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15: Pleural disease

OUTLINE

Anatomy, 193

Physiology, 194

Pleural Effusion, 196

Pathogenesis of Pleural Fluid Accumulation, 196

Etiology of Pleural Effusion, 196

Clinical Features, 198

Diagnostic Approach, 198

Treatment, 200

Pneumothorax, 200

Etiology and Pathogenesis, 201

Pathophysiology, 201

Clinical Features, 202

Diagnostic Approach, 202

Treatment, 203

Malignant Mesothelioma, 204

In moving from the lung to other structures that are part of the process of respiration, we next consider the adjacent pleura. In clinical medicine, the pleura is important not only because diseases of the lung commonly cause secondary abnormalities in the pleura, but also because the pleura is a major site of disease in its own right. Not infrequently, pleural disease is a manifestation of a multisystem process that is inflammatory, autoimmune, or malignant.

In this chapter, the anatomy of the pleura is discussed, followed by a presentation of several physiologic principles of fluid formation and absorption by the pleura and a discussion of two types of abnormalities that affect the pleura: liquid in the pleural space (pleural effusion) and air in the pleural space (pneumothorax). The chapter concludes with a brief discussion of a primary malignancy of the pleura, malignant mesothelioma. A comprehensive treatment of all the disorders that affect the pleura is

beyond the scope of this text. Rather, this chapter aims to cover the major categories and give the reader

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an understanding of how different factors interact in producing pleural disease.

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 that coats the apposing surfaces and acts as a lubricant during lung movement with respiration. 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.

FIGURE 15.1 Anatomic features of pleura. The pleural space is located between

visceral and parietal pleural surfaces. The pleura lines surfaces of lung in contact

with chest wall (costal pleura) and mediastinal and diaphragmatic borders

(mediastinal and diaphragmatic pleura, respectively). Source: (From Lowell, J. R.

(1977). Pleural effusions: a comprehensive review (p. 77). Baltimore, MD:

University Park Press.)

The pleura lines the surfaces of the lung in direct contact with the chest wall and 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 into the lymphatic system. Sensory nerve endings in the parietal and diaphragmatic pleura 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 thoracic or right lymphatic duct, which empties 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.

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FIGURE 15.2 Schematic diagram of normal filtration and resorption of fluid in

pleural space. Solid arrow shows filtration of fluid from parietal pleural

microvessels into pleural space. Arrowhead indicates removal of fluid through

stomata and into parietal pleural lymphatics. Dashed arrows indicate a minor role

for filtration and resorption of fluid by visceral pleural microvessels.

Source: (Modified from Pistolesi, M., Miniati, M., & Giuntini, C. (1989). Pleural

liquid and solute exchange. American Review of Respiratory Disease, 140, 825–

847.)

The normally occurring liquid in the pleural space is a low-protein transudate produced by ultrafiltration 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 magnitudes 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: