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Bronchography
Bronchography, first described by Sicard and
Forrestier in 1922 [15], delineated the three forms of
bronchiectasis subsequently described in Reid's anatomical classification [16]. It was unpleasant for the patient,
lead to a temporary impairment of ventilation [17, 18]
and was occasionally associated with allergic and foreign
body reactions to the contrast media. Combining bronchography with fibre optic bronchoscopy was a major
advance, permitting the clearance of secretions before
the accurate instillation of contrast medium [19].
However, even for those experienced in the technique,
underfilling of bronchial segments with contrast medium
was still a limitation.
The interpretation of bronchographic abnormalities is
also problematic, as shown in a study of 27 patients by
Currie et al [ 9 ] . They found disagreement regarding the
diagnosis of bronchiectasis in 22% of lobes considered
by one or other of two readers to contain bronchiectasis.
Despite these difficulties, bronchography was until
recently the investigation of choice for the diagnosis of
bronchiectasis and the gold standard against which the
current best imaging technique, CT, has been compared
[10, 20-24].
Computed tomography of the chest
The first CT description of bronchiectasis was provided by Naidich et al in 1982 [25]. The study was
performed using 10 mm slices. The authors emphasized
the appearances of dilated bronchi, the visualization of
bronchi in the periphery of the lung and bronchial wall
thickening. They proposed that CT might replace bronchography in selected cases whilst raising possible limitations of the technique, in particular the poor definition
of bronchi which did not lie in the plane of the scan.
Subsequent investigators critically compared CT with
bronchography and found the sensitivity disappointingly
low. Silverman and Goodwin [10] used 10 mm thick
sections at 20 mm intervals and reported a sensitivity of
63% and a specificity of 100%. Cooke et al [20] used
10 mm contiguous sections and found a sensitivity of
66% and a specificity of 92%. Phillips et al [21] used
8 mm sections at 15 mm intervals and reported a sensitivity of 79% and a specificity of 99%, concluding that
CT was too insensitive to be a screening test for bronchiectasis and that bronchography was still the investigation of choice.
With the advent of HRCT, the sensitivity of the investigation improved to 82-97% [22-24]. Focal areas of
bronchiectasis shown on HRCT are sometimes not visible on bronchography [22, 24].
Technique is important in HRCT; the lungs should be
scanned from the apices to the diaphragm using a scan
thickness of 1-2 mm with a scan interval of 10 mm, with
additional slices at 5 mm intervals for areas of particular
concern. A scan time of 1 s or less is required to minimize
artefacts from cardiac or respiratory motion, which are
particularly troublesome at the lung bases and may be
further reduced by scanning the patient prone. Cranial
angulation of the scanning gantry (20-25) may be
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operative HRCT appearances with pathological examination of lung specimens resected for bronchiectasis [26].
They found that lack of bronchial tapering was 79%
sensitive for the diagnosis of bronchiectasis while bronchial dilatation alone was only 60% sensitive. This
difference was explained by the fact that the pulmonary
artery cannot always be identified because of peribronchial fibrosis. Changes in pulmonary artery diameter, such
as are seen in pulmonary hypertension and in hypoxic
vasoconstriction, may also lead to under or over diagnosis of bronchial dilatation. Abnormal bronchial tapering is therefore a more specific and sensitive sign than
bronchial dilatation alone.
Bronchial wall thickening
Bronchial wall thickening is another of the CT signs
originally described by Naidich [29] but it is an inconstant feature and is not a prerequisite for the diagnosis.
This sign is not specific to bronchiectasis as it is also
seen in asthmatics [33] and occasionally in asymptomatic smokers [34]. Kang et al [26] found a sensitivity
of 68% for the subjective appearance of bronchial wall
thickening in the diagnosis of bronchiectasis compared
with pathological examination post-resection. However,
interpreting these findings is confounded by there being
no accepted definition of bronchial wall thickening.
Remy-Jardin defined a bronchus as being thick walled
when the bronchial wall was at least twice as thick as
that of a normal bronchus [34]. Such an assessment is
limited when the abnormality is diffuse. Diederich et al
have defined a bronchus as thick walled if the internal
diameter is less than 80% of the external diameter [30]
and interobserver agreement on the presence of the sign
was good (K = 0.66). Whilst such a measurement is useful
if bronchi are of normal diameter or only slightly dilated,
wall thickness will be undercalled in markedly dilated
bronchi and may be overestimated when there is bronchoconstriction, for example with asthma.
An alternative method of scoring bronchial wall thickness is to compare it with the adjacent pulmonary artery.
This system was first described in cystic fibrosis [13]
with a scoring system of 1 to 3, where 1 represents
bronchial wall thickness equal to the diameter of the
adjacent pulmonary artery. This is too insensitive for use
in most patients with bronchiectasis in whom the degree
of thickening is considerably less. Reiff et al have developed the method and redefined the score of 1 as representing a bronchial wall thickness of half the diameter
of the accompanying artery [35]. This approach seems
promising, but they did not report the interobserver
variability of the sign defined in this way or describe the
frequency with which it was impossible to use the scoring
system when the artery was obscured by peribronchial
fibrosis.
The significance of bronchial wall thickening on
HRCT has not been established. While Kang et al have
described its sensitivity compared with pathological
examination, they did not describe the pathological correlates [26]. It has been suggested that it is evidence of
chronic and recurrent infection [13]. Compared with
patients with idiopathic or other specific causes for bronchiectasis, those with hypogammaglobulinaemia have
more pronounced bronchial wall thickening for a given
degree of bronchial dilatation [35]. In a study of patients
with chronic sputum production, we found that two
patients with hypogammaglobulinaemia had no bronchial dilatation but both had bronchial wall thickening
[36]. The balance between bronchial dilatation and wall
thickening may therefore be dependent on the degree of
immunocompetence and this may guide future investigations into the inflammatory processes which lead to
bronchiectasis.
Associations between clinical features and radiological
appearances
The three most important clinical features of bronchiectasis are chronic sputum production, usually with
infective exacerbations, airflow limitation and haemoptysis. Radiological investigation of the possibility of bronchiectasis is justified in patients presenting with these
features without apparent cause.
Chronic sputum production is commonly attributed
to chronic bronchitis due to airway damage caused by
cigarette smoking. However, it seems likely that many
patients with this symptom have bronchiectasis. Using
bronchography, Currie et al [9] studied 27 patients with
chronic sputum production and found bronchiectasis in
19 while accepting that referral for bronchography probably selected patients more likely to have bronchiectasis.
In a study using HRCT, we found that 27 of 40 patients
with chronic sputum production had bronchiectasis
[36]. The only features of the clinical history which
predicted the presence of bronchiectasis were the continual production of purulent sputum and childhood pertussis. Other features of the history which did not
differentiate between those with or without bronchiectasis included: the duration of symptoms, the volume of
sputum per day, haemoptysis and smoking history.
Auscultation of the chest was equally poor at distinguishing the two groups.
The association between airflow limitation and bronchiectasis is a determinant of outcome [37]. Two studies
have shown a highly significant negative correlation
between the forced expiratory volume in one second
(FEV1) and the extent of bronchiectasis on HRCT [36,
38]. The airflow limitation is thought to be produced
by sputum obstructing the airways [39] and by the
bronchiolitis which accompanies the large airways dilatation in the large majority of cases [26]. It is likely that
the narrowing and eventual obliteration of the peripheral
bronchial divisions has a greater impact on pulmonary
function than does bronchial dilatation [40].
When small airways are obliterated, collateral ventilation occurs during inspiration via the pores of Kohn
and maintains inflation in areas where the bronchioles
are obstructed. Airflow is obstructed during expiration
and the air is trapped. Hansell et al have shown air
trapping using expiratory scans performed with ultra fast
CT in subjects with bronchiectasis [41]. The degree of
air trapping was estimated by scoring the area of
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