Thoracic Imaging 2003 - Society of Thoracic Radiology

SUNDAY
80
Pleural Effusions
Gerald F. Abbott, M.D.
Rhode Island Hospital / Brown Medical School
Pleural effusion is a common manifestation of local and systemic
diseases that involve the thorax, affecting an estimated 1.3
million individuals each year. The most commonly associated
diseases are (in decreasing order of frequency) congestive heart
failure, bacterial pneumonia, malignancy, pulmonary thromboembolic
disease, cirrhosis, pancreatitis, collagen vascular disease,
and tuberculosis. Other etiologies include trauma, abdominal
disease, and iatrogenic causes.
In normal subjects, a small amount of pleural fluid (5-15 ml)
is present within the pleural space providing a frictionless surface
between the visceral and parietal layers of pleura as lung
volume changes during respiration. Normal pleural fluid forms
and flows from capillaries in the parietal pleural and is absorbed
via the visceral pleura.
A variety of factors can cause an imbalance in the formation
and absorption of pleural fluid: increased hydrostatic pressure,
decreased oncotic pressure, decreased pressure in the pleural
space, increased permeability of the microvascular circulation,
and impaired lymphatic drainage. Fluid may also move from
the peritoneal space into the pleural space through diaphragmatic
lymphatics or anatomic defects in the diaphragm.
Patients with pleural effusion may be asymptomatic (15%)
or have dull aching pain, cough, and dyspnea. Large effusions
may displace the mediastinum and cause respiratory distress.
The history and physical examination are important elements in
guiding the evaluation of pleural effusions. Dullness to percussion
and decreased or absent breath sounds are characteristic
features in many patients with pleural effusion. Other physical
findings may suggest the etiology (e.g. distended neck veins and
peripheral edema in CHF).
Thoracentesis is usually performed to evaluate pleural effusions
of unknown etiology. The extracted fluid is examined for
its gross appearance and odor and submitted for biochemical
analysis, white blood cell and red blood cell counts, gram and
acid-fast stains, and cytologic evaluation. Invasive diagnostic
procedures including closed, open, or thoracoscopic biopsy, are
sometimes necessary to establish a diagnosis.
Clinically, most pleural effusions are categorized as transudates
or exudates using the criteria established by Light.
Exudates have one or more of the following characteristics: 1)
fluid-to-serum protein ratio > 0.5; 2) pleural fluid LDH > 200
IU; and 3) fluid-to-serum LDH ratio > 0.6. Transudates have
none of those characteristics. Such categorization may be combined
with clinical and other laboratory findings to establish a
differential diagnosis.
Transudative pleural effusions are characteristically caused
by systemic factors that alter pleural fluid formation or absorption.
The most common causes of transudative effusions are
CHF, cirrhosis, and pulmonary embolism. Exudative effusions
result from diseases that alter the pleural surfaces. The most
common causes are pneumonia, cancer, and pulmonary
embolism. If analysis reveals a transudative pleural effusion, the
cause of the systemic disorder can be treated and the pleura
does not require further investigation. When an exudative effusion
is found, further investigation of the pleura is warranted to
determine the etiology of the pleural disease.
Malignant pleural effusions occur in patients with primary or
metastatic neoplasia involving the thorax, but most frequently in
those with a primary tumor that is extrapulmonary. The most
common tumors related to malignant effusions are pulmonary,
ovarian, and gastric carcinomas and lymphoma.
Pleural effusions associated with pneumonia (parapneumonic)
occur in 40% of cases and are usually serous exudates that
resolve. Empyema (pus in the pleural space) may develop as a
complication of a parapneumonic effusion. Most empyemas are
secondary to spread from a pneumonic focus in the adjacent
lung or by formation of a bronchopleural fistula. Affected
patients are usually febrile and have an elevated white blood cell
count.
A variety of other etiologies are associated with pleural effusion.
Systemic lupus erythematosus and rheumatoid disease are
the most common causes of pleural effusions in connective tissue
disease. Benign asbestos-related effusions occur in 3% of
asbestos exposed individuals and are dose-related.
Other fluids may accumulate within the pleural space including
blood (hemothorax) and chyle (chylothorax). It is important
to distinguish between chylothorax and pseudochylous effusions.
Both look milky white on gross inspection, but are different
in their composition and in the mechanisms responsible for
their formation. The fluid of a chylothorax contains triglycerides
whereas pseudochylous effusions are rich in cholesterol.
Chylothorax typically occurs in the setting of trauma or tumor.
In approximately 50% of cases, chylothorax is a complication of
thoracic or mediastinal tumor. Postoperative chylothorax usually
appears within the week following surgery; post-traumatic chylothorax
develops over a longer time period, often a month.
Pseudochylous effusions are rare and are associated with longstanding
chronic pleural effusion (e.g. tuberculous pleurisy,
rheumatoid pleural effusion).
Imaging features
In the upright patient, small pleural effusions manifest as
blunting of the costophrenic sulcus, detectable on the lateral
chest radiograph with amounts as small as 25-50 ml and on the
frontal radiograph with accumulations of 200 ml. The ipsilateral
diaphragm is obscured by effusions of approximately 500 mll.
Most effusions are freely mobile in the pleural space and decubitus
radiographs may detect effusions as small as 5 ml.
Larger effusions manifest as dense opacities that obliterate
the costophrenic angle on both PA and lateral chest radiographs.
The peripheral aspect of these opacities characteristically
extends cephalad in the upright patient and forms a “meniscus”.
In supine patients, pleural effusions manifest as a veil-like
opacity that does not obscure the pulmonary vascular structures.
The margin of the ipsilateral hemidiaphragm may be hazy and
indistinct, the affected costophrenic angle is obscured, and with
sufficient accumulation (>500 ml) an “apical cap” is formed and
fluid may extend into interlobar fissures.
Atypical radiographic manifestations of pleural effusions
include subpulmonic (infrapulmonary) effusions, “pseudotumors”
formed by fluid accumulating within interlobar fissures,
and diaphragmatic inversion by large effusions. Air within a
pleural fluid collection should prompt consideration of the following
entities: bronchopleural fistula, hydropneumothorax,
trauma, esophageal rupture, and the presence of gas-forming
organisms.
Pleural effusions may become loculated and form mass-like
opacities that appear fixed and nonmobile, often with edges that
are better defined than freely mobile effusions. Empyemas
cause smooth thickening of the visceral and parietal pleura surrounding
the abnormal fluid collection and manifest as the “splt
pleura” sign on CT imaging.