Most empyemas develop from an underlying pulmonary infection and are thought to be secondary to subclinical aspiration of organisms in the dependent portions of the affected lung.15 Alcohol abuse is a recognized risk factor for pleural empyema, primarily because of the increased incidence of aspiration pneumonia. 17 Klebsiella pneumoniae empyema may occur in alcoholic males with multiple host defense defects that impair containment of or perception of disease until it is well advanced. 18 Immunocompromised patients are prone to pleural involvement with fungal or aerobic gram-negative bacillary infection. In patients with a malignancy, fungal or tuberculous foci may be reactivated, and empyema develops. Fungal or mycobacterial empyema may also develop in transplant recipients and patients with AIDS. The most common organisms in healthy adults, children, or patients who have had chest trauma or surgery include Streptococcus pneumoniae and Streptococcus pyogenes.1 l8 Other bacterial isolates include gram-negative aerobic bacilli in hospitalized patients and anaerobes such as fusiform bacilli, Bacteroides, anaerobic Streptococcus, and Clostridium species.
Pleural empyema represents a continuum of disease ranging from thin pleural fluid microscopically contaminated by organisms to gross pus in the pleural space. Approximately 20 to 30 percent of patients with bacterial pneumonia develop a radiographically apparent pleural effusion. 11 The stages of a parapneumonic empyema are exudative, fibrinopurulent, and organizing. In the early phase, the effusion is thin, watery, and easily drained by thoracostomy. In the exudative and intermediate fibrinopurulent stages, the lung retains its compliance and capacity to fully expand. As infection progresses, the initially serous fluid becomes thick and purulent with organisms, fibrin, and white blood cells. In the fibrinopurulent stage, the deposition of fibrin on the parietal pleura retards the resorption of blood, preventing access to lymphatics and retarding fluid resorption.19 Fibrin deposition in the presence of bacteria provides an ideal environment for the development of pleural empyema. Over a period of 4 to 6 weeks after the start of an empyema, the fibrin layer becomes organized and forms a thick peel (the thickened pleura that develops around a pleural empyema) in the chronic organizing phase.16 Early management of empyema may prevent the progression of this process to the more advanced stages, where multiple loculations and scarring complicate drainage.
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