Indian Journal of Tuberculosis

153
AN UNUSUAL CASE OF A PLEURAL EFFUSION WITH AN ABDOMINAL MASS
Preetam R Acharya
1
, Rameshchandra Sahoo
2
and Poornima Baliga
3
1. Assistant Professor 2. Professor & Head 3. Professor
Department of Tuberculosis and Respiratory Diseases, Kasturba Medical College & Hospital, Attavara, Mangalore (Karnataka).
Correspondence: Dr. Preetam R. Acharya, Department of Tuberculosis & Respiratory Diseases, Kasturba Medical College & Hospital, N. G. Road,
Attavara, Mangalore 575 001 (Karnataka); E-mail: [email protected]; Telephone (land): (0824) 2445858; Telephone (mobile): 9448953430;
Fax: (0824) 2428379
(Received on 10.12.2007. Accepted after revision on 22.4.2008)
Summary: A 38-year old man presented to us with a left sided pleural effusion. Pleural fluid was aspirated and analysis
revealed it to be an exudate with predominant lymphocytes and an elevated ADA level. He was discharged on anti-
tuberculous treatment. Patient returned with re-accumulation of pleural fluid. Computed tomography done in our
institute picked up not only parenchymal disease in the lung which was not evident on chest radiographs but also picked
up an abdominal mass in the left renal fossa. Pathological examination of excised mass revealed its tuberculous nature.
The repeated recollection of pleural fluid was attributed to a paradoxical response; the patient was reassured and his
anti-tuberculous treatment continued. Recognition of the fact that evidence of tuberculosis at distant sites may occasionally
be needed to substantiate the diagnosis of tuberculous pleural effusion in a difficult and bacteriologically negative case
prompted us to report this case.
Key words: Tuberculous Pleural Effusion, Paradoxical Response, Incidentaloma
[Indian J Tuberc 2008; 55: 153-156]
INTRODUCTION
Establishing Tuberculosis as the cause of
pleural effusion can be difficult at times. The
diagnosis of Tuberculous Pleuritis is commonly
made from

observation of granulomas in pleural
biopsy specimens or a culture

positive for
Mycobacterium Tuberculosis from pleural tissue or
pleural fluid. However, the diagnosis can be
uncertain or missed in bacteriologically negative
cases. Proof of co-existing pulmonary tuberculosis
or getting evidence of the presence of
mycobacterium at other extra-pulmonary sites may
indicate dissemination and establish sufficient
grounds for institution of anti-tuberculous treatment
in an otherwise microbiologically negative case.
CASE REPORT
A-38-year old man presented to us with
left sided pleuritic chest pain and exertional
breathlessness (Medical Research Council Grade
I) for last seven days. He also had cough with
minimal expectoration for a month. He denied
having had haemoptysis, fever, chills or night
sweats. On review of systems, the patient
reported that he had lost some weight since last
one month. He had no past history of respiratory
disease and was a non-smoker. Family history for
pulmonary tuberculosis was positive in an elder
sibling who had completed a course of anti-
tuberculous treatment 15 years back.
Respiratory system examination was
suggestive of a left sided pleural effusion. Chest
radiograph revealed a moderate left sided pleural
effusion with contra lateral tracheal shift and no
evidence of any parenchymal abnormalities (Fig.1).
Routine blood investigations like haemogram, ESR,
fasting blood glucose, total bilirubin, transaminases
and creatinine were all within normal limits. Human
immuno-deficiency virus (HIV) ELISA was negative.
Three samples of sputum examined for AFB by Ziehl-
Neelsen method were negative. Thoracentesis was
done and serosanguinous fluid aspirated. Pleural fluid
was an exudate (Protein: 7.1 gm/dl) with a leukocyte
count of 4,800 cells/cumm and a lymphocyte
differential of 95 %. Pleural fluid examination by
Gram stain and ZN stain were negative. AFB culture
of the pleural fluid sample did not show any
Case Report
Indian Journal of Tuberculosis
154
mycobacterial colonies at the end of eight weeks of
incubation. Cytological examination of pleural fluid
was negative for malignant cells. Pleural fluid
adenosine deaminase (ADA) levels were elevated
(patient value: 122.61 iu/L, normal: up to 36.0
iu/L). A provisional diagnosis of tuberculous pleural
effusion was made and the patient discharged on
a four drug antituberculous regimen consisting
of Isoniazid, Rifampicin, Ethambutol and
Pyrazineamide (HERZ).
Over a period of next four weeks, our
patient did not show any improvement. A chest
radiograph taken at follow-up at this point showed
re-accumulation of pleural fluid. A closed pleural
biopsy was inconclusive. Pleural fluid
carcinoembryonic antigen (CEA) was normal (1.7).
Pleural fluid was re-aspirated and a contrast
enhanced computed tomography of chest was
advised. This revealed calcified nodular opacities in
apices of both the lungs. Additionally, a hypo dense
Fig. 1: Chest radiograph showing left sided effusion
Fig. 3: Chest radiograph at treatment end.
Fig. 2: Follow-up chest radiograph at 12 weeks
Fig. 4: Image showing granulomas consisting of
epitheloid cells and Langhans giant cells
(H & E X10)
PREETAM R ACHARYA ET AL
Indian Journal of Tuberculosis
155
enhancing mass lesion with a few areas of hyper
intensity was seen to arise from the upper pole of
the left kidney. CT guided biopsy and FNAC was
done from the mass which showed only necrotic
material.
Because of the rapid re-accumulation of
pleural fluid despite regular anti-tuberculous
treatment, a decision was taken to surgically
explore the abdomen and excise the mass to rule
out a malignant etiology. Surgical exploration
revealed a pale brown mass measuring
approximately 874 cms not involving the
kidney. The mass was excised in its entirety.
Histopathological examination revealed caseating
granulomas consisting of epitheloid cells,
Langhans giant cells and mature lymphocytes
suggesting tuberculosis (Fig.4).
The presence of caseating granulomas in
the excised mass in addition to the pleural fluid
characteristics helped us to substantiate our initial
diagnosis of tuberculous pleural effusion. Patient
was asked to continue his anti-tuberculous drugs.
Follow-up at regular intervals and serial chest
radiographs (Fig.2, Fig.3) have not revealed any
further re-accumulation of pleural fluid.
DISCUSSION
Pleural effusions can occur in any form
of pulmonary tuberculosis. It is a well-known fact
that neither the clinical features nor any of the
imaging modalities are of much help in the
diagnosis of a tuberculous pleural effusion. Co-
existing parenchymal disease detected
radiographically in about one third of the patients
with an effusion serves as a marker of active
pulmonary tuberculosis. Computed tomography
of chest may show lymphadenopathy, pulmonary
infiltrates or cavitation not seen on chest
radiographs; which although non-specific, may
help to distinguish tuberculous pleurisy from other
causes like malignancy
1
.
The onus of proving tuberculosis as a cause
of pleural effusion rests on microbiological (smear/
culture), and histological analysis of aspirated pleural
fluid and biopsied pleural tissue. Mycobacteria are
seen in pleural fluid only in 10 - 20 % of cases
whereas a culture though positive in 25 - 50 % of
the cases takes a minimum of 6-8 weeks by
conventional methods to be of any clinical utility.
Pleural biopsy will show granulomas in the parietal
pleura in 50 80 % of patients and if cultured will
grow mycobacterium in 55 80% of the cases
2
.
High levels of pleural fluid ADA (The reported cut-
off value for PADA varies from 47 to 60 U/l) may
be helpful in distinguishing tuberculous effusions
from malignant effusions. Several reports have
suggested that an elevated pleural fluid

ADA level
predicts tuberculous pleuritis with a sensitivity

of
90 to 100% and a specificity of 89 to 100%
3
.
However, controversy surrounds the use of elevated
pleural fluid ADA as a diagnostic aid for tuberculous
effusion
4
.
Treatment with anti-tuberculous drugs is
the mainstay of management of extra pulmonary
tuberculosis. The term paradoxical response refers
to enlargement of old lesions or

unexpected
appearance of new lesions during anti-tuberculous
therapy. Re-crudescence of fever, enlarging
adenopathies, worsening of pulmonary infiltrates,
pleural effusion, ascites and appearance of
intracranial tuberculomas have all been described.
An incidence of 16% of paradoxical worsening of
tuberculous effusion following the start of anti-
tuberculous treatment has been observed
5,6
. Such a
paradoxical worsening can occur in both HIV
uninfected and infected starting TB therapy. The
syndrome poses a diagnostic challenge since the
apparent clinical deterioration may raise the suspicion
of drug resistant tuberculosis, non- compliance to
prescribed regimen or presence of a concomitant
disorder unrelated to TB. These patients generally
need no alteration in their drug regimen.
An incidentaloma is a tumor (-oma) found
by coincidence (- incidental). The widespread use
of ultrasound, CT and MRI has resulted in the
incidental discovery of asymptomatic adrenal
masses. Adrenal incidentaloma is not a single
pathological entity and the differential diagnosis
includes adenoma, adrenocortical carcinoma,
phaeochromocytoma, metastases, Cushings
PLEURAL EFFUSION WITH AN ABDOMINAL MASS
Indian Journal of Tuberculosis
156
syndrome, primary aldosteronism etc.The incidental
adrenal masses may also be infiltrative disease, fungal
and tuberculous granulomas , hemorrhage and lesions
that masquerade as adrenal but arise from adjacent
organs (e.g. kidneys, pancreas, gall bladder, spleen,
lymph nodes). The adrenal gland is also a common
site for metastases from the breast, lung, renal,
melanoma, lymphoma
7
. Tuberculosis may affect many
of the endocrine glands the commonest being the
adrenal gland; acute tuberculosis adrenalitis producing
mass-like enlargement of the gland
8
. Ultrasonography
and computed tomography do not always differentiate
between adrenal and extra-adrenal masses and between
malignancy and non-malignancy; surgical excision
therefore seems to be desirable in such cases
9
.
In our patient, CT thorax was requested
for purpose of evaluating lung parenchymal
abnormalities. The upper abdominal cuts in the CT
helped us to pick up the incidental adrenal mass.
Unfortunately, transcutaneous needle biopsy of
adrenal mass proved to be inconclusive prompting
us to subject the patient to exploratory laparatomy
with excision of the mass in its entirety. Histological
examination of the excised mass showed features
suggesting tuberculosis. Considering the pleural
fluid characteristics i. e. exudate with
lymphocytic predominance and a high pleural
fluid ADA levels, the diagnosis of tuberculous
pleural effusion was substantiated. In
retrospect, the increase in effusion size on
anti-tuberculous treatment may be attributed
to Immune reconstitution syndrome a
syndrome of paradoxical worsening known to
occur during treatment with ATT. Our
assumption is strengthened by the fact that
the patient has completed treatment and has
had no recurrence of the effusion on follow-
up.
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PREETAM R ACHARYA ET AL