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7/23/2019 Journal Radiology Chest TB
http://slidepdf.com/reader/full/journal-radiology-chest-tb 1/25
[Downloaded free from http://www.ijri.org on Thursday, October 22, 2!", #$:
%&.'(.!&%.2%()
*hest +adiology
Chest tuberculosis: Radiological review and imagingrecommendations
shu -eith halla, nur 0oyal, +andeep 0uleria!, run 1umar 0upta
Departments of +adiodiagnosis, and !$ulmonary edicine, ll #ndia #nstitute of edical
-ciences, 3ew Delhi, #ndia
*orrespondence: Dr. shu -eith halla, Department of +adiodiagnosis, ll #ndia
#nstitute of edical -ciences, nsari 3agar, 3ew Delhi‐ !!24, #ndia. 5
‐mail:
ashubhalla!6yahoo.com
Abstract
*hest tuberculosis 7*T8 is a widespread problem, especially in our country where it is
one of the leading causes of mortality. The article re9iews the imaging findings in *T
on 9arious modalities. e also attempt to categori;e the findings into those definiti9e for
acti9e T, indeterminate for disease acti9ity, and those indicating healed T. Though
9arious radiological modalities are widely used in e9aluation of such patients, no imaging
guidelines e<ist for the use of these modalities in diagnosis and follow‐up. *onse=uently,
imaging is not optimally utili;ed and patients are often unnecessarily subjected to
repeated *T e<aminations, which is undesirable. ased on the a9ailable literature and our
e<perience, we propose certain recommendations delineating the role of imaging in the
diagnosis and follow‐up of such patients. The authors recogni;e that this is an e9ol9ing
field and there may be future re9isions depending on emergence of new e9idence.
Key words: *hest radiograph> chest tuberculosis 7pulmonary, nodal and pleural8>
computed tomography> imaging recommendations> T acti9e
Background
The current guidelines for diagnosis of adult chest tuberculosis 7T8 are based primarily
on the demonstration of acid‐fast bacilli 7?8 on sputum microscopy. *hest radiograph
7*@+8 finds its place in sputum‐negati9e patients not responding to a course of
antibiotics. Though computed tomography 7*T8 is fre=uently employed in the diagnosis
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and follow‐up of T, it does not find a
place in the national and international
guidelines. Aiterature is lacing and no
consensus e<ists on use of ultrasound
7B-08, *T, and magnetic resonance
imaging 7+#8 in such patients. ith
#ndia ha9ing a large burden of T, it is
important to ha9e established imaging
criteria and recommendations.
-putum smear results tae se9eral days
while culture results need se9eral wees.
[!) This limits the diagnostic
efficiency of these con9entionalapproaches and fre=uently causes delays
in isolating infectious patients.[2) These
tests also suffer from low sensiti9ity.
ecause of these limitations, imaging
plays an important role in e9aluation of
chest T 7*T8 patients and *T is more
sensiti9e than *@+ in this regard.[%,()
?or optimal management, the
radiologists are often e<pected to deli9er important information, while limiting the
radiation e<posure and costs to the
patients.
Epidemiology: Global Scenario and
ndian !erspective
T is a global health problem and the
second leading infectious cause of death,
after human immunodeficiency 9irus
7C#8. s per the orld Cealth
Organi;ation 7CO8 reports, &.! million
cases of T were notified by national T
programs in 2!2, of which ".( million
were new cases.[") Of these, 2." million
had sputum smear ‐ positi9e pulmonary
T 7$T8, !.4 million had sputum
smear ‐negati9e $T, and .E million had
e<trapulmonary T 75$T8> case type
was unnown in the remaining cases.[")
#ndia accounted for 2&F of total cases of T worldwide in 2!2.[") T is one of
the leading causes of mortality in #ndia,
illing two persons e9ery % min, nearly
! e9ery day.[&) The number of T
deaths is disappointingly large, gi9en
that the majority of
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!.(!%/4'!‐
%2&.!&!(%!
these are pre9entable and that curati9e
regimens ha9e been a9ailable for a long
time now.
Chest &B
T can affect any organ system,
although manifestations are most
commonly related to the chest. The
lungs are the most common and oftenthe initial site of in9ol9ement. *hest
in9ol9ement is most commonly
pulmonary, followed by lymph nodal
and pleural disease 7latter two are
included under 5$T8. *hest wall,
cardiac, breast, and seletal in9ol9ement
7/23/2019 Journal Radiology Chest TB
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can also occur in the thora<> howe9er,
these are beyond the scope of the current
re9iew. #n the current re9iew, we discuss
the most common types of *T, namely
$T and 5$T 7pleural/lymph nodal8.
*ough greater than 2 wees is the
primary criterion to suspect $T.
$atients of $T/5$T also present with
fe9er, loss of appetite and loss of weight,
chest pain or dyspnea.
Role o' imaging in C&B
G Diagnosis
GTreatment e9aluation‐ response
assessment, residual
acti9ity
GDetection of disease complications /
se=uelae.
maging modalities
G *@+ H -putum smear microscopy,
culture for ?, and *@+ postero‐
anterior 7$8 9iew are the initial
in9estigations performed in adults
suspected to ha9e T. *@+ is fre=uently
employed as the initial test to e9aluate
une<plained cough. #t is the primary
modality for diagnosis and follow‐up,
and may be the only imaging re=uired in
sputum‐ positi9e cases. picogram /
lordotic 9iew 7for lung apices8 and
lateral 9iew are of limited utility and *T
is the ne<t in9estigation in case of
e=ui9ocal *@+. *@+ is useful to loo
for any e9idence of $T as well as toidentify other abnormalities responsible
for the symptoms. Table ! delineates the
indications of *@+
G B-0 ‐ -onography is 9ery useful for
pleural effusion detection,
characteri;ation, guiding drainage, and
follow‐up. Differentiating minimal
effusion from residual thicening is a
common indication. B-0 can also beused to e9aluate associated
hepatosplenomegaly, ascites, and
abdominal lymphadenopathy
G *T chest ‐ ulti‐detector *T 7D*T8
is an important tool in the detection of
radiographically occult disease,
differential diagnosis of parenchymal
lesions,[') e9aluation of mediastinal
lymph nodes 7A3s8, assessing disease
acti9ity, and e9aluating complications. #t
not only enables earlier and more
accurate diagnosis of pulmonary lesions,
but also can be used to differentiate the
etiologies of pneumonia.[',E) *T
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enables e9aluation of bronchiectasis,
ca9itation, associated fungal balls, and
assessment of necrosis in the A3s,
identifying pleural/airway/diaphragmatic
pathologies and e9aluating 9isuali;ed
bones. *ontrast‐enhanced *T 7*5*T8 is
the in9estigation of choice for e9aluation
of mediastinal A3s and also aids in
depicting pleural enhancement in
empyema. Cigh‐resolution *T 7C+*T8
reconstructions are especially useful to
detect miliary and centrilobular nodules,
ground‐glass opacities, and air ‐trapping.
Table ! outlines the 9arious situations
where *T chest is recommended. The
9alue of *T lies in the fact that it enables
one to suggest a diagnosis of T in patients with negati9e sputum e<amination and those
without sputum production [as occurs in the follow‐up of patients on anti‐tuberculosis
therapy 7TT8 or at presentation) non‐in9asi9ely. oreo9er, *T findings may permit
empirical initiation of TT until the time culture results are obtained[4)
G +#‐
+# is a problem‐
sol9ing modality and con9entional se=uences 7T! and T2images8 should be combined with diffusion‐weighted imaging 7D#8 and subtracted
contrast‐enhanced 7*58 imaging for optimal e9aluation. #t can be used to better e9aluate
mediastinal nodes and assess disease acti9ity in case of mediastinal nodes/fibrosis. -ince
it is free from ioni;ing radiation,
+# can be employed for follow‐up of mediastinal nodal disease in young patients to
reduce radiation e<posure. $resence of diffusion restriction in the A3s and peripheral
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enhancement suggest acti9e disease. +# has been pro9en to be superior to non ‐contrast
*T in the e9aluation of mediastinal nodes, pleural abnormalities, and presence of
caseation.[!) #t may ser9e as a reasonable alternati9e to *T for lung parenchymal
e9aluation in pregnant patients.[!) *ost and a9ailability issues are the main limitations
G $ositron emission tomography‐*T ‐ fluorodeo<yglucose ‐ positron emission
tomography 7?D0‐$5T8 plays an important role in the wor ‐up of patients with pyre<ia
of unnown origin 7$BO8, owing to its high sensiti9ity in the detection of infection,
inflammation, and malignancy.[!!) cti9e T shows increased uptae with high
standardi;ed uptae 9alues 7-Bs8 and
may pose as a cancer mimic.[!2) $5T
may help in assessing the disease
acti9ity and response to therapy.[!!)Though it is not specific for T, ?D0‐
$5T *T can guide biopsy from acti9e
sites, assess complete disease e<tent, and
detect occult distant in9ol9ement. The
use of $5T *T in e9aluation of benign
diseases is, howe9er, limited due to high
radiation e<posures in9ol9ed.
!rimary and !ost‐primary &B
*T is con9entionally di9ided into
primary and post‐ primary 7or
reacti9ation8 T 7$$T8, each with
corresponding radiological patterns,
albeit with considerable o9erlap. The
radiological features depend on age,
underlying immune status, and prior
e<posure. ?igure ! depicts the natural
history and progression of the disease.
$rimary T is ac=uired by inhalation of
airborne organisms and occurs in
patients not pre9iously e<posed to
Mycobacterium tuberculosis. #t
commonly affects infants and children in
endemic areas. Cowe9er, primary T is
now increasingly encountered in adult
patients, accounting
(igure ): 3atural history of chesttuberculosis
for 2%‐%(F of all adult cases and e9en
more in non‐endemic areas.[!%,!() The
primary parenchymal focus is nown as
the 0hon focus and the combination of
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0hon focus and enlarged draining A3s
constitutes the primary comple<: The
+ane or 0hon comple<.[!")
$rimary T may in9ol9e lung
parenchyma, A3s, tracheobronchial tree,
and pleura. *lassically, four entities are
described: 0angliopulmonary T, T
pleuritis, miliary T, and
tracheobronchial T.[!") Only the
gangliopulmonary form is characteristic
of primary T and the rest may be seen
in post‐ primary disease as well.
Gangliopulmonary TB is characteri;ed by the presence of mediastinal and/or
hilar A3 enlargement with associated
parenchymal abnormalities. A3
enlargement is seen in up to 4&F
children and (%F adults with primary
T.[!&‐!E) +ight paratracheal, hilar, and
subcarinal regions are the most common
sites of nodal in9ol9ement, though other
sites may also be affected. ilateraladenopathy occurs in %!F cases.[!')
The pre9alence of adenopathy decreases
with age.[!') *T is better than *@+ in
detection and characteri;ation of
thoracic A3 enlargement.[!4) On *5*T
scan, the enlarged A3s show highly
characteristic, but not pathogonomic,
Irim signJ attributed to low‐density
center surrounded by a peripheral rim
enhancement.[2) This rim sign may
also be seen with atypical mycobacteria,
histoplasmosis, metastases 7from
head/nec/testicular malignancy8, and
lymphoma.[!") Ceterogeneous
enhancement may also be seen.
Comogeneous enhancement is more
commonly found in pediatric age group.[!4) ssociated lung infiltrates are seen
on the same side as nodal enlargement in
two‐thirds of pediatric cases of primary
$T.[!') $arenchymal opacities are
usually located in the peripheral
subpleural regions. They may be
difficult to see on radiographs> thus, *T
is often re=uired to detect these subtle
parenchymal infiltrates.[2!) *@+s may
be normal in !"F of cases.[22) *ontrary
to the age‐related decrease in occurrence
of lymphadenopathy, the pre9alence of
radiographically detectable lung
in9ol9ement is higher in older children
and adults,[!',!E) so much so that
primary infection in adults fre=uently
manifests as parenchymal consolidation
without adenopathy. On *T, the air ‐space consolidation in primary T is
dense, homogeneous, and well‐defined.
$arenchymal disease in primary T
commonly affects the middle and lower
lung ;ones on *@+, corresponding to
the middle lobe, basal segments of lower
lobes, and anterior segments of upper
lobes.
0enerally, the primary disease is self ‐
limiting and immune‐competent persons
remain asymptomatic. ?re=uently, the
only radiological e9idence of primary
T is a combination of parenchymal scar
7Kcalcified8 and calcified hilar and/or
paratracheal A3s. *omplications of
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gangliopulmonary T include
perforation of an enlarged A3 into a
bronchus, bronchial compression due to
adenopathy leading to retro‐obstructi9e
pneumonia, and/or atelectasis. The latter
is usually right sided, with obstruction
occurring at the le9el of the right lobar
bronchus or bronchus intermedius.[2%)
#n "‐!F patients of primary T, the
infection is progressi9e and
hematogenous dissemination occurs> this
is termed progressi9e primary T,
manifestations of which are identical to
$$T.[4)
$$T occurs in pre9iously sensiti;ed
patients and results either from re‐
infection or from reacti9ation of dormant
bacilli in primary infection 74F of
cases8 owing to immunosuppression,
malnutrition, senility, and debilitation.
[2(,2") Thus, $$T occurs predominantly
in adolescents and adults and usually
begins with necroti;ing consolidation
followed by transbronchial spread.[4)
$$T is characteri;ed by: !. Ai=uefaction
of caseous necrosis, 2. formation of
ca9ities, %. progressi9e fibrosis and lung
destruction, and (. bronchogenic spread.
[!") pico‐ posterior segments of the
upper lobes and superior segments of the
lower lobes are the usual sites of in9ol9ement.[!") #nitially, there is
li=uefaction of regions of caseous
necrosis, which then communicate with
the tracheobronchial tree to form
ca9ities. *oughing may result in
bronchogenic spread to other lung
segments and/or may be a source of
infection for other patients 9ia inhalation
of bacilli‐laden droplets. ?ibro‐
atelectasis is common, especially of the
upper lobes with retraction of the hilum,
mediastinal shift, pulling up of
diaphragm, and compensatory
hyperinflation of the normal lung
segments. ssociated pleural thicening,
especially of the lung apices, may be
e9ident along with e<trapleural fat
proliferation. 5nd‐stage T may cause
complete destruction of the lung
parenchyma resulting from a
combination of parenchymal and airwayin9ol9ement. *ontrary to the pre9ious
notions, recent studies[2&) suggest that
children and adolescents are also e=ually
prone to de9elop destructi9e lung
changes with se9ere se=uelae, similar to
$$T. The similar location and
morphology of parenchymal changes
obser9ed in children blurs the distinction
between primary and reacti9ation T.
#maging in $$T often shows e<tensi9e
abnormalities in predisposed locations.
[2') ?eatures of acti9e endobronchial
infection ‐ consolidations, al9eolar
opacities on *@+, clustered nodules,
centrilobular nodules on *T ‐ are
hallmars of acti9e $$T. ronchogenic
spread is e9ident radiographically in
2F of cases and manifests as multiple,ill‐defined micronodules, in segmental
or lobar distribution, distant from the site
of ca9itation and usually in9ol9ing the
lower lung ;ones.[2E) On *T scan, it is
identified in 4"F of cases maing
C+*T the imaging modality of choice to
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detect early bronchogenic spread.[%,24)
Typical findings include 2‐ to (‐mm
centrilobular nodules and Itree‐in‐ budJ
branching opacities 7sharply marginated
linear branching opacities aroundterminal and respiratory bronchioles8.[%)
*a9itation is also characteristic of $$T,
radiographically
e9ident in (F of cases, and walls may
be thin and smooth or thic and nodular.
Thic ‐walled ca9ities and ca9ities with
surrounding consolidation indicate
acti9e infection, while thin‐walled
ca9ities suggest healed infection.[4)
Thin‐walled ca9ities may be difficult to
differentiate from bullae, cysts, or
pneumatoceles. ir ‐fluid le9els in the
ca9ity occur in !F of cases and can be
due to superimposed bacterial or fungal
infection.[!&,2E) ?ibro‐ parenchymal
lesions causing distortion of lung
parenchyma and cicatricial
bronchiectasis de9elop with healing of
acti9e infection.
Tuberculous ca9ities can rupture into
pleural space, resulting in empyema and
e9en bronchopleural fistula. 5rosion into
the pulmonary artery branches can lead
to massi9e hemoptysis 7+asmussen
pseudoaneurysm8. 5rosion into systemic
9essels or pulmonary 9eins can lead to
hematogenous dissemination and miliary
T. Cealing of $$T occurs with fibrosis
and calcification.
Radiological patterns encountered in
both primary and*or post‐primary
C&B
Miliary TB
iliary T results from hematogenous
dissemination of the T bacilli leading
to the de9elopment of innumerable small
granulomas in lungs and other organs.Though classically encountered in
children, the incidence in adults is
increasing.[!",2&) 5arly in the course of
the disease, *@+ may be normal in 2"‐
(F of cases.[%) *T, especially C+*T,
can demonstrate miliary disease before it
becomes radiographically apparent.
$resence of !‐% mm nodules, both
sharply and poorly defined, diffusely
spread in random distribution in both
lungs, often associated with interstitial
septal thicening is characteristic.[2")
There may be some basal predominance
due to gra9ity‐dependent increased
blood flow to the lung bases. #nitially,
the foci are about ! mm in diameter.
Bntreated, they may reach %‐" mm in
si;e and may become confluent, presenting a Isnow‐stormJ appearance.
Pleural involvement
#n9ol9ement of the pleura is one of the
most common forms of 5$T and is
more common in the primary disease. #n
case of primary T, it manifests as
unilateral free large effusion, without
loculations. #t occurs %‐& months after
infection, as a result of delayed
hypersensiti9ity response to
mycobacterial antigens.[!") #t is often
asymptomatic and microbiological
analyses are often negati9e. Though rare
in children, it is common in adolescents
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and young adults. $leural in9ol9ement
can be seen in up to %EF cases of
primary T and up to !EF cases of $$T.
[!&) #n $$T, effusion is usually small,
loculated, and associated with parenchymal lesions. -ince it originates
from rupture of a ca9ity into the pleural
space, cultures are usually positi9e
because a larger number of bacilli are
found in the pleural space.[%!) The
e<udati9e effusion in $$T de9elops in
three phases. The first phase is the
e<udati9e phase where *5*T typically
shows smooth thicening and
enhancement of the 9isceral and parietal
pleura with loculated effusion within
7split pleura sign8. [!") There may be
septations and echogenic debris within,
which are better appreciated on B-0.
The latter are more characteristic of the
second phase, the fibrino‐ purulent stage.
t this time, the effusion may consist
entirely of pus 7empyema8 when there
may be associated rib crowding onimaging and 9olume loss as well. This
empyema may brea through the parietal
pleura to form a subcutaneous abscess
7empyema necessitans8. ppearance of
air ‐fluid le9el in empyema suggests
communication with the bronchial tree
7bronchopleural fistula8. The latter
presents as increasing e<pectoration, air
in the pleural space, and changing air ‐
fluid le9el. *T is the in9estigation of
choice and may demonstrate the e<act
site of communication between the
pleural space and the bronchial tree or
lung parenchyma.[%2)
The final phase is the organi;ing phase
and includes chronic empyema and
fibrothora<. *hronic empyemas appear
as persistent focal fluid collections with
pleural thicening and calcification with
e<trapleural fat proliferation.
?ibrothora< manifests as diffuse pleural
thicening with 9olume loss, but without
effusion, and suggests inacti9ity. $leural
thicening and calcifications are the
fre=uently encountered features of
healed T.
hen *@+ suggests pleural effusion,
thoracocentesis and pleural fluid analysis
7biochemical, cytological, and
microscopic e<amination8 should be
done. #n addition, sputum induction for
? and culture is recommended in all
patients suspected to ha9e T pleurisy.
[%%) -traw‐colored fluid with large
number of cells 7in hundreds>
predominantly mononuclear8, high
protein le9el 7L% g/dl8, and ele9ated
adenosine deaminase 7D8 le9els
suggest T.[%() D le9els greater than
( B/l in the pleural fluid ha9e a high
predicti9e 9alue in areas with high T
pre9alence, and the specificity of this
en;yme increases if the e<udate is
predominantly lymphocytic.[%%) $leural
biopsy may be performed when the
thoracocentesis findings are
inconclusi9e.
Tracheobronchial TB
Tracheobronchial in9ol9ement occurs in
2‐(F of patients with $T.[%") #t
usually occurs as a complication of
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primary T, originating from perforation
of an in9ol9ed A3 into a bronchus,
though it may occur in $$T as well by
ascending endobronchial spread.[!")
Aymphatic submucosal spread andhematogenous infection may also be
responsible. *T in acute
tracheobronchitis may re9eal
circumferential narrowing of the
in9ol9ed segment associated with
smooth or irregular wall thicening.
[%&,%') bnormal enhancement and
adjacent adenopathy may also be seen.
Aess commonly, ulcerated polypoid
mass or peribronchial soft tissue cuff
may be seen.[%') #n9ol9ement of the
small airways is in the form of acute
bronchiolitis with centrilobular Itree‐in‐
budJ nodules.
This granulomatous in9ol9ement of the
tracheobronchial tree can ulcerate, which
on healing produces fibrotic
bronchostenosis and post‐obstructi9e
bronchiectasis. Aong segment
in9ol9ement is common and left main
bronchus is most fre=uently in9ol9ed.
[%") These bronchial strictures can lead
to lobar or segmental collapse which
may be e9ident on *@+. Cowe9er, the
more common cause of bronchiectasis in
T is cicatricial bronchiectasis as a
result of destructionHfibrosis of lung
parenchyma. *alcified peribronchial
A3s can erode into or cause distortion of
adjacent bronchus 7more common on the
right side8, producing broncholiths.
$resence of calcium near an area of lung
collapse may be a subtle indicator of
broncholithiasis.[%E) -econdary
amyloidosis may also de9elop in this
bacground of chronic inflammation.
Tuberculoma
Tuberculomas are persistent nodules or
mass‐lie lesions which can be seen in
both primary T and $$T. $ulmonary
tuberculomas can range in si;e from
being subcentimetric to " cm in
diameter, and may be solitary or
multiple. They are most often the result
of healed primary T and are usually
smooth‐walled and sharply defined. The
majority of these lesions remain stable in
si;e and may calcify. 3odular or diffuse
calcification can be seen in 2‐%F of
tuberculomas.[%4) *a9itation is seen in
!‐"F of cases. #n EF of cases, small
round opacities 7satellite lesions8 may be
obser9ed in the immediate 9icinity of the
main lesion.[!")
Complications o' C&B
arious complications can occur. These
include
G$arenchymal complications
Gspergilloma coloni;ation in pre‐
e<isting tuberculous
ca9ities. -uch patients may also presentwith hemoptysis as the dominant
symptom
GDestructi9e lung changes
G-car carcinoma ‐ co‐e<istence or
secondary de9elopment of malignancy
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Girway complications ‐
tracheobronchial in9ol9ement 7including
broncholithiasis and secondary
amyloidosis8
Gascular complications7pseudoaneurysms, hypertrophied
bronchial arteries, and systemic
collaterals8, which present with
hemoptysis
G$leural complications 7chronic
empyema, fibrothora<, bronchopleural
fistula, and pneumothora<8G ediastinal
complications: ediastinal fibrosis,
esophageal in9ol9ement 7in the form of
strictures, traction di9erticulae, or
fistulae8, pericarditis, pneumothora<, and
spondylodisitis.
maging 'indings o' active C&B
The imaging findings of acti9e *T are
presented in Table 2 and ?igures 2 and %.
&able +: ndicators o' C&B disease
activity on C,R and C&
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* 5
(igure + -A.E/: *hest radiographs in
acti9e T. 78 *@+ depicts +T upper
;one consolidation with prominent +Thilum. 78 *@+ in a different patient
shows multiple coalescent airMspace
nodules in +T upper ;one. 7*8 *@+ in adifferent patient shows multiple illM
defined reticuloMnodular lesions in both
lungs with basal predominance,suggesti9e of miliary T. 7D8 *@+ in a
different patient shows acti9e postM
primary T. *a9ity with surrounding
consolidation is seen in AT upper ;one.-cattered airMspace nodules are seen in
both lungs with left hilar adenopathy. 758
There is +TMsided loculated pleuraleffusion with multiple airMspace nodules
scattered in both lungs
normal *@+ has a high negati9e
predicti9e 9alue for the presence of
acti9e T. On the other hand, presence
of characteristic radiographic findings inappropriate clinical setting may be
sufficient to diagnose T e9en in the
absence of sputum positi9ity> and no
further in9estigation is re=uired. 59en
then, disease acti9ity may not be
accurately assessed by radiographs and
the fre=uency of false‐negati9es is
higher in C#‐ positi9e patients.[2(‐2&)
Temporal change o9er serial radiographs
is fre=uently employed to assess
response to TT and e9olution of newlesions may suggest reacti9ation in the
proper clinical setting. 3o significant
radiographic change o9er (‐ to &‐month
inter9al is termed Iradiographically
stableJ disease and generally indicates
disease inacti9ity.[4)
?ollowing are the imaging findings
which suggest acti9e T:
G *onsolidation: usually located in lung
apices and/or superior segments of lower
lobes.[() *T is more sensiti9e and can
detect subtle and smaller consolidations.
$resence of consolidation is non‐specific
for the etiology of infection>
ne9ertheless, consolidation with
ipsilateral hilar/paratracheal A3
enlargement is strongly suggesti9e of T. On *T, the majority of
consolidations are peribronchial or
subpleural in location. *onsolidations
in9ol9ing multiple lung segments are
more liely to ha9e positi9e ? smear
results.[(!) *onsolidations in the basal
segments of lower lobes are unliely to
be associated with T, though they may
be seen in elderly patients.[(2)
Aobular consolidations fa9or T, while other
bacterial infections are more liely to
present with segmental
consolidation[(%)
G Thic ‐ walled ca9ity: thic ‐walled
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ca9ities are fre=uently seen in patients
with early acti9e T and represent
necroti;ing consolidation in the early
stage. *a9ities, consolidations, and
nodules in the upper lung fields suggest
acti9e T in se9eral prediction
models[(!,(()
(igure 0 -A.G/: *hest *T in acti9e T.78 Aung window 7window center M&
CB, width !2 CB8 of chest *T depicts
centrilobular and clustered nodules in posterior segment of +T upper lobe,
suggesting acti9e endobronchialinfection. 78 Aung window of chest *Tin a different patient shows ca9ity with
surrounding consolidation in
apicoposterior segment of AT upper lobe.
ultiple centrilobular nodules with treeMinMbud branching pattern are also seen.
7*8 -agittal multiplanar *T reformat
lung window shows segmentalconsolidations in +T upper lobe. 7D8
<ial *T section lung window 7in the
same patient as in ?igure !c8 in miliaryT shows multiple tiny discrete nodules
randomly distributed in both lungs. 758
<ial *5*T mediastinal window
7window center ( CB, width ( CB8shows conglomerate rimMenhancing
lymphadenopathy in paratracheal
locations and multiple enlarged lymph
nodes in pre9ascular location as well
showing central necrosis. 7?8 <ial
*5*T mediastinal window shows +TMsided effusion with enhancing layers of
pleura 7split pleura sign8 and rib
crowding suggesti9e of empyema. 708<ial nonMcontrast *T mediastinal
window shows ATMsided free effusion
• *a9ity with air ‐fluid le9els: air ‐fluid
le9els in tuberculous ca9ities ha9e
been reported to be an indicator of
superimposed bacterial or fungal
infection[4)
• cinar / centrilobular nodules
7bronchogenic spread8: ill‐defined
fluffy air ‐space nodular opacities 7"‐
! mm8 are indicators of acti9e
disease on *@+s.[%) These nodules
may coalesce, resulting in focal area
of bronchopneumonia. *T features
of endobronchially disseminated T
include centrilobular nodules and
sharply marginated linear branching
opacities 7tree‐
in‐
bud sign8 alongwith bronchial wall thicening and
narrowing. These indicate acti9e
disease and correspond to bronchitis
of the small airways. $resence of
centrilobular nodules and tree‐in‐ bud
appearance on *T is more sensiti9e
than radiographs in detection of
acti9e endobronchial disease.[(")
Other causes of tree‐in‐ bud nodules
include infections 7bacterial, fungal,
9iral, or parasitic8, bronchiolitis,
aspiration or inhalation of foreign
substances, connecti9e tissue
disorders, and neoplastic pulmonary
emboli
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• *lustered nodules: Aarge nodular
opacities 7!‐( cm8 may result due
to coalescence of smaller
nodules. These usually ha9e
irregular margins and are
surrounded by tiny satellite
nodules. These may appear as
nodular patches or masses on
*@+. -uch nodule clusters,
especially in a peribronchial
distribution are an indicator of
acti9e disease.[(,(!) Aarger
nodules 7L! cm8 are seen in
1aposiNs sarcoma 7in C#8 and
lymphoma.[(&) Aarge nodules
with surrounding ground‐glass
and internal ca9itation fa9or a
diagnosis of fungal
infections[(&)
• iliary nodules: -mall 7!‐%
mm8, well‐defined, randomly
distributed nodules that indicate
hematogenous spread of
infection. These may be
inconspicuous on radiographs
and e9ident only on C+*T,
which may also show associated
septal thicening[(')
• +im‐enhancing A3s: 5nlarged
A3s 7short a<is dimension L!
cm8 with peripheral rimenhancement and central low
attenuation suggest acti9e
disease, while homogeneous and
calcified nodes represent inacti9e
disease.[(E) Aow attenuation
areas ha9e a pathological
correspondence to caseous
necrosis and are thus a reliable
indicator of disease acti9ity.
*onglomeration of A3s and
obscuration of perinodal fat are
also associated with acti9e
disease.[!4) Comogeneously
enhancing lymphadenopathy
without calcification poses a
diagnostic dilemma. iral and
fungal infections are less liely
to be associated with
lymphadenopathy, thus presence
of enlarged A3s fa9ors
T[(4,")
• $leural effusion or empyema:
Bnilateral free effusion and
empyema suggest acti9e disease,
while isolated pleural thicening
with or without calcification
indicates healed T. #t may be
borne in mind that imaging
modalities lie *@+ and *T
ser9e to detect and locali;e thedisease,[%() and based on site
and morphology of findings,
diagnosis of acti9e T may be
suggested. Definiti9e diagnosis
of acti9e T still re=uires
isolation and identification of M.
tuberculosis, especially if the
clinical/laboratory profile is
e=ui9ocal. Table 2 delineates
features which are definiti9e of
acti9e T [?igures 2 and %),
definiti9e for healed T
7se=uelae8 [?igure (), and
features indeterminate for disease
acti9ity [?igure "). ?igure &
demonstrates e<amples of
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complications in *T. hen *T
features indicate T but are
indeterminate for disease acti9ity,
then other criteria lie
bronchoal9eolar la9age [A)
7in case of parenchymal
in9ol9ement8, laboratory
parameters 7erythrocyte
sedimentation rate 5-+, *‐
reacti9e protein *+$, total and
differential leuocyte counts
TA*, DA* respecti9ely, and
antou< test8, sampling for A3s,
thoracocentesis for effusion,
clinical response, and follow‐
upmay be employed to resol9e the
ambiguity. ?ollowing features are
not specific for T and further
wor ‐up to e<clude other
diagnoses lie non‐tubercular
infections, non‐infectious
diseases 7lie sarcoidosis,
(igure 1 -A.(/: #maging features of healed T. 78 *@+ shows thinM walled
ca9ity in left upper ;one. reas of fibroM bronchiectasis and fibrocalcific lesionsare seen in left upper ;one, +T upper and
mid ;ones. 78 <ial *T lung window
7window center M& CB, width !2CB8 shows clustered thinMwalled ca9ities
in superior segment +T lower lobe. 7*8
*@+ shows 9olume loss in both upper
;ones with apical pleural thicening,
pulled hila, fibroMbronchiectasis, and
calcific foci. 7D8 *@+ shows fibroM bronchiectasis both upper ;ones. 758
*5*T mediastinal window 7window
center ( CB, width ( CB8 showsleftMsided pleural thicening and focal
pla=ueMlie calcifications. 7?8 *T lung
window section in endMstage lungdisease shows collapse and
bronchiectasis in9ol9ing the left lung
with ipsilateral mediastinal shift and rib
crowding.
serositis8, and e9en malignancies
7lymphoma, carcinoma8 should be
undertaen:
G *onsolidation without ipsilateral
lymphadenopathyG #maging features of
acti9e endobronchial infection in the
non‐typical locationsG #maging features
of acti9e endobronchial infection in the
presence of T se=uelae. These may
represent superimposed secondary
infection 7usually pyogenic8 or
reacti9ation T
G Thic ‐walled ca9ity may be seen in
malignancyG ilateral hilar
lymphadenopathy. *ommonly seen in
sarcoidosis and lymphomaG 3ecrotic
mediastinal A3s may also occur in
malignancies and fungal infectionsG
ilateral free effusion is more liely to
be non‐infecti9e in etiology 7serositis /
underlying heart, li9er, or renal disease8.
maging Signs o' 2ealing -&B
Se3uelae/
The imaging signs of healing 7T
se=uelae8 are presented in Table 2 and
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?igures ( and '.
#maging findings in patients with T
se=uelae include broncho9ascular
distortion, fibro‐ parenchymal lesions,
bronchiectasis, emphysema, and fibro‐
atelectatic bands indicati9e of prior
infection with scarring.[4) Thin‐walled
ca9ities and well‐defined nodules may
persist for a long time after completion
of TT. The former may get coloni;ed
by saprophytic fungi 7aspergilloma8 and
the latter may get calcified. *alcified
mediastinal A3s and pleural thicening
7with/without calcification8 are alsoimaging
(igure 4 -A.C/: #maging featuresindeterminate for disease acti9ity in
*T. 78 <ial *T lung window
7window center M& CB, width !2CB8 shows consolidation in basal
segments of left lower lobe. 3o
ipsilateral adenopathy, no ca9itation wasseen. 78 *5*T mediastinal window
7window center ( CB, width ( CB8
shows ca9ity with airMfluid le9el in +T
upper lobe. 3ote is also made of bronchiectasis and apical pleural
thicening. 7*8 <ial *5*T mediastinal
window shows small discretehomogeneous lymph node in +T hilar
location, measuring ! mm in short
a<is dimension 7-D8. This node wasunchanged in si;e and morphology after
complete course of TT
features of healed T. Tuberculomas and
small calcified lung nodules also suggest
prior infection.
#maging features of healed T may bedetected incidentally or patients may
only ha9e some minor symptoms. #n
such cases, no further imaging is
re=uired, especially if a comparison with
prior imaging suggests stability of
findings, and symptomatic management
is done. Cowe9er, if the symptoms are
se9ere and refractory, then an initial *T
is usually done for comprehensi9e
assessment of lungs, A3s, and pleura.
ased on this, definiti9e management
7surgery for locali;ed fibro‐
bronchiectatic disease8 or palliati9e
measures may be undertaen [bronchial
artery emboli;ation 758 for
hemoptysis, bronchoscopy‐guided or
percutaneous antifungal instillation for
persistent fungal ball in pre‐e<isting
tuberculous ca9ities). The initial *T also
ser9es to rule out any reacti9ation or to
detect any superimposed bacterial
infection.
!ersistent lesions at the end o'
treatment
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$ersistent lesions on *@+ at the end of
treatment indicate residual lesions in
which case acti9ity needs to be resol9ed
using imaging and/or laboratory
parameters. The residual inacti9e lesions
do not re=uire any treatment, whereas in
case of partial or no response, treatment
is prolonged
(igure 5 -A.E/: #maging findings in
tuberculous complications. 78 <ial *T
lung window 7window center M& CB,width !2 CB8 shows thinM walledca9ities in both upper lobes and presence
of aspergilloma in +T upper lobe ca9ity.
78 <ial *5*T mediastinal window7window center ( CB, width ( CB8
shows contrastMfilled pseudoaneurym
7arrow8 arising from the superior di9ision of +T pulmonary artery
7+asmussen aneurysm8 in the
bacground of fibroMca9itary lesions in
both upper lobes. 7*8 <ial *5*Tmediastinal window shows chronic
empyema AT side with 9olume loss and
pleural calcifications. 7D8 *oronal *Tlung window depicts abnormal
communication of pleural space with
bronchial tree suggesting a bronchopleural fistula. 758 <ial *5*T
mediastinal window shows calcified A3
in +T hilum causing postM obstructi9e
atelectasis of +T middle lobe
and follow‐up is repeated after e<tension
of intensi9e phase/continuation phase7#$/*$8 as per the re9ised national
tuberculosis control program 7+3T*$8
guidelines. 3o further imaging/treatment
is re=uired when *@+ or *T is
definiti9e for healed T. -econdly,
persistent lesions may represent drug‐
resistant T, in which case sampling and
drug susceptibility testing is
recommended. ppearance of new
lesions or reappearance of radio‐
opacities may represent reacti9ation T
or superimposed bacterial infections.
Thirdly, persistent lesions may suggest
the possibility of alternati9e diagnoses
and additional wor ‐up may be
undertaen to in9estigate the patient for
the same.
Recommendations
Imaging algorithm for diagnosis of
CTB
?igure E depicts the proposed algorithm.
s per the +3T*$, any person with
cough for 2 or more wees is a $T
suspect.["!) $resence of fe9er,
une<plained loss of appetite/weight, and
recent contact with an infectious patient
further raise the suspicion. #n addition to
sputum smear e<amination, all such
patients should be subjected to a *@+,
where9er feasible. *@+ has been
justified as an initial in9estigation in the
e9aluation of childhood T as well.[%()
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*@+ is also desirable in a patient
suspected/diagnosed to ha9e
e<trathoracic T, as a baseline wor ‐up.
(igure 6: #maging worMup of
symptomatic patients suspected/detectedto ha9e T se=uelae
#f the patient is sputum smear positi9e,
TT can be started irrespecti9e of the
*@+ findings. Though *@+ is liely to
be abnormal in majority of such cases,
up to 4F patients with culture‐confirmed
$T can ha9e normal radiographs, more
so in case of C#‐infected population.
["2) 59en then, initial *@+ ser9es as a
reference standard for comparison with
future studies.
#n case of sputum negati9ity or inability
of the patient to produce sputum, *@+
ser9es a pi9otal role in guiding
management. #f the radiographic
findings suggest acti9e T, TT may be
started if the clinical/laboratory profile is
also concordant. #n case the latter is
e=ui9ocal and not specific for T,
confirmation with *5*T is needed.
*5*T is also indicated when the *@+ is
indeterminate for disease acti9ity. #f the
*@+ suggests healed T, then as
delineated in ?igure ', comparison with
prior imaging is desirable to document
stability, failing which a *T is usually
done to confirm absence of acti9e
infection. #t may be noted that the initial
*T e9aluation in a *T suspect should
be a contrast‐enhanced study. #n addition
to being more sensiti9e, *5*T is
especially useful to characteri;e
mediastinal A3s, effusion, and to
confirm the parenchymal findings. #n the
unusual scenario of negati9e sputum and
normal *@+ in a *T suspect, *5*T
may still be undertaen if the clinical
suspicion is strong> howe9er, other
in9estigations may also be donedepending on the dominant symptom
7bronchoscopy/B-0 abdomen8.
ased on the *5*T findings, the
radiologist should categori;e the patient
into one of the three categories [?igure
4). *T may be definiti9e for acti9e T,
wherein TT can be started. $resence of
e9en a single imaging criterion of
acti9ity in a suspected case of T issufficient to diagnose acti9e disease and
warrants TT. Demonstration of ? is
desirable and adds supporti9e e9idence,
but is not mandatory. Cowe9er, if
clinically T is not the most liely
possibility, then single criterion of
acti9ity needs to be confirmed
bacteriologically or other supporti9e
e9idence may be sought 7blood/pleural
fluid parameters, pathological
confirmation8. #f the *T features suggest
healed T 7and there is no e9idence of
acti9e infection8, then based on
symptoms, palliati9e/ definiti9e
treatment is undertaen. #n case *5*T is
indeterminate for disease acti9ity, other
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parameters lie A, lab parameters, or
sampling come to rescue. $atient is
wored up for alternati9e diagnosis if
*5*T findings do not suggest T.
Imaging indicators of active TB, healed
TB, and features indeterminate for
disease activityTable 2 enumerates the
imaging features of disease acti9ity on
*@+ and *T.
#n a diagnosed case of *T, these
features help in assessing the disease
acti9ity at the time of presentation and
during follow‐up. #maging features
indeterminate for disease acti9ity include
e=ui9ocal radiographic findings, signs of
acti9e endobronchial infection in non‐
predisposed locations, and non‐specific
e9idence of acti9e infection 7which may
suggest superimposed secondary
infections8.
(igure 7: ?lowchart depicting the role
of imaging in diagnosis of *T 7Plab
profile includes hematological parameters lie 5-+, *+$, TA*, DA*,
and antou< test8
(igure 8: ?lowchart demonstrating the
stratification of patients after *T. ased
on *T findings, the patient should becategori;ed into either acti9e T, healed
T, or indeterminate for disease acti9ity
(igure )9: #maging protocol for followM
up of $T and mediastinal nodal T 7#$Q #ntensi9e phase8
(igure )): #maging protocol for followM
up of pleural T 7#$ Q #ntensi9e phase8
Protocol for follow‐up
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?igures ! and !! show the protocol for
follow‐up of *T patients.
ith compliant treatment, clinical
impro9ement is e<pected within 2‐(
wees. ?ollow‐up is done at the end of
#$ and *$. #n case of no response,
follow‐up is repeated after e<tension of
#$/*$ as per the +3T*$
guidelines/institute protocol. #f the
patient was sputum‐smear positi9e to
begin with, then follow‐up is usually
done with sputum‐smear e<amination.
Cowe9er, problems arise when such
patients become unable to producesputum but other symptoms persist.
lso, if sputum becomes negati9e but
clinical impro9ement is discordant, then
imaging pro9ides a 9iable option for
response assessment.
?igure ! depicts the imaging protocol
for follow‐up of pulmonary and nodal
types of *T. *@+ is done at the
completion of #$ of the treatmentregimen. #f there is significant resolution
of findings or *@+ depicts only
se=uelae of prior infection, then no
further imaging is needed e9en at the
end of treatment regimen, pro9ided there
is clinical impro9ement as well. This is
e9en applicable to those cases where
initial disease was e9ident only on *T.
-cenario 2 7partial response8 merits a
*@+ at the completion of TT course. #f at the end of treatment, *@+ is
consistent with scenario !, then TT can
be stopped. Cowe9er, if there is scenario
2 at the end of treatment, then the *$
may be prolonged depending on clinical
and laboratory parameters. #n case of no
definite response on *@+ and absence
of clinical impro9ement 7scenario %8, *T
may be done to assess disease acti9ity.
3on‐contrast *T 7with C+*T
reconstructions8 is sufficient for follow‐
up of solely parenchymal lesions, but
contrast administration is re=uired for
follow‐up of nodal disease. #$ of TT
may be prolonged in case *T suggests
residual acti9e disease or if *T is
indeterminate but clinical and laboratory
parameters do not suggest any response.
#f the nodes persist at the completion of
treatment regimen, or *5*T is e=ui9ocal
for disease acti9ity, then multiparametric
+# may help. The latter, being a
radiation‐free alternati9e, can be
employed instead of *T for follow‐up in
young patients. #t may be noted that
residual nodes do not necessarily
indicate acti9e disease.[!4) #f there is
good clinical response after the
completion of treatment regimen with
significant reduction in A3 si;e
compared with the initial scan, then few
persistent A3s may not suggest acti9e
disease and can be ept on follow‐up.
?igure !! demonstrates the imaging
follow‐up in case of pleural T. The
main difference from follow‐up of
$T/nodal T is that B-0 is
recommended to loo for
loculations/thicening in case of no
response or partial response at the end of
#$, so that further management can be
decided accordingly.
Symptomatic TB sequelae
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The imaging features of T
se=uelae/healed T are presented in
Table 2.
$atients presenting with refractory
respiratory symptoms7persistent/recurrent cough,
e<pectoration, hemoptysis, dyspnea8,
with or without prior history of TT,
need e9aluation using *@+. ?igure '
demonstrates the imaging approach to
such patients. The same flowchart
should be followed for patients
incidentally detected to ha9e T
se=uelae on imaging and for those
clinically suspected to ha9e acti9e T
but were found to ha9e se=uelae on
*@+.
comparison with pre9ious radiographsor *T e<aminations 7if a9ailable8 is 9ery
important. #f *@+ suggests T se=uelae
and there are no new lesions compared
with pre9ious imaging, then no further
imaging is indicated unless some
inter9ention lie 5 is planned.
Cowe9er, if
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no prior imaging is a9ailable, then an
initial *5*T is usually done to confirm
the radiographic findings. *T findings of acti9e infection may suggest a
superimposed infection, usually bacterial
or reacti9ation T. #f the patient presents
with significant hemoptysis, then *T
thoracic angiography may be done to
map out the abnormal arteries in order to
plan for 5.
eporting template
structured reporting format for
reporting chest *T in a
suspected/follow‐up case of *T is
proposed in Table %.
Conclusion
#n this re9iew, we ha9e attempted to
summari;e the criteria to differentiate
acti9e T from se=uelae andacnowledge that in conditions where
imaging is indeterminate, other
parameters be taen into consideration.
Cowe9er, a discussion of non‐
radiological parameters is beyond the
scope of the current re9iew. e ha9e
attempted to formulate algorithms for
imaging recommendations in the
diagnosis and follow‐up of patients with
suspected/ pro9en *T. ?urther research
is, howe9er, re=uired for 9alidation of
these recommendations and the same
may be re9ised subject to emergence of
new information. The proposed
recommendations are not intended for
application in national programs/at
primary health care le9el, but are more
applicable to secondary and tertiary care
centers. #n fact, we e<pect that these
algorithms would enable judicious use of
imaging and reduce the number of
unnecessary *T e<aminations in the
diagnosis and follow‐up of these cases.
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O;tr 5, et al . $atterns of delays in diagnosis
amongst patients with smear ‐ positi9e pulmonary
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#m R0, #toh C, -him S-, Aee RC, hn R, Can*, et al . $ulmonary tuberculosis: *T findings‐
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!44%>!E&:&"%‐&.
Reong SR, Aee 1-. $ulmonary tuberculosis: Bp‐
to‐date imaging and management. R+ m R
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CO 0lobal tuberculosis report 2!%. 9ailablefrom: http://www. who.int/tb. [Aast accessed on
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#to #, #shida T, Togashi 1, 3iimi , 1oyama C,
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Ceussel *$, 1auc;or CB, Ceussel 0, ?ischer ,
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+aniga -, $arih 3, rora . #s C+*T reliable
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!. +i;;i 5, -chininaN , *ristofaro , 0oletti D,
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