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STEVEN A. SAHN, MD
ABSTRACT: Pleural fluid analysis in isolation may have or confident clinical diagnosis can be expected in up to
clinical value. To have the greatest diagnostic impact, 95% of patients. The information in this report should
the clinician must formulate a prethoracentesis diagno- allow the clinician to achieve this goal. KEY INDEX-
sis based on the clinical presentation, blood tests, and ING TERM: Pleural fluid analysis. [Am J Med Sci
radiographic imaging. With this approach, a definitive 2008;335(1):7–15.]
Table 1. Diagnoses That Can Be Established “Definitively” By Table 2. Appearance, Character, and Odor of Pleural Fluid
Pleural Fluid Analysis Helpful in Diagnosis
LDH of 0.82 (AUC, 0.89). This higher ratio should Table 5. Exudates With at Least 80% Lymphocytes
decrease the incidence of false exudates.
Disease Comment
Total Protein and LDH Acute lung rejection New or increased effusion 2–6 weeks
after transplant
The absolute concentrations of total protein and Chylothorax 2,000–20,000 lymphocytes/L;
LDH in effusions may provide additional diagnostic lymphoma most common cause
Lymphoma Often 100% of nucleated cells are
value. For example, a tuberculous pleural effusion lymphocytes; diagnostic yield on
rarely has a total protein concentration ⬍4.0 g/dL, cytology or pleural biopsy higher
whereas total protein concentrations in malignancy with non-Hodgkin lymphoma
and parapneumonic effusions present with a wider Post–coronary artery Occurs ⬎2 months after surgery; not
range.2 A total protein concentration of ⱖ7.0 g/dL bypass graft associated with trapped lung
Rheumatoid pleurisy May be associated with unexpandable
suggests Waldenström macroglobulinemia,17 multi- (chronic) lung
ple myeloma18 or a cholesterol effusion.9 Pleural Sarcoidosis Usually ⬎90% lymphocytes
fluid LDH concentration greater than three times Tuberculous effusion Most common cause of lymphocyte
the upper limits of normal of the serum LDH (⬎1000 predominant exudate; usually 90%
to 95% lymphocytes
IU/L) is typically seen only in complicated parap- Yellow nail syndrome Typically a discordant exudate (by
neumonic effusions or empyema,19,20 rheumatoid protein only); occurs in 36% during
pleurisy,21 or pleural paragonimiasis.22 course of disease
Nucleated Cells
The total nucleated cell count alone is rarely di- shortly after the onset of symptoms, ie, acute bacte-
agnostic but may provide useful information.1,2,23 rial pneumonia, acute pulmonary embolism with in-
Most exudates have ⬎1000 nucleated cells/L, while farction, and acute pancreatitis. In contrast, with the
transudates have a few hundred cells/L. Pleural insidious onset of disease, as with malignancy and
fluid nucleated cell counts ⬎10,000/L are seen tuberculosis, a lymphocyte-predominant exudate is
most commonly with parapneumonic effusions, found. Transudative effusions are never neutrophil
acute pancreatitis, subdiaphragmatic hepatic or predominant and typically have ⬍5% neutrophils;
splenic abscess, and splenic infarction. Nucleated when the neutrophils percentage is ⬎10% to 15%, a
cell counts ⬎10,000/L at times can occur with pul- second diagnosis is likely. Transudative effusions are
monary infarction, post– cardiac injury syndrome, mononuclear cell predominant, a combination of lym-
and lupus pleuritis. When the nucleated cell count is phocytes, macrophages, and mesothelial cells.
⬎50,000/L, the differential diagnosis is limited to a When the lymphocyte population exceeds 80% of
complicated parapneumonic effusion and empyema the total nucleated cells, the differential diagnosis of
and rarely acute pancreatitis and pulmonary infarc- the exudate can narrowed to the diagnoses listed in
tion. Chronic exudates typically have nucleated cell Table 5.2,4 All typically have lymphocyte populations
counts ⬍5000/L, as seen with a tuberculous pleural ⱖ80%; however, the lymphocyte population can be
effusion24 and malignancy.25 When pus is aspirated less on occasion but virtually never ⬍50%. In con-
from the pleural space (empyema), the nucleated trast to most patients with lymphoma, only about
cell count may be as low as a few hundred cells per 60% of patients with metastatic carcinoma to the
microliter because the neutrophils have undergone pleura have a majority of lymphocytes, usually in
autolysis from the harsh pleural environment of the range of 50% to 75% of the total nucleated cell
acidosis and low oxygen tension. count. A lymphocyte predominant exudate is the
The predominant cell population is determined by most appropriate indication for percutaneous pleu-
the cause and phase of the pleural injury and the ral biopsy, which is the most sensitive (75% to 85%)
timing of thoracentesis in relation to the onset of diagnostic test for tuberculous pleural effusion24
pleural injury. The acute response to most pleural with the exception of thoracoscopy.
injury, whether infectious, immunologic or possibly Pleural fluid eosinophilia is defined as a pleural
malignant, is the attraction of neutrophils to the fluid eosinophil count ⬎10% of the total nucleated
pleural space, initiated by the chemotaxin interleu- cell count. It appears that bone marrow eosinophils
kin-8.26,27 Within 72 hours after the cessation of are attracted to the pleural space primarily by in-
acute pleural injury, mononuclear cells enter the terleukin-5.29 Causes of pleural fluid eosinophilia
pleural space from the peripheral blood and become are shown in Table 6.4 The most common are pneu-
the predominant cell as macrophages.28 This macro- mothorax and hemothorax. Eosinophilic pleuritis is
phage predominance is subsequently replaced by a common, early finding in patients requiring tho-
lymphocytes in effusions that persist for greater racotomy or thoracoscopy for treatment of spontane-
than 2 weeks. Therefore, a neutrophil-predomi- ous pneumothorax.30 In contrast to the rapid move-
nant exudate is the rule when the patient presents ment of eosinophils into pleural tissue and pleural
Table 6. Exudates With Greater Than 10% Eosinophils (PFE) agnosis of malignancy; however, recent studies have
Disease Comment
shown that the prevalence of malignancy is similar
in both eosinophilic and noneosinophilic pleural ef-
BAPE 30% incidence of PFE; up to 50% fusions.35
eosinophils/total nucleated cells Pleural fluid macrophages, which originate from
Carcinoma Prevalence of PFE similar in malignant the blood monocyte, are of no diagnostic value.28
and nonmalignant effusions Mesothelial cells are exfoliated into normal pleu-
Churg-Strauss High PF eosinophil counts; associated
syndrome with blood eosinophilia ral fluid in small numbers. Although common in
Drug-induced Dantrolene, bromocriptine, transudative effusions and some exudates, me-
nitrofurantoin, valproic acid sothelial cells are rarely found in tuberculous
Fungal disease Histoplasmosis, coccidioidomycosis pleural effusion, because of the extensive pleural
Hemothorax PFE develops 1–2 weeks after involvement from the hypersensitivity reaction to
hemothorax
Lymphoma Hodgkin disease tuberculin proteins that inhibits mesothelial shed-
Parasitic disease Paragonimiasis, hydatid disease, ding.31,36 A paucity of mesothelial cells is also the
amebiasis, ascariasis typical finding in other inflammatory processes,
Pneumothorax Effusion in 10% to 20%; tissue such as empyema, chemical pleurodesis, rheuma-
eosinophilia and PFE occur
within hours toid pleuritis, and chronic malignant effusions.31
Pulmonary embolism Associated with infarction and A large number of plasma cells in pleural fluid
hemorrhagic effusion suggests pleural involvement with multiple myeloma,
Sarcoid Rare while a small number of plasma cells is nondiagnostic
Tuberculous effusion Rare and has been observed in several nonmalignant con-
BAPE, Benign asbestos pleural effusion. ditions.31 A few basophils are occasionally found in
pleural fluid and are of no clinical significance. How-
ever, when basophils represent ⬎10% of the nucleated
fluid after pneumothorax, after hemothorax eosino- cells, leukemic involvement of the pleura is likely.31
phils do not appear in pleural fluid for 1 to 2
weeks.31,32 Furthermore, pleural fluid eosinophilia Pleural Fluid PH and Glucose
is associated with peripheral blood eosinophilia fol-
lowing hemothorax that does not clear until the A limited number of diagnoses are associated with
pleural fluid resolves.32 About 30% of patients with pleural fluid acidosis, defined as a pleural fluid pH
benign asbestos pleural effusion have pleural fluid ⬍7.30, which should only be measured with a
eosinophilia, which can reach a level of 50% of the blood gas analyzer (Table 7).37,38 Pleural fluid pH
nucleated cells.33,34 It was previously believed that decreases because 1) there is an increased meta-
pleural fluid eosinophilia virtually excluded the di- bolic activity in pleural fluid as a result of neutro-
Table 7. Incidence, Pleural Fluid Range, and Clinical Comments on Diseases With Pleural Fluid Acidosis (pH ⬍7.30)
Estimated Incidence
Disease of pH ⬍7.30 (%) Range of pH Comments
Complicated parapneumonic 100 7.29–7.10 Nonpurulent effusion that usually requires pleural
effusion space drainage
Esophageal rupture 100 6.80–5.00 pH 6.00 and high salivary amylase
Rheumatoid pleurisy (chronic) 100 7.15–6.80 Associated with glucose ⬍30 mg/dL and LDH
⬎1000 IU/L
Malignant effusion 30–40 7.50–6.90 pH ⬍7.30: worse survival, increased yield on
cytology and pleural biopsy, poorer response to
pleurodesis
Lupus pleuritis 15–20 7.40–6.85 Associated with low glucose; diagnosis by LE cells
in PF
Tuberculous effusion 10–20 7.40–6.95 Associated with low glucose; when pH low, range
between 7.29 and 7.10; pleura severely
abnormal
Hemothorax ⬍10 7.50–7.17 Occurs when PF hematocrit approaches blood
hematocrit and pleura severely injured
Pancreaticopleural fistula Rare 7.50–7.28 Occurs with very high amylase and severe pleural
injury
Pulmonary infarction Rare 7.52–7.29 Occurs with grossly bloody PF and extensive
pleural injury
Diaphragmatic hernia with Single report 7.15 Acid products of infarcted bowel overwhelm efflux
capacity of pleura
phil phagocytes and bacterial metabolism (empy- A low pleural fluid pH (⬍7.30) is seen in approx-
ema); 2) the pleural membrane is abnormal (fibrotic imately one-third of patients presenting with a ma-
or inflamed) and impairs the efflux of hydrogen lignant pleural effusion.43 A low pleural fluid pH in
ions and CO2 from the pleural space into the this setting suggests that the patients will have a
circulation (rheumatoid pleurisy)38; and 3) a com- positive cytologic examination on initial testing, a
bination of the 2 mechanisms. The presence of a shorter survival time, and a poorer response to
low pleural fluid pH is helpful diagnostically and chemical pleurodesis than those with a pH ⬎7.30.43
also provides prognostic information. In the only The explanation for these findings is related to the
study of acid-base characteristics of normal hu- advanced stage of malignant pleural metastasis that
man pleural fluid, pleural fluid pH was measured inhibits the end products of glycolysis, CO2 and
at 7.64, 0.23 pH units greater than the simulta- lactic acid, from exiting the pleural space.38 How-
neously measured blood pH.39 We and others have ever, finding a low pH is not an absolute contrain-
measured an alkaline pH of ⬃7.60 in normal ani- dication to pleurodesis but should be considered in
the decision making.
mals.40,41 It appears that a bicarbonate gradient
In the normal physiologic state, pleural fluid and
between pleural fluid and blood explains the alka-
blood glucose concentrations are equivalent, as glu-
line pH of normal pleural fluid. Human transuda- cose is of low molecular weight and moves from
tive effusions have a pleural fluid pH ranging from blood to pleural fluid by simple diffusion across the
7.45 to 7.55. The vast majority of exudative effu- endothelial and mesothelial membranes. Diseases
sions have pH values that range from 7.45 to 7.30. with low pleural fluid pH may also have a low
Pleural fluid pH provides prognostic information pleural fluid glucose concentration, defined as ⬍60
and helps guide therapy in parapneumonic and ma- mg/dL or a pleural fluid/serum glucose ratio of
lignant effusions. A meta-analysis examined the ⬍0.5.44 As noted in Table 8, the only diagnoses with
prognostic value of pleural fluid pH in patients with a glucose of 0 mg/dL are chronic rheumatoid pleu-
parapneumonic effusions.42 Using ROC (receiver op- risy and empyema.
erator characteristics) analysis, it was observed that
pleural fluid pH was lower in patients who had a
complicated course and required pleural space Amylase
drainage. The primary studies recommended vari- An increased pleural fluid amylase, defined as
ous cut points for a complicated effusion that varied either a value greater than the upper limits of nor-
from 7.10 to 7.30. Although no single pH value can mal serum or a pleural fluid/serum amylase ratio
be used as a definitive cut-point for classifying pa- ⬎1.0, is found with pancreatic disease,45– 47 esopha-
tients into complicated and uncomplicated parap- geal rupture,48 –50 and malignancy.51,52 Both acute
neumonic effusions, pleural fluid pH should serve as pancreatitis and a pancreaticopleural fistula can
adjunctive information that should be combined cause an amylase-rich pleural effusion, the latter
with the clinicians’ judgment in determining the often showing amylase levels ⬎100,000 IU/L.53 An
need for pleural space drainage. increased pleural fluid amylase concentration occurs
Table 8. Incidence, Range of Glucose Concentration, and Clinical Comments on Diseases With Low Pleural Fluid Glucose
Rheumatoid pleurisy 85–90% 0–118 Glucose ⬍30 mg/dL in 75%; PF triad of glucose
⬍30 mg/dL, pH 7.00 and LDH ⬎1000 IU/L;
may precede articular manifestations by 3
years
Empyema 80–90% 0–145 Low glucose not as sensitive marker as low pH
but correlation of glucose and pH is strong
Esophageal rupture 40–50% 15–120 Characteristic pH of 6.00 and high pleural fluid
amylase (salivary)
Malignant effusion 30–40% 15–167 Low glucose concentration with chronic effusion
in far-advanced pleural malignancy
Lupus pleuritis 20–30% 32–160 Transient; associated with severe pleural
inflammation; LE cells diagnostic
Tuberculous effusion 20–30% 10–140 No correlation between low glucose and clinical
course or pleural bacteriology
Table 9. Differentiating a Cholesterol Pleural Effusion From a 90% of patients with a known malignancy.57,58 The
Chylothorax reasons for this variability include 1) the effusion
Chylothorax Cholesterol may be paramalignant, which is defined as a pleu-
ral effusion associated with a known malignancy
Incidence Uncommon (2%) Rare but malignant cells cannot be detected in the
Causes NHL, trauma, Lung entrapment: TB, pleural fluid or pleural tissue, and the effusion
surgery, LAM RA, empyema results from another mechanism (ie, atelectasis)59;
Onset Acute to subacute Insidious; develops over
years
2) the type of tumor (high positivity with adeno-
Symptoms Dyspnea None; dyspnea carcinoma and low in Hodgkin lymphoma)60,61; 3)
Appearance Serous, turbid, Milky; satin-like sheen the number of specimens submitted (yields tend to
milky, bloody increase with additional specimens owing to exfo-
Pleural fluid ⬎80% lymphocytes; Chol/TG ⬎1; PMNs; TP liation of fresher cells)61; 4) the stage of pleural
analysis TG/Chol ⬎1 ⬎5 g/dL
Diagnosis TG ⬎110 mg/dL; Cholesterol ⬎250 mg/dL; involvement (the more advanced stage the higher
chylomicrons; 300–1500 mg/dL the diagnostic yield); and 5) the interest and ex-
cholesterol 60–200 cholesterol crystals pertise of the cytopathologist.
mg/dL
Treatment Underlying disease; Observe, decortication
pleurodesis, Flow Cytometry
thoracic duct
ligation, octreotide Flow cytometry can be helpful in the diagnosis of
lymphoma of the pleura, as it can specifically
NHL, Non-Hodgkin lymphoma. define lymphocyte surface markers.62 It can define
the clonality of a population of lymphocytes to
determine whether the cells are from T- or B-cell
in 10 –14% of patients with a malignant pleural effu- lineage. Therefore, flow cytometry is most helpful
sion; on isoenzyme analysis, salivary-type amylase is in patients with a lymphocyte-predominant pleu-
predominant.47,52 Adenocarcinoma of the lung is the ral effusion when lymphoma is in the differential
most common malignancy associated with a salivary diagnosis.
amylase-rich pleural effusion, followed by adenocarci-
noma of the ovary.47,52 Adenocarcinoma cells have Conclusion
been documented to secrete a salivary-like isoamy-
lase.52 Esophageal rupture is also characterized by the For pleural fluid analysis to be most valuable, the
presence of pleural fluid salivary isoamylase.48 –50 clinician must have a well thought-out pre-thoracen-
tesis diagnosis based on the history, physical exami-
Triglycerides and Cholesterol nation, ancillary laboratory findings, and radiographic
imaging. With a presumptive clinical diagnosis in con-
There are 2 types of lipid pleural effusions, cert with a good working knowledge of pleural fluid
chylothorax and a cholesterol effusion, also termed analysis, a definitive or confident clinical diagnosis can
chyliform effusion or pseudochylothorax (Table 9). be determined in up to 95% of patients. Without this
A chylothorax represents leakage of chyle into the approach, the clinician may be left with an unaccept-
pleural space from the thoracic duct or one of its able number of problematic or undiagnosed pleural
major tributaries.54,55 The most frequent cause of effusions.
a chylothorax is malignancy, most commonly non-
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