Adult Chest Surgery

Chapter 106. Overview 

The spectrum of benign conditions that affect the pleural spaces includes infectious, inflammatory, spontaneous, and traumatic etiologies. The pleural space represents one of the body's potential spaces and thus can be occupied pathologically by liquid, gas, or solid components, all of which can alter respiratory function. This chapter provides a brief overview of the clinical presentation, diagnosis, etiology, and treatment of benign pleural conditions. Since malignant diseases that affect the pleura are covered in Part 13 (see Overview), for the purposes of our discussion, these pathologies are described only in the context of understanding how to confirm a benign diagnosis.

ANATOMY AND PHYSIOLOGY

The pleural space is defined anatomically by a double-layered sac that covers the lung and lines the chest wall, diaphragm, and mediastinum. The sac is lined by mesothelial cells. The pleural layer itself is composed of a monolayer of mesothelial cells supported by a thin membrane of collagen and elastin connective tissue.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 the parietal pleura, is adjacent to the chest wall, mediastinum, and diaphragm (Fig. 106-1). An analogous representation of this configuration can be created by invaginating an inflated balloon with one's fist (Fig. 106-2). 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.

Figure 106-1.

 

A. The double-layered pleural sac mimics the topography of the lungs, including the fissures. The exterior surface exposed to the chest wall, diaphragm, and mediastinum is termed the parietal pleura. The interior surface adjacent to lung is called visceral pleura. B. The transition between parietal and visceral pleura occurs at the hilum. C. The anterior and posterior leaves of the visceral pleura fuse together at the inferior pulmonary ligament.

 

Figure 106-2.

 

There are two pleural sacs, one covering each lobe of the lung. The anatomy of this double-layered structure can be best appreciated by imagining one's fist invaginating a balloon. The hilum is at the wrist.

 

The pleural space develops between the fourth and seventh weeks of gestation. The lateral plate of the embryologic mesoderm differentiates into the splanchnopleurae, which give rise to the parietal pleura and the somatopleurae, 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. It is interesting to note that in elephants, the pleural space is filled with a dense connective tissue, presumably as a result of the evolutionary pressures of living in water and the physiologic requirements of snorkel-breathing in such an environment.The transmission of pressures across the pleural space to the lung alveoli in a snorkeling elephant would result in transudation of fluid from the pleural microvessels or frank rupture into the pleural space if it existed as a true potential space. In humans, the pleural space pressures range from –2 to –40 cm H2O as the lung expands from its functional residual capacity to maximum inspiration.Pathologic conditions that affect lung or chest wall likewise affect pleural surface pressures. With the upright posture of humans, there also exists a vertical gradient of pleural pressure that may account for differential effects on regional lung expansion in conjunction with the complex interactions of gravity and the mechanical forces of the expanding lung, thoracic cavity, and abdomen.Without the pressure constraints of snorkel-breathing, the human maintains the pleura as a potential space. Optimal coupling of the lung to the forces developed by the chest wall and diaphragmatic excursion is maintained by a small amount of pleural fluid.The volume of this fluid is approximately 1 mL in the normal state.This fluid also lubricates the pleural space, permitting the visceral pleural surface to slide smoothly against the parietal pleura as the lung expands and contracts. The composition of the pleural fluid is primarily protein, with a smattering of cells (e.g., mesothelial cells, monocytes, and lymphocytes).3–5 Hyaluronan (i.e., hyaluronic acid) acts as a boundary coating on pleural mesothelial cells, in addition to being present in pleural fluid,and may be involved in pleural lubrication and dissipation of frictional forces during lung movement, although this role remains somewhat controversial.4

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 arteries3,4,7 (Fig. 106-3). Similarly, the parietal pleural is innervated by the intercostal nerves.

Figure 106-3.

 

The pleura receives its blood supply from two sources. The parietal pleura is sustained by the intercostal arteries, whereas the visceral pleura is sustained by both bronchial and pulmonary arteries.

 

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 forgoing 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 Chap. 113). The lymphatic capillaries of the pleura are found within the submesothelial connective tissue. The parietal pleura also has 1- to 6-m stomata that facilitate drainage into the submesothelial lymphatic lacunae and from there through intercostal, mammary, and mediastinal lymphatics into the thoracic duct8,9(Fig. 106-4).

Figure 106-4.

 

A cross-section of the pleural space reveals important features of lymphatic drainage. Note the 1- to 6-m stomata in the parietal pleura, which facilitate drainage into the submesothelial lymphatic lacunae.

DIFFERENTIAL DIAGNOSIS

In the differential diagnosis of pleural space disease are included abnormalities of liquid, gas, and solid. Table 106-1 lists the various benign diagnoses of the pleural space, grouped by physical states. Consideration of extrathoracic disease also must be given because the upper intraabdominal contents may be found above the level of the costal margin as the diaphragm relaxes to 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.10 With 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.11 Other examples include recurrent pancreatitis that may fistulize to the pleural space.12

Table 106-1. Etiologies of Pleural Effusion

Frequency

Transudate

Exudate

Very common

Left ventricular failure

Malignancy

 

Cirrhosis

Parapneumonic effusions

 

Hypoalbuminemia

Empyema

Less common

Hypothyroidism

Lung infarction

 

Nephrotic syndrome

Rheumatoid arthritis

 

Mitral stenosis

Autoimmune disorders

 

Pulmonary embolism

Pancreatitis

 

 

Benign asbestos effusion

 

 

Post-myocardial infarction syndrome

Rare

Constrictive pericarditis

Yellow nail syndrome

 

Urinothorax

Medications

 

Superior vena cava syndrome

Fungal infections

 

Ovarian hyperstimulation

 

 

Meigs' syndrome

 

 

DIAGNOSTIC WORKUP

The workup of a pleural abnormality begins with a complete history and physical examination. Local symptoms of benign conditions include dyspnea, cough, and chest pain. Associated systemic symptoms such as fever or night sweats should be elicited while obtaining the history.

The complaint of chest pain should be elucidated 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 is related to inflammation or frank infection in some benign conditions such as hemothorax, parapneumonic effusion, or empyema (i.e., purulent fluid in the pleural space). On the other hand, changes in the intrapleural pressures and stretching of parietal pleural surfaces on the chest wall or diaphragm account for sensations of discomfort in cases of pneumothorax. The evolution of the pain sensations 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. The chest pain would have occurred as the ensuing mediastinitis then decompressed and contaminated the left chest.

Dyspnea may reflect a true decrement in 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 Chap. 93). A history of hemoptysis, weight loss, and heavy tobacco use in a patient with a pleural effusion would be suspicious for a malignant effusion (see Part 13, Overview). The specific presentation of individual benign pleural diseases or conditions is described below.

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. 106-5). 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.13 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.

Figure 106-5.

 
 
 

A. Spontaneous pneumothorax in the right pleural space. Note the absence of lung markings in the right hemithorax. Inset shows a coned down view of the pleural edge of the collapsed right lung (white arrows). B. Right-sided hemothorax. This example of fluid in the pleural space is notable for a meniscus at the costophrenic sulcus. C. Fibrothorax. The arrow points to an area of opacification that represents the thickest portion of the chronic empyema cavity. At operation, the full extent of the fibrothorax ranged from the upper third of the hemithorax to the hemidiaphragm, as suggested by the more bland opacity seen on this plain film.

 

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 (see Fig. 106-5A , 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.14,15 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 pneumothorax may be noted as the "deep sulcus sign," where the lateral sulcus is sharper and more lucent on the affected side or as a luceny over the right or left upper quadrants.16,17

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.18 CT scanning is also more sensitive for the detection of pneumothoraces.19,20 Distinguishing between exudative and transudative pleural effusions is not reliably accomplished with CT scanning alone.21 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.

MRI of the chest is useful in the workup of malignant disease because it demonstrates tumor invasivity and thus resectability. It has a sensitivity of up to 100% and a specificity of up to 93% in the detection of malignant disease during a workup of pleural masses.22 Its role in the workup of benign disease is less clear. Although it is not accurate in distinguishing between exudate and transudate, MRI can detect hemothorax reasonably well.23In practice, however, it is unlikely to be necessary to determine that diagnosis in most clinical circumstances.

Ultrasound is less sensitive than CT scanning for the detection of pleural fluid and pneumothorax,19,20,24 although it may have increased specificity for distinguishing pleural thickening from pleural fluid.25 Ultrasound is also a portable tool, which has implications in the rapid assessment of critically ill patients in the trauma or intensive care settings. Compared with plain radiography, ultrasound is more sensitive for detecting and quantifying pleural fluid.26,27 Moreover, further invasive investigation of the pleural fluid via thoracentesis is facilitated with real-time guidance by ultrasonography.25

Thoracentesis represents the first invasive modality in the workup of pleural effusions. The British Thoracic Society guidelines for workup of a unilateral pleural effusion are depicted in Fig. 106-6. The first goal of pleural fluid analysis is to distinguish between exudative effusions (e.g., cloudy serum signifying disease of the pleura itself) and transudative effusions (e.g., clear serum but abnormally high concentration). The different diagnoses associated with each type of effusion are listed in Table 106-2. It is important to keep in mind that clinical judgment can eliminate the need to subject the patient to the risk of an unnecessary invasive test. For example, a pleural effusion arising in the setting of known left ventricular failure is likely to represent a transudate. Scheurich and colleagues performed a prospective analysis of 33 patients with a pleural effusion and found that the clinical judgment of the physician was correct in predicting a transudative effusion in 16 of 16 cases and in 15 of 17 exudative effusions.28

Figure 106-6.

 

Flow diagram for workup of unilateral pleural effusion based on British Thoracic Society guidelines.

Table 106-2. Causes of Secondary Spontaneous Pneumothorax

Airway disease

Chronic obstructive pulmonary disease

Cystic fibrosis

Acute severe asthma

Infectious lung disease

Pneumocystis carinii pneumonia

Tuberculosis

Necrotizing pneumonia

Interstitial lung disease

Sarcoidosis

Idiopathic pulmonary fibrosis

Histiocytosis X

Lymphangioleiomyomatosis

Connective-tissue disease

Rheumatoid arthritis

Ankylosing spondylitis

Polymyositis/Dermatomyositis

Scleroderma

Marfan's syndrome

Ehlers-Danlos syndrome

Cancer

Lung cancer

Sarcoma

 

Used with permission from ref. 39.

At the Beth Israel Deaconess Medical Center, we adhere to British Thoracic Society guidelines for the workup of these effusions, and if a diagnostic thoracentesis is required, these procedures are always performed with real-time ultrasound guidance. As recommended, the fluid is then sent in three separate tubes for pleural chemistries [e.g., lactate dehydrogenase (LDH), pH, and protein], microbiologic analysis (e.g., aerobic and anaerobic culture, Gram stain, fungal culture, and AFB stain and culture), as well as cytology. Light's criteria are used to determine whether the fluid is transudative or exudative (pleural:serum LDH > 0.6, pleural:serum protein > 0.5, or pleural LDH > two-thirds of upper normal serum value).29 While other assays have been described to distinguish exudates from transudates, Light's criteria have been validated and in clinical practice remain a mainstay of the workup.30 It is important to remember that the data may not return as classic profiles of malignant or benign disease. Certain data will "trump" others. For example, the finding of malignant cells on cytology yields a definitive diagnosis of malignant pleural effusion regardless of the protein and LDH levels. Similarly, the finding of pleural food particles suggests viscus (esophageal) perforation, independent of other findings. Other specific analyses can be run on the fluid, depending on the clinical situation. For example, the presence of milky fluid, suggestive of chylous effusion, would prompt the addition of a triglyceride level to the fluid analysis. Amylase levels of the pleural fluid specimen may be determined in suspected cases of pancreatic disease, keeping in mind that malignancy, esophageal rupture, tuberculosis, abdominal trauma, uremia, and radiation pleuritis also have been found to be associated with increased levels of amylase.31

In cases of exudative effusion, when the diagnosis is still suspect, a pleural biopsy is warranted.32 The preferred route at our institution is by means of VATS. This is done under general anesthesia, with single-lung ventilation on the nonaffected side. The exploration and biopsy usually can be accomplished through a single 12-mm port. It is important to bear in mind that the pleural tissue obtained should be sent for both pathologic and microbiologic analysis.

SPECIFIC DIAGNOSES

Empyema

Empyema is defined as a collection of pus in the pleural space. In cases associated with pneumonia, there is a continuum from simple parapneumonic effusion to complex parapneumonic effusion to empyema. Parapneumonic effusion is defined as any effusion found in association with pneumonia.33 The stages of evolution of these effusions have been described: exudative, fibrinopurulent, and organizing.34 A simple parapneumonic effusion may resolve with proper antibiotic therapy of the underlying pneumonia. A complex parapneumonic effusion is one that demonstrates a pH greater than 7.20, LDH greater than three times the normal serum LDH value, glucose less than 60 mg/dL, and positive bacterial cultures. These should be drained, but since loculations inevitably form, it is increasingly more difficult to achieve complete drainage with a tube alone. Progression to the thick, fibrous "rind" of the third stage necessitates a decortication procedure to free the lung of the rind and allow full reexpansion (Fig. 106-7). An algorithm to assess and treat patients with pneumonia who are discovered to have a pleural effusion is depicted in Fig. 106-8. Thoracentesis should be performed, and pleural chemistries, microbiology, and a postthoracentesis plain radiograph should be assessed to determine whether the effusion demonstrates poor prognostic factors. If there are poor prognostic factors, our preference is to perform early VATS drainage. In a prospective, randomized trial, Wait and colleagues demonstrated better outcomes, as measured by primary treatment success, shorter duration of chest tube drainage, and shorter hospital stay, when comparing early VATS drainage with tube thoracostomy and fibrinolytic therapy.35 Antibiotic penetration into empyemas is variable and less likely to sterilize anything more advanced than the earliest stages of a developing empyema.36

Figure 106-7.

 
 

Fibrothorax. A. CT scan demonstrating the chronic empyema cavity with a hypodense center (fluid) and a thick rind peripherally (white arrow). B. Postoperative chest film showing full expansion of the left lung (compare with Fig. 106-1C ).

 

Figure 106-8.

 

Algorithm for workup and treatment of parapneumonic effusion. (Reproduced with permission from Maskell NA, Butland RJ: BTS guidelines for the investigation of a unilateral pleural effusion in adults. Thorax 58:8–17S, 2003.)

There exists debate regarding the use of fibrinolytic therapy to optimize drainage of infected pleural fluid. The largest prospective trial (MIST1) was reported in 2005 and randomized 430 patients to receive placebo or intrapleural streptokinase in conjunction with chest tube drainage of infected pleural fluid.32 There did not appear to be an advantage over placebo in terms of need for surgery, mortality, or length of stay. The next most recent trial was significantly smaller (44 patients, 2004), but it did show a difference in length of stay and freedom from surgery.37 A meta-analysis of the five randomized, controlled trials on fibrinolytic therapy did not support the use of fibrinolytics in cases of complicated parapneumonic effusion or empyema. The authors do raise the caveat that the comparatively large size of the MIST1 trial may skew the interpretation and that there exists heterogeneity in the trials that complicates the meta-analysis.38 At this point, fibrinolytic therapy should be reserved for patients in whom surgical drainage is not an option because of comorbidities or the availability of surgery. The medical management of empyema and other nonmalignant pleural effusions is reviewed in Chapter 107.

Other routes of infection of the pleural space exist, including traumatic, direct extension of infectious processes in the abdomen or neck, and iatrogenic (i.e., surgical or interventional). For additional detail about the surgical management of empyema, see Chapter 93. Aggressive drainage remains the key to treatment for most of these conditions.

Pneumothorax

The nonspontaneous causes of pneumothorax include trauma, iatrogenic etiologies such as inadvertent laceration of the lung during central venous line placement or intentional biopsy of the lung parenchyma, and postoperative air leak. Primary spontaneous pneumothorax refers to cases that arise in previously healthy lungs, whereas secondary spontaneous pneumothorax occurs in patients with chronic obstructive pulmonary disease, cystic fibrosis, and other lung pathologies39 (see Table 106-2). The pathophysiology of both primary and secondary causes has not been well established, but the rupture of peripheral blebs or bullae is thought to be the underlying cause of primary spontaneous cases.40

Once identified, pneumothorax must treated with consideration of the patient's underlying condition. An intubated patient who is subject to positive-pressure ventilation will require closed drainage of the pleural space to prevent an unpredictable evolution of a small pneumothorax into a large or tension pneumothorax with respiratory or hemodynamic effects. Similarly, a patient with underlying lung disease and poor pulmonary reserve may tolerate less well a pneumothorax that might be treated conservatively with observation in a healthy patient with normal lungs. Treatment strategies include observation, aspiration, chest tube drainage, chemical pleurodesis, and surgical resection of the underlying pathology (i.e., blebectomy) with or without mechanical or chemical pleurodesis. These will be discussed in greater detail in Chapter 107.

Chylothorax

A pleural fluid triglyceride level greater than 110 mg/dL is diagnostic of chylothorax. The fluid is also rich in lymphocytes, as detected on cell counting. It is suggested by the presence of milky fluid that on centrifugation does not layer, as might be expected with turbid exudative fluid from an empyema.41 This visual confirmation can be enhanced by feeding the patient a fat-rich meal before the investigation. Once the chylous effusion is in a collecting system, such as that into which a chest tube drains, there is an immiscible quality to it that allows identification of the milky effluent even after the meal has been digested and the lymphatic fluid begins again to run clear. The etiology of chylothorax includes traumatic/iatrogenic sequelae and medical conditions such as lymphoma, chylous ascites, and lymphatic abnormalities.42

Conservative management includes closed drainage of the pleural space with a chest tube, strict nonenteral nutrition or medium-chain triglyceride feedings, careful observation of nutrition status, and surveillance for infections. Unfortunately, conservative management may fail in up to 48% of patients.43 Somatostatin and etilefrine have been used as medical adjuncts to conservative management with some success.44,45 Percutaneous embolization of the thoracic duct also has been used.46 However, the mainstay of treatment involves VATS ligation of the duct. This technique is discussed in Chapter 113.

SUMMARY

The spectrum of benign pleural disease is large and must be approached with a careful diagnostic algorithm depending on the clinical situation and the type of abnormality encountered—solid, liquid, or gas.

EDITOR'S COMMENT

The pleural space has shaped our surgical approaches to diseases of the chest; a fact that is painfully apparent when the space is obliterated by disease or prior surgery. The function of the pleural space is an intriguing topic for speculation, but a reasonable hypothesis is that this space contributes to the mechanical coupling of respiratory muscle function with alveolar gas exchange.

–SJM

REFERENCES

1. Oldmixon EH, Hoppin FG Jr: Comparison of amounts of collagen and elastin in pleura and parenchyma of dog lung. J Appl Physiol 56:1383–8, 1984. [PubMed: 6725092]

2. West JB: Why doesn't the elephant have a pleural space? News Physiol Sci 17:47–50, 2002. [PubMed: 11909991]

3. Agostini E: Mechanics of the pleural space. Physiol Rev 52:57–128, 1972. 

4. Lai-Fook SJ: Pleural mechanics and fluid exchange. Physiol Rev 84:385–410, 2004. [PubMed: 15044678]

5. Light R, Erozan Y, Ball WJ: Cells in pleural fluid: Their value in differential diagnosis. Arch Intern Med 132:854–60, 1973. [PubMed: 4757257]

6. Laurent TC, Fraser JR: Hyaluronan. FASEB J 6:2397–404, 1992. [PubMed: 1563592]

7. Deffebach ME, Charan NB, Lakshminarayan S, Butler J: The bronchial circulation: Small, but a vital attribute of the lung. Am Rev Respir Dis 135:463–81, 1987. [PubMed: 3544986]

8. Wang NS: The preformed stomas connecting the pleural cavity and the lymphatics in the parietal pleura. Am Rev Respir Dis 111:12–20, 1975. [PubMed: 1111395]

9. Zocchi L: Physiology and pathophysiology of pleural fluid turnover. Eur Respir J 20:1545–58, 2002. [PubMed: 12503717]

10. Oestmann JW, Bridenbaugh S, Eggeling I: Gallstone migration into the pleural space. Am J Gastroenterol 95:836–7, 2000. [PubMed: 10710103]

11. Huang PM, Chang YL, Yang CY, Lee YC: The morphology of diaphragmatic defects in hepatic hydrothorax: Thoracoscopic finding. J Thorac Cardiovasc Surg 130:141–5, 2005. [PubMed: 15999054]

12. Uchiyama T, Suzuki T, Adachi A, et al: Pancreatic pleural effusion: Case report and review of 113 cases in Japan. Am J Gastroenterol 87:387–91, 1992. [PubMed: 1539580]

13. Blackmore CC, Black WC, Dallas RV, Crow HC: Pleural fluid volume estimation: A chest radiograph prediction rule. Acad Radiol 3:103–9, 1996. [PubMed: 8796649]

14. Beres RA, Goodman LR: Pneumothorax: Detection with upright versus decubitus radiography. Radiology 186:19–22, 1993. [PubMed: 8416563]

15. Carr JJ, Reed JC, Choplin RH, et al: Plain and computed radiography for detecting experimentally induced pneumothorax in cadavers: Implications for detection in patients. Radiology 183:193–9, 1992. [PubMed: 1549671]

16. Gordon R: The deep sulcus sign. Radiology 136:25–7, 1980. [PubMed: 7384513]

17. Tocino IM, Miller MH, Fairfax WR: Distribution of pneumothorax in the supine and semirecumbent critically ill adult. AJR 144:901–5, 1985. [PubMed: 3872573]

18. Kim EA, Lee KS, Shim YM, et al: Radiographic and CT findings in complications following pulmonary resection. Radiographics 22:67–86, 2002. [PubMed: 11796900]

19. Rowan KR, Kirkpatrick AW, Liu D, et al: Traumatic pneumothorax detection with thoracic US: Correlation with chest radiography and CT—Initial experience. Radiology 225:210–4, 2002. [PubMed: 12355007]

20. Wall SD, Federle MP, Jeffrey RB, Brett CM: CT diagnosis of unsuspected pneumothorax after blunt abdominal trauma. AJR 141:919–21, 1983. [PubMed: 6605061]

21. Nandalur KR, Hardie AH, Bollampally SR, et al: Accuracy of computed tomography attenuation values in the characterization of pleural fluid: An ROC study. Acad Radiol 12:987–91, 2005. [PubMed: 16087093]

22. Hierholzer J, Luo L, Bittner RC, et al: MRI and CT in the differential diagnosis of pleural disease. Chest 118:604–9, 2000. [PubMed: 10988179]

23. Tscholakoff D, Sechtem U, de Geer G, et al: Evaluation of pleural and pericardial effusions by magnetic resonance imaging. Eur J Radiol 7:169–74, 1987. [PubMed: 3653108]

24. Yu CJ, Yang PC, Wu HD, et al: Ultrasound study in unilateral hemithorax opacification: Image comparison with computed tomography. Am Rev Respir Dis 147:430–4, 1993. [PubMed: 8430970]

25. Feller-Kopman D: Ultrasound-guided thoracentesis. Chest 129:1709–14, 2006. [PubMed: 16778292]

26. Eibenberger KL, Dock WI, Ammann ME, et al: Quantification of pleural effusions: Sonography versus radiography. Radiology 191:681–4, 1994. [PubMed: 8184046]

27. Gryminski J, Krakowka P, Lypacewicz G: The diagnosis of pleural effusion by ultrasonic and radiologic techniques. Chest 70:33–7, 1976. [PubMed: 1277928]

28. Scheurich JW, Keuer SP, Graham DY: Pleural effusion: Comparison of clinical judgment and Light's criteria in determining the cause. South Med J 82:1487–91, 1989. [PubMed: 2595416]

29. Light RW, Macgregor MI, Luchsinger PC, Ball WC Jr: Pleural effusions: The diagnostic separation of transudates and exudates. Ann Intern Med 77:507–13, 1972. [PubMed: 4642731]

30. Heffner JE, Brown LK, Barbieri CA: Diagnostic value of tests that discriminate between exudative and transudative pleural effusions: Primary Study Investigators. Chest 111:970–80, 1997. [PubMed: 9106577]

31. Villena V, Perez V, Pozo F, et al: Amylase levels in pleural effusions: A consecutive unselected series of 841 patients. Chest 121:470–4, 2002. [PubMed: 11834659]

32. Maskell NA, Davies CW, Nunn AJ, et al: UK controlled trial of intrapleural streptokinase for pleural infection. N Engl J Med 352:865–74, 2005. [PubMed: 15745977]

33. Light RW: Parapneumonic effusions and empyema. Proc Am Thorac Soc 3:75–80, 2006. [PubMed: 16493154]

34. Andrews N, Parker E, Shaw R, et al: Management of nontuberculous empyema. Am Rev Respir Dis 85:935–6, 1962. 

35. Wait MA, Sharma S, Hohn J, Dal Nogare A: A randomized trial of empyema therapy. Chest 111:1548–51, 1997. [PubMed: 9187172]

36. Teixeira LR, Sasse SA, Villarino MA, et al: Antibiotic levels in empyemic pleural fluid. Chest 117:1734–9, 2000. [PubMed: 10858410]

37. Diacon AH, Theron J, Schuurmans MM, et al: Intrapleural streptokinase for empyema and complicated parapneumonic effusions. Am J Respir Crit Care Med 170:49–53, 2004. [PubMed: 15044206]

38. Tokuda Y, Matsushima D, Stein GH, Miyagi S: Intrapleural fibrinolytic agents for empyema and complicated parapneumonic effusions: A meta-analysis. Chest 129:783–90, 2006. [PubMed: 16537882]

39. Tschopp JM, Rami-Porta R, Noppen M, Astoul P: Management of spontaneous pneumothorax: State of the art. Eur Respir J 28:637–50, 2006. [PubMed: 16946095]

40. Ayed AK, Chandrasekaran C, Sukumar M: Video-assisted thoracoscopic surgery for primary spontaneous pneumothorax: Clinicopathological correlation. Eur J Cardiothorac Surg 29:221–5, 2006. [PubMed: 16376095]

41. Maskell NA, Butland RJ: BTS guidelines for the investigation of a unilateral pleural effusion in adults. Thorax 58:8–17S, 2003. 

42. Doerr CH, Allen MS, Nichols FC 3rd, Ryu JH: Etiology of chylothorax in 203 patients. Mayo Clin Proc 80:867–70, 2005. [PubMed: 16007891]

43. Lapp GC, Brown DH, Gullane PJ, McKneally M: Thoracoscopic management of chylous fistulae. Am J Otolaryngol 19:257–62, 1998. [PubMed: 9692635]

44. Cannizzaro V, Frey B, Bernet-Buettiker V: The role of somatostatin in the treatment of persistent chylothorax in children. Eur J Cardiothorac Surg 30:49–53, 2006. [PubMed: 16725334]

45. Guillem P, Billeret V, Houcke ML, Triboulet JP: Successful management of post-esophagectomy chylothorax/chyloperitoneum by etilefrine. Dis Esophagus 12:155–6, 1999. [PubMed: 10466051]

46. Cope C: Management of chylothorax via percutaneous embolization. Curr Opin Pulm Med 10:311–4, 2004. [PubMed: 15220758]



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