Beruflich Dokumente
Kultur Dokumente
23]
Chest Radiology
Correspondence: Dr.Ashu Seith Bhalla,Department of Radiodiagnosis, All India Institute of Medical Sciences, Ansari Nagar,
NewDelhi110029, India. Email:ashubhalla1@yahoo.com
Abstract
Chest tuberculosis(CTB) is a widespread problem, especially in our country where it is one of the leading causes of mortality. The article
reviews the imaging findings in CTB on various modalities. We also attempt to categorize the findings into those definitive for active TB,
indeterminate for disease activity, and those indicating healed TB. Though various radiological modalities are widely used in evaluation
of such patients, no imaging guidelines exist for the use of these modalities in diagnosis and followup. Consequently, imaging is not
optimally utilized and patients are often unnecessarily subjected to repeated CT examinations, which is undesirable. Based on the available
literature and our experience, we propose certain recommendations delineating the role of imaging in the diagnosis and followup of such
patients. The authors recognize that this is an evolving field and there may be future revisions depending on emergence of new evidence.
Key words: Chest radiograph; chest tuberculosis(pulmonary, nodal and pleural); computed tomography; imaging recommendations;
TB active
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these are preventable and that curative regimens have been USG Sonography is very useful for pleural effusion
available for a long time now. detection, characterization, guiding drainage, and
followup. Differentiating minimal effusion from
Chest TB residual thickening is a common indication. USG can
also be used to evaluate associated hepatosplenomegaly,
TB can affect any organ system, although manifestations are ascites, and abdominal lymphadenopathy
most commonly related to the chest. The lungs are the most CT chestMultidetector CT(MDCT) is an important
common and often the initial site of involvement. Chest tool in the detection of radiographically occult disease,
involvement is most commonly pulmonary, followed by differential diagnosis of parenchymal lesions, [7]
lymph nodal and pleural disease(latter two are included evaluation of mediastinal lymph nodes(LNs), assessing
under EPTB). Chest wall, cardiac, breast, and skeletal disease activity, and evaluating complications. It not
involvement can also occur in the thorax; however, these only enables earlier and more accurate diagnosis of
are beyond the scope of the current review. In the current pulmonary lesions, but also can be used to differentiate
review, we discuss the most common types of CTB, namely the etiologies of pneumonia.[7,8] CT enables evaluation
PTB and EPTB(pleural/lymph nodal). Cough greater than of bronchiectasis, cavitation, associated fungal balls,
2weeks is the primary criterion to suspect PTB. Patients of and assessment of necrosis in the LNs, identifying
PTB/EPTB also present with fever, loss of appetite and loss pleural/airway/diaphragmatic pathologies and
of weight, chest pain or dyspnea. evaluating visualized bones. Contrastenhanced
CT(CECT) is the investigation of choice for evaluation
Role of imaging in CTB of mediastinal LNs and also aids in depicting pleural
Diagnosis enhancement in empyema. Highresolution CT(HRCT)
Treatment evaluation response assessment, residual reconstructions are especially useful to detect miliary
activity and centrilobular nodules, groundglass opacities, and
Detection of disease complications/sequelae. airtrapping. Table1 outlines the various situations
where CT chest is recommended. The value of CT lies in
Imaging modalities the fact that it enables one to suggest a diagnosis of TB
CXRSputum smear microscopy, culture for AFB, in patients with negative sputum examination and those
and CXR posteroanterior(PA) view are the initial without sputum production[as occurs in the followup
investigations performed in adults suspected to have TB. of patients on antituberculosis therapy(ATT) or at
CXR is frequently employed as the initial test to evaluate presentation] noninvasively. Moreover, CT findings
unexplained cough. It is the primary modality for may permit empirical initiation of ATT until the time
diagnosis and followup, and may be the only imaging culture results are obtained[9]
required in sputumpositive cases. Apicogram/lordotic MRI MRI is a problemsolving modality and
view(for lung apices) and lateral view are of limited conventional sequences(T1 and T2W images) should be
utility and CT is the next investigation in case of combined with diffusionweighted imaging(DWI) and
equivocal CXR. CXR is useful to look for any evidence subtracted contrastenhanced(CE) imaging for optimal
of PTB as well as to identify other abnormalities evaluation. It can be used to better evaluate mediastinal
responsible for the symptoms. Table1 delineates the nodes and assess disease activity in case of mediastinal
indications of CXR nodes/fibrosis. Since it is free from ionizing radiation,
Table1: Indications of doing a chest radiograph and CT(in the context of CTB)
When to do chest radiograph? When to do CT?
Evaluation of patients suspected to have TB Evaluation of patients suspected to have TB
Evaluation of patients with unexplained cough and expectoration For diagnosis of CTB in case of sputum negative patient with equivocal
CXR or/and equivocal clinical profile)
Evaluation of unexplained fever or constitutional symptoms Initial CECT for complete disease assessment in patients suspected to
(loss of appetite or weight) have additional extrathoracic involvement
In a patient suspected/diagnosed to have extrathoracic TB, as a baseline workup In a diagnosed case of CTB for assessment of disease activity in case of
In a diagnosed case of CTB Persistent lesions(pulmonary/nodal/effusion) on CXR
After the completion of intensive phase, for assessing treatment response Radiographic worsening
After the completion of treatment regimen in selected cases(refer flowcharts) Equivocal CXR in absence of clinical response
After any intervention(chest tube, etc.) In evaluation of symptomatic patients with suspected TB sequelae: when
no prior radiographs available for comparison or if evolution of new findings
In evaluation of symptomatic patients Imaging of suspected complications of TB
(e.g hemoptysis, dyspnea, cough with expectoration) with past history of TB
CT: Computed tomography, CTB: Chest tuberculosis, TB: Tuberculosis, CXR: Chest radiograph
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MRI can be employed for followup of mediastinal for 2334% of all adult cases and even more in nonendemic
nodal disease in young patients to reduce radiation areas.[13,14] The primary parenchymal focus is known as
exposure. Presence of diffusion restriction in the LNs the Ghon focus and the combination of Ghon focus and
and peripheral enhancement suggest active disease. MRI enlarged draining LNs constitutes the primary complex:
has been proven to be superior to noncontrast CT in the The Ranke or Ghon complex.[15]
evaluation of mediastinal nodes, pleural abnormalities,
and presence of caseation.[10] It may serve as a reasonable Primary TB may involve lung parenchyma, LNs,
alternative to CT for lung parenchymal evaluation in tracheobronchial tree, and pleura. Classically, four entities
pregnant patients.[10] Cost and availability issues are the are described: Gangliopulmonary TB, TB pleuritis, miliary
main limitations TB, andtracheobronchialTB.[15] Only the gangliopulmonary
Positron emission tomographyCT fluorodeoxyglucose form is characteristic of primary TB and the rest may be seen
positron emission tomography (FDGPET) plays in postprimary disease as well.
an important role in the workup of patients with
pyrexia of unknown origin (PUO), owing to its high Gangliopulmonary TB is characterized by the presence of
sensitivity in the detection of infection, inflammation, mediastinal and/or hilar LN enlargement with associated
and malignancy.[11] Active TB shows increased uptake parenchymal abnormalities. LN enlargement is seen in up
with high standardized uptake values (SUVs) and may to 96% children and 43% adults with primary TB.[1618] Right
pose as a cancer mimic.[12] PET may help in assessing paratracheal, hilar, and subcarinal regions are the most
the disease activity and response to therapy.[11] Though common sites of nodal involvement, though other sites may
it is not specific for TB, FDGPET CT can guide biopsy also be affected. Bilateral adenopathy occurs in 31% cases.[17]
from active sites, assess complete disease extent, and The prevalence of adenopathy decreases with age.[17] CT
detect occult distant involvement. The use of PET CT in is better than CXR in detection and characterization of
evaluation of benign diseases is, however, limited due thoracic LN enlargement.[19] On CECT scan, the enlarged
to high radiation exposures involved. LNs show highly characteristic, but not pathogonomic,
rim sign attributed to lowdensity center surrounded
Primary and Postprimary TB by a peripheral rim enhancement.[20] This rim sign may
also be seen with atypical mycobacteria, histoplasmosis,
CTB is conventionally divided into primary and metastases(from head/neck/testicular malignancy), and
postprimary(or reactivation) TB(PPT), each with lymphoma.[15] Heterogeneous enhancement may also be
corresponding radiological patterns, albeit with seen. Homogeneous enhancement is more commonly found
considerable overlap. The radiological features depend in pediatric age group.[19] Associated lung infiltrates are
on age, underlying immune status, and prior exposure. seen on the same side as nodal enlargement in twothirds of
Figure1 depicts the natural history and progression of pediatric cases of primary PTB.[17] Parenchymal opacities are
the disease. usually located in the peripheral subpleural regions. They
may be difficult to see on radiographs; thus, CT is often
Primary TB is acquired by inhalation of airborne required to detect these subtle parenchymal infiltrates.[21]
organisms and occurs in patients not previously exposed CXRs may be normal in 15% of cases.[22] Contrary to the
to Mycobacterium tuberculosis. It commonly affects infants agerelated decrease in occurrence of lymphadenopathy, the
and children in endemic areas. However, primary TB is prevalence of radiographically detectable lung involvement
now increasingly encountered in adult patients, accounting is higher in older children and adults,[17,18] so much so
that primary infection in adults frequently manifests
as parenchymal consolidation without adenopathy. On
CT, the airspace consolidation in primary TB is dense,
homogeneous, and well-defined. Parenchymal disease in
primary TB commonly affects the middle and lower lung
zones on CXR, corresponding to the middle lobe, basal
segments of lower lobes, and anterior segments of upper
lobes.
adenopathy leading to retroobstructive pneumonia, and/or evident in 40% of cases, and walls may be thin and smooth
atelectasis. The latter is usually right sided, with obstruction or thick and nodular. Thickwalled cavities and cavities with
occurring at the level of the right lobar bronchus or bronchus surrounding consolidation indicate active infection, while
intermedius.[23] In 510% patients of primary TB, the infection thinwalled cavities suggest healed infection.[9]Thinwalled
is progressive and hematogenous dissemination occurs; this cavities may be difficult to differentiate from bullae, cysts,
is termed progressive primary TB, manifestations of which or pneumatoceles. Airfluid levels in the cavity occur in 10%
are identical to PPT.[9] of cases and can be due to superimposed bacterial or fungal
infection.[16,28] Fibroparenchymal lesions causing distortion
PPT occurs in previously sensitized patients and of lung parenchyma and cicatricial bronchiectasis develop
results either from reinfection or from reactivation with healing of active infection.
of dormant bacilli in primary infection(90% of cases)
owing to immunosuppression, malnutrition, senility, Tuberculous cavities can rupture into pleural space,
and debilitation.[24,25] Thus, PPT occurs predominantly in resulting in empyema and even bronchopleural fistula.
adolescents and adults and usually begins with necrotizing Erosion into the pulmonary artery branches can lead
consolidation followed by transbronchial spread.[9] to massive hemoptysis(Rasmussen pseudoaneurysm).
Erosion into systemic vessels or pulmonary veins can lead
PPT is characterized by: 1. Liquefaction of caseous necrosis, to hematogenous dissemination and miliary TB. Healing of
2. formation of cavities, 3. progressive fibrosis and lung PPT occurs with fibrosis and calcification.
destruction, and 4. bronchogenic spread.[15] Apicoposterior
segments of the upper lobes and superior segments of the Radiological patterns encountered in both primary and/or
lower lobes are the usual sites of involvement.[15] Initially, postprimary CTB
there is liquefaction of regions of caseous necrosis, which Miliary TB
then communicate with the tracheobronchial tree to form Miliary TB results from hematogenous dissemination of
cavities.Coughing may result in bronchogenic spread to the TB bacilli leading to the development of innumerable
other lung segments and/or may be a source of infection small granulomas in lungs and other organs. Though
for other patients via inhalation of bacilli-laden droplets. classically encountered in children, the incidence in
Fibroatelectasis is common, especially of the upper lobes adults is increasing.[15,26] Early in the course of the disease,
with retraction of the hilum, mediastinal shift, pulling up of CXR may be normal in 2540% of cases.[30] CT, especially
diaphragm, and compensatory hyperinflation of the normal HRCT, can demonstrate miliary disease before it becomes
lung segments. Associated pleural thickening, especially of radiographically apparent. Presence of 13mm nodules,
the lung apices, may be evident along with extrapleural fat both sharply and poorly defined, diffusely spread in
proliferation. Endstage TB may cause complete destruction random distribution in both lungs, often associated with
of the lung parenchyma resulting from a combination of interstitial septal thickening is characteristic.[25] There may
parenchymal and airway involvement. Contrary to the be some basal predominance due to gravitydependent
previous notions, recent studies[26] suggest that children and increased blood flow to the lung bases. Initially, the foci
adolescents are also equally prone to develop destructive are about 1mm in diameter. Untreated, they may reach
lung changes with severe sequelae, similar to PPT. The 35 mm in size and may become confluent, presenting a
similar location and morphology of parenchymal changes snowstorm appearance.
observed in children blurs the distinction between primary
and reactivation TB. Pleural involvement
Involvement of the pleura is one of the most common forms
Imaging in PPT often shows extensive abnormalities in of EPTB and is more common in the primary disease. In case
predisposed locations.[27] Features of active endobronchial of primary TB, it manifests as unilateral free large effusion,
infectionconsolidations, alveolar opacities on CXR, without loculations. It occurs 36months after infection, as a
clustered nodules, centrilobular nodules on CTare result of delayed hypersensitivity response to mycobacterial
hallmarks of active PPT. Bronchogenic spread is evident antigens.[15] It is often asymptomatic and microbiological
radiographically in 20% of cases and manifests as multiple, analyses are often negative. Though rare in children,
illdefined micronodules, in segmental or lobar distribution, it is common in adolescents and young adults. Pleural
distant from the site of cavitation and usually involving involvement can be seen in up to 38% cases of primary TB
the lower lung zones.[28] On CT scan, it is identified in 95% and up to 18% cases of PPT.[16] In PPT, effusion is usually
of cases making HRCT the imaging modality of choice small, loculated, and associated with parenchymal lesions.
to detect early bronchogenic spread.[3,29] Typical findings Since it originates from rupture of a cavity into the pleural
include 2to 4mm centrilobular nodules and treeinbud space, cultures are usually positive because a larger number
branching opacities(sharply marginated linear branching of bacilli are found in the pleural space.[31] The exudative
opacities around terminal and respiratory bronchioles).[3] effusion in PPT develops in three phases. The first phase is
Cavitation is also characteristic of PPT, radiographically the exudative phase where CECT typically shows smooth
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thickening and enhancement of the visceral and parietal This granulomatous involvement of the tracheobronchial
pleura with loculated effusion within (split pleura sign). tree can ulcerate, which on healing produces fibrotic
[15]
There may be septations and echogenic debris within, bronchostenosis and postobstructive bronchiectasis.
which are better appreciated on USG. The latter are more Long segment involvement is common and left
characteristic of the second phase, the fibrinopurulent main bronchus is most frequently involved. [35] These
stage. At this time, the effusion may consist entirely of bronchial strictures can lead to lobar or segmental
pus(empyema) when there may be associated rib crowding collapse which may be evident on CXR. However, the
on imaging and volume loss as well. This empyema may more common cause of bronchiectasis in TB is cicatricial
break through the parietal pleura to form a subcutaneous bronchiectasis as a result of destructionfibrosis of lung
abscess (empyema necessitans). Appearance of airfluid parenchyma. Calcified peribronchial LNs can erode
level in empyema suggests communication with the into or cause distortion of adjacent bronchus(more
bronchial tree(bronchopleural fistula). The latter presents common on the right side), producing broncholiths.
as increasing expectoration, air in the pleural space, and Presence of calcium near an area of lung collapse may
changing airfluid level. CT is the investigation of choice be a subtle indicator of broncholithiasis. [38] Secondary
and may demonstrate the exact site of communication amyloidosis may also develop in this background of
between the pleural space and the bronchial tree or lung chronic inflammation.
parenchyma.[32]
Tuberculoma
The final phase is the organizing phase and includes chronic
Tuberculomas are persistent nodules or masslike lesions
empyema and fibrothorax. Chronic empyemas appear as
which can be seen in both primary TB and PPT. Pulmonary
persistent focal fluid collections with pleural thickening and
tuberculomas can range in size from being subcentimetric
calcification with extrapleural fat proliferation. Fibrothorax
to 5cm in diameter, and may be solitary or multiple. They
manifests as diffuse pleural thickening with volume loss,
are most often the result of healed primary TB and are
but without effusion, and suggests inactivity. Pleural
usually smoothwalled and sharply defined. The majority
thickening and calcifications are the frequently encountered
of these lesions remain stable in size and may calcify.
features of healed TB.
Nodular or diffuse calcification can be seen in 2030% of
tuberculomas.[39] Cavitation is seen in 1050% of cases. In
When CXR suggests pleural effusion, thoracocentesis
and pleural fluid analysis (biochemical, cytological, and 80% of cases, small round opacities(satellite lesions) may
microscopic examination) should be done. In addition, be observed in the immediate vicinity of the main lesion.[15]
sputum induction for AFB and culture is recommended in
Complications of CTB
all patients suspected to have TB pleurisy.[33] Strawcolored
Various complications can occur. These include
fluid with large number of cells(in hundreds; predominantly
mononuclear), high protein level(>3g/dl), and elevated Parenchymal complications
adenosine deaminase (ADA) levels suggest TB.[34] ADA Aspergilloma colonization in preexisting tuberculous
levels greater than 40 U/l in the pleural fluid have a high cavities. Such patients may also present with hemoptysis
predictive value in areas with high TB prevalence, and as the dominant symptom
the specificity of this enzyme increases if the exudate Destructive lung changes
is predominantly lymphocytic.[33] Pleural biopsy may Scar carcinomacoexistence or secondary development
be performed when the thoracocentesis findings are of malignancy
inconclusive. A i r w a y c o m p l i c a t i o n s t r a c h e o b r o n c h i a l
involvement(including broncholithiasis and secondary
Tracheobronchial TB amyloidosis)
Tracheobronchial involvement occurs in 24% of patients Va s c u l a r c o m p l i c a t i o n s ( p s e u d o a n e u r y s m s ,
with PTB.[35] It usually occurs as a complication of primary hypertrophied bronchial arteries, and systemic
TB, originating from perforation of an involved LN into a collaterals), which present with hemoptysis
bronchus, though it may occur in PPT as well by ascending Pleural complications(chronic empyema, fibrothorax,
endobronchial spread.[15] Lymphatic submucosal spread and bronchopleural fistula, and pneumothorax)
hematogenous infection may also be responsible. CT in acute Mediastinal complications: Mediastinal fibrosis,
tracheobronchitis may reveal circumferential narrowing of esophageal involvement(in the form of strictures, traction
the involved segment associated with smooth or irregular diverticulae, or fistulae), pericarditis, pneumothorax,
wall thickening.[36,37] Abnormal enhancement and adjacent and spondylodiskitis.
adenopathy may also be seen. Less commonly, ulcerated
polypoid mass or peribronchial soft tissue cuff may be Imaging findings of active CTB
seen.[37] Involvement of the small airways is in the form of The imaging findings of active CTB are presented in Table2
acute bronchiolitis with centrilobular treeinbud nodules. and Figures2 and 3.
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A B C
A B
D E F
Figure 4 (A-F): Imaging features of healed TB. (A) CXR shows thin-
walled cavity in left upper zone. Areas of fibro-bronchiectasis and
fibrocalcific lesions are seen in left upper zone, RT upper and mid zones.
(B) Axial CT lung window (window center -600 HU, width 1200 HU)
shows clustered thin-walled cavities in superior segment RT lower lobe.
(C) CXR shows volume loss in both upper zones with apical pleural
thickening, pulled hila, fibro-bronchiectasis, and calcific foci. (D) CXR
shows fibro-bronchiectasis both upper zones. (E) CECT mediastinal
window (window center 40 HU, width 400 HU) shows left-sided pleural
thickening and focal plaque-like calcifications. (F) CT lung window C
section in end-stage lung disease shows collapse and bronchiectasis Figure 5 (A-C): Imaging features indeterminate for disease activity
involving the left lung with ipsilateral mediastinal shift and rib crowding in CTB. (A) Axial CT lung window (window center -600 HU, width
1200 HU) shows consolidation in basal segments of left lower lobe. No
ipsilateral adenopathy, no cavitation was seen. (B) CECT mediastinal
serositis), and even malignancies(lymphoma, carcinoma) window (window center 40 HU, width 400 HU) shows cavity with air-fluid
should be undertaken: level in RT upper lobe. Note is also made of bronchiectasis and apical
Consolidation without ipsilateral lymphadenopathy pleural thickening. (C) Axial CECT mediastinal window shows small
Imaging features of active endobronchial infection in discrete homogeneous lymph node in RT hilar location, measuring ~10
mm in short axis dimension (SAD). This node was unchanged in size
the nontypical locations and morphology after complete course of ATT
Imaging features of active endobronchial infection
in the presence of TB sequelae. These may represent features of healed TB. Tuberculomas and small calcified
superimposed secondary infection(usually pyogenic)
lung nodules also suggest prior infection.
or reactivation TB
Thickwalled cavity may be seen in malignancy
Imaging features of healed TB may be detected incidentally
Bilateral hilar lymphadenopathy. Commonly seen in
or patients may only have some minor symptoms. In
sarcoidosis and lymphoma
such cases, no further imaging is required, especially if
Necrotic mediastinal LNs may also occur in malignancies
a comparison with prior imaging suggests stability of
and fungal infections
findings, and symptomatic management is done. However,
Bilateral free effusion is more likely to be noninfective
in etiology(serositis/underlying heart, liver, or renal if the symptoms are severe and refractory, then an initial CT
disease). is usually done for comprehensive assessment of lungs, LNs,
and pleura. Based on this, definitive management(surgery for
Imaging Signs of Healing(TB Sequelae) localized fibrobronchiectatic disease) or palliative measures
may be undertaken[bronchial artery embolization(BAE)
The imaging signs of healing(TB sequelae) are presented for hemoptysis, bronchoscopyguided or percutaneous
in Table2 and Figures4 and 7. antifungal instillation for persistent fungal ball in
preexisting tuberculous cavities]. The initial CT also serves
Imaging findings in patients with TB sequelae include to rule out any reactivation or to detect any superimposed
bronchovascular distortion, fibroparenchymal lesions, bacterial infection.
bronchiectasis, emphysema, and fibroatelectatic bands
indicative of prior infection with scarring.[9] Thinwalled Persistent lesions at the end of treatment
cavities and welldefined nodules may persist for a long Persistent lesions on CXR at the end of treatment indicate
time after completion of ATT. The former may get colonized residual lesions in which case activity needs to be resolved
by saprophytic fungi (aspergilloma) and the latter may using imaging and/or laboratory parameters. The residual
get calcified. Calcified mediastinal LNs and pleural inactive lesions do not require any treatment, whereas
thickening (with/without calcification) are also imaging in case of partial or no response, treatment is prolonged
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A B
C D
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or other supportive evidence may be sought(blood/pleural active endobronchial infection in nonpredisposed locations,
fluid parameters, pathological confirmation). If the CT and nonspecific evidence of active infection(which may
features suggest healed TB(and there is no evidence of suggest superimposed secondary infections).
active infection), then based on symptoms, palliative/
definitive treatment is undertaken. In case CECT is Protocol for followup
indeterminate for disease activity, other parameters like Figures 10 and 11 show the protocol for followup of CTB
BAL, lab parameters, or sampling come to rescue. Patient patients.
is worked up for alternative diagnosis if CECT findings do
not suggest TB. With compliant treatment, clinical improvement is expected
within 24weeks. Followup is done at the end of IP and CP.
Imaging indicators of active TB, healed TB, and features In case of no response, followup is repeated after extension
indeterminate for disease activity of IP/CP as per the RNTCP guidelines/institute protocol. If
Table2 enumerates the imaging features of disease activity the patient was sputumsmear positive to begin with, then
on CXR and CT. followup is usually done with sputum-smear examination.
However, problems arise when such patients become unable to
In a diagnosed case of CTB, these features help in assessing
produce sputum but other symptoms persist. Also, if sputum
the disease activity at the time of presentation and during
becomes negative but clinical improvement is discordant, then
followup. Imaging features indeterminate for disease
imaging provides a viable option for response assessment.
activity include equivocal radiographic findings, signs of
Figure10 depicts the imaging protocol for followup
of pulmonary and nodal types of CTB. CXR is done at
the completion of IP of the treatment regimen. If there
Figure 10: Imaging protocol for follow-up of PTB and mediastinal nodal Figure 11: Imaging protocol for follow-up of pleural TB (IP = Intensive
TB (IP = Intensive phase) phase)
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Source of Support: Nil, Conflict of Interest: None declared.
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