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P leural infection associated with pneumonia is a potentially lethal disease afflicting more than 60,000 patients annually in the United States. The incidence continues to rise, and the mortality rate exceeds that of myocardial infarction. Five thousand years ago, the Egyptian physician Imhotep first described pleural space disease,4 and Hippocrates in 400 BC was credited for recognizing that prompt drainage of the infected pleural space is essential.5 When these infections become loculated, they are no longer amenable to tube thoracostomy and operative decortication is required. To understand the pathophysiology of a complicated parapneumonic effusion, it is instructive to review the anatomy of the pleural and cytologic players maintaining homeostasis in this unique space. The pleural cavity arises from the coelom that also forms the pericardium and peritoneum. The pleural cavity is lined by mesothelial cells surrounded by a layer of connective tissue, macula cribiformis, which is then encased in two layers of elastic tissue. Visceral mesothelium is intricately connected to the lung parenchyma, whereas the parietal layer is more loosely connected to the thoracic structures separated by a variable fatty layer. The parietal pleura has specialized areas known as stoma, and an extensive lymphatic network exists below which is the predominant route of fluid resorption. Under normal conditions, it is estimated that each pleural cavity generates 0.2 to 0.4 mL/kg per hour. The fluid originates predominantly from the parietal capillaries because of hydrostatic pressure, augmented by the negative pressure of the pleural space. Less fluid is produced by the visceral pleura because the hydrostatic pressure is attenuated by pulmonary venous drainage. However, the visceral surface will add more pleural fluid with increased pulmonary interstitial pressure. The capacity for pleural fluid absorption is thought to exceed 500 mL of fluid from each cavity with an intact lymphatic system. Thus, the net accumulation of pleural fluid is the result of a dynamic system of fluid production and absorption. Recent ultrasound studies of healthy individuals suggest that less than 4 mm of dependent pleural fluid should be considered normal. Complicated parapneumonic effusions, and ultimately empyemas, develop in three conceptual phases. The early phase is a sterile effusion caused by parenchymal inflammation that activates mesothelial cells and enhances capillary permeability, termed exudative (days 2Y5). This is thought to be driven by proinflammatory cytokines, including interleukin 8 and tumor necrosis factor->.8 Ultimately, the volume of fluid traversing into the pleural cavity exceeds the capacity to reabsorb the fluid and an effusion develops. The second phase is termed fibropurulent, which is initiated by bacterial infection (days 5Y10). At this point, the immune system is activated and the once hypocoagulable environment is changed dramatically. Bacterial and neutrophil activity acidify the fluid, consume glucose, increase protein content, and release lactate dehydrogenase (LDH) from cellular apoptosis and necrosis. The environment now becomes hypercoagulable because of the integrated responses of the innate immune and coagulation systems. These findings are directly relevant to the evolution of complicated effusions because the exuberant fibrin deposition is a concerted effort to control progressive infection. The final state of a complicated effusion is referred to as the organization phase (days 10Y21). Fibroblasts migrate into the pleural space and create a dense fibrotic lining of the visceral and parietal surfaces. This phase is thought to be driven by regenerative cytokines, for example, transforming growth factor-A and platelet-derived growth factor released primarily from activated mesothelial cells. The net result is a progressive rind that encases the lung, reducing ventilatory capacity and sequestering bacteria. The objective of this management algorithm for parapneumonic fluid collections (Fig. 1) is to outline cost-effective diagnostic and therapeutic interventions in the surgical intensive care unit (SICU) based on the pathologic state of the pleural cavity. These guidelines are derived from the published experience with adult populations, but conceptually, the same principles apply to the pediatric age group.17Y20

Western Trauma Association Critical Decisions in Trauma