Pleural Diseases.
The pleurae
The potential space between the
parietal and visceral pleurae serves as a coupling system between the lung and
the chest wall, and normally contains a small amount of fluid A negative
pleural pressure is maintained by the dynamic tension between the chest wall
and the lung (Chapter 3). Both pleurae have a systemic blood supply and
lymphatics, although lymphatic drainage of the pleural space is predominantly
via the parietal pleura. Fluid flux through the pleural space is determined by
Starling's relationship between microvascular pressures, oncotic pressures,
permeability and surface area. Normally, there is net filtration of
transudative (protein-poor) fluid into the pleural space that is balanced by
resorption via the parietal lymphatics.
Pneumothorax is an important
condition that occurs when air enters the pleural space and pleural pressure
rises to atmospheric pressure; pneumothorax is discussed in detail in Chapter
35.
Chylothorax is due to
accumulation of triglyceride-rich lymph in the pleural space, generally as the
result of damage to the thoracic duct causing leakage into the pleural space,
for example due to trauma or carcinoma.
Empyema is accumulation of
pus.
Pleurisy is a term commonly
used to describe the sharp localized pain arising from any disease of the
pleura. It is made worse by deep inspiration and coughing.
Pathophysiology
Most diseases of the pleura present
with pleural effusion, which can be detected on chest X-ray (CXR) when more
than 300 mL of fluid is present (Fig. 32b). Effusions are due to excessive flui
formation or inadequate fluid clearance. Symptoms develop if the fluid is inflammatory
or if pulmonary mechanics are compromised. Thus, the most common symptoms of a
pleural effusion are pleuritic chest pain, dull aching pain, fullness of the
chest or dyspnoea. Physical examination reveals decreased breath sounds,
dullness to percussion, decreased tactile or vocal fremitus. If there is
inflammation there may be a fric- tion rub. Compressive atelectasis (partial
lung collapse) may cause bronchial breath sounds. It is useful to categorize
pleural effusions as transudative or exudative (Fig. 32a).
Transudative effusions are
usually due to an imbalance in Starling's forces across normal pleural
membranes, have protein-poor fluid are often bilateral and are not associated
with fever, pleuritic pain or tenderness to palpation. The most common cause of
a transudative effusion is congestive heart failure. Other causes include
cirrhosis with ascites, nephrotic syndrome, pericardial disease or peritoneal
dialysis.
Exudative effusions imply
disease of the pleura or the adjacent lung and are characterized by an
increased protein, lactate dehydrogenase (LDH), cholesterol or white blood cell
count (WBC) (Fig. 32a). The differential diagnosis of exudative effusions is
broad, including infection, malignancy, autoimmune disease, oesophageal
perforation and pancreatitis.
Diagnostic evaluation of pleural
effusion should include measurement of pleural aspirate cell count with
differential, pH, protein, LDH, cholesterol and glucose. These studies usually
distinguish exudates from transudates and will often suggest a specifi
diagnosis. For example, extremely low glucose is typical for empyema,
malignancy, tuberculosis (Chapter 38), rheumatoid arthritis, systemic lupus evry
thematosus (SLE) or oesophageal perforation. If clinically indicated, a specifi
diagnosis may be obtained from microbiological stains and culture,
cytopathology, amylase, triglycerides and measurement of antinuclear antibody
(ANA) titre. Although all patients with SLE have a positive ANA titre in the
pleural f uid, it is also present in a significant proportion ( 5%) of other
effusions; these may be related to malignancy.
Treatment is for the
underlying condition, but persistent or reaccumulating effusions can be drained
to dryness (slowly so as to avoid severe pain).
Specific Conditions
Pneumonia (Chapters 36 and
37) commonly causes parapneumonic pleural effusions. These effusions are
usually sterile exudates with a neutrophilic leukocytosis and require only
treatment of the pneumonia to resolve. However, if bacteria invade the pleural
space, a complicated parapneumonic effusion or empyema will develop. These effusions
are characterized by a low pH and extensive fibri deposition causing flui
loculation and require adequate open or closed drainage for healing.
Streptococcus pneumoniae, Staphylococcus aureus, Gramnegative bacteria and
anaerobes commonly cause complicated effusions.
Tuberculosis pleurisy occurs when a subpleural focus
of primary infection ruptures into the pleural space, causing a delayed
hypersensitivity response. Subsequently, an exudative effusion with a lympho-
cytic leukocytosis, a paucity of macrophages and an elevated adenosine
deaminase will develop. Patients develop fever, dyspnoea, pleuritic pain and a
positive tuberculin response (Chapter 38). Granulomatous inflammatio is seen on
pleural biopsy, and culture of pleural tissue has the highest diagnostic yield.
Primary lung malignancies or metastases to the lung may cause
pleural effusions by direct invasion or by obstruction of parietal lymphatic
drainage. Malignant effusions are mostly exudative (90%), often with a very
high LDH, low pH and low glucose. Cytology of the pleural flui has a high
diagnostic yield. Symptomatic pleural effusions may respond to therapy for the
underlying malignancy, although palliative obliteration of the pleural space
(pleurodesis) is often necessary to relieve dyspnoea or chest pain.
Mesothelioma is an uncommon
malignancy that originates in the pleura and/or peritoneum (Chapter 33). Over
75% of cases develop 20-30 years after occupational asbestos exposure. Asbestos
may also cause benign pleural effusions or calcifie plaques on the parietal
pleura in the lower lungs or along the diaphragmatic surface. Mesothelioma
typically develops in men aged 50-70 years, presenting with insidi- ous
dyspnoea and aching chest pain. CXRs usually show unilateral pleural effusion
(Fig. 32b), and computed tomography (CT) shows lumpy f brotic encasement of the
pleural space (Fig. 32c). Pleural f uid cytology is not usually diagnostic.
Thoracoscopic biopsies have the highest yield. Treatment is generally
palliative, including pleurodesis. The prognosis is poor, with a median survival
of approximately year.
