Fatal asthma in a subject sensitized to t luene diisocyanate. Am Rev Respir Dis 1988; 137:1494-1498 Hudson P, Cartier A, Pineau L, et al: Follow-up of occupational asthma caused by c 2b and various agents. J Allergy Clin Immunol 1985; 76:682-688
ntibiotics for Pneumonia CUTE PULMONARY INFECIION continues to cause substantial morbidity and mortality even in immunocompetent patients. Although a sputum Gram's stain may be immediately available and, if of good quality and showing a predominant organism, may help focus therapy, rapid and definitive identification of the specific etiologic agent(s) responsible for a pneumonia is often difficult. For these reasons, empiric antibiotic therapy is usually instituted concurrent with attempts at diagnosis. Epidemiologic factors are helpful in choosing a reasonable regimen. A recent multicenter study of patients admitted for com-
munity-acquired pneumonia to a private community hospital, a university hospital, and a Department of Veterans Affairs hospital reported the four most common etiologic
Epitomes Important Advances in Clinical Medicine
Chest Diseases The Council on Scientific Affairs of the California Medical Association presents the following inventory of items ofprogress in chest diseases. Each item, in the judgment of a panel of knowledgeable physicians, has recently become reasonably firmly established, both as to scientific fact and important clinical significance. The items are presented in simple epitome, and an authoritative reference, both to the item itself and to the subject as a whole, is generally given for those who may be unfamiliar with a particular item. The purpose is to assist busy practitioners, students, researchers, or scholars to stay abreast of these items ofprogress in chest diseases that have recently achieved a substantial degree ofauthoritative acceptance, whether in their own field of special interest or another. The items ofprogress listed below were selected by the Advisory Panel to the Section on Chest Diseases of the California Medical Association, and the summaries were prepared under its direction. Reprint requests to Division of Scientific and Educational Activities, California Medical Association, PO Box 7690, San Francisco, CA 94120-7690
Occupational Asthma WHILE THE OVERALL prevalence of occupational asthma is unknown, it is estimated that from 5% to 15% of all cases of asthma in workers is attributable to workplace exposures. Occupational asthma can be defined as a variable airflow limitation caused by a specific agent in the workplace. Variable and sometimes chronic airflow limitation can result from sensitization to, pharmacologic effects of, recurrent inflammation from, or direct irritation by agents in the workplace. The treatment of occupational asthma may differ depending on its cause. The cornerstone of management is early diagnosis and identification of the offending agent, but diagnosis is not easy and often involves the investigation of exposure conditions at the workplace combined with an objective confirmation of exposure-related changes in lung function. It is a common misconception that occupational asthma caused by a worker's sensitivity to a specific agent-for example, toluene diisocyanate or laboratory animal proteinresolves after the worker is removed from further exposure to that agent. Although occupational asthma often resolves with this intervention, the results of several longitudinal studies indicate that most persons continue to have some degree of persistent asthma years after removal from exposure. Factors associated with a more favorable result are a short duration of symptoms before diagnosis and relatively normal lung function and mild, nonspecific airway hyperresponsiveness at diagnosis. Early diagnosis and removal from exposure may prevent or lessen persistent asthma and the resulting impairment or disability. Workers who continue in jobs that expose them to an agent to which they are sensitized tend to have increased respiratory symptoms, a progressive loss of ventilatory function, and increased airway responsiveness. This deterioration may occur despite suppressing symptoms with medication or reducing the intensity of exposure by using respiratory protective gear. Several deaths have been reported among workers with isocyanate-induced asthma who continued to work in jobs that involved exposure to that agent. Some patients with occupational asthma cannot change jobs because of financial constraints. In such cases, vigorous
efforts to reduce exposure to the lowest possible level are required. Product substitution, enclosure of specific work processes, and improved ventilation are preferable to the use of respirators, which are cumbersome, uncomfortable, and may leak. If respirators are to be used, however, patients must be medically certified, fit-tested, and properly trained to wear them. Careful monitoring can help assess the eff ctiveness of interventions to reduce exposure. Serial meas rements of peak expiratory flow rates can document a y recurrent subclinical bronchospasm, and serial methacl oline challenge can assess whether the level of airway re sponsiveness is increasing. Patients with evidence of bronc] iospasm or an accelerated annual rate of decline in ventilatc ry function should be strongly encouraged to change jobs. Drug therapy for occupational asthma is the same as that f r persons with nonoccupational asthma, but treatment with d gs cannot substitute for eliminating exposure. JOHN R. BALMES, MD San Francisco, California
REFERENCES Balmes JR: Surveillance for occupational asthma. Occup Med 1991; 6:101-1 10 Chan-Yeung M: Occupational asthma. Chest 1990; 98(suppl): 148S- 161S Fabbri LM, Danieli D, Crescioli S, et al: Fatal asthma in a subject sensitized to t luene diisocyanate. Am Rev Respir Dis 1988; 137:1494-1498 Hudson P, Cartier A, Pineau L, et al: Follow-up of occupational asthma caused by c 2b and various agents. J Allergy Clin Immunol 1985; 76:682-688
ntibiotics for Pneumonia CUTE PULMONARY INFECIION continues to cause substantial morbidity and mortality even in immunocompetent patients. Although a sputum Gram's stain may be immediately available and, if of good quality and showing a predominant organism, may help focus therapy, rapid and definitive identification of the specific etiologic agent(s) responsible for a pneumonia is often difficult. For these reasons, empiric antibiotic therapy is usually instituted concurrent with attempts at diagnosis. Epidemiologic factors are helpful in choosing a reasonable regimen. A recent multicenter study of patients admitted for com-
munity-acquired pneumonia to a private community hospital, a university hospital, and a Department of Veterans Affairs hospital reported the four most common etiologic
