Pediatric tB radiology FOR CLINICIANS by Kim C. Smith, MD, MPH, Susan D. John, MD

Produced by Heartland National TB Center. Consultation to healthcare providers at
2303 SE Military Drive, San Antonio, TX 78223 by

This product produced with funds awarded Kim C. Smith, MD, MPH
by the Centers for Disease Control & Prevention (CDC)

About the Authors

Kim Connelly Smith, MD, MpH, is a Professor of Pediatrics at the University of Texas Health

Science Center at Houston Medical School. She is the director of the Children's Tuberculosis

Clinics at Children's Memorial Hermann and Lyndon B. Johnson Hospitals in Houston, Texas.

Susan D. John, MD, is the Chair of Diagnostic and Interventional Imaging and Professor of

Diagnostic Imagining and Pediatrics at the University of Texas Health Science Center at Houston

Medical School.


James B. McAuley, MD, MPH
Ewell Clarke, MD
Alan Schlesinger, MD
Barbara Seaworth, MD
Andrea T. Cruz, MD, MPH
Lisa Y. Armitige, MD, PhD
Jeffrey R. Starke, MD

Thanks to Stephanie McAlpin and Creative Blend Design for artistic design and Dwight C. Andrews

for Photography.

Table of Contents:

Introduction 3

Learning Objectives 3

Chapter I: Basics of Normal Chest Radiographs in Children 5
Infant chest radiograph 5
Child and adolescent chest radiographs 8

Chapter II: Basic patterns of disease 11
Air space opacities 11
Central peribronchial opacities 15
Interstitial opacities 16
Hilar opacities 17
Pleural opacities 18

Chapter III: Pediatric Intrathoracic Tuberculosis 21
Primary disease 22
Ghon complex 23
Hilar Lymphadenopathy 26
Considerations for CT in Children with TB 29
Complications of lymphadnopathy 33
Tuberculosis pneumonia 39
Miliary tuberculosis 40
Pleural effusions 43
Air filled cysts 47
Congenital tuberculosis 55
Healed intrathoracic disease 55

Chapter IV: Pediatric Extrapulmonary Tuberculosis 57
Central Nervous System tuberculosis 57
Abdominal tuberculosis 66
Musculoskeletal tuberculosis 70
Pericardial Tuberculosis 78

Chapter V: Other diseases that can mimic tuberculosis 79

Chapter VI: Clinical Case Studies 87

References 105

Tuberculosis is one of the leading infectious diseases in developing countries, with an
estimated 40% of people infected. Globalization, mobility and immigration continue
to diversify populations throughout the world. TB can present with a myriad of clinical
findings in children ranging from asymptomatic to life threatening disease. The diagnosis
is often more difficult to recognize in children than in adults. Radiographic findings remain
one of the most important diagnostic tools for pediatric TB, yet the abnormalities can be
subtle and the findings in children do not follow patterns typical of adult disease.

This book for clinicians shows and describes examples of radiographic abnormalities
common in pediatric tuberculosis, emphasizing pulmonary, lymphatic and meningeal
disease. The utility of CT scan and MRI in pediatric TB are also discussed. Radiographs
and case studies are used as illustrations throughout the book.

Learning Objectives

Understand normal findings and variation in chest radiographs by age

Recognize basic pulmonary disease patterns in child chest radiographs

Become familiar with the spectrum of pediatric TB including primary, miliary,
lymph node, extrapulmonary and healed disease

Understand the value of CT in children with TB

Become familiar with the expected clinical evolution of radiographs in children
with TB during and after treatment

Recognize typical MRI findings in children with central nervous system TB

Appreciate other diseases that can mimic TB radiographically

Basics of Normal Chest Radiographs in Children

Infant Chest Radiograph

The anatomic differences in the chest of infants below the age of 1 year are significant
and can confuse the inexperienced observer who is investigating the possible diagnosis
of tuberculosis. As with other solid organs in the body, the heart appears relatively
large in relationship to the overall size of the chest during infancy. The thymus gland
is large during the first years of life in infants and young children. Because the thymus
gland is soft tissue in nature, it has the same density on radiographs as the heart
that is composed of soft tissue and fluid. The thymus gland sits anterosuperior to the
heart and is contiguous with it, causing the two structures to be indistinguishable on
radiographs. The combination of a normal large thymus gland and the heart can cause
the cardiomediastinal silhouette to appear abnormally large (Figure 1), so the observer must
be aware of this complicating factor when interpreting chest radiographs in infants.

Figure 1.
Normal thymus gland in an infant. Prominent tissue in the anterior mediastinum represents normal
thymus gland. Buckling of the trachea to the right is a normal phenomenon when the infant exhales
and does not indicate displacement by the thymus gland.

Page 6


Basics of Normal Chest Radiographs in Children (continued)
Use of a comparative ratio of cardiac to thoracic diameter on radiographs in children is
less reliable than in adults, but the general rule of thumb is that the diameter of the heart
in the infant and young child is equal to or less than approximately 55% of the thoracic
diameter. The aortic arch is usually relatively small in infancy and is often not clearly
visible behind the thymus gland.

Radiographs of good technical quality are essential when evaluating the chest and are
sometimes challenging to obtain. The radiograph should be taken in an adequate degree
of inspiration, producing lungs that are equally distended with air. When radiographs
are obtained in a suboptimal phase of inspiration, the amount of air within the lungs
is decreased causing the lungs to appear more opaque than normal. The degree of
opacity of the lungs on an expiratory radiograph in a young infant can be quite striking
as the pulmonary compliance is very good and end expiratory volumes can be small.
The absence of visible air within the trachea and mainstem bronchi can be a clue to the
expiratory nature of a radiograph (Figure 2). Be aware that the trachea elevates during
expiration and can have a buckled appearance, usually displaced to the right (see Figure 1).
This deviation from the usual straight position of the trachea over the right side of the
spine may suggest mass effect, but don't be fooled by this finding.

Fig 2.
Expiratory radiograph. Note that the lungs appear small in volume and hazy in density. No air
is visible in the tracheobronchial tree, indicating that the image was obtained near the end of

Page 7


Basics of Normal Chest Radiographs in Children (continued)
The lung hilum is a difficult area to evaluate in infants. The pulmonary vasculature is
relatively small during infancy, and a prominent thymus gland can obscure the central
vasculature. Lateral views of the chest are helpful. Linear vascular markings should be
visible coursing towards the hila, but no nodular opacities should be seen.

Straight positioning is also important in chest radiography. When the patient is rotated
toward one side on a radiograph, important areas of the chest and lungs can be obscured
by the heart and mediastinum (Figure 3). Overall density of the lungs can appear artificially
asymmetrical with rotated positioning, mimicking pathology. The thymus can simulate
atelectasis or pulmonary infiltrates, especially in a rotated radiograph such as Figure 3.
Asymmetry of the skeletal structures in the chest is good evidence that the positioning
of the patient is suboptimal.

Figure 3.
Rotated positioning. When the patient is rotated on the radiograph, anterior mediastinal

structures such as thymus gland are projected over portions of the lung and obscure


Page 8


Basics of Normal Chest Radiographs in Children (continued)

Child and adolescent chest radiographs

As a child grows beyond infancy, the thymus gland decreases in size, but some thymic
tissue may be visible on radiographs up to 5 or 6 years of age. The rate of thymic
regression is variable between individuals. The central pulmonary vasculature becomes
more easily visible and more prominent as the child grows. The left lung hilum continues
to be more difficult to evaluate than the right lung hilum throughout childhood.

As the thymus gland regresses, the main pulmonary artery and the aorta become visible
as discrete bulges in the contour of the left side of the cardiac and mediastinal border
(Figure 4A). The azygous vein appears as a small round opacity to the right of the trachea
just above the takeoff of the right mainstem bronchus. Normal pulmonary vessels are
usually not seen clearly in the outer 1/3 of lungs because of their small size.
Good inspiratory radiographs continue to be a challenge until the child reaches a
cooperative age, usually around 4-5 years. Therefore, the lungs may not appear as
large in young children as they do in older children and adolescents who can obey the
command to "take a deep breath and hold it."

Fig 4A.
Normal chest (older child). PA view. Aorta, main pulmonary artery, azygos vein.

Page 9


Basics of Normal Chest Radiographs in Children (continued)
The lateral view of the chest is important for complete evaluation of normal structures
and pathology. The lungs should be assessed for any focal areas of increased opacity.
The lung bases contain a larger volume of air than the upper lungs and, therefore,
should be slightly blacker. This can be observed by looking at the spine on lateral view,
which should appear blacker in the lower thoracic region than in the upper chest. The
pulmonary vessels radiate as thin linear structures from the region of the lung hilum.
The right pulmonary artery is normally seen as a round structure anterior to the trachea
on lateral view and should not be mistaken for a mass or a lymph node (Figure 4B). Once
the thymus gland has regressed, the retrosternal region of the chest on lateral view
should appear black.

The hemidiaphragms have a slightly domed contour on both PA and lateral views when
the lungs are normally inflated. The right hemidiaphragm usually sits slightly higher
than the left hemidiaphragm because of the underlying liver. The angles formed by the
juncture of the ribs and the margins of the hemidiaphragms (costophrenic angles) should
be fairly deep and sharply pointed.

Figure 4B.
Lateral view. Right pulmonary artery.

Page 11

Basic Patterns of Disease

Air Space Opacities

Pulmonary conditions that involve primarily the alveolar air space consist mainly of space
occupying pathologies, air space collapse (atelectasis), and lung masses or nodules. All
of these abnormalities cause some degree of opacification of the lung that is usually
homogeneous in density, unless fat or calcifications are also present.

Conditions that fill the lung with fluid, such as bacterial pneumonia or pulmonary edema,
displace the air from the alveolus causing it to appear white (or less black) on the radiograph.
Often the bronchioles or bronchi in the area remain filled with air and are black (ie, air
bronchogram). Pneumonia tends to be located in one or more focal areas within a lung,
whereas pulmonary edema is more likely to be distributed evenly in both lungs. The portions
of the lung affected by such air space abnormalities usually maintain their volume and can
even become larger than the unaffected parts of the lung (Figure 5).

Figure 5A.
Bacterial pneumonia. Dense consolidation involves only the right upper lobe of the lung.

Page 12

Basic Patterns of Disease (continued)

Figure 5B.
Lateral radiograph, same patient. The horizontal fissure remains in a normal position, indicating

a space occupying process with no volume loss.

Page 13


Basic Patterns of Disease (continued)
Areas of the lung that become collapsed also become white because of the absence
of normal air in the alveolar space. However, atelectasis differs from space-occupying
conditions in that the volume of a collapsed portion of the lung will be decreased. The
loss of volume causes near-by structures (eg., fissures, hemidiaphragm, trachea) to shift
toward the side of volume loss (Figure 6), an important finding to distinguish atelectasis from
lung consolidation. When atelectasis is caused by a bronchial obstruction, the affected
bronchus will also be opaque, so air bronchograms are less common with atelectasis than
with pneumonia in children.

Figure 6.
Right upper lobe atelectasis. Note that the horizontal fissure on the right is elevated
indicating volume loss in the right upper lobe.

Page 14


Basic Patterns of Disease (continued)
Lung masses or nodules cause the same kind of increased opacity in the alveolar space
as pneumonia or atelectasis, except that they have a more well-defined contour in most
cases. Large pulmonary masses are quite rare in infancy and childhood, and most apparent
pulmonary masses in these age groups represent congenital or developmental abnormalities
such as pulmonary sequestration or congenital bronchopulmonary malformations. Smaller
nodules or masses are usually caused by infections or occasional congenital or acquired
lung cysts. Be aware that a bacterial pneumonia can sometimes have a round, well-defined
appearance in children that mimics a pulmonary mass (Figure 7). Pulmonary neoplasms in
childhood are exceedingly rare.

Figure 7A.
Round pneumonia. Note the rounded solid opacity in the left lower lobe on PA .

Figure 7B.
Lateral view. Bacterial pneumonia in children sometimes appears round and well-defined resembling
a pulmonary mass.

Page 15


Basic Patterns of Disease (continued)
Central peribronchial opacities

Conditions that primarily affect the trachea and smaller airways can sometimes cause
radiographic abnormalities in the lungs. Viral lower respiratory tract infection is a common
cause of such a lung pattern. Tracheobronchial infections and inflammatory conditions
are associated with mild edema that can leak into the peribronchial and interstitial spaces
to cause ill-defined, hazy or streaky increased opacity in the central parahilar regions of
the lungs. The abnormal opacities are bilateral and symmetrical (Figure 8), distinguishing
them from the localized, more peripheral opacities that characterize bacterial pneumonia.
Similar opacities can be seen chronically in the lungs of children with chronic bronchial
diseases such as chronic aspiration or cystic fibrosis.

Figure 8
Viral respiratory tract infection.
Note the central, ill-defined, parahilar peribronchial opacities, typical of viral bronchiolitis

infection in children.

Page 16


Basic Patterns of Disease (continued)
Interstitial opacities

Conditions that involve the lung interstitium (ie., pulmonary edema, viral infections,

pneumonitis), create a net-like pattern that reflects thickening of the interstitial lung spaces
(Figure 9). As interstitial processes become more severe, the interstitial markings can begin to
restrict the size of the alveolar space, and the decreased air in the space will cause the lung

appear hazy. When interstitial disease is very severe, the air spaces can be so compromised
that the pattern on radiographs resembles air space consolidation such as that seen in

Figure 9
Interstitial lung pattern in a child with lymphocytic interstitial pneumonitis. The thickened

interstitial markings create a net-like pattern in the lungs.

Page 17


Basic Patterns of Disease (continued)
Hilar opacities

Abnormal hilar opacities most commonly represent lymphadenopathy in infants and
children. Identifying hilar lymphadenopathy can be difficult in infants because of overlying
thymus gland. In some patients, prominent central pulmonary vessels can resemble lymph
nodes. The most reliable clue to the correct identification of hilar lymphadenopathy is a
convex appearance to the opacities in the hilar region between the radiating vessels on PA
view (Figure 10A) and discrete rounded opacities in the lung hilum on lateral view (Figure 10B).
Hilar lymph nodes are most common and most easily visible in the subcarinal region on
lateral view.

Figure 10B.
On lateral view, the round lymph node is visible at the lower margin of the lung hilum .

Figure 10A.
Hilar lymphadenopathy. The enlarged right hilar lymph nodes create a convex shadow between the
hilar vessels . Note the straight margin of the normal pulmonary vessels on the left.

Page 18


Basic Patterns of Disease (continued)
Pleural opacities

Abnormal radiographic findings related to the pleural space in infants and children are most

often caused by pleural effusions or other types of fluid filling the pleural space. Since fluids

all have the same density on radiographs, it is usually not possible to determine the type of

pleural fluid from the appearance on the images. Transudates tend to be free-flowing and will be

larger in the dependent portions of the pleural space on upright views (Figure 11A). Small

pleural effusions may cause only slight blunting of the costophrenic angle (Figure 11B). On

supine radiographs, free-flowing pleural effusions will layer posteriorly, causing a generalized

increase in haziness over the affected hemithorax. Lateral decubitus radiographs can help

distinguish free flowing from loculated pleural fluid (Figure 11C). Fluid that tends to be

loculated, such as empyema or hemothorax, will usually cause uneven areas of thickening in the

pleural space around the periphery of the lung (Figure 12). Decubitus views with the affected

side of the chest down may help by demonstrating lack of movement of the pleural fluid in

loculated collections. Ultrasound is a safe and effective imaging modality to help localize and

characterize pleural fluid collections in children.

Figure 11A.
Pleural effusion. This free-flowing pleural effusion is larger in the base of the hemithorax
and decreases in size superiorly.

Page 19

Basic Patterns of Disease (continued)

Figure 11B.
Note blunting of the costophrenic angle by a small effusion.

Figure 11C.
A left lateral decubitus radiograph in the same patient as 11A shows the free flowing nature of

the pleural fluid.

Page 20

Basic Patterns of Disease (continued) Basic Patterns of Disease (continued)

Fig 12A.
Loculated pleural fluid (empyema). Radiograph shows a convex contour of the fluid collection in

the left pleural space.

Figure 12B.
CT of the same patient reveals multiple loculated pleural fluid collections on the left.

Page 21


Pediatric Intrathoracic Tuberculosis

The diagnosis of intrathoracic TB in children depends largely on the interpretation of the
chest radiograph since clinical diagnostic features are often nonspecific, AFB smears
and cultures for TB are usually negative and half of children with disease identified in
industrialized nations may be asymptomatic.1,2 Both posterioanterior (PA) and lateral
chest views are important for optimal visualization in pediatric patients since a relatively
wide mediastinum may hide enlarged hilar and/or paratracheal lymph nodes. Findings on
imaging reflect the natural progression of infection to either latent TB, primary disease
or disseminated disease depending on the response of the host and the clinical stage at
the time of evaluation.

A normal chest radiograph in a clinically well child with a positive tuberculin skin test or
interferon-gamma releasing assay (IGRA) is the standard for the diagnosis of latent TB
infection (LTBI). Clinical trials over decades have demonstrated the efficacy of treatment
of children diagnosed with LTBI with isoniazid to prevent progression to TB disease.

Page 22


Pediatric Intrathoracic Tuberculosis (continued)
Primary disease

In primary TB, the chest radiograph usually shows hilar lymphadenopathy and/
or pulmonary air space opacities.3 Primary TB may be seen in any age group but is
most common in younger children, before the age of adolescence. A review of TB
disease in teens found that only 10% had radiologic findings of primary disease with
lymphadenopathy.4 Adolescents are more likely to have adult-like TB with cavitary
disease. Lymphohematogenous spread following infection is typical and may progress to
disseminated disease. In many cases, the primary lung focus will resolve undetected and
the infection can remain dormant as LTBI. The risk of disease progression and disease
severity depend on host factors including the age of the child when the infection occurs.
Infants have the highest risk of disease progression as well as more severe forms of
disease. Children 5 years of age and less and teenagers have a higher risk of progression
of TB disease when compared to children infected between 6-10 years of age.(Table 1)

Table 1. Risk of progression to
TB disease by age in untreated patients with LTBI 1, 3

Age at Infection Risk of TB Disease
Birth-12 months 43-50%
1-5 years 20-25%
6-10 years 2%
11-15 years 16%
Healthy Adults 5-10% lifetime risk
HIV Infected Adults 30-50% lifetime risk

The radiographic appearance of primary TB typically includes enlargement of regional
lymph nodes, with or without a small localized focus of air space consolidation. In the
absence of clinical symptoms, the subtle changes of primary TB may be difficult to detect
radiographically. Unlike adult reactivation disease, pediatric primary TB is characteristically
pauci-bacillary and non-cavitary. The primary focus is reported in the right chest
more commonly, although it may occur anywhere in the lungs. Due to the mediastinal
lymphatic drainage, right sided adenopathy normally accompanies right lung primary
opacities whereas bilateral lymphadenopathy is often seen with left sided opacities.5
Hilar lymphadenopathy is the hallmark of pediatric tuberculosis and is often the only
radiographic finding.

Page 23


Pediatric Intrathoracic Tuberculosis (continued)
Ghon complex

The Ghon focus is the primary site of infection in the lung which usually occurs in
the subpleural alveolar space as a small hazy, solid or ill-defined opacity (Figure 13).
This transient inflammatory response is frequently followed by regional lymph node
enlargement. The combination of the Ghon focus (primary parenchymal infiltrate) and local
lymph node involvement is called the Ghon or primary complex (Figure 14).1,3,5 The pulmonary
lesion is often short-lived or may be hidden, with only mild pleural reaction. The size of
the Ghon complex may be variable or radiographically subclinical depending on the degree
of infection, host response and timing of evaluation. Local progression or intrabronchial
spread can occur.

Figure 13A.
Ghon focus. When visible on radiographs, the Ghon focus usually appears as a small hazy

Figure 13B.
Lateral view of Ghon focus.

Page 24


Pediatric Intrathoracic Tuberculosis (continued)

Figure 13C.
Radiograph in a different child shows a larger and denser area of consolidaton resulting from

primary TB.

Figure 13D.
Denser consolidation in primary TB.

Page 25


Pediatric Intrathoracic Tuberculosis (continued)

Fig 14.
Ghon complex. PA radiograph of a child with primary TB shows airspace consolidation in the right

lower lung that partially obscures lymphadenopathy in the right lung hilum .

Page 26


Pediatric Intrathoracic Tuberculosis (continued)
Hilar Lymphadenopathy

Intrathoracic lymphadenopathy is the most common and characteristic radiographic
finding of primary tuberculosis in children. Enlargement of the intrathoracic lymph nodes
represents a local inflammatory response following pulmonary infection and may be the
only radiographic finding in 50% of pediatric cases. TB lymphadenopathy is typical in
children less than 5 years of age. Unilateral involvement is more common than bilateral
disease on plain radiographs. Lymphadenopathy should be visible on posteroanterior (PA)
and lateral chest radiographs (see Figure 10). Lateral views are important since enlarged
nodes may be hidden on a single PA view due to the relatively wider mediastinal silhouette
in children (Figure 15). Central pulmonary vessels are part of the normal hilar structures that
must be recognized and distinguished from lymphadenopathy (Figure 16).


Figure 15A.
Hidden hilar lymphadenopathy. Left hilar enlarged lymph nodes are partially hidden by the thymus

gland on this rotated radiograph.

Figure 15B.
A better positioned radiograph of the same patient makes the lymphadenopathy easier to see.

Page 27

Pediatric Intrathoracic Tuberculosis (continued)

Figure 16A.
Hilar lymphadenopathy versus normal vessels. Lateral radiograph shows normal linear vessels
emanating from the lung hilum.

Figure 16B.
Lateral radiograph of a different child shows nodular opacity in the lower hilum representing

Page 28


Pediatric Intrathoracic Tuberculosis (continued)
In some cases, lymphadenopathy may be difficult to detect with confidence on plain
chest radiographs. The normal thymus gland can be large in infants and can appear
indistinguishable from paratracheal or anterior mediastinal lymph nodes, sometimes
requiring further imaging with CT (Figure 17). Ultrasonography has been suggested as another
modality for the detection of mediastinal lymphadenopathy, although not commonly used.6

TB lymphadenopathy gradually decreases in size after 3 months of treatment, but in some
cases there can be a paradoxical, transient increase in lymph node size in the first period
of therapy.7 In some cases, hilar lymphadenopathy can be visible on radiographs for
years. Pre-chemotherapy studies documented the natural history of pediatric tuberculosis
describing the resolution of hilar lymph nodes within 6 months in 40%, 1 year in 30% and up
to 4 years for the remainder of children followed with no antibiotic treatment.1,3,8

Figure 17A.
Hilar and mediastinal lymphadenopathy on CT. Contrast enhanced CT images help to distinguish

mediastinal lymph node from adjacent enhanced vessels. Normal prominent thymus gland (T)

enhances homogeneously in this young child.

Figure 17B.
Another CT image of the same child with primary TB shows enlarged lymph nodes in the right hilar

and subcarinal regions .

Page 29

Pediatric Intrathoracic Tuberculosis (continued)
Considerations for CT in Children

A normal chest radiograph in an otherwise healthy child with a positive tuberculin skin
test or interferon-gamma release blood assay is the hallmark of latent TB infection. Chest
CT is not indicated for further evaluation of a normal plain chest radiograph in a healthy
appearing child being assessed for tuberculosis. Normal chest radiographs are occasionally
reported in children with clinically suspected TB and positive gastric aspirate or sputum
cultures (3-4%).9,10 Small air space opacities may be detected on repeat chest radiograph a
few days later or on CT scan. For patients with clinical symptoms of disease but no findings
on radiographs, CT becomes an important consideration. Since CT improves detection of
lymphadenopathy, it is used in many research publications.11,12,13 Even with CT, detection
of intrathoracic lymphadenopathy can be difficult with less than perfect agreement
demonstrated between radiologists.14,15

The increased cost and higher radiation exposure with CT must be taken into consideration.
Infants and children are more vulnerable to the effects of radiation because of more
rapidly dividing cells and longer remaining life span.16 One CT scan of the chest delivers
a radiation dose equal to approximately 150 chest radiographs. CT techniques should be
adjusted for the smaller size of children to reduce radiation exposure. Chest CT for TB
should be performed with intravenous contrast to help distinguish normal structures from
lymphadenopathy (Figure 18). Newer generation multidetector CT scanners provide better
resolution than older single detector scanners.

Page 30


Pediatric Intrathoracic Tuberculosis (continued)

Figure 18A.
Radiograph of a child with tuberculosis shows dense consolidation in the left upper lobe, masking

the presence of lymphadenopathy.

Page 31


Pediatric Intrathoracic Tuberculosis (continued)

Figure 18B.
CT performed without intravenous contrast shows only heterogeneous consolidation. The mediastinal

structures and vessels are not distinguishable without contrast.


Figure 18C.
Contrast-enhanced CT of the same child better identifies anterior mediastinal low attenuation

lymph nodes with peripheral enhancement , with a large area of adjacent lung consolidation.

Page 32


Pediatric Intrathoracic Tuberculosis (continued)
Tuberculous lymphadenopathy often shows a characteristic pattern on CT consisting of a
low-attenuation center surrounded by a thin, sometimes interrupted rim of enhancement
(Figure 19).11,12 Bilateral hilar involvement is more commonly seen on CT compared to plain
radiographs. Reported sites of lymphadenopathy on CT, include subcarinal (90%), hilar
(bilateral 72%), anterior mediastinal, pericarinal, right paratracheal and multiple sites
(96%) on chest CT among children with TB.11 Calcification is less common in children with
TB than in adults (Figure 20). Calcification, a later finding, is more easily seen on CT than on
radiographs but can be masked by contrast enhancement.

Fig 19A.
Mediastinal lymphadenopathy with overlying thymus gland. Plain radiograph in this infant shows

prominent tissue in the right paratracheal region that could represent normal thymus gland.

Figure 19B.
Contrast enhanced CT shows retrocaval lymphadenopathy with characteristic thin, slightly

interrupted rim of contrast enhancement.

Page 33


Pediatric Intrathoracic Tuberculosis (continued)

Figure 20.
Calcified lymphadenopathy. Note the densely calcified nodule representing a lymph node in the

left mediastinum or hilum .

Complications of lymphadenopathy

Intrathoracic lymphadenopathy may lead to complications as a result of partial or complete
airway obstruction or erosion into airways. Partial bronchial obstruction secondary to
compression by lymphadenopathy or luminal narrowing by endobronchial granulomas can
cause a ball-valve phenomenon that results in progressive over inflation of a portion of the
lung (Figure 21). Atelectasis may be seen with complete extrinsic compression or intrinsic
endobronchial involvement causing obstruction (Figure 22, 23). Rarely, erosion may result in
intrabronchial spread with patchy consolidation affecting multiple distal lung segments
(Figure 24).17 Bronchiectasis may result, especially after extensive TB disease or in cases
with severe secondary pulmonary infections such as viral bronchiolitis, pertussis or other

Page 34


Pediatric Intrathoracic Tuberculosis (continued)

Figure 21.
Obstructive emphysema caused by hilar lymphadenopathy. Overinflation of the left lung is the

result of partial obstruction of the left mainstem bronchus by adjacent hilar lymphadenopathy.

Figure 22A.
Progressive atelectasis in a child with primary TB. This initial radiograph shows prominent
bilateral hilar lymphadenopathy.

Page 35


Pediatric Intrathoracic Tuberculosis (continued)

Figure 22B.
Radiograph taken one month later shows well-defined opacity in the left lower lobe representing
atelectasis and hyperinflation of the left upper lobe.

Figure 22C.
Atelectasis has progressed to collapse of the entire left lung in the same child one week later.

Page 36

Pediatric Intrathoracic Tuberculosis (continued) Pediatric Intrathoracic Tuberculosis (continued)

Figure 23A.
Mild atelectasis with TB. Radiograph in a child shows vague haziness in the left mid lung.

Figure 23B.
Lateral view of the same child reveals elongated opacity in the lingula with bowing of the

oblique fissure toward the opacity indicating volume loss. Nodular opacity in the left hilar
region on both PA and lateral views suggests lymphadenopathy.

Page 37


Pediatric Intrathoracic Tuberculosis (continued)

Figure 23C.
Another child with ill-defined hazy opacity in the left upper lung

Figure 23D.
Linear subsegmental atelectasis is apparent on the lateral view of this child.

Page 38


Pediatric Intrathoracic Tuberculosis (continued)

Figure 24.
Endobronchial spread of TB in an adolescent. Note the extensive linear and nodular opacities in

the left upper lobe
("bronchopneumonia "pattern) caused when infected material ruptures into a bronchus.

Page 39


Pediatric Intrathoracic Tuberculosis (continued)
Tuberculous pneumonia

Pulmonary parenchymal involvement in TB occurs in children but is less common.
Alveolar disease varies from small areas of homogeneous consolidation to large, dense
lobar consolidations or multifocal opacities (Figure 25). Lung involvement can occur in
any lobe and does not have a predilection for the lung apices as in the adult reactivation
form of tuberculosis. Cavitation is very uncommon, usually only seen in adolescents with
reactivation disease and occasionally in infants with extensive disease.

Figure 25.
Tuberculous pneumonia. The large area of consolidation in the right lower lung is caused by

progressive primary TB
pulmonary disease.

Page 40


Pediatric Intrathoracic Tuberculosis (continued) Pediatric Intrathoracic Tuberculosis (continued)
Miliary Tuberculosis

Miliary TB classically occurs as small, diffuse, nodular opacities evenly distributed
throughout all lung fields to the periphery, characteristic of hematogenous dissemination
(Figure 26). Although the name "miliary" implies that the nodules are tiny like millet seeds,
the size of the nodules in miliary disease in children may vary from 1-2 mm nodules to
large coalescing ill defined patches (Figure 27). Early miliary TB may be difficult to see
radiographically but becomes more easily visible over the course of a few days. CT may
more clearly demonstrate the nodules in subtle cases (Figure 28) and has been described
to show ground-glass opacification with early miliary disease.18,19 High resolution CT
in children with acute disseminated TB may show variation in size, distribution and
concentration of nodular opacities. Coalescence of nodules and interstitial thickening can
be variable.20 Tuberculosis should always be suspected when miliary infiltrates are seen.

Figure 26.
Miliary TB. The lungs are diffusely studded with small, uniformly sized nodules, consistent
with hematogenous dissemination.

Figure 27A.
Miliary TB. Early miliary disease in this child causes subtle tiny nodules distributed evenly

through the lung.

Page 41

Pediatric Intrathoracic Tuberculosis (continued)

Figure 27B.
Another child with more numerous tiny miliary nodules.

Figure 27C.
The nodules in this child are slightly larger than typical miliary nodules.

Page 42

Pediatric Intrathoracic Tuberculosis (continued)

Another child with tiny nodules that are so numerous that they appear confluent and resemble

alveolar disease.

Figure 28.
Miliary TB. Tiny miliary nodules are often more easily visualized on CT lung windows.


Page 43


Pediatric Intrathoracic Tuberculosis (continued)
Pleural effusions

Pleural effusion is an uncommon presenting finding in children with tuberculosis, reported in

1.8% of pediatric cases in the United States between 1993-200321 and 3.9% of cases reviewed in

Cape Town, South Africa.22 More commonly pleural effusion in children is a result of other

bacterial pathogens which cause pneumonia. Tuberculous pleural effusions are rare in young

children but are more frequent in adolescents and in boys (Figure 29).23 Most TB pleural

effusions are unilateral (92%) and are typically associated with parenchymal involvement

(69%)(Figure 30).24 The size of the effusion may vary from quite small to very large but

typically affects less than 2/3rds of the hemithorax.25 Culture and AFB smear of pleural fluid

caused by TB has a low yield and is usually not diagnostic, although analysis of the type of

fluid may be useful. The fluid is most commonly transudative secondary to a hypersensitivity

response. Resolution usually occurs within 1-4 weeks although a small amount of fluid may persist

for longer.24 Punch biopsy of the pleura examining histopathology and culture has been shown to

have a higher yield than pleural fluid cultures for TB. Chest ultrasound and/or CT can

characterize pleural fluid as free flowing or septated and loculated (Figure 31). Loculated

pleural fluid collections usually represent exudates and are much more likely to be caused by

other types of bacterial pneumonia. Pleural effusion can rarely be a complication of

intra-abdominal tuberculosis.

Page 44

Pediatric Intrathoracic Tuberculosis (continued)

Figure 29A.
Pleural effusion in an adolescent with TB. The large left sided pleural fluid collection
shows the typical "meniscus" sign that indicates a non-loculated pleural effusion .
The effusion hides any consolidation that might be present in the underlying lower lung.
The effusion was initially presumed to represent a bacterial empyema.

Figure 29B.
CT of the same patient shows the large effusion with a single enlarged subcarinal lymph
node . The diagnosis of TB was made upon thoracentesis. Figure 30A. Pulmonary tuberculosis
with pleural effusion. Radiographic findings include a moderate size left pleural effusion
(black arrow) and patchy air space opacities in the right upper lobe (white arrows).

Page 45


Pediatric Intrathoracic Tuberculosis (continued)

Figure 30B.
CT of the same patient better defines the pleural effusion and bilateral lung consolidations (C)

on soft tissue windows.

Figure 30C.
CT with lung windows shows the patchy, slightly nodular pattern of the right upper lobe opacities


Page 46


Pediatric Intrathoracic Tuberculosis (continued)

Figure 31 A.
TB with loculated pleural effusion. PA radiograph shows that the right pleural effusion

compresses the lung in an uneven manner , suggesting loculations within the effusion.

Figure 31B.
On CT of this patient, the irregular margin of the pleural surface is more evident. The effusion

was accompanied by mediastinal lymphadenopathy .

Page 47


Pediatric Intrathoracic Tuberculosis (continued)
Air filled cysts

Cavities are air-filled cysts that occur in an area of lung parenchymal destruction with
a persistent bronchial connection. Cavities generally arise within an area of alveolar
consolidation and persist after the consolidation resolves (Figure 32).

Figure 32A.
Primary TB with
The initial radiograph on
this child shows a large
area of consolidation
in the right parahilar

Figure 32B.
reveal gradual
development of
multiple air-filled
cavities within
the consolidation

Page 48


Pediatric Intrathoracic Tuberculosis (continued)
Figure 32C.
Follow up radiographs show progression of the air-filled cavities.

Page 49


Pediatric Intrathoracic Tuberculosis (continued)
Alveolar opacification and cavitation occur occasionally in infants and in
immunosuppressed children, including those infected with HIV.1,2,5,26 Cavitation is seen with
increased frequency in older children and teens compared to younger children, in most
cases representing reactivation disease typical of adult TB disease (Figure 33).

Cavities should be distinguished from pneumatoceles that are more common in pediatric
patients (Figure 34). Pneumatoceles are thin-walled cysts that probably result from partial,
ball-valve bronchial occlusion that leads to temporary progressive over-inflation of local
alveolar groups. Most pneumatoceles resolve within days to weeks as the disease that
caused them subsides, but the time to resolution is variable (Figure 35). Cavities differ in that
they have thicker walls and heal over months to years often resulting in permanent scaring.

Figure 33.
16 year old with TB. Note the patchy and nodular bilateral upper lobe opacities and bilateral

air-filled cavities . The findings are characteristic of the reactivation form of tuberculosis.

Page 50


Pediatric Intrathoracic Tuberculosis (continued)

Figure 34A.
Pneumatoceles in TB. A small air-filled cyst that developed within the tuberculous lung
focus in this young child is a pneumatocele . The thin wall is obscured by the surrounding lung

Figure 34B.
The isolated pneumatocele in nother child shows the characteristic thin wall of these air-filled
cysts .

Page 51


Pediatric Intrathoracic Tuberculosis (continued)

Figure 35A.
Congenital TB. This 5 week old infant presented initially with multiple areas of lung

consolidation, small nodular lung opacities and bilateral pleural effusions. A left hilar mass
consistent with lymphadenopathy suggested the diagnosis of TB.

Figure 35B.
Several weeks later, the lung consolidations resolved and were replaced by large air-filled cysts

that persisted until the time of discharge

Page 52


Pediatric Intrathoracic Tuberculosis (continued)

Figure 35C.
A radiograph obtained at the time of a follow-up clinic visit several months later revealed

complete resolution of the cysts with little, if any visible scarring, suggesting that the cysts

represented pneumatoceles.

Page 53


Pediatric Intrathoracic Tuberculosis (continued)
Upper lobe consolidation and cavitation are more common in postprimary pulmonary TB.
These patients may have evidence of prior pulmonary TB and apical pleural thickening.
Lymphadenopathy and pleural effusions are not usually seen in patients with postprimary
disease.27 Three possible mechanisms have been proposed for development of cavitary
TB in children: 1) classical upper lobe, unilateral postprimary TB; 2) progressive primary TB
with multiple bilateral cavitary lesions; and, 3) cavitary lesions secondary to mediastinal
lymph nodes causing airway compression with distal collapse and consolidation.28

Endobronchial TB may be a complication of cavitary disease, representing spread via the
airways following caseous necrosis into bronchial walls. The tree-in-bud appearance of
centrilobular nodules and branching centrilobular areas of opacity is caused by bronchiolar
wall thickening and filling of bronchioles with fluid, pus, or mucus (Figure 36). The finding in
patients with TB is indicative of endobronchial spread of infection.

Figure 36A.
Pulmonary TB in adolescent with gastrointestinal malignancy. The chest radiograph shows a mild
reticulonodular pattern that is difficult to characterize .

Page 54


Pediatric Intrathoracic Tuberculosis (continued)

Figure 36B.
Chest CT shows a "treein-bud" pattern that is not specific but can be seen with TB .
Bronchoalveolar lavage revealed acid-fast bacilli in this patient.

Page 55


Pediatric Intrathoracic Tuberculosis (continued)
Congenital Tuberculosis

Congenital tuberculosis is a rare form of primary disease caused by prenatal transmission
of TB from the mother to the fetus through the umbilical vein or amniotic fluid. For this
to occur, hematogenous spread, disseminated disease or uterine involvement during
pregnancy would be the most likely mechanisms. Infants with congenital TB may have
clinical symptoms at birth but usually present within the first 2-3 weeks of life. Disease
after 1 month of age is more likely to have been acquired post-natally. Chest radiographic
findings may resemble other more common types of neonatal pneumonia. Findings of
intrathoracic lymphadenopathy, evidence of liver involvement (usual site of entry), or a
miliary pattern of pneumonia are all supportive of tuberculosis. Unless the mother has
evidence of uterine, placental or disseminated TB disease, it can be difficult to distinguish
congenital transmission from respiratory transmission soon after birth. In either case,
TB in the neonatal period is often a rapidly progressive, disseminated, extensive and life
threatening disease (see Figure 35).

Healed intrathoracic disease

Abnormal chest radiograph findings regress more slowly in patients with tuberculosis
than in other more common types of pneumonia. Even with treatment, little change
may occur in the first 3 months after the initial diagnosis. The primary complex may
remain visible for 6-8 months and sometimes as long as 2 years.3 Frequent radiographs
are not necessary unless the clinical condition deteriorates or raises concerns about
complications. There are no evidence-based guidelines for follow up radiographs for
children with TB, but some experts recommend films at beginning of treatment, 2 months
after initiation, at the end of treatment and 2 months after completion of medication.29
Other experts recommend films at the time of diagnosis and the conclusion of therapy
unless clinical symptoms dictate otherwise. The severity of the disease and immune
response of the patient influence the degree of radiographic resolution. Thirty to 40% of
pediatric patients may still have visible mediastinal lymphadenpathy at the conclusion of

Calcification is indicative of healed disease and is a relatively rare finding in children
treated for TB (Figure 37). Calcification of the pulmonary focus and/or lymph nodes is more
common in cases that were not diagnosed or treated. Uncomplicated primary disease
often heals with no signs of fibrosis, scaring or calcification.30 Calcification may form in
the lymph nodes or the Ghon focus between 6 months to 4 years after infection.1,2,5 CT
can detect calcification not visible on plain radiographs and has been reported in 15-20%
of children with healed TB.12,31,32 One study published in 1970 found partial or complete
clearing of calcifications in the lungs and lymph nodes in many children over a 10-17 year
period of follow up.32

Page 56


Pediatric Intrathoracic Tuberculosis (continued)
Bronchiectasis can result from TB pneumonia. The earliest radiographic finding of
bronchiectasis is bronchial wall thickening resulting in a "tram track" pattern, followed later
by bronchiolar dilation and eventually a cystic honeycomb pattern. Chest CT is a much more
sensitive examination for the detection of bronchiectasis in the earlier stages.33

Healing of cavitary lesions may result in fibrosis, volume loss and anatomic distortion.
Cavitation caused by caseating pneumonia often leads to fibrosis with resolution and is
more common among teens and adults.

Figure 37A.
Calcified lymph nodes with TB. Early calcifications in this right paratracheal lymphadenopathy
are difficult to see on radiographs.

Figure 37B.
A different patient with miliary TB shows calcifications in a left hilar lymph node and small
left upper lobe granuloma .

Figure 37C.
Another child with peripheral calcifications in a large retrocaval lymph node .

Page 57


Pediatric Extrapulmonary Tuberculosis

Central Nervous System TB

Tuberculosis can involve the meninges or the parenchyma of the cerebrum, cerebellum,
brainstem, or spinal cord. Tuberculous meningitis is generally more common in
children than adults, especially infants.34 Like most forms of extrapulmonary TB,
spread to the brain and meninges is typically hematogenous. Up to 50% of patients
with miliary TB may have central nervous system involvement. Local spread from the
middle ear, mastoid or the calvarium occasionally can occur. The most common clinical
manifestation is diffuse meningitis. But focal disease, infarction and hydrocephalus are
possible complications. An intense inflammatory response, which may paradoxically
worsen during the first month of therapy, contributes to morbidity and complications.

Brain CT findings of tuberculous meningitis are subtle to absent in many cases. Intense
basal contrast enhancement is the most common finding on CT and MRI in early cases
(Figure 38 A,B). The findings on head CT most suggestive of tuberculous meningitis (TBM)
is marked contrast enhancement outlining the basal cisterns or basal enhancement.35 A
study of 37 children with culture confirmed TBM reported 89% with basal enhancement,
68% with hydrocephalus, 62% with parenchymal infarcts and 13.5% with tuberculoma.36
These authors summarized 17 studies reporting CT findings in children with TBM. The
results are compared in Table 2. Basilar enhancement is not specific for TBM and can be
seen in other disease processes like fungal meningitis, sarcoidosis and
syphilis.37, 38 The findi ngs are more difficult to see on non-contrast CT scans, however
in some cases, hyperdensity is visible in the basal cisterns, representing high density
exudates (Figure 38C). This finding has been reported to be highly specific for TBM.37

Page 58

Pediatric Extrapulmonary Tuberculosis (continued) Pediatric Extrapulmonary Tuberculosis


Figure 38B.
Gadolinium-enhanced MRI image of the same child shows similar basilar enhancement. The
dark flow void of the vessels of the circle of Willis surrounded by the inflammatory
exudates creates a double line of enhancement.

Figure 38A.
TB meningitis. Contrast-enhanced CT image shows pronounced enhancement in the basal cisterns
in this child with TB meningitis.

Page 59


Pediatric Extrapulmonary Tuberculosis (continued)

Figure 38C.
Non-contrast enhanced CT image shows high attenuation surrounding the basal cisterns and
Circle of Willis , representing dense tuberculous exudates.

Comparison of CT findings in children with TB meningitis

Study Artopoulos
Total Patients 9
Children # 9
Hydrocephalus (%) 100
Basal enhancement (%) 11
Infarcts (%) 44
Tuberculoma (%) 56

Study Bhargava
Total Patients 60
Children # 36
Hydrocephalus (%) 83
Basal enhancement (%) 82
Infarcts (%) 28
Tuberculoma (%) 10

Study Farinha
Total Patients 33
Children # 33
Hydrocephalus (%) 94
Basal enhancement (%) 93
Infarcts (%) 33
Tuberculoma (%) 15

Study Kingsley
Total Patients 25
Children # 12
Hydrocephalus (%) 72
Basal enhancement (%)
Infarcts (%) 67
Tuberculoma (%)

Study Kumar
Total Patients 94
Children # 94
Hydrocephalus (%) 81
Basal enhancement (%) 83
Infarcts (%) 19
Tuberculoma (%) 24

Study Leiguarda
Total Patients 65
Children # 65
Hydrocephalus (%) 89
Basal enhancement (%) 69
Infarcts (%) 38
Tuberculoma (%) 27

Study Patwari
Total Patients 136
Children # 136
Hydrocephalus (%) 32
Basal enhancement (%)
Infarcts (%) 13
Tuberculoma (%) 27

Study Waeker
Total Patients 30
Children # 30
Hydrocephalus (%) 100
Basal enhancement (%) 37
Infarcts (%) 37
Tuberculoma (%)

Study Andronikou
Total Patients 37
Children # 37
Hydrocephalus (%) 68
Basal enhancement (%) 89
Infarcts (%) 62
Tuberculoma (%) 13.5

Study Altunbasak
Total Patients 52
Children # 52
Hydrocephalus (%) 98
Basal enhancement (%) 52
Infarcts (%) 25
Tuberculoma (%)

Study De
Total Patients 21
Children # 21
Hydrocephalus (%) 76
Basal enhancement (%) 67
Infarcts (%) 50
Tuberculoma (%) 10

Study Kemaloglu
Total Patients 156
Children # 156
Hydrocephalus (%)
Basal enhancement (%) 46
Infarcts (%) 22
Tuberculoma (%) 4

Study Ozates
Total Patients 289
Children # 214
Hydrocephalus (%) 80
Basal enhancement (%) 15
Infarcts (%) 14
Tuberculoma (%) 4

Study Tung
Total Patients 7
Children # 7
Hydrocephalus (%) 100
Basal enhancement (%) 14
Infarcts (%) 29
Tuberculoma (%)

Study Upadhyaya
Total Patients 59
Children # 59
Hydrocephalus (%) 100
Basal enhancement (%)
Infarcts (%) 6
Tuberculoma (%) 8

Study Schoeman
Total Patients 198
Children # 198
Hydrocephalus (%) 83
Basal enhancement (%) 75
Infarcts (%) 38
Tuberculoma (%) 11


Adapted from Andronikou S. Pediatr Radiol. 2004 34(11):876-85. 36

Page 60


Pediatric Extrapulmonary Tuberculosis (continued)
Objective radiographic CT and MRI criteria for the presence of basal enhancement in children
with TBM may have high sensitivity and specificity when more than one criterion is present.54
The useful findings include: 1) filling of the CSF spaces around the vessels with contrast, 2)
double lines of enhancement in the middle cerebral artery cisterns, 3) enhancement along
the frontal lobe and uncus of the temporal lobe at the supracellar cistern, 4) enhancement of
the infundibular recess of the third ventricle, 5) nodular enhancement of the vessels, and 6)
asymmetrical vascular enhancement.37,54 Early follow up head CT within 1-4 weeks of initial CT
may be of value in detecting new findings including hydrocephalus, cerebral infarcts and basal
enhancement which may be of diagnostic and/or prognostic benefit.55 MRI is more sensitive for
detection of infarcts and is generally of more value (Figure 39).56

Figure 39A.
Brain infarcts secondary to TB mengitis. Contrast enhanced MRI images show scattered focal areas
of enhancement secondary to post-infectious infarcts.

Figure 39B.
Infarcts shown in contrast enhanced MRI.

Page 61

Pediatric Extrapulmonary Tuberculosis (continued)
Tuberculoma is the most common form of localized TB CNS disease. The tuberculous
mass usually measures less than 2 cm in diameter and is rarely calcified (Figure 40).
Tuberculomas can mimic neoplasms. CNS abscess is uncommon with TB. Intravenous
contrast is important on CT and MRI scans to show enhancement patterns. TB lesions
are usually of low density with ring enhancement (Figure 41), and the cerebral hemisphere
is the most common location. These lesions exhibit mass effect with surrounding edema,
but no mural nodules are present.57

Figure 40A.
Axial T2 weighted MRI image shows loculated fluid collection in the left mesial temporal and
hypothalamic regions with mass effect on the third ventricle and midbrain

Page 62

Pediatric Extrapulmonary Tuberculosis (continued)

Figure 40B.
Coronal T2 weighted image of same lesion.

Figure 40C.
Contrast-enhanced axial image shows intense leptomeningeal enhancement in the basal cisterns and

midbrain, surrounding the non-enhancing loculated abscess.

Page 63


Pediatric Extrapulmonary Tuberculosis (continued)

Figure 41.
Tuberculomas. Multiple small ring enhancing lesions in the cerebellum represent tuberculomas.

Page 64


Pediatric Extrapulmonary Tuberculosis (continued)
Tuberculous otomastoiditis can be a result of hematogenous spread or direct extension
from the upper respiratory tract (Figure 42). CT or MRI demonstrates opacification of the
mastoid air cells and the middle ear space. Damage to the middle ear structures may

Figure 42A.
Tuberculous otomastoiditis. T2-weighted MRI shows inflammatory edema in the right mastoid air

cells, with a central non-enhanced area representing an abscess .

Page 65


Pediatric Extrapulmonary Tuberculosis (continued)

Figure 42B.
Gadolinium-enhanced MRI images show enhancement in the mastoid air cells.

Figure 42C.
A ring enhancing lesion in the cerebellum.

Page 66


Pediatric Extrapulmonary Tuberculosis (continued)

Abdominal Tuberculosis

Abdominal TB is less common in children than adults. The majority (64%) of children
with abdominal tuberculosis also have pulmonary disease.58 Lymphadenopathy can
occur throughout the abdomen with para-aortic, mesenteric, and periportal lymph nodes
most commonly involved (Figure 43). Peripheral lymph node enhancement can occur,
similar to that seen in thoracic tuberculous lymphadenopathy. Calcification is more likely
in abdominal tuberculous than in thoracic lymph node disease in children. Abdominal
and pelvic CT and MRI are equally effective for identifying abnormal lymph nodes in the
abdomen and pelvis. Intravenous contrast enhancement is necessary to distinguish
lyphadenopathy caused by tuberculosis from normal intra-abdominal structures.

Figure 43A.
Abdominal TB lymphadenopathy. Multiple enlarged mesenteric lymph nodes show peripheral

enhancement typical of tuberculous lymphadenopathy.

Figure 43B.
A larger lesion in the right lower quadrant of the same patient has a low attenuation center and

a thin rim of peripheral enhancement, suggestive of an abscess.

Page 67

Pediatric Extrapulmonary Tuberculosis (continued)
Solid organ lesions are usually granulomas or microabscesses and appear as either
calcified or low attenuation lesions on CT. Lesions in the liver or spleen on MRI are low
intensity on T1 weighted images and high intensity on T2 weighted sequences. Both
CT and MRI may show mild enhancement around the periphery of the lesions. High
frequency ultrasound is a sensitive method for detecting small tuberculous lesions in the
liver or spleen. The lesions are hypoechoic and multiple (Figure 44).

Figure 44.
Splenic lesions. The hypoechoic, round lesions of varying sizes seen on ultrasound may represent

granulomas or microabscesses.

Page 68


Pediatric Extrapulmonary Tuberculosis (continued)
Less common types of abdominal involvement include tuberculous peritonitis and
ileocolitis. Peritonitis is accompanied by ascites that may have high attenuation values
on CT (Figure 45). Ultrasound identifies the fluid but the findings cannot distinguish TB
peritonitis from other causes of ascites and peritonitis. Bowel involvement usually
occurs in the ileocecal region and is manifest by bowel wall thickening or inflammatory
phlegmon (Figure 46).59

Figure 45A.
Tuberculous peritonitis. Contrast-enhanced CT shows a large amount of free intraperitoneal fluid

(F). Enhancement of the peritoneal surface indicates peritonitis.

Page 69

Pediatric Extrapulmonary Tuberculosis (continued)

Figure 45B.
T2-weighted MRI shows the high signal intensity peritoneal fluid.

Figure 46.
Bowel involvement with TB. Note thickening of the wall of the cecum and stranding in the adjacent
intra-abdominal fat indicating edema.

Page 70


Pediatric Extrapulmonary Tuberculosis (continued)
Musculoskeletal Tuberculosis

Skeletal involvement in children is uncommon, occurring in 1-2% of all pediatric TB
cases. Hematogenous dissemination to bone is the origin of the infection, but the
primary pulmonary site is usually occult. Tuberculous bone lesions start as caseating
granuloma, then progress to trabecular and cortical destruction. Subperiosteal spread
and soft tissue involvement are late findings. The spine is a common site of bone
involvement. The infection is hematogenously deposited in the anterior aspect of the
vertebral body and often spreads to the disc, subligamentous space and soft tissues
(Figure 47). The posterior elements are seldom involved. Eighty-five percent of patients
with spinal TB will have multiple contiguous vertebrae involvement. MRI of the spine is
critical in children with spinal tuberculosis, because paravertebral and epidural abcesses
are common and can lead to cord compression (Figure 48). Infection can also spread along
the iliopsoas muscle into the groin or chest. After healing, kyphotic gibbus deformity
can remain60,61 but this complication is uncommon in developed countries (see Figure 47C).

Figure 47A. TB spondylitis. AP radiograph of the thoracic spine shows bilateral paraspinal soft
tissue masses (short arrows) surrounding a narrowed disc space. Note the calcified mediastinal

lymph nodes.

Page 71

Pediatric Extrapulmonary Tuberculosis (continued)

Figure 47B.
Coronal T2-weighted MRI image of this patient shows large subligamentous abscess collections
(black arrows) surrounding multiple vertebral bodies with abnormal signal intensity and a

narrowed and low signal disc space (white arrows).

Figure 47C.
Lateral spine radiograph in this patient shows vertebral endplate destruction and angular

kyphosis (gibbus deformity).

Page 72


Pediatric Extrapulmonary Tuberculosis (continued)

Figure 48A.
TB spondylitis. AP radiograph of the lower thoracic spine shows thickening of the paraspinal

stripes bilaterally, consistent with paraspinal mass or abscess (short arrows). The T 7-8
and T 8-9 disc spaces are narrowed and the right pedicle of T8 appears partially destroyed.

Figure 48B.
Coronal T2-weighted MRI image shows extensive paraspinal subligamentous abscess and abnormal disc

Page 73


Pediatric Extrapulmonary Tuberculosis (continued)

Figure 48C.
Sagittal T2-weighted MRI image shows the predominantly anterior location of the paraspinal
abscess . Abscess also involves the disc and vertebral bodies. Note compromise of the spinal
canal and mild kyphotic deformity.

Page 74


Pediatric Extrapulmonary Tuberculosis (continued)
Joints are the second most frequent location for pediatric musculoskeletal involvement.
Tuberculous arthritis is usually monoarticular often involving the hips and knees.62 Joint
effusions are the most common finding and may be visible in the knees, elbows or ankles
on radiographs. Effusions in other joints may be detected with ultrasound. Periarticular
demineralization can also occur. Joint narrowing, ankylosis and overgrown epiphyses are
characteristic but late findings.

TB osteomyelitis beyond the spine is rare and is usually a solitary lesion (Figure 49). Like
all hematogenously disseminated osteomyelitis in children, tuberculosis infection is
initially deposited in the long bone metaphyses and metaphyseal equivalent areas of
bone such as the iliac bone adjacent to the sacroiliac joint. In some cases the infection
can spread across physis to the epiphysis. The most commonly seen sites include the
skull, hands, feet and ribs. Rarely other sites may be involved (Figure 50). TB bone lesions
are most often cystic but permeative lesions have been seen. The typical radiographic
appearance of the cystic lesion is usually a well-defined osteolytic lesion with mild
surrounding sclerosis and bone expansion. Infiltrative lesions have a "moth-eaten"
appearance with ill-defined margins. A similar appearance occurs with other types of
infection such as fungal or chronic pyogenic infections or with tumors such as Ewing
sarcoma. When the skull is involved, the parietal bone is most frequently affected. Skull
lesions are usually discrete, well-circumscribed osteolytic lesions (Figure 51A). Associated
subgaleal swelling is seen in 92% of patients (Figure 51B).

Page 75


Pediatric Extrapulmonary Tuberculosis (continued)

Figure 49A.
TB osteomyelitis. A well-defined osteolytic lesion with a thin sclerotic rim is present in the

medial aspect of the distal femoral metaphysis (black arrow), associated with widening of the

adjacent physis and a large soft tissue mass over the medial knee (white arrow).

Figure 49B.
Coronal STIR MRI image shows high signal intensity in the bone lesion, which involves the medial

growth plate. High signal is also present in the soft tissues.

Page 76


Pediatric Extrapulmonary Tuberculosis (continued)

Figure 50A.
TB of the sternum. Contrast-enhanced CT image shows destruction of the manubrium with surrounding
fluid collections with peripheral enhancement representing abscesses.

Fig 49C.
Coronal post-Gadolinium image shows peripheral enhancement surrounding the abscesses in the
bone and soft tissues.

Page 77


Pediatric Extrapulmonary Tuberculosis (continued)

Figure 50B.
A lower image of the same patient shows a large retrosternal abscess with adjacent anterior

mediastinal lymphadenopathy.

Page 78

Pediatric Extrapulmonary Tuberculosis (continued)

Figure 51A.
TB of the skull. CT with bone windows reveals the well-defined margins of the osteolytic defect .

Figure 51B.
Contrast-enhanced head CT of the same patient shows the enhancing abscesses overlying the defect
and in the epidural space.

Pericardial Tuberculosis

The pericardium is a rare but potentially life-threatening site for extrapulmonary
tuberculosis disease. Pericardial effusion is the only visible manifestation of the
infection, creating an enlarged and globular cardiac silhouette on radiographs.
Echocardiography is the most sensitive method for detection of pericardial fluid, but
there are no specific findings in tubercular disease.

Page 79


Other Diseases That Can Mimic Tuberculosis

Tuberculosis has been called the great imitator considering the variety of presentations
and clinical manifestations of the disease. Unilateral hilar or paratracheal
lymphadenopathy is strongly associated with mycobacterial disease in children.
A few other clinical entities may result in similar radiographic findings but are less
common depending on the epidemiology in a given region. Conditions including other
infections, immune deficiency diseases and neoplastic diseases can cause intrathoracic
lymphadenopathy on chest imaging. Childhood lymphoma and leukemia may present
with medistinal lymphadenopathy often with bilateral involvement including multiple
nodes in different sites (Figure 52). TB lymphadenopathy is usually limited to a few nodes
within a localized region, but may occasionally involve multiple sites. Although not a
common finding with mycoplasma pneumonia, unilateral hilar lymphadenopathy similar
to TB has been reported (Figure 53). 63 Severe mycoplasma infections may produce
lymphocytic exudative effusions that can be confused with TB.64 Other causes of
thoracic lymphadenopathy in children such as viral or fungal infections and sarcoidosis
are more likely to show bilateral disease than tuberculosis (Figure 54).


Figure 52.
Lymphoma. Left hilar and bilateral mediastinal masses in this adolescent with Hodgkin lymphoma

have an appearance similar to lymphadenopathy seen with TB.

Page 80

Other Diseases That Can Mimic Tuberculosis (continued)

Figure 53A.
Mycoplasma infection. PA radiograph shows nodular prominence in the right lung hilum , consistent

with lymphadenopathy. The lungs are clear.

Figure 53B.
Lateral radiograph verifies an enlarged node in the infrahilar region.

Page 81


Other Diseases That Can Mimic Tuberculosis (continued)

Figure 54.
Mediastinal lymphadenopathy with cysticercosis. Multiple enhancing anterior mediastinal lymph

nodes in a child with disseminated cysticercosis, resembling TB.

Page 82


Other Diseases That Can Mimic Tuberculosis (continued)
Pulmonary consolidative opacities are seen with many lung infections and cannot be
distinguished from TB radiographically. Diffuse micronodular or miliary patterns as well
as cavitary pneumonias are highly suggestive of TB but can sometimes be caused by
other infections. MRSA is an increasingly common cause of multiple cavitary nodules in
children (Figure 55). Pleural effusion, a nonspecific inflammatory response to pneumonia,
is more common in adults with TB than in pediatric disease. Adolescents have a higher
incidence of TB pleural effusions than younger children. More often, pleural effusions
are seen with Staphlococcus aureus and Streptococcus pneumonia, especially in areas
with a low incidence of TB. Viral, fungal and parasitic infections, nontuberculous
mycobacteria, Pneumocystis jirovecii and aspiration pneumonia may present with
pulmonary findings similar to TB. Severe allergic bronchopulmonary aspergillosis
may show nodular pulmonary densities and air space opacities on chest radiograph
masquerading as pulmonary TB. On biopsy, acute and chronic inflammation, necrotizing
granulomas, giant cells, eosinophilia, and rare hyphal elements are described with
aspergillosis.65 Thoracic actinomycosis may mimic TB with pulmonary consolidation,
pleural effusion, or mediastinal involvement.66 Detailed clinical information, other
diagnostic tests and cultures are usually necessary to make the final diagnosis.
Lymphocytic interstitial pneumonitis (LIP) (Figure 56) and opportunistic infections can
look like TB and cause diagnostic confusion.67, 68 Pulmonary blastomycosis, endemic
to Canada and the upper Midwest of the United States, has a variety of radiology
manifestations that can imitate TB including miliary disease, consolidation, and cavitary
lesions. Lymphadenopathy, pleural effusion and calcification are rarely seen with
blastomycosis.69 Other granulomatous diseases such as histoplasmosis and sarcoidosis
can cause hilar lymphadenopathy and sometimes diffuse reticulondular opacities that
are indistinguishable from TB on plain radiographs.70

Page 83


Other Diseases That Can Mimic Tuberculosis (continued)

Figure 55B.
Chest CT on the same patient shows cavitation within nodules that was not apparent on


Figure 55A.
MRSA cavitary nodules. Chest radiograph shows multiple pulmonary nodules, one of which contains

an air-fluid level indicating cavitation.

Page 84


Other Diseases That Can Mimic Tuberculosis (continued)

Figure 56.
Interstitial disease mimics miliary TB. The fine reticulonodular pattern in the lung of this

adolescent with lymphocytic interstitial pneumonitis (LIP) could be mistaken for a miliary

pattern of TB.

Page 85


Other Diseases That Can Mimic Tuberculosis (continued)
Noninfectious conditions such as cystic fibrosis, dyskinetic cilia syndrome and chronic
granulomatous disease may lead to long term or recurrent infections and inflammatory
conditions resulting in findings confused with TB (Figure 57). Reticulonodular patterns can
be seen with Langerhans cell histiocytosis, rheumatoid lung disease, pulmonary fibrosis
or rarely lymphatic spread of cancer. Wegener granulomatosis, a systemic vasculitis,
can present with diffuse, nodular pulmonary granulomatous disease sometimes mistaken
for TB. Epidemiologic information, clinical findings, cultures, biopsy and pathologic
examination may be required to elucidate the final diagnosis.

Figure 57.
Chronic granulomatous disease. Chest radiographs show small, bilateral pulmonary nodules (short

arrows), right paratracheal lymphadenopathy , and bilateral areas of atelectasis, similar to what

might be seen with TB.

Page 87

Clinical Cases


A 12-year-old Hispanic male was exposed to his father who had AFB smear positive
pulmonary TB. The child's tuberculin skin test measured 6 mm induration (> 5 mm is
considered positive among household contacts). The patient had no symptoms and
a normal physical examination. See initial chest radiograph (Figure 58). The primary
physician read the initial radiograph as normal and started isoniazid for LTBI. Look for
the subtle abnormal finding on the chest radiograph (Figure 59).

Figure 58. Case 1.

Page 88


Clinical Cases (continued)

Upon follow up 6 weeks later the child was ill with fever, cough and weight loss. A
repeat chest radiograph showed a large pleural effusion (Figure 60). The patient required
hospitalization, video-assisted thorascopic surgery (VATS) and a chest tube. AFB
smears and TB cultures were negative. Routine cultures were also negative. The clinical
symptoms and findings on the chest radiograph resolved with tuberculosis treatment (Figure
61). This case emphasizes the importance of documentation of the final interpretation of
the radiograph, as subtle abnormalities can be missed by inexperienced observers.

Figure 59. Case 1.
Chest radiograph shows blunting of the left costophrenic angle by a small pleural effusion.

Figure 60A. Case 1.
Follow-up chest radiograph 6 weeks later shows a large left pleural effusion .

Figure 60B.
A left lateral decubitus view on the same date shows that most of the fluid shifts within the
pleural space when the patient is in the decubitus positon, indicating a predominantly free-
flowing effusion.

Page 89

Clinical Cases (continued)

Figure 60C.
Axial CT image shows a left pleural effusion with no visible pleural enhancement or evidence of
loculation. Note lymphadenopathy in the subcarinal region.

Figure 61. Case 1.
After therapy, the left pleural effusion resolves completely.

Page 90


Clinical Cases (continued)


A 4-month-old infant was exposed to an adult with cavitary pulmonary TB, AFB smear
and culture positive. The infant's initial TB skin test measured 0 mm. Two weeks later
the baby developed symptoms of cough, fever and tachypnea. Chest radiograph at that
time is shown (Figure 62).

Figure 62. Case 2.
The initial radiograph shows extensive alveolar opacity in the right lung and a small right

pleural effusion .

Page 91


Clinical Cases (continued)

The child was hospitalized with respiratory distress. Repeat TB skin test measured 12
mm induration. Early morning gastric aspirates were AFB smear and culture positive for
TB. Cerebral spinal fluid (CSF) showed elevated white blood cells of 26 with lymphocyte
predominance and the CSF protein was elevated at 98, consistent with TB meningitis.
The brain MRI was normal with no evidence of inflammation or infarcts. One month
after initiation of treatment the patient developed respiratory distress and repeat chest
radiograph is shown (Figure 63). The patient was treated for 12 months with standard TB
medications and had a full recovery.

Figure 63. Case 2.
A radiograph obtained one month later continues to show a large area of consolidation in the

right lung. New tiny miliary
nodules are seen in both lungs .

Page 92


Clinical Cases (continued)


A 10-year-old Hispanic boy had a 2 month history of nontender cervical
lymphadenopathy measuring 5 cm on examination.

The patient was born in Mexico and had BCG vaccination at birth. He was healthy with no
significant past medical history. The physical examination was normal except for cervical
lymphadenopathy and a 1 cm supraclavicular lymph node. The TB skin test measured 15
mm induration. The chest radiograph is shown (Figure 64).

Biopsy of the supraclavicular and cervical lymph nodes showed Hodgkin's lymphoma
on pathology and no evidence of TB. AFB smear and culture for tuberculosis were
negative. The child was successfully treated for Hodgkin's lymphoma. He also completed
treatment with isoniazid for latent TB infection.

Figure 64. Case 3.
PA chest radiograph shows a large, lobulated mass in the anterior superior mediastinum.


Page 93


Clinical Cases (continued)

A 6-month-old Hispanic infant came to the emergency room with a 2 week history of
upper respiratory symptoms, cough, congestion and fever. The chest radiograph is
shown (Figure 65). On physical examination the infant had left hemiparesis and deviated
lateral gaze.

Figure 65. Case 4.
PA chest radiograph shows consolidation in the lingula on the left , accompanied by diffuse lung
haziness and numerous tiny miliary nodules.

Page 94


Clinical Cases (continued)

The CSF showed elevated white blood cells of 64 with lymphocytic predominance and
elevated CSF protein of 108 consistent with TB meningitis. The brain MRI is shown
(Figure 66). The patient was started on standard 4 drug TB medications and treated for
12 months. Steroids were given during the first month of treatment. The diagnosis of
TB meningitis was based on clinical findings including the MRI. Cultures from gastric
aspirates and CSF were negative for TB.

Follow up image 3 months after treatment was started is shown (Figure 67). After
completion of treatment, mild gross motor deficits and left sided weakness persisted.
But the patient was able to walk, use the hands and arms and had an otherwise normal
developmental assessment.

Figure 66A. Case 4.
Axial contrast-enhanced T1-weighted MRI image reveals leptomeningeal enhancement (large
arrow) and numerous small enhancing nodules in the brain and brainstem (small arrows).

Page 95


Clinical Cases (continued)

Figure 67. Case 4.
Follow-up axial MRI image obtained 3 months later shows resolution of the brain nodules but

residual abnormal signal in the right cerebral infarct.

Figure 66B.
Same MRI sequence at a different level shows gyriform enhancement on the right (large arrow)

indicating infarction. Multiple ring enhancing nodules are present (small arrows).

Page 96


Clinical Cases (continued)

A 15-year-old boy had a 1 month history of fever, 25 pound weight loss and night sweats.
The physical examination was significant for cervical lymphadenopathy, and the TB skin
test measured 0 mm induration. The chest radiograph was normal.

Evaluation included a negative HIV test, a normal CBC and peripheral smear. An
interferon gamma release assay (IGRA) blood test for TB was positive, indicating TB
infection or disease. CT of the abdomen and neck showed lymphadenopathy (Fig 68
A,B). Biopsy of the cervical lymph node was positive on AFB smear and TB culture.
Pathology from the lymph node biopsy was consistent with TB lymphadenitis and
showed no evidence of cancer. The patient was treated for 9 months for disseminated
TB disease with resolution of symptoms and a full recovery.

Figure 68A. Case 5.
Contrast-enhanced CT of the abdomen shows enlarged lymph nodes with ring enhancement.

Figure 68B.
Contrast CT of the neck in the same patient also shows enlarged lymph nodes with characteristic
peripheral enhancement.

Page 97


Clinical Cases (continued)


A 3-year-old boy presented with chronic pain and swelling of the left knee. Plain
radiographs and MRI of the leg are shown (Figure 69).

A biopsy of the lesion for malignancy versus osteomyelitis reveled granulomatous
osteomyelitis and cultures grew TB. 71 The tuberculin skin test measured 20 mm
induration. There were no known risk factors for TB, but contact investigation identified
a source case with pulmonary TB. The patient was treated for 12 months for TB
osteomyelitis with standard therapy.

Figure 69A. Case 6.
AP radiograph of the right knee shows well-defined osteolytic defect with sclerotic margins and
widening of the adjacent physis. Focal soft tissue swelling is present in the medial soft tissues

over the knee.


Figure 69B.
Coronal post-Gadolinium image shows peripheral enhancement surrounding the abscesses in the bone

and soft tissues.

Page 98


Clinical Cases (continued)


A 15-year-old girl presented with a 3 week history of pleuritic chest pain, tachypnea,
shortness of breath, high fever, productive cough, hemoptysis, night sweats and an
18 pound weight loss. She was treated with levaquin followed by azithromycin for
pneumonia. The chest radiograph is shown (Figure 70).

An extensive evaluation including a biopsy of the lung showed necrotizing granulomatous
process with rare multi-nucleated giant cells and no evidence of malignancy. AFB stains
and cultures were negative. The tuberculin skin test was negative and an IGRA blood
assay for TB was negative. There was no known TB exposure or risk factors. A positive
antineutrophil cytoplasmatic autoantibody test (C-ANCA) confirmed the diagnosis of
Wegener granulomatosis. This systemic vasculitis is rarely encountered in children and
may present with pulmonary infiltrates and cavitary lung disease. The most common
presentation includes sinusitis, fever epistaxis and hematuria.

Figure 70. Case 7.
PA chest radiograph shows a large nodular opacity in the right upper lobe , with smaller

opacities scattered elsewhere in the lungs (short arrows).

Page 99


Clinical Cases (continued)


A 4-month-old Hispanic girl was evaluated for a pulmonary mass on chest radiograph
(Figure 71). The initial differential diagnostic considerations included pneumonia, thymus,
central obstructive process, or congenital agenesis of left upper lobe. Chest CT is shown
(Figure 72). Tuberculin skin test measured 18 mm induration. Pulmonary TB disease was
diagnosed in the child's mother. Gastric aspirates from the infant were AFB smear
positive and the culture grew TB. The child was treated with standard therapy and follow
up radiographs showed gradual resolution (Figure 73).

Figure 71. Case 8.
PA chest radiograph shows a large area of air space consolidation in the left upper lobe without

shift of the

Page 100


Clinical Cases (continued)


Figure 72B.
Another image from the same CT scan shows peripherally enhancing lymphadenopathy in the

subcarinal and left hilar regions .

Figure 72A. Case 8.
Contrast enhanced CT image shows the left upper lobe consolidation with an area of lower
attenuation and peripheral enhancement near the mediastinum that could represent an area of

necrosis or an enhancing lymph node.

Page 101


Clinical Cases (continued)


Figure 73. Case 8.
A follow-up radiograph obtained 6 months later shows improvement in the left upper lobe

consolidation, with mild residual opacity.

Page 102


Clinical Cases (continued)

An 8-year-old boy was followed for chronic eosinophilic inflammation of the urinary
bladder (eosinophilic cystitis). Prior to starting steroid therapy he had a negative
tuberculin skin test that measured 0 mm. There were no risk factors for TB. An initial
chest radiograph from the referring clinic was reported as "normal except for aortic
calcification." Steroids were started for treatment of the cystitis and a follow up chest
radiograph is shown (Figure 74).

Repeat TB skin test was negative. An IGRA blood assay for TB was positive. Sputum and
urine samples were positive for TB. The patient was treated for 12 months with standard
therapy and follow up chest radiograph is shown (Figure 75).

Figure 74. Case 9.
PA chest radiograph shows a fine diffuse miliary nodular pattern in the lungs. Calcified lymph
nodes are present in the left mediastinum, which were mistaken for aortic calcifications on the

earlier radiograph.

Figure 75. Case 9.
A post-treatment radiograph shows decreased size of the calcified lymphadenopathy (white arrow)

with a tiny calcified granuloma in the left upper lobe (black arrow). The miliary nodules have


Page 103


Clinical Cases (continued)
CASE 10.

A 15-month-old boy was seen for fever, a 3 week history of draining otitis media and acute

mastoiditis. He developed seizures and cerebral spinal fluid showed 360 WBC, 67% lymphocytes, and

CSF protein of 210, consistent with meningitis. There were no risk factors for TB and the

tuberculin skin test was negative, measuring 0 mm. Chest radiograph was normal. An IGRA blood

assay for TB was positive. Brain MRI is shown (Figure 76). The patient developed hydrocephalus

and ischemic infarcts as complications of TB meningitis. Cultures of the cerebral spinal fluid

grew TB. The patient was treated with standard therapy for 12 months, including steroids during

the first month.

Figure 76A. Case 10.
Contrast enhanced MRI shows abnormal signal in the right mastoid air cells with enhancement.

Figure 76B.
The same MRI at a different level reveals a small ring-enhancing nodule in the right occipital
lobe .

Page 104


Tuberculosis is an important disease worldwide and is sometimes difficult to recognize in

children who do not follow the same patterns of disease as adults. In children the lungs, lymph

nodes or central nervous system are more commonly involved. In general, radiographic findings may

be suggestive but often are not specific for TB. Characteristic patterns in children with TB

include unilateral hilar lymphadenopathy with or without consolidation and miliary disease.

Cavitary lesions are uncommon except in adolescents who may demonstrate findings similar to adult

disease. Contrast CT and/or MRI are the best diagnostic imaging modalities for extrapulmonary

disease. Pediatric TB may present with confusing and difficult to interpret clinical information.

Radiographic images are among the most important diagnostic tools.

Page 105



Marais BJ, Gie RP, Schaaf HS, et al. The natural history of childhood intra-thoracic tuberculosis

– a critical review of the literature from
the prechemotherapy era. Int J Tuberc Lung Dis. 2004;8:392-402.

Gie R. Diagnostic atlas of intrathoracic tuberculosis in children: A guide for low income

countries 2003. International Union Against
Tuberculosis and Lung Disease, Paris, France, 1-55, 2003.

Miller FJ, Seal RM, Taylor MD. Tuberculosis in children. J and A Churchill Ltd, London, UK, 1963.

Weber HC, Beyers N, Gie RP, et al. The clinical and radiological features of tuberculosis in

adolescents. Ann Trop Paediatr. 2000;20, 5-10.

Lincoln EM, Sewell EM. Tuberculosis in children. McGraw-Hill, New York, pp 1-327, 1963.

Bosch-Marcet J, Serres-Creixams X, Borras-Perez V, et al. Value of sonography for follow-up of

mediastinal lymphadenopathy in children
with tuberculosis. Journal of Clinical Ultrasound. 2007 Mar-Apr;35(3):118-124.

Im J-G, Itoh H, Shim Y-S, et al. Pulmonary tuberculosis: CT findings-early active disease and

sequential changes with antituberculous
therapy. Radiology. 1993;186:653-660.

Bentley FJ, Grzybowski S, Benjamin B. Tuberculosis in childhood and adolescence. The National

Association for the Prevention of
Tuberculosis. London, England: Waterlow and Sons Ltd, 1954:1-213 and 238-253.

Schaaf HS, Beyers N, Gie RP, et al. Respiratory tuberculosis in childhood: the diagnostic value

of clinical features and special investigations.
Pediatr Infect Dis J. 1995 Mar;14(3):189-94.

Milkovic D, Richter D, Zoricic-Letoja I, Raos M, Koneul I. Chest radiography findings in primary

pulmonary tuberculosis in children. Coll
Antropol. 2005 Jun;29(1):271-276.

Neu N, Saiman l, San Gabriel P, et al. Diagnosis of pediatric tuberculosis in the modern era.

Pediatr Infect Dis J. 1999 Feb;18(2):122-126.

Andronikou S, Joseph E, Lucas S, et al. CT scanning for the detection of tuberculous mediastinal

and hilar lymphadenopathy in children.
Pediatr Rad. 2004 Mar; 34(3):232-6.

Delacourt C, Mani TM Bonnerot V, et al. Computed tomography with normal chest radiograph in

tuberculous infection. 1993, Arch Dis Child.

Andronikou S, Brauer B, Galpin J, et al. Interobserver variability in the detection of

mediastinal and hilar lymph nodes on CT in children with
suspected pulmonary tuberculosis. Pediatr Radiol. 2005 35:425-28.

Du Toit G, Swingler G, Iloni K. Obeserver variation in detecting lymphadenopathy on chest

radiograph. Int J Tubercu Lung Dis. 2002

Donnelly LF, Emery KH, Brody AS, et al. Minimizing radiation dose for pediatric body applications

of single-detector helical CT: strategies at
a large children's hospital. AJR AM J Roentgenol. 2001 Feb;176(2):303-6.

Marais BJ, Gie RP, Schaaf HS, et al. A proposed radiological classification of childhood

intra-thoracic tuberculosis. Pediatr Radiol. 2004

Im JG, Itoh H, Han MC. CT of pulmonary tuberculosis. Seminars in Ultrasound CT MR. 1995


Kosaka N, Sakai T, Uematsu H, et al. Specific high-resolution computed tomography findings

associated with sputm smear-positive
pulmonary tuberculosis. Journal of Computer Assisted Tomography. 2005 Nov-Dec;29(6):801-4.

Jamieson DH, Cremin BJ. High resolution CT of the lings in acute disseminated tuberculosis and a

pediatric radiology perspective of the
term "miliary". Pediatr Radiol. 1993;23(5):380-3.

Baumann MH, Nolan R, Ptrini M, et al. Pleural tuberculosis in the United States: incidence and

drug resistance. Chest. 2007; 131:1125-1132.

Theart AC, Marais BJ, Gie RP, et al. Criteria used for the diagnosis of childhood tuberculosis at

primary health care level in a high-burden,
urban setting. International Journal of Tuberculosis and Lung Disease. 2005 Nov;9(11):1210-1214.

Enarson DA, Dorken E, Grzybowski S. Tuberculosis pleurisy. Can Med Assoc J. 1982;126:493-5.

Chiu CY, Wu JH, Wong KS. Clinical spectrum of tuberculous pleural effusion in children. Pediatr

Int. 2007 Jun;49(3):359-62.

Andreu J, Caceres J, Pallisa E, Martinez-Rodriguez M. Radiological manifestations of
pulmonary tuberculosis. European Jouranl of Radiology 2004;51:139-149.

Schaaf HS, Marais BJ, Whitelaw A, et al. Culture-confirmed childhood tuberculosis in Cape Town,

South Africa: a review of 596 cases. BMC
Infect Dis. 2007 Nov 29;7:140.

Page 106


Shewchuk JR, Reed MH. Pediatric postprimary pulmonary tuberculosis. Pediatr Radiol. 2002


Griffith-Richards SB, Goussard P, Andronikou S, et al. Cavitating pulmonary tuberculosis in

children: correlating radiology with pathogenesis.
Pediatr Radiol. 2007 Aug;37(8):798-804.

Kisembo HN, Kawooya MG. Zirembuzi G, Okwera A. Serial chest radiographs in the management of

children with a clinical suspicion of
pulmonary tuberculosis. Journal of Tropical Pediatrics. 2001 Oct:47;276-283.

Fish RH, Pagel W. The morbid anatomy of epituberculosis. J Path Bact. 1938; 47:593-601.

Kim WS, Moon WK, Kim IO, et al. Pulmonary tuberculosis in children: evaluation with CT. AJR Am J


Morrison JB. Resorption of calcification in primary pulmonary tuberculosis. Thorax. 1970;25:


Tsao PC, Lin PY. Clinical spectrum of bronchiectasis in children. Act Paediatr Taiwan. 2002


Garg RK. Tuberculous meningitis. Acta Neurol Scand. 2010 Aug 1;122(2):75-90.

Theron S, Andronikou S, Grobbelaar M, et al. Localized basal meningeal enhancement in tuberculous

meningitis. Pediatr Radiol. 2006

Andronikou S, Smith B, Hatherhill M, Douis H, Wilmsgurst J. Definitive neuroradiological

diagnositic features of tuberculous meningitis in
children. Pediatr Radiol. 2004 Nov;34(11):876-85.

Bernaerts A, Vanhoenacker FM, Parizel PM, et al. Tuberculosis of the central nervous system:

overview of neuroradiologic findings. Eur
Radiol. 2003 13(8):1876-1890.

Kumar R, Kohli N, Thavnani H, et al. Value of CT scan in the diagnosis of meningitis. Indian

Pediatr. 1996;33:465-468.

Artopoulos J, Chalemis Z, Christopoulos S, et al. Sequential computed tomography in tuberculous

meningitis in infants and children. Comput
Radiol. 1984 8:271-277.

Bhargava S, Gupta AK, Tandon PN. Tuberculous meningitis – a CT study. Br J Radiol. 1982


Farinha NJ, Razali KA, Holzel H, et al. Tuberculosis of the central nervous system in children: a

20-year survey. J Infect. 2000 41:61-68.

Kingsley DP, Hnedrickse WA, Kendall BE, et al. Tuberculous meningitis: role of CT in management

and prognosis. J Neurol Neurosurg
Psychiatry. 1987 50:30-36.

Kumar R, Singh SN, Kohli N. A diagnostic rule for tuberculous meningitis. Arch Dis Child.


Leiguarda R, Berthier M, Starkstein S, et al. Ischaemic infarction in 25 children with

tuberculous meningitis. Stroke. 1988 19:200-204.

Patwari AK, Aneja S, Ravi RN, et al. Convulsions in tuberculous meningitis. J Trop Pediatr. 1996


Waeker NJ, Connor JD. Central nervous system tuberculosis in children: a review of 30 cases.

Pediatri Infect Dis J. 1990 9:539-543.

Altunbasak S, Alhan E, Baytok V, et al. Tuberculous meningitis in children. Acta Paediatr Jpn.

1994 36:480-484.

De JK, Bagchi S, Bhadra UK, et al. Computerised tomographic study of tuberculous meningitis in

children. J Indian Med Assoc. 2002 42:91-97.

Kemaloglu S, Ozkan U, Bukte Y, et al. Timing of shunt surgery in childhood tuberculous meningitis

with hydrocephalus. Pediatr Neurosurg.
2002 37:194-198.

Ozates M, Kemaloglu S, Gurkan F, et al. CT of the brain in tuberculous meningitis. Acta Radiol.

2000 41:13-17.

Tung Y-R, Lai M-C, Lui C-C, et al. Tuberculous meningitis in infancy. Pediatr Neurol. 2002


Upadhyaya P, Bhargava S, Sundaram KR, et al. Hydrocephalus caused by tuberculous meningitis:

clinical picture, CT findings and results of
shunt surgery. Z Kinderchir. 1983 38 [Suppl 2]:76-79.

Scheoman JF, Van Zyl LE, Laubscher JA, et al. Serial CT scanning in childhood tuberculous

meningitis: prognostic features in 198 cases. J
Child Neurol. 1995 10:320-329.

Przybojewski S, Andronikou S, Wilmshurst J. Objective CT criteria to determine the presence of

abnormal basal enhancement in children with
suspected tuberculous meningitis. Pediatr Radiol. 2006 Jul;36(7):687-96.

Andronikou S, Wieselthaler N, Smith B, et al. Value of early follow-up CT in paediatric

tuberculous meningitis. Pediatr Radiol. 2005

Pienaar M, Andronikou S, van Toorn R. MRI to demonstrate diagnostic features and complications of

TMB not seen with CT. Childs Nerv Syst.
2009 25:941-947.

du Plessis J, Andronikou S, Wieselthaler N, et al. CT features of tuberculous intracranial

abscesses in children. Pediatr Radiol. 2007

Saczek KB, Schaaf HS, Voss M, Cotton MF, Moore SW. Diagnostic dilemmas in abdominal tuberculosis

in children.
Pediatr Surg Int. 2001;17:111-15.

Andronikou S, Welman CJ, Kader E. The CT features of abdominal tuberculosis in children. Pediatr

Radiol. 2002 Feb;32(2):75-81.

Page 107


Harisinghani MG, McLoud TC, Shepard J-A, et al. Tuberculosis from head to toe. Radiographics.


Andronikou S, Jadwat S, Douis H. Patterns of disease on MRI in 53 children with tuberculous

spondylitis and the role of gadolinium. Pediatric
Radiol. 2002 Nov;32(11):798-805.

Teklali Y, El Alami ZF, El Madhi T, Gourinda H, Miri A. Peripheral osteoarticular tuberculosis in

children: 106 case-reports. Joint Bone Spine.
2003 Aug;70(4):282-6.

Hsieh S, Kuo Y, Chern M, et al. Mycoplasma pneumonia: clinical and radiographic features in 39

children. Pediatr Int. 2007 49:363-367.

Wang RS. Wang SY, Hsieh KS, et al. Necrotizing pneumonitis caused by Mycoplasma pneumoniae in

pediatric patients: report of five cases and
review of literature. Pediatr Infect Dis J. 2004;23:564-7.

Ragosta KG, Clayton JA, Cambareri CB, Domachowske JB. Allergic bronchopulmonary aspergillosis

masquerading as pulmonary tuberculosis.
Pediatr Infect Dis J. 2004 Jun;23(6):582-4.

Ng KK, Cheng YF, Ko SF, et al. CT findings of pediatric thoracic actinomycosis: report of four

cases. J Formos Med Assoc.
1992 Mar;91(3):346-50.

Graham SM, Coulter JB, Gilks CF. Pulmonary disease in HIV-infected children. Int J Tuberc Lung

Dis. 2001 5:12-23.

Rennert WP, Kilner D, Hale M. Tuberculosis in children dying with HIV-related lung disease:

clinical-pathological correlations. Int J Tuberc Lung
Dis. 2002 6:806-813.

Fang W, Washington L, Kumar N. Imaging manifestations of blastomcycosis: a pulmonary infection

with potential dissemination.
Radiographics. 2007 May-Jun;27(3):641-655.

Singh M, Kothur K. Pulmonary sarcoidoisis masqueratding as tuberculosis. Indian Pediatrics. 2007


Lemme SD, Kevin RA, Cannon CP, et al. Primary tuberculosis of bone mimicking a lytic bone tumor.

J Pediatric Hematology Oncology. 2007