Anatomy

The term pleura refers to the thin lining layer on the outer surface of the lung (visceral pleura), the corresponding lining layer on the inner surface of the chest wall (parietal pleura), and the space between them (pleural space) (Fig. 15-1). Because the visceral and parietal pleural surfaces normally touch each other, the space between them is usually only a potential space. It contains a thin layer of serous fluid coating the apposing surfaces. When air or a larger amount of fluid accumulates in the pleural space, the visceral and parietal pleural surfaces are separated, and the space between the lung and the chest wall becomes more apparent.

The pleura lines not only the surfaces of the lung in direct contact with the chest wall but also the diaphragmatic and mediastinal borders of the lung. These surfaces are called the diaphragmatic and mediastinal pleura, respectively (see Fig. 15-1). Visceral pleura also separates the lobes of the lung from each other; therefore, the major and minor fissures are defined by two apposing visceral pleural surfaces.

Each of the two pleural surfaces, visceral and parietal, is a thin membrane, the surface of which consists of specific lining cells called mesothelial cells. Beneath the mesothelial cell layer is a thin layer of connective tissue. Blood vessels and lymphatic vessels course throughout the connective tissue and are important in the dynamics of liquid formation and resorption in the pleural space. On the parietal but not the visceral pleural surface, openings called stomata are located between the mesothelial cells. Each stoma leads to lymphatic channels, allowing a passageway for liquid from the pleural space to the lymphatic system. Sensory nerve endings in the parietal and diaphragmatic pleura apparently are responsible for the characteristic “pleuritic chest pain” arising from the pleura.

Blood vessels supplying the parietal pleural surface originate from the systemic arterial circulation, primarily the intercostal arteries. Venous blood from the parietal pleura drains to the systemic venous system. The visceral pleura is also supplied primarily by systemic arteries, specifically branches of the bronchial arterial circulation. However, unlike the parietal pleura, the visceral pleura has venous drainage into the pulmonary venous system. Depending on their location, the lymphatic vessels that drain the pleural surfaces transport their fluid contents to different lymph nodes. Ultimately, any liquid transported by the lymphatic channels finds its way to the right lymphatic or thoracic ducts, which empty into the systemic venous circulation.

Physiology

The pleural space normally contains only a small quantity of liquid (≈10 mL), which lubricates the apposing surfaces of the visceral and parietal pleurae. According to the current concept of pleural fluid formation and resorption, formation of fluid is ongoing primarily from the parietal pleural surface, and fluid is resorbed through the stomata into the lymphatic channels of the parietal pleura (Fig. 15-2). The normal rates of formation and resorption of fluid, which must be equal if the quantity of fluid within the pleural space is not changing, are believed to be approximately 15 to 20 mL/day.

The normally occurring liquid in the pleural space is an ultrafiltrate from the pleural capillaries. Several different forces either promote or oppose fluid filtration. The net movement of fluid from the pleural capillaries to the pleural space depends on the magnitude of these counterbalancing forces. The hydrostatic pressure in the capillary promotes movement of fluid out of the vessel and into the pericapillary space, whereas the colloid osmotic pressure (the osmotic pressure exerted by protein drawing in fluid) hinders movement of liquid out of the capillary. Likewise, hydrostatic and colloid osmotic pressures in the pericapillary space comprise the opposing forces that act on liquid within the pericapillary region.

The effect of these forces is summarized in the Starling equation, which describes the movement of fluid between vascular and extravascular compartments of any part of the body, not just the pleura:

where K = filtration coefficient (a function of the permeability of the pleural surface), P = hydrostatic pressure, COP = colloid osmotic pressure, σ = measure of capillary permeability to protein (called the reflection coefficient), and the subscripts c and is refer to the capillary and pericapillary interstitial space, respectively. In this case, the pericapillary interstitial space is essentially the pleural space; therefore, P_is and COP_is refer to intrapleural pressure and the colloid osmotic pressure of pleural fluid, respectively. The intrapleural pressure—that is, the hydrostatic pressure within the pleural space—is negative, reflecting the outward elastic recoil of the chest wall and the inward elastic recoil of the lung.

When values obtained by direct measurement or by estimation are put into the Starling equation, a net pressure of approximately 9 cm H₂O favors movement of fluid from the parietal pleura to the pleural space. The critical factor responsible for the forces favoring formation of pleural fluid is the difference between the positive hydrostatic pressure in the pleural capillaries and the negative hydrostatic pressure within the pleural space.

Applying the same equation to fluid filtration from the visceral pleura is more difficult. The visceral pleural capillaries are supplied mainly by the systemic arterial circulation but are drained into the pulmonary venous circulation rather than the systemic venous circulation. Although currently unknown, the hydrostatic pressure in the visceral pleural capillaries is estimated to be less than in the parietal pleural capillaries. As a result, the driving pressure for formation of pleural fluid is normally greater at the parietal than at the visceral pleural surface, and most of the small amount of normal pleural fluid is thought to originate from filtration through the systemic capillaries of the parietal pleura.

Resorption of pleural fluid, including protein and cells in the fluid, occurs through the stomata between mesothelial cells on the parietal pleural surface. The fluid enters lymphatic channels, and valves within these channels ensure unidirectional flow. Movement of fluid through the valved lymphatics is believed to be aided by respiratory motion. When pleural fluid formation is increased, as occurs in many of the pathologic states to be discussed, the parietal pleural lymphatics are capable of increasing their flow substantially to accommodate at least some of the excess fluid formed.

Pleural Effusion

In the normal individual, resorption of pleural fluid maintains pace with pleural fluid formation, so fluid does not accumulate. However, a variety of diseases affect the forces governing pleural fluid filtration and resorption, resulting in fluid formation exceeding fluid removal—that is, development of pleural effusion. The pathogenesis (dynamics) of fluid accumulation is discussed first, followed by a consideration of some of the etiologic factors, clinical features, and diagnostic approaches to pleural effusions.