CHAPTER 77
Pleural Disease
Joshua M. Kosowsky and Heidi H. Kimberly
Pleural disease is commonly encountered in the emergency
department (ED). Presentations range in severity from asymp-
tomatic pleural effusion to tension pneumothorax. This chapter
reviews the two most common nontraumatic pleural problems:
spontaneous pneumothorax and pleural inflammation with effu-
sion. Pleural space problems associated with trauma are discussed
in Chapter 45, and the approach to a patient with pleuritic chest
pain in Chapter 26.
SPONTANEOUS
PNEUMOTHORAX
Perspective
Under normal conditions, the visceral and parietal pleurae lie
in close apposition, with only a potential space between them.
Pneumothorax is defined as the presence of free air in the intra-
pleural space. A spontaneous pneumothorax occurs in the absence
of any external precipitating factor, either traumatic or iatrogenic.
Primary spontaneous pneumothorax occurs in individuals without
clinically apparent lung disease. Secondary spontaneous pneumo-
thorax arises in the context of an underlying pulmonary disease
process.
The incidence of primary spontaneous pneumothorax is
approximately 15 cases per 100,000 population per year among
men and 5 cases per 100,000 population per year among women.1,2
Primary spontaneous pneumothorax typically occurs in healthy
young men of taller than average height. Factors associated with
primary spontaneous pneumothorax include cigarette smoking
and changes in ambient atmospheric pressure. Familial patterns
suggest an inherited propensity in some cases of primary sponta-
neous pneumothorax. Mitral valve prolapse and Marfan syndrome
are associated with spontaneous pneumothorax in the absence of
clinically apparent lung disease.
Approximately one third of spontaneous pneumothoraces
occur in the context of underlying pulmonary disease (Box 77-1).
The incidence of secondary spontaneous pneumothorax is three
times higher in men. The most common condition associated with
secondary spontaneous pneumothorax is chronic obstructive pul-
monary disease (COPD), which accounts for nearly 70% of cases.
Patients with severe COPD (e.g., with forced expiratory volume
in 1 second below 1L) are at highest risk. The incidence of spon-
taneous pneumothorax among patients hospitalized for emphy-
sema is 0.8% and for asthma 0.3%.
Spontaneous pneumothorax occurs in approximately 2%
of patients with acquired immunodeficiency syndrome, almost
always in the setting of Pneumocystis jiroveci (previously known as
Pneumocystis carinii) pneumonia.
988
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Malignancy is another common cause of secondary spontane-
ous pneumothorax. The occurrence of spontaneous pneumotho-
rax in a patient with known malignancy should suggest lung
metastases. In developing countries, tuberculosis and lung abscess
remain leading causes of secondary spontaneous pneumothorax.
Catamenial pneumothorax is a rare condition in which recur-
rent spontaneous pneumothorax occurs in association with
menses (typically within 72 hours of onset). Although it is termed
thoracic endometriosis syndrome and often responds to ovulation-
suppressing medications, the exact cause of catamenial pneumo-
thorax is uncertain.
Spontaneous pneumothorax is rare in childhood. The princi-
ples of diagnosis, imaging, treatment, and surgical management
for pediatric primary spontaneous pneumothorax are similar to
those for adult pneumothorax.1
Pathophysiologic Principles
Normally, intrapleural pressure is negative (less than atmospheric),
fluctuating from 10mmHg to 12mmHg during inspiration
to approximately 4mmHg during expiration. Intrabronchial
and intra-alveolar pressures are negative during inspiration (1 to
3mmHg) and positive during expiration (+1 to +3mmHg).
The alveolar walls and visceral pleura form a barrier that separates
the intrapleural and intra-alveolar spaces and maintains the pres-
sure gradient. If a defect occurs in this barrier, air enters the
pleural space until either the pressures equalize or the communi-
cation seals.
With the loss of negative intrapleural pressure in one hemitho-
rax, the ipsilateral lung collapses. A large pneumothorax results in
restrictive ventilation impairment, with reduced vital capacity,
functional residual capacity, and total lung capacity. Shunting of
blood through nonventilated lung tissue may result in acute
hypoxemia, although over time this effect is mitigated by compen-
satory vasoconstriction in the collapsed lung.
In tension pneumothorax, the alveolar-pleural defect acts as a
one-way valve, allowing air to pass into the pleural space during
inspiration and trapping it there during expiration (Fig. 77-1).
This trapping leads to progressive accumulation of intrapleural
air and increasingly positive intrapleural pressure, causing com-
pression of the contralateral lung with asphyxia and worsening
hypoxia. Intrapleural pressure exceeding 15 to 20mmHg impairs
venous return to the heart. If the situation is allowed to progress,
cardiovascular collapse and death ensue.
In primary spontaneous pneumothorax, disruption of the
alveolar-pleural barrier occurs when a subpleural bulla (or bleb),
typically located at the lung apex, ruptures into the pleural space.
Subpleural bullae are found in almost all patients who undergo
 Chapter 77 / Pleural Disease 989

Causes of Secondary Spontaneous shortness of breath, extreme dyspnea is uncommon in the absence
BOX 77-1 Pneumothorax of underlying lung disease or tension pneumothorax. Cough is
present in a few individuals. Occasionally, patients are asymptom-
Airway Disease atic or have only nonspecific complaints. Patients may wait several
Chronic obstructive pulmonary disease days before they seek medical attention, and a significant number
Asthma
delay presentation for 1 week or more. Without treatment, symp-
Cystic fibrosis
toms often resolve spontaneously within 24 to 72 hours, although
Infections the pneumothorax is still present.
Necrotizing bacterial pneumonia, lung abscess Physical findings tend to correlate with the degree of symptoms.
Pneumocystis jiroveci pneumonia A mild sinus tachycardia is the most common physical finding.
Tuberculosis With a large pneumothorax, decreased or absent breath sounds
Interstitial Lung Disease with hyper-resonance to percussion may be present. Other
Sarcoidosis classic signs include unilateral enlargement of the hemithorax,
Idiopathic pulmonary fibrosis decreased excursion with respirations, absent tactile fremitus, and
Lymphangiomyomatosis inferior displacement of the liver or spleen. Absence of any or all
Tuberous sclerosis of these findings does not exclude pneumothorax, however, and a
Pneumoconioses
chest radiograph should be obtained when pneumothorax is
Neoplasms suspected.
Primary lung cancers With tension pneumothorax, signs of asphyxia and decreased
Pulmonary or pleural metastases cardiac output develop. Tachycardia (often >120beats/min) and
Miscellaneous hypoxia are common. Hypotension is a late and ominous finding.
Connective tissue diseases Distention of the jugular veins is common but may be difficult to
Pulmonary infarction detect. Displacement of the trachea to the contralateral side is
Endometriosis, catamenial pneumothorax classically described but is an uncommon finding, usually occur-
ring only in the immediately preterminal phase of the pneumo-
thorax, if at all. Its absence should not be considered evidence that
a tension phenomenon is not present.
In patients with significant underlying lung disease, pneumo-
thorax manifests differently. Because of poor pulmonary reserve,
dyspnea is nearly universal, even when the pneumothorax is small,
and symptoms tend not to resolve on their own. Physical findings,
such as hyperexpansion and distant breath sounds, often overlap
considerably with the underlying lung disease, making the clinical
diagnosis difficult. For this reason the diagnosis of pneumothorax
should be considered whenever a patient with COPD experiences
an exacerbation of dyspnea.
Although suggested by the patients history and physical exami-
Inspiration Expiration nation, the diagnosis of pneumothorax is generally made with the
Figure 77-1. Tension pneumothorax with total collapse of the right chest radiograph. The classic radiographic appearance is that of a
lung and shift of mediastinal structures to the left. Air is forced into thin, visceral pleural line lying parallel to the chest wall, separated
the pleural space during inspiration and cannot escape during by a radiolucent band devoid of lung markings. The average
expiration. width of this band can be used to estimate the size of the pneu-
mothorax with a fair degree of accuracy (Fig. 77-2). In general,
however, it is more reasonable simply to characterize the pneumo-
surgical treatment for primary spontaneous pneumothorax and thorax as small, moderate, large, or total. The estimated size of the
are identified on computed tomography (CT) of the chest in 90% pneumothorax and the patients clinical status can be useful in
of cases. The cause of these bullae may be related to degradation guiding management decisions.
of elastic fibers within the lung and an imbalance in the protease- Tension pneumothorax is a clinical diagnosis, and delay in
antiprotease and oxidant-antioxidant systems.2 treatment to obtain radiographic confirmation is inadvisable.
In the case of secondary spontaneous pneumothorax, the When the diagnosis of tension pneumothorax is not apparent
underlying lung disease weakens the alveolar-pleural barrier. In clinically and a chest radiograph is obtained, the classic appear-
patients with P. jiroveci pneumonia, the cytotoxic effects of ance is one of complete lung collapse with gross distention of the
repeated episodes of inflammation lead to bullous and cystic thoracic cavity on the affected side and shift of mediastinal struc-
changes. In patients with COPD, chronic exposure to cigarette tures across the midline (Fig. 77-3A). In patients with underlying
smoke results in the development of large, thin-walled bullae that pulmonary disease, however, pleural adhesions and lack of lung
are at an increased risk for rupture. Other factors, including elasticity may mask the fact that a pneumothorax is under signifi-
increased intrabronchial and intra-alveolar pressures generated by cant positive pressure.
bronchospasm and coughing, also play a role. When pneumothorax is suspected but not seen on a standard
chest radiograph, an expiratory film may be obtained. Theoreti-
Clinical Features cally, the volumes of the lungs and the chest cavity are reduced
during expiration so that the relative size of the pneumothorax is
Symptoms of primary spontaneous pneumothorax typically enhanced. Although expiratory films are occasionally helpful in
begin suddenly while the individual is at rest. Ipsilateral chest pain identifying a small apical pneumothorax, their routine use does
and dyspnea are the most common symptoms. At the outset, the not improve diagnostic yield. In critically ill patients for whom
pain is typically pleuritic in nature (i.e., often described as sharp only a supine chest radiograph can be obtained, the finding of a
and made worse with deep inspiration), but it often evolves over deep sulcus (i.e., a deep lateral costophrenic angle) can suggest
time into a dull, steady ache. Although patients frequently describe the presence of pneumothorax on that side (see Fig. 77-3A).

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990 PART III Medicine and Surgery / Section Two Pulmonary System
A

Thoracic

Average interpleural distance (%)

Upper 5
cage
half 0.5 10
B

Pneumothorax size (cm)

Collapsed of 1.0
lung 15
lung 1.5
20
2.0
25
2.5
3.0 30
C Lower 35
half 3.5
of 4.0 40
lung 4.5 45
Figure 77-2. Determining the size of a
pneumothorax. Calculation of average interpleural 5.0 50
distance to predict pneumothorax size. PA,
posteroanterior. Lateral view PA view

Subcutaneous
tissue

Rib
Rib
Pleural line
Rib
Rib shadow
shadow

B
Figure 77-3. A, Radiograph of tension pneumothorax with mediastinal shift to left. B, Ultrasound demonstrating location of pleural line. Lung
sliding is dynamic and visualized in real time as shimmering or sliding of the pleural line.

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Special care should be taken in viewing the chest radiographs
of patients with underlying lung disease. In patients with COPD,
the relative paucity of lung markings makes pneumothorax more
difficult to detect. At the same time, giant bullae may simulate the
radiographic appearance of pneumothorax. A clue to differentiat-
ing a pneumothorax from a giant bulla is that the former tends to
run parallel to the chest wall, whereas the latter tends to have a
more concave appearance. When the diagnosis is unclear, CT can
differentiate between the two entities.
Chest CT is considered the gold standard for the diagnosis of
pneumothorax; however, it requires that patients be stable enough
for transport. Although portable chest radiography is convenient
and commonly used, it has poor overall sensitivity.3 Point-of-care
thoracic ultrasound is a rapid and accurate diagnostic aid per-
formed and interpreted by the clinician at the bedside.4,5 Bedside
thoracic ultrasound is more sensitive than a supine chest radio-
graph for the diagnosis of pneumothorax and avoids ionizing
radiation.6,7 In addition to routine use for the diagnosis of both
traumatic and spontaneous pneumothorax, thoracic ultrasound
can be used to evaluate for postprocedural pneumothorax and for
the diagnosis of occult pneumothorax in critically ill patients.8,9 In
normal lung the closely opposed visceral and parietal pleura create
the appearance of shimmering or sliding of the pleural interface
during respiration. Assessment for pneumothorax is optimally
performed with a high-frequency linear probe to most accurately
visualize the lung sliding at the pleural line (see Fig. 77-3B). In
supine patients, air rises; scanning a few interspaces on the anterior
chest wall along the midclavicular line can effectively evaluate the
most likely areas for pneumothorax. Extending the examination to
the lateral chest wall can help identify the lung point or boundary
between normal lung and pneumothorax and is highly specific for
the detection of pneumothorax.10 Visualization of lung sliding at
the pleural line effectively rules out pneumothorax in the area
being scanned. A small pneumothorax may not be detected with
ultrasound, and false-positive results can occur in patients with
blebs, pleural scarring, or severe acute respiratory distress syn-
drome (ARDS) or in single-lung intubation.
The differential diagnosis of pneumothorax includes numerous
conditions associated with chest pain and dyspnea. Among the
most important is pulmonary embolism, which may manifest in
similar fashion with unilateral pleuritic chest pain. Most pleural-
based processes (pneumonia, embolism, tumor) have characteris-
tic radiographic findings. Rarely, pneumothorax may mimic an
acute myocardial infarction with electrocardiographic changes
simulating an acute injury pattern.
Spontaneous pneumomediastinum is a closely related clinical
entity, diagnosed by the presence of subcutaneous emphysema
and the finding of mediastinal air on chest radiography. In con-
trast to spontaneous pneumothorax, spontaneous pneumomedi-
astinum typically occurs during exertion, particularly after a
strenuous Valsalva maneuver. Most cases of spontaneous pneumo-
mediastinum occur in the absence of known underlying disease
and have a benign course. Secondary causes of pneumomediasti-
num (e.g., Boerhaaves syndrome) are more serious, and treatment
is aimed at the underlying disorder.
Spontaneous hemopneumothorax is a rare but potentially
serious condition that occurs when collapse of the lung is associ-
ated with rupture of a vessel in a parietopleural adhesion. The
clinical presentation is similar to that of spontaneous pneumotho-
rax but may be accompanied by symptoms and signs of hemor-
rhagic shock. Treatment entails large-caliber tube thoracostomy to
evacuate the pleural space, reexpand the lung, and tamponade
bleeding.
Pneumothorax has a readily available, highly reliable confirma-
tory diagnostic test (i.e., chest radiography). Absence of a pneu-
mothorax on chest radiography should prompt a search for an
alternative diagnosis.
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Chapter 77 / Pleural Disease 991
Management
Whether in the field or in the ED, if the clinical circumstances
suggest tension pneumothorax, treatment should be initiated
without awaiting further cardiovascular compromise or definitive
diagnosis by chest radiography. As soon as tension pneumothorax
is suspected, the pleural space should be decompressed. This
decompression may be accomplished by insertion of an intrave-
nous catheter or by immediate tube thoracostomy, depending on
the availability of equipment and the expertise of the providers.
The diagnosis is confirmed by the hiss of air escaping under posi-
tive pressure as the needle or chest tube enters the pleural space.
Needle decompression is only a temporizing procedure, and defin-
itive management requires prompt tube thoracostomy. In mor-
bidly obese patients, the needle and catheter may be of insufficient
length to reach the pleural space, and a longer needle may be
required.
The management of spontaneous pneumothorax has two
goals: (1) to evacuate air from the pleural space, and (2) to prevent
recurrence. Pursuit of the latter goal extends beyond the realm of
the ED but may influence the initial approach to management.
Therapeutic options for treatment of pneumothorax range from
simple observation or aspiration with a catheter to video-assisted
thoracoscopic surgery or thoracotomy. Decisions should be indi-
vidualized and consider several factors, including size of the pneu-
mothorax, severity of signs, presence of underlying pulmonary
disease, other comorbidities, history of previous pneumothoraces,
patient reliability, degree and persistence of the air leak, and avail-
able follow-up monitoring.
For otherwise healthy, young patients with a small primary
spontaneous pneumothorax (i.e., <20% of the hemithorax), and
minimal symptoms, observation alone may be appropriate. The
intrinsic reabsorption rate ranges from 1 to 2% per day, a rate that
is accelerated by a factor of 4 with the administration of 100%
oxygen. By lowering the alveolar partial pressure of nitrogen, sup-
plemental oxygen increases the rate at which air diffuses across
the pleural-alveolar barrier. Admission to the hospital generally
is not required for a patient with a small pneumothorax and
no hemodynamic disturbance or hypoxia. Although there are
no evidence-based guidelines, we recommend observing these
patients in the ED for a 4- to 6-hour period. This observation
period also can occur in an ED-based observation unit. A repeat
chest radiograph obtained before discharge confirms that there is
no interval worsening in the size of the pneumothorax. Discharged
patients should be able to return to an ED if they worsen and
should undergo telephone or in-person follow-up with a primary
care provider in 24 to 48 hours. Air travel and underwater diving
must be avoided until the pneumothorax has completely resolved.
Patients who are not able to follow up with a primary care physi-
cian in the desired interval are advised to return to the ED for
follow-up evaluation.
For primary spontaneous pneumothoraces that are larger in
size (i.e., 20% of the hemithorax), aspiration with an intravenous
catheter may be attempted. If 6 hours after aspiration the chest
radiograph shows no reaccumulation of the pneumothorax,
the catheter is removed and the patient can be discharged home,
with the same caveats that apply to patients managed with obser-
vation alone.
Although there is no universal agreement on the optimal treat-
ment of patients with a first episode of primary spontaneous
pneumothorax, data suggest that aspiration may be equally effec-
tive as chest tube drainage and clearly causes much less patient
discomfort.11 Advantages of simple aspiration include low mor-
bidity, lack of invasiveness, and overall cost savings, with reported
rates of successful outcome ranging from 45 to 71%.12 Success is
less likely when the patient is older than 50 years or the volume
of air aspirated exceeds 2.5L, suggesting a continuing air leak. If
992 PART III Medicine and Surgery / Section Two Pulmonary System
aspiration fails to reexpand the lung fully, the catheter can be
attached to a water-seal device or to a one-way Heimlich valve and
managed like a small-caliber chest tube.
Most recurrent spontaneous pneumothoraces should be
managed with tube thoracostomy because less invasive approaches
(i.e., observation or simple aspiration) are associated with signifi-
cantly lower success rates.13 Similarly, patients who have respira-
tory distress, have tension physiology, or are likely to require
mechanical ventilation should undergo tube thoracostomy to
reexpand the lung definitively. Also, if there is significant pleural
fluid (hemothorax or hydrothorax), tube thoracostomy is required.
Finally, tube thoracostomy may be considered in uncomplicated
cases of primary spontaneous pneumothorax either as a first-line
intervention or after a less invasive approach (i.e., observation or
simple aspiration) fails.
For most primary spontaneous pneumothoraces, placement of
a small-caliber (7-14F) tube is generally sufficient because air
leakage tends to be minimal. Small-caliber tubes are easy to insert,
are well tolerated by patients, and leave only a small scar after
removal. Complications associated with small-caliber tubes
include kinking, malposition, inadvertent removal, occlusion by
pleural fluid or clotted blood, and large persistent air leaks. For
secondary spontaneous pneumothorax, a standard size (20-28F)
thoracostomy tube is recommended. When there is detectable
pleural fluid or an anticipated need for mechanical ventilation, a
larger tube size (28F) is required.
After insertion, the tube is attached to a water-seal device and
left in place until the lung has reexpanded fully and the air leak
has ceased. A Heimlich valve, which consists of a one-way flutter
valve covered in transparent plastic, can be used in place of a
water-seal device and allows unhindered ambulation. Specific
complications associated with the use of a Heimlich valve include
accidental disconnection and occlusion by fluid.
Routine application of suction neither increases the rate at
which the lung reexpands nor improves patient outcome and is
no longer recommended. The use of suction (with a pressure of
20cm H2O) is reserved for situations in which the lung fails to
reexpand after drainage through a water-seal device or Heimlich
valve for 24 to 48 hours.
In most cases, chest tube management requires hospital admis-
sion, although outpatient management of spontaneous pneumo-
thorax with a small-caliber tube and Heimlich device also is
reasonable in a stable, responsible patient with good follow-up
availability. Common complications of chest tube placement
include incorrect placement, pleural infection, and prolonged
pain. Reexpansion pulmonary edema and reexpansion hypoten-
sion are rare occurrences after rapid evacuation of large
pneumothoraces.
Outcome
Most spontaneous pneumothoraces resolve within 7 days of tube
thoracostomy. Air leaks that persist for longer than 2 days are less
likely to resolve on their own. If an air leak persists beyond 4 to
7 days, tube thoracostomy is considered to have failed, and surgical
intervention generally is recommended.
Failure of tube thoracostomy is more common with secondary
spontaneous pneumothoraces because these tend to be associated
with larger and more persistent air leaks. In the setting of COPD,
healing of the alveolar-pleural barrier may be impaired by chronic
inflammatory changes and loss of vascularity in pulmonary tissue.
The success rate also decreases substantially with recurrent epi-
sodes of pneumothorax, declining from 91% for treatment of a
first pneumothorax to 52% for treatment of a first recurrence and
to 15% for treatment of a second recurrence.14
Recurrences of spontaneous pneumothorax are common. The
risk of recurrence after a primary spontaneous pneumothorax is
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approximately one in three, with studies reporting rates of 16 to
50%.15 Younger age, lower weight-to-height ratio, and a history of
smoking are associated with an increased rate of recurrence.
Recurrence rates after a secondary spontaneous pneumothorax
are slightly higher (39-47%).2
Recurrences may be life-threatening for patients with serious
underlying lung disease, and intervention is advocated to prevent
recurrence as part of the initial approach to secondary spontane-
ous pneumothorax. In contrast, for patients with primary spon-
taneous pneumothorax, interventions typically are not considered
until after a second ipsilateral pneumothorax. Preventive treat-
ment also is recommended for patients who plan to continue
activities such as flying or diving that increase the risk of serious
complications if a pneumothorax recurs. CT can be used in
primary spontaneous pneumothorax to detect emphysematous
changes, predict the likelihood of recurrence, and guide interven-
tion decisions.
A variety of operative and nonoperative interventions prevent
recurrences. One strategy promotes adherence of parietal and vis-
ceral pleura, which obliterates the pleural space. Pleurodesis can
be accomplished by mechanical pleural abrasion or by instillation
of sclerosing agents. Another strategy involves resection of apical
bullae or other lesions at risk for causing recurrences. Often the
two strategies are combined. Minimally invasive procedures, such
as video-assisted thoracoscopic surgery, allow for resection of
bullae and pleurodesis. Patients with extensive bullae may require
thoracotomy for wider visualization of lesions. Success rates are
generally good, ranging from 86 to 100%.
PLEURAL INFLAMMATION
AND EFFUSION
Perspective
Under normal circumstances, a thin layer of fluid lies between the
visceral and the parietal pleurae. Pleural effusion implies the pres-
ence of an abnormally large amount of fluid in the pleural space.
Pleural effusions are relatively common. The most common cause
of pleural effusions in Western countries is congestive heart failure,
followed by malignancy, bacterial pneumonia, and pulmonary
embolism. In other countries, tuberculosis is the leading cause of
pleural effusions. Other conditions commonly associated with
pleural effusions include viral infections of the lung parenchyma
or pleura, uremia, myxedema, cirrhosis, nephrotic syndrome,
ovarian hyperstimulation syndrome, collagen vascular diseases
(e.g., systemic lupus erythematosus, rheumatoid arthritis), and
intra-abdominal processes (e.g., acute pancreatitis, subphrenic
abscess, ascites). Esophageal perforation is a rare but uniquely
morbid cause of a pleural effusion.
Pleuritis (also referred to as pleurisy) is a nonspecific term
denoting inflammation of the pleura. Pleuritis can occur with or
without significant exudation of fluid into the pleural space. Pleu-
ritis is a common presentation for a range of disease processes,
from self-limited viral syndromes to more serious acute condi-
tions, such as pneumonia and pulmonary embolism, to chronic
illnesses, such as systemic lupus erythematosus and other connec-
tive tissue diseases.
A pleural effusion associated with bacterial pneumonia, bron-
chiectasis, or lung abscess is called a parapneumonic effusion. The
term complicated parapneumonic effusion refers to parapneumonic
effusions that require tube thoracostomy for their resolution. The
diagnosis of empyema (or pus in the pleural space) requires the
presence of bacteria on Gram staining of the pleural fluid.
Fluid anatomically confined and not freely flowing in the
pleural space is termed a loculated effusion. Loculated effusions
occur when there are adhesions between the visceral and the pari-
etal pleurae. Hemothorax and chylothorax (i.e., from rupture of
 Chapter 77 / Pleural Disease 993
Pleural
Chest wall space Lung
Systemic capillary Pulmonary capillary

Hydro- 30 11
static
pressure 5 5
(cm H2O) 35 16

Colloid
osmotic
pressure 34 34
(cm H2O) 8 8
26 26
Figure 77-4. Diagram representing pressures
involved in formation and absorption of pleural
fluid. (Adapted from Fraser RG, etal: Diagnosis
of Diseases of the Chest, 3rd ed. Philadelphia,
9 10 WB Saunders, 1988.)

the thoracic duct) are special instances of pleural effusion that are
approached separately. BOX 77-2 Causes of Pleural Effusion
Transudates
Pathophysiologic Principles Congestive heart failure
Cirrhosis with ascites
Pleural fluid is produced from systemic capillaries at the parietal Nephrotic syndrome
pleural surface and absorbed into pulmonary capillaries at the Hypoalbuminemia
visceral pleural surface. Lymphatics also play an important role Myxedema
in removing pleural fluid. Movement of fluid across the pleural Peritoneal dialysis
surfaces is governed by Starlings law. Under normal circum- Glomerulonephritis
stances, the direction of pleural fluid flow is largely governed by Superior vena cava obstruction
the difference in hydrostatic pressure between the systemic and Pulmonary embolism
the pulmonary circulations (Fig. 77-4). Pleural fluid exists in a Exudates
dynamic equilibrium in which influx equals efflux, with approxi- Infections
mately 1L of fluid traversing the pleural space in 24 hours. Under Bacterial pneumonia
normal conditions, the amount of fluid that remains in the pleural Bronchiectasis
space is small (~0.1-0.2mL/kg body weight) and clinically Lung abscess
or radiographically undetectable. Pleural effusion develops Tuberculosis
whenever influx of fluid into the pleural space exceeds efflux. Viral illness
Numerous disorders can lead to formation of a pleural effusion. Neoplasms
Pleural effusions classically are divided into two groups Primary lung cancer
transudates and exudatesaccording to the composition of the Mesothelioma
pleural fluid (Box 77-2). Pulmonary or pleural metastases
Transudates are essentially ultrafiltrates of plasma, containing Lymphoma
very little protein. A transudative effusion develops when there is Connective Tissue Disease
an increase in the hydrostatic pressure or decrease in the oncotic Rheumatoid arthritis
pressure within pleural microvessels. The primary cause of Systemic lupus erythematosus
increased hydrostatic pressure is congestive heart failure, which is Abdominal or Gastrointestinal Disorders
responsible for about 90% of transudative effusions. In hepatic Pancreatitis
cirrhosis and nephrotic syndrome, increased hydrostatic pressure Subphrenic abscess
is combined with loss of plasma oncotic pressure because of sig- Esophageal rupture
nificant decreases in serum albumin. Patients with severe malnu- Abdominal surgery
trition may develop transudative effusions resulting from severe
Miscellaneous Conditions
isolated hypoalbuminemia. Pulmonary infarction
Exudates contain relatively high amounts of protein, reflecting Uremia
an abnormality of the pleura itself. An exudative effusion is the Drug reactions
result of increased membrane permeability or defective lymphatic Postpartum
drainage. Any pulmonary or pleural process associated with Chylothorax
inflammation can result in an exudative effusion. In the absence
of clinically apparent effusion, pleuritic symptoms may still be
present. Pleurisy without pleural effusion is typical of most viral reflect alterations in pleural permeability and problems with lym-
pleuritis, for example. The most common form of an exudative phatic drainage. Exudative effusions also may arise in response
effusion is a parapneumonic effusion, in which infection of the to inflammatory abdominal processes, such as pancreatitis or
adjacent lung elicits an intense inflammatory response in pleura, subphrenic abscess, presumably owing to altered permeability of
disrupting normal membrane permeability. Malignant effusions the diaphragm itself. Exudative effusions may be reabsorbed or
are the second most common form of exudative effusion and often organize into fibrous tissue, resulting in pleural adhesions.

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994 PART III Medicine and Surgery / Section Two Pulmonary System
Some pleural effusions can manifest as either transudates or
exudates or may have characteristics of both. In the case of pul-
monary embolism, the pathogenesis of pleural effusion is often
multifactorial, reflecting increased pulmonary vascular pressure (a
transudative process) and ischemia and breakdown of the pleural
membrane (an exudative process).
Massive effusions (>1.5-2L) are most commonly associated
with malignancy but also can arise in the setting of congestive
heart failure, cirrhosis, and other conditions. Massive effusions
may restrict respiratory movement, compress the lungs, and result
in intrapulmonary shunting. In extremely rare cases, tension
hydrothorax can develop, with mediastinal shift and circulatory
embarrassment.
Clinical Features
Symptoms associated with pleural effusion are most often caused
by the underlying disease process and not the effusion itself. Small
pleural effusions often are entirely asymptomatic. A new or enlarg-
ing pleural effusion may be heralded by localized pain or pain
referred to the shoulder. Viral pleuritis and pulmonary infarction
commonly are associated with pleuritic chest pain. When the
volume of pleural fluid reaches 500mL, dyspnea on exertion or at
rest may occur as a result of compromised pulmonary function.
The patients history often helps to establish the diagnosis for
pleural effusion or pleural inflammation. A history of congestive
heart failure, liver disease, uremia, or malignancy can direct subse-
quent evaluation. The pain of viral pleuritis usually is preceded by
several days of a typical viral prodrome, with low-grade fever, sore
throat, and other upper respiratory or constitutional symptoms. In
the absence of such prodromal symptoms, an alternate cause for
pleuritis such as pulmonary embolism should be considered.
Physical findings depend on the size of the effusion but are
often either dominated or obscured by the underlying disease
process. Classic physical signs of pleural effusion include dimin-
ished breath sounds, dullness to percussion, decreased tactile
fremitus, and occasionally a localized pleural friction rub. The
simple technique of auscultatory percussion (i.e., percussing
the chest while listening for a dullness with the stethoscope) may
be even more sensitive and specific for the physical diagnosis of
pleural effusion. Egophony and enhanced breath sounds can often
be appreciated at the superior border of the effusion because of
underlying atelectatic lung tissue. In the setting of pleuritis, a
pleural friction rub may be appreciated. With massive effusions,
signs of mediastinal shift may be present.
Chest radiography confirms the clinical suspicion of pleural
effusion and occasionally reveals a pleural effusion as an incidental
finding. The classic radiographic appearance of a pleural effusion
is blunting of the costophrenic angle on the upright chest radio-
graph. On a frontal (anteroposterior or posteroanterior) projec-
tion, a volume of 250 to 500mL of pleural fluid is required before
radiographic demonstration is possible. A lesser amount of fluid
may be visible in the posterior costophrenic gutter on a lateral
projection. With larger effusions, the hemidiaphragm is obscured,
and an upwardly concave meniscus may be seen because pleural
fluid has a tendency to layer higher laterally than centrally. Pleural
fluid can extend up a major fissure and appear as a homogeneous
density in the lower two thirds of the lung field. Massive pleural
effusion can appear as a totally opacified hemithorax.
In the recumbent patient, free pleural fluid gravitates superiorly,
laterally, and posteriorly and may not be clearly discernible on a
supine radiograph. If the effusion is large enough, diffuse haziness
or partial opacification of a hemithorax may be seen. Other find-
ings on the supine radiograph may include apical capping, oblit-
eration of the hemidiaphragm, and a widened minor fissure. The
radiographic appearance of pleural effusions can be confusing.
Subpulmonic effusions (fluid collections between the lung base
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and the diaphragm) can be difficult to diagnose, often simulating
an elevated hemidiaphragm. Clues to the presence of a subpul-
monic effusion include shifting of the apparent dome of the dia-
phragm toward the lateral chest wall and, when located on the left
side, an increase in the distance between the gastric bubble and
aerated lung. Loculated fluid in a fissure may assume a fusiform
appearance and can simulate a mass (Fig. 77-5A and B). Such
fluid pseudotumors are common in patients with congestive
heart failure.
Other imaging techniques, such as ultrasound and CT, may be
helpful in localizing and quantifying effusions and characterizing
underlying lung processes. Bedside thoracic ultrasound is particu-
larly helpful because it is more sensitive than chest radiography
and can be used to guide thoracentesis in real time.16,17 It decreases
the risk of complications during thoracentesis, even in mechani-
cally ventilated patients.18 Sonographically, pleural effusions are
typically visualized as hypoechoic fluid located above the dia-
phragm and can be visualized with a curvilinear probe in the
midaxillary line (Fig. 77-5C). Not all pleural fluid is hypoechoic,
however, and both hemothorax and pyothorax can appear hetero-
geneous. Ultrasound guidance for thoracentesis is best performed
with the patient sitting upright using either a curved or linear
probe. The largest fluid pocket is visualized, and a measurement
is taken to estimate the depth the needle will need to be advanced.
The procedure can be static, with the ultrasound used to mark the
location for drainage, or dynamic, in which the procedure is per-
formed with real-time visualization of the needle. Often, com-
pressed lung or pleural adhesions can be visualized within the
effusion, and careful observation of these findings as well as the
location of the diaphragm, liver, or spleen can aid in the correct
localization for thoracentesis or tube thoracostomy.
Pulmonary embolism easily can be overlooked in the workup
of a pleural effusion. A patient with an otherwise unexplained
pleural effusion in a setting of predisposing conditions or signs
and symptoms of pulmonary embolism should be evaluated as
described in Chapter 88.19 Pleural effusion resulting from pulmo-
nary embolism typically is small, occupying less than one third of
the hemithorax, but dyspnea often is disproportionately severe for
the size of effusion present.
An unexplained pleural effusion requires further investigation,
but not necessarily on an emergency basis. Unless there is suspi-
cion of an immediately life-threatening condition such as
empyema or hemothorax, pleural fluid evaluation may be deferred
to an inpatient or outpatient setting. The primary goal of pleural
fluid analysis is to distinguish between transudative and exudative
effusions. Transudative effusion usually is found in patients
with known underlying disorders (e.g., congestive heart failure,
nephrotic syndrome), whereas the presence of an exudate requires
a detailed diagnostic evaluation. Although numerous alternative
measurements have been proposed, Lights criteria remain a
widely accepted means of differentiating transudates and exudates
(Box 77-3).20
In the presence of an exudative effusion, additional pleural fluid
analyses further classify the effusion. A pleural fluid pH of less
than 7.3 is associated with parapneumonic effusions, malignan-
cies, rheumatoid effusions, tuberculosis, and systemic acidosis. A
pH of less than 7.0 strongly suggests empyema (or esophageal
rupture). A pleural fluid pH of less than 7.0 and glucose less than
50mg/dL are reasonable indications for tube thoracostomy.
Normal pleural fluid contains less than 1000 white blood
cells/mm3; exudative pleural fluid may contain over 10,000 white
blood cells/mm3. Although the absolute cell count has limited
diagnostic value, a predominance of neutrophils suggests an acute
process, such as pneumonia, pulmonary embolus, or acute tuber-
culous pleuritis. A predominance of monocytes or lymphocytes
suggests a more chronic process, such as malignancy or established
tuberculosis. Pleural fluid from any patient with an undiagnosed
 Chapter 77 / Pleural Disease 995

A B

Diaphragm

Pleural
effusion Liver
Lung

C
Figure 77-5. A and B, Radiographs of pleural effusion along major and minor fissures. C, Ultrasound image of the right upper quadrant
demonstrating the typical hypoechoic appearance of a pleural effusion.

Lights Criteria for Differentiating Transudates
BOX 77-3 from Exudates
Pleural fluid is considered an exudate if one or more of the
following conditions are met:
1. Pleural fluid protein level: serum protein level exceeds 0.5
2. Pleural fluid lactate dehydrogenase (LDH) level: serum
LDH level exceeds 0.6
3. Pleural fluid LDH level exceeds 2 3 (upper limit of normal
for serum LDH level)
From Light RW, etal: Pleural effusions: The diagnostic separation of transudates
and exudates. Ann Intern Med 77:507, 1972.
exudative pleural effusion should undergo Gram staining
and culture for bacteria (aerobic and anaerobic), mycobacteria,
and fungi.
In the absence of a traumatic tap, bloody fluid suggests trauma,
neoplasm, or pulmonary infarction. If the hematocrit of the
pleural fluid is more than 50% that of the peripheral blood, the
effusion is, by definition, a hemothorax. Atraumatic hemothorax
is relatively rare but can occur with spontaneous rupture of a
tumor or blood vessel (e.g., ruptured aortic aneurysm).
If the diagnosis of a malignant pleural effusion is being consid-
ered, pleural fluid should be submitted for cytologic examination.
Contrary to popular perception, the sensitivity for diagnosis of
pleural malignancy does not depend on the volume of pleural
fluid extracted during thoracentesis.21 Cytologic analysis provides
the diagnosis of cancer in a majority of malignant effusions.
Management
In patients with large effusions, urgent therapeutic thoracentesis
may stabilize respiratory or circulatory status. The presence of
empyema necessitates insertion of a chest tube to drain the pleural
space adequately and prevent the development of loculations. If
an effusion is already loculated, streptokinase or urokinase can be
injected by a thoracic surgeon, pulmonologist, or interventional
radiologist into the pleural space in an attempt to dissolve adhe-
sions and allow fluid to drain freely. Hemothorax requires tube
thoracostomy to evacuate the pleural space, quantify bleeding, and
allow apposition of the two pleural surfaces to tamponade hemor-
rhage. If bleeding exceeds 200mL/hr, thoracotomy should be
considered.
In most other cases, the decision to proceed with therapeutic
thoracentesis in the ED can be individualized. For example,

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996 PART III Medicine and Surgery / Section Two Pulmonary System
therapeutic thoracentesis may be considered in patients with
known, recurrent malignant effusion, in whom symptomatic relief
may permit discharge. Thoracentesis under ultrasound guidance
decreases complications and should be used when possible.
Pain relief is an important consideration in the management
of patients with significant pleuritic pain. Nonsteroidal anti-
inflammatory drugs are relatively successful in treating pleural
pain. Opioid analgesia is safe and effective, but care should be
exercised in debilitated patients or patients with severe lung
disease because of potential respiratory depression.
Relative contraindications to thoracentesis include coagulopa-
thy and other bleeding disorders. Thoracentesis may be safe with
a prolonged prothrombin time in the absence of active bleeding.22
Pleural adhesions, suggested by a prior history of empyema, rep-
resent a relative contraindication to thoracentesis because of
the high risk of pneumothorax associated with blind needle
insertion.
After thoracentesis has been completed, a chest radiograph
should be obtained to evaluate for an iatrogenic pneumothorax.
Other potential complications of thoracentesis include hemotho-
rax, lung laceration, shearing of the catheter tip, and infection.
Transient hypoxia caused by ventilation-perfusion mismatch often
occurs, whereas unilateral, postexpansion pulmonary edema is
rare except when large volumes (>1500mL) are drained in one
session. Hypotension also can occur after removal of a large
volume of fluid, particularly in patients who are already intravas-
cularly volume depleted.
Outcome
Some pleural effusions reflect little clinical significance. For
example, small pleural effusions are common after abdominal
surgery and in the postpartum state and resolve spontaneously
within a few days. Viral pleuritis, with or without effusion, is
generally self-limited and resolves without specific treatment.
For patients with congestive heart failure, pleural effusions gen-
erally respond well to diuretic therapy. If a significant effusion
persists despite several days of aggressive diuresis, a diagnostic
thoracentesis should be considered.
Pleural effusions associated with malignancy are a significant
cause of morbidity in patients with advanced cancer. The presence
of a malignant effusion indicates disseminated disease, and most
of the malignancies that cause pleural effusionsmainly lung or
breast carcinoma and lymphomaare not curable at this stage.
Therapeutic thoracentesis can relieve dyspnea in the short term,
but malignant effusions tend to be recurrent, often rapidly so.
Management strategies include chemical or mechanical pleurode-
sis to obliterate the pleural space or placement of a pleuroperito-
neal shunt to provide continual drainage. Control of pleural
effusions can improve quality of life in these patients.
Parapneumonic effusions contribute significantly to the mor-
bidity and mortality of pneumonia. Therefore the presence of a
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parapneumonic effusion may influence the decision to hospitalize
a patient with community-acquired pneumonia.23 Empyema can
develop in 5 to 10% of patients with a parapneumonic effusion,
but in most cases, it responds well to parenteral antibiotics and
pleural drainage. Early surgical drainage results in shorter hospital
stays and may be more cost-effective than conservative manage-
ment.24 In nearly 20% of pleural effusions, no definitive diagnosis
can be established even after extensive investigation. A sizable
percentage of these effusions may be caused by viral infections,
and most resolve spontaneously without sequelae.
KEY CONCEPTS
Point of care thoracic ultrasound can be used to rule out
pneumothorax with greater sensitivity than a portable supine
chest x-ray examination. Chest CT is the gold standard for
diagnosis of pneumothorax.
For healthy, young patients with a small (<20%) primary
spontaneous pneumothorax, observation alone (with
administration of 100% oxygen) is an appropriate treatment
option; for larger symptomatic pneumothoraces, simple
aspiration with an intravenous catheter is often successful.
In most cases of secondary spontaneous pneumothorax, tube
thoracostomy should be considered because less invasive
approaches are associated with lower rates of success.
Routine application of suction after tube thoracostomy is no
longer recommended and does not accelerate lung
reexpansion.
The most common cause of pleural effusions in Western
countries is congestive heart failure, followed by malignancy
and bacterial pneumonia; however, the diagnosis of
pulmonary embolism should not be overlooked in a patient
with pleural effusion of unknown cause.
Therapeutic thoracentesis is indicated for the relief of acute
respiratory or cardiovascular compromise and should be
performed under ultrasound guidance if possible.
The clearest indication for diagnostic thoracentesis in the ED
is to diagnose immediately life-threatening conditions, such
as empyema or esophageal rupture in a toxic patient; in most
other cases, diagnostic thoracentesis to distinguish between
transudative and exudative processes can be deferred.
On a frontal (anteroposterior or posteroanterior) projection, a
volume of 250 to 500mL of pleural fluid is required before
radiographic demonstration is possible. A smaller amount of
fluid may be visible in the posterior costophrenic gutter on a
lateral projection. Subpulmonic effusions (fluid collections
between the lung base and the diaphragm) can be difficult
to diagnose, often simulating an elevated hemidiaphragm.
The references for this chapter can be found online by
accessing the accompanying Expert Consult website.

References
1. Shaw KS, Prasil P, Nguyen LT, Laberge JM: Pediatric spontaneous
pneumothorax. Semin Pediatr Surg 2003; 12:55.
2. Sahn SA, Heffner JE: Spontaneous pneumothorax. N Engl J Med 2000;
342:868.
3. Ball CG, et al: Factors related to the failure of radiographic recognition
of occult posttraumatic pneumothoraces. Am J Surg 2005; 189:541-546.
4. Lichtenstein D: Pneumothorax. In: Lichtenstein D, ed. Whole Body
Ultrasound in the Critically Ill. New York: Springer; 2010:163-179.
5. Moore CL, Copel JA: Point-of-care ultrasonography. N Engl J Med 2011;
364:749-757.
6. Kirkpatrick AW, et al: Hand-held thoracic sonography for detecting
post-traumatic pneumothoraces: The Extended Focused Assessment
with Sonography for Trauma (EFAST). J Trauma 2004; 57:288-295.
7. Wilkerson RG, Stone MB: Sensitivity of bedside ultrasound and supine
anteroposterior chest radiographs for the identification of
pneumothorax after blunt trauma. Acad Emerg Med 2010; 17:11-17.
8. Vezzani A, et al: Ultrasound localization of central vein catheter and
detection of postprocedural pneumothorax: An alternative to chest
radiography. Crit Care Med 2009; 38:533-538.
9. Lichtenstein DA, et al: Ultrasound diagnosis of occult pneumothorax.
Crit Care Med 2005; 33:1231-1238.
10. Lichtenstein D, Mezire G, Biderman P, Gepner A: The lung point: An
ultrasound sign specific to pneumothorax. Intensive Care Med 2000;
26:1434-1440.
11. Noppen M, Alexander P, Driesen P, Slabbynck H, Verstraeten A: Manual
aspiration versus chest tube drainage in first episodes of primary
spontaneous pneumothorax: A multicenter, prospective, randomized
pilot study. Am J Respir Crit Care Med 2002; 165:1240.
12. Packham S, Jaiswal P: Spontaneous pneumothorax: Use of aspiration
and outcomes of management by respiratory and general physicians.
Postgrad Med J 2003; 79:345.
Downloaded from ClinicalKey.com at Universitas Hasanuddin April 12, 2016.
For personal use only. No other uses without permission. Copyright 2016. Elsevier Inc. All rights reserved.
Chapter 77 / Pleural Disease 996.e1
13. Soulsby T: British Thoracic Society guidelines for the management of
spontaneous pneumothorax: Do we comply with them and do they
work? J Accid Emerg Med 1998; 15:317.
14. Jain SK, Al-Kattan KM, Hamdy MG: Spontaneous pneumothorax:
Determinants of surgical intervention. J Cardiovasc Surg 1998; 39:107.
15. Schramel FM, Postmus PE, Vanderschueren RG: Current aspects of
spontaneous pneumothorax. Eur Respir J 1997; 10:1372.
16. Gordon CE, Feller-Kopman D, Balk EM, Smetana GW: Pneumothorax
following thoracentesis: A systematic review and meta-analysis. Arch
Intern Med 2010; 170:332-339.
17. Lichtenstein D: Pleural effusion. In: Lichtenstein D, ed. Whole Body
Ultrasound in the Critically Ill. New York: Springer; 2010:129-138.
18. Mayo PH, Goltz HR, Tafreshi M, Doelken P: Safety of ultrasound-guided
thoracentesis in patients receiving mechanical ventilation. Chest 2004;
125:1059-1062.
19. Light RW: Pleural effusion due to pulmonary emboli. Curr Opin Pulm
Med 2001; 7:198.
20. Light RW, Macgregor MI, Luchsinger PC, Ball WC Jr: Pleural effusions:
The diagnostic separation of transudates and exudates. Ann Intern Med
1972; 77:507.
21. Sallach SM, Sallach JA, Vasquez E, Schultz L, Kvale P: Volume of pleural
fluid required for diagnosis of pleural malignancy. Chest 2002; 122:1913.
22. McVay PA, Toy PT: Lack of increased bleeding after paracentesis and
thoracentesis in patients with mild coagulation abnormalities.
Transfusion 1991; 31:164.
23. Fine MJ, et al: A prediction rule to identify low-risk patients with
community-acquired pneumonia. N Engl J Med 1997; 336:243.
24. Lim TK: Management of parapneumonic pleural effusion. Curr Opin
Pulm Med 2001; 7:193.