Download as pdf or txt
Download as pdf or txt
You are on page 1of 7

1361

Review

American Journal of Roentgenology 1995.164:1361-1367.

CT in Adults with Tuberculosis


of the Chest:
Findings and Role in Management
Kyung

Soo

Lee1

and Jung-Gi

Chest radiography remains the firstimaging technique in


the evaluation
of thoracic
tuberculosis.
Conventional
and
high-resolution
CT (1-2-mm
collimation,
high-spatial-frequency
reconstruction
algorithm)
may be needed for further
evaluation of known or suspected tuberculosis in the thorax.
The purpose of this review is to describe the characteristic
CT findings of various forms of tuberculous involvement of
the thorax in adults and to assess the role of CT in the diagnosis and management
of the disease.
CT Findings
Involving

the Lung

Parenchyma

Primaiy
tuberculosis.-The
decreasing exposure to Mycobacterium
tuberculosis
in childhood,
because of public health
measures
and the advent of antituberculous chemotherapy,
has resulted in later initialexposure to tuberculosis and an
increased likelihood of susceptibility to tuberculosis during

Received

November

28, 1994:

1 Department

of Diagnostic

2Department

of Diagnostic

AJR 1995;164:1361-1367

accepted

Imaging,
Radiology,

Characteristic

1m2

The frequency of tuberculosis


decreased continuously
until
1 985, when the trend reversed, mainly because of the large
number of cases in patients with AIDS [1-3]. Pulmonary
tuberculosis remains a common disease In North America, particularly In groups such as the socioeconomlcally
disadvantaged,
the elderly, chronically
debilitated
patients, immigrants,
refugees, and prisoners (1-3]. The prevalence and incidence of the
disease are still high in endemic areas [4].

Tuberculosis

Article

after

revision

Samsung

Medical

Seoul

National

0361-803)(/95/i646-1361

January
Center,
University

American

adulthood
[5-7]. Therefore,
tuberculosis
in adults frequently
appears
initially with the findings
of primary tuberculosis,
as
in children.
Primary
tuberculosis
usually presents
in association
with
lobar pneumonia
combined
with radiologically
recognizable
enlargement
of lymph nodes in the hilum or the mediastinum.
The site of primary tuberculosis
in the lungs reflects areas of
greatestventilation;
the most common sites are the middle lobe,
the lower lobes, or the anterior segment of an upper lobe [5].
The typical
appearance
of primary
tuberculosis
on CT
scans is air-space consolidation.
The consolidation
is usually
homogeneous,
dense, and well defined. It is anatomically
confined to a segment
(Fig. 1) or, more commonly,
to a lobe. With
progression,
especially
in patients
who are immunocompromised, have diabetes,
or are taking corticosteroids,
lobar or
segmental
pneumonia
may break down into multiple cavities.
Nonsegmental
distribution
of lesions also occurs [8]. Primary
tuberculosis
appears as a solitary cavitary lesion in about 10%
of patients [9]. On CT scans, the wall ofthe cavity can be thick
or thin and smooth or irregular. An air-fluid
level in the cavity is
common.
Acute bronchogenic
spread of tuberculosis
occurs
from breakdown
of a lobar infection
or from rupture
of an
infected lymph node into the bronchus.
The disease disseminates widely to the other bronchial
segments
or other lobes of
either lung. Typical CT findings in bronchogenic
spread of pulmonary tuberculosis
are centrilobular
branching
linear structure, relatively
poorly
defined
centnlobular
peribronchiolar

31, 1995.
50, Irwon-Dong,
College
Roentgen

Kangnam-Ku,

of Medicine,
Ray Society

Seoul

135-230,

28, Yongon-Dong,

South

Chongno-Ku,

Korea.

Address

Seoul

correspondence

110-744,

to K. S. Lee.

South Korea.

1362

LEE

nodules
2-3 mm in size, acinar shadows
4-10 mm in size,
and large lobular consolidations
[9] (Fig. 2).
Miliary tuberculosis.-In
2-6% of primary tuberculosis,
the
lymphohematogenous
dissemination
of massive
numbers
of
viable
organisms
results
in clinical
and radiographic
evidence of miliary tuberculosis
[1 5, 10, 11]. Miliary tuberculosis can occur in postprimary
tuberculosis
when the hosts
defense
mechanism
is overwhelmed.
In the early stage of miliary
tuberculosis,
chest radiographs may appear normal. Follow-up
radiographs
obtained
a week or more later usually
show a poorly defined
haze
through
both lungs. Typical nodules of 1-2 mm become
recognizable
even later. As the infection
progresses,
the miliary
nodules
coalesce.
Cavitation
may occasionally
occur in the
nodules
[5]. Adult respiratory
distress
syndrome
can be a
complication
of miliary tuberculosis
[6].
High-resolution
CT scans show poorly or well-defined
1-2mm nodules widely disseminated
through
the lungs in association with diffuse reticulation
[8] (Fig. 3). McGuinness
et al.
[12] reported
high-resolution
CT findings
of miliary lung disease in nine patients.
A mixture of both sharply
and poorly
defined
1-3-mm
nodules was seen in all cases, many of the
latter having an appearance
indistinguishable
from air-space
nodules.
Other features
attributable
to the presence
of nodules included
nodular
interlobular
septa, nodular irregularity
of vessels,
subpleural
dots, and studded
fissures.
Diffuse
intra- and interlobular
septal thickening
also proved common,
appearing in eight patients (91%). CT findings of miliary
tuberculosis appear to be due to granulomatous
foci developing in a seemingly
random distribution
involving
both pulmonary air space and the interstitium.
Postprimaiytuberculosis.-Postprimary
tuberculosis
results
from reactivation
of a previously
dormant
primary infection
in
90% of cases; a minority of cases represent
a continuation
of

American Journal of Roentgenology 1995.164:1361-1367.

AND

IM

AJR:164,

June

1995

the primary disease [5, 13]. Rarely, postprimary


tuberculosis
is
an exogenous
superinfection
on an inactive
or even active
original infection
(true reinfection).
The postprimary
tubercubus pattern also occurs in patients
previously
immunized
by
bacille Calmette-Gu#{233}rin (BCG) vaccine [4].
The most commonly
involved
parts of the lungs in postprimary disease
are the apical and posterior
segments
of an
upper
lobe. When
postprimary
tuberculosis
involves
the
anterior
segment
of an upper lobe or basilar segment
of a
lower lobe by parenchymal
disease,
it may be misdiagnosed
radiographically
as another bacterial
infection
[10]. Nonetheless, in most of these cases, cavitary or fibronodular
disease
is present in typical locations,
and in many of these patients
there is also residual
radiographic
evidence
of the previous
primary
disease-subtle
but helpful
adjunctive
findings
in
correctly
diagnosing
tuberculosis.
Im et al. [14] evaluated
the high-resolution
CT findings
of
newly diagnosed
active postprimary
pulmonary
tuberculosis
in
41 patients. The findings were centrilobular
lesions appearing
as a nodule or a branching
linear structure
(95%), bronchial
wall thickening
(73%), a poorly defined nodule (61%), a cavity
(51 %), and lobular consolidation
(41 %) (Fig. 4A). On CTpathologic
correlation,
the centrilobular
nodules on CT scans
denote the inflammatory
lesion in the bronchioles
and peribronchiolar
alveoli on histologic
examination.
The caseous
material occupying
the bronchiolar
lumen and alveolar
ducts
appeared
with branching
linear subacinar
structure
finer than
the centrilobular
type of nodule. Large areas of consolidation
on pathologic
examination
manifested
as areas of lobular and
lobar consolidation
on CT scans. Lobular consolidation
consisted of centrally located granulomas
that contained
caseation
necrosis
and marginal
nonspecific
inflammation;
the area of
inflammation
appeared
relatively
less dense than the area of
central granuloma
with caseation
necrosis.

Fig. 1 .-Primary
tuberculosis
appearing
as
segmental
consolidation
In 27-year-old
woman.
Thin-section
(1.5-mm
collimation)
CT scan obtamed at level of bronchus
Intermedius
shows
segmental
consolidation
In anterior
segment
of
right upper lobe of lung. Small variable-sized
nodular lesions are also observed
lateral to segmental consolidation.
Fig. 2.-Bronchogenlc
spread
of pulmonary
tuberculosis
In 29-year-old
man. Thin-section
(1 .5-mm collimation)
CT scan obtained
at level of
bronchus
intermedius
shows foci of nodular lesions markedly
variable
In size in anterior
segment of right upper lobe and superior
segment
of left lower lobe of lung. Lesions consist of
branching
linear structures
(arrowheads),
2-3mm poorly defined centrilobular
perlbronchlolar
nodules
(straight
arrows),
4-10-mm
acinar
shadows
(curved
arrows), and larger lobular
consolidation.
Fig. 3.-Millary
tuberculosis
In 29-year-old
woman.
Thin-section
(1 .5-mm
collimation)
CT
scan obtained
at level of right upper lobar bronchus shows 1-4-mm
nodular lesions throughout
lung.
Also
note
Irregular
nodular
vessels
(arrows)
and studded
fissure (arrowheads).

American Journal of Roentgenology 1995.164:1361-1367.

AJR:164,

June

1995

CT

OF

TUBERCULOSIS

On follow-up CT examinations,
gradual disappearance
of lobular consolidation,
poorly defined nodules, and centnlobular
nodules or branching
linear lesions were seen, in that order.
Resolution oflobular consolidation
began usually atthe periphery,
with eventualtransformation
into a poorly defined nodule, followed
by the appearance
of a centrilobular
nodule or branching
linear
lesion. Centrilobular
nodules or branching
linear structures seen
on initial CT scans gradually decreased
in prevalence
and were
no longer observed after 12 months of treatment. Compared
with
centrilobular
lesions, cavities healed and disappeared
by obliteration with more residual fibrotic changes (linear or stellate).
On the other hand, the findings
of inactive or stable-state
pulmonary
tuberculosis
on high-resolution
CT scans include
areas of irregular
lines and calcified
nodules along with distortion
of bronchovascular
bundles,
bronchiectasis,
and
pericicatrical
emphysema
[14] (Figs. 4B and 5).
Determination
of disease activity in patients with pulmonary
tuberculosis
usually depends on the detection of acid-fast bacilli
on culture of sputum or bronchoalveolar
lavage fluid. However,
because
acid-fast
bacilli are found in a limited number
of
patients (20-55%)
with active pulmonary
disease [15, 16] and
chest radiographs
are commonly
classified
as indeterminate,
the diagnosis
of disease activity is important.
CT scans, especially high-resolution
CT scans, are superior
to chest radiographs
for assessing
the disease
activity
of postprimary
tuberculosis.
To compare the performance
of high-resolution
CT
scans with that of chest radiographs
in the assessment
of the
disease
activity of pulmonary
tuberculosis,
Song et al. (presented at the Society of Thoracic
Radiology
meeting,
March
1993) reviewed
chest radiographs
and high-resolution
CT
scans from 52 patients with active tuberculosis and 31 patients
with inactive
tuberculosis.
Four board-certified
radiologists
assessed
both the chest radiographs
and the CT scans, and
their observations
were plotted on a receiver operating
characteristic (ROC) curve. The mean area under the ROC curve for
high-resolution
CT was significantly
larger than that for chest

Fig. 4.-Active

OF THE

CHEST

radiography.
These researchers
concluded
that high-resolution
CT is helpful in judging the activity oftuberculosis
when findings
of bacteriologic
studies are negative and the activity cannot be
determined
by chest radiography
alone.
Tuberculoma.-Tuberculoma
is a round or oval granuloma
caused by acid-fast
bacilli, encapsulated
by connective
tissue
[18]. The pathogenesis
of tuberculomas
is controversial.
They
may result from a bronchial
infection that has been localized
and sealed off. A healed, filled-in
cavity and a rounded-off,
contracted
healing tuberculous
lesion are the reported possible mechanisms
of tuberculoma
formation
[17, 18].
The tuberculomas
on CT scans are usually regular and
smooth in outline but may have a rough edge. Cavitation
in the
lesion or surrounding
satellite nodule(s) (Fig. 6) can be seen on
CT scans. The lesions are usually low in attenuation
and show no
or minimal enhancement
with administration
of contrast medium
[9]. Calcification
in the tuberculomas
is found in 20-30%
of the
lesions and is usually nodular and diffuse [19]. Rarely, tuberculoma appears with a CT halo sign (halo of ground-glass
attenuation surrounding
the nodule) in patients with hemoptysis
[20].
Chronic infection and the destroyedlung.-ln
an incompetent
immune state (when the cellular immune response of patients is
lowered), multiple foci oftuberculosis
throughout
the lungs may
persist with a fibrotic cavitating
pattern. Radiologically,
there are
multiple small cavities, with a variable degree of alveolar clouding around each lesion [5, 21] (Fig. 7). In chronic infection,
a
nonspecific
radiologic
pattern of interstitial fibrosis, severe and
widespread
throughout
both lungs, is occasionally
encountered,
diagnosed
only by open lung biopsy [5].
Complete
destruction
of the whole or a major part of a lung is
not an uncommon
end stage of tuberculosis.
It may result from
a progressive primary infection or from prolonged cavitation,
reinfection,
spread, and subsequent
fibrosis. In the majority of
patients, this is unilateral
and involves the upper lobe. Bronchiectasis
isalmost always associated. Marked elevation of the
hilum occurs with compensatory
lower lobe hyperexpansion.

cavitary
pulmonary
tuberculosis
in 36-year-old
woman.
(1 .5-mm collimation)
CT scan obtained
at level of distal trachea shows cavltary lesion with air-fluid
level In right upper lobe of lung. Surrounding
nodular lesions have similar pattern
to those in Figure 2. Also note tuberculous
lesions In left upper lobe of lung.
B, CT scan at 1-year follow-up
obtained
at similar level after completion
of chemotherapy
shows
fibrotic lung lesion with areas of irregular
lines and distortion
of central and peripheral
bronchovascular bundles.
Areas of pericicatrical
emphysema
(arrowheads) are also observed.
These findings
suggest
stable state of pulmonary
tuberculosis.

A, Thin-section

1363

Fig. 5.-Stable
pulmonary
tuberculosis
in 52year-old
man who received
antituberculous
chemotherapy
for 9 months.
Thin-section
(1 .5-mm
collimation)
CT scan obtained
at level of thoraclc
Inlet shows areas of irregular
lines, parenchymal
bands,
irregular
nodules,
and emphysema
In
right upper lobe of lung. These findings
suggest
tuberculous
lesions are stable in their activity.

LEE

1364

American Journal of Roentgenology 1995.164:1361-1367.

Aiiway

Tuberculosis

Airway involvement
in tuberculosis
has been reported in 1020% of all patients with pulmonary tuberculosis
[22, 23]. The airways can be involved secondarily
by the spread of the organism
within the airway lumen or along peribronchial
lymphatic channels
from an area of cavitation or localized tuberculous
pneumonia.
They can also be involved by direct extension of infection from a
contiguous
lymph node orfrom the parenchyma
itself [24, 25].
On CT scans, the bronchi show stenosis with wall thickening, obstruction
with a peribronchial
cuff of soft tissue (Fig.
8), stenosis
or obstruction
with tuberculous
Iymphadenitis
(Fig. 9), or an intraluminal
polypoid
mass of low attenuation
[4, 26]. The lung parenchyma
distal to the bronchial
lesion is
involved
with segmental
atelectasis
or consolidation,
cavities, or a round area of low attenuation,
suggesting
mucoid
impaction
distal to the obstructed
bronchus
on CT scans [4].
Bronchial tuberculosis
may cause a diagnostic problem in that
there are overlapping
features
with bronchogenic
carcinoma
both on radiographs
and CT scans (Figs. 8 and 9). Thickening
of
the bronchial
wall in tuberculous
bronchitis
may simulate the
findings
of early bronchogenic
carcinoma.
The presence
of
enlarged lymph nodes lying close to the stenotic bronchus with
low attenuation
on enhanced
CT scans, when combined
with
peripheral
parenchymal
atelectasis
or consolidation,
may mimic
the findings of lung cancer by showing differential enhancement
between
a central tumor mass and an atelectatic
distal lung.
Because of these overlapping features between bronchial tuberculosis
and bronchogenic
carcinoma,
bronchoscopy
should
always be performed
to confirm the diagnosis.

AND

IM

Tuberculosis

Tuberculous
mediastinal
lymphadenitis,
often
associated
pulmonary
lesion (the primary complex),
quent manifestation
of primary
tuberculosis.
The
common
in postprimary
tuberculosis
[27].

Fig. 6.-Large
tuberculoma
In 64-year-old
man. Thin-section
(1.5-mm
collimation)
CT scan
obtained
at level of thoraclc
Inlet shows 36-mm
mass containing
internal cavitation
In right apex
of lung. Calcified
and uncalcified
satellite
nodules are also observed
In surrounding
area.

with an
is a frelesion is

June

1995

Im et al. [27] assessed


CT scans of 23 patients
with a
mediastinal
or hilar tuberculous
lymphadenitis.
The right
paratracheal
and tracheobronchial
nodes were preponderantly involved.
On enhanced
CT scans, nodes larger than 2
cm in diameter
invariably
showed central areas of low attenuation and peripheral
rim enhancement
(1 9 patients,
83%)
(Fig. 1 0). Enhanced
walls were usually irregular in thickness.
In a small number
of patients,
solid (1 patient, 4%) or calcified nodes (5 patients,
22%) could be observed.
Moon et al. [28] analyzed the initial and follow-up
CT scans
obtained in 58 consecutive
patients who had mediastinal
lymphadenitis
and who were treated with antituberculous
chemotherapy for 18 months. CT patterns of the initial lesions before
treatment were categorized
into four types: solid; peripheral
rimenhancing
with central low attenuation;
extranodally
extensive;
and calcified.
Prompt response
(decreased
size of the lymph
nodes within the first 3 months and no residual nodes after 1
year) was usually seen in the peripheral
rim-enhancing
type with
central low attenuation
(20/36 patients, 56%) and the extranodally extensive type (6/9 patients, 67%). Slow (decrease
in size
after 3 months but residual lesion after 1 year) or no (no change
in size after treatment)
response was observed
in the solid (6/8
patients, 75%) and calcified (4/5 patients, 80%) types. Interestingly, in nine of 36 patients with peripheral rim-enhancing
lesions
with central low attenuation,
temporary
increase
but ultimate
decrease of nodal size was noted. The investigators
concluded
that response to chemotherapy
could be predicted on the basis
of CT findings in patients with tuberculous
lymphadenitis.

Pleural
Mediastinal

AJR:164,

Tuberculosis

Pleural effusion occurs in about 10% of all new cases of tuberculosis infection [5]. The frequency
is higher in adult patients with
AIDS [4]. Tuberculous
effusion appears either as free pleuralfluid
or as loculated
effusion. Although
the lymph nodes may be
enlarged,
a pulmonary
lesion is seldom seen on a radiograph

Fig. 7.-Chronic
active pulmonary
tuberculosis In 20-year-old
woman.
ThIn-section
(1.5-mm
collimation)
CT scan obtained
at subcarlnal
level
shows extensive
lesions containing
areas of nodules and consolidation.
Nodules
are variable
in
size. Also note cavity with areas of surrounding
nodular consolidation
in right upper lobe of lung.

Fig. 8.-Bronchial
tuberculosis
In 38-year-old
woman.
Enhanced
conventional
(10-mm collimation) CT scan obtained
at subcarinal
level shows
obstruction
of left upper
lobar bronchus
with
peribronchial
cuff
of soft
tissue
(arrows).
Atelectasis
of left upper lobe of lung Is associated. Also note calcified
tuberculoma
In superior
segment
of left lower lobe of lung.

AJR:164,

June

1995

CT

OF

TUBERCULOSIS

when a pleural effusion is present [4, 29, 30]. However, a lung


focus is usually found on pathologic examination
[4, 30].
In acute tuberculous
effusion, a CT scan may show parenchymal cavitation
(including
a small subpleural
cavity), the site
of communication
between
the cavity and the pleural space,
parenchymal
infiltrates,
and hilar adenopathy
as well as fluid
collection
in the pleural cavity [30] (Fig. 11). Hulnick et al. [30]
observed
subpleural
parenchymal
cavitation
in 8/14 patients
(57%) with pleural tuberculosis
on CT scans. Thin, regular
pleural thickening
can be shown on CT scans.
In chronic
tuberculous
empyema,
CT scans show a focal fluid collection
in association
with pleural thickening
and calcification
(Fig.
12). In these cases, the presence
of residual pleural fluid signifies active infection.
Additionally,
CT scans may show the
complication
of chronic tuberculous
empyema,
including bronchopleural
fistula and cold abscess (empyema
necessitatis)
in
the chest wall. Fibrothorax
with diffuse pleural thickening
without effusion on CT scans indicates the disease is inactive [30].

American Journal of Roentgenology 1995.164:1361-1367.

Pericardial

Tuberculosis

Involvement
of the pericardium
by nodal rupture is common
in pericardial
tuberculosis
because of the close anatomic
relationship between the mediastinal
lymph nodes and the postenor pericardial
sac. The pericardium
can also be involved
in
miliary spread of the disease [9].
When the pericardium
is involved
with tuberculosis
by
nodal rupture,
lymphadenopathy
and pericardial
thickening
with or without
effusion
may be seen on CT scans [9] (Fig.
13). When the pericardium
is involved with miliary tuberculosis, the evidence
of parenchymal
miliary disease
along with
pericardial
effusion can be observed.
In the chronic constrictive
stage of pericardial
tuberculosis
in adults, pericardial
thickening
by more than 3 mm is seen
with or without pericardial
effusion.
Secondary
signs of dilatation of the inferior vena cava (more than 3 cm in diameter)

Fig. 9.-Bronchial
tuberculosis
associated
with
lymphadenitis
In 60-year-old
woman.
Enhanced
conventional
(10-mm
collimation)
CT scan obtained at subcarinal
level shows stenosis of lingular segmental
bronchus
with hilar adenopathy.
On
bronchoscopy,
lingular
segmental
bronchus
showed narrowing
with active inflammation.
Also
note subcarlnal
adenopathy
and parenchymal
lesions both In left upper and lower lobes of lung.

OF

THE

1365

CHEST

and acute angulation


or sinus configuration
of the interventricular
septum
are usually associated.
Visceral
pericardial
calcification
may occur at the atrioventricular
grooves,
interventricular
grooves,
or especially
the crux of the heart (the
intersection
of the walls separating
the right and left sides
and the atrial and ventricular
heart chambers).
Parietal pencardial
calcification
may range from focal patches
to large
uniform plaques on CT scans [31].

Chest

Wall Tuberculosis

Tuberculous
rib involvement
may occur either by direct
extension
from a pleuropulmonary
tuberculous
lesion or from
hematogenous
spread from a distant focus. CT findings
of
costal tuberculosis
are soft-tissue
lesions with low attenuation
showing rim enhancement
on enhanced
scans, with or without
bone destruction
(Fig. 13). Lee et al. [32] reviewed
the CT
findings of 13 tuberculous
rib lesions in eight patients. On CT
scans, all rib lesions showed
a juxtacostal
soft-tissue
mass
with central low attenuation
and peripheral
rim enhancement.
Only four of 13 lesions demonstrated
bone destruction:
two
were osteolytic
expansile
lesions with cortical disruption
and
two were mild cortical irregularities.
In addition to ribs, other components
of the chest wall can
be involved with tuberculosis.
Adler et al. [33] reviewed the CT
findings in four patients with documented
tuberculous
infection
of the chest wall. In their cases, the ribs were involved
in two
patients,
the costal cartilage
in one, and the stennoclavicular
joint in one. The CT findings were osseous
and cartilaginous
destruction
in four patients, soft-tissue
masses with calcification in two, and rim enhancement
of a soft-tissue
mass following IV administration
of contrast
medium
in two. They
concluded
that the chest wall tuberculosis
is characterized
by
bone or costal cartilage
destruction
and soft-tissue
masses
that may demonstrate
calcification
or rim enhancement.

Fig. 10.-Tuberculous
lymphadenltis
In 29year-old
man. Enhanced
CT scan obtained
at level of distal trachea
shows enlarged
lymph node
in paratracheal
area. Node shows central low attenuation
with rim enhancement.
Also notice
small node in left lower paratracheal
region.

Fig. 11.-Tuberculous
effusion
in 48-year-old
man. Enhanced
thin-section
(1 .5-mm
collimation) CT scan obtained
at ventricular
level shows
pleural effusion
in right hemithorax.
Enhancing
parietal
pleura
is evenly
thickened.
Passive
atelectasis
Is observed
in peripheral
lung. Small
cavitary
lesion (arrow) in right middle
lobe of
lung abuts right major fissure.

1366

LEE

American Journal of Roentgenology 1995.164:1361-1367.

Fig. 12.-Chronic
tuberculous
empyema
In
48-year-old
man. Conventional
(10-mm
collimation) CT scan obtained
at liver dome shows pleural calcification.
Small
amount
of
pleural
effusion
(arrows) is associated.
Also note thickened ribs in left hemithorax.

in Patients

IM

AJR:164,

June

1995

Fig. 13.-Progressive
primary tuberculosis
involving
chest wall and pericardlum
In 18-year-old
woman.
A, Enhanced
conventional
(10-mm collimation)
CT scan obtained
at level of thoracic
inlet shows
fluid collection
in right thoracic
inlet with peripheral
rim enhancement.
Destruction
of right first rib
Is noted anteriorly.
Also note irregular-shaped
tuberculoma
In left upper lobe of lung.
B, CT scan obtained at level of bronchus intermedlus
shows extensive
pericardial
thickening
(solid arrows).
Enlarged
left hilar nodes (open arrows) are also observed.
Also note consolidation
in superior segment
of left lower lobe of lung.

The findings of tuberculous


spondylitis
are characterized
by
a predilection
for the midthoracic
spine, vertebral
destruction
with gibbus deformity,
disk collapse,
and calcified
paraspinal
abscesses
[34] (Fig. 14). On CT scans, encroachment
on the
spinal canal and cord is well shown, as is the presence
of
large paraspinal
abscess.
Tuberculosis

AND

with AIDS

An association
between
tuberculosis
and HIV infection
is
evident;
in one study [35], nearly 25% of patients with AIDS
had tuberculosis.
To determine the difference in disease patterns on CT scans
between seropositive
and seronegative
patients, Leung et al. [36]
reviewed the CT scans of 33 HIV-seropositive
patients with culture-proved
tuberculosis
infection along with 33 age-, race-, and
sex-matched seronegative
control subjects. HIV-positive
patients
had a higher prevalence of lymphadenopathy
(p < .01), miliary disease (p < .01), and extrapulmonary
manifestations
(p < .01). The
prevalence
of consolidation
(p < .01),cavitation (p < .01), and
reactivation-like
disease distribution
(p < .01) occurred
less frequently in seropositive
patients. The researchers concluded that

seropositive
patients had a lower prevalence
of localized parenchymal disease and a higher prevalence ofdisseminated
disease.
HIV-infected
patients with tuberculosis
and mediastinal
adenopathy have lower CD4 cell counts than do those without adenopathy. In patients
with lower CD4 cell counts
(<50/mm3),
progressive
primary tuberculosis
that is characterized
by mediastinal adenopathy
may be more likely to develop
(Fig. 15),
whereas
in patients with higher CD4 cell counts (>100/mm3),
postprimary
tuberculosis
may be more likely to develop [37, 38].
In contrast with the findings of mediastinal
adenopathy,
pleural
effusions are more common
in HIV-infected
patients with more
than 1 00 CD4 cells/mm3
[39].
Role

of CT in Diagnosis

and Treatment

Many patients with thoracic tuberculosis


do not need CT in
the initial diagnosis of thoracic tuberculosis.
CT can help identify
or confirm the presence of findings that may be used to suggest
the diagnosis of tuberculosis
when the radiographic
findings are
inconspicuous
but when tuberculosis
is suspected
clinically.
CT is helpful
in the diagnosis
of miliary tuberculosis
in
patients with fever of unknown
origin and a chest radiograph

Fig. 14.-Tuberculous
spondylltis
In 52-yearold man. Conventional
(10-mm
collimation)
CT
scan obtained
at ventricular
level shows
bony
destruction
of vertebral
body with formation
of
soft-tissue
mass. Left pleural effusion
and small
amount
of pericardlal
effusion
are associated.
Also note partial ateiectasls
of left lower lobe,
right middle
lobe, and lingular
segment
of left
upper lobe of lung.
Fig. 15.-Tuberculosis
In 32-year-old
patient
with AIDS. CT scan obtained
at main bronchus
level shows
extensive
mediastlnal
adenopathy
with central low attenuation.
Consolidations
are
also observed
in superior
segment
of left lower
lobe and superior
lingular segment
of left upper
lobe of lung. Also note mediastinal
gas in preaortic area, caused by esophagomedlastinal
flstula.

AJR:164,

June

1995

CT

OF

TUBERCULOSIS

that is normal.
It can help identify or confirm the presence
of
adenopathy
and lead to the diagnosis
oftuberculous
mediastinitis by showing
the lymph nodes of central low attenuation
with peripheral
rim enhancement
on enhanced
scans.
In
HIV-positive
patients,
findings
of low-attenuation
nodes are
sufficient
to warrant
instituting
empiric antituberculous
chemotherapy
[40]. The role of CT in the evaluation
of tubercubus pleurisy
may be to suggest
the diagnosis
before it is
evident
using other imaging techniques.
CT can define focal
areas of subpleural
nodule or cavitation
that are undetectable on routine chest radiographs.
In tuberculous
penicarditis, CT may enable diagnosis
at an early stage by showing
the nature and amount
of effusion,
the thickened
penicardium, and associated
pulmonary
parenchymal
tuberculous
lesions
on mediastinal
lymphadenitis
abutting
the penicardium. CT is also used to direct bronchoscopy
and to locate
appropriate
sites for biopsy [4, 22-26].
CT can display
complications
of lymphadenitis
including
esophagomediastinal
or esophagobronchial
fistula [41 42]. It is
also helpful in the diagnosis
and in the evaluation
of the extent
of cold abscess
in the chest wall, which is a complication
of
tuberculous
pleurisy. In constrictive
pericarditis,
CT can differentiate the constrictive
pericarditis
from restrictive cardiomyopathy
by showing the thickened
pericardium
by more than 3 mm [31].
CT, especially
high-resolution
CT, is superior to chest radiognaphy in assessing
tuberculosis
activity. Parenchymal
lesions
having a centrilobular
branching
linear structure,
centrilobular
peribronchiolar
nodules, acinar shadows, and large lobular consolidations
are considered
active. Cavities, the most important
radiologic evidence of activity, can be well depicted on CT scans.

American Journal of Roentgenology 1995.164:1361-1367.

OF

of primary

15.

16.
17.
18.
19.

20.
21

22.
23.
24.
25.
26.
27.
28.

29.
30.
31

32.

6. Choyke PL, Sostmen


HD, Curtis AM, et al. Adult-onset
pulmonary
tuberculosis. Radiology 1983:148:357-362
7. Miller WT, McGregor
AR. Tuberculosis:
frequency
of unusual radiographic
findings. AJR 1978;1 30:867-875
8. Ikezoe J, Kakeuchi
N, Johkoh T, et al. CT appearance
of pulmonary
tuberculosis
in diabetic
and immunocompromised
patients:
comparison
with
patients who had no underlying
disease. AJR 1992:159:1175-1179
9. Lee KS, Song KS, Lim TH, Kim PN, Kim IV, Lee BH. Adult-onset
pulmonary tuberculosis:
findings
on chest radiographs
and CT scans. AJR
1993:160:753-758
10. Woodring
JH, Vandiviere
HM, Fried AM, Dillon HL, Williams
TD, Melvin
1G. Update:
the radiographic features
of pulmonary
tuberculosis.
AJR
1986;146:497-506
11. Geppert
EF, Left A. The pathogenesis
of pulmonary
and miliary tuberculosis. Arch Intern Med1979:139:1381-1383
12. McGuinness
G, Naidich
DP, Jagirdar
J, Leitman B, McCauley
Dl. High
resolution
CT findings
in miliary lung disease.
J Comput Assist Tomogr
1992:16:384-390
13. Stead WW, Kerby GR, Schluetter
DP, Jordahi CW. The clinical spectrum

CHEST

tuberculosis

1367

in adults:

confusion

with

reinfection

in the patho-

genesis of chronic tuberculosis.


Ann Intern Med 1968;68:731-745
14. Im J-G, Itoh H, Shim Y-S, et al. Pulmonary
tuberculosis:
CT findings-

REFERENCES
1 . Buckner CB, Walker CW. Radiologic
manifestations
of adult tuberculosis.
J Thorac Imaging 1990;5:28-37
2. Centers for Disease Control. Tuberculosis,
final data: United States, 1986.
MMWR
1988:36:817-820
3. Miller WI Tuberculosis
in the 1990s. RadiolClin
NorthAm
1994;32:649-661
4. Lee KS, Kim YH, Kim WS, Hwang SH, Kim PN, Lee BH. Endobronchial
tuberculosis:
CT features.
J ComputAssist
Tomogr 1991:15:424-428
5. Palmer
PES. Pulmonary
tuberculosis:
usual and unusual
radiographic
presentations.
Semin Roentgenol
1979:14:204-243

THE

33.
34.
35.
36.

37.

38.

39.
40.

41

42.

eariy active disease and sequential


change with antituberculous
therapy.
Radiology
1993:186:653-660
Hong YP, Kwon DW, Kim Si. Tuberculosis
in Korea. In: Hong YP, ed. Management
of tuberculosis.
Seoul,
South Korea:
Ministry
of Health and
Social Affairs, Korean Academy
of Tuberculosis,
1990:3-4
Chan W, Chia M, Lee LK, et al. Bacteriological
measures
for the detection of
cases ofpulmonary
tuberculosis.
Bull WorldHealth
Organ 1971:45: 551-558
Bleyer JM, Marks JH. Tuberculomas
and hamartomas
of the lung. AJR
1957:77:101 3-1 022
Sochocky
S. Tuberculoma
ofthe lung. Am Rev Tubercle 1958:78:403-410
Lee KS, Kim HT, Cho WS, Kim PN, Bae WK, Kim IV. Active solitary tuberculoma of the lung: CT and clinical findings.
J Korean Radiol Soc 1993;
29:1200-1207
(Korean)
Gaeta M, Volta 5, Stroscio 5, Romeo P, Pandolfo
I. CT halo sign in pulmonary tuberculoma.
J Comput Assist Tomogr 1992:16:827-828
Fraser AG, Pare JAP, Pare PD, Fraser AS, Genereux
GP. Diagnosis
of diseases ofthe chest. 3rd ed. Vol 2. Philadelphia:
Saunders,
1989:897-910
Lukomsky GI, Tetarchenko
yE. Bronchology.
St. Louis: Mosby, 1979:287-305
Jokinen K, Palva T, Nuutinen
J. Bronchial
findings in pulmonary
tuberculosis. Clin Otolaryngol
1977;2:139-148
Ip MSM, So SY, Lam WK, Mok CK. Endobronchial
tuberculosis
revisited.
Chest 1986:89:727-730
Smith LS, Schillaci
RF, Sarlin AF. Endobronchial
tuberculosis:
serial
fiberoptic
bronchoscopy
and natural history. Chest 1987;91:644-647
Choe KO, Jeong HJ, Sohn HY. Tuberculous
bronchial
stenosis:
CT findings in 28 cases. AJR 1990;155:971-976
Im J-G, Song KS, Kang HS, et al. Mediastinal
tuberculous
lymphadenitis:
CT manifestations.
Radiology
1987:164:115-119
Moon WK, Im J-G, Kim HC, et al. Analysis
of CT pattems
and treatment
response
in patients with mediastinal
tuberculous
lymphadenitis.
J Korean
Radiol Soc 1993:29:995-1001
(Korean)
Medlar EM. The behavior
of pulmonary
tuberculosis
lesion: a pathologic
study (part II). Am Rev Respir Dis 1955:71:1-244
Hulnick DH, Naidich DP, McCauley
Dl. Pleural tuberculosis
evaluated
by
computed
tomography.
Radiology
1 983; 149:759-765
Suchet IB, Horwitz TA. CT in tuberculous
constrictive
pericarditis.
J ComputAssist
Tomogrl992;16:391-400
Lee G, Im J-G, Kim JS, Kang HS, Han MC. Tuberculosis
of the ribs: CT
appearance.
J ComputAssist
Tomogr 1993:17:363-366
Adler BD, Padley SP, Muller NL. Tuberculosis
of the chest wall: CT findings. J ComputAssist
Tomogrl993;17:271-273
Sharif HS, Aideyan
OA, Clark DC. Brucellar
and tuberculous
spondylitis:
comparative
imaging features.
Radiology
1989;171:419-425
Goodman
PC. Pulmonary
tuberculosis
in patients with acquired
immunodeficiency
syndrome.
J Thorac Imaging 1990;5:38-45
Leung AN, Brauner
MW, Gamsu G, et al. Pulmonary
tuberculosis:
comparison of CT findings
in HIV-positive
and seronegative
patients.
Radiology 1993;189(p):153
Shafer AW, Chirgwin
KD, Glatt AE, Dahdouh
MA, Landesman
SH, Suster
B. HIV prevalence,
immunosuppression,
and drug resistance
in patients
with tuberculosis
in an area endemic for AIDS. AIDS 19915:399-405
Jones BE, Young 5MM, Antoniskis
D, Davidson
PT, Kramer F, Barnes PF.
Relationship
of the manifestations
of tuberculosis
to CD4 cell counts in
patients with human immunodeficiency
virus infection. Am Rev Respir Dis
1993:148:1292-1297
ElIner JJ, Barnes PF, Wallis AS, Modlin AL. The immunology
of tubercubus pleurisy. Semin Respirlnfect
1988;3:335-342
Pastores SM, Naidich DP, Aranda CP, McGuinness
G, Aom WN. Intrathoracic adenopathy
associated
with pulmonary
tuberculosis
in patients with
human immunodeficiency
virus infection.
Chest 1993;1 03:1433-1437
Williford
ME, Thompson
WM, Hamilton JD, Postlethwait
AW. Esophageal
tuberculosis:
findings on barium swallow and computed
tomography.
Gastrointest Radiol 1983:8:119-122
Im J-G, Kim JH, Han MC, Kim C-W. Computed
tomography
of esophagomediastinal
fistula in tuberculous
mediastinal
lymphadenitis.
J Comput
Assist Tomogr 1990;14:89-92

You might also like