Despite being studied for over 100 years, the physiology of pleural fluid formation and absorption is still controversial. The most recent accepted model of pleural fluid exchange in the normal state involves formation by filtration through the pleural microvas-cular endothelium and absorption via stomata in the parietal pleura that drain into subpleural lymphatic vessels. The formation of fluid is powered by the pressure gradient between the microvasculature and pleural space, while absorption is aided by respiratory motion. There is a continuous exchange of water and low-molecular-weight solute across both visceral and parietal pleura, but this is not believed to lead to net fluid absorption.
Since the microvascular endothelium is semiper-meable, the protein content of the pleural fluid is lower than in the serum. Both albumin and the globulin fraction in the pleural fluid are believed to originate from the serum via diffusion;’ however, some protein can form within the pleural space, such as LDH from pleural fluid leukocytes. The proteins are also cleared via the subpleural lymphatic vessels.
In the abnormal state, pleural fluid can collect for a number of reasons, which lead to increased fluid formation, decreased fluid absorption, or both. Tran-sudative causes for effusion usually occur with an intact microvascular endothelium, and therefore the gradient between serum and fluid protein is maintained.