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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 imaging recommendations 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 followup 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 acidfast bacilli 7?8 on sputum microscopy. *hest radiograph 7*@+8 finds its place in sputumnegati9e patients not responding to a course of antibiotics. Though computed tomography 7*T8 is fre=uently employed in the diagnosis

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Page 1: Journal Radiology Chest TB

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

Access this article online

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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

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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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