Exudative Pleural Effusion: Approach to Management

The normal pleural space contains approximately 1 ml of fluid. Pleural fluid is filtered in the parietal pleural compartment from the systemic capillaries down a small pressure gradient into the pleural space. Pleural fluid secretion is greatest at the apex while absorption is maximum towards the diaphragm and mediastinum, where the parietal lymphatics are concentrated. The fluid is drained out predominantly through the stomata of the parietal lymphatics lying between the parietal mesothelial cells. These stomata merge into small lymphatic channels which, in turn, form larger vessels ultimately drain into the mediastinal lymph nodes. The parietal stomata possess valve-like structures to guarantee a unidirectional flow of fluid out of the pleural space1. The lymphatic drainage system can cope with up to several hundred milliliters of additional fluid per day without the development of an effusion. Therefore any pleural effusion represents a severe imbalance of pleural fluid formation and/or drainage capacity. In case of congestive heart failure, even a small pleural effusion signals a severe pulmonary fluid overload. The visceral pleura does not play a significant role in pleural fluid turnover. One implication of pleural fluid dynamics is that, despite statements to the contrary, effusions in CCF do not indicate right heart failure. It is actually a function of elevated pulmonary capillary wedge pressures rather than to pulmonary artery or right heart pressures2. This is due to left ventricular dysfunction with pathological flow of interstitial pulmonary fluid into the pleural space across the visceral side. In animal models of cardiogenic pulmonary edema, it has been shown that up to 25% of the edema fluid flows via the visceral pleura into the pleural space. Therapeutic centesis hence has a role in CCF by reducing systemic fluid overload and thus contributing to a decrease in pulmonary capillary pressures.