Flashcards in Twenty Six Deck (22):
What is the pleural space like? What is it composed of? What determines how much fluid enters in and out? How much fluid normally enters the pleural space in a day? How much fluid is normally contained within the pleural space? How does fluid leave the pleural space?
The pleural space is a low-pressure environment between the
parietal pleura that covers the inner surface of the ribs and thoracic
musculature, and the visceral pleura covering the lungs’
external regions. These have a combined surface area of about
4,000 cm2. The forces regulating pleural fl uid formation by
the parietal and visceral pleura are summarized by the Starling’s
equation (as established in Chaps. 7 and 19):
Notably, the protein refl ection coeffi cient σ defi nes the
barrier function of the pleural membranes, such that decreases
in σ typifi ed by infl ammatory conditions correlate with
increased permeability to protein (see also Chap. 28). The
intravascular concentration of albumin (MW ≈ 65 KDa) is the
primary determinant of serum colloid osmotic pressure.
The normal entry rate of pleural fl uid into the pleural space
in humans is considered to be approximately 0.5 mL/h or 12 mL/day, and this pleural fl uid derives from microvascular
fi ltration governed by Starling’s forces across both the parietal
pleura and visceral pleura. Although a degree of fl uid reabsorption
occurs within both the parietal and visceral pleura membranes,
actual pleural fl uid reabsorption from the pleural space
itself occurs via lymphatic stomata in the parietal pleura (Fig.
29.1). Thus, at any time the total volume of pleural fl uid in normal
individuals is 0.1-0.2 mL/kg, or approximately 10-20 mL
in a 70 kg subject. These parietal pleural lymphatic stomata are
fenestrated openings in the mesothelial cell layer that average
10-12 μm in diameter, and are especially prevalent in dependent
regions of the pleural space, especially on the diaphragmatic
surface and in the mediastinal regions (Fig. 29.2).
List 7 mechanisms for pleural effusions along with a clinical example for each.
Increased Pmv in parietal pleural microvessels
Congestive heart failure
Decreased πmv in blood
Cirrhosis, nephrotic syndrome
Increased permeability of pleural microvessels
Infl ammation, infection, tumor
Decreased lymphatic drainage
Lymphoma, yellow nail syndrome
Decreased perimicrovascular pressure
Atelectasis, trapped lung
Transdiaphragmatic fl ow ofperitoneal fl uid
Iatrogenic fl uid instillation
Misdirected central venous catheters
What is critical in guiding the diagnostic workup of a pt. with a pleural effusion? What do the symptoms depend on? What are the main symp. of a pleural effusion? What can change that clinical presentation? What are the primary physical findings in a patient wiht pleural effusion?
A comprehensive medical history and physical exam of the chest are critical elements in guiding the diagnostic workup of a patient with a pleural effusion. Symptoms related to a pleural effusion depend on its size and the state of underlying
lung function. Shortness of breath at rest and on exertion, as well as cough are the main symptoms. However, the clinical presentation can be dominated by other respiratory symptoms
if there is coexisting asthma, COPD, or pneumonia. The primary physical fi ndings in patients with a pleural effusion are dullness to percussion over the affected area, decreased tactile fremitus, diminished breath sounds, and occasionally egophony at the upper level of large effusions (Chap. 14). Very large pleural effusions can be associated with bulging of the intercostal spaces or contralateral shift of the mediastinum.
Describe how to use radiographic evaluation to evaluate a pneumothorax? What is usually seen? What views are important? Is chest CT useful?
Radiographic evaluation is important in confi rming the presence
of a pleural effusion, as well as in formulating the most
likely differential diagnostic possibilities. On upright chest radiographic
frontal views, larger pleural effusions usually manifest as a meniscus-shaped density in the costophrenic sulcus
(Fig. 29.3); smaller effusions may appear only as blunting of
the costophrenic sulcus in upright views. Generally, at least
300-500 mL of fl uid in the pleural space is required for visualization
on x-ray. Accordingly, lateral views are useful for
confi rmation, as are supine portable AP fi lms that can disclose
free-fl owing effusions as unilateral increases in radiographic
density because of gravitational layering of the fl uid over the
In such situations, pleural effusions are manifest as a diffuse,
generalized haziness over the ipsilateral lung fi eld with
visible underlying lung vascular markings, together with
absence of other signs of pulmonary consolidation such as air
bronchograms (Chap. 15). The main value of lateral decubitus
fi lms is to confi rm the presence of a pleural effusion as
well as to evaluate the possibility of a loculated fl uid collection.
Fluid that is free-fl owing will layer to a thickness of at
least 10 mm on such decubitus views, in contrast to loculated
fl uid collections that have a similar appearance and shape
regardless of the patient’s position. Chest CT imaging is the
most sensitive method to detect pleural fl uid collections and
pleural disease (Chap. 15). Pleural effusions can easily be
identifi ed by their homogeneous lower density with variable
degrees of lung compression (Fig. 29.4).
Explain what the indications for diagnostic thoracocentesis are? Explain how this would apply to a CHF pt. with a pleural effusion?
The main indication for thoracentesis (Fig. 19.6) is a clinically
signifi cant pleural effusion of unknown or unclear etiology
by medical history, physical exam, and chest imaging studies.
Not all effusions require diagnostic thoracentesis. For
example, in a patient with bilateral pleural effusions and overt
clinical evidence of CHF without fever, chest pain, or dyspnea
out of proportion to the size of the effusion, transudative
effusions are most likely, especially if they regress during the
fi rst several days of diuretic therapy and other cardiac-targeted
treatments. In this setting, the lack of at least a partial resolution
of the pleural effusion, or the fi nding of unilateral effusions,
or the presence of fever and/or chest pain are indications for
What are transudative pleural effusions? What is the fluid like? Generally, what are their two causes? Specifically, what is the main cause and how does it usually occur? How else does it occur? What are the signs and symptoms that accompany it?
Transudative pleural effusions are caused by two primary
mechanisms: (1) increases in the hydrostatic pressure (eg,
PMV) of pleural membrane microvessels; and (2) decreases
in serum colloid osmotic pressure (eg, πMV). In other words,
the pleural membranes themselves are not diseased in a subject
with a simple transudative pleural effusion. Accordingly,
transudative effusions are characterized by low pleural fl uid
concentrations of constituent plasma proteins (principally
albumin), as well as other plasma biomarkers such as lactate
dehydrogenase (LDH) and cholesterol when pleural fl uid is
sampled by diagnostic thoracentesis. By extension, pleural
fl uid/serum ratios for these substances are also low, in contradistinction
to exudative effusions (Table 29.2).
The most common cause of a transudative pleural effusion
is congestive heart failure (CHF), with approximately
500,000 effusions from this condition diagnosed annually in
the United States. Effusions in CHF are principally due to
elevations in the microvascular hydrostatic pressure within
pleural microvessels, and they are bilateral with the right side
fl uid volume greater than the left side in 85% of patients These effusions are usually accompanied by clinically overt
symptoms and signs of left ventricular dysfunction, including
bilateral inspiratory lung crackles. In ~5% of patients, isolated
left side transudative pleural effusions occur. The nephrotic
syndrome is associated with small to moderate pleural effusions
in about 20% of patients (Fig. 29.5). The primary cause
of effusions in nephrotic syndrome is a decrease in serum colloid
osmotic pressure, particularly when serum albumin concentrations
What is hepatic hydrothorax? What happens in it? What causes it? What is the effusion normally like? How is it diagnosed? How is it treated?
Hepatic hydrothorax is observed in 5%-10% of patients
with cirrhotic liver disease and portal venous hypertension.
Such eff usions are typically transudative, owing to transdiaphragmatic
movement of abdominal ascitic fl uid
from the peritoneal compartment to the pleural space
via diaphragmatic openings. Thus they are generally,
but not uniformly, associated with clinically detectable
ascites. Hepatic hydrothorax is unilateral and right-sided
in approximately 50%-80% of patients; bilateral and
isolated left-sided eff usions occur in approximately 15% of
patients. Patients with hepatic hydrothorax usually have
other stigmata of chronic liver disease, such as jaundice
and liver function test abnormalities. The diagnosis of
hepatic hydrothorax can be confi rmed if necessary by a
radionuclide scan in which tracer that is injected into the
peritoneal compartment appears within 2 hours in the
pleural space. Treatment is directed toward the underlying
cirrhotic condition with sodium restriction, diuretic therapy, and other adjunctive measures. Refractory hepatic
hydrothorax occurs in approximately 10% of patients.
This condition generally improves after a transjugular
intrahepatic portosystemic shunt (TIPS) that lowers
portal venous pressure and hence, the rate of peritoneal
What is an exudative pleural effusion like? What is the most frequent cause? What are 3 categories of this most frequent cause?
Exudative pleural effusions primarily result from increased
permeability of microvessels in the pleural membranes (ie,
an increased value of σ). Accordingly, pleural fl uid concentrations
of protein and other plasma biomarkers are elevated,
as are their ratios (Table 29.2). The most frequent cause of
an exudative fl uid is a parapneumonic effusion, which occurs
in about 40%-50% of bacterial pneumonias (Chaps. 34 and
35). Annually, between 250,000 and 500,000 parapneumonic
effusions develop in hospitalized patients in the United States.
Parapneumonic pleural effusions are categorized into three
main groups: (1) uncomplicated parapneumonic effusions;
(2) complicated parapneumonic effusions; and (3) thoracic
empyema. Each of these is briefl y reviewed below.
What are uncomplicated parapneumonic effusions? What are they like? How are they treated?
An uncomplicated parapneumonic effusion is an exudative,
free-fl owing pleural effusion that develops in conjunction
with infectious pneumonia (Chaps. 34-36). These effusions are
generally small and resolve completely following appropriate antimicrobial therapy directed at the pneumonia. Consequently
the majority of parapneumonic pleural effusions are
What is a complicated parapneumonic effusion? How is operationally defined? What is the prognosis like? What can compicate them? What is a trapped lung? What are complicated parapneumonic effusions associated with clinically? What is the pleural fluid analysis like?
However, approximately 10%-15% do evolve
into complicated parapneumonic effusions that are operationally
defi ned as those that require pleural space drainage
for resolution. These are associated with signifi cant morbidity
and mortality if not managed appropriately, because of the
development of intrapleural adhesions, persistently trapped
loculated fl uids, and development of trapped lung. The latter
situation refers to a restriction of normal lung expansion
because of fi brous thickening of the visceral pleura. Clinical
features that predispose to, or are indicative of a complicated
parapneumonic effusion include protracted respiratory symptoms
(eg, 7-10 days to several weeks) despite antimicrobial
therapy. Complicated parapneumonic effusions are also associated
clinically with large effusions that occupy >40%-50%
of a hemithorax, with those that contain loculated or multiloculated
fl uid collections on chest CT scan with a thickened or
enhancing visceral pleura, where intrapleural air-fl uid levels
are discernible, or when anaerobic pulmonary infections are
accompanied by pleural effusion (Fig. 29.6). Pleural fl uid
analyses showing a pH 1,000 U/L, and a
pleural fl uid glucose
What are thoracic empyema?
represents overt pus in the pleural space and is most often the
end result of a complicated parapneumonic effusion.
What the 3 recognized stages in the development of a complicated parapneumonic effusion? What happens in each? What are the clinical implications?
There are three recognized stages in the development of
complicated parapneumonic effusions, and these carry important
patient care implications. In the early exudative or capillary
leak stage lasting 2-5 days following the onset of the pleural
effusion, the effusion is usually amenable to simple drainage
by tube thoracostomy (Chap. 19). The fi brino purulent or
bacterial invasion stage extends for 3-14 days from onset, and
the organizational or empyema stage from 10 to 21 days.
Because of the rapid conversion from a free-fl owing effusion during the exudative phase of a complicated para pneumonic
effusion to the loculated, infected fl uids of the fi brinopurulent
phase, it is strongly recommended that all patients with parapneumonic
pleural effusions undergo diagnostic thoracentesis.
This procedure both evaluates the patient for the possibility
of a complicated parapneumonic effusion and documents the
need for drainage of the pleural space, in addition to prompt
initiation of antimicrobial therapy.
What are pleural effusions caused by neoplastic extension usually like? How should this be confirmed? Why?
Pleural effusions associated with extension of neoplastic
disease to the pleural space are typically exudative in nature
because of pleural infl ammation that increases pleural membrane
permeability, as well as fi brin deposition that limits the
rate of egress of fl uid out of the pleural space via lymphatic
drainage. However, patients with neoplastic disease may have
multiple reasons to have a pleural effusion of both exudative
and transudative causes. Thus, diagnostic thoracentesis is
always indicated to help distinguish among these possibilities
What is BAPE? What is the cause? What is the pathophysiology? What can hint towards this diagnosis? How is this diagnosis made? What other lung abnormalities is it associated with?
Benign asbestos pleural effusion (BAPE) is an exudative
fl uid collection resulting from prior exposure to asbestos. It is
characterized by a long latency period averaging 20-25 years
and is initiated by inhalational exposure and deposition of
asbestos fi bers within the respiratory bronchioles and alveolar
ducts. Because of their straight, linear structure and peripheral
lung deposition, amphibole asbestos fi bers are most associated
with BAPE. Following fi ber inhalation, an ensuing macrophagedriven
infl ammatory reaction extends outward to the pleural
space, where cytokines including TNF-α are released along
with growth factors, proteases, and reactive nitrogen and
oxygen species, culminating in oxidative DNA damage and
pleural infl ammation. Because there are no unique diagnostic
features of BAPE on pleural fl uid and cellular analyses, it
remains a diagnosis of exclusion. However, previous asbestosis
exposure suggesting the possibility of BAPE is commonly
manifested as calcifi c or noncalcifi c parietal plaques in the
mid-thoracic regions or involving the diaphragmatic pleura
(Chap. 23). Asbestos-related parenchymal abnormalities may
coexist, such as nodular or reticular opacities
What is yellow nail syndrome? How is it characterized?
nail syndrome is a rare disorder of lymphatic vessels characterized
by recurrent exudative pleural effusions, lymphedema
and yellowish discoloration of the nails.
What is the presentation of postpericardial injury syndrome? When does it develop? What is another name for it? What is the pathophys? What is the treatment?
The postpericardial injury syndrome has a relatively acute
presentation with dyspnea, fever, symptoms of pericarditis,
pleuritic chest pain, and an exudative pleural eff usion that
is typically left-sided. This syndrome develops in the setting
of previous cardiac surgery, myocardial infarction, or cardiac
instrumentation such as percutaneous coronary intervention
or pacemaker implantation. The condition is also referred to
as Dressler syndrome when it occurs following myocardial
infarction and persists for several weeks to months. It is
associated with autoantibodies directed against cardiac
tissue. Treatment with nonsteroidal anti-infl ammatory
agents as well as glucocorticoids is generally eff ective.
List 7 causes of transudative effusions?
Transudative Eff usions
Congestive heart failure
Peritoneal dialysis fl uid
Exudative Eff usions
Complicated parapneumonic eff usion
Benign asbestos pleural eff usion
Connective tissue disease
Postpericardial injury syndrome
Yellow nail syndrome
How are pleural effusions treated?
The approach to pleural effusions should employ a Bayesian
analysis in which the prethoracentesis probability of specifi c
disorders based on the clinical presentation should be considered,
after which the results of postthoracentesis pleural fl uid
analysis should be integrated to arrive at a list of focused diagnostic
possibilities. Regardless of this Bayesian approach or
the likelihood of a transudative effusion, thoracentesis should
be performed in patients with dyspnea and respiratory compromise
with the intent to remove as much fl uid as possible
(albeit generally ≤1,500 mL per procedure). Pleural effusions
associated with CHF are frequently proportional to the severity
of pulmonary edema and similarly respond to diuretic therapy
and other targeted cardiac therapies. Lack of improvement of
a pleural effusion that was presumed to be secondary to CHF
despite clinical evidence of an overall therapeutic response
should trigger reevaluation of the working diagnosis.
Antibiotic therapy for the underlying pneumonia generally
resolves uncomplicated parapneumonic effusions without
the need for drainage by a chest tube (tube thoracostomy). A
positive Gram stain of pleural fl uid for microorganisms or a positive
pleural fl uid microbial culture in a patient with an exudative
pleural effusion is an indication for tube thoracostomy and
pleural drainage. By extension, the fi nding of pus on thoracentesis
mandates immediate pleural space drainage. Antimicrobial
therapy alone is never adequate treatment of a closed pleural
space infection. When a chest tube is placed for treatment of a
complicated parapneumonic effusion, the tube can be removed
when <100 mL of fl uid drains in a 24-hour period. Loculated
pleural fl uid collections can frequently be successfully accessed
by ultrasound-guided thoracentesis. Smaller accumulations and/
or multiple-infected loculations can be successfully addressed
by CT-guided percutaneous catheter drainage. Thoracoscopy
and/or video-assisted thoracoscopic surgery (VATS) may be
required to lyse extensive intrapleural adhesions (Chap. 18).
What is a hemothorax? What causes it? What are the signs/symptoms? How should it be treated?
A hemothorax refers to blood in the pleural space, and is most
commonly the result of penetrating or nonpenetrating trauma or of excessive anticoagulation. Symptoms and physical fi ndings
in a patient with a hemothorax are generally similar to those of
a patient with a pleural effusion. Hemothorax usually requires
drainage with larger caliber chest tubes to avoid development
of a fi brinous visceral pleural peel and causing trapped lung. In
trauma or postoperative patients, both the patient’s clinical status
and drainage should be monitored frequently for clotting or
excessive bleeding (eg, ≥200 mL/h) which can result in hypovolemia
and cardiopulmonary compromise.
What is a pneumothorax? What are some possible causes? What is the resolution rate like? What does it depend on? What is the treatment like for small pneumothoraces? Larger ones?
A pneumothorax is defi ned as air or other gas in the pleural
space. It can occur unexpectedly as a primary spontaneous
pneumothorax (Fig. 29.7), as discussed for congenital emphysematous
bullae (Chaps. 20 and 37). Spontaneous pneumothorax
also may follow trauma to the parietal or visceral pleura,
or rarely, arise from the presence of gas-forming organisms in
the pleural space. In this context, a bronchopleural (BP) fi stula
is an abnormal connection between the tracheobronchial tree
or lungs and the pleural space, resulting in pneumothorax. A
characteristic feature of a BP fi stula is continued intrapleural
air leakage following chest tube insertion.
The resolution rate of a pneumothorax is mainly dependent
on the partial pressure gradient for nitrogen between
pleural gas and the venous blood. Assuming that no further
air enters the pleural space, the average resolution rate of a
pneumothorax in a subject breathing ambient room air withoutpleural aspiration or drainage is approximately 5% of its volume per day. In such subjects, breathing enriched O2
mixtures enhances the resolution rate of a pneumothorax by
reducing the Pn2 in blood and thereby enlarging the partial
pressure gradient for reabsorption. Small pneumothoraces (eg,
<15% of hemithoracic volume) in asymptomatic patients are
frequently observed medically for their progression or resolution.
However, larger pneumothoraces require the insertion of
small caliber chest tubes (≤28 French gauge) connected to an
underwater seal drainage with applied suction. Chest tubes for
pneumothoraces are left in place until at least 24 hours after
the leak has sealed as confi rmed radiographically.
What is reexpansion pulmonary edema? What settings does it occur in? What are the symptoms?
Reexpansion pulmonary edema is a rare and dramatic
unilateral lung complication associated with pulmonary
edema and alveolar consolidation that can occur within
24 hours following the rapid reexpansion of a chronically
collapsed lung. It is most typically observed after the
removal of a large amount of air from a pneumothorax
or fl uid from a pleural eff usion. The edema may progress for 24-48 hours and last for 5-6 days. Symptoms of this
complication include rapidly progressive dyspnea and
cough; arterial O2 desaturation and hypoxemia may ensue.