Anatomy and pathophysiology

Pleural effusion is a common development with pleural disorders and frequently indicates a significant underlying systemic disease. The parietal and visceral pleura comprise the serous membranes which line the pleural space. These membranes consist of a single layer of mesothelial cells 20 to 40 ^m wide and 0.1 to 0.4 ^m thick. Microvilli, which line the pleural surface, increase the functional surface area tremendously, thereby enhancing membrane transport and decreasing pleural friction. The pleura is composed of two membranes which differ both anatomically and functionally. The visceral pleura lines the lungs, mediastinum, diaphragm, and inner surface of the chest wall. It is thin, elastic, and tightly connected to the lung via fibrous extensions of connective tissue, and it reabsorbs fluid from the pleural space. In contrast, the parietal pleura is a thick membrane loosely attached to the underlying chest wall. Blood supplied by systemic capillaries to the parietal pleura creates a hydrostatic gradient which allows net movement of fluid from the parietal pleura into the pleural space. Oncotic pressures of visceral pleural fluid create the driving force which allows fluid reabsorption from the pleural space to the visceral pleura (as much as 5 to 10 l/day).

Pleural membranes are permeable to gas; however the pleural space remains gas free. This is due to a gradient between the partial pressure of gas in the pleural space and venous blood. Normal partial pressures of venous gas in the parietal pleura are as follows: oxygen, 40 mmHg (5.3 kPa); carbon dioxide, 46 mmHg (6.1 kPa); nitrogen, 673 mmHg (89.7 kPa); water, 47 mmHg (6.3 kPa). The total of these partial pressures (706 mmHg (94.1 kPa)) is approximately 50 mmHg (6.7 kPa) less than atmospheric pressure.

Pleural effusions result when there is a breakdown in the balance between hydrostatic and cellular osmotic forces. In the normal physiological state the balance between these forces creates a gradient where absorption of pleural fluid by the visceral pleura is favored. The rate of fluid formation and reabsorption depends on Starling forces, pleural lymphatics, and pleural surface area. Although this gradient allows large volumes of fluid flux into the pleural space, the visceral pleura reabsorbs almost all of the fluid. Only a small volume of pleural fluid (0.1-0.2 ml/kg body weight) is maintained. Pleural and systemic disease processes may result in a change in the normal balance and, as the equilibrium is shifted, accumulation of pleural fluid occurs.

Blood supply to the parietal pleura is systemic. Thus the mean capillary hydrostatic pressure in the parietal pleura is about 30 cmH 2O. The blood supply to the visceral pleura is pulmonary, with a mean capillary hydrostatic pressure of 6 to 10 cmH 2O. Lymphatic supply to the pleura is responsible for absorption of protein and particulate material. The pleural membranes have an effective lymphatic network which decreases the protein content of pleural fluid to about 100 mg/100 cm 3 This lymphatic drainage normally removes about 600 ml of fluid from the pleural space every day. Hydrostatic forces between the pleural space and parietal pleura are positive and exceed the oncotic forces. Thus there is a net flux of fluid from the chest wall into the pleural space. In contrast, the visceral pleura has a hydrostatic pressure which is less than the oncotic gradient and reabsorption of pleural fluid to the visceral pleura is favored.

Several mechanisms are responsible for breakdown of the normal physiological balance which keeps the pleural space free of fluid. An increase in hydrostatic pressure in the pulmonary capillaries decreases pleural fluid uptake. Inflammatory processes or neoplasms can increase capillary permeability resulting in a flux of fluid into the pleural space. Neoplastic cells, protein, and inflammatory products increase the colloid oncotic pressure of the plural fluid, decreasing the reabsorptive effect of the visceral pleura. Systemic hypoalbuminemia decreases pleural capillary osmotic pressure. The flux of fluid out of the parietal pleura is increased, while fluid uptake by the visceral pleura is decreased, leaving lymphatic reabsorption as the major route for fluid reabsorption. Obstruction of lymphatics decreases absorption of protein, cells, and particulate matter by the visceral pleura, which may result in pleural effusions.

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