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Mechanisms of pleural liquid accumulation in disease

Author: V Courtney Broaddus, MD
Section Editor: Talmadge E King, Jr, MD
Deputy Editor: Geraldine Finlay, MD

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Dec 2019. | This topic last updated: Feb 27, 2018.

INTRODUCTION

In the normal pleural space, there is a steady state in which there is a roughly equal rate of the
formation (entry) and absorption (exit) of liquid (figure 1). (See "Mechanisms of pleural liquid
turnover in the normal state".) This balance must be disturbed in order to produce a pleural
effusion. Thus, there must be an increase in entry rate and/or a reduction in exit rate. It is likely that
both mechanisms contribute to effusion formation for the following reasons:

● An isolated increase in entry rate, unless large and sustained, is unlikely to cause a
clinically significant effusion because the absorbing pleural lymphatics have a large reserve
capacity to deal with excess pleural liquid. If, for example, artificial hydrothoraces are instilled
into the pleural space of awake sheep, the exit rate can increase to 0.28 mL/kg per hour,
which is 28 times the baseline rate [1].

● An isolated decrease in exit rate is also unlikely to cause a large effusion because the
normal entry rate is low. Even if the exit of liquid ceased entirely, accumulation of liquid would
take many days to become evident. As an example, the normal entry rate of 0.01 mL/kg per
hour is equivalent to a total of 12 mL/day in a 50 kg woman; at this rate of entry without any
exit of liquid, it would take more than one month days for 500 mL to accumulate in the pleural
space. Of note, the effusion would presumably be a transudate, since the normal liquid
entering the pleural space is low in protein.

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INCREASED FLUID ENTRY

Excess liquid filters out of systemic microvessels based on a balance of hydrostatic and osmotic
forces across a semipermeable membrane [2,3]. These forces are well described in the Starling
equation, in which the hydrostatic forces that force water out of the vessel are balanced by osmotic
forces that reabsorb water back into the vessel [4,5].

Flow = k x [(Pmv - Ppmv) - s (πmv - πpmv)]

In this equation, k is liquid conductance of the microvascular barrier, Pmv and Ppmv represent
hydrostatic pressure in the microvascular and perimicrovascular compartments, s is the reflection
coefficient for total protein and ranges from 0 (completely permeable) to 1 (completely
impermeable), and πmv and πpmv represent protein osmotic pressure in microvascular and
perimicrovascular liquids, respectively. In normal microvessels, there is ongoing filtration of a small
amount of low protein liquid. The flow from the microvessels can increase with changes in various
parameters of the Starling equation.

Increase in permeability — An increase in flow can be due to increases in either liquid

conductance (an increase in k) or protein permeability (a decrease in reflection coefficient). If the
endothelial barrier becomes more permeable to liquid and protein, for example, there will be an
increase in flow of a higher protein liquid. Because absorption does not alter the protein
concentration of pleural liquid, pleural liquid with a high protein concentration indicates its origin
from a circulation across an area of increased permeability. (See "Mechanisms of pleural liquid
turnover in the normal state", section on 'Evidence for bulk flow'.)

Increase in microvascular pressure — An elevation in microvascular pressure (Pmv) is usually

induced by an elevation in venous pressure. Increases in arterial pressure are less likely to be
transmitted to the microvessels because of the high precapillary resistance and autoregulation of
arteriolar tone.

Elevations in systemic venous pressure (which would mostly affect the parietal pleura) can lead to
an increase in pleural liquid formation. If vascular permeability were unchanged, the increased flow
would be associated with a greater sieving of proteins, leading to a filtrate with a lower protein
concentration than normal (with a pleural liquid-to-serum protein ratio of less than 0.15).

Of course, most effusions formed due to increased microvascular pressures, ie, transudative
effusions, have a pleural liquid-to-serum protein ratio much higher than this, between 0.4 and 0.5.
This fact demonstrates that most liquid must arise from a source other than the systemic
circulation of the pleural membranes. The likely source is the large non-systemic circulation

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adjacent to the pleural space, namely the pulmonary circulation of the nearby lung. In the normal
state, lung interstitial liquid, eg, lymph, filtered from the low pressure pulmonary circulation has a
protein concentration ratio (lung to serum protein concentration ratio) of 0.7, but with increased
flow due to increased pulmonary microvascular pressures, this ratio falls to 0.4-0.5 [6]. As shown
in studies of anesthetized sheep, this lung interstitial edema liquid is the likely source of the
majority of the hydrostatic pleural effusion [7].

How does the lung edema liquid reach the pleural space? When the rate of filtrate formation
exceeds the absorptive capacity of the lung lymphatics, the filtrate accumulates in the
peribronchovascular spaces ("cuffs") [8]. Once in these interstitial spaces, the liquid is not
accessible to lung lymphatics [9]. Thus, although the lymphatics are undeniably important in
removing liquid as it is filtered from the pulmonary circulation, they cannot account for the
clearance of already established edema from the lung [10]. This interstitial edema probably leaves
the lung by flowing in response to pressure gradients along the interstitial spaces (interlobular
septae, peribronchovascular bundles and visceral pleura) of the lung toward either the
mediastinum or the pleural space. The entry of large amounts of lung interstitial liquid into the
pleural space will elevate the overall protein concentration of the pleural liquid, giving a ratio of
0.40-0.50, the expected range for a transudative effusion [7].

Decrease in pleural pressure — A decrease in pleural pressure, as seen with significant

atelectasis, may alter the balance of forces described in the Starling equation by reducing the
pressures surrounding the nearby microvessels. This decrease in perimicrovascular pressures
(Ppmv) can enhance filtration across the microvascular barrier of a low protein liquid (with a pleural
liquid-to-serum protein ratio of less than 0.15). Thus, fluid will accumulate until the pressure
balance is restored; the decreased pleural pressure is the likely explanation for the formation of
pleural effusions in the setting of atelectasis.

Decrease in plasma osmotic pressure — Hypoproteinemia (due to hypoalbuminemia) will

decrease the plasma oncotic pressure (πmv), thereby increasing the forces favoring filtration until
the balance is restored. By itself, hypoproteinemia can probably induce small effusions with a low
protein concentration. In addition, hypoproteinemia can lower the threshold for effusion formation
when other Starling forces are changed. In a study of hospitalized patients with AIDS, for example,
hypoproteinemia alone was the apparent cause of 19 percent of all pleural effusions [11]. However,
together with other factors, a lower serum protein concentration may have contributed to effusion
formation in many more patients, because, in general, the patients with effusions had a lower
serum albumin concentration than those without effusion (2.5 versus 3.4 g/dL). In another study,
hypoalbuminemia may have enhanced the size of pleural effusions, perhaps by shifting the
balance toward increased filtration; in children with parapneumonic pleural effusions, those with

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large effusions had a lower mean serum albumin concentration than those with small effusions (2.7
versus 3.7 g/dL) [12]. Thus, while a low albumin concentration may be an infrequent cause of
effusions by itself, it may contribute to effusion formation by other causes.

DECREASED FLUID EXIT

A decrease in exit rate indicates a reduction in clearance of fluid from the pleural space, a
clearance that largely takes place via the parietal pleural lymphatics. Because lymphatic function is
poorly understood, much of this discussion is speculative. Unlike blood vessels, lymphatic vessels
have one-way valves. Lymph is propelled actively by rhythmic muscular contractions of lymphatic
smooth muscle and passively by compressions from the respiratory motions of the chest wall. In
addition, flow is affected by lymphatic patency, availability of liquid, and the pressures influencing
filling (pleural pressure) and emptying (systemic venous pressure) of lymphatics [13,14].

Intrinsic factors — A number of factors can interfere with or inhibit the ability of lymphatics to
contract, including:

● Cytokines and products of inflammation (eg, endotoxins)

● Endocrine abnormalities (eg, hypothyroidism)
● Injury due to radiation or drugs (eg, chemotherapeutic agents)
● Infiltration of lymphatics by cancer
● Anatomic abnormalities (eg, yellow nail syndrome)

Extrinsic factors — Multiple extrinsic factors can inhibit lymphatic function although the
lymphatics themselves are normal. These include:

● Limitation of respiratory motion (eg, diaphragm paralysis, lung collapse, pneumothorax)

● Mechanical compression of lymphatics (eg, pleural fibrosis, pleural granulomas)

● Blockage of lymphatic stomata (eg, fibrin deposition on pleural surface, pleural malignancy)

● Decreased intrapleural pressure (eg, atelectasis)

● Increased systemic venous pressure – Acutely, increases in venous pressure may decrease
lymphatic flow because of the higher downstream pressures; chronically, the lymphatics may
be able to adapt.

● Decreased availability of fluid at the lymphatics – After pneumothorax, for example, fluid may
not remain in contact with lymphatic stomata and may accumulate at the dependent portion of

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the pleural space as a small effusion.

EFFUSION FORMATION AND DISEASE STATES

As discussed above, no single mechanism is likely to explain the development of a pleural

effusion. It is likely that, for many effusions, multiple factors contribute to effusion formation. In
addition, an alteration of one mechanism can lower the threshold for effusion formation later by
another mechanism. Thus, a decreased exit rate due to malignant infiltration or fibrosis of
lymphatics can gradually reduce the capacity of the lymphatics to drain pleural liquid. As long as
the entry rate remains low, an effusion may not form; however, if the entry rate should increase, the
limitation of the exit rate would reduce the ability of the lymphatics to handle the increased fluid
and an effusion could then accumulate.

There are some data on the entry and exit rates of pleural liquid in patients with pleural effusions.
In two early studies of the turnover of pleural liquid in effusions of patients with a variety of different
diseases, the entry rates were highest in tuberculosis but similar among the other disorders
[15,16]. The exit rates were low in malignant and tuberculous effusions compared to the rates in
effusions due to cardiac failure and pulmonary embolism. In one study, for example, calculated
lymphatic flow for patients with pulmonary embolism was 0.18 mL/kg per h, which is similar to the
maximal exit rate measured for sheep (0.28 mL/kg per h); in comparison, lymphatic flow was lower
in the patients with carcinoma or tuberculosis (0.06 and 0.08 mL/kg per h, respectively) [16].
Interestingly, the entry rate decreased and the exit rate increased after therapy with prednisone in
patients with tuberculosis.

EFFUSION FORMATION BY SITE

Most effusions form due to abnormalities at thoracic sites such as the pleural membranes, lungs,
mediastinum, or diaphragm. On occasion, effusions can develop from abnormalities at other sites
such as the central nervous system, kidney, or pancreas.

Pleura — Direct involvement of pleural membranes by disease can lead to a pleural effusion by
increasing the formation of liquid and interfering with parietal pleural lymphatic function (figure 2).
Hydrostatic pressure elevations can also increase filtration from the pleural membrane
microvessels.

● Malignancy – Malignant effusions are probably caused by both mechanisms, increased entry
plus decreased exit of fluid. There are patients with rapid entry rates, which can be recognized

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clinically because the effusion accumulates rapidly after drainage or has a high chest tube
drainage rate. In this setting, the tumor has presumably extensively infiltrated pleural
capillaries, leading to increased filtration, or is producing cytokines, such as vascular
endothelial growth factor (VEGF), that increase capillary permeability [17,18]. One study
indicated that the mast cell may be the key cell producing cytokines, such as tryptase AB1
and IL1 beta, leading to increased permeability [19]. Decreased plasma osmotic pressure or
decreased pleural pressure could contribute to the enhanced entry of liquid.

On the other hand, malignancy may lead to effusion formation by infiltrating the draining
lymphatics or lymph nodes, thereby decreasing the exit rate. In some cases of lymphatic
involvement, the decrease in the exit rate appears to be an important mechanism of effusion
formation because the effusions can resolve after mediastinal irradiation of involved lymph
nodes. In certain malignant effusions, extrapleural involvement of draining lymphatics may be
the sole mechanism of effusion formation. Such an isolated exit block may explain the
existence of transudative effusions, which have been described in approximately 10 percent of
patients with malignant effusions [20].

● Tuberculosis – Tuberculosis involves the pleural membranes with a granulomatous reaction

that may lead to both an increased entry rate and decreased exit rate of liquid. The high
protein concentration of tuberculous pleural effusions indicates its origin from capillaries
involved with an intense inflammation [16]. The exit rate, on the other hand, has been found to
be low in both patients and animals with experimental models of BCG pleurisy [15,16,21]. The
low exit rate may indicate that inflammation of the parietal pleural by tuberculosis is extensive
and intense enough to compromise pleural lymphatic function.

For patients with pleural malignancy or tuberculosis, the synergistic combination of increased entry
and decreased exit of liquid may explain the massive effusions that can accumulate.

Pleural microvessel hydrostatic pressure elevation — An increase in the microvascular

pressure of pleural vessels can increase filtration in a variety of ways. Systemic venous pressure
elevation both increases filtration from the parietal pleural microvessels and decreases lymphatic
drainage into the venous system (figure 3). In comparison, an elevation in pulmonary venous
pressure increases filtration from the visceral pleura.

● Pulmonary embolism – Pulmonary embolism can increase entry rates of liquid by injuring
pulmonary and adjacent pleural systemic circulations, by elevating hydrostatic pressures in
pulmonary veins and/or systemic veins, and perhaps by lowering pleural pressure due to
atelectasis. Pulmonary embolism may also decrease exit rates of pleural liquid by increasing
the systemic venous pressure (thereby hindering lymphatic drainage) or perhaps by

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decreasing pleural pressure (thereby hindering lymphatic filling). The observation that all
effusions due to pulmonary embolism were exudates suggests a key role for vascular injury
[22]; however, hydrostatic pressure changes probably also contribute to the formation of the
effusions. One retrospective study comparing patients with PE found that those with effusions
were more likely to have more severe PE and pulmonary infarction than those without
effusions [23]. As in acute lung injury, when microvessels are injured, small changes in
hydrostatic pressure can have a large effect on fluid flux.

● Superior vena cava syndrome – The mechanism of effusion formation in patients with the
superior vena cava syndrome has only been studied in a few cases [24]. Apparently, the entry
rate of liquid into the pleural space is increased. The most detailed study has been in one
patient who was shown to have a transudative effusion with flow through the thoracostomy
tube of approximately 500 mL/day [25]. In another study of volume-loaded dogs, an elevation
in systemic venous pressure for two hours plus a decrease in plasma osmotic pressure led to
a significant increase in pleural liquid entry and formation of an effusion [26].

The exit rate may also be decreased acutely since the lymphatics must pump against a higher
downstream pressure. With chronic pressure elevations, however, the lymphatics may adapt
and resume a more normal capacity. In a series of 27 patients with chronic systemic venous
pressure elevation due to pulmonary hypertension, for example, no effusions were found on
ultrasonography [27]. More recently, small effusions have been noted to be common in
patients with elevated right sided pressures and right heart failure due to idiopathic pulmonary
hypertension. It is possible that even these small effusions were generated by the interference
of the right heart in left heart function [28].

● Brachiocephalic venous obstruction – This entity has been identified as a cause of persistent,
sometimes intractable transudative effusions. In particular, the obstruction, often developing in
a patient undergoing hemodialysis, is thought to increase pleural microvascular hydrostatic
pressure, and thereby increase pleural liquid formation and decrease lymphatic clearance
[29]. The effusion can resolve after angioplasty of the occluded vessel [30,31].

Lung — The lung is a potentially large source of liquid immediately adjacent to the pleural space.
Lung interstitial liquid can move into the pleural space along a pressure gradient and across leaky
pleural membranes (figure 4) [32].

● Acute lung injury – From animal studies in which injury is limited to the lung, it is clear that
large amounts of lung liquid can move into the pleural space. After chemical or hyperoxia-
induced lung injury in animals, for example, an increased permeability lung edema developed
and was followed by high protein pleural effusions in approximately two hours [33-35]. With

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hyperoxic lung injury in rats, the movement of liquid from lung to pleural space could be traced
by the movement of a specific marker [36]. In sheep given intravenous oleic acid, liquid
leaving the lung across the visceral pleura could be collected in a surrounding bag and
quantified as representing almost 20 percent of the lung edema [35].

These observations suggest that pleural effusions should be common in patients with acute
lung injury. In a radiographic study of patients with pulmonary edema, for example, pleural
effusions were found to be as common in patients with acute lung injury (36 percent) as in
patients with hydrostatic pulmonary edema (40 percent) [37]. Other lung injuries, such as
pneumonia or pulmonary embolism, can also result in effusion formation due to the movement
of high protein lung interstitial liquid into the pleural space.

● Hydrostatic pulmonary edema – In heart failure, in contrast to lung injury, the abnormalities
are not limited to the lung; as a result, identification of the source of the pleural liquid is more
difficult. An elevation in systemic venous and pulmonary venous pressures can lead to
increased filtration from both pleural membranes, decreased absorption via pleural
lymphatics, and increased filtration into the lung with movement of lung edema into the pleural
space.

Several studies suggest that the contribution of lung edema may be the most important. In an
experimental study in which pressures were elevated in the systemic venous, the pulmonary
venous, or both circulations, the most liquid appeared after systemic pressure elevation [26].
However, this study lasted only two hours and lung edema takes at least two hours to
accumulate and then to flow to the pleural space [7,33,35]. It is therefore likely that the
contribution from the lung was not yet evident. The observation in a clinical study of patients
with heart failure that the presence of pleural effusions by ultrasound correlated better with
elevated pulmonary venous pressures than systemic venous pressures is compatible with the
importance of a lung contribution [38], although a visceral pleural contribution cannot be
excluded. A later study of patients with pulmonary hypertension showed that isolated
increases in systemic venous pressure, at least when chronic, did not cause edema formation
[27].

Studies in anesthetized sheep addressed the contribution of the lung (and visceral pleura)
more directly by isolating the lung in an impermeable bag [7]. Lung edema was created by
volume loading to elevate the pulmonary capillary wedge pressure by 10, 20 or 30 cmH2O.
Liquid began to leak from the lung, and by two hours after stable pressure elevation, the lung
liquid flow had reached a steady state. The lung liquid had the same protein concentration as
lung lymph and interstitial liquid later harvested from peribronchovascular spaces ("cuffs").

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The amount of liquid flowing from the lung could account for the pleural effusions found in
other closed-chest volume loaded sheep. The edema that cleared the lung into the pleural
space accounted for almost 23 to 29 percent of all edema formed. Thus, the contribution of
the pleural route to edema clearance appears to be similar for hydrostatic edema and for the
increased permeability edema formed due to acute lung injury [35]. These observations
suggest that the pleural route of edema clearance may be an important additional safety factor
protecting against alveolar flooding.

The protein concentration in the transudative effusions seen with heart failure also argues
strongly that the effusions consist mostly of lung interstitial liquid. As discussed above, liquid
derived from increased filtration across systemic vessels would be expected to have a very
low protein concentration with a pleura-to-serum protein concentration ratio of less than 0.15.
However, transudative effusions have a higher protein concentration ratio (approximately 0.40
to 0.50), similar to the ratio in pulmonary filtrate (eg, in lung lymph) [7].

The protein concentration of pleural fluid and the pleural/serum protein concentration ratio can
increase with acute diuretic therapy, so that a true transudate may yield indices suggestive of
an exudate [39-41]. Although not all studies have shown a change from transudative to
exudative chemistries following diuresis [42], this phenomenon must be considered when
interpreting pleural chemistries in patients following a significant diuresis [43].

Extrapleural or extrapulmonary — Excess liquid from any tissue in the body may find its way to
the pleural space by passive flow toward the low pressure of the pleural space. Then, once
adjacent to the pleural membranes, the excess fluid could move into the pleural space, either via
holes or tears in the mediastinal pleura or diaphragm or via direct flow across the permeable
pleural membranes.

● Mediastinum – Effusions have been described following mediastinal inflammation due to

esophageal variceal sclerotherapy and esophageal perforation. Chyle can also collect in the
mediastinum from a break in the thoracic duct and can then decompress by draining into the
pleural space, producing a chylothorax (see "Etiology, clinical presentation, and diagnosis of
chylothorax"). Fluid from a pancreatic pseudocyst can also flow via pressure gradients into the
mediastinum and then decompress into the pleural space. Usually decompression of the
mediastinal collection is achieved when there is flow into one pleural space and thus, these
effusions tend to be unilateral.

● Diaphragm – Liquid can cross the diaphragm by diffusion or by movement across

macroscopic holes, either acquired or congenital. Peritoneal liquid can potentially reach the
pleural space by diffusion across the two mesothelial layers, a process which would likely be

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slow. Peritoneal fluid can also move rapidly across the diaphragm through acquired or
congenital defects in the diaphragm [44]. The defects apparently form at points of weakness in
the muscular webbing of the diaphragm. Based on observations during video-assisted
thoracoscopy (VATS), the defects have various morphologies from blebs to fenestrations [45].
They may be missed, even on direct inspection of the diaphragm, unless pressure is applied
to expand them.

Although some have speculated that liquid might cross the diaphragm via lymphatics, there is no
evidence for the existence of direct lymphatic channels connecting the peritoneal and pleural
spaces across the diaphragm [46,47]. In studies in which radiocontrast dye is instilled into the
peritoneal space, the dye clearly drains into lymphatics that travel to the mediastinum; no dye
enters the pleural space. Therefore, the only likely mechanism for rapid movement of liquid across
the diaphragm is through actual defects in the diaphragm [44].

SUMMARY AND RECOMMENDATIONS

● Most effusions are likely caused by a combination of increased pleural fluid formation and
decreased pleural fluid clearance. (See 'Increased fluid entry' above.)

● The protein concentration of pleural liquid is a clue to its formation since protein concentration
is not altered by absorption of pleural liquid via lymphatics. (See 'Increase in permeability'
above.)

● Elevations in either systemic venous pressure (affecting the parietal pleura) or pulmonary
venous pressure (affecting the visceral pleura) can lead to an increase in pleural liquid
formation and the development of a pleural effusion. (See 'Increase in microvascular pressure'
above.)

● Transudative effusions from heart failure are likely caused by entry of lung edema (lung
interstitial fluid) into the pleural space. Interstitial edema probably leaves the lung by flowing
down pressure gradients along the interstitial spaces of the lung (interlobular septae,
peribronchovascular bundles and visceral pleura) toward either the mediastinum or the pleural
space. (See 'Increase in microvascular pressure' above.)

● Hypoproteinemia (due to hypoalbuminemia) decreases the plasma oncotic pressure, thereby

increasing the forces favoring filtration. By itself, hypoproteinemia may result in small effusions
but, when other Starling forces are changed (eg, increased central venous pressure),
hypoproteinemia lowers the threshold for effusion formation. (See 'Decrease in plasma

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osmotic pressure' above.)

● A reduction in lymphatic function will decrease the absorption rate of pleural liquid. Impairment
in lymphatic function may be caused by intrinsic factors (eg, hypothyroidism, cancer
infiltration, yellow nail syndrome) or extrinsic factors (eg, decreased respiratory motion from
diaphragmatic paralysis, perilymphatic granulomas or cancer). (See 'Decreased fluid exit'
above.)

● In certain malignant effusions, extrapleural infiltration of draining lymphatics may be the sole
mechanism of effusion formation. Such an isolated exit block may explain the existence of
transudative effusions in approximately 10 percent of patients with malignant effusions. (See
'Pleura' above.)

● Pleural effusions can form from excess liquid generated anywhere in the body (lungs,
mediastinum, abdomen, retroperitoneum) that moves toward the subatmospheric pressure of
the pleural space and across the leaky mesothelium or across defects in the diaphragm or
mediastinal pleura. (See 'Effusion formation by site' above.)

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GRAPHICS

Pathways of pleural liquid turnover

Schematic representation of the pathways of normal pleural liquid turnover. Pleural

liquid appears to originate from the systemic vessels of both the parietal and
visceral pleural membranes (dashed arrows). The parietal vessels (intercostal
microvessels) are thought to be of primary importance because they are closer to
the pleural space and have a higher filtration pressure than the bronchial
microvessels of the visceral pleura. Pleural liquid is initially partially reabsorbed by
the microvessels; the remaining fluid exits the pleural space via the lymphatic
stomata in the parietal pleura (solid arrow).

Graphic 62020 Version 2.0

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Pathways of pleural fluid accumulation in pleurisy

Schematic representation of the pathways of pleural liquid accumulation in

pleurisy. Direct involvement of pleural membranes by disease increases the
formation of liquid from the intercostal and bronchial arteries (solid arrows) and
interferes with parietal pleural lymphatic fluid removal (dashed open arrow).

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Pleural fluid formation with increased systemic venous

pressure

Schematic representation of pleural fluid formation with increased venous

pressure. An elevation in systemic venous pressure both increases filtration from
the parietal pleural microvessels (the intercostal arteries, solid arrows) and
decreases lymphatic drainage into the venous system (dashed open arrow).
Filtration from visceral pleural microvessels (the bronchial arteries) is unaffected
(dashed solid arrows). In comparison, an elevation in pulmonary venous pressure
would increase filtration from the visceral pleural microvessels.

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Pleural fluid accumulation in interstitial pulmonary edema

Schematic representation of the mechanism of pleural fluid accumulation in

interstitial pulmonary edema. Lung interstitial liquid can move into the pleural
space along a pressure gradient and across leaky pleural membranes (heavy solid
arrow). Lymphatic fluid removal is able to increase, but not sufficiently to prevent
fluid accumulation in the pleura.

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