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Current Respiratory Medicine Reviews, 2012, 8, 314-321
314
Malignant Pleural Effusion Evaluation and Management
Jed A. Gorden* and Joelle Thirsk Fathi
Swedish Cancer Institute, 1101 Madison Ave, Seattle, WA 98104, USA
Abstract: Malignant pleural effusion represents advanced disease. Management is determined by the patient’s
performance status, symptoms and degree of lung re expansion after pleural fluid drainage. The goal of management is
control of patient symptoms, with minimum morbidity and maximum patient independence. Pleural fluid evacuation and
long term palliation can be achieved by either chemical pleurodesis or patient controlled drainage with a tunneled pleural
catheter. Thoughtful patient evaluation is critical to choosing the appropriate palliative option for each individual with
malignant pleural effusion.
Keywords: Malignant effusions, pleurodesis, thoracoscopy, tunneled pleural catheter.
INTRODUCTION
(A)
A pleural effusion is defined as a malignant pleural
effusion by the presence of malignant cells in the pleural
fluid and an increase in the volume of pleural fluid [1] (Fig.
1). Malignant pleural effusions (MPE) occur in patients with
advanced malignancies and are most commonly associated
with lung, breast, gastric, and ovarian cancers, as well as
lymphoma. Breast and lung primaries are associated with
nearly 75% of MPE [2] (lung cancers accounting for 35%45% and metastatic breast cancers for 25% of all malignant
pleural effusions) [3]. Malignant pleural effusions represent
22% of all pleural effusions, and in 20% of these patients
MPE is the first clinical presentation of their malignancy [4].
Malignant pleural effusions are an immense contribution
to the morbidity experienced by cancer patients, and their
management often requires repeated interventions and
repeated hospital admissions. Over the years, the annual
incidence of MPE has grown as the number of cancer
survivors has increased, with at least 150,000 annual cases
seen in the US [5-7]. Women constitute a larger portion of
this MPE population due to the prevalence of breast cancer
and secondary risk of MPE in breast cancer victims.
(B)
A malignant pleural effusion is an ominous clinical
indicator and represents advanced stage neoplasm. The
prognosis of patients affected with MPE is usually poor with
a reported median survival of 6 months [8]. Patient survival
is influenced by the type of neoplasm, the functional status
of the patient at time of diagnosis, and the responsiveness of
the underlying neoplasm to treatment [9-13].
ANATOMY AND PHYSIOLOGY OF THE PLEURAL
LINING AND SPACE
The pleural space (or cavity) is a self-contained space
that is defined by the visceral and parietal pleural
membranes, with the visceral membrane lining each lung
and fissures and the parietal membrane lining the chest wall,
diaphragm, pericardium and mediastinum [14]. The pleural
space is a potential space between the two surfaces and
*Address correspondence to this author at the Swedish Cancer Institute,
1101 Madison Ave, Seattle, WA 98104, USA; Tel: (206) 215-6800;
Fax: (206)215-6801; E-mail: [email protected]
1875-6387/12 $58.00+.00
Fig. (1). (A) Normal pleural space with normal visceral and parietal
pleural surfaces. (B) Malignant pleural space with tumor studding
the visceral pleura, the parietal pleura and pleural effusion present.
usually contains less than 1 ml of lubricating fluid [15, 16].
These smooth membranes facilitate the movement of the
lung within the pleural space through secretion and
absorption of pleural fluid.
The lubricated pleural membranes are divided into five
cellular layers: a single mesothelial cellular layer, the subendothelial connective tissue and basal lamina, a thin
superficial sub-elastic layer, a sub-connective tissue layer
and a deep fibro-elastic layer [15].
© 2012 Bentham Science Publishers
Malignant Pleural Effusion Evaluation and Management
The mesothelial layer has secretory and absorption
capabilities; this layer synthesizes glycosaminoglycans and
surfactant that deliver lubrication for the parietal and visceral
pleural membranes [15]. The primary function of the
mesothelial cells is to reduce the friction between the mobile
organs including the lung and the chest wall; it is also
integral to membrane transport [17].
The sub-endothelial connective tissue layer of the pleura
is a complex structure that lies beneath the mesothelial
cellular layer and functions as an anchoring structure. This
lining is a strong contributor to the low oncotic pressure of
the pleural space and the resulting negative pleural pressure
that allows the lung to expand [17].
The fourth layer, known as the loose connective tissue
layer, contains adipose tissue, fibroblasts, mast cells, blood
vessels, nerves and lymphatics; the fifth layer, known as the
deep fibroelastic layer, is typically an adherent layer to the
presiding structures including the lung, mediastinum,
diaphragm, ribs or intercostals muscles [15].
The parietal pleura also possess stomata that communicate directly with the lymphatic system. These stomata are
openings in the mesothelial cells that aid in the absorption
(i.e. egress and removal) of pleural fluid, protein, and cells
[18].
PHYSIOLOGY OF PLEURAL FLUID
Pleural fluid is a low protein interstitial fluid that
promotes the lung mechanics of respiration. As the lung
expands and contracts during respiration, pleural fluid is the
lubricant that allows the lung to slide, reducing friction.
Pleural fluid is normally produced and absorbed at a
relatively slow rate of 0.01ml/kg/h. This amounts to the
presence of less than 1ml in the pleural space at any given
time, and a total production of approximately 17 ml/day [4,
18, 19].
The maximal absorptive capacity of the pleura is 0.2-0.3
ml/kg/h, and once absorbed, the fluid is then drained into the
lymphatic system [4]. Fluid volume is kept constant by a
combination of Starling forces, the oncotic pressure in the
circulation, and the negative pressure in the lymphatics of
the lungs [15, 20].
A sub-atmospheric pressure exists in the pleural space as
compared to the sub-pleural space creating a negative
pressure gradient from the pleural interstitium to the pleural
space. This pressure gradient coupled with the porous
qualities of the mesothelium facilitates the continual
production of pleural fluid, absorption of concentrated
pleural fluid through the mesothelium, passage through the
parietal stomata, and ultimate drainage into the lymphatic
system [15, 18].
LUNG AND PLEURAL LYMPHATIC SYSTEM
The lymphatic drainage system for the lungs and pleura
is an expansive network of endothelium lined lymphatic
vessels within the loose sub-pleural connective tissue. This
lymphatic network runs the surface of the lungs and
penetrates them while communicating with the inter-lobar
septa [17, 21, 22].
Current Respiratory Medicine Reviews, 2012, Vol. 8, No. 4
315
The pleural space thus resides between the pulmonary
(visceral) and the parietal pleura lymphatic circulations [17,
23]. The visceral and parietal pleura possess their own
groups of lymph nodes, but here we will consider only those
nodal groups of the parietal pleura.
The sternal, intercostal, mediastinal and diaphragmatic
nodes comprise the parietal pleural lymph node groups.
These nodal groups are large contributors to the pleural
lymphatic system, and play a significant role in the drainage
of pleural fluid into the interstitial space, in both healthy and
diseased states [17, 23].
The pleural lymphatics directly drain the pleura via the
mesothelium at the parietal stomata. The direct anatomical
connections between the pleural space to the parietal
stomata, the lumen to the lymphatics, and the negative
pressure within the lymphatic drainage system are vital in
successful space drainage, and are responsible for the
majority of the pleural fluid drainage [17, 18, 22]. Due to a
greater thickness and lower water and solute permeability,
there is limited drainage via the visceral pleura. The visceral
pleural drainage that does occur is noted to be greatest at the
lower lobes where the visceral pleural lymphatics are the
most abundant [22, 24].
The negative pressure within the pulmonary lymphatics
facilitates fluid drainage through the parietal pleura. The
lymphatic drainage system can increase absorption to
accommodate up to a 28-fold increase in pleural fluid
volume [18, 22, 24].
PROPERTIES OF MALIGNANT PLEURAL EFFUSION
Malignant pleural effusions are most often characterized
chemically as exudative pleural effusions [25]. There are
numerous mechanisms in which a malignancy can contribute
to the formation of an MPE. In many cases, the malignancy
causes inflammation, subsequent increased pleural permeability, and enhanced production of pleural fluid and resulting accumulation of an effusion.
Malignancy can also impair the pleura via direct pleural
invasion resulting in an increased pleural effusion. If the
mediastinal lymph nodes are involved, the pleural lymphatic
drainage system will be impaired, decreasing outflow and
resulting in increased fluid accumulation. Cases where the
thoracic duct is interrupted by malignancy can be the most
challenging to manage as chyle is continuously produced and
floods the pleural space resulting in a rapidly reoccurring
large volume chylothorax [7, 26, 27].
Lymphatic drainage disruption also occurs when there is
fibrosis induced by chemotherapy or radiation therapy;
fibrosis results in decreased absorption and increased
accumulation of pleural fluid [7, 26-28].
CLINICAL PRESENTATION
PLEURAL EFFUSION
OF
MALIGNANT
Symptoms of pleural fluid accumulation are associated
with patient physiology and not fluid volume. Pleural fluid
can cause changes in chest wall mechanics, restrictive lung
disease and mediastinal shift. Patients with compromised
pulmonary or cardiac function can be symptomatic with
small volumes of fluid in the pleural space, other patients
316 Current Respiratory Medicine Reviews, 2012, Vol. 8, No. 4
can tolerate larger volumes before symptoms are detected [7,
29, 30].
Dyspnea is the most common symptom of MPE:
symptoms can be positional with patients complaining of
increased symptoms when they lie down or bend over to tie
their shoes. Dyspnea is often worsened with exertion.
Malignant pleural effusion can also be accompanied by
fever, pleuritic chest pain, non–productive cough, or chest
pressure [7, 31]. First time symptoms in association with a
physical exam suspicious for an effusion, including
decreased breath sounds or dullness to percussion, warrant a
work up including radiographic imaging (CXR; often
followed by CT or ultrasound).
PLEURAL SPACE EVALUATION
The full work-up of MPE begins with an ultrasound
guided thoracentesis and drainage of the pleural fluid
collection. The pleural space should be analyzed by
ultrasound. This allows for assessment of pleural anatomy
including pleural or diaphragmatic masses, pleural space
septations, and for the most accurate localization of the
pleural fluid allowing for a safe thoracentesis [32, 33].
EVACUATION OF THE PLEURAL SPACE
Pleural fluid should be drained completely or to the
extent tolerated. Indications for stopping pleural fluid
drainage include chest pain or pressure and difficulty
breathing experienced by the patient as fluid is being
removed. Pleural manometry has been studied as a tool to
diagnose lung entrapment and to determine the safest fluid
volume to extract [34, 35].
Evacuation of the pleural space allows for the assessment
of lung entrapment vs trapped lung. Entrapped lung
describes a lung that fails to expand due to visceral pleural
thickening, endobronchial blockage or increase in lung
elastic recoil from interstitial disease; this is pathophysiologically different from trapped lung, which is a restrictive
visceral pleural peel that prevents re-expansion [36, 37].
Entrapped or trapped lung will not fully re-expand after
evacuation of the effusion (Fig. 2) and will need to be
accounted for in any long-term palliative management
strategy.
Gorden and Fathi
EVALUATION OF THE PLEURAL FLUID
The pleural fluid should be sent for laboratory evaluation
including: glucose, LDH, total protein, cell count and
differential as well as cytology. A malignant pleural effusion
is often exudative and lymphocyte predominant. The
diagnostic yield of pleural fluid cytology ranges from
20-80% depending on the cancer type, with breast being the
highest yield and sarcoma the lowest [15]; additional
maneuvers may be required to confirm the diagnosis of a
malignant pleural effusion. If the malignant nature of the
pleural effusion cannot be confirmed by fluid evaluation
alone, a pleural biopsy can be obtained by either VideoAssisted Thoracic Surgery (VATS) or single port semi-rigid
thoracoscopy, often termed medical thoracoscopy [38]. Both
tools allow for the visual inspection of the pleural surfaces
and for pleural biopsy, allowing for generous tissue samples,
which can be used to prove the diagnosis, identify the
underlying malignancy type and even possibly assess for
mutation analysis for possible tailored systemic therapy.
Pleural biopsies should only be considered if it has been
determined that the findings will impact the treatment plan.
A patient with a known advanced malignancy and a recurrent
symptomatic effusion may require palliation only, and an
invasive diagnostic procedure may not be necessary to guide
therapy.
TREATMENT STRATEGY
Malignant pleural effusion represents an advanced
disease state and treatment should be tailored to the
individual patient and must take into account their condition,
prognosis, performance status, and future expectations and
goals of treatment. Any therapeutic intervention should
conform to the principles of palliative care:
1.
The intervention should be rapid and effective at
controlling the symptoms.
2.
It should have low associated morbidity and
mortality.
3.
It should require minimal follow-up.
4.
The intervention should maximize independence,
comfort and quality of life.
CLINICAL OPTIONS FOR THE MANAGEMENT OF
MALIGNANT PLEURAL EFFUSION
There are three fundamental mechanisms for controlling
recurrent malignant pleural effusions: repeat thoracentesis,
evacuation and pleurodesis, or placement of a tunneled
pleural catheter (TPC).
THORACENTESIS
Fig. (2). Lung entrapment: Failure of the lung to re expand
following lung insufflation at the time of VATS.
A thoracentesis is a proven safe and effective tool for
removing pleural fluid and eliminating symptoms. It is best
reserved for rapid symptom palliation and assessment of
lung re-expansion after drainage. Thoracentesis provide no
lasting protection from pleural fluid re-accumulation and
may need to be repeated every time symptoms recur as the
pleural fluid re-accumulates; this often translates into
patients needing repeated visits to the ER or clinic for
drainage while tethering them to the medical community and
Malignant Pleural Effusion Evaluation and Management
diminishing their independence. For most patients,
thoracentesis does not provide long-term palliation for
recurrent MPE. There are also theoretical concerns that
repeated thoracentesis can lead to loculations and potential
lung entrapment.
POTENTIAL COMPLICATIONS OF THORACENTESIS
Thoracentesis can be safely performed in the outpatient
setting. Principle risks include bleeding and pneumothorax.
In some centers it is not required to stop patient
anticoagulation prior to thoracentesis. The risk of
pneumothorax is small and was decreased by the use of
ultrasound. The incidence of pneumothorax is about 10%
and drops to 4% when ultrasound guidance is used [29, 39,
40]. After uneventful thoracentesis, when the clinician does
not identify a complication, a post procedure X-ray is not
required [28].
If the symptoms of MPE are relieved after thoracentesis
and the symptomatic MPE recurs, then a long-term
management strategy must be considered. Thoracentesis as a
primary palliative tool should probably be reserved only for
the most end-stage patients when dyspnea interferes with the
palliative goals of a comfortable and dignified end of life.
Thoracentesis can also be used to identify patients whose
symptoms will not be relieved by pleural space evacuation
and in whom a more definitive and often invasive procedure
will not be required.
PLEURODESIS
Pleurodesis is established by fusing the visceral and
parietal pleural surfaces and thus eliminating the very space
in which pleural fluid may accumulate. To consider
pleurodesis the lung must re-expand after pleural fluid
evacuation, thereby placing the two pleural surfaces in
contact. Pleurodesis can be cautiously considered if the lung
fails to completely re-expand after drainage. A significant reexpansion though incomplete may at times suffice to attempt
pleurodesis as long as enough visceral-parietal pleural
contact is achieved. In such a scenario, re-accumulation of a
smaller but hopefully asymptomatic effusion is the target.
Unfortunately no guidelines exist for what constitutes
“enough” lung re-expansion. If after pleural fluid evacuation
an isolated space persists, one could consider this strategy in
the fit, well informed patient.
Fusion of the visceral and parietal surfaces is achieved by
introducing a chemical irritant into the pleural space and
promoting an inflammatory response to ensue. Many agents
have been used to fuse the pleural space, including talc,
povidone-iodine, doxycycline, hypertonic dextrose, and
other sclerosants [7, 31, 41]; talc is clearly favored over
other sclerosing agents in multiple trials [26].
Sclerosants can be introduced in the pleural space via
large or small-bore chest tubes or by VATS or medical
thoracoscopy [27, 42-44]. Contrary to popular belief,
following intrapleural chemical instillation, patients do not
require side-to-side rotation to disperse the sclerosant as
natural respiratory movements will disperse it throughout the
pleural surface [45]. The manner with which sclerosants are
Current Respiratory Medicine Reviews, 2012, Vol. 8, No. 4
317
introduced in the pleural space does not appear critical as
shown in a large randomized phase III CALGB trial where
no difference in overall pleurodesis rates was seen between
VATS talc and bedside talc slurry via chest tube [42].
Pleurodesis is very effective at achieving fusion, with
successful pleurodesis rates reported at 67-84%, but the need
for re-intervention is not insignificant at 16% [30].
The major limitation of pleurodesis relates to periprocedure pain and the requirements for hospitalization.
Following sclerosant instillation, pleurodesis requires chest
tube drainage of the space to keep the two pleural surfaces in
apposition and to allow optimal adhesion to occur. Hospital
length-of-stay varies anywhere from 3-10 days, following
pleurodesis [30, 44, 46].
POTENTIAL COMPLICATIONS OF PLEURODESIS
Pulmonary complications with talc pleurodesis have been
reported including the development of Acute Respiratory
Distress Syndrome [7, 26, 47, 48]. This risk is related to talc
particle size and even when allowing the use of talc
containing small particles, the risk has been mitigated by
limiting talc instillation to no more than 4 grams. The most
reported side effects from pleurodesis include: pain, dyspnea
and fever [43]. Thirty day mortality rates vary; in the
CALGB phase III trial, a 20% - 30 day mortality rate was
seen, emphasizing the importance of patient selection and
adherence to palliative principles [11, 42]. Various
approaches have been tried to minimize the morbidity of
pleurodesis [49], but the procedure still requires a hospital
stay and may be painful.
Pleurodesis is limited to the specific population where
the lung re-expands and should not be considered for
patients with lung entrapment regardless of their
performance status except in limited circumstances. The
main advantage of pleurodesis however, is that it is a onetime procedure and when successful, patients do not require
persistent care of their effusion. Early cost effectiveness data
suggests for patients with 12 month or greater survival,
bedside pleurodesis is favorable over Tunneled Pleural
Catheter (TPC) or VATS pleurodesis [50].
TUNNELED IN-DWELLING PLEURAL CATHETERS
The tunneled pleural catheter was first approved for
patient placement by the FDA in 1997. The catheter consists
of an intra-pleural component, a tunneled subcutaneous
portion, a fibrous subcutaneous cuff (which prevents
migration), and an external access section. At the proximal
end of the catheter is a one-way valve, which permits safe
pleural space drainage (Fig. 3). Because the TPC allows for
repeated patient controlled access and drainage of the pleural
fluid, it can be used to palliate patients with lung entrapment
as well as those with complete lung expansion. The TPC is
usually placed in an outpatient or bedside procedure, by the
Seldinger technique, but can be placed in adjunct to a
diagnostic VATS or medical thoracoscopy. The minimally
invasive nature of catheter placement allows it to be used to
palliate a spectrum of patients with varying performance
statuses, and is unique in that it can be offered to frail
patients with diminished performance status.
318 Current Respiratory Medicine Reviews, 2012, Vol. 8, No. 4
(A)
(B)
Gorden and Fathi
The TPC can be placed in the ambulatory setting and
immediately managed by supportive caregivers, without
requirement for hospitalization. In our experience, when placed
in hospitalized patients the mean post procedure length of stay
was 3 days, significantly less than the 6 days required after
pleurodesis; most placed on an outpatient basis required no
hospitalization [30, 46]. In multiple trials the TPC has been
shown to palliate the clinical symptoms of MPE with improved
dyspnea scores [51-53]. In published series, TPC achieve
pleurodesis in approximately 50% of patients but this “bonus”
effect cannot be determined apriori. The average time to auto
pleurodesis after catheter placement exceeds 40 days [54, 55].
Successful pleurodesis does allow for removal of the TPC but
this will not be achieved in all patients and should not be
established as an expectation of placement. Tunneled pleural
catheter provides durable palliation with limited need for reintervention. In our series, TPCs required significantly less need
for ipsilateral re-intervention when compared to talc pleurodesis
(2% vs 16% ) [30].
Tunneled pleural catheters require on-going management
and active drainage for symptom palliation. Because TPCs
require continued engagement, placement must be considered as
part of a program and not as isolated procedures. A tunneled
pleural catheter program requires a supportive team to ensure
maximum palliation and to provide post-procedure support for
the patient and caregiver. The education must begin before
insertion and followed up for first drainage with the caregiver
present. It requires participation of physicians, allied health
professionals and/or nurses, a willing patient, and an able
caregiver structure. TPC management also requires assistance
for drainage and dressing changes: this can often be provided by
a family member or visiting caregiver. Additionally, an
important part of the TPC program staff is to secure insurance
approval and initiate the supply chain for drainage equipment.
(C)
Fig. (3). (A) Tunneled pleural catheter with intra-thoracic portion,
tunneled portion, fibrous cuff and external portion with one way
valve and cap. Disposable pleural drainage bottle and tubing for
tunneled pleural catheter. (B) Tunneled pleural catheter with
external thoracic portion and one way valve with cap showing. (C)
CT Scout image of a tunneled pleural catheter in the pleural space.
Patients with TPC should be given a drainage schedule:
currently no established drainage schedules exist and it is
unknown if drainage frequency impacts the pleurodesis rate.
Patients should be drained frequently enough to preempt
symptoms and should be taught to drain the maximum
comfortable volume of fluid per session. Painful drainage is
most commonly associated with lung entrapment, and drainage
should be interrupted if pain results. Patients must be educated
that the volume of fluid drained is not important, and that the
palliative effect of fluid drainage is really what matters.
Complications of TPC are rare, reported deep infection rates
are less than 5% [51, 55]. Occlusion of the TPC is rare and can
be potentially managed with the instillation of a small
dose/volume of thrombolytic. Tunneled pleural catheter
placement supports an active functional lifestyle. Patients
should be encouraged to participate in all their usual activities
including active sports, travel, work, and showering. The only
specific activity limitations are those activities which result in
submerging the catheter; swimming, scuba diving, snorkeling,
hot tubs or baths. Early cost effective data supports the use of
TPC for patients with more limited life expectancy, i.e. 3
months or less [50].
CONCLUSION
Malignant pleural effusions represent an advanced state
of malignancy and a significant barrier to a good quality of
Malignant Pleural Effusion Evaluation and Management
Current Respiratory Medicine Reviews, 2012, Vol. 8, No. 4
life. The development of a strategy for managing MPE requires education and engagement of the patient and their
caregiver. Any strategy to control the symptoms of MPE
must adhere to defined palliative goals: 1. The intervention
should be rapid and effective at controlling dyspnea. 2. The
intervention should have low - associated morbidity and
mortality; 3. The intervention should require minimal followup; 4. The intervention should maximize independence and
quality of life.
presence of pleural fluid adds an increased symptom layer to
their diminished baseline.
Three strategies exist for managing MPE: thoracentesis,
pleurodesis and tunneled pleural catheter placement. We
propose an algorithm for the management of MPE, (Fig. 4)
[30]. Thoracentesis is an excellent diagnostic tool to
differentiate patients with lung entrapment from those whose
lung will fully expand, and to identify patients whose
symptoms will not improve despite pleural space evacuation.
This is the first branch point in deciding on palliative
options. Thoracentesis usually provides no durable symptom
relief and in that regard is often a sub-optimal long-term
palliative option. Tunneled pleural catheters can be placed in
patients with full lung re-expansion post evacuation as well
as in those with lung entrapment. The placement of TPC
Palliation of MPE must be tailored to the individual
patient; some patients remain active despite their diagnosis
of malignancy and experience significant loss of function
when pleural fluid is present, and become once again highly
functional when it is evacuated. Other patients are
significantly impaired by their diagnosis of cancer and the
Symptomatic pleural effusion in a
patient with cancer
Thoracentesis
Relief of symptoms,
followed by recurrent
symptomatic effusion?
No
No further
intervention.
Yes
Was the tap diagnostic
of cancer?
No
Pleural biopsy, if it will change
management. Palliative therapy
(TPC or pleurodesis) at the time of
biopsy.
Yes
Does the lung fully
reexpand on CXR?
Yes
TPC or pleurodesis.
319
No
TPC
Fig. (4). Proposed algorithm for evaluation and management of malignant pleural effusion [30].
320 Current Respiratory Medicine Reviews, 2012, Vol. 8, No. 4
carries low morbidity risks, requires no or limited
hospitalization and provides durable relief of symptoms.
Tunneled pleural catheter requires on-going self-directed
drainage to palliate symptoms and support from caregivers.
Tunneled pleural catheter can be placed in both frail and
active patients and supports a fully functional lifestyle.
Pleurodesis is only compatible with patients who have
complete lung expansion and requires hospitalization of 4-6
days with chest tube suction and drainage during this period.
After successful pleurodesis patients do not require on-going
maintenance or care giver support.
For a frail population with MPE, both those with lung
entrapment and complete lung expansion, we favor TPC due
to its lower morbidity and durable palliation. For patients
with better performance status, a reasonable life-expectancy
and complete or majority lung re-expansion, it remains an
individual decision between the informed patient and their
caregiver team with regards to the choice of TPC or
pleurodesis.
ACKNOWLEDGEMENT
Declared none.
Gorden and Fathi
[14]
[15]
[16]
[17]
[18]
[19]
[20]
[21]
[22]
[23]
[24]
[25]
[26]
[27]
CONFLICT OF INTEREST
Declared none.
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Received: April 24, 2012
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Revised: May 1, 2012
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Accepted: June 2, 2012