Pleural Effusion Accp

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Evaluation of the Patient with a Pleural EffusionPCCSU Article | 01.15.08

By Steven A. Sahn, MD, FCCP

Dr.Sahn is Professor of Medicine and Director, Division of Pulmonary, Critical Care, Allergy and Sleep

Medicine, Medical University of South Carolina, Charleston, SC.

Dr.Sahn has disclosed no significant relationships with the companies/organizations whose products or

services may be discussed within this chapter.

Objectives

1. To understand the diagnostic value of pleural analysis.

2. To appreciate the value of pleural pH in narrowing the differential diagnosis of the exudate.

Key words: pleural effusion; pleural fluid analysis

Pleural effusions are a common occurrence that involve all specialities of medicine and surgery. The

annual incidence of new pleural effusions in the United States is estimated to be at least 1.5

million. 1 Thoracentesis is a relatively simple diagnostic procedure that can be performed in the office, at

the bedside, in the ICU, or in a dedicated procedure suite. Pleural fluid analysis in isolation may result in

only a small percentage of diagnoses with a high clinical likelihood that provides a strong argument for

generating a prethoracentesis diagnosis. If the clinician obtains a thorough history, performs a careful

physical examination, orders appropriate blood tests, and interprets the chest images thoughtfully prior

to thoracentesis, the likelihood of determining a likely clinical, if not definitive, diagnosis is greatly

enhanced. In this chapter, I will not only discuss discriminating information from the pleural fluid

analysis but also will address salient features of the history, physical examination, and radiographic

imaging that should lead to a logical prethoracentesis differential diagnosis.

History

Patients may be symptomatic or asymptomatic on presentation with a pleural effusion. Diagnoses in

which patients typically do not present with symptoms are listed in Table 1. For example, about half of

the patients with rheumatoid pleural effusion are asymptomatic,2 and 60 to 70% of patients with benign

asbestos pleural effusion (BAPE) have no symptoms.3 In contrast, as shown in Table 2, patients with

bacterial pneumonia, lupus pleuritis,4

postcardiac injury syndrome (PCIS),5

and congestive heart failure

virtually always have symptoms in association with their pleural effusions.

Dyspnea and chest pain are the most common symptoms of patients with a pleural effusion. Those with

a small pleural effusion and normal underlying lungs may have no perceptible symptoms. In contrast,

patients may present with a massive pleural effusion associated with contralateral mediastinal shift,

leading to dyspnea at rest. Pleuritic chest pain is the cardinal symptom of pleural inflammation and is


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typically accompanied by a pleural effusion.6 Pleuritic chest pain varies with the intensity of the

inflammation. Patients have described pleuritic chest pain as "stabbing," "shooting," or having a "stitch

in the side." This type of pain is exacerbated by deep inspiration, cough, or sneezing. Pleuritic chest pain

may be focused over the precise location of the inflammation or may be referred. With costal pleural

inflammation, the pain tends to be localized directly over the site of pleural involvement and is often

associated with tenderness on pressure and cutaneous hypersensitivity. When the lateral, anterior, and

portions of the posterior diaphragm are inflamed, pain is perceived diffusely over the lower thorax, back,

and abdomen. In contrast, inflammation of the central portion of the diaphragmatic pleura does not

result in local pain; pain is referred to the ipsilateral posterior neck, shoulder, and trapezius muscle.Central diaphragmatic pleural inflammation causes referred pain because the sensory fibers of the

phrenic nerve enter the spinal cord at the C4 level, which is the usual entry point of sensation from the

shoulder.6

Although the number of drugs associated with pleural disease is significantly fewer than those that are

presumed to cause parenchymal lung disease, drugs should always be considered as a possible cause of

a pleural effusion or pleural fibrosis, especially when the etiology of the effusion is problematic. 7 Some of

the drugs that have been associated with a pleural effusion, in more than a single case, include

bromocriptine, cyclophosphamide, dantrolene, isotretinoin, mesalamine, methotrexate, mitomycin,

nitrofurantoin, practolol, procarbazine, and valproic acid.

Physical Examination

Pleural fluid interferes with sound transmission from the lung to the stethoscope, as it separates thelung from the chest wall. Physical signs of a pleural effusion depend on the volume of pleural fluid and

the degree of lung compression. The status of the underlying lung and the patency of the bronchial tree

will modulate the physical findings. The physical examination results will be essentially normal when the

fluid volume is


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Bilateral effusions are most commonly transudates, as seen with congestive heart failure, nephrotic

syndrome, hypoalbuminemia, and constrictive pericarditis. The cardiac silhouette is virtually always

enlarged in congestive heart failure but may be of normal size with nephrotic syndrome and constrictive

pericarditis.16

Bilateral pleural effusions with a normal heart size are most likely related to malignancy

from a nonlung primary but can also occur with lupus pleuritis, rheumatoid pleurisy, hepatic

hydrothorax, and hypoalbuminemia.16

A chest radiograph with interstitial infiltrates raises the differential diagnosis of congestive heart failure,

rheumatoid disease,11 asbestos pleuropulmonary disease,3 lymphangiticcarcinomatosis,17lymphangioleiomyomatosis, 18 viral and mycoplasma

pneumonia,19

sarcoidosis,20

and Pneumocystis cariniipneumonia.21

Pleural effusions associated with

multiple pulmonary nodules suggest cancer (most common), Wegener granulomatosis,22

rheumatoid

disease,11 septic pulmonary emboli,23 sarcoidosis,20 or tularemia.24

Pleural Fluid Analysis

Virtually all patients with a newly discovered pleural effusion should undergo thoracentesis to confirm a

diagnosis. Exceptions include the patient who has typical congestive heart failure with a clinical diagnosis

that does not raise suspicion for an alternative diagnosis or a pleural effusion that is extremely small, as

with viral pleurisy. Observation is warranted in the previously mentioned examples; however, if the

clinical situation worsens or is atypical, a thoracentesis should be performed without delay. For example,

if a patient with congestive heart failure has pleuritic chest pain, fever, a unilateral effusion, a left

effusion greater than the right effusion, a normal cardiac silhouette, or an oxygen tension valve out of

proportion to the clinical situation, a thoracentesis should be done immediately.25 In a prospective studyof 129 patients with pleural effusion published 20 years ago, thoracentesis provided a definitive

diagnosis in only 18% and a presumptive diagnosis in 55%.26

In the remaining 27% of patients, the

pleural fluid findings were not helpful diagnostically because the values were compatible with two or

more clinical possibilities. However, in a number of these patients, the findings excluded possible

diagnoses, such as empyema. Over the years, health-care professionals have become better educated

about pleural fluid analysis; in conjunction with the clinical presentation, this should enable a definitive

or confident presumptive diagnosis in close to 95% of patients. Table 3 enumerates the diseases where

a diagnosis can be established "definitively" by pleural fluid analysis.27

Positive cytologic findings, pus in

the pleural space, or isolation of an organism from the fluid is obviously diagnostic. However, finding a

low pH and a high salivary amylase in the pleural fluid establishes the diagnosis of esophageal rupture in

the absence of malignancy. Other examples are the characteristic cytologic findings in a patient with

rheumatoid pleurisy28 or finding 2-transferrin in the pleural fluid,29 diagnostic for a duropleural fistula.


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Observation

The initial diagnostic step is to closely examine the pleural fluid as it is aspirated from the pleural space.

The color, character, and odor of the fluid may either be diagnostic or helpful in diagnosis (Table

4).27 Clear, straw-colored fluid suggests a transudate, but a paucicellular exudate cannot be excluded.

Sanguinous fluid (hematocrit value


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The character of the fluid can also suggest a diagnosis. If pus is aspirated, an empyema is established.

Pus is determined by the gross appearance of the fluid, which is a thick, viscous, yellow-white, opaque

fluid. If the pus has a putrid odor, an anaerobic infection is confirmed. If the pleural fluid appears to

contain debris, rheumatoid pleurisy with exfoliation of rheumatoid nodules from the visceral pleural

surface into the pleural space is a likely cause.28 If pleural fluid smells like ammonia, the diagnosis is

urinothorax, which is caused by obstructive uropathy.36

Exudates vs Transudates

The next deductive step in evaluating patients with a pleural effusion is to determine whether the

effusion is an exudate or transudate. Patients with transudative effusions have normal pleurae and

limited diagnostic possibilities, and the effusion is formed because hydrostatic pressures increase or

oncotic pressure decreases, or a combination of the two (Table 5).1,25 Rare causes of transudates

develop from an extravascular origin (pleural effusions of extravascular origin) and include urinothorax,

duropleural fistula, peritoneal dialysis, and extravascular migration of a central venous catheter withsaline infusion.35 In contrast, exudative effusions have a more extensive differential diagnosis, as these

effusions are caused by inflammation, infection, malignancy, and lymphatic abnormalities (Table 6).25,27


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It is important to distinguish between a transudate and an exudate accurately. The detection of an

exudative pleural effusion warrants additional diagnostic testing in most patients to determine the

underlying cause. Conversely, the patients clinical presentation is usually sufficient to determine the

cause of a transudative effusion without further testing.

An exudative effusion is defined by the presence of a high concentration of large, molecular weight

proteins compared with transudates. Although several tests have been suggested to separate

transudates from exudates, the two tests that appear to have the highest specificity and sensitivity are

the pleural fluid-to-serum total protein ratio and the pleural fluid LDH (lactate dehydrogenase) compared

with the upper limits of the normal serum LDH.37

The total protein ratio can be used because the pleural

fluid and serum values are related; however, because there is no correlation between pleural fluid and

serum LDH, the previously mentioned ratio should be used instead.38

If the pleural fluid-to-serum total

protein ratio is >0.50 or the pleural fluid LDH is >0.67 of the upper limit of normal serum LDH, the fluid

is most likely an exudate. If both total protein and LDH ratios are 0.50 and 0.67, respectively, the fluid

is most likely a transudate.1

Subsequent validation studies using pooled data from several primary

investigations reported that the above criteria have a sensitivity of 98% and a specificity of 74% inidentifying an exudative pleural effusion.

1However, the closer the values are to the cut-point, the fluid is

likely to be either a transudate or an exudate, while the further the value is from the cut-point, the more

likely the fluid is to be a transudate or an exudate. It should be recognized that treatment of the patient

may affect pleural fluid values; for example, in patients with congestive heart failure treated with

diuretics, either the protein or LDH ratio may be increased from the transudative range prior to diuresis

to the exudative range following diuresis. A more recent study by Joseph and colleagues,39 using

receiver operating characteristic curve analysis, found that the test with the highest sensitivity and

specificity for separating transudates and exudates was a pleural fluid LDH compared with the upper

limit of the normal serum LDH ratio of 0.82 (AUC = 0.89); this higher ratio decreases the incidence of

false exudates.


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Total Protein and LDH

The absolute concentrations of total protein and LDH may be of some diagnostic value. For example, a

tuberculous pleural effusion rarely has a total protein concentration 1,000 IU/L) for the serum LDH is typically seen only in complicated parapneumonic effusions

or empyema,42,43 rheumatoid pleurisy,44or pleural paragonimiasis.45

Nucleated Cells

The total nucleated cell count is rarely diagnostic but may provide useful information.1,25,46 Mostexudates have >1,000 nucleated cells/L, while transudates have a few hundred cells per microliter.

Pleural fluid nucleated cell counts >10,000/L are seen most commonly with parapneumonic effusions,

acute pancreatitis, subdiaphragmatic abscesses, liver, hepatic and splenic abscesses, and splenic

infarction. Nucleated cell counts >10,000/L at times can occur with pulmonary infarction, PCIS, and

lupus pleuritis. When the nucleated cell count is >50,000/L, the differential is limited to a complicated

parapneumonic effusion and empyema and rarely with acute pancreatitis and pulmonary infarction.

Chronic exudates typically have nucleated cell counts


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The predominant cell population is determined by the type of pleural injury and the timing of

thoracentesis in relation to the acute pleural injury. The acute response to any pleural injury, whether

infectious, immunologic, or malignant, is the attraction of neutrophils to the pleural space, initiated by

the chemotaxin interleukin-8.48,49

Within 72 h following the cessation of acute pleural injury,

mononuclear cells enter the pleural space from the peripheral blood and become the predominant

cells.50 This macrophage predominance is subsequently replaced by lymphocytes in effusions that persist

for >2 weeks. Therefore, a neutrophil-predominant exudate is the rule when the patient presents shortly

after the onset of symptoms, ie, acute bacterial pneumonia, acute pulmonary embolism with infarction,

and acute pancreatitis. In contrast, with the insidious onset of disease, as with malignancy andtuberculosis, a lymphocyte-predominant exudate is found. Transudative effusions are never neutrophil-

predominant (usually 10 to 15%, a second

diagnosis is likely. Transudative effusions are mononuclear-cell-predominant, a combination of

lymphocytes, macrophages, and mesothelial cells.

When the lymphocyte population is >80% of the total nucleated cells, the differential diagnosis of the

exudate is narrowed to those entities shown in Table 7.25,27 All the diagnoses listed in the table typically

have lymphocyte populations 80%; the lymphocyte population can occasionally be less but virtually

never 10% of the total nucleated

cell count. It appears that bone marrow eosinophils are attracted to the pleural space primarily by

interleukin-5.52Causes of PFE are shown in Table 8.27 The most common causes are pneumothorax and

hemothorax. Eosinophilicpleuritis is a common, early finding in patients requiring thoractomy or

thoracoscopy for treatment of spontaneous pneumothorax.53

In contrast to the rapid movement of

eosinophils into the pleura and pleural fluid in pneumothorax, eosinophils do not appear in the pleural

space for 1 to 2 weeks following hemothorax.54Furthermore, PFE is associated with peripheral blood

eosinophilia following trauma that does not clear until the pleural fluid resolves.55

About 30% of patients

with BAPE have PFE, which, at times, totals 50% of the nucleated cells. 56,57 It was previously thought


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that PFE virtually excluded the diagnosis of malignancy; however, recent studies have shown that the

prevalence of malignancy is similar in both eosinophilic and noneosinophilic pleural effusions. 58

Pleural fluid macrophages, which originate from the blood monocyte, are of no diagnostic

value.50 Mesothelial cells are exfoliated into normal pleural fluid in small numbers. Although common in

transudative effusions and some exudates, mesothelial cells are rarely found in tuberculous pleural

effusion, because of the extensive pleural involvement from the hypersensitivity reaction to tuberculin

proteins that inhibits mesothelial shedding.54,59 The paucity of mesothelial cells is also the typical finding

in other inflammatory processes, such as empyema, chemical pleurodesis, rheumatoid pleuritis, andchronic malignant effusions.54

A large number of plasma cells in pleural fluid suggests pleural involvement with multiple myeloma,

while a small number of plasma cells isnondiagnostic and has been observed in several nonmalignant

conditions.54

A few basophils are occasionally found in pleural fluid and are of no clinical significance.

However, when basophils represent >10% of the nucleated cells, leukemic involvement of the pleura is

likely.54

Pleural Fluid pH and GlucoseA limited number of diagnoses are associated with pleural fluid acidosis, which is defined as a pleural

fluid pH


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ranging from 7.45 to 7.55. The vast majority of exudative effusions have pH values that range from

7.45 to 7.30, while a small number of exudates are associated with pleural fluid acidosis (pH


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parapneumonic effusions.65 Using receiver operating characteristic curve analysis, it was observed that

the pleural fluid pH was lower in patients who had a complicated course and required pleural space

drainage. The primary studies recommended various cut-points for a complicated effusion that varied

from 7.10 to 7.30. While no single pH value can be used as a definitive cut-point for classifying patients

as having complicated or uncomplicated parapneumonic effusions, the pleural fluid pH serves as

adjunctive information that should be combined with the clinicians judgment in determining the need for

pleural space drainage.

A low pleural fluid pH (7.30.66

The explanation for these findings is related to the advanced

stage of malignant pleural metastasis that inhibits the end products of glycolysis from exiting the pleural

space.61

Finding a low pH is not an absolute contraindication to pleurodesis but should be considered in

the decision when contemplating treatment.

In the normal physiologic state, pleural fluid and blood glucose concentrations are equivalent, as glucose

is of low molecular weight and moves from blood to pleural fluid by simple diffusion across the

endothelial and mesothelial membranes. The same diseases associated with low pleural fluid pH also

have a low pleural fluid glucose concentration, which is defined as


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Amylase

An increased pleural fluid amylase level, defined as either a value greater than the upper limits of

normal serum or a pleural fluid/serum amylase ratio >1.0, is found with pancreatic disease,68-

71esophageal rupture,

72-74and malignancy.

70,75,76Both acute pancreatitis and a pancreaticopleural fistula

can cause an amylase-rich pleural effusion, the latter often having amylase levels >100,000 IU/L.75 An

increased pleural fluid amylase concentration occurs in 10 to 14% of patients with a malignant pleural

effusion. On isoenzyme analysis, the amylase in these malignant effusions is virtually all salivary-type.68,70,76 Adenocarcinoma of the lung is the most common malignancy associated with a salivary

amylase-rich pleural effusion followed by adenocarcinoma of the ovary.70,76

It has been demonstrated

that adenocarcinoma cells secrete a salivary-like isoamylase.75

Esophageal rupture is also characterized

by the presence of pleural fluid salivary isoamylase.

Triglycerides and Cholesterol

There are two types of lipid pleural effusions, chylothorax and a cholesterol effusion, also called a

chyliform effusion or pseudochylothorax. Table 11 provides detailed information that clearly

demonstrates the differences between these two lipid effusions. A chylothorax represents leakage of

chyle into the pleural space from the thoracic duct or one of its major tributaries.77,78

The most common

cause of a chylothorax is lymphoma, most commonly non-Hodgkin lymphoma. A cholesterol effusion is a

chronic form of lung entrapment that is most commonly associated with rheumatoid pleurisy and

tuberculosis.32,79

The diagnosis of chylothorax is highly likely when the pleural fluid triglyceride

concentration is >110 mg/dL and is highly unlikely if the triglyceride concentration is


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malignant cells cannot be detected in pleural fluid or pleural tissue and the effusion results from another

mechanism (ie, atelectasis)82; (2) the type of tumor (high adenocarcinoma positivity and low in Hodgkin

lymphoma)83,84; (3) the number of specimens submitted (yields tend to increase with additional

specimens, owing to exfoliation of fresher cells)84

; (4) the stage of pleural involvement (the more

advanced stage, the higher the diagnostic yield); and (5) the interest and expertise of the

cytopathologist.

Flow Cytometry

Flow cytometry can be helpful in the diagnosis of lymphoma of the pleura. Flow cytometry canspecifically define lymphocyte surface markers.85 Therefore, it can define clonality of a population of

lymphocytes to determine whether the cells are from T- or B-cell lineage. Therefore, flow cytometery is

most helpful in patients with a lymphocyte-predominant pleural effusion when lymphoma is in the

differential diagnosis.

Conclusion

For pleural fluid analysis to be most valuable, the clinician must have a solid prethoracentesis diagnosis

based on a patients history, physical examination, laboratory findings, and radiographic imaging. With a

presumptive clinical diagnosis in concert with a good working knowledge of pleural fluid analysis, a

definitive or confident clinical diagnosis can be determined in 95% of patients. Without this approach,

the clinician may be left with an unacceptable number of problematic or undiagnosed pleural effusions.

Poststudy Questions

References

1. Light RW. Pleural diseases. 4th ed. Baltimore, MD: Lippincott, Williams and Wilkins, 2001

2. Carr DT, Mayne JG. Pleurisy with effusion in rheumatoid arthritis, with reference to the low concentration of

glucose in pleural fluid. Am Rev Respir Dis 1962; 85:345-3503. Epler GR, McLoud TC, Gaensler EA. Prevalence and incidence of benign asbestos pleural effusion in aworking

population. JAMA 1982; 247:617-622

4. Good JT Jr, King TE, Antony VB, et al. Lupus pleuritis: clinical features and pleural fluid characteristics withspecial reference to pleural fluid antinuclear antibody titers. Chest 1983; 84:714-718

5. Stelzner TJ, King TE, Antony VB, et al. The pleuropulmonary manifestations of the postcardiac injury syndrome.Chest 1983; 84:383-387

6. Sahn SA, Heffner JE. Approach to the patient with pleurisy. In: Kelley WN, ed. Textbook of internal medicine.2nd ed. Philadelphia, PA: JB Lippincott Company, 1991; 1887-1890

7. Sahn SA. Drug-induced pleural disease. In: Camus P, Rosenow E, eds. Drug- induced iatrogenic lung disease.London, UK: Hodder Arnold. In press

8. Hopkins HU. Principles and methods of physical diagnosis. 3rd ed. Philadelphia, PA: WB Saunders, 1965; 202-230

9. Berger HW, Mejia E. Tuberculous pleurisy. Chest 1973; 63:88-92

10. Alptekin F. An epidemic of pleurisy with effusion in Bitl is, Turkey: a study of 559 cases. US Armed Forces Med J1958; 9:1-11

11. Walker WC, Wright V. Pulmonary lesions in rheumatoid arthritis. Medicine 1968; 47:501-519

12. Maher GG, Berger HW. Massive pleural effusions: malignant and non-malignant causes in 46 patients. Am RevRespir Dis 1972; 105:458-460

13. Lieberson M. Diagnostic significance of the mediastinal profile in massive unilateral pleural effusions. Am RevRespir Dis 1963; 88:176-180


14/16

14. Heller RM, Janower ML, Weber AL. The radiological manifestations of malignant pleural mesothelioma. Am JRoentengol 1971; 108:53-59

15. Lorch DG, Sahn SA. Pleural effusions due to diseases below the diaphragm. SemRespir Med 1987; 9:75-85

16. Rabin CB, Blackman NS. Bilateral pleural effusions: its significance in association with a heart of normal size. JMt Sinai Hosp 1957; 24:45-53

17. Janower ML, Blennerhassett JB. Lymphangitic spread of metastatic cancer to the lung: a radiologic-pathologicclassification. Radiology 1971; 101:267-273

18. Taylor JR, Ryu J, Colby TV, et al. Lymphangioleiomyomatosis: clinical course in 32 patients. N Engl J Med1990; 323:1254-1260

19. Fine NL, Smith LR, Sheedy PF. Frequency of pleural effusions in mycoplasma and viral pneumonias. N Engl JMed 1970; 283:790-793

20. Soskel NT, Sharma OP. Pleural involvement in sarcoidosis: case presentation and detailed review of theliterature. SeminRespir Med 1992; 13:492-514

21. Horowitz ML, Schiff M, Samuels J, et al. Pneumocystis cariniipleural effusion: pathogenesis and pleural fluidanalysis. Am Rev Respir Dis 1993; 148:232-234

22. Maguire R, Fauchi AS, Doppman JL, et al. Unusual radiographic features of Wegeners granulomatosis. Am JRoentengol 1978; 130:233-238

23. Gumbs RV, McCauley DI. Hilar and mediastinaladenopathy in septic pulmonary embolic disease. Radiology1982; 142:313-315

24. Rubin SA. Radiographic spectrum of pleuropulmonarytularemia. Am J Roentengol 1978; 131:277-281

25. Sahn SA. The pleura. Am Rev Respir Dis 1988; 138:184-234

26. Collins TR, Sahn SA. Thoracentesis: complications, patient experience and diagnostic value. Chest 1987;91:817-822

27. Sahn SA. The diagnostic value of pleural fluid analysis. SeminRespirCrit Care Med 1995; 16:269-278

28. Nosanchuk JS, Naylor B. A unique cytologic picture in pleural fluid from patients with rheumatoid arthritis. Am JClinPathol 1968; 50:330-335

29. Skedros D, Cass S, Hirsch B, et al. Beta-2 transferrin assay in clinical management of cerebral spinal fluid andperilymphatic fluid leaks. J Otolaryngol 1993; 22:341-344

30. Joseph J, Sahn SA. Thoracic endometriosis syndrome: new observations from an analysis of 110 cases. Am JMed 1996; 100:164-170

31. Doerr C, Allen M, Nichols FR, et al. Etiology of chylothorax in 203 patients. Mayo ClinProc 2005; 80:867-870

32. Coe JE, Aikawa JK. Cholesterol pleural effusion. Arch Intern Med 1961; 108:763-774

33. Lillington GA, Carr DT, Mayne JG. Rheumatoid pleurisy with effusion. Arch Intern Med 1971; 128:764-768

34. Strange C, Allen ML, Freedland P, et al. Biliopleural fistula as a complication of percutaneous biliary drainage:experimental evidence for pleural inflammation. Am Rev Respir Dis 1988; 137:959-96l

35. Sahn SA. Pleural effusions of extravascular origin (PEEVO). Clin Chest Med 2006; 27:285-308

36. Stark DD, Shanes JG, Baron RL, et al. Biochemical features of urinothorax. Arch Intern Med 1982; 42:1503-1511

37. Light RW, MacGregor I, Lusinger PC, et al. Pleural effusion: the diagnostic separation of transudates andexudates. Ann Intern Med 1972; 77:507-513

38. Heffner JE, Brown LK, Barbieri C. Diagnostic value of tests that discriminate between exudative andtransudative pleural effusions. Chest 1997; 111:970-979

39. Joseph J, Badrinath P, Basran G, et al. Is the pleural fluid transudate or exudate? A revisit of the diagnosticcriteria. Thorax 2001; 56:867-870

40. Winterbauer RH, Riggins RC, Griesman FA, et al. Pleuropulmonary manifestations ofWaldentrmsmacroglobulinemia. Chest 1974; 66:368-375

41. Rodriguez JN, Pereira A, Martinez JC, et al. Pleural effusion and multiple myeloma. Chest 1994; 105:622-624

42. Light RW, Girard WM, Jenkinson SG, et al. Parapneumonic effusions. Am J Med 1980; 69:507-511

43. Potts DE, Levin DC, Sahn SA. Pleural fluid pH and parapneumonic effusions. Chest 1976; 70:328-331

44. Pettersson T, Klockers M, Helmstrom PE. Chemical and immunological features of pleural effusions:comparison between rheumatoid arthritis and other diseases. Thorax 1982; 37:354-361


15/16

45. Johnson JR, Falk A, Iber C, et al. Paragonomyacis in the United States: a report of 9 cases in Hmongimmigrants. Chest 1982; 82:168-171

46. Light RW, Erozan YS, Ball WC. Cells in pleural fluid: their value in differential diagnosis. Arch Intern Med 1973;132:854-860

47. Pettersson T, Riska H. Diagnostic value of total and differential leukocyte counts in pleural effusions. Acta MedScand 1981; 210:129-135

48. Antony VB, Repine JE, Sahn SA. Experimental models of inflammation in the plerual space. In: Chretien J,Bignon J, Hirsch A, eds. The pleura in health and disease. New York, NY: Marcel Dekker, 1985; 253-266

49. Antony VB, Godbey SW, Kunkel SL, et al. Recruitment of inflammatory cells to the pleural space chemotaticcytokines, IL8, and monocyte chemotatic peptide 1 in human pleural fluid. J Immunol 1993; 151:7216-7223

50. Antony VB, Sahn SA, Antony AC, et al. Bacillus calmette-guerin stimulated neutrophils release chemotaxins formonocytes in rabbit pleural spaces and in vitro. J Clin Invest 1985; 76:1514-1521

51. Yam LT. Diagnostic significance of lymphocytes in pleural effusions. Ann Intern Med 1967; 66:972-982

52. Nakamura Y, Ozaki T, Kamei T, et al. Factors that stimulate proliferation and survival of eosinophils ineosinophilic pleural effusion: relationship to granulocytes/macrophage colony stimulating factor, interleuken-5,and interleuken-5. Am Rev Cell MolBiol 1993; 8:605-611

53. Askin FB, McCann BG, Kuhn C. Reactive eosinophilicpleurit is. Arch Pathol Lab Med 1997; 101:187-191

54. Spriggs AI, Boddington MM. The cytology of effusions. 2nd ed. New York, NY: Grunn and Stratton, 1968

55. Maltais F, Laberge F, Cormier Y. Blood hyper-eosinophilia in the course of posttraumatic pleural effusion. Chest

1990; 98:348-351

56. Mattson SB. Monosymptomatic exudative pleurisy in persons exposed to asbestos dust. Scand J Respir Dis1997; 56:263-272

57. Hillerdal G, Ozesmi M. Benign asbestos pleural effusion: 73 exudates in 60 patients. Eur J Respir Dis 1987;71:113-121

58. Rubins JB, Rubins HB. Etiology and prognostic significance of eosinophilic pleural effusions: a prospectivestudy. Chest 1996; 110:1271-1274

59. Hurwitz S, Leiman G, Shapiro C. Mesothelial cells in pleural fluid: TB or not TB? S Afr Med J 1980; 57:938-939

60. Good JT, Taryle DA, Maulitz RM, et al. The diagnostic value of pleural fluid pH. Chest 1980; 78:55-59

61. Sahn SA. Pleural fluid pH in the normal state and in diseases affecting the pleural space. In: Chretien J, BignonJ, Hirsch A, eds. The pleura in health and disease. New York, NY: Marcel Dekker, 1985; 253-266

62. Yamada S. Uberdieseroseflussigkeit in der plerachohle der gesunden menschen. Z GesExp Med 1933; 90:343-

348

63. Sahn SA, Willcox ML, Good JT Jr, et al. Characteristics of normal rabbit pleural fluid: physiologic andbiochemical implications. Lung 1979; 156:63-69

64. Rolf LL, Travis DM. Pleural fluid-plasma bicarbonate gradients in oxygen-toxic and normal rats. J Physiol 1973;224:857-861

65. Heffner JE, Brown LK, Barbieri C. Pleural fluid chemical analysis in parapneumonic effusions: a meta-analysis.Am J RespirCrit Care Med 1995; 51:1700-1708

66. Sahn SA, Good JT Jr. Pleural fluid pH in malignant effusions: diagnostic, prognostic, and therapeuticimplications. Ann Intern Med 1988; 108:345-349

67. Sahn SA. Pathogenesis and clinical features of diseases associated with a low pleural fluid glucose. In: ChretienJ, Bignon J, Hirsch A, eds. The pleural in health and disease. New York, NY: Marcel Dekker, 1985; 267-285

68. Light RW, Ball WC Jr. Glucose and amylase in pleural effusions. JAMA 1973; 225:257-260

69. Kaye MD. Pleuropulmonary complications of pancreatitis. Thorax 1968; 23:297-306

70. Joseph J, Viney S, Beck P, et al. A prospective study of amylase-rich pleural effusion with special reference toamylase isoenzyme analysis. Chest 1992; 102:1455-1459

71. Rockey DC, Cello JP. Pancreaticopleural fistula: a report of 7 cases and review of the literature. Medicine 1990;69:332-334

72. Maulitz RM, Good JT Jr, Kaplan RL, et al. The pleuropulmonary consequences of esophageal rupture in anexperimental model. Am Rev Respir Dis 1979; 120:363-367

73. Abbott OA, Mansour KA, Logan WD Jr, et al. A traumatic so-called "spontaneous" rupture of the esophagus: areview of 47 personal cases with comments on the new method of surgical therapy. J ThoracCardiov Sur 1970;59:67-83


16/16

74. Sherr HP, Light RW, Morson MH, et al. Origin of pleural fluid amylase in esophageal rupture. Ann Intern Med1972; 76:75-76

75. Ende N. Studies of amylase activity in pleural effusions and ascites. Cancer 1960; 13:283-287

76. Kramer MR, Sepero RJ, Pitchenik AE. High amylase in neoplasm-related pleural effusions. Ann Intern Med1989; 110:567-569

77. Staats BA, Ellefson RD, Budahn LL, et al. The lipoprotein profile of chylous and non-chylous pleural effusions.Mayo ClinProc 1980; 55:700-704

78. Teba L, Dedhia AT, Bowen R, et al. Chylothorax review. Crit Care Med 1985; 13:49-52

79. Hamm H, Pfalzer B, Fabell H. Lipoprotein analysis in a chyloform pleural effusion: implications for pathogenesisand diagnosis. Respiration 1991; 58:294-300

80. Grunze H. The comparitive diagnostic accuracy, efficiency, and specificity of cytologic techniques used in thediagnosis of malignant neoplasm and serous effusions of the pleuroperitoneal cavities. ActaCytol 1964; 8:150-164

81. Jarvi OH, Kunnas RJ, Laitio MT, et al. The accuracy and significance of cytologic cancer diagnosis of pleuraleffusions. ActaCytol 1972; 16:152-157

82. Sahn SA. Malignant pleural effusions. SeminRespir Med 1987; 9:43-53

83. Naylor B, Schmidt RW. The case for exfoliator cytology of serous effusions. Lancet 1964; 1:711-712

84. Melamed MR. The cytologic presentation of malignant lymphomas in related diseases and effusions. Cancer1963; 16:413-431

85. Moriarty AT, Wiersema L, Snyder W, et al. Immunophenotyping of cytologic specimens by flow cytometry.DiagnCytopathol 1993; 9:252

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