10.

TUBERCULOUS
PLEURAL EFFUSION
(PLEURITIS TUBERCULOSA)

PLEURAL DISEASES SERIES 08

BY WIDIRAHARDJO
 10. TUBERCULOUS PLEURAL EFFUSION (PLEURITIS TUBERCULOSA)

The diagnosis of pleuritis tuberculosa

should be considered in any patient
with an exudative pleural effusion.

PATHOGENESIS AND
PATHOPHYSIOLOGIC FEATURES
If occurs in the absence of
radiologically apparent TB, it may be
the sequel to a primary infection 6 to
12 weeks previously or it may
represent reactivation TB.
 10. TUBERCULOUS PLEURAL EFFUSION (PLEURITIS TUBERCULOSA)

The tuberculous pleural effusion is thought to

result from rupture of a subpleural caseos focus
in the lung into the pleuraI space.
It appears that delayed hypersensitivity plays a
large role in the pathogenesis of tuberculous
pleural effusion that initiated when tuberculous
protein gains access to the pleural space.
The mycobacterial cultures of the pleural fluid
from most patients with tuberculous pleural
effusions are negative.
But the pleural effusion in patients with AIDS is
related to pleural invasion by the mycobacteria
rather than to delayed hypersensitivity. The fact
that smears and cultures are more often
positive in the human immunodeficiency virus
(HIV) patient.
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The neutrophil appears to play a key role in the

development of pleuritis tuberculosa for the
first 24 hours.
The neutrophils in the pleural space appear to
secrete a monocyte chemotaxin that recruits
monocytes to the pleural space and thereby
contributes to the formation of granulomas.
After this period, lymphocytes are the
predominant cells in the pleural fluid.
When the lymphocytes first appear in the
pleural fluid approximately on day 3, they do
not respond to PPD. From day 5 onward,
however, reactivity to PPD is found in most
cases.
 10. TUBERCULOUS PLEURAL EFFUSION (PLEURITIS TUBERCULOSA)

The development of the tuberculous

pleural effusion is that the delayed
hypersensitivity reaction increases
the permeability of the pleural
capillaries to protein, and result in a
much higher rate of pleural fluid
formation.
The inflammatory reaction in the
parietal pleura impedes the
lymphatic drainage from the pleural
space.
 10. TUBERCULOUS PLEURAL EFFUSION (PLEURITIS TUBERCULOSA)

INCIDENCE
In northern Spain, TB was the most common
etiology of pleural effusion, accounting for
25% of all pleural effusions.
In Saudi Arabia demonstrated that TB
accounting for 37% of all pleural effusions.
In the United States, the annual incidence of
pleuritis tuberculosa has been estimated to be
approximately 1,000 cases, and it is said that
3% to 5% of patients with TB will have
pleuritis tuberculosa.
 10. TUBERCULOUS PLEURAL EFFUSION (PLEURITIS TUBERCULOSA)

CLINICAL MANIFESTATIONS
Pleuritis tuberculosa most commonly
manifests as an acute illness, the initial
symptoms less than 1 week.
Most patients have a cough, usually
nonproductive; chest pain, usually pleuritic;
and febrile.
In general, patients with pleuritis tuberculosa
are younger (between 31 50 year) than
patients with parenchymal TB.
 10. TUBERCULOUS PLEURAL EFFUSION (PLEURITIS TUBERCULOSA)

Usually unilateral and can be of any

size.
In approximately 20% of patients
coexisting parenchymal disease is
radiologically visible and pleural
effusion is almost always on the side
of the parenchymal infiltrate.
 10. TUBERCULOUS PLEURAL EFFUSION (PLEURITIS TUBERCULOSA)

NATURAL HISTORY OF UNTREATED

PLEURITIS TUBERCULOSA
Without treatment, pleuritis
tuberculosa usually resolves
spontaneously, only to return (43%
to 65%) as active TB at a later date.
 10. TUBERCULOUS PLEURAL EFFUSION (PLEURITIS TUBERCULOSA)

DIAGNOSIS
The diagnosis depends on the
demonstration of tubercle bacilli in the
sputum, pleural fluid, or pleural biopsy
specimen, or the demonstration of
granulomas in the pleura.
Also be established with elevated levels of
adenosine deaminase (ADA) or interferon-
gamma in the pleural fluid.
Most patients do not have leukocytosis.
 10. TUBERCULOUS PLEURAL EFFUSION (PLEURITIS TUBERCULOSA)

The chest radiograph usually demonstrates

only the pleural fluid, but approximately
only 20% of the patients also have a
parenchymal infiltrate due to TB or hilar or
mediastinal lymphadenopathy as shown in
CT.

Tuberculin Skin Testing

In the past, the tuberculin skin test was an
important diagnostic. However, a negative
skin test does not rule out the diagnosis of
pleuritis tuberculosa.
 10. TUBERCULOUS PLEURAL EFFUSION (PLEURITIS TUBERCULOSA)

Pleural Fluid Analysis

The fluid is invariably an exudate.
In most patients, the pleural fluid
differential white blood cell (WBC) count
reveals more than 50% small
lymphocytes.
If eosinophils are found in the pleural
fluid in significant numbers (> 10%),
one can virtually exclude the diagnosis
of tuberculous pleuritis, unless the
patient has a pneumothorax or has had a
previous thoracentesis.
 10. TUBERCULOUS PLEURAL EFFUSION (PLEURITIS TUBERCULOSA)

Adenosine Deaminase (ADA) level above 70

U/L had TB and level below 40 U/L had no TB.
In general, the two main diseases other than
tuberculous pleuritis that are associated with
a high pleural fluid ADA are empyema and
rheumatoid pleuritis that do not have pleural
fluid lymphocytosis.
Interferon-Gamma is produced by the CD4+
lymphocytes, pleural fluid cutoff level of 3.7
IU/mL yielded a sensitivity of 0.98 and a
specificity of 0.98.
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Polymerase Chain Reaction is certainly not

superior to either the pleural fluid ADA or
interferon-gamma levels in establishing
the diagnosis of pleuritis tuberculosa, in
which the sensitivity and specificity were
81% and 100%.
Sputum Smears and Cultures studies were
positive in 52%.
Pleural Fluid Stains are not indicated as a
routine smear, because they are usually
negative, unless the patient has a
tuberculous empyema.
 10. TUBERCULOUS PLEURAL EFFUSION (PLEURITIS TUBERCULOSA)

Pleural fluid cultures should be

obtained, positive for mycobacteria
in fewer than 40%.
Pleural Biopsy showed granulomas
80%, the acid-fast stain of the
biopsy was positive in 25.8%, the
culture of the biopsy tissue was
positive in 56% to 91%.
 10. TUBERCULOUS PLEURAL EFFUSION (PLEURITIS TUBERCULOSA)

TREATMENT
The treatment of tuberculous
pleuritis has three goals:
1. To prevent the subsequent
development of active TB,
2. To relieve the patient symptoms,
3. To prevent the development of a
fibrothorax.
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The recommendations for the treatment of all

pulmonary and extrapulmonary TB are the
initial phase should consist of a 2-month
period of isoniazid (INH), rifampin,
pyrazinamide and ethambutol.
The second phase of the treatment should be
INH and rifampin given for 4 months.
Directly observed therapy (DOT) is
recommended.
The penetration of INH into pleural fluid was
excellent, but the penetration of pyrazinamide
was very poor, whereas the penetration of
rifampin was intermediate.
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With treatment, the average patient becomes

afebrile within 2 weeks, but temperature
elevations may persist for as long as 2 months.
If a therapeutic thoracentesis is performed at
the same time that antituberculous therapy is
initiated, most patients become afebrile within
5 days.
The mean duration for complete resorption of
the pleural fluid is approximately 6 weeks, but
it can be as long as 12 weeks.
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The incidence of pleural thickening at 6

to 12 months after beginning treatment
is approximately 50%.
Administration of corticosteroids: 80 mg
of prednisone every other day until the
acute symptoms, influence the degree
of residual pleural thickening at 6 or 12
months after therapy was initiated.
If the patient is dyspneic from a large
pleural effusion, a therapeutic
thoracentesis should be performed.
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Surgery (decortication) should not

be performed early for pleural
thickening, be considered until the
patient has undergone treatment for
at least 6 months.
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TUBERCULOUS BRONCHOPLEURAL FISTULA

These fistulas are usually seen in patients with
old, healed TB, and especially in patients with
a previous therapeutic pneumothorax who
were never treated with chemotherapy.
Superinfection of the pleural space by bacteria
sometimes occurs.
The fistula can be confirmed by the injection of
methylene blue or a radiopaque dye into the
pleural space and then observing whether the
dye appears in the sputum or in the
tracheobronchial tree.
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A tuberculous bronchopleural fistula is

dangerous to the patient for three reasons:
1. Bacteria to gain acess to the pleural
space and to cause pleural infection
2. The pleural space becomes
superinfected, the patient is at risk to a
fulminant pneumonia cause by entrance
material from the pleural space.
3. The tuberculous bacilli in the pleural
space are likely to become resistant to
anti tuberculosis drug.
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The initial treatment of tuberculous

bronchopleural fistulas should be the
institution of appropriate
antituberculous chemotherapy in
addition to the insertion of chest
tubes.
Before a definitive surgical procedure
is attempted, the patient should be
given antituberculous chemotherapy
for 90 to 120 days, or until sputum
tests become negative for AFB.
 10. TUBERCULOUS PLEURAL EFFUSION (PLEURITIS TUBERCULOSA)

Definitive surgical treatment consists

of decortication, which sometimes
must be combined with
thoracoplasty, with an operative
mortality rate of 20%.
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TUBERCULOUS EMPYEMA
Tuberculous empyema is characterized by
purulent pleural fluid that is loaded with tu-
berculous organisms on AFB stains.
It usually develops in fibrous scar tissue
resulting pleurisy, artificial pneumothorax, or
thoracoplasty.
The patient usually has a subacute or chronic
illness characterized by fatigue, low-grade
fever, and weight loss. On rare occasions, a
tuberculous empyema may produce empyema
necessitatis, where the empyema ruptures
through the chest wall.
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Treatment is difficult, decortication,

extrapleural pneumonectomy, and
thoracoplasty have all been
recommended.