SYMPOSIA
Multidetector High-resolution Computed
Tomography of the Lungs
Protocols and Applications
Baskaran Sundaram, MD, Aamer R. Chughtai, MD, and Ella A. Kazerooni, MD, MS
Abstract: Advances in computed tomography (CT) scanner techno-
logy have made isotropic volumetric, multiplanar high-resolution
lung imaging possible in a single breath-hold, a significant advance
over the incremental high-resolution CT (HRCT) technique in
which noncontiguous images sampled the lung, but lacked anatomic
continuity. HRCT of the lungs is an established imaging technique
for the diagnosis and management of interstitial lung disease,
emphysema, and small airway disease, providing a noninvasive
detailed evaluation of the lung parenchyma, and providing infor-
mation about the lungs as a whole and focally. In addition to
having a high degree of specificity for diagnosing conditions such as
emphysema, sarcoidosis, usual interstitial pneumonitis, Langer-
hans cell histiocytosis, and small airway disease, there is a growing
body of medical evidence to support the use of HRCT findings
or diagnosis to predict patient prognosis. In this article, we review
the technique, advantages, and clinical applications of the current
HRCT technique.
Key Words: high-resolution computed tomography, lungs, interstitial
lung disease, technique, protocols
(J Thorac Imaging 2010;25:125–141)
A dvances in multidetector computed tomography (CT)
have made volumetric, high-resolution CT (HRCT)
possible in a single breath-hold, even for patients with
shortness of breath, one of the most frequent symptoms in
patients undergoing lung evaluation. HRCT of the lungs
has become the in vivo gold standard for evaluating the
lung parenchyma and airways. Its superiority over conven-
tional chest radiography and standard chest CT is well
established. Fortunately, imaging of the lung parenchyma
with CT requires relatively fewer x-ray photons to generate
diagnostic quality images compared with other parts of the
body, thus making ‘‘low-dose’’ thoracic CT more straight-
forward. As with all applications of CT today, every effort
should be made to reduce radiation exposure following the
ALARA principle of ‘‘as low as reasonably achievable.’’1
The use of HRCT as part of a multidisciplinary
approach by pulmonary medicine specialists, radiologists,
and pathologists to evaluate patients with diffuse lung
disease (DLD) has been shown to be helpful in arriving at
the correct final diagnosis of DLD.2 It has also been shown
From the Department of Radiology, University of Michigan Health
System, Ann Arbor, MI.
Reprints: Baskaran Sundaram, MD, Department of Radiology,
University of Michigan Health System, Cardiovascular Center
#5481, 1500 East Medical Center Drive, Ann Arbor, MI 48109-
5868 (e-mail: sundbask@med.umich.edu).
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J Thorac Imaging  Volume 25, Number 2, May 2010
that the HRCT lung findings in interstitial lung diseases
may have survival implications for patients.3,4
In this review, we aim to illustrate various aspects of
HRCT, including technical aspects, radiation exposure,
lung anatomy relevant to HRCT, and clinical utility for
diagnosing and managing various lung diseases.
IMAGE ACQUISITION AND EVALUATION
The primary objective of HRCT is to obtain optimal
spatial resolution for accurate anatomic depiction of the
lung parenchyma and the evaluation of the extent and
distribution of lung abnormalities. This allows accurate
depiction of fine lung detail and also helps avoid many
pitfalls of incremental scanning, such as difficulty in differ-
entiating small lung nodules from vessels and bronchiecta-
sis from true honeycombing. The technique used should
be reproducible for accurate comparison and follow-up.
Although it is important to maintain optimal image quality,
radiation exposure should be kept to the minimum necessary
to obtain images of sufficient diagnostic quality, through
meticulous attention to the technical parameters used.
There are many different ways in which an HRCT
examination can be obtained, which can be tailored to the
suspected or known disease process. Common to all HRCT
protocols are thin collimation of 1.5 mm or less, coupled
with a high spatial frequency reconstruction algorithm, to
maximize fine lung detail. The 2 most widely used methods
are the incremental acquisition technique, in which axial images
are obtained at 1 to 2 cm increments throughout the lungs,
and volumetric acquisition, in which the entire lungs are
imaged helically in a continuous manner. The incremental
method was mostly used before CT scanners of 16 detectors
or more became widely available, permitting consistent
single breath-hold imaging of the entire lungs at thin
collimation and without tube cooling issues routinely due to
increased scanning speed.5
Data Acquisition
HRCT protocols usually consist of several acquisi-
tions, optimized to evaluate the lung parenchyma for DLD
and airway disease by combining differences in breath
holding and patient positioning. Our current standard
HRCT protocol consists of a volumetric inspiratory supine
acquisition, incremental expiratory supine acquisition, and
incremental inspiratory prone acquisition, which permits
evaluation of both infiltrative and obstructive lung diseases.
CT Scanning Parameters
General technical parameters for HRCT include 100 to
120 kVp at 40 to 100 mAs. The technique can be modified
according to patient body habitus, using the body mass
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index or circumference of the thorax. Higher milliampere
seconds and kilovolt peak are used for larger patients and
lower values for smaller-sized patients and for the pediatric
population, balancing image noise and radiation exposure
with sufficient diagnostic quality. Thin collimation of 1.5 mm
or less is important in HRCT to reduce the volume-
averaging artifacts and increase the spatial resolution in
the images, enabling us to visualize subtle lung findings.
Although thinner collimation of 0.5 to 0.6 mm is available
currently on many CT scanners, it has not yet been shown
to provide additional clinically relevant information over the
more commonly used 1 to 1.5 mm collimation for HRCT. A
fast CT gantry rotation time, often sub-second, is also ideal
to reduce motion artifacts.6 Typically, the 360-degree
rotation time for current CT scanners is of the order of
350 to 500 ms.7 Patients are comfortably able to hold their
breath for that amount of short volumetric acquisitions,
which reduces respiratory motion artifacts. Cardiac motion
artifacts are also reduced, as a typical left ventricular
diastole lasts about 500 ms.8
Patient Positioning and Respiratory Phase
Most thoracic imaging, including HRCT, is obtained
with the patient in a supine position, the standard anatomic
position for thoracic CT examinations. Prone images are
important, both when the nondependent lung parenchyma
is normal on the supine images to distinguish between
dependent atelectasis versus mild lung disease and to elimi-
nate superimposed atelectasis, which may make disease
seem more severe than it really is, by exaggerating ground-
glass opacity (GGO). Images are usually obtained following
several breaths in and out, with the patient holding his or
her breath in deep inspiration to allow optimal tissue
FIGURE 1. A and B, Volumetric HRCT. Focal thin-walled multiple cystic lesions in the right upper lobe on an axial HRCT image suggest
centrilobular emphysema or cystic lung disease or early honeycombing (arrow in A). Coronal reconstruction image from the volumetric
HRCT examination clearly shows focal bronchiectasis (curved arrow in B).
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J Thorac Imaging  Volume 25, Number 2, May 2010
contrast within the lung parenchyma between normal
aerated tissue, normal anatomy, and disease. If the patient
is not able to hold his or her breath and remain motionless
during the scan, the images may be suboptimal for the
evaluation of the lungs. In this situation, the scan can be
obtained in 2 consecutive but shorter acquisitions to reduce
the duration of breath-hold. The scan direction can also be
modified to scan in the caudal-to-cranial direction, the
reverse of most examinations, so that the lower lung images
are acquired first, in the event the patient exhales, as motion
at the lung bases with the movement of the diaphragm
creates more artifacts than exhaling while scanning the lung
apices. A less ideal solution is to increase the pitch or table
speed to reduce the total imaging time, at the expense of
spatial resolution, as this results in an increase in effective
slice thickness.8 Images can also be obtained during
dynamic expiration or at static end-expiration to evaluate
for air trapping in the lung parenchyma as evidence of small
airway disease and tracheobronchomalacia of the central
airway.
Image Reconstruction Plane, Interslice Gap,
and Algorithm
Volumetric acquisitions are reconstructed using over-
lapping or continuous increments with no interslice gaps.
This is advantageous for detecting and comparing small
lung nodules or tracing small airways to, respectively,
differentiate them from blood vessels and honeycombing
(Fig. 1).9 The reconstruction algorithm is the filter applied
to the raw data set for image reconstruction. Conventional
imaging is obtained with low spatial frequency and low
noise algorithm for soft tissue reconstruction. A high
special frequency algorithm is typically applied for HRCT
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image reconstruction, which increases spatial resolution,
providing edge enhancement and higher contrast, which
reduces image smoothing and increases image noise.10
Image Evaluation
Images are usually reviewed on a picture archiving and
communication systems or image review workstation. The
choice of window width and level settings is important,
particularly when comparing examinations. Typically, the
window level used ranges from 500 to 600 HU, with a
window width of 1500 to 2000 HU. The window settings can
be modified in individual cases to depict finer detail. Images
may be viewed in a 2-dimensional (axial, coronal, and sagittal
planes) and a 3-dimensional manner (volume-rendered
images, maximum and minimum intensity projections).11
Multiplanar viewing may help to better appreciate the exact
and predominant distribution of parenchymal disease, with
coronal images mimicking a frontal chest radiographic
image, and sagittal images mimicking a lateral radiographic
image.12 Sliding slab maximum intensity projection images
aid in the detection of small pulmonary nodules.13 Pulmo-
nary micronodules and their orientation to the secondary
pulmonary lobule anatomy may be better appreciated with
volumetric data sets that permit rotation of the anatomy
under review into the best plane.14,15 Similarly, even subtle
emphysema may be better appreciated with sliding minimum
intensity projection images than with routine HRCT
views.15,16
HRCT LUNG ANATOMY
The smallest functional unit displayed on HRCT
images is the secondary pulmonary lobule (Fig. 2).17,18
The secondary pulmonary lobule is a polygonal structure, 1
FIGURE 2. Schematic illustration of secondary pulmonary lobule.
Secondary pulmonary lobules are bounded by interlobular septa
(arrows), which contain the pulmonary veins (red). The central
bronchovascular core is composed of a pulmonary artery (curved
arrow) and accompanying terminal airway (arrowhead). The
terminal bronchovascular core is surrounded by clusters of
pulmonary acini (A), where gas exchange takes place.
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Multidetector HRCT of Lungs
to 4 cm in diameter, and bounded by the interlobular septa.
Interlobular septa contain pulmonary veins that collect
oxygenated blood from the pulmonary acini. Each second-
ary pulmonary lobule contains 3 to 24 acini clustered
together beyond the terminal bronchiole. The central
bronchovascular core of each lobule has several terminal
bronchioles, each with an adjacent small pulmonary artery.
The terminal bronchioles bifurcate into clusters of pulmonary
acini, each of which is a collection of alveoli. Lymphatics are
present both around the central bronchovascular structures
and within the interlobular septae. Generally, in normal
secondary pulmonary lobules, it is difficult to visualize most
of these structures on HRCT, with the exception of the
terminal pulmonary artery branches as a small nodule in the
centrilobular location. More specifically, Murata et al,19
using 4 inflation-fixed lungs obtained from autopsy, showed
that HRCT is capable of showing normal pulmonary artery
branches as small as 200 mm in diameter, and noted that the
distance between these vessels and the lobule border ranges
from 3 to 5 mm.
Understanding the HRCT findings in relation to the
secondary pulmonary lobule architecture is important to
categorize interstitial lung disease for the purposes of
differential diagnosis. HRCT abnormalities in DLD may
be categorized as primarily linear, nodular, high- or low-
attenuation lesions. On the basis of the distribution of these
abnormalities in relation to the secondary pulmonary
lobule, lung nodules can be further subcategorized as
centrilobular, perilymphatic, or random. The predominant
group of nodules and their distribution may suggest specific
diseases, such as acute hypersensitivity pneumonitis (HP)
or respiratory bronchiolitis (centrilobular), sarcoidosis
(perilymphatic), and military infections or tumors (ran-
dom). HRCT abnormalities can be described in a standard-
ized manner using the glossary of terms described by the
Fleischner society.20
RADIATION EXPOSURE
Radiation exposure from a CT examination is based
on many variables, including both patient-related factors
and CT technical parameters. Whether a helical or
nonhelical technique is used, the goal is to obtain images
of sufficient diagnostic quality using radiation exposures
that are as low as reasonably achievable.1 Mayo et al21
reported that the skin radiation dose using specific scanning
parameters of 120 kVp, 200 mA, and 2 seconds of gantry
rotation time and incremental HRCT technique with a 10-
mm to 20-mm gap between HRCT slices results in much
lower radiation exposure than routine helical CT. Similarly,
van der Bruggen-Bogaarts et al22 reported that the effective
radiation exposure is 6.5 times lower for axial nonvolu-
metric HRCT than helical CT. As radiation exposure
during CT scanning has a linear relationship with CT
scanner tube current, many investigators have attempted to
reduce the tube current and have now established the utility
of low-dose helical chest CT examinations.23,24
The inherent high contrast difference between the air
within the alveoli of the lung and lung tissue has made
lower-dose thoracic CT examinations possible, and at lower
exposure levels than possible for CT examinations of other
body parts.25 Lowering tube current may degrade image
quality by decreasing the signal-to-noise ratio, probably
more so in helical volumetric HRCT than axial HRCT,
leading to concerns about image quality.26 However,
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Sundaram et al
Zwirewich et al25 evaluated a low radiation exposure
HRCT examination technique (20 mA, 2 s rotation speed,
120 kVp, 1.5-mm collimation), showing equal diagnostic
quality to a higher radiation exposure HRCT examination
technique (200 mA, 2 s rotation speed, 120 kVp, 1.5-mm
collimation). Leswick et al26 compared radiation exposure
between routine helical chest CT (1.25 mm 8, 130 mAs,
120 kVp, and 0.875 pitch) and nonvolumetric HRCT
(1.25 mm  10, 170 mAs, and 120 kVp) and a combination
CT acquisition (1.25 mm  8, 225 mAs, 120 kV, and 0.875
pitch) that was used to generate contiguous 5-mm and 1.25-
mm axial images. Initially, they established that 225 mAs
helical CT had a similar noise index to an axial nonvolu-
metric HRCT after testing a female water phantom at
various 10-mA increments. They reported that combination
CT acquisition resulted in higher radiation exposure to the
central chest (33% higher; P=0.001), breast (25% higher;
P<0.05), and total body (32% higher; P<0.001), and
lower average radiation exposure to the ovaries (25%
lower; P<0.01), which, presumably, was secondary to
shorter scanning time.
CLINICAL APPLICATIONS
Diffuse Lung Disease
HRCT is a well-established technique to evaluate for
DLD in advanced disease, early-stage disease, or even
preclinical disease.27,28 As with almost all diagnostic tests,
a normal HRCT may not exclude DLD.29 Although there
may be no major differences in diagnosing DLD using
either an incremental HRCT scan at regular increments or
even fewer HRCT images, let alone helical technique in
cases of sufficient severity to warrant surgical biopsy, the
impact of incremental versus helical HRCT on sensitivity
for disease or specific diagnosis has not been evaluated.30 It
is important to understand that the information obtained
from HRCT is used for many different reasons, from
differential diagnosis to the evaluation of disease activity,
FIGURE 3. A and B, A 92-year-old man with increasing shortness of breath over 6 months. A, Axial and (B) coronal HRCT images show
bilateral, subpleural, and lower-lung-predominant classic honeycombing (arrow), representing a definite UIP pattern.
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J Thorac Imaging  Volume 25, Number 2, May 2010
and evaluating temporal change in disease with treatment.
In addition, many patients with DLD are at increased risk
for lung malignancy31–34; therefore, being able to consis-
tently view and evaluate these nodules on the serial HRCT
examinations these patients may undergo over time is very
important.
DLD categorization has continued to evolve over the
years, as our understanding of these diseases improves
through the process of scientific inquiry. The international
multidisciplinary consensus statement from the American
Thoracic Society and European Respiratory Society
classifies DLD into discrete groups as follows: (a)
idiopathic: idiopathic pulmonary fibrosis usual interstitial
pneumonitis (UIP), desquamative interstitial pneumonitis
(DIP), acute interstitial pneumonitis, nonspecific interstitial
pneumonitis (NSIP), respiratory bronchiolitis-interstitial
lung disease (RB-ILD), cryptogenic organizing pneumonia
(COP), and lymphocytic interstitial pneumonits (LIP);
(b) secondary (such as collagen vascular disease or drugs);
(c) granulomatous disease (such as sarcoid); and (d) other
forms (cystic lung diseases).35
Idiopathic Interstitial Pneumonia
DLDs with no identifiable etiology are considered
idiopathic. To report HRCT, particularly of the UIP and
NSIP group of patients, we have developed a reporting
system of 3 patterns: definite UIP in cases when honey-
combing is the dominant feature (Fig. 3), probable UIP
when honeycombing is a nondominant finding (Fig. 4),
and an NSIP-like pattern (Fig. 5) when there is no honey-
combing. In our clinical practice, we also developed and
validated a semiquantification grading system to assess
DLD at baseline and over time (Table 1).36
The HRCT finding of lower-lung-predominant, sub-
pleural honeycombing is strongly associated with the
pathologic diagnosis of UIP.37 Moreover, this pattern
of abnormality on HRCT has such a high specificity that
it obviates the need for surgical lung biopsy.4,38 The
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FIGURE 4. A and B, A 75-year-old man with progressive declining pulmonary functions. His HRCT showed scattered subpleural patches
of minor foci of honeycomb (arrows) and lower-lung-dominant interlobular septal thickening, traction bronchiectasis, and minimal
GGO, suggesting probable UIP pattern. Surgical lung biopsy confirmed UIP.

limitation of this pattern is that many patients with UIP
have an ‘‘NSIP-like’’ appearance, dominated by septal lines
and GGO in the absence of honeycombing, such that this
pattern has limited sensitivity for UIP. In fact, for patients
with an NSIP-like pattern on HRCT, it has been shown
that the diagnosis of NSIP versus UIP is almost equally
likely at surgical lung biopsy.4 Hence, in the absence of
typical HRCT findings of UIP, tissue diagnosis is advised
to confirm the diagnosis.4
Similarly, HRCT features of chronic HP could also
significantly overlap with UIP. A patchy distribution of the
same pattern of UIP HRCT findings should raise suspicion
of chronic HP, particularly in the context of upper-lung-
dominant distribution. Pathologically, a combination of
relatively lesser cellularity, temporal heterogeneity, honey-
combing, and fibroblastic foci suggests UIP and not chronic
HP. Despite the large size of the pathologic specimens
obtained during surgical lung biopsy, sampling error still
exists in diagnosing DLD. Hence, we emphasize incorpor-
ating HRCT findings, clinical and lung functional informa-
tion, and histopathologic information in a multidisciplinary
manner to arrive at the correct DLD diagnosis.2

FIGURE 5. A and B, A 60-year-old woman with lower-lung-dominant bilateral ground-glass attenuation lesion and traction
bronchiecatasis (arrow) and no honeycombing, suggesting an NSIP pattern. Subsequent surgical lung biopsy diagnosis was UIP.

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GGO can assist with diagnosis.41 Some of the other idiopathic

TABLE 1. Our Current Semiquantitative HRCT Scoring System of interstitial pneumonia are covered in the subsequent segments.
Diffuse Interstitial Lung Disease
Alveolar Score Secondary DLD: Collagen Vascular Diseases
(Ground Glass) Score Interstitial Score Collagen vascular diseases such as scleroderma,
None 0 None rheumatoid arthritis (RA), systemic lupus erythematosis,
<5% of the lobe 1 Septal thickening dermatomyositis, polymyositis, Sjögren syndrome, and
(no honeycombing) mixed connective disease may produce DLD. Secondary
Up to 25% of the lobe 2 Honeycombing up to DLD also has an HRCT pattern similar to idiopathic DLD
25% of the lobe described above. Ancillary findings may be useful to
26% to 49% of the lobe 3 Honeycombing 26% to determine the etiology of DLD. For example, a patulous
49% of the lobe
50% to 75% of the lobe 4 Honeycombing 50% to
esophagus suggests esophageal dysmotility and scleroder-
75% of the lobe ma, and erosive bone changes suggest RA.
>75% of the lobe 5 Honeycombing >75% The common HRCT patterns described in these
of the lobe patients are UIP, NSIP-like, COP, diffuse alveolar damage,
and nodular lesions. DLD may be seen in either a limited or
diffuse form of scleroderma. Pathologically, the vast majo-
rity of scleroderma lung patients have fibrosis42 and an
It is important to differentiate true from false NSIP-like pattern on HRCT.43 Patients with RA lung may
honeycombing. Subpleural bronchiectasis or emphysema have a combination of ILD features such as UIP, bronchial
can simulate honeycombing on incremental images; using thickening, nodules, constrictive bronchiolitis, DIP, and
volumetric images can help to recognize the communication patchy consolidation representing COP. Dermatomyositis
with the adjacent dilated airways (Fig. 1). Another area for and polymyositis patients may have patterns of COP, UIP,
confusion is the collision of the upper-lung-predominant and diffuse alveolar damage on HRCT.
emphysema with the DLD pattern of the lower-lung- Patients with Sjögren syndrome may pathologically have
predominant pattern of septal lines and GGO, creating a pulmonary fibrosis, LIP (Fig. 7), lymphoma, pseudolym-
‘‘pseudo-honeycombing appearance’’ that can be recog- phoma, amyloidosis, bronchopneumonia, panbronchiolitis,
nized by its appearance in the subpleural lung midway from and/or COP.44,45 HRCT may show GGO and reticular and
apex to base, rather than extending upward from the more nodular opacities, and the patterns may be NSIP, UIP, LIP,
caudal aspect of the lungs (Fig. 6). and COP.46 The specific HRCT manifestations of Sjögren
Unlike honeycombing, GGO is a relatively nonspecific syndrome and multisystem connective tissue disorder have not
HRCT finding. In the context of DLD, it may represent yet been well established.
alveolitis or even fibrosis below the resolution of HRCT.39
In the latter, identifying bronchiectasis within the GGO is Sarcoidosis
a feature that can help distinguish inflammatory GGO HRCT of pulmonary sarcoidosis may show characteris-
from fibrosis.40 In addition, the anatomic distribution of tic peribronchovascular distribution of nodules with diffuse

FIGURE 6. A and B, A 50-year-old patient with heavy smoking history and cough with progressive decline in pulmonary function. Axial
HRCT image (A) shows severe upper-lung-dominant paraseptal emphysema and adjacent apparent honeycombing. Coronal
reconstruction (B) clearly illustrates the collision of severe upper lung paraseptal emphysema with lower-lung GGO mixed with
interlobular septal thickening, creating a pseudo-honeycombing (arrow) appearance. Surgical pathology confirmed desquamative
interstitial lung disease.

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FIGURE 7. A and B, A 59-year-old woman with scleroderma presenting with worsening exertional breathlessness. Axial (A) and
coronal reformatted images (B) from her HRCT illustrate lower-lung-dominant interstitial lung disease as evidenced by GGO,
interlobular septal thickening, and traction bronchiectasis (arrow). There were also thin-walled pulmonary cysts (curved arrow). Her
lower esophagus (arrowhead) also was dilated due to scleroderma-induced esophageal dysmotility. Appearances are felt to be
characteristic of LIP.

thickening, GGO, bronchiectasis, focal consolidation, lung
nodules, parenchymal distortion, lines, honeycombing, and
mediastinal enlarged lymph nodes (Fig. 8). Typically, the
central and upper lungs are involved. Depending upon the
stage of the disease process, severity, activity, and therapy,
these patients may have a combination of the above-
mentioned findings. Air trapping in sarcoidosis is common,
seen in 95% of HRCT examinations in 1 series of
21 patients, and correlates with small airway disease found
on pulmonary function tests. Furthermore, as shown in

FIGURE 8. A and B, A 50-year-old man with chronic cough and abnormal hila on chest radiograph. HRCT shows (A) enlarged lymph
nodes (arrow in A) in the mediastinum and bilateral hila with peribronchovascular nodules (arrowhead in B) and thickening (curved
arrow in B), characteristic of sarcoidosis. Transbronchial biopsy revealed multiple epithelioid granulomas in the alveolar parenchyma and
bronchial wall, confirming sarcoidosis.

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Sundaram et al
one study of 29 patients with sarcoidosis, the mean extent
of nodules and consolidation on HRCT reflects disease
activity, as quantified by 67 Gallium scintography, broncho-
alveolar lavage, and serum angiotensin converting enzyme
assay.47 In contrast, HRCT findings of GGO, nodularity,
septal thickening, traction bronchiectasis, and parenchymal
distortion do not correlate well with lung function.48 The
small nodules seen on HRCT have been shown to
correspond to granulomas on surgical lung biopsy, whereas
resting lung function in these same patients correlates
poorly with the presence and extent of disease on HRCT.49
Patients with sarcoidosis, who predominantly have GGO
and consolidation on their initial HRCT, may have a poor
prognosis compared with other patients with sarcoidosis
with progressive decline in their lung function.50
Cystic Lung Disease
Simple lung cysts are uniform, approximately 1 to
2 cm or less in diameter, thin-walled, air-containing lesions
with usually no mural nodules or wall thickening. Simple
lung cysts are sometimes confused with emphysema,
honeycombing, and cavitary lung disease within preexisting
disease such as cystic malignancy, infection, and granulo-
ma. In contrast to cysts, emphysema has no perceptible
wall, and honeycombing lesions are thick and irregularly
walled. Lymphangiomyomatosis (LAM; Fig. 9) is a disease
characterized by the proliferation of smooth muscle in the
wall of lymphatic channels, which occludes lymphatic flow
resulting in rupture of these channels, hence the finding of
associated chylous pleural effusions. Subsequently, cystic
lung lesions develop because of obstruction of the terminal
bronchioles that are surrounded by these abnormal
lymphatic vessels. The cysts in LAM are usually fairly
FIGURE 9. A and B, A 83-year-old woman with clinical features of reactive airway disease and obstructive pulmonary function tests.
HRCT shows multiple thin-walled lung cysts (arrow) that were evenly distributed from lung apex to base, and from center to periphery
of the lungs.
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J Thorac Imaging  Volume 25, Number 2, May 2010
uniform in size and are uniformly distributed throughout
the lungs, both apex to base, and axial to peripheral lung.
Some patients may have associated enlarged lymph nodes.
LAM is a disease that occurs mainly in women of child-
bearing age.
Langerhans cell histiocytosis (LCH; Fig. 10) is another
cystic lung disease that can be differentiated from LAM in
many ways. The cysts in LCH are usually irregular in shape
and size, and associated with small irregular nodules that
are also of varying size and may be cavitary. LCH is one of
the smoking-related lung diseases, all of which are more
common in the upper lungs, where there is relatively less
ventilation and perfusion, allowing for greater concentra-
tion of the toxins from inhaled smoke and relatively less
macrophage delivery.
A few other cystic lung diseases deserve mention,
including lung cysts in the context of Sjögren disease or
HIV infection, which represent LIP,51 and cysts in chronic
Pneumocytsis jiroveci pneumonia.52
Airway Disease
CT is the noninvasive imaging of choice for diagnosing
both large and small airway disease. Multidetector HRCT
can both image the anatomy of the airways in multi-
dimensional planes, which has eliminated diagnostic
bronchography, and also identify secondary evidence of
airway disease in the form of air trapping (Fig. 11) on
expiratory images. Sometimes, the latter is the earliest
evidence of small airway disease, at a stage when the small
airways appear morphologically normal.
The common manifestations of small airway disease
are bronchiectasis, bronchial wall thickening, and air
trapping. Bronchiectasis is generally divided into 3 types:
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FIGURE 10. A and B, A 35-year-old woman with a 30 pack-year smoking history and pituitary insufficiency underwent HRCT to evaluate
for possible sarcoidosis. Axial HRCT (A) showed upper- and central-lung-predominant innumerable centrilobular ground-glass
attenuation nodules (arrow), cysts (curved arrow), and emphysema (arrowhead). Surgical lung biopsy suggested respiratory
bronchiolitis-associated interstitial lung disease. She successfully stopped smoking. HRCT obtained 22 months later (B) showed
significant resolution of nodules. Her pulmonary function test parameters had also significantly improved. The pituitary findings were
presumed to be due to pituitary eosinophilic granulomatosis.

cylindrical, varicose, and cystic. If one assumes that the
pulmonary arteries are normal in size, a bronchus that is
larger in cross-section than the adjacent artery is considered
abnormally dilated. This has been referred to as the signet
ring sign or pearl ring sign. Caution should be used when
applying this criterion at high altitudes where there is
normally some degree of vasoconstriction, so that the
arteries may be smaller than the bronchi in the normal
state.53
Large airway diseases include infection (bacterial,
mycobacterial, viral, fungal), mucociliary dysfunction (cystic
fibrosis, Kartagener syndrome) (Fig. 12), congenital dis-
orders (Mounier-Kuhn syndrome, Williams-Campbell syn-
drome, bronchopulmonary sequestration), immune disorders
(AIDS, hypogammaglobulinemia), postobstructive (tumor,
foreign body), collagen vascular disorders (RA, Sjögren
syndrome, ankylosing spondilitis, relapsing polychondritis),
aspiration, asthma, and sarcoidosis.54 HRCT findings of
bronchiectasis, bronchial wall thickening, air trapping, and
mucoid impaction may overlap among these. However, in
many conditions, the distribution of abnormalities and associa-
ted features may narrow the differential diagnosis. For
example, the central airway abnormalities with glove-finger
appearance of central mucous plugging abnormali-
ties suggest allergic bronchopulmonary aspergillosis.55
Similarly, an upper lung distribution of bronchiectasis sug-
gests cystic fibrosis.56 Mounier-Kuhn syndrome is tracheo-
megaly, often associated with bronchiectasis.57
Small airway diseases may be primary or secondary
to the interstitial disease with bronchiolar involvement.58
The primary bronchiolar diseases include constrictive
bronchiolitis, acute bronchiolitis, diffuse panbronchiolitis,
RB-ILD, and follicular bronchiolitis. Secondary bronchio-
lar diseases due to interstitial lung disease include HP, RB,
DIP, and COP. Among the primary bronchiolar diseases,
the HRCT features overlap and include bronchiectasis,
bronchiolectasis, airway wall thickening, mucoid impaction
resulting in centrilobular nodules, tree-in-bud appearance,
and air trapping.
The utility of a volumetric HRCT over nonvolumetric
scans to diagnose bronchiectasis was shown as early as
1994 by Engeler et al.59 More recently, Lucidarme et al60
reported the added benefit of volumetric HRCT over
incremental HRCT in diagnosing bronchiectasis in 50
consecutive patients. Incremental HRCT images (120 kV,
175 mAs, 1.5-mm collimation at 10-mm intervals of the
entire lungs) and volumetric HRCT images (120 kV, and
150 mAs, 3-mm collimation, 4.8 mm/s table increments with
a pitch of 1.6; from 15 mm above the carina down to the
bases of the lung) were compared independently for
bronchiectasis by 3 observers in both blinded and consensus
manner. The extent of bronchiectasis detected was more
extensive with volumetric HRCT in segments through the
distal bronchi (k=0.77; P<10 9) compared with incre-
mental HRCT (k=0.27; P=not significant). It is impor-
tant to note that in their study the measured skin radiation

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Sundaram et al J Thorac Imaging  Volume 25, Number 2, May 2010

FIGURE 11. A and B, A 50-year-old woman with proven sarcoidosis and a restrictive small airway disease pattern on pulmonary function
tests. HRCT images obtained at end inspiration (A) shows unremarkable lung parenchyma and an image during end expiration (B)
shows alternative high-attenuating and low-attenuating lower-lung parenchyma, suggesting air trapping evident in the left lower lobe.

exposure was 3.4 times higher in volumetric than in Emphysema Analysis

incremental HRCT. Dodd et al61 also reported the
improved performance of volumetric HRCT imaging in
detecting bronchiectasis in a series of 61 patients. Volu-
metric HRCT (1-mm thickness, 15-mm table speed per
rotation, 0.5-s gantry rotation time, 120 kVp, and 130 mAs,
reconstructed using bone algorithm) images at full inspira-
tion from lung apex to base and simulated incremental
HRCT (1-mm slices at 10-mm intervals) images were
generated from the volumetric HRCT, with the latter
showing a higher prevalence of bronchiectasis (P<0.0001;
good consensus interobserver agreement values), greater
extent of bronchiectasis within a lobe (P<0.0001; very
good consensus interobserver agreement values), and higher
severity (P<0.0001; good consensus interobserver agree-
ment values) of bronchiectasis. Using consensus volumetric
HRCT findings as the gold standard, performance of incre-
mental HRCT for detecting bronchiectasis was as follows:
prevalence 42%; sensitivity 71% (95% confidence interval
=64-78%); specificity 93% (95% confidence interval=
90-96%); and positive and negative predictive values,
88% and 81%, respectively.
Beyond medical therapy and pulmonary rehabilita-
tion, the treatment options for severe emphysema include
lung transplantation and surgery designed to improve respi-
ratory mechanics, including lung volume reduction surgery
(LVRS), bullectomy, and endobronchial valve proce-
dures.62 HRCT plays a key role in patient selection for
these procedures as the best in vivo tool to evaluate regional
emphysema severity and distribution and to evaluate for
potential comorbid conditions. LVRS has been shown to
have a short-term and long-term impact on clinical and
functional parameters, with positive long-term outcome
being debatable.63,64 Preoperative emphysema quantifica-
tion by HRCT is shown to correlate with postoperative
outcome. More specifically, patients with severe emphyse-
ma homogenously distributed from lung apex to base have
been identified to have high mortality after LVRS,65–69
whereas patients with upper-lung-predominant emphyse-
ma, often referred to as heterogeneous emphysema, have
the best outcome. This is one of the most important criteria
for selecting patients to undergo LVRS.66,67,70,71 The role
of HRCT in emphysema in this setting is to evaluate the

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J Thorac Imaging  Volume 25, Number 2, May 2010
FIGURE 12. A and B, A 21-year-old man with a known history of cystic fibrosis was evaluated for bilateral lung transplantation. As part of
his workup, HRCT was performed that showed bilateral upper-lung bronchiectasis of varying degrees (arrow) with mucoid impacted
thick-walled bronchi (curved arrow). In addition, there were areas of mosaic attenuation and bilateral hyperinflated lungs due to fixed
air trapping.
severity and distribution of emphysema, and the presence of
bronchiectasis and related findings such as pulmonary
artery enlargement and potential lung malignancy.
Preoperative assessment of the degree and quantity of
emphysema may be performed easily with HRCT images
(Fig. 13). HRCT quantification is a sensitive tool for
assessing longitudinal changes in emphysema and following
specific therapy.72–74 Using computer attenuation-based
analysis, referred to as the density mask technique, the
range of lung tissue that is abnormally low in attenuation
values can be quantified as emphysema. This has been
shown to correlate well with the pathologic grade of
emphysema.75 Different HRCT reconstruction algorithms
impact density mask-based emphysema quantification, as
does slice thickness.76 Recently, lung texture-based quantifi-
cation has been shown to correlate better with pulmonary
function tests than the density mask technique.77 Some
have suggested that a simple visual score may be just as
reliable as sophisticated analysis in the quantitative analysis
of emphysema78; however, this may be too gross to evaluate
for short-term changes in disease, as it lacks sufficient
reliably reproducible detailed analysis. Recent studies
suggest that objective emphysema quantification with
attenuation thresholds may perform better than subjective
assessment.79,80 Although there may be some relationship
between the objective and subjective emphysema assess-
ment for its severity and distribution, there is higher repeat-
ability of the quantitative CT indices using volumetric
imaging of the entire lungs.78,81,82 In addition, CT emphysema
quantification based on attenuation values seems to have
a high predictability of gas transfer reduction; however, the
elastic recoil has not been thought to be correlated.83
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Multidetector HRCT of Lungs
Infection
The role of HRCT in diagnosing pulmonary infections
is well known, particularly atypical and typical infections in
immunocompromised patients.84–91 HRCT reliably diagno-
ses Pneumocysitis jiroveci pneumonia based on certain
findings such as nodular or patchy GGO, diffuse GGO in
the upper lungs with or without reticulations, and lung
cysts (Fig. 14).87,92 Patients with cytomegalovirus pneumo-
nia after bone marrow transplantation have bilateral
asymmetric GGO, air space opacities, and centrilobular
nodules.89 Although the halo sign is most commonly
associated with invasive pulmonary aspergillosis, other
infections should be kept in mind, particularly Candida.90
HRCT has also been shown to be useful in early diagnosis of
even unusual infections such as severe acute respiratory
syndrome-associated coronavirus pneumonia.85 HRCT find-
ings may also have prognostic significance in patients with
pulmonary infections. For example, a study reports that
HRCT findings such as atelectasis, cavities, and pleural
thickening are shown to predict responders to infection
among patients with mycobacterium avium complex.93
Similarly, another study reported that HRCT findings
predict disease progression in patients with culture-positive
non-mycobacterial tuberculosis with underlying cystic
fibrosis.94
Smoking-related Interstitial Lung Diseases
Smoking-related interstitial lung diseases include LCH,
RB, and DIP. LCH was discussed earlier in the section
on cystic lung diseases. RB is characterized on HRCT
as upper-lung-predominant centrilobular GGO nodules,
similar to acute HP. When patients with an RB are
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Sundaram et al J Thorac Imaging  Volume 25, Number 2, May 2010

FIGURE 13. A to D, A 71-year-old woman with prior significant smoking history undergoing evaluation for exertional breathlessness.
Pulmonary function tests suggested severe emphysema. A, Coronal and (B) sagittal HRCT images show severe emphysema in the upper lungs
(arrows) and mild emphysema in the lower lungs (arrowheads). Density mask technique using 920 HU showed that (C) 84.6% of the upper
lungs is emphysema and (D) 37.2% of the lower lungs, with an upper versus lower lung emphysema ratio of 2.3. She successfully underwent
bilateral upper lobe LVRS.

symptomatic, usually dyspnea, the same finding is con-
sidered to represent RB-ILD. Patients with DIP have
lower-lung-predominant GGO. RB, RB-ILD, and DIP have
a significant overlap in their HRCT features, suggesting that
they reflect various time frames of the same disease process.95
Asymptomatic healthy smokers are known to have
abnormal lungs on HRCT.96 Similarly, patients with a
second-hand smoking exposure have been shown to have
subclinical DIP and RB-ILD, with GGO and irregular/
linear opacities on HRCT (Figs. 6, 15).97 Low attenuation
areas on HRCT significantly correlate with abnormal
pulmonary function tests,98 and air trapping may even
precede these abnormalities.99 HRCT measurements of
airway thickening inversely correlate with airflow limitation
and cumulative smoking history.100 A 5-year longitudinal
HRCT study of smokers showed that continued smoking
results in increasing upper lung disease, and that the rate of
disease progression does not slow down in the first few years
after smoking cessation.101
Occupational Lung Diseases
Chronic dust exposures are known to result in ILDs,
including silicosis, coal worker’s pneumoconiosis, graphite
pneumoconiosis, asbestosis, talcosis, welder’s lung, beryl-
liosis, aluminum lung, hard metal lung disease, HP, and
chemical pneumonitis. In silicosis, small, less than 1 cm,
discrete solid nodules are found predominantly in the upper
lungs and may increase in size over time, or coalesce to
form large, partly calcified, conglomerate masses with
architectural distortion and upward retraction of lung hilar
structures, associated with enlarged thoracic lymph nodes
that may have eggshell calcifications. Coal workers with

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J Thorac Imaging  Volume 25, Number 2, May 2010 Multidetector HRCT of Lungs

FIGURE 14. A and B, A 44-year-old woman with HIV and low CD4 cell count presents with 4 months of cough, dyspnea on exertion,
and unintentional weight loss. Her HRCT showed bilateral upper- and central-lung-dominant central ground-glass attenuation (arrow)
and minimal interlobular septal thickening, characteristic of Pneumocystis jiroveci pneumonia. She was successfully treated with
sulfamethoxazole and trimethoprim.

rheumatoid disease may develop lung nodules even after
low levels of dust exposures, known as Caplan syndrome.
Similarly, systemic sclerosis is reported to occur more often
in patients with silicosis, a condition known as Erasmus
syndrome.102 The HRCT appearance of graphite pneumo-
coniosis is similar to coal worker’s pneumoconiosis.
Asbestos exposure-related ILD is referred to as
asbestosis, and is characterized by lower-lung-predominant,
peripheral interlobular septa thickening, subpleural bands,
parenchymal lines, and honeycombing when severe. Asbes-
tosis is often seen with asbestos-related calcified and
noncalcified pleural plaques (Fig. 16).
Intravenous drug abuse of oral medications containing
magnesium silicate, aluminum, and iron can produce
pulmonary talcosis, which appears on HRCT as diffuse
fine nodules and GGO. The inhalation of metallic iron

FIGURE 15. A and B, A 25-year-old woman with significant smoking history had recent onset of breathlessness. Her HRCT showed fluffy
centrilobular ground-glass nodules (arrow). Findings were considered to be characteristic of respiratory bronchiolitis.

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Sundaram et al J Thorac Imaging  Volume 25, Number 2, May 2010

FIGURE 16. A and B, An 80-year-old veteran with significant occupational asbestos exposure during construction work. He has
progressive dyspnea and increasing oxygen requirement. His pulmonary function tests revealed a restrictive pattern. His HRCT shows
bilateral focal dense pleural calcified plaques (arrows) and lower-lung-dominant interstitial lung disease as evidenced by GGO,
interlobular septal thickening (curved arrow), and traction bronchiectasis (arrowhead).

or iron oxide fumes along with other metallic dusts that
have a fibrogenic potential may result in welder’s lung,
with centrilobular micronodules in the central mid-lungs.
Berylliosis has many similarities to sarcoidosis, including
parenchymal nodules distributed along the bronchovascu-
lar bundles in the upper lungs. Patients with aluminum
toxicity manifest on HRCT as a reticulonodular interstitial
fibrosis pattern, mainly in the upper lungs.
Patients exposed to organic dust may develop HP.
Depending on the etiology, this may be called farmer’s
lung, bird-fancier lung, mushroom worker’s lung, and
bagassosis. In the acute and subacute form of the
disease, HRCT shows upper-lung-dominant/ill-defined
centrilobular GGO nodules, whereas in the chronic
phase, HRCT shows evidence of interstitial fibrosis,
with irregular septal thickening, traction bronchiectasis,
GGO, and honeycombing, the same findings seen with
UIP, but in a patchy, geographic or mosaic-like distribu-
tion, rather than the lower lung subpleural distribution of
UIP (Fig. 17). Often, the radiologist recognizing this
pattern is the first to suggest chronic HP, and should
recommend that an extensive exposure history be taken.

FIGURE 17. A 50-year-old woman with progressive breathlessness and abnormal pulmonary function tests. Her axial (A) and coronal (B)
HRCT images showed diffuse centrilobular ground-glass attenuation nodules (arrow). In addition, there were areas of lobular sparing
and fixed air trapping (curved arrow). The appearances were thought to be characteristic of HP. Later, pathologic diagnosis of talc
inhalation pneumonitis was made.

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J Thorac Imaging  Volume 25, Number 2, May 2010
Expiratory images may also show areas of air trapping in
these patients.
CONCLUSIONS
In conclusion, recent advancements in CT techniques
have made volumetric lung imaging possible in a reliable
and reproducible manner in a single breath-hold. It is
important to be cognizant of the radiation dose in HRCT,
and appropriate clinical use of HRCT is recommended as
per the ALARA principle. Current HRCT imaging has
become the noninvasive gold standard for the evaluation of
DLD, emphysema, and small and large airway disease.
Using HRCT alone, a specific diagnosis can often be made.
Even in cases in which the HRCT findings are atypical or
nonspecific, it can direct surgical lung biopsy to the areas of
greatest yield. HRCT features may also predict the surgical
and overall outcome in some DLDs. A multidisciplinary
approach to the DLD is a critical element in arriving at the
final correct diagnosis.
REFERENCES
1. Cascade PN, Webster EW, Kazerooni EA. Ineffective use of
radiology: the hidden cost. AJR Am J Roentgenol. 1998;170:
561–564.
2. Flaherty KR, King TE Jr, Raghu G, et al. Idiopathic
interstitial pneumonia: what is the effect of a multidisciplinary
approach to diagnosis? Am J Respir Crit Care Med. 2004;170:
904–910.
3. Goh NS, Desai SR, Veeraraghavan S, et al. Interstitial lung
disease in systemic sclerosis: a simple staging system. Am J
Respir Crit Care Med. 2008;177:1248–1254.
4. Flaherty KR, Thwaite EL, Kazerooni EA, et al. Radiological
versus histological diagnosis in UIP and NSIP: survival impli-
cations. Thorax. 2003;58:143–148.
5. Dawn SK, Gotway MB, Webb WR. Multidetector-row spiral
computed tomography in the diagnosis of thoracic diseases.
Respir Care. 2001;46:912–921.
6. Rubin GD, Leung AN, Robertson VJ, et al. Thoracic spiral
CT: influence of subsecond gantry rotation on image quality.
Radiology. 1998;208:771–776.
7. Remy-Jardin M, Tillie-Leblond I, Szapiro D, et al. CT
angiography of pulmonary embolism in patients with under-
lying respiratory disease: impact of multislice CT on image
quality and negative predictive value. Eur Radiol. 2002;12:
1971–1978.
8. Remy-Jardin M, Dumont P, Remy J. High-resolution compu-
ted tomography techniques in diffuse parenchymal lung
disease and their application to clinical practice. Semin Respir
Crit Care Med. 2003;24:333–346.
9. Schoepf UJ, Bruening RD, Hong C, et al. Multislice helical
CT of focal and diffuse lung disease: comprehensive diagnosis
with reconstruction of contiguous and high-resolution CT
sections from a single thin-collimation scan. AJR Am J
Roentgenol. 2001;177:179–184.
10. Mayo JR, Webb WR, Gould R, et al. High-resolution CT of
the lungs: an optimal approach. Radiology. 1987;163:507–510.
11. Beigelman-Aubry C, Hill C, Guibal A, et al. Multi-detector
row CT and postprocessing techniques in the assessment of
diffuse lung disease. Radiographics. 2005;25:1639–1652.
12. Remy-Jardin M, Campistron P, Amara A, et al. Usefulness of
coronal reformations in the diagnostic evaluation of infiltra-
tive lung disease. J Comput Assist Tomogr. 2003;27:266–273.
13. Kawel N, Seifert B, Luetolf M, et al. Effect of slab thickness
on the CT detection of pulmonary nodules: use of sliding thin-
slab maximum intensity projection and volume rendering.
AJR Am J Roentgenol. 2009;192:1324–1329.
14. Remy-Jardin M, Remy J, Artaud D, et al. Diffuse infiltrative
lung disease: clinical value of sliding-thin-slab maximum
r 2010 Lippincott Williams & Wilkins
Multidetector HRCT of Lungs
intensity projection ct scans in the detection of mild micro-
nodular patterns. Radiology. 1996;200:333–339.
15. Bhalla M, Naidich DP, McGuinness G, et al. Diffuse lung
disease: assessment with helical CT—preliminary observations
of the role of maximum and minimum intensity projection
images. Radiology. 1996;200:341–347.
16. Remy-Jardin M, Remy J, Gosselin B, et al. Sliding thin slab,
minimum intensity projection technique in the diagnosis of
emphysema: histopathologic-CT correlation. Radiology. 1996;
200:665–671.
17. Griffin CB, Primack SL. High-resolution CT: normal ana-
tomy, techniques, and pitfalls. Radiol Clin North Am. 2001;39:
1073–1090.
18. Webb WR. Thin-section CT of the secondary pulmonary
lobule: anatomy and the image—the 2004 Fleischner lecture.
Radiology. 2006;239:322–338.
19. Murata K, Itoh H, Todo G, et al. Centrilobular lesions of the
lung: demonstration by high-resolution CT and pathologic
correlation. Radiology. 1986;161:641–645.
20. Hansell DM, Bankier AA, MacMahon H, et al. Fleischner
society: glossary of terms for thoracic imaging. Radiology.
2008;246:697–722.
21. Mayo JR, Jackson SA, Muller NL. High-resolution CT of
the chest: radiation dose. AJR Am J Roentgenol. 1993;160:
479–481.
22. van der Bruggen-Bogaarts BA, Broerse JJ, Lammers JW,
et al. Radiation exposure in standard and high-resolution
chest CT scans. Chest. 1995;107:113–115.
23. Jung KJ, Lee KS, Kim SY, et al. Low-dose, volumetric helical
CT: image quality, radiation dose, and usefulness for
evaluation of bronchiectasis. Invest Radiol. 2000;35:557–563.
24. Yi CA, Lee KS, Kim TS, et al. Multidetector CT of bronchi-
ectasis: effect of radiation dose on image quality. AJR Am J
Roentgenol. 2003;181:501–505.
25. Zwirewich CV, Mayo JR, Muller NL. Low-dose high-
resolution CT of lung parenchyma. Radiology. 1991;180:
413–417.
26. Leswick DA, Webster ST, Wilcox BA, et al. Radiation cost of
helical high-resolution chest CT. AJR Am J Roentgenol. 2005;
184:742–745.
27. Afeltra A, Zennaro D, Garzia P, et al. Prevalence of intersti-
tial lung involvement in patients with connective tissue
diseases assessed with high-resolution computed tomography.
Scand J Rheumatol. 2006;35:388–394.
28. Gochuico BR, Avila NA, Chow CK, et al. Progressive pre-
clinical interstitial lung disease in rheumatoid arthritis. Arch
Intern Med. 2008;168:159–166.
29. Orens JB, Kazerooni EA, Martinez FJ, et al. The sensitivity
of high-resolution CT in detecting idiopathic pulmonary
fibrosis proved by open lung biopsy. A prospective study.
Chest. 1995;108:109–115.
30. Sundaram B, Gross BH, Oh E, et al. Reader accuracy and
confidence in diagnosing diffuse lung disease on high-resolu-
tion computed tomography of the lungs: impact of sampling
frequency. Acta Radiol. 2008;49:870–875.
31. Hubbard R, Venn A, Lewis S, et al. Lung cancer and crypto-
genic fibrosing alveolitis. A population-based cohort study.
Am J Respir Crit Care Med. 2000;161:5–8.
32. Daniels CE, Jett JR. Does interstitial lung disease predispose
to lung cancer? Curr Opin Pulm Med. 2005;11:431–437.
33. Lee HJ, Im JG, Ahn JM, et al. Lung cancer in patients with
idiopathic pulmonary fibrosis: CT findings. J Comput Assist
Tomogr. 1996;20:979–982.
34. Kishi K, Homma S, Kurosaki A, et al. High-resolution
computed tomography findings of lung cancer associated with
idiopathic pulmonary fibrosis. J Comput Assist Tomogr. 2006;
30:95–99.
35. Demedts M, Costabel U. Ats/Ers International multidisci-
plinary consensus classification of the idiopathic interstitial
pneumonias. Eur Respir J. 2002;19:794–796.
36. Kazerooni EA, Martinez FJ, Flint A, et al. Thin-section
CT obtained at 10-mm increments versus limited three-level
www.thoracicimaging.com | 139
Sundaram et al
thin-section CT for idiopathic pulmonary fibrosis: correlation
with pathologic scoring. AJR Am J Roentgenol. 1997;169:
977–983.
37. Hunninghake GW, Lynch DA, Galvin JR, et al. Radiologic
findings are strongly associated with a pathologic diagnosis of
usual interstitial pneumonia. Chest. 2003;124:1215–1223.
38. Raghu G, Mageto YN, Lockhart D, et al. The accuracy of the
clinical diagnosis of new-onset idiopathic pulmonary fibrosis
and other interstitial lung disease: a prospective study. Chest.
1999;116:1168–1174.
39. Leung AN, Miller RR, Muller NL. Parenchymal opacifica-
tion in chronic infiltrative lung diseases: CT-pathologic
correlation. Radiology. 1993;188:209–214.
40. Remy-Jardin M, Giraud F, Remy J, et al. Importance of
ground-glass attenuation in chronic diffuse infiltrative
lung disease: pathologic-CT correlation. Radiology. 1993;189:
693–698.
41. Sundaram B, Gross BH, Martinez FJ, et al. Accuracy of high-
resolution CT in the diagnosis of diffuse lung disease: effect
of predominance and distribution of findings. AJR Am J
Roentgenol. 2008;191:1032–1039.
42. Steen VD, Owens GR, Fino GJ, et al. Pulmonary involve-
ment in systemic sclerosis (Scleroderma). Arthritis Rheum.
1985;28:759–767.
43. Bouros D, Wells AU, Nicholson AG, et al. Histopathologic
subsets of fibrosing alveolitis in patients with systemic
sclerosis and their relationship to outcome. Am J Respir Crit
Care Med. 2002;165:1581–1586.
44. Strimlan CV, Rosenow EC III, Divertie MB, et al. Pulmonary
manifestations of Sjogren’s syndrome. Chest. 1976;70:354–361.
45. Wright JL, Cagle P, Churg A, et al. Diseases of the small
airways. Am Rev Respir Dis. 1992;146:240–262.
46. Parambil JG, Myers JL, Lindell RM, et al. Interstitial lung
disease in primary Sjogren syndrome. Chest. 2006;130:
1489–1495.
47. Leung AN, Brauner MW, Caillat-Vigneron N, et al. Sarco-
idosis activity: correlation of HRCT findings with those of
67ga scanning, bronchoalveolar lavage, and serum angioten-
sin-converting enzyme assay. J Comput Assist Tomogr.
1998;22:229–234.
48. Davies CW, Tasker AD, Padley SP, et al. Air trapping in
sarcoidosis on computed tomography: correlation with lung
function. Clin Radiol. 2000;55:217–221.
49. Lynch DA, Webb WR, Gamsu G, et al. Computed tomo-
graphy in pulmonary sarcoidosis. J Comput Assist Tomogr.
1989;13:405–410.
50. Akira M, Kozuka T, Inoue Y, et al. Long-term follow-up CT
scan evaluation in patients with pulmonary sarcoidosis.
Chest. 2005;127:185–191.
51. Ryu JHSwensen SJ. Cystic and cavitary lung diseases: focal
and diffuse. Mayo Clin Proc. 2003;78:744–752.
52. Boiselle PM, Crans CA Jr, Kaplan MA. The changing face
of pneumocystis carinii pneumonia in aids patients. AJR Am
J Roentgenol. 1999;172:1301–1309.
53. Ouellette H. The signet ring sign. Radiology. 1999;212:67–68.
54. McGuinness G, Naidich DP. CT of airways disease and
bronchiectasis. Radiol Clin North Am. 2002;40:1–19.
55. Kalil ME, Fernandes AL, Curzel AC, et al. Allergic broncho-
pulmonary aspergillosis presenting a glove-finger shadow in
radiographic images. J Bras Pneumol. 2006;32:472–475.
56. Helbich TH, Heinz-Peer G, Eichler I, et al. Cystic fibrosis: CT
assessment of lung involvement in children and adults.
Radiology. 1999;213:537–544.
57. Katz I, Levine M, Herman P. Tracheobronchiomegaly. The
Mounier-Kuhn syndrome. Am J Roentgenol Radium Ther
Nucl Med. 1962;88:1084–1094.
58. Ryu JH, Myers JL, Swensen SJ. Bronchiolar disorders. Am J
Respir Crit Care Med. 2003;168:1277–1292.
59. Engeler CE, Tashjian JH, Engeler CM, et al. Volumetric high-
resolution CT in the diagnosis of interstitial lung disease and
bronchiectasis: diagnostic accuracy and radiation dose. AJR
Am J Roentgenol. 1994;163:31–35.
140 | www.thoracicimaging.com
J Thorac Imaging  Volume 25, Number 2, May 2010
60. Lucidarme O, Grenier P, Coche E, et al. Bronchiectasis:
comparative assessment with thin-section ct and helical CT.
Radiology. 1996;200:673–679.
61. Dodd JD, Souza CA, Muller NL. Conventional high-
resolution CT versus helical high-resolution Mdct in the
detection of bronchiectasis. AJR Am J Roentgenol. 2006;187:
414–420.
62. Brasileiro FC, Vargas FS, Kavakama JI, et al. High-
resolution CT scan in the evaluation of exercise-induced
interstitial pulmonary edema in cardiac patients. Chest. 1997;
111:1577–1582.
63. Flaherty KR, Kazerooni EA, Curtis JL, et al. Short-term and
long-term outcomes after bilateral lung volume reduction
surgery: prediction by quantitative CT. Chest. 2001;119:
1337–1346.
64. Gelb AF, McKenna RJ Jr, Brenner M, et al. Lung function 4
years after lung volume reduction surgery for emphysema.
Chest. 1999;116:1608–1615.
65. Geddes D, Davies M, Koyama H, et al. Effect of lung-
volume-reduction surgery in patients with severe emphysema.
N Engl J Med. 2000;343:239–245.
66. National Emphysema Treatment Trial Research Group.
Patients at high risk of death after lung-volume-reduction
surgery. N Engl J Med. 2001;345:1075–1083.
67. Fishman A, Martinez F, Naunheim K, et al. A randomized
trial comparing lung-volume-reduction surgery with medical
therapy for severe emphysema. N Engl J Med. 2003;348:
2059–2073.
68. Pakhale SS, Gutierrez C. Lung-volume—reduction surgery.
N Engl J Med. 2003;349:999–1000; author reply 1999–1000.
69. Ramsey SD, Berry K, Etzioni R, et al. Cost effectiveness of
lung-volume-reduction surgery for patients with severe
emphysema. N Engl J Med. 2003;348:2092–2102.
70. Algranti E, Mendonca EM, DeCapitani EM, et al. Non-
malignant asbestos-related diseases in Brazilian asbestos-
cement workers. Am J Ind Med. 2001;40:240–254.
71. McKenna RJ Jr, Brenner M, Fischel RJ, et al. Patient
selection criteria for lung volume reduction surgery. J Thorac
Cardiovasc Surg. 1997;114:957–964; discussion 964–957.
72. Dowson LJ, Guest PJ, Stockley RA. Longitudinal changes in
physiological, radiological, and health status measurements in
alpha(1)-antitrypsin deficiency and factors associated with
decline. Am J Respir Crit Care Med. 2001;164:1805–1809.
73. D’Andrilli A, Vismara L, Rolla M, et al. Computed tomogra-
phy with volume rendering for the evaluation of parenchymal
hyperinflation after bronchoscopic lung volume reduction.
Eur J Cardiothorac Surg. 2009;35:403–407.
74. Dirksen A, Piitulainen E, Parr DG, et al. Exploring the role of
CT densitometry: a randomised study of augmentation
therapy in alpha-1 antitrypsin deficiency. Eur Respir J. 2009;
33:1345–1353.
75. Muller NL, Staples CA, Miller RR, et al. ‘‘Density mask’’. An
objective method to quantitate emphysema using computed
tomography. Chest. 1988;94:782–787.
76. Boedeker KL, McNitt-Gray MF, Rogers SR, et al. Emphy-
sema: effect of reconstruction algorithm on CT imaging
measures. Radiology. 2004;232:295–301.
77. Park YS, Seo JB, Kim N, et al. Texture-based quantification
of pulmonary emphysema on high-resolution computed
tomography: comparison with density-based quantification
and correlation with pulmonary function test. Invest Radiol.
2008;43:395–402.
78. Zompatori M, Battaglia M, Rimondi MR, et al. Quantitative
assessment of pulmonary emphysema with computerized
tomography. Comparison of the visual score and high resolu-
tion computerized tomography, expiratory density mask with
spiral computerized tomography and respiratory function
tests. Radiol Med. 1997;93:374–381.
79. Hersh CP, Washko GR, Jacobson FL, et al. Interobserver
variability in the determination of upper lobe-predominant
emphysema. Chest. 2007;131:424–431.
r 2010 Lippincott Williams & Wilkins
J Thorac Imaging  Volume 25, Number 2, May 2010
80. Stavngaard T, Shaker SB, Bach KS, et al. Quantitative
assessment of regional emphysema distribution in patients
with chronic obstructive pulmonary disease (COPD). Acta
Radiol. 2006;47:914–921.
81. Hunsaker AR, Ingenito EP, Reilly JJ, et al. Lung volume
reduction surgery for emphysema: correlation of CT and V/Q
imaging with physiologic mechanisms of improvement in lung
function. Radiology. 2002;222:491–498.
82. Gierada DS, Yusen RD, Pilgram TK, et al. Repeatability of
quantitative CT indexes of emphysema in patients evaluated
for lung volume reduction surgery. Radiology. 2001;220:
448–454.
83. Baldi S, Miniati M, Bellina CR, et al. Relationship between
extent of pulmonary emphysema by high-resolution compu-
ted tomography and lung elastic recoil in patients with
chronic obstructive pulmonary disease. Am J Respir Crit Care
Med. 2001;164:585–589.
84. Bayramoglu S, Cimilli T, Aksoy S, et al. The role of HRCT
versus CXR in children with recurrent pulmonary infections.
Clin Imaging. 2005;29:317–324.
85. Hui JY, Hon TY, Yang MK, et al. High-resolution computed
tomography is useful for early diagnosis of severe acute
respiratory syndrome-associated coronavirus pneumonia in
patients with normal chest radiographs. J Comput Assist
Tomogr. 2004;28:1–9.
86. D’Arienzo P, Giampalma E, Lavecchia MA, et al. Role of
HRCT in the identification of atypical pulmonary myco-
bacteriosis. Radiol Med. 2002;103:158–170.
87. Hidalgo A, Falco V, Mauleon S, et al. Accuracy of high-
resolution CT in distinguishing between pneumocystis carinii
pneumonia and non- pneumocystis carinii pneumonia in aids
patients. Eur Radiol. 2003;13:1179–1184.
88. Syrjala H, Broas M, Suramo I, et al. High-resolution com-
puted tomography for the diagnosis of community-acquired
pneumonia. Clin Infect Dis. 1998;27:358–363.
89. Gasparetto EL, Ono SE, Escuissato D, et al. Cytomegalovirus
pneumonia after bone marrow transplantation: high resolu-
tion CT findings. Br J Radiol. 2004;77:724–727.
90. Althoff Souza C, Muller NL, Marchiori E, et al. Pulmonary
invasive aspergillosis and candidiasis in immunocompromised
patients: a comparative study of the high-resolution CT
findings. J Thorac Imaging. 2006;21:184–189.
91. Franquet T. High-resolution computed tomography (HRCT)
of lung infections in non-aids immunocompromised patients.
Eur Radiol. 2006;16:707–718.
r 2010 Lippincott Williams & Wilkins
Multidetector HRCT of Lungs
92. Gruden JF, Huang L, Turner J, et al. High-resolution CT in
the evaluation of clinically suspected pneumocystis carinii
pneumonia in aids patients with normal, equivocal, or non-
specific radiographic findings. AJR Am J Roentgenol. 1997;169:
967–975.
93. Kuroishi S, Nakamura Y, Hayakawa H, et al. Mycobacteri-
um avium complex disease: prognostic implication of high-
resolution computed tomography findings. Eur Respir J.
2008;32:147–152.
94. Olivier KN, Weber DJ, Lee JH, et al. Nontuberculous
mycobacteria. II: nested-cohort study of impact on cystic
fibrosis lung disease. Am J Respir Crit Care Med. 2003;167:
835–840.
95. Vassallo R, Jensen EA, Colby TV, et al. The overlap between
respiratory bronchiolitis and desquamative interstitial pneu-
monia in pulmonary Langerhans cell histiocytosis: high-
resolution CT, histologic, and functional correlations. Chest.
2003;124:1199–1205.
96. Clark KD, Wardrobe-Wong N, Elliott JJ, et al. Patterns of
lung disease in a ‘‘Normal’’ smoking population: are emphy-
sema and airflow obstruction found together? Chest. 2001;
120:743–747.
97. Vierikko T, Jarvenpaa R, Uitti J, et al. The effects of
secondhand smoke exposure on HRCT findings among
asbestos-exposed workers. Respir Med. 2008;102:658–664.
98. Betsuyaku T, Yoshioka A, Nishimura M, et al. Pulmonary
function is diminished in older asymptomatic smokers and
ex-smokers with low attenuation areas on high-resolution
computed tomography. Respiration. 1996;63:333–338.
99. Verschakelen JA, Scheinbaum K, Bogaert J, et al. Expiratory
CT in cigarette smokers: correlation between areas of decrea-
sed lung attenuation, pulmonary function tests and smoking
history. Eur Radiol. 1998;8:1391–1399.
100. Deveci F, Murat A, Turgut T, et al. Airway wall thickness in
patients with COPD and healthy current smokers and healthy
non-smokers: assessment with high resolution computed
tomographic scanning. Respiration. 2004;71:602–610.
101. Soejima K, Yamaguchi K, Kohda E, et al. Longitudinal
follow-up study of smoking-induced lung density changes
by high-resolution computed tomography. Am J Respir Crit
Care Med. 2000;161:1264–1273.
102. Remy-Jardin M, Remy J, Farre I, et al. Computed tomo-
graphic evaluation of silicosis and coal workers’ pneumoco-
niosis. Radiol Clin North Am. 1992;30:1155–1176.
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