Pleural Disease

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15

Pleural Disease

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, immune, or malignant.

This chapter discusses the anatomy of the pleura, 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). 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 an understanding of how different factors interact in producing pleural disease. The primary malignancy of the pleura, mesothelioma, is discussed in Chapter 21, which deals with neoplastic disease of the thorax.

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:

image

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, Pis and COPis 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.

The Starling equation can be applied to the parietal pleura:

Pc = 30 cm H2O

Pis (mean intrapleural pressure) = − 5 cm H2O

COPc = 32 cm H2O

COPis = 6 cm H2O

σ = 1, K = 1

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.

Fluid movement at parietal pleura = [30 − (−5)] − 1(32 − 6) = 9 cm H2O

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 fluid is filtered from the parietal pleura into the pleural space and reabsorbed through stomata into the parietal pleural lymphatics.

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.

Pathogenesis of Pleural Fluid Accumulation

In theory, a change in magnitude of any of the factors in the Starling equation can cause sufficient imbalance of pleural fluid dynamics to result in pleural fluid accumulation. In practice, it is easiest to divide these changes into two categories: (1) alteration of the permeability of the pleural surface (i.e., changes in the filtration coefficient [K] and reflection coefficient [σ] such that the pleura is more permeable to fluid and larger-molecular-weight components of blood, including proteins) and (2) alteration in the driving pressure, encompassing a change in hydrostatic or colloid osmotic pressures of the parietal or visceral pleura, without any change in pleural permeability.

The most common types of disease causing a change in the filtration and reflection coefficients are inflammatory or neoplastic diseases involving the pleura. In these circumstances, the pleural surface becomes more permeable to proteins, so the accumulated fluid has a relatively high protein content. This type of fluid, because of a change in permeability and its association with a relatively high protein content, is termed an exudate.

Increased permeability of the pleural surface is associated with exudative pleural fluid. Changes in pleural hydrostatic or colloid osmotic pressures are associated with transudative pleural fluid.

In contrast, an increase in hydrostatic pressure within pleural capillaries (as might be seen with high pulmonary venous pressure from congestive heart failure) or a decrease in plasma colloid osmotic pressure (as in hypoproteinemia) results in accumulation of fluid with a low protein content because the pleural barrier is still relatively impermeable to the movement of proteins. This type of fluid, because of a change in the driving pressure (without increased permeability) and the presence of a low protein content, is termed a transudate.

Another general mechanism accounting for some pleural effusions reflects neither altered permeability nor altered driving pressure. Rather, the fluid originates in the peritoneum as ascitic fluid and travels to the pleural space primarily via small diaphragmatic defects and perhaps also by diaphragmatic lymphatics. Considering that intrapleural pressure is more negative than intraperitoneal pressure, it is not surprising that fluid moves from the peritoneum to the pleural space when such defects exist.

Interference with the resorptive process for pleural fluid can contribute to development of effusions. This is seen primarily with blockage of the lymphatic drainage from the pleural space, as may occur when tumor cells invade the lymphatic channels or draining lymph nodes.

Etiology of Pleural Effusion

The numerous causes of pleural fluid accumulation are best divided into transudative and exudative categories (Table 15-1). This distinction is generally easy to make and is most important in guiding the physician along the best route for further evaluation. Transudative fluid usually implies that the pathologic process does not primarily involve the pleural surfaces, whereas exudative fluid often suggests that the pleura is affected by the disease process causing the effusion.

Transudative Pleural Fluid

Most frequently, transudative pleural fluid is associated with heart failure. Although traditionally the explanation has been that an elevation of hydrostatic pressure in the pleural capillaries was responsible for increased flux of fluid from these vessels into the pleural space, more recent data suggest an alternative explanation. The source of pleural fluid in congestive heart failure appears primarily to be liquid leaking out of the pulmonary capillaries and accumulating in the lung interstitium. This interstitial fluid then leaks across the visceral pleura and into the pleural space, akin to leakage of fluid from the surface of a wet sponge. On the basis of clinical studies, pulmonary venous hypertension (with left-sided heart failure) leading to increased hydrostatic pressure in the pulmonary capillaries appears to be a more important factor contributing to effusions than systemic venous hypertension (with right-sided failure). Pleural effusion is particularly likely to occur when both ventricles are failing and pulmonary and systemic venous hypertension coexist.

Patients with hypoproteinemia have decreased plasma colloid osmotic pressure, and pleural fluid may develop because hydrostatic pressure in pleural capillaries now is less opposed by the osmotic pressure provided by plasma proteins. The most common circumstance resulting in hypoproteinemia and pleural effusion is nephrotic syndrome, with excessive renal losses of protein.

Movement of transudative ascitic fluid through diaphragmatic defects and into the pleural space appears to be the most important mechanism for the pleural effusions sometimes seen in liver disease, especially cirrhosis. Although patients also may have decreased hepatic synthesis of protein, hypoproteinemia has only a minor role in the pathogenesis of these effusions.

Ascitic fluid may travel through diaphragmatic defects into the pleural space.

Exudative Pleural Fluid

Exudative pleural fluid generally implies an increase in permeability of pleural surfaces, allowing protein and fluid to more readily enter the pleural space. Although a wide variety of processes can result in exudative pleural effusions, the two main etiologic categories are inflammatory and neoplastic disease. Inflammatory processes often originate within the lung but extend to the visceral pleural surface. Infection (especially bacterial pneumonia and tuberculosis) and pulmonary embolism (often with infarction) are two common examples. In the case of pneumonia extending to the pleural surface, an associated pleural effusion is called a parapneumonic effusion. When the effusion itself harbors organisms or has the appearance of pus (as a result of an exuberant inflammatory response with many thousands of neutrophils), the effusion is called an empyema, or more properly, empyema thoracis. Although infection within the pleural space is commonly secondary to pneumonia, empyema also may result from infection introduced through the chest wall, as occurs with trauma or surgery involving the thorax.

In tuberculosis, a subpleural focus of infection may rupture into the pleural space, with an ensuing inflammatory response of the pleura (with or without growth of the tubercle bacilli within the pleural space). In some cases, the pulmonary focus is not apparent, and pleural involvement is the major manifestation of tuberculosis within the thorax.

Other forms of inflammatory disease affecting the pleura primarily involve the pleural surface as opposed to the lung. Several connective tissue diseases, particularly systemic lupus erythematosus and rheumatoid arthritis, are associated with pleural involvement that is independent of changes within the pulmonary parenchyma. Inflammatory processes below the diaphragm, such as pancreatitis and subphrenic abscess, are often accompanied by “sympathetic” pleural inflammation and development of an exudative pleural effusion. With these disorders, inflammation of the diaphragm itself may lead to increased permeability of vessels in the diaphragmatic pleura and leakage of fluid into the pleural space. When ascites is present, as is common in pancreatitis, transport of fluid from the abdomen through defects in the diaphragm may contribute to pleural fluid accumulation.

Malignancy may cause pleural effusion by several mechanisms, but the resulting fluid is generally exudative in nature. Commonly, malignant cells are found on the pleural surface, arriving there either by direct extension from an intrapulmonary malignancy or by hematogenous (bloodstream) dissemination from a distant source. In other cases, lymphatic channels or lymph nodes are blocked by foci of tumor, impairing the normal lymphatic clearance mechanism for protein and fluid from the pleural space. In these latter cases, malignant cells are generally not found on examination of the pleural fluid.

A host of other disorders may have pleural effusion as a clinical manifestation. The list includes such varied processes as hypothyroidism, benign ovarian tumors (Meigs’ syndrome), asbestos exposure, and primary disorders of the lymphatic channels. Detailed discussion of the various disorders with potential for pleural fluid accumulation can be found in the references at the end of this chapter.

Clinical Features

A patient with pleural fluid may or may not have symptoms caused by the pleural disease. Whether symptoms are present depends on the size of the effusion(s) and nature of the underlying process. Inflammatory processes affecting the pleura frequently result in pleuritic chest pain—that is, sharp pain aggravated by respiration. When an effusion is large, patients may experience dyspnea resulting from compression of the underlying lung. With small- or moderate-sized effusions, a patient with otherwise normal lungs generally does not have dyspnea just from the presence of fluid in the pleural space. When the pleural fluid has an inflammatory nature or is frankly infected, fever is commonly present.

On physical examination of the chest, the region overlying the effusion is dull to percussion. Breath sounds are usually decreased in this region as a result of fluid in the pleural space interfering with the transmission of breath sounds from the lung to the chest wall. However, at the upper level of the effusion, egophony and other findings usually associated with consolidation may be heard as manifestations of increased transmission of sound resulting from compression (atelectasis) of the underlying lung parenchyma. A scratchy pleural friction rub may be present, particularly with an inflammatory process involving the pleural surfaces.

Common clinical features with pleural effusion(s) are:

Symptoms: pleuritic chest pain, dyspnea

Physical signs: dullness, decreased breath sounds, egophony at upper level, pleural friction rub

Diagnostic Approach

Posteroanterior and lateral chest radiographs are clearly most important in the initial evaluation of the patient with suspected pleural effusion (Fig. 15-3). With a small effusion, blunting of the normally sharp angle between the diaphragm and chest wall (costophrenic angle) is seen. Often this blunting is first apparent on inspection of the posterior costophrenic angle on the lateral radiograph, because this is the most dependent area of the pleural space. With a larger effusion, a homogeneous opacity of liquid density appears and is most obvious at the lung base(s) when the patient is upright. The fluid may track along the lateral chest wall, forming a meniscus. Computed tomography (CT) scanning of the chest is more sensitive than plain film in detecting pleural effusions (Fig. 15-4). Small free-flowing effusions will be seen posteriorly at the bases of the lung, and track up the lung fields posteriorly and laterally as the effusion becomes larger.

When certain inflammatory effusions persist for a time, fluid may no longer be free-flowing within the pleural space as fibrous bands of tissue (loculations) form within the pleura. In such circumstances, fluid is not necessarily positioned as expected from the effects of gravity, and atypical appearances may be found. To detect whether fluid is free-flowing or whether small costophrenic angle densities represent pleural fluid, a lateral decubitus chest radiograph may be extremely useful. In this view, the patient lies on a side, and free-flowing fluid shifts position to line the most dependent part of the pleural space (Fig. 15-5).

Ultrasonography is another technique frequently used to evaluate the presence and location of pleural fluid. When pleural fluid is present, a characteristic echo-free space can be detected between the chest wall and lung. Ultrasonography is particularly useful in locating a loculated effusion or a small effusion not apparent on physical examination and in guiding the physician to a suitable site for thoracentesis.

When pleural fluid is present and the etiologic diagnosis is uncertain, sampling the fluid by thoracentesis (withdrawal of fluid through a needle or catheter) allows determination of the cellular and chemical characteristics of the fluid. These features define whether the fluid is transudative or exudative and frequently give other clues about the cause. Although different criteria have been used, the most common criteria include the levels of protein and the enzyme lactate dehydrogenase (LDH) within the fluid, both in absolute numbers and relative to the corresponding values in serum. Exudative fluid has high levels of protein, LDH, or both, whereas transudative fluid has low levels of protein and LDH.

An exudative effusion is defined by one or more of the following:

Pleural fluid obtained by thoracentesis is routinely analyzed for absolute numbers and types of cellular constituents, for bacteria (by stains and cultures), and for glucose level. In many cases, amylase level and pH value of the pleural fluid are measured. Special slides are prepared for cytologic examination, and a search for malignant cells is made. Detailed discussions of the findings in different disorders can be found in the references at the end of this chapter.

In some cases, pleural tissue is sampled by closed pleural biopsy, generally performed with a relatively large cutting needle inserted through the skin of the chest wall. Histologic examination of this tissue is most useful for demonstrating granulomas of tuberculosis but also can reveal implants of tumor cells from a malignant process in some cases. Pleural tissue also can be obtained under direct vision with the aid of a thoracoscope passed through the chest wall and into the pleural space; this has become the most definitive method for evaluating the pleural space for malignant implants.

Pulmonary function tests are generally not part of the routine evaluation of patients with pleural effusion. However, a significant effusion may impair lung expansion sufficiently to cause a restrictive pattern (with decreased lung volumes) on pulmonary function testing.

Treatment

Treatment of pleural effusion depends entirely on the nature of the underlying process and usually is directed at this process rather than the effusion itself. In cases with a high likelihood of the effusion eventuating in extensive fibrosis or loculation of the pleural space (e.g., with an empyema or a hemothorax [blood in the pleural space, often secondary to trauma]), the fluid is drained with a catheter or a larger bore tube inserted into the pleural space. If loculation has already occurred, thoracoscopy or an open surgical approach may be necessary to break up fibrous adhesions and allow effective drainage of the fluid and full reexpansion of the lung.

In other cases with recurrent large effusions causing dyspnea, especially malignant effusions, the fluid is initially drained with a tube passed into the pleural space, and an irritating agent (e.g., talc or a tetracycline derivative) is instilled via the tube into the pleural space to induce inflammation and cause the visceral and parietal pleural surfaces to become adherent. This process of sclerosis (also called pleurodesis) eliminates the pleural space and, if effective, prevents recurrence of pleural effusion on the side where the procedure was performed. When the effusion is loculated or pleurodesis via a chest tube is unsuccessful, the procedure can be performed under general anesthesia through a thoracoscope.

Pneumothorax

Air is not normally present between the visceral and parietal pleural surfaces, but it can be introduced into the pleural space by a break in the surface of either pleural membrane, creating a pneumothorax. Because pressure within the pleural space is subatmospheric, air readily enters the space if there is any communication with air at atmospheric pressure.

Etiology and Pathogenesis

When a pneumothorax is created by entry of air through the chest wall and parietal pleura, the most common causes are (1) trauma (e.g., knife or gunshot wound) and (2) introduction of air via a needle, catheter, or incision through the chest wall and into the pleural space. Alternatively, air may enter the pleura through a break in the visceral pleura, allowing communication between the airways or alveoli and the pleural space. Examples of the latter circumstance include rupture of a subpleural air pocket (e.g., bleb, cyst, or bulla) into the pleural space or necrosis of the lung adjacent to the pleura by a destructive pneumonia or neoplasm.

A pneumothorax can result from a break in the parietal pleura (e.g., from trauma, needle or catheter insertion) or in the visceral pleura (e.g., from rupture of a subpleural air pocket, necrosis of lung adjacent to the pleura).

In some cases, a reason for the pneumothorax is apparent, such as an underlying abnormality in the lung, a form of lung disease known to be associated with subpleural air pockets (emphysema or interstitial lung disease with honeycombing and subpleural cysts), or destruction of lung tissue adjacent to the pleural surface (necrotizing pneumonia or neoplasm). Pneumothorax in these clinical settings is said to be secondary to the known lung disease.

In patients with AIDS, pneumothorax can develop as a complication of pulmonary infection with Pneumocystis jiroveci (formerly called Pneumocystis carinii), presumably because of necrosis or cyst formation adjacent to the visceral pleura.

In contrast, other patients do not have a defined abnormality of the lung adjacent to the pleura and therefore are said to have a primary spontaneous pneumothorax. Even in this latter circumstance, patients frequently have small subpleural pockets of air (blebs), especially at the lung apices, that have gone unrecognized clinically and on routine radiographic examination. If a bleb eventually ruptures, air is released from the lung parenchyma into the pleural space, creating a pneumothorax.

Patients who receive positive pressure to the tracheobronchial tree and alveoli (e.g., with mechanical ventilation) are subject to development of a pneumothorax. In this case, as a result of positive pressure, a preexisting subpleural bleb may rupture, or air may rupture through an alveolar wall into the interstitial space, track through the lung parenchyma to the subpleural surface, and then rupture into the pleural space. Alternatively, and perhaps more commonly, the air following alveolar rupture tracks retrograde to the mediastinum alongside blood vessels and airways and produces a pneumomediastinum (see Chapter 16). A pneumothorax can result when air ruptures through the mediastinal pleura into the pleural space.

Pathophysiology

The pathophysiologic consequences of a pneumothorax are variable, ranging from none to the development of acute cardiovascular collapse. The size of the pneumothorax (i.e., amount of air within the pleural space) is an important determinant of the clinical effects. Because the lung is enclosed within a relatively rigid chest wall, accumulation of a substantial amount of pleural air is accompanied by collapse of the underlying lung parenchyma. In extreme cases, air in the pleural space occupies almost the entire hemithorax, and the lung is totally collapsed and functionless until the air is resorbed or removed.

Air in the pleural space is generally under atmospheric or subatmospheric pressure. In some cases the air may be under positive pressure, creating a tension pneumothorax. This tension within the pleural space is believed to occur as a result of a “one-way valve” mechanism by which air is free to enter the pleural space during inspiration, but the site of entry is closed during expiration. Therefore, only unidirectional movement of air into the pleural space is permitted, the intrapleural pressure increases, and the underlying lung collapses further. When pleural pressure is sufficiently high, the mediastinum and trachea may be shifted away from the side of the pneumothorax. In extreme cases, cardiovascular collapse and respiratory failure may result, with a marked fall in cardiac output and blood pressure. These hemodynamic changes are commonly stated to result from inhibition of venous return into the superior and inferior venae cavae as a consequence of positive intrathoracic pressure. However, in animal models, the predominant pathophysiologic explanation is progressive respiratory failure with severe hypoxemia and ventilatory compromise. Whatever the mechanism, emergent treatment is necessary to release the air under tension and reverse the process. A particularly important risk factor for development of a tension pneumothorax is positive-pressure ventilation with a mechanical ventilator. When a pneumothorax occurs in this situation, the ventilator may continue to introduce air under high pressure through the site of rupture in the visceral pleura.

A tension pneumothorax may be associated with total collapse of the underlying lung, mediastinal shift, and cardiovascular collapse.

For most cases of pneumothorax, after the site of entry into the pleural space is closed, the air is spontaneously resorbed. The reason is that the pressure of gases in the air in a pneumothorax is higher than the combined partial pressure of gases in surrounding venous or capillary blood. For example, air within the pleural space might have a pressure a few millimeters of mercury below atmospheric pressure, or approximately 755 to 758 mm Hg. In contrast, gas pressures in mixed venous blood are approximately as follows: PO2 = 40 mm Hg, PCO2 = 46 mm Hg, PN2 = 573 mm Hg, and PH2O = 47 mm Hg. Therefore, the total gas pressure in mixed venous blood is 706 mm Hg, which is approximately 50 mm Hg below that of air in the pleural space. Consequently, there is a gradient for diffusion of gas from the pleural space into mixed venous blood. With continued diffusion of gas in this direction, the size of the pneumothorax is slowly reduced, the gas pressures within the pleural space are maintained, and the gradient favoring absorption of gas continues until all the air is resorbed.

If pure O2 is administered to the patient with a pneumothorax, the process of resorption can be hastened. In arterial blood, most of the nitrogen is replaced by O2. As a result, PN2 in the capillary blood surrounding the pneumothorax becomes quite low, and the gradient for resorption of nitrogen from the pleural space has been increased considerably. At the same time, although arterial PO2 is high after inhalation of pure O2, PO2 falls substantially in capillary and venous blood because of O2 consumption by the tissues. Therefore, a large partial pressure gradient from pleural gas to pleural capillary blood remains for O2 as well. The net result is that O2 administration favors more rapid resorption of nitrogen (the main component of gas in the pneumothorax) without significantly compromising the gradient promoting resorption of O2.

When a pneumothorax is causing important clinical problems, the physician need not wait for spontaneous resorption of the air, but can actively remove the air with a needle, catheter, or tube inserted into the pleural space.

Clinical Features

In many cases, the patient has obvious risk factors for developing a pneumothorax (e.g., predisposing underlying lung disease, receiving positive-pressure ventilation with a mechanical ventilator). Interestingly, the group of patients in whom a primary spontaneous pneumothorax develops shows a striking predominance of males. In addition, the patients are often smokers, are young adults, and frequently are tall and thin.

Clinical features of pneumothorax are:

Symptoms: chest pain, dyspnea

Physical signs: asymmetric (decreased) breath sounds, hyperresonance, tracheal deviation (tension), ↓ blood pressure (tension)

The most common complaint at the time of pneumothorax is acute onset of chest pain, dyspnea, or both, but some patients may be totally symptom free, particularly if the pneumothorax is small. On physical examination, findings depend to a large extent on the size of the pneumothorax. Because of decreased transmission of sound, breath sounds and tactile fremitus are diminished or absent. With a significant amount of air in the pleural space, increased resonance to percussion over the affected lung may be observed.

When the pneumothorax is under tension, the patient is often in acute distress, and a decrease in blood pressure or even frank cardiovascular collapse may be present. Palpation of the trachea frequently demonstrates deviation away from the side of the pneumothorax.

Diagnostic Approach

The diagnosis of pneumothorax is established or confirmed by chest radiograph. The characteristic finding is a curved line representing the edge of the lung (the visceral pleura) separated from the chest wall. Between the edge of the lung and the chest wall, the pleural space is lucent, and none of the normal vascular markings of the lung are seen in this region (Figs. 15-6 and 15-7). When the pneumothorax is small, separation of the visceral and parietal pleura appears on upright chest films only at the apex of the lung, where the pleural air generally accumulates first. If the pneumothorax is substantial, the lung loses a significant amount of volume and therefore has a greater density than usual.

When both fluid and air are present in the pleural space (hydropneumothorax), the fluid no longer appears as a meniscus tracking up along the lateral chest wall. Rather, the fluid falls to the most dependent part of the pleural space and appears as a liquid density with a perfectly horizontal upper border (see Fig. 15-7). Finally, when gas in the pleural space is under tension, evidence is often seen of structures (e.g., trachea and mediastinum) being “pushed” away from the side of the pneumothorax (Fig. 15-8).

Treatment

Treatment of a pneumothorax is determined by its size and the ensuing clinical consequences. With a small pneumothorax causing few symptoms, it is best to wait for spontaneous resolution. This process can be hastened by administration of 100% O2, which alters the partial pressures of gases in capillary blood, favoring resorption of pleural air. When the pneumothorax is large (i.e., involves >20% of the hemithorax) or the patient has significant clinical sequelae, the air is best removed, usually by a needle, catheter, or chest tube inserted into the pleural space. Occasionally, patients have recurrent spontaneous pneumothoraces that require obliteration of the pleural space by instilling agents, such as talc, into the pleura to promote pleural inflammation and sclerosis. Concomitant thoracoscopic resection of subpleural apical blebs is frequently performed.

If a patient has hemodynamic compromise because of a tension pneumothorax, a needle, catheter, or tube must be inserted immediately to relieve the pressure. When this technique is performed, the sound of air under pressure escaping from the pleural space can readily be heard. The most important results of decompression are improvements in gas exchange, venous return to the thorax, cardiac output, and arterial blood pressure.

References

General Reviews

Light, RW. Pleural diseases, ed 5. Philadelphia: Lippincott Williams & Wilkins; 2007.

Loddenkemper, R, Antony, VB. Pleural diseases. Eur Respir Mon. 2002;7(monograph 22):1–326.

Natanzon, A, Kronzon, I. Pericardial and pleural effusions in congestive heart failure—anatomical, pathophysiologic, and clinical considerations. Am J Med Sci. 2009;338:211–216.

Pistolesi, M, Miniati, M, Giuntini, C. Pleural liquid and solute exchange. Am Rev Respir Dis. 1989;140:825–847.

Qureshi, NR, Gleeson, FV. Imaging of pleural disease. Clin Chest Med. 2006;27:193–213.

Sahn, SA. Pleural disease. editor. Clin Chest Med. 2006;27:157–394.

Wiener-Kronish, JP, Broaddus, VC. Interrelationship of pleural and pulmonary interstitial liquid. Annu Rev Physiol. 1993;55:209–226.

Zocchi, L. Physiology and pathophysiology of pleural fluid turnover. Eur Respir J. 2002;20:1545–1558.

Pleural Effusion

Colice, GL. Medical and surgical treatment of parapneumonic effusions. An evidence-based guideline. Chest. 2000;18:1158–1171.

Heffner, JE, Klein, SJ, Hampson, C. Interventional management of pleural infections. Chest. 2009;136:1148–1159.

Heffner, JE. Discriminating between transudates and exudates. Clin Chest Med. 2006;27:241–252.

Heffner, JE. Management of the patient with a malignant pleural effusion. Semin Respir Crit Care Med. 2010;31:723–733.

Light, RW. Pleural effusion. N Engl J Med. 2002;346:1971–1977.

Light, RW. Parapneumonic effusions and empyema. Proc Am Thorac Soc. 2006;3:75–80.

Rahman, NM, Maskell, NA, West, A, et al. Intrapleural use of tissue plasminogen activator and DNAase in pleural infection. N Engl J Med. 2011;365:518–526.

Rodriguez-Panadero, F, Janssen, JP, Astoul, P. Thoracoscopy: general overview and place in the diagnosis and management of pleural effusion. Eur Respir J. 2006;28:409–422.

Sahn, SA. The value of pleural fluid analysis. Am J Med Sci. 2008;335:7–15.

Thomsen, TW, DeLaPena, J, Setnik, GS. Videos in clinical medicine: thoracentesis. N Engl J Med. 2006;355:e16.

Pneumothorax

Haynes, D, Baumann, MH. Management of pneumothorax. Semin Respir Crit Care Med. 2010;31:769–780.

Baumann, MH. Management of spontaneous pneumothorax. Clin Chest Med. 2006;27:369–381.

Leigh-Smith, S, Harris, T. Tension pneumothorax—time for a re-think? Emerg Med J. 2005;22:8–16.

O’Connor, AR, Morgan, WE. Radiological review of pneumothorax. BMJ. 2005;330:1493–1497.

Tschopp, JM, Rami-Porta, R, Noppen, M, Astoul, P. Management of spontaneous pneumothorax: state of the art. Eur Respir J. 2006;28:637–650.

Wakai, A, O’Sullivan, RG, McCabe, G. Simple aspiration versus intercostal tube drainage for primary spontaneous pneumothorax in adults. Cochrane Database Syst Rev. (1):2007. CD004479

Weissberg, D, Refaely, Y. Pneumothorax. Experience with 1,199 patients. Chest. 2000;117:1279–1285.

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