Pediatr Radiol (2017) 47:1237–1248

DOI 10.1007/s00247-017-3868-z

MINISYMPOSIUM: IMAGING OF CHILDHOOD TUBERCULOSIS

Standardized radiographic interpretation of thoracic

tuberculosis in children
Nathan David P. Concepcion 1,2 & Bernard F. Laya 1,2 & Savvas Andronikou 3 &
Pedro A. N. Daltro 4 & Marion O. Sanchez 5 & Jacqueline Austine U. Uy 1 &
Timothy Reynold U. Lim 2

Received: 27 January 2017 / Accepted: 9 April 2017 / Published online: 26 August 2017
# The Author(s) 2017. This article is an open access publication

Abstract There is a lack of standardized approach and termi- Introduction

nology to classify the diverse spectrum of manifestations in
tuberculosis. It is important to recognize the different clinical Numerous articles have been published regarding childhood
and radiographic patterns to guide treatment. As a result of tuberculosis but there is still a lack of standardized approach
changing epidemiology, there is considerable overlap in the and terminology to classify the diverse spectrum of manifes-
radiologic presentations of primary tuberculosis and post- tations in tuberculosis. It is important to recognize the differ-
primary tuberculosis. In this article we promote a standardized ent clinical and radiographic patterns because management of
approach in clinical and radiographic classification for chil- each condition is varied. A classification of disease manifes-
dren suspected of having or diagnosed with childhood tuber- tation that is common to all will help to facilitate communica-
culosis. We propose standardized terms to diminish confusion tion and understanding among scientific communities.
and miscommunication, which can affect management. In ad- Generally the pathological changes in childhood tuberculosis
dition, we present pitfalls and limitations of imaging. are pauci-bacillary, and thus the diagnosis of intrathoracic tuber-
culosis depends largely on chest imaging [1]. Pulmonary tuber-
Keywords Children . Computed tomography . Ghon focus . culosis has been classically classified as primary tuberculosis in
Progressive primary tuberculosis . Radiography . Tuberculosis children and post-primary tuberculosis in adults. However, be-
cause of the changing epidemiology there is a considerable
overlap in the radiologic presentations of these entities [2].
In this article we promote a standardized combined clinical
* Savvas Andronikou and radiographic approach for children suspected of having or
doctor.andronikou@gmail.com
diagnosed with childhood tuberculosis. We propose standard-
ized terms to diminish confusion and miscommunication,
1
Section of Pediatric Radiology, Institute of Radiology, which can affect management. In addition, we present pitfalls
St. Luke’s Medical Center, Bonifacio Global City, and limitations of imaging in childhood tuberculosis diagno-
Taguig City, Philippines
sis. The atypical radiologic patterns seen in immunocompro-
2
Section of Pediatric Radiology, Institute of Radiology, mised children, however, are not discussed in this article.
St. Luke’s Medical Center, Quezon City, Philippines
3
Department of Paediatric Radiology,
Bristol Royal Hospital for Children and the University of Bristol,
Bristol, UK
Clinical categories for intrathoracic tuberculosis
4
in children [3–5]
Section of Pediatric Radiology,
Clínica de Diagnóstico por Imagem, Rio de Janeiro,
Brazil Intrathoracic tuberculosis has been classified based on clini-
5
Section of Pediatric Pulmonology,
cal, laboratory and radiologic evidence. The child should pres-
Institute of Pulmonary Medicine, St. Luke’s Medical Center, ent at least one sign or symptom suggestive of tuberculosis but
Quezon City, Philippines without any other plausible etiology. These signs and
1238 Pediatr Radiol (2017) 47:1237–1248

symptoms include any of (a) persistent cough; (b) weight if no alternative diagnosis is established or not tuberculosis if
loss/failure to thrive; (c) persistent unexplained fever, or (d) an alternative diagnosis is established such as cardiac disease,
persistent, unexplained lethargy or reduced activity. The fol- foreign body aspiration or asthma. Those who have docu-
lowing sections are definitions that have been proposed to mented exposure or close contact with a known tuberculosis
indicate the degree of certainty of the diagnosis of patient but are asymptomatic and have negative tuberculin
tuberculosis. skin test and chest radiography are considered tuberculosis
exposed. No treatment is necessary for these children.
Confirmed tuberculosis Tuberculous infection and tuberculous disease have to be
differentiated because treatments for these two entities are
Tuberculosis is confirmed when the culture from a specimen different. We propose simple definitions. When a child has a
representative of intrathoracic disease (e.g., sputum, positive tuberculin skin test but does not show any of the
nasopharyngeal/gastric aspirate, pleural fluid) is positive, probable tuberculosis symptoms and has a normal chest radio-
and more recently when Xpert MTB/RIF — a rapid test to graph, this might be classified as tuberculous infection and
simultaneously detect Mycobacterium tuberculosis and resis- could be treated with one-drug therapy [9]. However when
tance to rifampicin — from any specimen is positive. the findings in the chest radiographs are consistent with tuber-
The Xpert MTB/RIF is not only sensitive and specific for culosis, this is considered tuberculous disease and warrants
diagnosing pediatric pulmonary mycobacterial tuberculosis treatment with at least three drugs [9–11]. In the next sections
but is also effective in detecting rifampicin resistance [6, 7]. we discuss chest radiography findings that are consistent with
The World Health Organization in 2013 [8] strongly recom- tuberculous disease seen in possible or probable tuberculosis.
mended Xpert MTB/RIF for use rather than conventional mi-
croscopy, culture and drug-susceptibility testing as the initial
diagnostic test in children suspected of having multidrug- Primary pulmonary tuberculous disease
resistant-tuberculosis or human immunodeficiency virus
(HIV)-associated tuberculosis. This test can also be used (con- The major route of Mycobacterium tuberculosis infection is
ditional recommendation) rather than conventional microsco- by inhalation [1]. Infection begins when infected droplets are
py and culture as the initial diagnostic test in all children deposited in the terminal airway or alveoli, followed by a
suspected of having tuberculosis. localized parenchymal inflammation or pneumonic process
called the primary (Ghon) focus. There is then spread via
Probable tuberculosis draining lymphatic vessels, usually to the ipsilateral central
or regional lymph nodes, which then enlarge. The upper lobes
Children in this category have chest radiographs showing drain to the ipsilateral paratracheal nodes, while the rest of the
findings consistent with intrathoracic tuberculosis disease, lung drains to the perihilar nodes. The parenchymal focus and
and at least one of the following: the enlarged lymph nodes are called the primary (Ranke or
Ghon) complex [1, 2, 12–17] (Figs. 1 and 2).
(a) positive clinical response to anti-tuberculosis therapy, Incubation can be up to 6 weeks from exposure, during
(b) documented exposure/close contact with a known tuber- which time chest radiographs are normal. After 1–3 months
culosis patient, or from exposure, hilar or mediastinal adenopathy can be visual-
(c) positive tuberculin skin test or interferon-gamma release ized in 50–70% of cases [18–20]. Primary tuberculosis re-
assay. flects a patient’s conversion from insensitivity to having the
antigens of the tubercle bacilli [2, 14].
Regional (perihilar or paratracheal) lymphadenopathy is
Possible tuberculosis the radiologic hallmark of primary infection in childhood [1,
13] (Figs. 3 and 4). Anteroposterior and lateral views are re-
There are two scenarios in this category. One is when the chest quired for optimal lymph node visualization [13, 21], but it
radiograph is not consistent with tuberculous disease, but at can remain difficult to visualize enlarged lymph nodes with
least one of the criteria in the prior section is present. The other certainty [1, 22]. The most common sites of nodal involve-
possibility is when the chest radiography is consistent with ment are the right paratracheal and hilar regions [13, 17].
tuberculosis disease but none of the criteria in the prior section The prevalence of adenopathy decreases with age; it is
is present. 100% in children <3 years of age and 88% in older children.
Some children are symptomatic but have chest radiography The prevalence of parenchymal involvement detectable on
findings that are not consistent with tuberculous disease and radiographs, however, is significantly lower in children
have none of the criteria mentioned in probable tuberculosis. <3 years of age (51%) as compared with that in older chil-
These children are categorized as either unlikely tuberculosis dren (78%) [13].
Pediatr Radiol (2017) 47:1237–1248 1239

Fig. 1 Diagram of a Ghon focus (yellow) and associated lymphadenopathy Fig. 3 Diagram of isolated lymphadenopathy (green)
(green). This is the so-called primary complex

If the child is immunocompetent, the lesions heal and be- infection via the airways, lymphatics or bloodstream [15, 16].
come dormant while still causing continuous antigenic stimu- Clinically active tuberculous disease can develop within
lation for maintenance of hypersensitivity to tuberculous anti- 5 years after infection. This is called progressive primary tu-
gen. Thus the tuberculin skin test is positive in 95% of cases. berculosis [2, 24].
This has been referred to as latent tuberculous infection. The
caseating necrosis within the Ghon focus and infected lymph
node frequently calcifies [1, 2]. Calcification can occur from Progressive primary tuberculous disease
6 months to 4 years after infection, occurring earlier in young
children [1]. The parenchymal focus, called pulmonary Progression from infection to disease usually occurs within
tuberculomas (Fig. 5), which are identified radiographically, 1 year after the primary infection in more than 90% of cases.
represent sharply defined ovoid granulomas, solitary or mul- It is bimodal in age distribution, with children younger than
tiple, ranging in size from 0.4 cm to 5 cm in diameter [2, 23]. 5 years and adolescents being at increased risk [1, 17, 25].
Children with latent tuberculous infection can be treated with Early disease progression can happen 2–6 months from
a one-drug therapy provided there was no prior treatment. exposure, when homogeneous consolidation can occur
If immunity is inadequate, the disease progresses either (Fig. 6). Obstructive atelectasis or overinflation can result from
locally or in other parts of the lung or body, with spread of compression by an adjacent enlarged node. Distribution is

Fig. 2 Chest radiographs in a 5-

year-old girl with primary
tuberculous disease. a, b
Anteroposterior (a) and lateral (b)
views show a middle lobe opacity
(asterisk) with right hilar
lymphadenopathy (arrow)
1240 Pediatr Radiol (2017) 47:1237–1248

Fig. 4 Chest radiographs in a 1-

year-old boy with primary
tuberculous disease and
lymphadenopathy. a, b
Anteroposterior (a) and lateral (b)
views show hilar
lymphadenopathy (arrows) on the
right without ipsilateral lung
abnormality. A left retrocardiac
opacity (asterisk) is noted

typically on the right side at the level of the right lobar bron- phrenic nerve might also be affected, producing
chus or bronchus intermedius. Fibrosis and destruction of the tracheoesophageal fistula, chylothorax and diaphragmatic pal-
lung parenchyma result in traction bronchiectasis and forma- sy, respectively [1, 18–20]. Hematogenous miliary dissemina-
tion of cavities (Fig. 7), respectively [2]. This is known as tion can also occur in this stage.
progressive Ghon focus [18–20].
Three possible mechanisms are involved in the formation Miliary tuberculosis
of cavities: (1) progressive primary spread of disease with
extensive and bilateral pulmonary cavities, (2) cavities Miliary tuberculosis is seen in 8% of cases [25], usually in the
caused by bronchial obstruction by lymph nodes or (3) younger age group because of immature immune function
post-primary tuberculosis showing cavities that are usually [28]. It is an acute hematogenously disseminated infection
single and unilateral in the upper lobe. These have fairly presenting as innumerable ≤2-mm non-calcified nodules
equal incidence [26]. scattered in both lungs [1, 2, 18–20, 28–30] (Figs. 8 and 9).
Lymph nodes can continue to enlarge 4–12 months from There is no pathognomonic finding for tuberculosis except for
exposure and can cause progression of the disease affecting miliary tuberculosis [28], and it can be seen in primary and
the airways, pleura and pericardium, which are discussed in post-primary disease [2].
the next sections. On contrast-enhanced CT, involved lymph In 25–40% cases, chest radiographs are initially normal [1,
nodes often measure more than 2 cm and show a very char- 30]. CT is more sensitive for miliary disease before it becomes
acteristic, but not pathognomonic, rim sign consisting of a radiographically apparent. The tiny nodules can be sharply or
low-density center surrounded by a peripheral enhancing rim poorly defined, and are seen in a diffuse, random distribution,
[17, 22, 27] (Fig. 6). The esophagus, lymphatic duct and often with intra- and interlobular septal thickening [16].

Fig. 5 Ghon focus in a 7-year-

old boy. a Anteroposterior chest
radiograph shows a Ghon focus
(arrow) in the right lower lobe. b
Non-enhanced axial chest CT
demonstrates the focus, which is
calcified (arrow)
Pediatr Radiol (2017) 47:1237–1248 1241

Fig. 6 Primary progressive tuberculous disease in a 15-month-old boy.

Axial contrast-enhanced CT image shows progressive Ghon focus
(asterisk) in the right middle lobe and progressive hilar
lymphadenopathy (arrow). The enlarged lymph node demonstrates the
characteristic central necrosis with peripheral enhancement (rim sign)

Lymphobronchial/lymphotracheobronchial tuberculosis Fig. 7 Diagram shows a progressive Ghon focus (circle) with cavitation
and associated lobar consolidation
Lymphobronchial or lymphotracheobronchial involvement is
a complication in 2–4% of tuberculosis cases [2, 31].
Lymphadenopathy is seen in chest radiographs in 63–95%
[26] and on CT in up to 96–100% of tracheobronchial tuber- The obstructive infiltrates can be resorbed or calcify,
culosis cases [32, 33]. The enlarged nodes compress the adja- fibrose with traction bronchiectasis (Fig. 13) or cause lung
cent trachea or bronchi, causing luminal narrowing and destruction [2]. There is often excessive inflammation, which
resulting in lung hyperinflation from partial obstruction with can result in dense alveolar consolidation and eventual paren-
check-valve effect (Fig. 10), or atelectasis due to a complete chymal breakdown [1]. Cicatricial bronchostenosis can man-
obstruction (Figs. 11 and 12). These nodes subsequently ifest as concentric narrowing, uniform wall thickening, and
erode, perforate and discharge caseous material into the air- involvement of a long bronchial segment after healing [31].
ways manifesting as obstructive pneumonia [1, 2, 13, 14,
17–20, 33–36]. Lymphogenic and hematogenous spread into
the large airways have also been reported [2].
Radiographic manifestations in lymphotracheobronchial
tuberculosis are nonspecific, and a normal chest radiograph
does not rule out airway involvement. Involvement of the
central airways can be easily missed on radiographs.
Persistent segmental or lobar collapse, lobar hyperinflation
and obstructive pneumonia are seen as complications of the
airway compression [31, 33].
Enhancement and enlargement (usually >2 cm) of ad-
jacent mediastinal lymph nodes are common findings at
CT in the active stage of stenosis. The enlarged lymph
nodes are commonly identified in the subcarinal [37],
paratracheal and perihilar (infrahilar) regions closely abut-
ting or compressing the airways [33].
The most commonly involved airway is the bronchus
intermedius, followed by the left main bronchus and trachea
[37]. Bronchial narrowing can be smooth or irregular, with
mural thickening [33, 38]. Smooth bronchial narrowing is
caused by compression by an adjacent node, and the irregular
narrowing correlates with significant mucosal irregularity, ca- Fig. 8 Diagram of miliary tuberculosis (white dots) with
seation, granuloma formation or even perforation [33]. lymphadenopathy (green)
1242 Pediatr Radiol (2017) 47:1237–1248

Fig. 9 Miliary tuberculosis in a

14-year-old boy. a, b Focused
anteroposterior chest radiograph
(a) and axial contrast-enhanced
CT (b) of the upper lobes show
innumerable 2-mm or smaller
discrete nodules

Pleural tuberculous disease The effusion can complicate into an exudative effusion,
empyema or infiltration of the thoracic duct [18–20].
Another site of extrapulmonary involvement, aside from Contrast-enhanced CT scan shows smooth thickening of vis-
lymph nodes, is the pleurae [25]. Its prevalence increases ceral and parietal pleura (“split-pleura” sign) [40]. An Air-
with age. Pleural effusion (Figs. 14 and 15) most often fluid level in the pleural space indicates presence of
results from obstruction of the lymphatic drainage or hy- bronchopleural fistula [41]. The empyema can also spread
persensitivity reaction than from direct seeding into the beyond the parietal pleura to produce a subcutaneous abscess,
pleura. This explains why pleural fluid cultures are mostly called empyema necessitatis [42].
negative [28]. Spread to the pleura might also come from
a caseating granuloma near the pleura or via hematoge- Pericardial disease
nous dissemination [2].
As a complication of primary tuberculosis, pleural involve- Tuberculous pericarditis is a relatively uncommon complica-
ment is most frequently observed in older children and ado- tion of primary tuberculosis. It has been reported in 1% of
lescents. It can occur 3–6 months after infection and is some- cases. It is commonly caused by direct extension of lymph
times asymptomatic [2]. It is also typically appreciated in as- nodes into the posterior pericardial sac [28], although miliary
sociation with parenchymal or nodal disease [39]. Pleural ef- spread has been reported [28, 43]. CT shows lymphadenopa-
fusions are associated with air-space consolidation in 29% and thy and pericardial thickening with or without effusion.
could be bilateral or loculated in 6% of cases [17]. This is Constrictive pericarditis with fibrous or calcified pericardial
usually self-limiting and prognosis is good. Residual pleural thickening of usually >3 mm occur in about 10% of patients
calcifications appear in some cases [2].

Fig. 10 Diagram of lymphobronchial tuberculosis with partial Fig. 11 Diagram of lymphobronchial tuberculosis with complete
obstruction of the lower lobe bronchus by enlarged lymph nodes obstruction by enlarged lymph nodes (green) of the right main
(green) and secondary lobar hyperinflation (blue) bronchus, resulting in right lung atelectasis
Pediatr Radiol (2017) 47:1237–1248 1243

Fig. 12 Primary progressive

lymphobronchial tuberculous
disease in a 6-year-old boy. a
Anteroposterior chest radiograph
shows left lung collapse. b
Volume-rendered CT shows
occlusion of the left mainstem
bronchus caused by
lymphobronchial disease

[43]. Pericardial effusion (Figs. 15, 16 and 17), commonly observed in the pediatric age group, mostly in adolescents [2,
serous type [28], can result in globular enlargement of the 13]. It is considered a late disease progression of the primary
heart shadow (water bottle sign) [1]. infection, which can occur 8–24 months from exposure and in
children as young as 8 years [18–20].
The most commonly affected locations are the apical and
Post-primary tuberculosis posterior segments of the upper lobes and the apical segment
of the lower lobes because of higher oxygen tension (Fig. 18).
Post-primary tuberculosis is also known as adult-type, reacti- Initially there might be cloudy opacification in a segment before
vation or secondary tuberculosis and sometimes phthisis [2]. coalescence and parenchymal breakdown. Complications in-
This results from the reactivation of dormant foci. It is further clude cavitation, bronchogenic spread with bronchopneumonic
consolidation, exudative pleuritis, cicatrization atelectasis of the

Fig. 13 Diagram of bronchiectasis (beaded black lumina) as a

complication of tuberculosis
Note enlarged lymph nodes (green) Fig. 14 Diagram of pleural effusion as a complication of tuberculosis
1244 Pediatr Radiol (2017) 47:1237–1248

Fig. 15 Pleural effusion and

cardiac involvement in a 10-year-
old girl with primary progressive
tuberculous disease. a
Posteroanterior chest radiograph
shows an enlarged cardiac
shadow (arrowheads) with
pleural effusion (asterisk) on the
left. b Follow-up axial contrast-
enhanced CT image demonstrates
bilateral pleural effusions
(asterisks) and pericardial
effusion (arrows)

upper lobe with retraction of hilum and formation of traction 4 mm with linear branching opacities (“tree-in-bud” sign)
bronchiectasis [1, 2, 44–46]. Lymph node enlargement is not which represent caseous necrosis at and around terminal and
common in comparison to primary tuberculosis [18–20]. respiratory bronchioles [49] (Fig. 20). Complete destruction
Cavitation is radiographically evident in 40% of cases of of the entire lung or a large part of a lung is not uncommon in
post-primary disease. The walls of the cavities might appear the end stage of tuberculosis. Secondary pyogenic or fungal
thin and smooth or thick and nodular. It is difficult to distin- infection can occur [47]. Miliary tuberculosis and
guish thin-walled cavities from bullae, cysts or pneumatoceles. tuberculomas might also be encountered in post-primary tu-
Cystic bronchiectasis should also be considered when multiple berculosis [2, 50].
cavities are present [47] (Figs. 18 and 19).
In 20% of post-primary tuberculosis cases, bronchogenic
spread appears on radiographs as multiple, ill-defined Approach to classification of intrathoracic
micronodules in a segmental or lobar distribution, typically tuberculosis
in the lower-lung zones [48]. High-resolution CT, the modal-
ity of choice, demonstrates centrilobular nodules ranging 2– We adapted the clinical and laboratory components of the
classification from Graham et al. [3], Moyo et al. [4] and
Triasih [5]. An imaging approach to interpretation is summa-
rized in Fig. 21. The radiologic side of the algorithm is based
on the pathological processes that occur in tuberculosis that
result in various complications.

Fig. 17 Tuberculous pericarditis in a 6-year-old boy. Anteroposterior

Fig. 16 Diagram of pericardial effusion (green) as a complication of radiograph of the chest shows globular enlargement (arrows) of the
tuberculosis cardiac silhouette (water bottle sign)
Pediatr Radiol (2017) 47:1237–1248 1245

Pitfalls and limitations of imaging

Chest radiography is the primary screening tool in children

suspected of having tuberculosis. It has, however, high intra-
and inter-observer variability, with 74% specificity and 39%
sensitivity [51] even in the best technical quality radiographs.
A normal chest radiograph does not rule out tuberculosis [52].
CT offers excellent anatomical visualization [53], but because
of its high cost and the higher radiation exposure, it is reserved
for complicated cases [18].
Lymphadenopathy is the most common abnormality noted
in children with primary tuberculosis [13], but it is not patho-
gnomonic of tuberculosis because other infectious processes
can present with lymphadenopathy. Large pulmonary vessels
are sometimes erroneously identified as lymph nodes, leading
to over-diagnosis. The inter-observer agreement is low (kappa
−0.03 to 0.25) [5]. Knowledge and familiarization of the hilar
anatomy are prerequisites prior to interpretation [52].
Fig. 18 Diagram of a post-primary tuberculosis with upper lobe The abnormalities seen on chest radiographs resolve grad-
predominance ually and can worsen despite clinical improvement.
Lymphadenopathy and parenchymal disease without or with
calcifications can also persist for many months and even years
Whenever a child comes in for workup for a possible even after proper treatment. Re-treatment might not be neces-
tuberculous infection or disease, it is important to be sary, especially if the child is asymptomatic. Moreover, the
aware of the terminology and pathological pathways. calcifications do not equate with healed tuberculosis because
The diagnosis or impression of the imaging findings these can indicate latency [52].
should contain the main pathology (i.e. primary tubercu-
lous infection, primary progressive tuberculous disease or
post-primary tuberculous disease), followed by the vari- Conclusion
ous complications present (e.g., primary progressive tu-
berculosis with tracheobronchial involvement and pleural Radiologic interpretation of pulmonary tuberculosis remains
disease; Fig. 21). challenging. Classically, tuberculosis is classified as primary

Fig. 19 Post-primary
tuberculosis in a 14-year-old girl.
a, b Posteroanterior chest
radiograph (a) and volume-
rendered CT (b) show cavitations,
traction and cystic bronchiectasis
in the right lung
1246 Pediatr Radiol (2017) 47:1237–1248

Fig. 20 Post-primary
tuberculous disease with
bronchogenic spread in a 15-year-
old girl. a Posteroanterior chest
radiograph of shows ill-defined
infiltrates in the left upper lobe
(encircled). b Coronal
reconstruction CT image
demonstrates multiple
centrilobular nodules (arrows)
with linear branching opacities
(tree-in-bud sign)

and post-primary tuberculosis, but the typical radiologic pat- infection and disease because treatments are different. The
terns are now complicated by overlapping imaging character- proposed standardized clinical and radiographic classification
istics as well as occurrence of atypical features seen in immu- presented in this paper aims to provide helpful guides in the
nocompromised children. It is important to differentiate proper nomenclature of suspected tuberculosis patients. The

Fig. 21 This is the proposed approach to classify intrathoracic complications present (e.g., primary progressive tuberculosis with
tuberculosis in children. It includes clinical, laboratory and radiologic lymphobronchial involvement and pleural disease). CXR chest
(in black background) components. The imaging characteristics follow radiograph, IGRA interferon-gamma release assay, LTBI latent
the pathological processes and the possible complications that occur. The tuberculous infection, TB tuberculosis/tuberculous, TST tuberculin skin
impression of the imaging findings should contain the main pathology test, Xpert MTB/RIF test to detect Mycobacterium tuberculosis and
(i.e. primary tuberculosis infection, primary progressive tuberculous resistance to rifampicin [8]
disease or post-primary tuberculous disease) followed by the various
Pediatr Radiol (2017) 47:1237–1248 1247

pitfalls and limitations of imaging likewise caution both clini- 15. Miller WT, Miller WT Jr (1993) Tuberculosis in the normal host:
radiological findings. Semin Roentgenol 28:109–118
cians and radiologists to avoid erroneous interpretations and
16. Leung AN (1999) Pulmonary tuberculosis: the essentials.
over-diagnosis of childhood tuberculosis. Radiology 210:307–322
17. Kim WS, Choi J II, Kim I-O et al (2006) Pulmonary tuberculosis in
Compliance with ethical standards infants: radiographic and CT findings. AJR Am J Roentgenol 187:
1024–1033
Conflicts of interest None 18. Perez-Velez CM, Marais BJ (2012) Tuberculosis in children. N
Engl J Med 367:348–361
Open Access This article is distributed under the terms of the Creative 19. Lincoln EM, Sewell EM (1963) Tuberculosis in children. McGraw-
Commons Attribution 4.0 International License (http:// Hill, New York, pp 1–315
creativecommons.org/licenses/by/4.0/), which permits unrestricted use, 20. Wallgren A (1948) The time-table of tuberculosis. Tubercle 29:
distribution, and reproduction in any medium, provided you give appro- 245–251
priate credit to the original author(s) and the source, provide a link to the 21. Lamont AC, Cremin BJ, Pelteret RM et al (1986) Radiological
Creative Commons license, and indicate if changes were made. patterns of pulmonary tuberculosis in the paediatric age group.
Pediatr Radiol 16:2–7
22. Andronikou S, Joseph E, Lucas S et al (2004) CT scanning for the
detection of tuberculous mediastinal and hilar lymphadenopathy in
References children. Pediatr Radiol 34:232–236
23. Lee KS, Song KS, Lim TH et al (1993) Adult-onset pulmonary
tuberculosis: findings on chest radiographs and CT scans. AJR
1. Marais BJ, Gie RP, Simon Schaaf H et al (2004) A proposed radio-
Am J Roentgenol 160:753–758
logical classification of childhood intra-thoracic tuberculosis.
24. McAdams HP, Erasmus J, Winter JA et al (1995) Radiologic mani-
Pediatr Radiol 34:886–894
festations of pulmonary tuberculosis. Radiol Clin N Am 33:655–678
2. Van Dyck J, Vanhoenacker FM, Van den Brande P et al (2003)
25. Sanchez MO, Mendoza AR, Laya BF et al (2011) Primary progres-
Imaging of pulmonary tuberculosis. Eur Radiol 13:1771–1785
sive tuberculosis in children: radiographic patterns in correlation
3. Graham SM, Ahmed T, Amanullah F et al (2012) Evaluation of
with clinical presentation and microbiologic studies. St. Luke’s J
tuberculosis diagnostics in children: 1. Proposed clinical case defi-
Med 7:59–68
nitions for classification of intrathoracic tuberculosis disease.
26. Griffith-Richards SB, Goussard P, Andronikou S et al (2007)
Consensus from an expert panel. J Infect Dis 205:S199–S208
Cavitating pulmonary tuberculosis in children: correlating radiolo-
4. Moyo S, Verver S, Hawkridge A et al (2012) Tuberculosis case
gy with pathogenesis. Pediatr Radiol 37:798–804
finding for vaccine trials in young children in high-incidence set-
27. Kim WS, Moon WK, Kim IO et al (1997) Pulmonary tuberculosis
tings: a randomized trial. Int J Tuberc Lung Dis 16:185–191
in children: CT evaluation. AJR Am J Roentgenol 168:1005–1009
5. Triasih R, Robertson C, De campo J et al (2015) An evaluation of 28. Pulido KGC, Laya BF, Villamor CP et al (2011) Radiographic
chest x-ray in the context of community-based screening of child patterns of active pulmonary tuberculosis disease in Filipino pedi-
tuberculosis contacts. Int J Tuberc Lung Dis 19:1428–1434 atric patients and their correlation with symptoms, length of hospi-
6. Wang XW, Pappoe F, Huang Y et al (2015) Xpert MTB/RIF assay tal confinement and clinical dispositions. St. Luke’s J Med 7:21–32
for pulmonary tuberculosis and rifampicin resistance in children: a 29. Tuddenham WJ (1984) Glossary of terms of thoracic radiology:
meta-analysis. Clin Lab 61:1775–1785 recommendations of the nomenclature Committee of the
7. Ardizzoni E, Fajardo E, Saranchuk P et al (2015) Implementing the Fleischner Society. AJR Am J Roentgenol 143:509–517
Xpert1MTB/RIF diagnostic test for tuberculosis and rifampicin re- 30. Kwong JS, Carignan S, Kang EY et al (1996) Miliary tuberculosis:
sistance: outcomes and lessons learned in 18 countries. PLoS One diagnostic accuracy of chest radiography. Chest 110:339–342
10:e0144656 31. Lee KS, Kim YH, Kim WS et al (1991) Endobronchial tuberculo-
8. World Health Organization (2013) Automated real-time nucleic sis: CT features. J Comput Assist Tomogr 15:424–428
acid amplification technology for rapid and simultaneous detection 32. Weber AL, Bird KT, Janower ML et al (1968) Primary tuberculosis
of tuberculosis and rifampicin resistance: Xpert MTB/RIF assay for in childhood with particular emphasis on changes affecting the tra-
the diagnosis of pulmonary and extrapulmonary TB in adults and cheobronchial tree. Am J Roentgenol Radium Therapy, Nucl Med
children: policy update. World Health Organization, Geneva 103:123–132
9. Centers for Disease Control and Prevention (2016) TB treatment for 33. Laya BF, Concepcion NDP, De la Eva RC et al (2011) Computed
children https://www.cdc.gov/tb/topic/treatment/children.htm. tomography with multiplanar reformation and 3D-volume rendering
Accessed 9 Jan 2017 technique in correlation with fiberoptic tracheobronchoscopy for tho-
10. Nahid P, Dorman SE, Alipanah N et al (2016) Official American racic evaluation of children with primary progressive tuberculosis
Thoracic Society/Centers for Disease Control and Prevention/ and tracheobronchial involvement. St Luke’s J Med 7:11–20
Infectious Diseases Society of America clinical practice guide- 34. Kashyap S, Mohapatra PR, Saini V et al (2003) Endobronchial
lines: treatment of drug-susceptible tuberculosis. Clin Infect Dis tuberculosis. Indian J Chest Dis Allied 45:247–256
63:e147–e195 35. Daly JF, Brown DS, Lincoln EM et al (1952) Endobronchial tuber-
11. Lu-Fong MT, How CH, Bañez MAP et al (2003) Philippine pedi- culosis in children. Dis Chest 22:380–398
atric Society handbook on childhood tuberculosis. Quezon City, 36. Smith LS, Schillaci RF, Sarlin RF et al (1987) Endobronchial tu-
Philippines berculosis: serial fiberoptic bronchoscopy and natural history. Chest
12. Goodwin RA, Des Prez RM (1983) Apical localization of pulmo- 91:649–657
nary tuberculosis, chronic pulmonary histoplasmosis and progres- 37. Lucas S, Andronikou S, Goussard P et al (2012) CT features of
sive massive fibrosis of the lung. Chest 83:801–805 lymphobronchial tuberculosis in children, including complications
13. Leung AN, Muller NL, Pineda PR et al (1992) Primary tuberculosis and associated abnormalities. Pediatr Radiol 42:923–931
in childhood: radiographic manifestations. Radiology 182:87–91 38. Moon WK, Im JG, Yeon KM et al (1997) Tuberculosis of central
14. Agrons GA, Markowitz RI, Kramer SS et al (1993) Pulmonary airways: CT findings of active and fibrotic disease. AJR Am J
tuberculosis in children. Semin Roentgenol 28:158–172 Roentgenol 169:649–653
1248 Pediatr Radiol (2017) 47:1237–1248

39. Choyke PL, Sostman HD, Curtis AM et al (1983) Adult-onset pul- 48. Hadlock FP, Park SK, Awe RJ et al (1980) Unusual radiographic
monary tuberculosis. Radiology 148:357–362 findings in adult pulmonary tuberculosis. AJR Am J Roentgenol
40. Yilmaz MU, Kumcuoglu Z, Utkaner G et al (1998) CT findings of 134:1015–1018
tuberculous pleurisy. Int J Tuberc Lung Dis 2:164–167 49. Im JG, Itoh H, Shim YS et al (1993) Pulmonary tuberculosis: CT
41. Woodring JH, Vandiviere HM, Fried AM et al (1986) Update: ra- findings — early active disease and sequential change with antitu-
diographic features of pulmonary tuberculosis. AJR Am J berculous therapy. Radiology 186:653–660
Roentgenol 146:497–506 50. Sochocky S (1958) Tuberculoma of the lung. Am Rev
42. Glicklich M, Mendelson DS, Gendal ES et al (1990) Tuberculous Tuberc 78:403–410
empyema necessitatis: CT findings. Clin Imaging 14:23–25 51. De Villiers RVP, Andronikou S, Van de Westhuizen S et al (2004)
43. Kim Y, Song KS, Goo JM et al (2001) Thoracic sequelae and Specificity and sensitivity of chest radiographs in the diagnosis of
complications of tuberculosis. Radiographics 21:839–858 paediatric pulmonary tuberculosis and the value of additional high-
44. Palmer PE (1979) Pulmonary tuberculosis: usual and unusual ra- kilovolt radiographs. Australas Radiol 48:148–153
diographic presentations. Semin Roentgenol 14:204–242 52. Laya BF (2011) Thoracic tuberculosis in children: pitfalls and
45. Im JG, Webb WR, Han MC et al (1991) Apical opacity associated dilemma in chest radiograph interpretation. St. Luke’s J Med
with pulmonary tuberculosis: high-resolution CT findings. 7:69–76
Radiology 178:727–731
53. Andronikou S, van Hoenacker FM, de Backer AI et al
46. Van den Brande P, Demedts M (1992) Pulmonary tuberculosis in
(2009) Advances in imaging chest tuberculosis: blurring of
the elderly: diagnostic difficulties. Eur J Med 1:224–229
differences between children and adults. Clin Chest Med 30:
47. Winer-Muram HT, Rubin SA (1990) Thoracic complications of
717–744
tuberculosis. J Thorac Imaging 5:46–63