Overview
The
role of computed tomography (CT) in the imaging of airway disease
increased after the development of lung high-resolution CT (HRCT). The
technical progress of thin-section acquisition, high-spatial-frequency
data reconstruction (ie, bone algorithm technique), and targeted
reconstruction has allowed the visualization of finer details on HRCT
scans; these details include airtrapping, measurable bronchial wall
thickening, atelectasis, centrilobular nodules due to mucous plugging,
and acinar nodules due to low-grade inflammatory changes.
[37, 38, 39]
King et al discuss details of HRCT methods for evaluating the airways in obstructive pulmonary disease.
[40] They discuss the technical features of HRCT and review its use in the assessment of obstructive airway disease.
See the asthma-related HRCT images below.
High-resolution
CT scan of the thorax obtained during inspiration demonstrates
airtrapping in a patient with asthma. Inspiratory findings are normal.
High-resolution
CT scan of the thorax obtained during expiration demonstrates a mosaic
pattern of lung attenuation in a patient with asthma. Lucent areas
(arrows) represent areas of airtrapping (same patient as in the previous
image).
Asthma.
High-resolution CT scan of the thorax obtained during inspiration in a
patient with recurrent left lower lobe pneumonia shows a bronchial
mucoepidermoid carcinoma (arrow).
Asthma.
High-resolution CT scan of the thorax obtained during expiration in a
patient with recurrent left lower lobe pneumonia shows a bronchial
mucoepidermoid carcinoma (same patient as in the previous image). Note
the normal increase in right lung attenuation during expiration (right
arrow). The left lung remains lucent, especially the upper lobe,
secondary to bronchial obstruction with airtrapping (left upper arrow).
The vasculature on the left is diminutive, secondary to reflex
vasoconstriction. Left pleural thickening and abnormal linear opacities
are noted in the left lower lobe; these are the result of prior episodes
of postobstructive pneumonia (left lower arrow).
Asthma.
High-resolution CT scan of the thorax demonstrates mild bronchial
thickening and dilatation in a patient with bilateral lung transplants
and bronchial asthma.
Asthma.
High-resolution CT scan of the thorax demonstrates central
bronchiectasis, a hallmark of allergic bronchopulmonary aspergillosis
(right arrow), and the peripheral tree-in-bud appearance of
centrilobular opacities (left arrow), which represent mucoid impaction
of the small bronchioles.
Baseline high-resolution CT scan of the thorax obtained during expiration in a patient with bronchial asthma.
Asthma.
High-resolution CT scan of the thorax obtained during expiration and
after a methacholine challenge in the same patient as in the previous
image. Note the greater degree of airtrapping in the posterior
subpleural aspects of the right upper lobe after methacholine is
administered.
Animal studies
In one study, the intact
lobes of pressurized canine lungs were evaluated with HRCT before and
after the administration of carbachol, a bronchoconstrictor.
Intermediate-sized airways had the most prominent decreases in luminal
area; 2- to 4-mm airways had a 56% reduction in diameter, and 4- to 6-mm
airways had a 59% reduction. Wall thickening was believed to result, in
part, from increased bronchial blood flow, edema, and smooth muscle
hyperplasia. The lower range of visibility was at the generally accepted
maximal diameter of small airways, that is, 2 mm.
[41]
Herold
et al established the usefulness of HRCT in measuring the bronchial
response to bronchoconstrictors in the setting of hyperreactivity.
Responses to aerosol isotonic sodium chloride solution and histamine
were assessed in anesthetized ventilated dogs and corrected for lung
volume. Airway cross-sectional area decreased by 43% after histamine
administration and by 26% after saline administration alone, but
intersubject and intrasubject variability was significant; the irritant
effect of the base aerosol was evident. Although airways as small as 1
mm were evaluated, the discrepancy between the response of large airways
(ie, bronchoconstriction) and small airways (ie, change in mean airway
pressure) could not be explained.
[42]
The
role of vascular engorgement and edema was evaluated with HRCT. Dogs
received 3 successive 50 mL/kg isotonic sodium chloride challenges or 2
successive 25 mL/kg blood infusions. This large sodium chloride load
caused more airway wall thickening and luminal narrowing than blood
alone. With sodium chloride, the luminal area and wall thickness were
68% and 150% of those at baseline, respectively; with blood, the results
were 81% and 108% of those of baseline, respectively. The findings were
not reversible within 30 minutes. Also, the findings were attributed to
edema in airway walls, but they were considered to have only a minor
role in the multiple causes of increased airway resistance in asthma and
left ventricular dysfunction.
[43] .
The
investigators then showed that, although the initial histamine
challenge narrowed the airways to 71% of their baseline luminal area,
the sodium chloride challenge alone (100 mL/kg) reduced the airway lumen
to 78% of its baseline size. Potentiation of the effect by combining
sodium chloride and histamine reduced the luminal area to 54% of its
baseline value. These findings were correlated with the known
exaggerated constrictor response to provocation in the setting of airway
edema
[44] .
Findings
from later studies of the role of inflammatory mediators in airway
hyperresponsiveness led to the conclusion that methacholine and
bradykinin, alone or combined, have only minor effects on
bronchoconstriction
[45]
Bronchial asthma
HRCT findings in bronchial asthma include the following:
Bronchial wall thickening
Bronchial dilatation
Cylindrical and varicose bronchiectasis
Reduced airway luminal area
Mucoid impaction of the bronchi
Centrilobular opacities, or bronchiolar impaction
Linear opacities
Airtrapping, as demonstrated or exacerbated with expiration
Mosaic lung attenuation, or focal and regional areas of decreased perfusions
Emphysema and airtrapping
Some
initial human studies involved emphysema scoring in patients with
asthma. Royle first described emphysema in severe asthma by using
radiographs in current or former smokers.
In the late 1980s, a
group evaluated the coexistence of emphysema and asthma findings using
HRCT. In comparing 10 nonsmoking patients with asthma with 10 matched
cigarette smokers with severe airflow obstruction, an emphysema grade of
0% was observed in the nonsmokers, and 100%, in smokers; the emphysema
score reflected vascular disruption, bullae, and low-attenuating areas.
Although all smokers with a TLC greater than 120% had at least some
emphysema, no nonsmoking patients with asthma had emphysema. The authors
concluded that, in patients with asthma, elevated TLC between attacks
can be explained by hyperinflation, which is entirely due to asthma and
not coexisting emphysema.
[46]
Paganin
et al studied airway remodeling in nonsmokers with allergic asthma and
in those with nonallergic asthma. On HRCT scans, the authors observed
emphysema, cylindrical and varicose bronchiectasis, bronchial wall
thickening (ie, bronchial recruitment), and linear opacities ("sequellar
line shadows"). The findings were significantly more prevalent in
individuals with nonallergic asthma than in individuals with allergic
asthma. Scores of the findings were significantly greater in both groups
and were associated with the severity and duration of asthma.
[47] Centrilobular
emphysema was most severe in individuals with severe nonallergic asthma
and was not observed in control subjects without asthma.
Whether
true emphysema exists in patients with asthma or whether only terminal
airspace enlargement is involved in bronchial asthma.
[48] the
severity of the findings appears to be correlated with the clinical
measures of severe asthma. Paganin et al suggested that some form of
airway remodeling accounted for the findings and that the process likely
differed in allergic asthma versus nonallergic asthma. An interesting
speculation is that interstitial emphysema and peribronchial fibrosis
may be the result of rupture of the dilated bronchial glands that are
present in bronchial asthma.
[49]
Confirming
earlier findings, authors from Japan also showed that smokers with
moderately severe asthma have a significantly higher emphysema score
(13.7% vs 2.3%) than that of nonsmokers. As expected, the diffusion
capacity was correlated with the emphysema score and the pack-years of
cigarette smoking. The authors concluded that, in smokers with asthma,
emphysema develops independent of the asthmatic condition.
[50] Determining
the difference between the 2 conditions may illuminate variations in
the decline of lung function and the prognosis.
The 10-year
mortality rate in patients with an emphysematous form of COPD (ie, 60%)
is substantially worse than that of atopic control subjects or
nonsmokers with known asthma (15%).
[51, 52] Therefore, differentiating between the 2 groups is important from an imaging point of view.
Findings
of a later study confirmed that a subgroup of individuals with asthma
who also had emphysema tended to smoke more than others and that they
have poorer lung function.
[53] In
this study, the patients with asthma were selected from a group with
suspected allergic bronchopulmonary aspergillosis (ABPA) who actually
did not have ABPA, cystic fibrosis, bronchiectasis, or immune
deficiency, as prior laboratory and HRCT findings revealed.
In
another study, a group of individuals with reversible asthma were
stratified in terms of absent, mild, or severe emphysema. Neither the
duration nor the severity of asthma was correlated with the presence of
emphysema, whereas smoking history, sex, and age were strongly
correlated. Patients with long-standing and partially reversible
bronchial asthma did not have emphysema if they were nonsmokers.
[54] The findings also were consistent with the observation that DLCO typically is preserved in nonsmokers with asthma.
The
correlation of airtrapping with pulmonary function was studied by using
HRCT in 74 patients with chronic airway disease, including asthma,
[55] and
it was found that on expiratory HRCT scans, the airtrapping and expired
volume scores were inversely correlated with FEV1, FEV1/FVC, and FEF25.
The TLC was not correlated with any of the imaging, age, sex, cigarette
smoking history, or visual HRCT scores. Airtrapping was found, even
when PFT results were normal; this finding suggests a complementary role
for HRCT in the functional evaluation of asthma. HRCT may be more
sensitive than PFT or DLCO alone in the evaluation of centrilobular and
panlobular emphysema.
[49]
By
the late 1980s, the HRCT features that were accepted as demonstrating
emphysema included low-attenuating regions, pulmonary vascular pruning,
distortion, disruption, and bullae. The use of an attenuation mask
allowed the semiautomated measurement of hypoattenuation in focal
regions of the lungs, with quantification in regions of interest, in
which other findings then were correlated.
[56]
Gevenois
et al demonstrated that the distribution of lung attenuation, as
visualized on CT scans, depends on the TLC and, to a lesser degree, age.
[57] However,
Biernacki et al showed a considerable overlap in lung attenuation, as
measured in Hounsfield units, in the evaluation of patients with chronic
asthma, patients with chronic bronchitis and emphysema, and control
subjects without asthma. The authors confirmed a correlation (
r
= 0.63) between TLC and the index of lung attenuation, although neither
lung attenuation nor TLC changed after PEFR improved with the use of a
nebulized adrenergic bronchodilator.
[58]
Ng
et al investigated airtrapping as an expression of small airway
narrowing. The authors examined 106 patients with small airway disease
and 19 healthy individuals. They found that decreased attenuation was
more prominent on expiratory HRCT scans than on inspiratory HRCT scans.
[59]
Quantitative
CT analysis also has promise. Newman et al demonstrated that patients
with asthma could be distinguished from individuals without asthma by
using machine calculations of the percentage of lung area near the
diaphragm with an attenuation less than –900 HU at end expiration.
[60] This
finding was true for both standard CT and HRCT, and it was correlated
with the degree of airtrapping, as measured with the FRC and RV. A
report of expiratory HRCT findings of airtrapping included inspiratory
scans that had normal findings and suggested that the most common
underlying causes of airtrapping were asthma and bronchiolitis
obliterans.
[61]
Additional
methods have emerged with the development of dynamic HRCT scanning.
With these methods, anatomic variations in bronchial obstruction can be
studied after a provocative challenge. For example, the temporal
development of airtrapping can be demonstrated with the successive,
rapid acquisition of CT images during expiration.
[62] .
Dynamic
CT scans demonstrate that the increase in attenuation in the dependent
and basilar portions of the lungs in individuals without asthma is
greater than that of individuals with asthma.
[63] Nevertheless,
images in 4 of 10 individuals without asthma also showed airtrapping
during rapid exhalation. Clinically, the usefulness of this modality is
yet to be determined.
Bronchiectasis and bronchial dilatation
Studies
of HRCT images in asthma consistently reveal the presence of
bronchiectasis in patients with asthma but not ABPA. In ABPA,
bronchiectasis often is considered part of the definition of the
disease. Dilated airways may take the form of cylindrical, varicose, or
cystic bronchiectasis. Park et al observed bronchial dilatation in 31%
of patients with asthma versus 7% of control subjects. The authors
measured bronchoarterial ratios but did not find a statistically
significant difference between the groups.
[64]
Lynch
et al showed that dilated bronchi, defined as bronchi that are larger
than accompanying arteries in which the tapering pattern is not lost,
were observed in 59% of the control subjects compared with 77% of the
patients with asthma. Other researchers found no or few such features in
control subjects. A decreased arterial diameter with hypoventilation
and hypoxic vasoconstriction, a sectioning artifact near the branching
arteries and bronchi, a bronchodilator effect on medium-sized airways,
and subclinical ABPA are potential explanations for the unexpectedly
high percentage of findings in control subjects. The authors discussed
CT scanner gantry tilting, as used in HRCT examination of patients with
bronchiectasis.
[65] They outlined their ability to follow the natural branching pattern of the bronchi in their plane.
[53]
The reported prevalence of dilated, normally tapering bronchi ranged from 18% with skin test results that were positive for
Aspergillus
species, which are common in patients with mild asthma, to almost 80%
in patients with moderately severe asthma. The varicose type, observed
in as many as 60% of patients, was considered to be more specific for
nonallergic asthma and severe asthma, whereas the cylindrical type
occurred in both allergic asthma and nonallergic asthma with varying
degrees of severity.
[47]
In
a study by Grenier et al, subsegmental and distal bronchiectasis was
more common in patients with asthma (29%) than in healthy volunteers
(7%). The changes were considered permanent, especially if they were
varicose or cystic; the prevalence of these changes and the number of
involved lobes increased with disease severity. The authors studied
interobserver variability and found that interobserver and intraobserver
agreement (k = 0.40) were clinically acceptable for bronchial wall
thickening, bronchial dilatation, small centrilobular opacities, and
decreased lung attenuation. Interobserver and intraobserver agreement
was not clinically acceptable with subtypes of bronchiectasis, such as
the cylindrical and varicose subtypes.
[66]
Investigators
in early studies used HRCT findings to prove that bronchial dilatation
was prevalent in 41% of the pulmonary lobes in 8 patients with asthma
who had clinical and immunologic evidence of ABPA and in 15% of lobes
studied in 8 patients with asthma who had positive skin test results for
only
Aspergillus fumigatus.[33] The
authors speculated that the unexpected findings in individuals with
asthma alone may have been due to steroidal suppression of immunologic
markers in these patients who actually had ABPA, non-
Aspergillus fungal disease, or cylindrical bronchiectasis.
Although
upper lobe involvement and bronchial wall thickening were considered
nonspecific findings, Neeld et al raised the awareness that asthma may
be more destructive than previously thought. Also, central
bronchiectasis in its various forms primarily may reflect the duration
of an inflammatory airway process rather than determine the difference
between ABPA and asthma per se.
[33]
Compared
with the value of the traditional modality of bronchography, the value
of thoracic HRCT in demonstrating central bronchiectasis in ABPA was
proven in all 21 patients with the disease and in most of the segments.
Central and peripheral bronchiectasis, but not peripheral bronchiectasis
alone, have been evaluated by using both chest radiography and HRCT
images as a diagnostic criteria for ABPA. Angus et al observed bronchial
dilatation in 82% of their 17 patients and in 41% of the affected lobes
in patients with ABPA versus 18% and 5%, respectively, in patients with
asthma and in those without ABPA. However, peripheral bronchiectasis
alone was not found in any of the patients with ABPA.
[67]
Mucoid
impaction is a well-defined finding in patients with ABPA. It may
appear as centrilobular bronchiolar plugging or have a tree-in-bud
appearance on HRCT scans. Mucoid impaction is believed to be one of the
physiologic origins of mosaic lung attenuation.
[10] Paganin
et al attributed the development of varying degrees of cylindrical
bronchiectasis to sequela of multifocal mucoid impactions and bronchial
hypersecretion in asthma
[47]
Grenier
et al found a 21% incidence of centrilobular opacities on HRCT scans
obtained in patients with asthma, compared with 5% in individuals
without asthma. The authors believed that these opacities and the
decreased lung attenuation can be related to the severity of asthma. The
authors studied intraobserver and interobserver variability and found
that, with bronchial wall thickening, bronchial dilatation, small
centrilobular opacities, and decreased lung attenuation, intraobserver
(k = 0.60-0.79) and interobserver (k = 0.40-0.64) agreement was
clinically acceptable.
[66]
Bronchial wall thickening
Carroll
et al found that, in cartilaginous airways, the total areas of the
inner wall and outer wall, smooth muscle, mucous gland, and cartilage
were greater in fatal cases of asthma than in control and nonfatal
cases.
[68] The
internal size of segmental to sixth-generation bronchi was studied in
healthy control subjects by using HRCT. Measurements ranged from 0.8-8
mm in diameter, with the use of 2-HU windows, 5X optical magnification,
and automated luminal area calculation. The authors used a 2-HU window
to clarify the edges of the bronchial walls to enhance the
reproducibility of the measurement.
[69]
Hudon
et al used HRCT to show that bronchial thickening in patients with
asthma and irreversible airflow obstruction was significantly greater
(2.4 mm) than that of patients with completely reversible asthma (2 mm)
despite the similar internal diameters of their airways.
[70]
Lynch
et al observed bronchial wall thickening on CXRs and HRCT scans in 71%
and 92% of individuals with asthma, respectively (vs HRCT in 19% of
control subjects). The authors' patient selection was somewhat biased
toward those with asthma complications and smokers (44%).
[53] As
discussed before, a decreased arterial diameter with hypoventilation
and hypoxic vasoconstriction, a sectioning artifact near branching
arteries and bronchi, a bronchodilator effect on medium airways, and
subclinical ABPA were considered to be potential explanations for the
unexpectedly high percentage of findings in control subjects.
Park
et al found bronchial wall thickening proportional to severity in 44%
of stable nonsmokers with asthma versus 4% of control subjects.
Bronchial wall thickening occurred in 83% of patients with severe
airflow obstruction versus 35% in patients with mild obstruction and 38%
in control subjects.
[64]
Grenier
et al found bronchial wall thickening in 82% of patients with asthma
versus 7% of control subjects; this finding established one of the
largest differentials between these groups, although the measurements
were solely subjective. Nevertheless, the method of measurement appeared
to be reliable in terms of intraobserver and interobserver variability.
[66] Others had similar findings.
[67, 71, 47, 72]
In
an autopsy study of individuals who died with asthma as well as those
who died from asthma, large airway and small airway thickening was
observed in individuals with lethal asthma, whereas small airway
thickening was observed only in nonlethal asthma.
[68]
Awadh
et al studied airway wall thickening and found no significant
difference in the ratio of wall thickness to outer diameter or the
percentage of wall area to the total outside cross-section in patients
with near-lethal asthmatic attacks versus patients with moderate asthma.
[73] Both
groups differed from patients with mild asthma and from individuals
without asthma. Nevertheless, even the group with mild asthma differed
from individuals without asthma; this finding confirming those of others
and demonstrating that individuals with mild asthma can have airway
thickening if the condition is chronic. The findings were present in
both the small airways (< 2 mm) and the larger airways (>2 mm).
The findings support the concept of chronic airway thickening in asthma
and the likelihood of airway remodeling; interstitial peribronchial
fibrosis; and, perhaps, parabronchial inflammation, which may cause
accompanying centrilobular emphysema.
Bronchial responsiveness
Okazawa
et al evaluated a known feature in patients with asthma, that is, the
exaggerated airway response to bronchoconstricting stimuli. Patients
with mild-to-moderate asthma and control subjects received a
methacholine challenge, and airway lumen narrowing was normalized for
FRC. In both groups, the site similar (small, < 2 mm; medium, >2
mm) and extent of airway luminal narrowing on HRCT scans were similar,
as were the reductions in FEV1 values. Only patients with asthma had
extensive small airway wall thickening without an increased airway wall
area; this finding did not change much after a bronchoconstrictor was
administered. Control subjects did not have wall thickening, and their
airway wall area decreased. The authors concluded that nonreversible
small airway wall thickening in patients with asthma contributed to an
exaggerated response of the small airways to stimuli.
[74]
In
the intermediate bronchi of individuals with asthma and fixed or partly
reversible obstruction, Boulet et al observed no difference in
bronchial wall thickness relative to the diameter compared with that of
control subjects. Small airways, in which asthma and COPD cause
substantial pathophysiologic changes, were not studied. The authors
suggested that mechanical properties of the airway wall were probably
more important than wall thickness in determining airway responsiveness.
[75]
In
another study of bronchoeffector agents, the appearance of the airways
on HRCT scans showed that airway internal luminal diameter slightly
decreased in individuals with mild asthma and that specific airway
resistance increased after methacholine administration; this effect
completely reversed after the bronchodilator agent albuterol was
administered, and an improvement compared with baseline values was even
observed. Airway wall thickness did not change in terms of the diameter,
and pulmonary functions did not change with treatment. The
investigators were able to quantify the changes in patients with asthma
and control subjects by using HRCT scans.
[76]
In
attempting to differentiate COPD from asthma with HRCT scans, Park et
al showed that bronchial walls were thicker in bronchial asthma (2.3 mm
thicker than normal) than in COPD (0.9 mm thicker than normal). However,
the ratio of wall thickness to luminal diameter was not correlated with
clinical features such as smoking history, duration of symptoms,
physiologic measures (eg, FEV1), specific airway conductance, and a
provocative concentration of the bronchoconstrictor methacholine. HRCT
findings of tubular bronchiectasis, emphysema, and mosaic lung
attenuation were correlated with a long history of asthma symptoms,
compromised lung function, and decreased bronchial hyper responsiveness.
[64] The
authors concluded that differentiating COPD from asthma is possible
from the data, although the usefulness of the data in individual cases
remains speculative.
Carr et al studied the role of the small
airways in severe asthma by using HRCT. Inspiratory and expiratory scans
were obtained with an electron-beam scanner. The mean decrease in the
expiratory-to-inspiratory cross-sectional area was measured: Findings
were 76% in patients versus 45% in control subjects. The results showed
marked initial inspiratory airway narrowing, and further narrowing with
expiration in patients with asthma was limited. The authors also found
that FEV1 was correlated with this narrowing and with CT features of
airtrapping, but not with features of airway wall thickening or airway
dilatation. Airtrapping was observed with and without overt
bronchiectasis in some lung regions; this finding led to the speculation
that small airway disease with airtrapping may precede bronchiectasis.
As previously shown, FEV1 and RV are correlated with end-expiratory
airtrapping in individuals with asthma.
[77]
Guckel
et al also evaluated the source of mosaic attenuation on HRCT scans and
observed the influence of oxygen administration on this appearance. In
22 patients with asthma who received a methacholine challenge, high-flow
oxygen administered by face mask at a rate of 12 L/min produced the
greatest increase in volume-corrected attenuation in regions of mosaic
attenuation, compared with the nasal administration of oxygen at a rate
of 5 L/min or the use of room air. The proposed and plausible
explanation is that hypoxic vasoconstriction, another known cause of
mosaic attenuation (airtrapping) besides bronchial narrowing, may
account for foci of decreased attenuation in patients with asthma.
[78]
In
addition, airtrapping is observed in some areas of bronchiectasis in
individuals with asthma due to weakness of the bronchiolar walls and
resultant airway collapse during exhalation.
[79] Ng
et al investigated airtrapping as an expression of small airway
narrowing on HRCT scans. The authors examined 106 patients with small
airway disease and 19 healthy individuals. They found that decreased
attenuation was more prominent on expiratory HRCT scans than on
inspiratory HRCT scans.
[59]
Effect of treatment
Paganin
et al found both reversible and irreversible findings on HRCT scans of
individuals with asthma. Mucoid impaction, acinar opacities, and lobar
collapse resolved within 2 weeks of treatment with oral steroids.
Bronchiectasis, bronchial wall thickening, linear opacities, and
emphysema were unchanged during that interval and were considered
permanent. While chest radiographs alone showed abnormal findings in 38%
of patients, CT demonstrated abnormal findings in 72% of patients, and
the authors concluded that patients with more severe asthma are more
likely to have irreversible abnormalities.
[71]
Grenier
et al also studied the effect of treatment in patients with asthma
without ABPA who had more mucoid impaction or lobar collapse on HRCT
scans than on chest radiographs alone. The features tended to resolve
with use of corticosteroids.
[66]
Another
study of bronchoeffector agents and the appearance of airways on HRCT
scans revealed that airway internal luminal diameter slightly decreased
and specific airway resistance increased after the administration of
methacholine in patients with mild asthma. These effects completely
reversed after the bronchodilator agent albuterol was administered, and
an improvement compared with baseline values was even observed. Airway
wall thickness did not change with treatment in these patients or in the
control subjects. In the control subjects, neither airway luminal
diameter nor pulmonary function changed. HRCT scans significantly aid in
quantifying the changes in patients with asthma and in control
subjects.
[76]
Goldin
et al examined 15 patients with asthma and 8 control subjects by using
spirometry and HRCT and by using a methacholine challenge and albuterol
inhalant reversal (see the images below). The authors showed a shift in
the frequency distribution curve of lung attenuation and small airway
cross-sectional area after bronchoprovocation; the findings reversed
after bronchodilators were administered. The findings were correlated
with changes in FEV1 in individuals with asthma and with a lack of
changes in control subjects.
[80]
Baseline high-resolution CT scan of the thorax obtained during expiration in a patient with bronchial asthma.
Asthma.
High-resolution CT scan of the thorax obtained during expiration and
after a methacholine challenge in the same patient as in the previous
image. Note the greater degree of airtrapping in the posterior
subpleural aspects of the right upper lobe after methacholine is
administered.
Asthma.
Graph demonstrates results in right upper lobe matched pairs before and
after a methacholine challenge. The resulting frequency distribution of
regional lung density in the midright upper lobe demonstrates a
leftward shift to lower attenuation after methacholine administration.
Courtesy of Jonathan Goldin, MD, University of California, Los Angeles.