Acs0404 Pleural Effusion

© 2006 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice
4 THORAX 4 PLEURAL EFFUSION — 1

4 PLEURAL EFFUSION
Rafael S. Andrade, M.D., and Michael Maddaus, M.D., F.A.C.S.

Approach to the Patient with a Pleural Effusion

Pleural effusion is a common problem in surgical practice. It cer) can raise the index of suspicion for an effusion and provide
results from perturbations of normal pleural fluid transport, which guidance regarding possible causes. Careful physical examination
are produced by three main mechanisms—abnormalities in of the chest can detect an effusion, and many physical signs may
Starling’s equilibrium, increased capillary and mesothelial perme- provide clues to the cause. Physical signs that are particularly useful
ability, and interference with lymphatic drainage. These mecha- for diagnostic purposes include jugular venous distention and tachy-
nisms are associated with a variety of different causes [see Table cardia (suggestive of congestive heart failure); lymphadenopathy,
1].1,2 Often, more than one mechanism is involved. An inflamma- digital clubbing, and localized bone tenderness (suggestive of lung
tory effusion, for instance, is marked by increases in capillary and cancer); and ascites (suggestive of ovarian tumors or cirrhosis).
mesothelial permeability, which lead to elevated intrapleural on- Pleural effusion can occur in a wide variety of clinical situations,
cotic pressure. however, and it often evades clinical detection by history and phys-
Pleural effusion is classified as either transudative or exudative, ical examination. Consequently, imaging tests are indispensable in
depending on the chemical composition of the fluid. A transudate the workup of a patient with a possible pleural effusion. Pleural
is an ultrafiltrate of serum and has a low total protein content (≤ 3 fluid analysis, pleural biopsy, and thoracoscopy may also be re-
g/dl); an exudate is the result of increased permeability and has a quired for evaluation.
high total protein content. Increased pleural permeability results
from complex inflammatory mediator interactions between the
mesothelium (whose cells play an active role in inflammation, Investigative Studies
phagocytosis, leukocyte migration, tissue repair, antigen presenta-
IMAGING
tion, coagulation, and fibrinolysis3,4) and the capillary endotheli-
um. The distinction between transudative and exudative pleural
effusion is clinically significant in that the two types of effusion Chest Radiography
have different causes [see Table 2].1,4 To be detectable on a standard upright posteroanterior chest
radiograph, an effusion must have a volume greater than 150 ml.
If the volume is 150 to 500 ml, the lateral costophrenic angle will
Clinical Evaluation be blunted; if the volume is greater than 500 ml, a meniscus will
A complete history, phys- be created.5,6 A lateral decubitus chest radiograph can detect an
ical examination, and clini- effusion as small as 5 ml. As a general rule, a layering effusion that
cal acuity are the initial tools is at least 1 cm thick is accessible to thoracentesis.6,7 A loculated
used for diagnosing pleural effusion may appear as a so-called pseudotumor on a chest radi-
effusion. Important facts ograph and typically will not layer freely on a lateral decubitus
from a patient’s history (e.g., radiograph. Subtle changes on an upright chest radiograph (e.g.,
respiratory symptoms, pain, accentuation of a fissure, elevation of a hemidiaphragm [see 4:6
extrathoracic symptoms, duration of symptoms, previous medical Paralyzed Diaphragm], or increased separation between the lung
conditions, and risk factors for cardiopulmonary diseases or can- and subdiaphragmatic gas [see Figure 1]) may also signal an effu-

Table 1 Pathophysiologic Mechanisms of Pleural Effusion

Mechanism Specific Alteration Cause

Increased capillary and lymphatic hydrostatic Increased venous pressure (e.g., biventricular
pressure heart failure, renal failure)

Decreased capillary oncotic pressure Hypoproteinemia (e.g., nephrotic syndrome)
Abnormality in Starling’s equilibrium
Decreased intrapleural hydrostatic pressure Ex vacuo effusion (e.g., atelectasis)

Inflammation (e.g., infection, cancer, autoim-
Increased intrapleural oncotic pressure
mune disease)

Increase in capillary and mesothelial Inflammation (e.g., infection, cancer, autoim-
Increased filtration
permeability mune disease)

Interference with lymphatic drainage Obstruction Cancer, structural abnormalities


Approach to the Patient with a
Pleural Effusion
Findings are adequate for diagnosis

Assess respiratory status.

Patient is not in respiratory distress Patient is in respiratory distress

Transudative effusion is Exudative effusion is Nature of effusion is unclear
suspected suspected

Treat underlying cause.

Suspected cause is PSI (PPE) Suspected cause is other Suspected cause is malignancy,
condition esophageal perforation,
hemothorax, or chylothorax
[See Table 3.]

Patient’s condition improves Patient’s condition does not mprove

Provide clinical and radiologic Treat with pleurodesis or long-term
follow-up. drainage.


Clinical evaluation and chest x-ray suggest pleural effusion

Findings are inadequate for diagnosis

Perform US or CT.

Pleural pathology is not complex Pleural pathology is complex

Perform VATS.

Perform thoracentesis (with or without
imaging guidance) or tube
thoracostomy.

Drainage is successful Drainage is unsuccessful

Analyze pleural fluid sample (total protein Perform VATS.
concentration, with or without LDH concentration).

Effusion is transudative Effusion is exudative


Suspected cause is PSI (PPE) Suspected cause is malignancy Suspected cause is nonmalignant
condition other than PSI (PPE)
[See Table 3.] Perform cytologic tests.
Perform cell count with differential.
Assess levels of triglycerides, cholesterol,
amylase, chylomicrons, rheumatoid factor,
and antinuclear antibodies.

Cytology is positive Cytology is negative

Treat malignancy (with or without Perform pleural biopsy.
pleurodesis or long-term drainage).
Test results are positive Test results are negative

Treat underlying cause Treat with pleurodesis or
(with or without pleurodesis long-term drainage.
Biopsy is positive Biopsy is negative or long-term drainage).

Treat malignancy (with or without
pleurodesis or long-term drainage).


Table 2 Causes of Transudative tween effusion and lung abscess, and for guiding and monitoring
and Exudative Pleural Effusion closed drainage of effusions.6,10,12,13
Magnetic Resonance Imaging
Type of Effusion Cause
Magnetic resonance imaging of the chest provides no useful
Congestive heart failure information beyond what can be obtained with CT scanning.
Cirrhosis MRI is neither efficient nor cost-effective in standard evaluation
Nephrotic syndrome of pleural effusion.12,14
Acute atelectasis
Transudative Renal failure THORACENTESIS
Peritoneal dialysis
If the cause of a pleural
Postoperative state
Myxedema
effusion cannot be explained
Postpartum state by the clinical circumstances
(e.g., congestive heart failure
Pneumonia or a recent surgical proce-
Malignancy
dure), diagnostic thoracen-
Infection
tesis [see Sidebar Techniques
Esophageal perforation
Hemothorax
of Bedside Thoracentesis and Tube Thoracostomy] is indicated.
Chylothorax Thoracentesis may also have therapeutic value, in that drainage of
Pseudochylothorax fluid may relieve dyspnea. Absolute contraindications to thoracen-
Connective tissue diseases tesis include lack of cooperation on the patient’s part, clinical insta-
Exudative Drug-induced pleuritis bility with hemodynamic or respiratory compromise, severe coag-
Pancreatitis ulopathy, and high-pressure ventilation. Relative contraindications
Uremia to thoracentesis include a nonlayering effusion, loculations, and
Postmyocardial infarction (Dressler syndrome) previous thoracic trauma, chest tube placement, or surgery.
Chronic atelectasis
A large effusion can be drained without any special imaging
Radiation therapy
guidance other than an upright lateral chest radiograph. Thora-
Asbestos exposure
Meigs syndrome
centesis for a small or loculated effusion is best done with ultra-
Ovarian hyperstimulation sound guidance; success rates are as high as 97%.15

Transudative or exudative Pulmonary embolus

sion. Additional findings on a standard chest radiograph (e.g., lat-
erality, the size of the cardiac silhouette, the position of the medi-
astinum, pulmonary parenchymal changes, pleural calcifications,
and osseous abnormalities) may point to a specific cause.
Supine chest radiographs are less sensitive than other chest
radiographs. With these images, suspicion of an effusion is trig-
gered by increased homogeneous density of the lower hemithorax,
loss of normal diaphragmatic silhouette, blunting of the lateral
costophrenic angle, or apical capping [see Figure 2].8
Ultrasonography
Chest ultrasonograms are more reliable for detecting and local-
izing small (5 to 100 ml) or loculated pleural effusions than chest
radiographs are.5,9,10 Ultrasonography is particularly helpful for
guiding thoracentesis for small-volume effusions and for assessing
pleural effusions in critically ill patients.6,11
Computed Tomography of the Chest
Computed tomography of the chest is a very sensitive tool for
evaluating pleural effusion. Free-flowing fluid causes a sickle-
shaped opacity in the most dependent portion of the thorax, and
even small effusions are readily detected [see Figure 3]. CT may
also reveal clues to the cause of the effusion, such as a fluid-fluid
level (suggestive of acute hemorrhage), pleural thickening and
enhancement (suggestive of pleural space infection [see Figure 4]),
calcified pleural plaques (suggestive of asbestosis), and diffuse
irregular nodularity and pleural thickening (suggestive of pleural
metastases or mesothelioma). CT is especially useful for charac- Figure 1 Posteroanterior chest radiograph of a patient with bilat-
terizing loculated effusions, for differentiating pleural thickening eral pleural effusion reveals costophrenic blunting and increased
or pleural masses from pleural effusion, for distinguishing be- separation between the left lung and subdiaphragmatic gas.


preferable to minimize the chance of edema. Additional potential
complications include so-called dry tap, vasovagal reaction, hem-
orrhage hypovolemia, and pleural space infection (PSI).10,16-18
PLEURAL FLUID ANALYSIS

Assessment of a pleural
fluid sample is guided, to
some extent, by the clinical
context in which the pleural
effusion occurs. When the
cause of the effusion is un-
known, evaluation of a pleu-
ral fluid sample typically in-
cludes measurement of total protein and lactic dehydrogenase
(LDH) concentrations, a cell count with differential, cause-specif-
ic testing, and microbiologic and cytologic analysis.
Biochemical Analysis of Pleural Fluid
A total protein concentration higher than 3 g/dl is generally
used as the main criterion for distinguishing a transudate from an
exudate; however, the use of this criterion may result in misclassi-
Figure 2 Supine chest radiograph of a patient with bilateral fication of as many as 15% of effusions. According to Light’s cri-
pleural effusion shows increased homogeneous density of the teria,19 which have a sensitivity of 99% and a specificity of 98% for
lower hemithoraces. identifying exudates, an effusion is an exudate if any of the follow-
ing three findings is present:
1. A pleural fluid–to–serum protein ratio higher than 0.5
2. A pleural fluid–to–serum LDH ratio higher than 0.6
3. A pleural fluid LDH concentration higher than two thirds of
the upper limit of the serum reference range
A 1997 meta-analysis of the diagnostic value of tests used to dis-
tinguish transudates from exudates did not find any test or com-
bination of tests to be clearly superior.20 The choice of a test for
this purpose is therefore a matter of individual preference. If only
one test is to be performed, measurement of the total protein con-
centration is the most practical choice, in view of its accuracy and
availability.

Figure 3 Chest CT shows a free-flowing, sickle-shaped right-
side effusion.

The incidence of complications associated with thoracentesis
varies, depending on the experience of the operator and on the use
of imaging guidance. Pneumothorax occurs in 3% to 20% of
patients, of whom approximately 20% require tube thoracostomy
[see Sidebar Techniques of Bedside Thoracentesis and Tube
Thoracostomy]. Patients commonly experience pain and cough
with lung reexpansion during drainage. Reexpansion pulmonary
edema is an uncommon complication that can occur with rapid
drainage of a large-volume effusion. It is common practice to drain
no more than 1 to 1.5 L at a time, even though no evidence sup-
ports this practice. Experimental data suggest that active aspira-
tion of fluid can cause high negative intrapleural pressures, poten- Figure 4 Chest CT of a patient with right-side empyema shows a
tially precipitating edema formation; gravity drainage may be loculated effusion. The pleura is enhanced with I.V. contrast.


Techniques of Bedside Thoracentesis and Tube Thoracostomy
Bedside Thoracentesis During preparation for chest tube placement, narcotics and sedatives
should be administered intravenously; additional doses should then be
Bedside thoracentesis should be performed on a bed or an examination administered at the beginning of and during the procedure.
table (as a safeguard if hypotension develops). The patient should be The ideal location for chest tube placement is determined by clinical
upright and seated (provided that he or she is awake and cooperative), and radiographic examination. The area is prepared and draped wide-
with the arms leaning comfortably on a bedside table and the back fac- ly, and a local anesthetic is used at a near-maximum dosage, with care
ing the surgeon. taken to anesthetize skin, subcutaneous tissue, muscle, and perios-
The proper intercostal space for catheter insertion is determined teum. A 1.5 cm skin incision is made, a soft tissue tunnel is created with
through physical examination and radiologic evaluation of the effusion; blunt instrument and finger dissection, the upper edge of the rib is
generally, the ninth or 10th intercostal space in the midscapular line is a identified clearly, and additional local anesthetic is applied to the per-
good choice. The area is prepared and anesthetized with 1% lidocaine, iosteum and the intercostal muscles. The subcutaneous tunnel should
3 to 5 mg/kg, with care taken not to injure the intercostal bundle. To con- generally be directed posteriorly so that the chest tube will sit along the
firm that the catheter is in the correct location, we recommend drawing a posterior chest wall and will not be trapped in a fissure. The intercostal
small amount of pleural fluid at the time of local anesthetic infiltration. muscle is pierced bluntly, and digital examination of the pleural space
Several thoracentesis kits with one-way valves are available. To minimize is performed to confirm that an intrapleural location has been reached
the risk of reexpansion pulmonary edema, fluid should be allowed to and to search for abnormalities such as adhesions or tumor implants.
drain by gravity, and drainage should not exceed 1.5 L. Frequently, a dry The chest tube is then directed to the desired location with the aid of a
cough and pleuritic pain develop as drainage approaches its end. To clamp. As with thoracentesis, fluid should be allowed to drain by gravi-
minimize anxiety, the patient should be warned about this possibility in ty, but drainage should not exceed 1.5 L. If the effusion exceeds 1.5 L,
advance. After the completion of thoracentesis, a chest radiograph the chest tube should be clamped and the remaining fluid allowed to
should be obtained. drain intermittently in 200 ml aliquots every 2 hours. Immediately after
completion of the procedure, a chest radiograph should be obtained to
Bedside Tube Thoracostomy
verify lung expansion and confirm the position of the chest tube. When
Bedside tube thoracostomy should be performed with the patient chest tube output falls below 200 ml/day and reexpansion of the lung
supine. The side on which the thoracostomy will be created should be is verified, pleurodesis should be performed. We recommend that pa-
elevated, and the patient’s ipsilateral arm should be abducted. Supple- tient-controlled analgesia be employed while the chest tube remains
mental oxygen should be supplied. Monitoring must include, at the in place.
least, continuous oxygen saturation plethysmography and intermittent The size of the chest tube is determined by the suspected cause and
measurement of blood pressure and heart rate. Tube thoracostomy is by the radiologic characteristics of the effusion. For a free-flowing tran-
potentially very painful; accordingly, in a nonemergency situation, every sudative effusion, a small (20 to 24 French) chest tube or even a pigtail
effort should be made to minimize pain and anxiety. We usually adminis- catheter usually suffices; for a thick exudative effusion or a hemothorax,
ter intravenous ketorolac about 30 to 60 minutes before the procedure. a tube as large as 40 French may be required.

Assessment of pleural fluid pH and glucose levels may be used are idiopathic. As a rule, the presence of mesothelial cells is of lit-
adjunctively for risk stratification in patients with PSI, but the clin- tle diagnostic value; the exception to this rule is that if such cells
ical utility of these measurements is not well established (see account for more than 5% of WBCs, a tuberculous effusion is
below).21 unlikely.23,27
There are numerous pleural fluid components whose concen-
trations can be measured to help determine the specific cause of a Microbiologic Tests
pleural effusion, such as triglycerides, chylomicrons, and choles- If a PSI is suspected, Gram staining and standard bacterial cul-
terol (to help diagnose chylothorax); amylase (to help diagnose tures are indicated. If tuberculous pleurisy is a possibility, acid-fast
esophageal perforation or pancreatitis); rheumatoid factor (to help stains and mycobacterial cultures should be performed. Fungal,
diagnose rheumatoid effusion); antinuclear antibodies (to help viral, and parasitic PSIs are uncommon; accordingly, special stains
diagnose lupus pleuritis); carcinoembryonic antigen (to help diag- and cultures for these conditions are indicated only if dictated by
nose malignancy); and adenosine deaminase (to help diagnose a specific clinical setting.28
tuberculous pleurisy).3,22-25
Cytologic Tests
Cell Counts Cytologic testing of pleural fluid is routinely performed when-
Analysis of the number and type of white blood cells (WBCs) ever the cause of an effusion is unclear. The diagnostic yield for
present in pleural fluid is often diagnostically useful. Pleural effu- malignancy varies depending on the stage of the disease, but it
sions can be categorized according to the type of WBC that is pre- generally is in the range of 50% to 60% (higher in patients with
dominant. Generally, pleural fluid neutrophilia points to acute bulky pleural tumors). Repeat cytologic testing may increase the
inflammation (e.g., from PSI or pulmonary infarction) as the yield to more than 70%,10,29 and testing of three or more samples
underlying cause; however, the presence of a neutrophilic effusion may increase the yield to 90%.30
does not exclude malignancy. Pleural fluid lymphocytosis, in
PLEURAL BIOPSY
which lymphocytes account for more than 50% of WBCs, most
frequently is indicative of malignancy (occurring in 50% of malig- In approximately 25% of patients with exudative effusion, the
nant effusions), tuberculosis (occurring in 15% to 20% of tuber- cause remains unknown after clinical evaluation, imaging, and
culous effusions), or chylothorax.26 Pleural fluid eosinophilia, in pleural fluid analysis. The next step in the evaluation of such
which eosinophils account for more than 10% of WBCs, can be patients is pleural biopsy.
caused by a wide variety of benign and malignant conditions— Percutaneous pleural biopsy is an infrequently used tool that
even, in some cases, by the mere presence of air or blood in the has a diagnostic yield of 57% for carcinoma. Its low yield for
pleural space. Approximately one third of eosinophilic effusions malignant effusion can be explained by the uneven distribution of


pleural metastases. For tuberculous pleurisy, however, the diag-
nostic yield of percutaneous pleural biopsy is 75%, and the yield
rises to 90% when this procedure is combined with pleural fluid
culture. In about 10% to 20% of patients with exudative pleural
effusion, laboratory analysis of pleural fluid and percutaneous
biopsy fail to produce a specific diagnosis.18 The contraindications
and complications associated with percutaneous pleural biopsy are
similar to those associated with thoracentesis.31
Video-assisted thoracoscopic surgery (VATS) is also employed
for pleural biopsy; its diagnostic yield in this setting is 92% for
malignancy and nearly 100% for tuberculous pleurisy. VATS is a
therapeutic procedure as well, allowing the surgeon to perform
pleurodesis, decortication, or pleurectomy if necessary. VATS
pleural biopsy is typically performed with the patient under gen-
eral anesthesia, but if the patient is highly debilitated, it can be
done with regional and local anesthesia.32 Procedure-specific com-
plications include hypoxemia, hemorrhage, prolonged air leakage,
subcutaneous emphysema, and empyema, each of which occurs at
a rate of about 2%. The mortality associated with diagnostic tho- Figure 5 Shown is a Pleurx catheter after placement and subcu-
racoscopy ranges from 0.01% to 0.09%.29,31 When VATS is per- taneous tunneling. The vacuum container is not connected.
formed to remove a suspected malignant lesion, a protective plas-
tic device is required to minimize the possibility of tumor seeding.
Incisional tumor seeding after a VATS biopsy is rare but can occur at Small-bore subcutaneously tunneled catheters may be em-
any time after the procedure (reported range, 2 weeks to 29 months).33 ployed for long-term management of malignant pleural effusions.
If mesothelioma is suspected, open lung biopsy (through a 5 to Two options are available: the Pleurx catheter (Denver
7 cm incision) is the preferred diagnostic procedure. Ideally, the Biomedical, Golden, Colorado) [see Figure 5] and the Tenckhoff
biopsy incision should be placed at the location of a potential tho- peritoneal dialysis catheter. Regardless of which option is chosen,
racotomy incision so that future excision of the biopsy scar can be the procedure is essentially the same: the catheter is inserted with
accomplished in a manner that minimizes the risk of local tumor the patient under local or general anesthesia, the patient is dis-
recurrence.34 charged on the same day or on the day after insertion, and the
pleural fluid is drained either according to a schedule or on an as-
needed basis. Small-bore tunneled catheters are comfortable, but
Management patients may object to having a permanent catheter or to under-
going home-based procedures. In 20% to 58% of patients with a
PLEURAL EFFUSION IN THE permanent catheter, pleurodesis develops within 4 to 6 weeks.
INTENSIVE CARE UNIT Catheter removal, if desired, is easily done in the office setting.
Pleural effusion develops Technical failures and infection may occur in as many as 20% of
in as many as 60% of inten- patients with permanent catheters, but such problems are easily
sive care unit patients who managed.36-39
are evaluated with ultraso- Pleuroperitoneal shunting has been advocated as an alternative
nography.11 When pleural effusion occurs in the ICU, drainage for long-term management of malignant pleural effusions. Ex-
should be liberally employed to optimize the patient’s hemody- perience with this mode of drainage is limited, however, and the
namic and respiratory status and to detect PSI early.Thoracentesis potential for technical complications is high.40,41
can be done in critically ill ventilator-dependent patients with the Recurrence of malignant pleural effusion is best prevented by
help of bedside ultrasonography. Chest tube thoracostomy does using sclerosants to induce pleurodesis. The sclerosant may be
not require ultrasonographic guidance and may be a safer choice instilled either via a bedside tube thoracostomy or thoracoscopi-
for patients on high-pressure ventilation. cally; a median hospitalization of 6.5 days is required.36 Of the var-
ious sclerosants available, talc is the most efficacious, with an over-
MALIGNANT PLEURAL EFFUSION all success rate of 80% to 96%.42,43 The ideal talc dose has not
Pleural effusion is associated with malignancy in 30% to 65% been determined; the usual dose is 4 or 5 g. Talc pleurodesis with
of patients, and approximately 75% of patients with malignant a 5 g dose has generally proved efficient and safe. For obvious rea-
effusion have lung or breast cancer.35 The principal aim of thera- sons, simultaneous bilateral talc instillation should be avoided.42 A
py is to relieve dyspnea and to limit the number of procedures and phase III intergroup study (CALGB 9334) that compared bedside
hospital days that patients with a limited life expectancy must talc slurry pleurodesis with thoracoscopic talc insufflation pleu-
endure. rodesis found no difference in outcome at 30 days; however, sub-
Drainage can be achieved by means of thoracentesis, chest tube group analysis revealed that thoracoscopic talc insufflation pleu-
placement, or VATS. Thoracentesis is a valuable option for initial rodesis was superior in patients with primary lung cancer or breast
patient evaluation, particularly in the office setting. Because malig- cancer.44 Thoracoscopically guided talc pleurodesis can be per-
nant pleural effusion recurs rapidly unless patients undergo effec- formed with an operative mortality of less than 1%.45,46
tive systemic or local treatment, repeat thoracentesis is generally Pain and fever are frequent side effects of talc pleurodesis, but
not recommended for anything other than urgent relief of symp- the main concern is the possible development of acute lung injury
toms. Chest tubes are placed primarily with the intention of per- (ALI) and respiratory failure. Respiratory failure occurs in approx-
forming bedside pleurodesis. imately 1% to 4% of patients.The cause of respiratory failure sec-


Table 3 Categorization of PPE by Risk of Poor Outcome

Risk of Poor
Pleural Space Anatomy Pleural Fluid Bacteriology Category Drainage
Outcome

Minimal free-flowing effusion (< 10 mm Culture and Gram stain results unknown 1 Very low No
on lateral decubitus x-ray)

Small to moderate free-flowing effusion (> 10 mm Negative culture and Gram stain 2 Low No
but < 50% hemithorax)

Large free-flowing effusion (> 50% hemithorax), loc- Positive culture or Gram stain 3 Moderate Yes
ulated effusion, or effusion with thickened pari-
etal pleura (as seen on contrast-enhanced CT) Pus 4 High Yes

ondary to talc pleurodesis is not clear and is probably related to In most patients, PSI is caused by bacteria.The most common
multiple factors (e.g., talc dose, talc absorption, underlying lung pathogens are Staphylococcus aureus, Streptococcus pneumoniae,
disease, reexpansion pulmonary edema, systemic inflammatory enteric gram-negative bacilli, and anaerobes. Approximately 30%
response, tumor burden, and lymphatic obstruction). There is no to 40% of cultures are polymicrobial. In a subgroup of patients,
definitive evidence that the talc dose is correlated with the inci- there is sterile pus in the pleural space, as a consequence either of
dence of ALI; respiratory failure has been reported even with a 2 previous antimicrobial therapy or of bacterial autolysis. The
g talc dose.42,47-51 pathogens identified vary according to the cause of PSI. For
Treatment of malignant pleural effusion must be individual- instance, S. aureus and S. pneumoniae predominate in PPE; S.
ized. The key factors governing the choice of treatment approach aureus, in postthoracotomy PSI; mixed oropharyngeal organisms,
are (1) the patient’s performance status, (2) the prognosis, (3) the in PSI resulting from esophageal perforation28; and acid-fast bac-
pleural tumor bulk, and (4) the ability of the lung to reexpand. teria, in tuberculous empyema.55
Patients who have poor performance status (e.g., those with
advanced tumors or significant comorbid conditions) or a very Parapneumonic Effusion
poor short-term prognosis should undergo the least invasive treat- PPE occurs in as many as 57% of patients hospitalized with
ment—namely, drainage only. Patients who have better function- pneumonia, and pneumonia accounts for 42% to 73% of cases of
al status and are expected to survive longer should undergo tho- PSI. In most cases, early PPE is effectively treated by timely
racoscopically guided talc pleurodesis. Intrathoracic tumor bulk is antibiotic therapy aimed at the underlying pneumonia.21,28
important in that a bulky pleural lesion will interfere with pleu- In 2000, a panel convened by the Health and Science Policy
rodesis. The lung’s ability to reexpand after drainage of a malig- Committee of the American College of Chest Physicians (ACCP)
nant effusion is significant because if the lung is atelectatic as a reviewed the available literature with the aim of developing an evi-
result of airway obstruction or trapped as a result of pleural seed- dence-based clinical practice guideline for the treatment of PPE.21
ing, no agent will be able to induce pleurodesis, and the best treat- The panel formulated a clear and relatively simple classification
ment will be long-term drainage. system that used pleural anatomy and bacteriology to stratify
patients according to the risk of a poor outcome [see Table 3]. It
PLEURAL SPACE INFECTION
then made therapeutic recommendations on the basis of this clas-
PSI can be caused by a variety of factors, including pneumonia, sification. Some authors have used pleural fluid chemistry test
trauma, and intrathoracic procedures. It has a wide clinical spec- results (e.g., pH and glucose concentration) as additional criteria
trum, ranging from a small parapneumonic effusion (PPE) to a for categorizing PPE; for example, a pleural fluid pH lower than
pus-filled pleural space (empyema) with respiratory compromise 7.20 or a glucose level lower than 60 mg/dl has been considered
and sepsis. (The terms PSI and PPE are often used interchange- suggestive of moderate risk. To date, however, the clinical utility
ably.) PSI can be classified either according to its pathophysiolog- and decision thresholds of pH and glucose values have not been
ic stage (exudative, fibrinopurulent, or organizing) or according to well defined. Accordingly, we prefer to omit pleural fluid chem-
its anatomic appearance (nonloculated versus loculated or non- istry from these guidelines.
complicated versus complicated). The term empyema is com- The ACCP Health and Science Policy Committee evaluated
monly reserved for the most advanced stage of PSI.52 six primary management approaches: no drainage, therapeutic
The pathophysiology of PSI or PPE can be divided into three thoracentesis, tube thoracostomy, fibrinolytic therapy, VATS, and
stages.The exudative stage is characterized by the development of open surgery. Overall, pooled outcomes favored patients treated
an exudative effusion secondary to increased pleural permeability; with fibrinolytics, VATS, and open surgery. However, the success
the pleural space is often sterile initially, but if it is left untreated, of an approach is related to the patient’s risk category. The rec-
bacterial infection is likely to ensue. The fibrinopurulent stage is ommendations for drainage in relation to risk category are gener-
marked by the progressive deposition of fibrin and the increasing al guidelines, based on level C and D evidence (with level C refer-
presence of WBCs; gradual angioblastic and fibroblastic prolifera- ring to historically controlled series and case series and level D to
tion leads to extensive fibrin deposits, and the effusion becomes expert opinion). With these recommendations (and their limita-
loculated (complicated). The organizing stage starts as early as 1 tions) in mind, treatment should be tailored to the specific situa-
week after infection, with increasing collagen deposition and lung tion of each patient.
entrapment. After 3 or 4 weeks, the organized collagen has formed
a peel, and the pleural fluid is grossly purulent. Eventually, dense Category 1 and 2 PPE PPE in categories 1 (very low risk)
fibrosis, contraction, and lung entrapment develop.53,54 and 2 (low risk) can be treated with antibiotic therapy directed at


the underlying pneumonia. Some patients with category 2 PPE Tuberculous PSI
may require drainage for relief of dyspnea through either thora- Pleural effusion is common in patients with clinically evident
centesis or tube thoracostomy. pulmonary tuberculosis. Most cases of tuberculous effusion are
secondary to hypersensitivity and resolve spontaneously. Tuber-
Category 3 and 4 PPE Drainage options for categories 3 culous empyema is relatively rare; it is typically the result of active
(moderate risk) and 4 (high risk) PPE include tube thoracostomy pleural infection by acid-fast bacteria.55
alone, tube thoracostomy with intrapleural fibrinolytic therapy, Tuberculous PSI is also treated in accordance with the general
VATS drainage, and open surgical drainage. These various ap-
treatment guidelines for bacterial PSI. Chronic tuberculous PSI
proaches are not mutually exclusive: in some cases, patient out-
may present specific problems, such as drug resistance and im-
comes may be optimized by combining them.56
paired ability (or even inability) to reexpand the lung. Surgical pro-
Tube thoracostomy alone may be appropriate for category 3
cedures performed to manage chronic tuberculous empyema
patients with free-flowing effusion.With loculated effusion, howev-
include VATS, standard open decortication, thoracoplasty, parietal
er, the key to successful therapy is breaking down the fibrin septa-
wall collapse, open drainage, myoplasty, and omentopexy.55
tions. Evidence from three small randomized, controlled trials sug-
gested that intrapleural fibrinolytic therapy has an advantage over CHYLOTHORAX AND PSEUDOCHYLOTHORAX
tube thoracostomy alone for patients with category 3 or 4 PPE; a
Chylothorax is the presence of chyle in the pleural space as a
large trial is being conducted to address this specific issue.53 To
consequence of blockage of or damage to the thoracic duct or one
date, only one randomized study, including 20 patients with cate-
of its tributaries.The rate at which chyle flows through the thoracic
gory 3 or 4 PPE, has compared VATS with fibrinolytic therapy.
duct can be higher than 100 ml/hr, and thus, large amounts of
The primary treatment success rate was significantly higher in the
chyle can leak into the pleural space.61 The principal causes of chy-
VATS treatment group, the duration of chest tube drainage was
lothorax are surgical trauma and malignancy (70% to 80% are
less, and the total hospital stay was shorter.57 VATS allows not only
adequate drainage and visualization of the pleural space but also caused by non-Hodgkin lymphoma).46,61,62 Congenital chylotho-
decortication of the lung if required; however, if decortication can- rax is more often due to malformation of the thoracic duct than to
not be thoroughly accomplished by means of VATS and satisfac- birth trauma.24
tory lung expansion cannot be achieved, a thoracotomy should be The diagnosis of chylothorax is made by measuring triglyceride
performed.58 levels in pleural fluid. Levels higher than 110 mg/dl are highly sug-
The principles of PPE treatment can be applied to PSI from any gestive of chylothorax; levels between 50 and 100 mg/dl are equiv-
cause, but in view of the paucity of reliable data, caution should be ocal; and levels lower than 50 mg/dl rule out chylothorax.24
exercised. A pleura-to-serum triglyceride ratio higher than 1 can be a useful
indicator63; the presence of chylomicrons is synonymous with
Posttraumatic PSI chylothorax.25
PSI occurs in about 1% to 5% of patients who have sustained Treatment of chylothorax depends on its cause and severity.
blunt or penetrating thoracic injury. The incidence of PSI in the Postoperative chylothorax may be treated initially with conserva-
setting of trauma increases with the number of chest tubes placed tive measures (e.g., with a nihil per os [NPO] regimen, total par-
and with the duration of chest tube drainage. The effect of an enteral nutrition, and administration of octreotide). However,
undrained hemothorax on the risk of PSI has not been complete- drainage totaling more than 500 ml/day is considered to predict
ly defined, and prophylactic antibiotics have not been shown to failure of conservative management. Thoracic duct ligation is the
reduce the incidence of PSI.52 surgical treatment of choice and can often be performed thoraco-
As noted (see above), the general guidelines for the treatment of scopically. To help identify the leak intraoperatively, it may be
PPE apply to the treatment of posttraumatic PSI. helpful to administer 100 to 200 ml of heavy cream or olive oil
orally 2 to 3 hours before the operation.64,65 Early surgical inter-
Iatrogenic PSI vention is important because the ongoing loss of lymph has sig-
Iatrogenic PSI develops when a preexisting pleural effusion is nificant effects on fluid homeostasis, nutrition, and immunocom-
inoculated with bacteria during an invasive procedure (e.g., thora- petence (secondary to lymphocyte loss). In the early postligation
centesis or tube thoracostomy). The presence of fluid in the pleu- period, medical management should be continued to allow any
ral space appears to be a prerequisite for infection.52 small leaks to seal. An alternative to surgical ligation that has
A bronchopleural fistula (BPF) is by definition a PSI and there- evoked some interest is transabdominal percutaneous emboliza-
fore has a similarly broad spectrum of clinical presentation. The tion of the thoracic duct. This technique requires significant
overall incidence of BPF after lobar resection is approximately 1%; expertise.66
it is somewhat higher after resections for inflammatory diseases Lymphoma-related chylothorax is caused principally by obstruc-
than after resections for cancer. The incidence of BPF after pneu- tion and usually develops on the left side [see Figure 6]. In a stiff and
monectomy varies, depending on the side on which the pneu- infiltrated duct, minor triggers (e.g., a Valsalva maneuver) can lead
monectomy was done, the indications for surgery, the extent of to duct rupture. Although patients with chylothorax often have
preoperative irradiation, and the comorbid conditions present. In extensive disease, supradiaphragmatic disease is not always present.
a report encompassing 464 pneumonectomies for cancer, the inci- Lymphoma-related chylothorax is best managed with thoracentesis
dence of BPF was 8.6% after right pneumonectomy and 2.3% and with therapy directed at the underlying cause. If first-line ther-
after left pneumonectomy. The overall incidence of postpneu- apy fails, thoracoscopic talc pleurodesis is recommended; a small
monectomy empyema (generally but not always secondary to a series reported 100% resolution of lymphoma-related chylothorax
BPF) is 1% to 3%.59,60 with thoracoscopic talc pleurodesis. If the chylothorax does not
PSI that is not associated with a BPF is treated in accordance respond to any of these approaches, it may respond to thoracic duct
with the treatment guidelines for PPE, but if a BPF is present, ligation or pleuroperitoneal shunting. Chylothorax in the presence
operative management is required. of lymphoma-related chylous ascites is a difficult problem that is


generally refractory to most forms of therapy (though pleurodesis is
occasionally successful).46,61,62,67,68
Pseudochylothorax is a rare disorder associated with the forma-
tion of persistent exudates that last for months or years. The most
common cause is tuberculosis; the second most common cause is
rheumatoid arthritis. Biochemical analysis of pleural fluid from
patients with pseudochylothorax reveals very high cholesterol lev-
els (> 200 mg/dl) and the presence of cholesterol crystals. Treat-
ment is generally conservative.24,25
IDIOPATHIC PERSISTENT PLEURAL EFFUSION

In a small percentage of patients, the cause of pleural effusion
remains unknown despite extensive diagnostic evaluation. Tuber-
culosis and other granulomatous diseases, malignancy, and pulmon-
ary embolism account for most cases of idiopathic effusion; those
causes are identified later in the course of the disease or at autopsy.
Other causes include constrictive pericarditis, subphrenic abscess,
connective tissue diseases, drug-induced pleuritis, peritoneal dial-
Figure 6 Chest CT shows left-side chylothorax secondary to ysis, and cirrhosis.23 In the management of persistent benign or
lymphoma. Subtle mediastinal lymphadenopathy obstructing the idiopathic effusion, talc pleurodesis has a high success rate and
thoracic duct (arrow) is apparent. minimal long-term implications.69,70

Discussion
Pleural Anatomy
of the venules, which suggests that the pleural mesothelial cell
The pleura is a continuous membrane that covers the parietal layer may be as leaky as the venular endothelium.3,4,72
and visceral surfaces of the thorax. In adults, it has an estimated
surface area of 2,000 cm2.71 Light microscopy shows the pleura to
have five layers: (1) a mesothelial cell layer; (2) a mesothelial con- Pleural Fluid Physiology
nective tissue layer with basal lamina; (3) a superficial elastic layer; The amount of pleural fluid in an adult is 1 to 10 ml and forms
(4) a loose connective tissue layer with adipose tissue, blood ves- a 10 µm–thick layer.1,3,71,72 Fluid exchange across the pleural sur-
sels, nerves, and lymphatic vessels; and (5) a deep fibroelastic face depends on three mechanisms: (1) passive filtration following
layer.The parietal pleura establishes a pleurolymphatic communi- Starling’s equilibrium, (2) active solute transport, and (3) lym-
cation on the diaphragm to allow clearance of large (> 1,000 nm) phatic clearance. In the normal pleura, Starling’s equilibrium
particles and cells from the normal pleural space.The structure of favors the flow of fluid in a parietal-to-visceral direction.71 The rate
this pleurolymphatic communication consists of stomata 2 to 12 at which fluid traverses the pleura ranges from 20 to 160 ml/day
µm in diameter, which overlie bulblike lymphatic channels (lacu- in adults; maximal lymphatic clearance is believed to be approxi-
nae) separated by a layer of loose connective tissue (the mem- mately 700 ml/day.2,71,73-76
brana cribriformis). The chemical composition of normal pleural fluid is similar to
Electron microscopy reveals microvilli on the mesothelial cell that of interstitial fluid.The protein concentration is typically 1 to
surface of the pleura. The main function of these microvilli is to 2 g/dl.The concentration of high-molecular-weight proteins (e.g.,
enmesh glycoproteins rich in hyaluronic acid for purposes of LDH) is approximately half that seen in serum. Cell counts in
lubrication.The structure of the intercellular junction in the meso- normal pleural fluid range from 1,400 to 4,500 cells/mm3; macro-
thelial cells of the pleura is similar to that in the endothelial cells phages account for the majority of the cells.3,72

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