PATHOPHYSIOLOGY OF PARAPNEUMONIC EFFUSION
IT is important to understand the pathophysiology of parapneumonic effusions. It is to prevent the complications associated with the organization of the effusion that determine how we manage parapneumonic effusions. It is not true that an uncomplicated effusion is any more difficult to sterilize than a pneumonia. Antibiotic penetration of the pleural space is very good.
An effusion evolves in
three phase. The initial phase is the accumulation of a small,
sterile effusion caused by the infection contiguous to the pleural space. Fortunately, many parapneumonic effusions do not progress beyond this stage and resolve as the pneumonia resolves.
The second stage occurs if bacteria and polymorphs enter the pleural fluid. The inflammatory response causes fibrin to be deposited along the visceral and parietal pleura that can lead to
loculation. Associated with this inflammation, the LDH rises while the pH and glucose fall.
If the fluid is
not drained, the
third stage will occur. Fibroblasts move in organizing the fluid into a pleural peel, making removal of fluid by a needle impossible. This pleural fluid will encase or trap the lung permanently impairing its ability to function. If the effusion is still infected, it will act as an
abscess. It then can drain through the chest wall, or disastrously into a bronchus forming a life threatening
broncho-pleural fistula.
If an effusion is noticed with a pneumonia, a lateral decubitus should be ordered as soon as possible. If it forms a layer greater than 10 ml in depth, a thoracentesis should be done on an urgent basis before the fluid has a chance to organize. The fluid should always be sent for glucose, LDH, total protein, pH, cell count, culture and gram stain. The pH can be obtained by sending the fluid to the lab in an arterial blood kit. If clinically warranted, fluid can be sent for amylase, TB, fungus and cytology.
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