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* * * * The development of empyema has been described as triphasic.[1,2] Empyema begins with an exudate as the pleura secretes protein-rich fluid in response to contamination. During this phase, the lung remains mobile within the fluid. The second phase, known as the fibrinopurulent phase, is characterized by the accumulation of large quantities of frank pus and fibrin. Fibrin deposition produces a thick pleural peel, which restricts the normal expansion of the lung and creates septa, causing loculation and entrapment. During this phase, the pleural fluid, pH, and glucose levels fall. During the third phase, called the organizing phase, the fibrous peel thickens and contracts, further restricting the movement and expansion of the lung. Pathophysiology Pleural effusions are nutritionally rich culture media with poor white blood corpuscles (WBC) defenses. The pleural space is normally sterile but readily colonized once pleural fluid is accumulated(5). Para-pneumonic effusions that occur in first 48-72 hours are small, sterile polymorphonuclear leucocytes (PMNS) predominant exudate with pleural fluid pH more than 7.30, glucose more than 60 mg/dl and LDH less than 500 IU/L (25-28). If pneumonia remains untreated, the amount of pleural fluid increases with time due to endothelial injury, increased localized permeability and edema. Bacteria invade pleural space and become persistent(29). Then comes fibrinopurulent phase characterized by an increased number of PMNS, a fall in pleural fluid pH and glucose with an increase in the pleural fluid LDH. The pleural fluid/serum glucose ratio decreases to less than 0.5 and the absolute concentration of glucose is usually less than 40 mg/dl because of increased glycolysis due to PMNS phago-cytosis and bacterial metabolism(30). As the end products of glucose metabolism, lactic acid and CO2 accumulate in the pleural space, the pH falls below 7.10 and the level of LDH increases above 1000 IU/L due to cell lysis. During this phase, ple
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