The pleural space represents one of the body’s potential spaces and can be affected pathologically by liquid, gas, or solid components, all of which can alter respiratory function. These processes may result from benign or malignant conditions, including infectious, inflammatory, or traumatic benign etiologies, as well as primary and secondary malignancies. This chapter provides a brief overview of the clinical presentation, diagnosis, etiology, and treatment of pleural conditions.

The pleural space lies within the layer of pleura that covers the lung and the pleural layer that lines the chest wall, diaphragm, and mediastinum. The pleural layers are composed of a monolayer of mesothelial cells supported by a thin membrane of collagen and elastin connective tissue.¹ The pleural surfaces are categorized as the visceral and parietal pleurae. The interior surface, termed the visceral pleura, covers the lung. The exterior surface, denoted by the parietal pleura, lines the chest wall, mediastinum, and diaphragm (Fig. 126-1). An analogous representation of this configuration can be created by invaginating an inflated balloon with one’s fist (Fig. 126-2). The portion of the balloon that covers the hand is analogous to the visceral pleural surface, and the exterior surface of the balloon represents the parietal pleural surface. The transition from visceral to parietal pleura occurs at the hilum of the lung. Inferior to the hilum, the anterior and posterior leaves of the visceral pleura fuse together at the inferior pulmonary ligament and anchor the medial aspect of the lower lobe to the mediastinum. The sulci, or sinuses, of the pleural space are defined by various structures: the upward bowing of the diaphragm into the hemithorax, the costophrenic sinus, the costomediastinal sinuses anteriorly and posteriorly, and the mediastinophrenic sinus medially. As the diaphragm descends with inspiration, these sinuses are occupied with inflated lung.

The pleural space develops between the fourth and seventh weeks of gestation. The lateral plate of the embryologic mesoderm differentiates into the splanchnopleure, which give rise to the parietal pleura and the somatopleure, which become the visceral pleura. At the end of the seventh week of gestation, the diaphragm has separated the pleural and pericardial compartments from the peritoneal compartment, and over the next month of embryologic development, the pleural space expands cranially and caudally to surround the developing pericardial sac.

As a potential space, the pleural space is capable of transferring the mechanical forces of the expanding hemithorax to the lung, permitting unimpeded inflation. Coupling of chest wall and diaphragmatic forces to the lung across the pleural space is facilitated by the presence of about 1 mL of pleural fluid. Composed primarily of protein, with a smattering of cells (e.g., mesothelial cells, monocytes, and lymphocytes), this physiologic pleural fluid may also facilitate smooth sliding of visceral and parietal pleural surfaces against one another as the lung volume changes.^2–5 Pressure within the pleural space ranges from -2 to -40 cm H₂O as the lung expands from its functional residual capacity to maximum inspiration.²

The blood supply of the pleura is divided between the systemic and pulmonary circulations. The parietal pleura is supplied largely by the intercostal arteries, whereas the visceral pleura is supplied by both bronchial and pulmonary arteries (Fig. 126-3).^2,3,6 Similarly, the parietal pleural is innervated by the intercostal nerves.

The lymphatic flux through the pleural space occurs through lymphatic channels within the visceral and parietal pleurae, as well as through the thoracic duct, which conveys the chyle generated by the intestinal lymphatics through the thoracic cavity to drain into the junction of the left jugular and left subclavian veins. The thoracic duct exhibits some variability in its course through the thorax, existing as duplicate ducts or foregoing the usual route between the aorta and azygos vein in the lower right hemithorax before it crosses to the left at the T4 level (see Chapter 133). The lymphatic capillaries of the pleura are found within the submesothelial connective tissue. The parietal pleura also has 1- to 6-μm stomata that facilitate drainage into the submesothelial lymphatic lacunae and from there through intercostal, mammary, and mediastinal lymphatics into the thoracic duct (Fig. 126-4).^7,8

Pleural space diseases can be grouped into abnormalities of liquid, solid, and gas, although there may be some overlap between physical states. Consideration of extrathoracic disease also must be given, since the upper intra-abdominal contents may be located above the level of the costal margin, while still below the dome of the diaphragm, especially after full exhalation. Subphrenic infections, gallbladder inflammation, and splenic rupture all can lead to pain in the lower chest on inspiration. Occasionally, infradiaphragmatic pathology can lead to a pleural process. There have been case reports of gallstones migrating into the pleural space.⁹ With the so-called hepatic hydrothorax, a transudate accumulates in the pleural space of cirrhotic patients as ascitic fluid fluxes across the diaphragm, possibly through blebs or fenestrations.¹⁰ Other examples include recurrent pancreatitis that may fistulize to the pleural space.¹¹

The workup of a pleural abnormality begins with a complete history and physical examination. A thorough review of systems should be taken including specific queries about local symptoms such as pain, dyspnea, or cough, as well as more systemic findings such as fevers, weight loss, or neurologic symptoms.

A complaint of chest pain should be explored further—is the pain pleuritic? Was there antecedent trauma? Does the pain radiate to the top of the shoulder or scapula or back? The sensation of pain by the afferent nerve fibers of the parietal pleura secondary to inflammation or infection may be observed with hemothorax, parapneumonic effusion, or empyema (i.e., purulent fluid in the pleural space). On the other hand, changes in intrapleural pressures and stretching of parietal pleural surfaces on the chest wall or diaphragm may account for sensations of discomfort in cases of pneumothorax. The time course of the pain also might yield insight into the pathologic process. For example, a history of retching followed by acute epigastric or substernal pain and then progression to left-sided chest pain would suggest an esophageal rupture with initial mediastinitis followed by contamination of the left chest.

Dyspnea may reflect a true decrement in the lung function if the pathologic process usurps a significant volume within the hemithorax. This can be seen in patients in whom fluid or solid volume prevents full lung expansion. The respiratory mechanics also can be disrupted, such as may occur in cases of pneumothorax, where there is an uncoupling of the mechanical forces of the chest wall and diaphragm from the lung, with a resulting diminution of lung volume caused by the lung’s intrinsic elastic recoil. However, dyspnea also may result without a significant loss of lung function. The sensation of incomplete chest expansion that accompanies some pleural processes may lead to dyspnea in the absence of hypoxia or hypoventilation.

A history of cough should be elicited to determine the characteristics of the sputum produced: color, odor, viscosity, amount, and frequency. A period of coughing that is productive of purulent sputum, in conjunction with a fever and chest pain, followed later by a persistent dry cough, may be an indication that a chronic empyema cavity has formed (see Chapter 107). A history of hemoptysis, weight loss, and heavy tobacco use in a patient with a pleural effusion would be suspicious for a malignant effusion or pleural malignancy.

A comprehensive physical examination often, but not always, corroborates the suspicions raised by an abnormal history. Auscultation, percussion, palpation, and testing for tactile fremitus or egophony all represent important aspects of the respiratory examination. It is equally important to detect pathology in other systems because the pleural space may represent only one manifestation of many in a particular disease. For example, a patient complaining of shortness of breath with stair climbing also may relate a long-standing history of joint pain and swelling. On examination, in addition to a dullness to percussion that shifts to the dependent aspects of the chest when the patient is moved from the sitting to the decubitus positions, one also might observe the severely gnarled joints and ulnar deviation of rheumatoid arthritis.

In practice, few diagnoses are made solely by physical examination. Radiologic examination of the pleural space is accomplished with plain chest radiographs, ultrasound, CT scan, and MRI. Plain films are usually the initial investigation of benign conditions from any of the three categories described earlier (Fig. 126-5). The scant volume of pleural fluid present in the healthy state is not visible on chest x-ray, but a pleural effusion of 50 mL should be detectable on a lateral chest film, evidenced as blunting of the posterior costophrenic sinus. A 200-mL effusion is evidenced by blunting of the lateral sulcus.¹² On anteroposterior (portable) films, often the meniscus of the pleural effusion is indistinct, and atelectatic or consolidated lung may contribute to the basilar opacification. An upright posteroanterior and lateral film is preferable because it should be technically superior, but even that technique still may not distinguish the fluid component of such a finding. In these cases, a lateral decubitus chest x-ray may be performed to assess the effusion, which should layer dependently if it is free flowing and not loculated.

A plain upright chest x-ray is also the mainstay of radiologic evaluation of pneumothorax. Small amounts of air in the pleural space may be detected by observing the visceral pleural line (Fig. 126-5, inset) or noting the absence of lung markings. In an otherwise normal pleural space, the first location of detectable pneumothorax is usually the apex. Thus, in most instances, an upright plain film is the appropriate study to order, although there is experimental evidence from cadaver studies that a lateral decubitus film may be even more sensitive.^13,14 The progressive collapse of the lung with increasing pneumothorax will continue to shorten the radial distances between the visceral pleural surfaces of the pulmonary lobes and the hilum. In a supine patient, the distribution of air within the pleural space is altered, and the pneumothorax may be noted as the “deep sulcus sign,” where the lateral sulcus is sharper and more lucent on the affected side or as lucency over the right or left upper quadrants.^15,16

Chest CT scanning increases the sensitivity of detection of solid, liquid, and gas within the pleural space. Fluid collections can be further characterized by measuring Hounsfield units to distinguish between simple effusions and hemothorax or evolving empyemas.¹⁷ CT scanning is also more sensitive for the detection of pneumothoraces.^18,19 It is worth stating that tension pneumothorax is not a diagnosis that should be made with CT or chest x-ray, but rather clinical assessment. Distinguishing between exudative and transudative pleural effusions is not reliably accomplished with CT scanning alone.²⁰ In terms of surgical planning, a chest CT scan can be extremely useful in planning video-assisted thoracic surgery (VATS) port sites or even thoracotomy to avoid lung adhesions and obtain optimal access to the intrapleural pathology.