Fluid movement = K[(Pc − Pis) − σ(COPc − COPis)] |
(Eq. 15.1) |
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
Fluid movement at parietal pleura = [30 − (−5)] − 1(32 − 6) = 9 cm H2O
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 (6.6 mm Hg) 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 primarily 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 can augment their flow substantially to accommodate some or all of the excess fluid formed.
The liquid normally lubricating the pleural surfaces 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
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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 both fluid and proteins, so the accumulated fluid has a relatively high protein content compared to normal pleural fluid. 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 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, formed because of a change in the driving pressure (without increased permeability) or 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 is drawn from the peritoneum into 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 itself is affected by the disease process causing the effusion.
TABLE 15.1
Major Causes of Pleural Effusion
Transudate
Increased hydrostatic pressure; “overflow” of liquid from the lung interstitium
• Heart failure
Decreased plasma oncotic pressure
• Nephrotic syndrome
Movement of transudative ascitic fluid through the diaphragm
• Cirrhosis
Exudate
Inflammatory
•Infection (tuberculosis, bacterial pneumonia)
•Pulmonary embolus (infarction)
•Connective tissue disease (lupus, rheumatoid arthritis)
•Adjacent to subdiaphragmatic disease (pancreatitis, subphrenic abscess)
Malignant
Transudative pleural fluid
Most frequently, transudative pleural fluid is associated with left ventricular failure. The source of pleural fluid in 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. Previously, it was thought that increased hydrostatic pressure in the parietal pleural capillaries, due to elevated right atrial pressure, was responsible for increased flux of fluid from these vessels into the pleural space. However, clinical studies indicate that pulmonary venous hypertension (with left-sided heart failure), leading to increased hydrostatic pressure in the pulmonary capillaries, is the more important factor contributing to effusions rather 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. In contrast, pleural effusion is rare in isolated right ventricular dysfunction.
Patients with hypoproteinemia have decreased plasma colloid osmotic pressure, and pleural fluid may accumulate because hydrostatic pressure in pleural capillaries now is less opposed by the osmotic
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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 diseases. 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 (due to 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 focus of infection adjacent to the pleura 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, either as a tuberculous empyema in advanced disease or as an inflammatory but largely sterile pleural effusion seen in early tuberculosis.
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 occurs 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 may occur 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 usually exudative. 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 become occluded 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 Suggested Readings 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), the rate of accumulation, the nature of the underlying process, and the degree of a given patient’s cardiopulmonary reserve. 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 smallor moderate-sized effusions, a patient with otherwise normal lungs may not have any symptoms 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 due to 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, bronchial breath sounds, 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): Symptoms: pleuritic chest pain, dyspnea
Physical signs: dullness to percussion, decreased breath sounds, egophony at upper level, pleural friction rub
Diagnostic approach
Posteroanterior and lateral chest radiographs are typically 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. Ultrasonography and computed tomography (CT) scanning of the chest are more sensitive than plain film in detecting pleural effusions (Fig. 15.4). With imaging for these studies performed in the supine position, 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.
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FIGURE 15.3 Posteroanterior (A) and lateral (B) chest radiographs demonstrating
left pleural effusion.
FIGURE 15.4 Chest computed tomography scan showing a left pleural effusion.
With the patient supine, the fluid lies posteriorly against the chest wall in the
dependent portion of the left hemithorax.
When inflammatory effusions persist for a time, fluid may no longer be free-flowing as fibrous bands of tissue (loculations) form within the pleural space. 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).
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FIGURE 15.5 Posteroanterior (A) chest radiograph suggesting presence of left
pleural effusion. Left lateral decubitus (B) chest radiograph of patient shown in A.
With patient lying on left side, pleural fluid (arrows) flows freely to dependent part
of pleural space adjacent to left lateral chest wall. Film is shown upright for
convenience of comparison with A.
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 a pleural effusion 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 rely on levels of protein and the enzyme lactate dehydrogenase (LDH) within the fluid. 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:
1.Pleural fluid/serum protein ratio > 0.5
2.Pleural fluid/serum LDH ratio > 0.6
3.Pleural fluid LDH > 2/3 × upper limit of normal serum LDH
Pleural fluid obtained by thoracentesis routinely is analyzed for absolute numbers and types of cellular constituents, for microorganisms (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 to search for malignant cells. Detailed discussions of the findings in different disorders can be found in the Suggested Readings at the end of this chapter.
When pleural tissue is needed for diagnostic purposes, it is most commonly obtained under direct vision with the aid of a thoracoscope passed through the chest wall and into the pleural space while the patient is under general anesthesia. Formerly, pleural tissue was often sampled by closed pleural biopsy, generally performed with a relatively large cutting needle inserted through the skin of the chest wall in an awake patient. Histologic examination of these small biopsies is most useful for demonstrating granulomas of tuberculosis but also can reveal implants of tumor cells from a malignant process in some cases.
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. If the effusion is likely to progress to 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]), a chest tube is placed through the chest wall into the pleural space to drain the fluid as completely as possible. 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.
When the effusion is recurrent and large enough to cause dyspnea, 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) is most commonly used for recurrent malignant effusions and, if effective, obliterates the pleural space and 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. Another option for management of a recurrent effusion is placement of a tunneled pleural catheter that can remain in place for many months and through which the
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