Classification of chronic airflow obstruction may be based on the site of the obstructing lesions. It is seldom that only one type of lesion is present, but one may often dominate. In chronic bronchitis, the major disease of large airways, chronic mucus hypersecretion, is reflected by an increase in size of bronchial mucous glands. This may be a factor in airway narrowing, especially with coexisting edema of the airway wall. Excess intralumenal mucus compounds the obstruction. Increased airways reactivity is present in 15 to 70 percent of patients with chronic airflow obstruction. Increased airway muscle and cartilage atrophy are features of chronic bronchitis, but the association of increased muscle with increased airway reactivity is poor. Inflammation of the small airways (bronchiolitis) is a significant complication for cigarette smokers and is an important cause of mild chronic airflow obstruction. Goblet cell metaplasia is a reflection of chronic small airways inflammation and, together with intralumenal mucus, is an important feature. Permanent narrowing of the small airways presumably results from inflammation with consequent fibrosis, while functional narrowing results from release of mediators of inflammation. Increased muscle mass is present in some cases. Distortion and irregularity of small airways related to emphysema are major factors in severe obstruction. Lesser degrees of emphysema may be associated with a diminished number of alveolar attachments and mild chronic airflow obstruction. Emphysema, the dominant lesion in patients with severe chronic airflow obstruction, results from parenchymal lesions. Centrilobular emphysema, in which the respiratory bronchioles are selectively or dominantly involved, is the most common form.(ABSTRACT TRUNCATED AT 250 WORDS)

Medical views in the United States on the effects of smoking have shifted dramatically since the published evidence in 1958 established the link between smoking and fatal disease. Today's physician should be a nonsmoking role model, whose workplace both directly and indirectly teaches smoking cessation skills. Publications on smoking cessation techniques from the National Institutes of Health along with intervention tools such as patient smoking history questionnaires are available free of charge to physicians. Patient histories are critical to the intervention process, for they provide essential clues and information about which stage in cessation of smoking the patient has already reached: precontemplation, contemplation, action, and maintenance. Different approaches and techniques are required at each stage. The most important objective for the physician with a patient at the stage of contemplating quitting is to initiate a conversation leading to a directive to quit, with benefits of quitting stressed as reinforcement. Actively motivated patients committed to quit dates may need both educational and pharmacologic support; issues such as nicotine dependence and withdrawal symptoms must be addressed. Pharmacologic therapy at this time may consist of substitution of nicotine-containing gum (nicotine polacrilex) for cigarettes. Used in sufficient, regular dosages, the nicotine gum has been found to help diminish withdrawal symptoms following smoking cessation. Other drug therapies are currently under study. For now, nicotine replacement therapy (where indicated) is to be used for at least three months, the period of greatest chance of relapse. The physician should continue to encourage patients who have quit smoking to forestall relapses, while tacitly understanding that the incidence of relapse is high in first-time quitters. Hospital inpatients provide an opportunity to initiate bedside smoking cessation programs. The hope is that, in the future, hospitals will involve the entire health team in comprehensive smoking cessation programs.

Chronic obstructive pulmonary disease (COPD) is extremely common; all primary care physicians should be able to manage this disorder. Probably 30 million Americans are afflicted with some stage of the disease. Assessment of COPD is based on symptoms and simple spirometric measurements that primary care physicians can perform in their offices. Early identification and intervention are vital to controlling COPD. Smoking cessation is most important. Aggressive pharmacologic therapy is also required. Bronchoactive drugs are more successful in improving airflow in patients in early stages of the disease than those with more advanced stages. The National Mucolytic Study Investigators' Meeting, focusing on the usage of iodinated glycerol (Organidin) in patients with moderate-to-advanced airflow obstruction from chronic bronchitis, has concluded that symptoms of the disease were improved in treated patients compared with patients receiving placebo. These results, based on a major double-blind, controlled clinical trial, will usher in a new approach to the treatment of patients with mucus clearance problems. It is now time to develop a nationwide strategy for involving all primary care physicians in the identification and treatment of patients with COPD.

The fifth leading cause of death in the United States, chronic obstructive respiratory conditions, cannot be cured but can be considerably ameliorated by appropriate management. Many patients with COPD have a combination of chronic bronchitis, asthma, and emphysema. While the damage due to emphysema is permanent, many of the pathophysiologic changes of asthma and bronchitis can be reversed to some extent, and such reversal should be a goal of therapy. Smoking cessation will help the patient more than any other medical treatment. Bronchodilator therapy is best given by inhalation from a metered dose inhaler and on a maintenance basis. Be sure to check inhaler technique. An anticholinergic agent, eg, ipratropium bromide, is probably most effective, but many patients prefer a beta 2-selective adrenergic agent. Xanthines are currently third choice but are very useful to cover nocturnal dyspnea. Corticosteroids are usually only used in acute exacerbations and then only for short courses. If prolonged use is required, however, the inhalation route minimizes side effects to which these patients are particularly prone. Antibiotics are also usually only used in exacerbations, but one can be liberal with them. Use the less expensive broad-spectrum options for ten days. Some clinicians believe that hydration is an effective expectorant. Mucolytic therapy is extensively used outside the United States. The appropriate role of mucolytic therapy in the treatment of bronchitis remains to be more fully explored. Low-flow oxygen is only used in the prevention or treatment of cor pulmonale when the PaO2 is persistently at or below 55, or with a rising hematocrit and right-sided cardiac changes. If used, oxygen is helpful only when given long term for at least 18 h per day, not on a prn basis. Cardiac glycosides are probably of little benefit, but diuretics have an important role in treatment of fluid retention. Pulmonary vasodilator therapy is still experimental, as is almitrine. Prophylaxis with pneumococcal vaccine and annual influenza vaccine is rational but has not been proven to be of value. Exercise and activity should be encouraged for all except those with frank congestive heart failure. The role of "breathing exercises" is currently being reevaluated. Surgery has almost no place in the management of COPD. Anesthesia often results in postoperative complications in this disease. Avoid all sedatives and tranquilizers.

If one includes all types of chronic generalized airways obstruction under the heading of "COPD," diagnosis of this condition requires only the demonstration of an obstructive ventilatory impairment on spirometric testing that persists despite maximum medical therapy. However, as generally used, the term COPD implies that upper airways obstruction and "specific" lung diseases that can produce an obstructive type of physiologic abnormality have been excluded. Examples of these exclusions include silicosis, sarcoidosis, and even advanced tuberculous disease. It is more difficult to determine the type of disease that is causing the chronic airways obstruction in patients with COPD as defined above. A severe and persistent form of asthma, sometimes called "chronic asthmatic bronchitis," can mimic the typical emphysematous form of COPD that is characteristic of heavy cigarette smokers. Since these types of chronic airflow obstruction differ in regard to their clinical courses, prognoses, and treatments, their distinction is clinically important. One should not be discouraged by the fact that some patients appear to have a mixed type of disorder. Features that help differentiate the various forms of chronic airways obstruction are described in this report, and recommendations are offered to help guide the practitioner in the workup indicated for patients thought to have any type of chronic airways obstruction. It is also emphasized that patients vary markedly in regard to the relative importance of readily reversible bronchospasm, airways inflammation, and mucus hypersecretion in producing their disability. Assessment of these factors is critical in determining clinical management.

Chronic bronchitis is characterized by mucociliary dysfunction resulting from structural and functional defects of cilia and the secretory apparatus. The combination of hypersecretion and ciliary impairment leads to disruption of mucociliary interaction and hence the accumulation of secretions in the lower airways. Cigarette smoke appears to play a critical role in the pathogenesis of chronic bronchitis-associated mucociliary dysfunction. While the excessive lower airway secretions may have only minor effects on the natural course of airflow obstruction, they could transiently compromise airway function during acute exacerbations. In addition, altered aerosol deposition in the airways resulting from excessive airway secretions could influence the airway responses to inhaled irritants and pharmacologic agents. There are currently no direct, non-invasive methods available to assess the quantity and distribution of airway secretions in vivo. Indirect indices such as cough frequency, sputum volume, respiratory function, and mucociliary clearance are nonspecific and subject to misinterpretation. The clinical utility of mucotropic pharmacologic agents and of physical maneuvers directed at removing excessive lower airway secretions is therefore difficult to evaluate objectively.

Sclerosing mediastinitis is an uncommon disease associated with a multiplicity of clinical syndromes. The cause of this disorder is probably an abnormal fibroproliferative response to an inflammatory stimulus, most commonly a granulomatous infection secondary to Histoplasma capsulatum. The pathophysiology of this disease is predicated on the encasement of mediastinal vital organ structures within a dense fibrotic mass. This mass appears to emanate from an invasive chronic inflammatory process causing erosion as well as external compression of these structures. The following case reports illustrate the diversity of this disease entity, representing a patient population from the Ohio River Valley, endemic for histoplasmosis. The purpose of this report is to elucidate the various clinical manifestations of sclerosing mediastinitis and to correlate the pathologic process with a rational approach to treatment.

Flexible bronchoscopy is an important diagnostic technique for study of pediatric patients with pulmonary problems. Many pitfalls await the unwary, but with experience and care, most can be overcome or circumvented.

We conducted retrospective chart and literature reviews to analyze the frequency and spectrum of causes of asymptomatic pleural effusion (APE). In our series, 16 percent of patients undergoing thoracentesis for PE were asymptomatic and the spectrum of causes was similar to that for symptomatic patients. Asymptomatic PEs were evenly distributed among transudates, exudates and indeterminate effusions. More symptomatic (S) PE were exudates, although the difference was not statistically significant (p greater than 0.1). In comparison to SPE, APE were more often free flowing and small. In both groups, the four most common diagnoses were malignancy, CHF, parapneumonic and postoperative effusions accounting for greater than 70 percent of each group. Review of the literature demonstrated the following associations with APE: recent childbirth or abdominal surgery, benign asbestos effusion, uremia, malignancy, and tuberculosis. In the uncomplicated postpartum or postoperative setting or in patients with typical findings of left ventricular failure, observation without diagnostic studies is appropriate. In all other situations, APE should be evaluated in traditional fashion. If thoracentesis is non-diagnostic and the effusion is an exudate, closed pleural biopsy and less often, fiberoptic bronchoscopy, should follow. Once malignant or granulomatous pleuritis has been excluded, it may be appropriate to observe for a period of time before proceeding to more invasive procedures.

Carbon monoxide poisoning is a major cause of illness and death in the United States. Most cases result from exposure to the internal combustion engine and to stoves burning fossil fuels. Most cases of accidental exposure are preventable if proper precautions are taken; however, when cases arise, their presenting signs and symptoms are nonspecific and often lead to a misdiagnosis resembling a flu-like viral illness. As a result, the incidence of acute CO poisoning is underestimated. The effects of CO poisoning are due to tissue hypoxia, with the CNS and the heart being the most susceptible target organs due to their high oxygen needs. Prolonged hypoxia due to high CO levels may lead to cardiac arrhythmias or arrest (or both) and a variety of neurologic sequelae. Treatment is directed toward the relief of tissue hypoxia and the removal of CO from the body. Severity of poisoning can be divided into three levels based on CO levels in the blood. Administration of normobaric 100 percent oxygen is the therapy of choice for most cases, while hyperbaric oxygen therapy is reserved for severe poisonings.

This review has examined the possible role of CMI in providing protection against three pathogens that can be opportunists in the lung. Monoclonal antibodies that identify the cellular components of the immune response and recombinant cytokines are important tools to better understand how pulmonary immunity is regulated. Although not discussed in detail, recombinant microbial antigens are useful for understanding various aspects of protective immunity and immunosuppression as well as for advancing vaccine development. There are important problems to address in order to continue steady progress in understanding pulmonary defenses, including some of those mentioned in this brief review. There should be an increased use of infectious models that more closely mimic naturally occurring infections, and comparisons should be made between results obtained with parenteral versus intrapulmonary routes of infection.