1964, Brit. J.

Radiol, 37, 344-357

P. Lesley Bidstrup
REFERENCES

SUMMARY

1. The known occupational causes of lung cancer are

listed.
2. The results of routine radiology in two groups of men
exposed in the past to the hazard of lung cancer in their
occupations are discussed.
3. The fact that a few men have survived and been able
to work for more than five years following operation indicates that routine radiology, combined with strict medical
supervision of persons at risk, is of value in the diagnosis
of lung cancer as an industrial disease.

GWYNNE MORGAN, J., 1958, Brit. J. industr. Med., 15,

224; 1963, personal communication.

NASH, F. A., MORGAN, M., and TOMPKINS, G.,

1961,

Lancet, 2, 46.
POSNER, E., MCDOWELL, L. A., and CROSS, K. W., 1959,

Brit. med.J., 1, 1213.

RAVEN, R. W., Cancer. Progress 1960. Industrial Aspects
81 (Butterworth & Co. (Publishers) Ltd., London).
STEWART, A., PENNYBACKER, W., and BARBER, R., 1962,

Brit. med.J., 2, 882.

The Annual Report of the Registrar-General for Scotland
for 1960. No. 106 (H.M.S.O., Edinburgh) 1961.

III. The radiology of chronic bronchitis

Contributed to the symposium on "Industrial pulmonary disease" at the Annual Congress of The British
Institute of Radiology, April 5, 1963

By G. D. Scarrow, M.D., M.Rad., D.M.R.D.

Department of Radiodiagnosis, University of Liverpool; Respiratory Unit, Whiston Hospital,
Prescot, Lanes.
In 1959 the Report of the conclusions of a Ciba that this pattern may be due to hyperaemia of the
Guest Committee on chronic pulmonary emphysema arterioles of the bronchial arteries in the walls of
and related conditions clearly defined the clinical the bronchi.
state of chronic bronchitis as chronic or recurrent
Very strong evidence to the contrary was provided
cough with expectoration which is not attributable by the exhaustive work of Simon and Reid (1958)
to conditions excluded from chronic non-specific who showed that the bronchial thickening and hylung disease. The words "chronic" or "recurrent" peraemia which occurred was of such dimensions as
may be defined as "occurring" on most days for at to be invisible on the normal radiograph.
least three months in the year during at least two
In 1953 Simon and Galbraith examined the plain
years. Infection is frequently but not necessarily radiographs of 857 patients with a clinical diagnosis
present. The same report also precisely lays down of chronic bronchitis and were unable to detect any
the definitions, classification and terminology for changes in the intra-pulmonary vascular pattern
the associated reversible and irreversible obstructive apart from those attributable to emphysema. In 41
lung disease and emphysema.
per cent of these cases they saw no radiological abUnfortunately no such easy radiological definition normality and throughout the series they saw no
exists and to describe specific radiological changes in generalised abnormal shadowing which might corchronic bronchitis and emphysema has been recog- respond to the larger bronchi or to peribronchial
nised as a most difficult task for nearly a quarter of a structures lying in juxtaposition to the vascular
century. Stuart Harris and Hanley in 1957 stated shadows.
that there are no radiological appearances which can
These observations may not be so true in the
be used in a positive diagnostic sense and they con- future when with a greater use of a multiline grid of
sider that the main value of radiography is to the Schmit type and short exposures in the region
exclude other lung diseases which may present a of 3 jjus, structures of the order of 0-3 mm can be
similar clinical picture. Nevertheless, it is rare to seen.
find a radiologist who will frankly admit that he
Perhaps the most valuable contribution by Simon
cannot recognise the chest radiograph of a chronic at that time was the recognition and detailed desbronchitic. In it he sees a variation from the normal cription of the specific bronchographic changes ocdifficult to describe and inconstant in appearance. curring in chronic bronchitis. Leopold and Seal in
Numerous attempts have been made to explain 1961 described a further type of peripheral pool
these changes more precisely and for many years a thought to be due to the opaque medium lying in the
theory of peribronchial thickening was in vogue space created by areas of centrilobular emphysema.
which was thought to give rise to a more dense lung
Diffuse interstitial reticulation has been observed
pattern than normal. Alternatively, it was thought by Lodge (1946), Simon (1958), Kerley (1962) and
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Industrial Pulmonary Disease

others to occur in the lower zones in some cases, but
doubt exists as to whether or not this finding is in
fact related to the Hamman-Rich syndrome.
Thus it is currently accepted that whereas the
bronchographic changes in chronic bronchitis may
be regarded as characteristic the diagnosis on the
plain radiograph depends on the recognition of the
presence of the concurrent emphysema.
This paper is based on the material passing through
a 1,000-bedded peripheral general hospital, part
acute and part geriatric, situated in south-west
Lancashire, one of the areas in which there is a high
incidence of the disease. The material has been collected from and includes the winter of 1957-58.
The hospital has for many years filled the role of
a local district hospital and has provided an opportunity for studying the radiological behaviour of the
disease for periods of a decade or more.
Other patients have been radiographed in connection with a therapeutic trial conducted by an
industrial medical officer in the same area.
In both instances the material is, of course, highly
selective, the hospital usually being concerned with
severe exacerbation of the advanced case. In the case
of the factory, the trial was conducted on known
chronic bronchitics with a bad sickness record.
Nevertheless, due to the high incidence of the disease in the area, the ordinary hospital intake for nonrelated conditions has provided material for the
study and integration of the radiology in the quiescent phase of the disease, and has also provided
chest radiographs of a similar age and environmental
group in which there is no clinical evidence of
bronchitis and emphysema.
The clinical diagnosis was supported in most
instances by pulmonary function tests, electrocardiograms and vector electrocardiograms, sputum examinations and blood counts, and in some instances
cardiac catheterisation.
For various reasons the radiological investigation
has been restricted to postero-anterior and lateral
radiographs of the chest in various stages of the
disease. In those cases where clinical or radiological
evidence pointed to the presence of pulmonary
arterial hypertension, tomograms were taken of the
right hilum and lung fields in the supine position
using a Philips Danatome and a multisection cassette. Occasional bronchograms and pulmonary
angiograms have been done where it was felt necessary to confirm or supplement evidence supplied by
the plain radiographs.
In cases where films were not available prior to
hospital admission every effort was made to obtain
a further radiograph of the patient during a period of

maximum clinical recovery, usually in the following

summer. These films were used for comparative
purposes to assess the changes occurring during exacerbations or any progressive deterioration. For
reference the film is termed the "summer" or "quiescent" film.
FACTORS INFLUENCING THE RADIOGRAPH

At an early stage it became apparent that there

were many factors which influenced the appearances
of the radiograph and these have been summarised as
follows:
(1) the physical build of the patient;
(2) the phase of respiration;
(3) the degree of radiological emphysema;
(4) superimposed acute or chronic infection;
(5) exacerbation or quiescence;
(6) the presence and degree of pulmonary arterial
hypertension;
(7) the presence of congestive cardiac failure;
(8) the presence of other illnesses common to the
age group;
(9) the presence of any significant degree of polycythaemia.
Some of these factors are variants associated with
the disease under review, others are extraneous
factors. The changes due to ischaemic heart disease,
systemic hypertension, fibroid tuberculosis, pneumoconiosis, chronic renal disease and other concurrent diseases must be recognised and discounted.
Similarly, recognising the known influences of
polycythaemia on the pulmonary vascular pattern,
blood counts were taken of the cases. Although a
mild polycythaemia was demonstrated in a number
of cases, in no instance was this thought to be sufficient to influence the radiograph.
The physical build of the patient and the presence
of deformities of the thoracic cage will determine the
shape and volume of the thorax. This in time may
influence the clinical course of the disease or may
modify the radiological appearances. Alternatively,
the shape and volume of the thorax may be the result
of chronic bronchitis and emphysema.
The effects of gross congenital deformities of the
ribs, kyphoscoliosis and other severe abnormalities
are well recognised and I do not wish to refer to
these in detail.
Perhaps of more pertinent interest are the possible
effects of what may be regarded as the normal variations in the physical characteristics of individuals.
In a tall thin hyposthenic patient emphysematous
changes in the lung fields may either be simulated or
exaggerated due to an early increase in the vertical
diameter of the chest which does not occur so readily

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G. D. Scarrow

FIG. 1.
An obese male, aged 52 years, admitted with dyspnoea, cyanosis, mental confusion, frothy sputum and oedema, the
clinical picture simulating cor pulmonale in congestive cardiac failure.
(A) Postero-anterior chest film showing a small volume thorax with congestive changes, de-aeration of the lower zones
and cardiac enlargement. There is no enlargement of the hilar vessels or other radiological evidence of pulmonary arterial
hypertension
(B) A subsequent tomogram seven days later shows some congestive enlargement of the intrapulmonary arteries and
veins but no evidence of pulmonary arterial hypertension.
(c) Postero-anterior film nine months later after considerable loss of weight. The chest is assuming a more normal
configuration. There is evidence of moderate lung damage and this was confirmed by pulmonary function test. An
electrocardiogram showed evidence of ischaemic heart disease.

in the short sthenic individual. The cardiac contour

is tall, narrow and vertical from an early stage.
Conversely, in the sthenic patient the relatively
high diaphragm tends to mask the radiological
changes of emphysema for a longer period if viewed
solely in the postero-anterior projection. The increase in the volume of the thoracic cage in these
cases initially occurs in the antero-posterior diameter with exaggerated anterior bowing of the sternum and an increasing kyphos. To a lesser extent
there is an increase in the transverse diameter of the
base. The heart does not readily assume the characteristic narrow vertical silhouette but it does
diminish in size and this feature of a small heart in
a large chest in a sthenic individual may be regarded
as a diagnostic pointer in these cases.
The height/weight/thoracic volume ratio also appears to be of significance. For a similar height and
weight one patient will have a large volume chest and
another a smaller than normal volume thorax. Although this aspect of the subject is still under
investigation the patient with the small volume
thorax appears to be more prone to develop chronic
infective lung disease, whereas in patients with a
large volume thorax the dominant characteristic is
a progressive emphysema.

Obesity is of great importance and in the extreme

can confuse and modify the course of the disease,
as in the so-called "Pickwick syndrome" (Figs. 1A,
1B, lc). The other varying factors are so intimately
bound up w7ith the features of the disease that they
will be discussed under the appropriate headings.
RADIOLOGICAL APPEARANCES

If the influence of these many variants is recognised then the radiographs of patients suffering from
chronic bronchitis and emphysema can be seen to
fall into fairly well defined categories. In the majority of cases the radiographs also bear some relation
to the severity of the disease and a progressive deterioration can be demonstrated. For convenience
the appearances may be described under two headings; those occurring in simple uncomplicated cases
of chronic bronchitis and emphysema and those occurring incases in which a significant degree of pulmonary arterial hypertension with or without
congestive cardiac failure has developed. In the first
category the radiographs may be divided into four
fairly clearly defined although overlapping groups.

346

A. SIMPLE UNCOMPLICATED CASES

Group 1
Those cases in which there is irrefutable clinical

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1964

Industrial Pulmonary Disease

evidence of chronic bronchitis but the chest radiograph shows little evident variation from the normal.

It may well be that these large volume chests with

relatively small hearts and normally distributed vasculature in patients with respiratory symptoms represent the stage of dilatation of the distal air spaces
prior to the development of centrilobular destruction
(Fig. 2).

Group 2
Those cases in which the radiological finding is
one of widespread diffuse emphysema.
Group 3
Those cases in which there is a mixture of chronic
inflammatory change in the lung fields interspersed
with areas of radiologically normal or hyperaemic
lung and areas of emphysema.

GROUP 2
Although these cases fulfil the clinical criteria for
chronic bronchitis, progressive breathlessness is
usually the main complaint and the infective episodes and exacerbations are not so frequent and not
so marked as in the other groups. The main radiological finding is one of widespread diffuse emphysema, which is more evenly distributed than in the
following groups. Recognisable inflammatory shadowing plays little part in the composition of the
films (Figs. 3A and 3B).
It is evident that a considerable discrepancy exists
between the radiological diagnosis of emphysema
and subsequent pathological findings. Nevertheless,

Group 4
Those cases in which there are extensive chronic
inflammatory changes in the lung fields, and these
are the dominant features of the radiograph.
GROUP 1
Great emphasis has always been given to the disparity between the clinical state of the patient and
the appearances of the chest film.
It is reasonable to suppose that in early and
moderate cases in which chronic bronchitis, that is
an excessive secretion of mucus with infective episodes, is the major pathology, with little in the way
of concurrent emphysema and structural damage to
the lung, then a chest radiograph must of necessity
appear normal in a quiescent phase.
The anomaly of the respiratory cripple with an
apparently normal chest film remains a problem.
However, reports are appearing in the literature of
such patients with little radiological change but
marked changes in the lung function tests (Fletcher,
Hugh-Jones, McNichol and Pride, 1963). Thus it
may be that a normal chest radiograph in the presence of a severe respiratory disability is not in fact
a radiological failure but of great diagnostic and
prognostic significance indicating disturbed alveolar
ventilation and gas tensions rather than destruction
of the lung.
It is perhaps of significance that in a group of 48
patients all classified as known chronic bronchitics
who were radiographed in connection with a therapeutic clinical trial I was unable to recognise any
definite abnormality in the lung fields in seven of the
cases.
Three of these chests were in all respects normal.
One had normal lung fields but evidence of ischaemic heart disease. The other four had large volume
chests relative to the height and weight of the patient
and a cardio-thoracic ratio of less than 0-4. There
was, however, no obvious change in the vascular
pattern of the lung fields.

FIG. 2.
Male, aged 59 years. Postero-anterior chest film showing a
large volume thorax. The diaphragm is below the anterior
end of the 7th rib and the heart and mediastinum are compressed. A lateral view confirmed the expanded thorax. The
vascular pattern of the lung fields is normally distributed
and there is plenty of background filling. Tomograms
showed normal vessels. The patient suffers severe disability
with an FEV of 1-2 1. and a forced vital capacity FVC of
2-5 1. The obstructive lung disease is irreversible.

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G. D. Scar row

A
FIG. 3.
B
(A) Diffuse confluent emphysema with little in the way of inflammatory shadowing.
(B) Same patient four years later admitted following a rapid deterioration in the clinical condition.

vessels and diminution in the degree of background

filling.
The distribution of the vasculature is even, discounting the variations due to the volumetric changes
in the thorax, and there is not the same degree of
local distortion of vessels which is seen in the following group. Bullae are normally absent.
The work of Laws and Heard (1962) stresses the
importance of the alterations in the pulmonary
vasculature in the radiological diagnosis of emphy(a) Changes due to the influence of the increased lung sema and I am in agreement that these are probably
the ultimate diagnostic criteria.
volume and rigidity on the adjacent structures
The thoracic wall is expanded, first in one and
then in all diameters. The diaphragm is depressed (c) Change in the heart size
There is usually a progressive diminution in the
and restricted in movement. The mediastinum is
compressed, producing a thin mediastinal shadow in size of the heart as the degree of emphysema prowhich the aortic knuckle is prominent and the main gresses. This is thought to be the result of three
divisions of the pulmonary arteries are clearly factors:
visible. The cardiac silhouette is tall, thin and (1) the descent of the diaphragm which elongates
narrow.
the heart;
(2) the increase of the intrathoracic pressure;
(3) a diminished right heart blood flow.
(b) Changes in the vascularity of the lung fields
The heart size tends to remain constant, other
The lung fields are diffusely hypertranslucent and
oligaemic due to narrowing of the peripheral lung than in periods of infective exacerbation when some
if the radiological criteria are strictly applied then it
is a fair assumption that a radiological diagnosis of
emphysema is likely to be confirmed pathologically,
whereas the absence of radiological evidence of
emphysema on the plain film does not necessarily
exclude its presence.
The radiological changes occurring in this group
of cases may be summarised under the following
headings.

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1964

Industrial Pulmonary Disease

enlargement occurs, until with the onset of congestive heart failure, with or without associated pulmonary arterial hypertension, the heart again enlarges,
sometimes dramatically.
GROUP 3
These are cases in which there is an uneven
distribution throughout the lung fields of emphysema, inflammatory changes, areas of normal lung
tissue and areas of overfilled lung tissue.
The effect of these elements on the radiograph is
to produce a disruption of the normal lung pattern
of very varying degree depending on the preponderance of one or other component (Fig. 4).
This is by far the most common finding in chronic
bronchitis. A slowly progressive deterioration occurs
manifest by a diminution of the amount of recognisable lung tissue and an increase in the extent and
degree of the abnormal elements.

FIG. 4.
An example of the type of radiological change occurring in
Group 3. The patient has suffered from chronic bronchitis
for over ten years. The radiograph shows a large volume
chest with emphysema of the left apex and the left lower
zone. Areas of chronic inflammatory shadowing are present
in both lower zones adjacent to the cardiophrenic angles,
and in the right mid-zone. In other areas the lung structure
and vasculature show an almost normal appearance.

GROUP 4
In these cases the extensive chronic inflammatory
changes in the lung fields are the dominant features
of the radiograph.
The changes are usually of two types, both of
which may be present in the same patient.
(1) Frank bronchiectatic areas.
(2) Chronic inflammatory shadowing disseminated
and dispersed between the emphysematous areas.
This shadowing is usually hard, discrete and nodular. The changes vary little over long periods irrespective of the clinical condition of the patient.
(Figs. 5A and 5B).
Chronic inflammatory shadowing may also take
the form of areas of fibrosis which produce bizarre
appearances and distortion of the lung.
BEHAVIOUR DURING AN ACUTE CHEST ILLNESS OR
EXACERBATION

This is recognised clinically by a deterioration

in the clinical condition of the patient, the presence
of purulent or mucopurulent sputum and an increase
in such symptoms as cough and dyspnoea. Pyrexia
may be present.
The first three groups show essentially similar
radiological behaviour as assessed against the quiescent or summer film. The following changes have
been observed.
1. One or more areas of consolidation and deaeration of segmental or greater distribution. More
rarely, the shadowing is more widespread and is of a
bronchopneumonic character. The areas of consolidation frequently recur over the years in the same
site leading eventually to frank bronchiectasis. Lobular collapse was seen only infrequently. Radiological
resolution is variable. The lesion may resolve progressively over two to three weeks or alternatively
residual shadowing may persist for many months
and possibly still be present on the "summer" film.
Of a series of 126 patients admitted during the
winter of 1958-59, 40 showed this type of change.
2. Changes in the vascular pattern of the lung
fields with or without associated evidence of pulmonary oedema. These changes consist of: (a) a lack of
definition of the intrapulmonary vessels which may
occur locally in one zone or diffusely throughout the
lung fields; or (b) an increase in the vascular pattern
of the lung fields which is a true increase in both the
size and number of the vessels visualised. This is
usually unevenly distributed and may occur to a
greater extent in one area than in another or be
restricted to one area (Figs. 6A and 6B).
The changes are most marked in those areas least
affected by the emphysema, where a pulmonary

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G. D. Scarrow

-v.

FIG. 5. (A) Postero-anterior film of a chronic bronchitic patient of many years standing. Over the
past five years the patient has had repeated infective episodes with inflammatory shadowing in both
lower and middle zones. Less resolution occurred with each infection until the present stage had
been reached when little change occurred in the appearances of the chest over long periods. Bronchograms in this case showed irregularity and dilation of many of the bronchii of the lower lobes.
(B) This patient has a similar clinical history to (A). Frank bronchiectatic changes have developed in
the base of the right upper lobe.
FIG. 6. (A) Summer film of a known chronic bronchitic of the "clean" type.
(B) Radiograph of the same patient in an exacerbation, showing an increase in the vascularity of the
lung fields, particularly in those areas where the emphysema is less marked.

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Pulmonary Industrial Disease

vascular pattern is still visible. Emphysematous bullae and the extent of the gross lung damage may often
be recognised more easily during an exacerbation
when these areas appear translucent and featureless
in an otherwise hyperaemic and infected lung.
Alternatively, emphysema recognised in the quiescent film is sometimes masked in an exacerbation
due to the easy distensibility of the pulmonary vascular bed and the presence of superimposed inflammatory changes.
The lung pattern may be disorganised, unusually
large vessels appearing in the periphery of the lung
field.
Where the changes are extreme, a miliary type of
mottling is present, generally or locally, due in part
to the number of vessels seen "end on" and possibly
in part to miliary pulmonary oedema (Fig. 7). Frank
intra-alveolar pulmonary oedema is occasionally
observed.
There is usually a small or moderate increase in
the size of the heart and the hilar vessels. There may
be associated bronchospasm with distension of the
thoracic cage.
With adequate treatment these changes resolve
quite quickly over a period of days, although the

clinical state may lag behind the radiological recovery.

Fifty-three patients in the series showed this type
of radiological pattern. In none of these cases wras
there any evidence at the time or subsequently of
left ventricular failure.
3. Seventeen cases presented with a pleural effusion usually unilateral and of no appreciable specific
characteristics.
4. Superimposed on the above changes in a number of the more advanced cases there was more
definite evidence of a transient pulmonary arterial
hypertension, manifest by right heart enlargement
and significant increase in the size of the pulmonary
artery and its main branches.
5. The 16 cases not included in the above figures
are unclassifiable for one reason or anotherusually
due to technical faults or concomitant disease.
It has been observed that the patients tend to behave in a similar manner in each episode, i.e. if they
show opacities in the lung fields in one exacerbation
they will tend to do so in the next exacerbation.
The fourth group of cases in which there is extensive chronic inflammatory shadowing do not show
such a marked radiological change in the lung fields
during an exacerbation due to the already extensive
shadowing. In some cases the exacerbation may be
reflected in the size of the cardiac outline, however,
which enlarges.
BEHAVIOUR OVER A LONG PERIOD

FIG. 7.
Known chronic bronchitic in an exacerbation showing
miliary mottling throughout the lung fields. The "summer"
film of this patient is shown in Fig. 4.

This is very variable. In those cases where the

disease becomes manifest following an acute chest
infection in a previously healthy adult, deterioration
rapidly takes place over a few years with increasing
emphysema and repeated infections. The patient
succumbs after a relatively short period either as a
result of infection or following the onset of cor
pulmonale.
The more usual picture is one of slow deterioration over the years (many patients give a history of
20 to 25 years), with either the infective element or
emphysema becoming the dominant chest characteristic. In the absence of a fatal intercurrent infection,
pulmonary arterial hypertension develops with episodes of cardiac failure. Nevertheless, the patient
may live for many years in this state.
Finally, there is a group of patients in whom the
disease appears to remain static both clinically and
radiologically for a decade or more. In these cases it
is difficult on occasion to distinguish between the
first and the last radiograph.

351

B. COMPLICATED CASES

Apart from complications due to diseases common

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G. D. Scarrow

to the age group such as systematic hypertension,

ischaemic heart disease and chronic renal disease,
many cases of chronic bronchitis admitted to hospital show clinical and radiological evidence of pulmonary arterial hypertension.

was clinical evidence of chronic cor pulmonale and

vector cardiographic evidence of right ventricular
hypertrophy.
Although in this group the clinical findings were
approximately the same in all the cases and were
basically those of cyanosis, dyspnoea, oedema and
PULMONARY ARTERIAL HYPERTENSION varying degrees of carbon dioxide narcosis, radioA series of patients has been studied who had logically the group showed a number of varying
clinical evidence of pulmonary arterial hypertension features.
and vector cardiographic evidence of right ventri- (a) The size and shape of the heart. It was soon
cular hypertrophy. In a proportion of these cases the appreciated that comparable degrees of cor pulmonpulmonary arterial hypertension was confirmed by ale in a similar clinical state could be present assocardiac catheterisation, and this aspect of the in- ciated with either an enlarged heart or with a small
vestigation will form the basis of a future communi- heart.
cation.
The cardio-thoracic ratio in the series varied from
In view of the well-established relationship be- 0-33 to 0-59. The majority of cases (19) had a cardiotween pulmonary arterial hypertension and enlarge- thoracic ratio less than 0-45, whilst in nine cases the
ment of the proximal divisions of the pulmonary cardio-thoracic ratio was greater than 0-5.
arteries, tomograms were done of the right hilum of
Variation in size also occurred in the individual
these patients in the supine position and arrested case during the various stages of exacerbation and
inspiration in an endeavour to study the changes in recovery, the heart enlarging during a period of
detail. A Philips Danatome was used in conjunction clinical deterioration whether or not this was associated with peripheral oedema.
with a multisection cassette.
The shape of the heart shows an undue preRadiological changes attributable to hypertension
in the lesser circulation were observed in two forms ponderance of the ventricular mass relative to the
heart as a whole, the mass being situated anteriorly
during the series:
in the region of the right ventricle. In the absence of
severe concurrent disease the left ventricle is normal
1. Transient pulmonary hypertension
Consistent with the findings of Mounsey, Ritz- in size or small.
The pulmonary conus may be a prominent feature
mann and Selverstone (1952) a transient form of
pulmonary arterial hypertension occurs in cases of of the radiograph during the whole of the period of
chronic bronchitis which have no demonstrable observation or may become apparent during a period
chronic cor pulmonale and show the following radio- of clinical deterioration, diminishing in size on the
logical changes:
patient's recovery. This variation occurs indepen(a) The heart enlarges and the pulmonary conus dently of any variation in the size of the pulmonary
arteries, which tends to remain fairly constant, once
becomes more prominent.
(b) The main pulmonary arteries enlarge as do their the state of cor pulmonale is established. The main
pulmonary arteries are not invariably symmetrically
proximal divisions.
(c) The periphery of the lung field tends to remain increased in size and the branches of the right and
oligaemic in those cases where there is diffuse left pulmonary arteries may not all show the same
emphysema, but where the emphysema is more degree of enlargement. The appearances probably
unevenly distributed the lung fields may show reflect the uneven distribution of the chronic bronareas of hyperaemia and of oligaemia inter- chitis and emphysema resulting in varying degrees
of destruction of the vascular bed.
spersed.
The right atrium may show a moderate degree of
(d) Fluoroscopy shows the heart to be thrustful and
active. There is an increased systolic expansion enlargement and in these cases there is fullness of
and opacification of the proximal divisions of the the superior vena cava and of the azygos vein.
pulmonary arteries.
In the absence of atheroma or systemic hyperA feature of the condition is the rapidity with tension the aorta was small and no selective enlargewhich the changes resolve and the chest radiograph ment was noted of the left auricle in any of the cases.
reverts to its basic state.
In comparable degrees of failure fluoroscopy revealed either a thrustful active heart with an associated increase in the haemodynamics of the right
2. Chronic cor pulmonale
A series of 34 cases was studied in which there outflow tract, the exaggerated systolic opacification
352

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1964

Industrial Pulmonary Disease

and expansion of the arteries extending well out into
the lung fields, or a quiet poorly contracting heart
with little ventricular thrust. A number of these
latter showed an exaggerated inspiratory increase in
cardiac volume on all borders similar to that described by Munk and Lederer (1954) in obstructive
laryngo-tracheitis in infants.
(b) The pulmonary vessels. Tomograms of the pulmonary vessels divided a series of 38 cases into three
fairly clearly defined groups.
1. In the first group, consisting of 17 cases, there
is a considerable enlargement of the main pulmonary
arteries and their proximal divisions. There is then
rapid attenuation of these vessels into small intrapulmonary vessels which may be tortuous and distorted.
Occasionally these changes become so marked
that the intrapulmonary vessels have a "nipped-off"
appearance adjacent to the hilum and numerous
small abnormal vessels appear in the lung fields.
Fluoroscopy in these cases shows the main pulmonary arteries to be still pulsatile.
The penetration of the vessels to the periphery of
the lung is poor although it is possible to recognise
abnormal sub-pleural vessels in some cases. The
pulmonary veins are small.
These cases are usually associated with small or
normal-sized hearts only five out of the 17 having
cardio-thoracic ratios significantly in excess of 0-5
(Figs. 8A and 8B).
2. In the second group, consisting of ten cases,
the main pulmonary arteries are enlarged and these
give rise to large, tortuous florid vessels extending
far out into the lung fields, and then attenuating into
small twigs which do not reach the periphery of the
lung.
These large vessels are usually clear-cut in a
relatively translucent lung field with little background filling but in three out of the ten cases
FIG. 8.
Established chronic bronchitis for 30 years. The clinical
state is now one of chronic cor pulmonale with episodes of
congestive cardiac failure. Vector electrocardiogram showed
right ventricular preponderance.
(A) Postero-anterior chest film taken in a period of clinical
remission. The heart is enlarged as is the main pulmonary
artery and its right and left branches. The normal lung
arborisations have largely disappeared except for a number
of vessels adjacent to the hila. The rest of the lung fields
are either oligaemic or show excessive background filling.
The aorta is small.
(B) A composite tracing of the tomograms shows great
disruption of the vessels in the outer two-thirds of the lung
fields. Both the arteries and veins are small and irregular in
distribution, shape and size. The upper and lower lobes are
approximately equally affected.

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G. D. Scarrow

FIG. 9.
A respiratory cripple with a history of chronic bronchitis
since childhood. The patient is in a state of chronic cor
pulmonale with attacks of congestive cardiac failure. The
films were taken in a period of clinical remission. Vector
electrocardiogram showed right ventricular preponderance.

(A) Postero-anterior chest film showing an enlarged heart,

prominent pulmonary conus and enlarged hilar vessels.
There is extensive lung destruction.
(B) Tomogram showing enlarged vessels extending out into
the lung fields but giving rise to few small branches.
(c) A composite tracing of the tomograms shows these
changes to be fairly evenly distributed throughout the lung
field.

numerous small abnormal vessels could also be

recognised in the lung field similar to the vessels
seen in some of the cases in the first group.
The pulmonary veins in both the upper and lower
lobes are enlarged.
In eight out of the ten cases the cardiothoracic
ratio was significantly in excess of 0-5. Fluoroscopy
may show the heart to be quiet or alternatively thrustful with systolic opacification of the vessels extending

far out into the lung fields (Figs. 9A, 9B, 9C, 10A,
10B).

3. The third group of 11 cases shows features

common to both the above groups in different parts
of the lung field. The pulmonary arteries and their
primary divisions are enlarged in all cases. Some of
the branches are normal or enlarged and tortuous,
whereas others are normal or small.
The same changes are not necessarily confined to

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Industrial Pulmonary Disease

A
FIG. 10.
B
Case of advanced pulmonary hypertension due to chronic bronchitis and emphysema. Vector electrocardiograms showed right ventricular preponderance.
(A) Postero-anterior chest film showing cardiac enlargement with slight prominence of the pulmonary conus and enlargement of the hilar vessels. There is extsnsive disruption of the lung architecture.

(B) The injected specimen of the left lung demonstrates enlarged patent pulmonary arteries with a
relative paucity of the small terminal branches.

the same lobe in different cases in the series. Pulsation is retained in those portions of the vessels proximal to the obliteration (Figs. 11A, 11B, 12A, 12B).
The size of the veins parallels that of the arteries,
being large where the arteries are large and small
where the arteries are small.

DISCUSSION

It has not been possible as yet to correlate the

differing pulmonary vascularity with any clearly
defined clinical syndromes, all the patients showing
similar clinical features. The appearances in the first
group are in conformity with the generally accepted
reaction of a vascular tree to a chronic hypertension,
namely a destruction and obliteration of the vascular
bed with thickening of the arterial walls, narrowing
of the lumen and finally obliteration of the arteries.
Tomograms following prolonged administration
of oxygen showed no appreciable change in the
appearances and similarly repeated tomograms over
the period of survival perhaps amounting to three to
four years again showed no material alteration.
The second group is more difficult to explain,

particularly in those cases in which there is a poor

cardiac thrust at rest. Recent cases have shown no
change in the tomographic appearances following
exercise although a marked increase in the pulmonary tension and heart rate occurred.
In both the above groups the paucity of small
peripheral vessels and the presence of abnormal
small vessels suggests that the normal vascular bed
is largely destroyed.
The third group of cases may demonstrate the
shunting of blood away from underventilated areas
of the lung by means of arteriolar spasm stimulated
by disturbed alveolar gas tensions. This process is
presumably reversible in the early stages but is
followed by organic obliteration with the development of hyperkinetic increased blood flow through
the less damaged areas in an attempt at compensation.
Although the role of thrombo-embolism has not
been fully assessed we have found no major emboli
in the cases coming to post-mortem.
It is apparent that many varied appearances are
found when groups of patients suffering from
chronic bronchitis are X-rayed. It is likely that a

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G. D. Scarrow

12a
number of conditions are included under this title
which will no doubt be more clearly defined in the
future.
The work of Ogilvie (1959), Platts, Hammond and
Stuart Harris (1960) and Fletcher et al. (1963) indi-

cates that these subdivisions are becoming recognised and explored. It may be that a radiological
survey will prove to be an easy method of classification in addition to excluding other forms of pulmonary disease.

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1964

Industrial Pulmonary Disease

FIG. 11. (opposite page)
Chronic obstructive lung disease and cor pulmonale. Episodes of congestive cardiac failure.
(A) Postero-anterior chest film showing extensive lung disease, enlargement of the pulmonary conus and the hilar vessels.
(B) A composite tracing of the tomograms shows large vessels to the upper lobe but small vessels to the lower lobe.
FIG. 12. (oppositepage)
A similar type of case to that shown in Fig. 11, of long standing chronic obstructive lung disease and cor pulmonale
(A) Postero-anterior chest film showing extensive lung disease with enlargement of the pulmonary conus and main hilar
vessels.
(B) A composite tracing of the tomograms in this case shows that it is the upper lobe vessels which are small and partially
obliterated, whereas the middle and lower lobe vessels are enlarged.

ACKNOWLEDGMENTS

I am indebted to Dr. Eric Sherwood Jones and Dr. I. K.

Brown, who have collaborated with me in the collection and
preparation of the material upon which this paper is based.

KERLEY, P., 1962, in A Text-book of X-ray Diagnosis,

3rd edn., Vol. II (eds. S. C. Shanks and P. Kerley) (Lewis,
London).
LAWS, J. W., and HEARD, B. E., 1962, Brit. J. Radiol, 35,

750.
LEOPOLD, J. G., and SEAL, R. M., 1961, Thorax, 16, 70.

SUMMARY

1. A number of factors influencing the appearances of

the radiograph in cases of chronic bronchitis and emphysema are discussed.
2. In simple uncomplicated cases of chronic bronchitis
the radiographs fall into four fairly clearly defined groups.
The radiological appearances of these groups are described.
3. Changes occurring in the radiograph during acute
exacerbation of cases of chronic bronchitis are described.
4. The behaviour of the radiological appearances over a
long period are discussed.
5. The radiological findings are described in cases of
chronic bronchitis complicated by congestive cardiac failure
and pulmonary arterial hypertension.

LODGE, T., 1946, Brit. J. Radiol, 19, 77.

MOUNSEY, J . P . D . , RlTZMANN, L . W . , SELVERSTONE,
N. J., BRISCOE, W. A., and MCLEMORE, G. A., 1952, Brit.

Heartjf., 14, 153.

MUNK, J., and LEDERER, K. T., 1954, Brit.J. Radiol., 27,

294.
OGILVIE, C. M., 1959, Thorax, 14, 113.
PLATTS, M. M., HAMMOND, J. D. S., and STUART HARRIS,

C. H., 1960, Quart J. Med., 29, 559.

SIMON, G., 1958, in Recent Trends in Chronic Bronchitis
(ed. N. C. Oswald) (Lloyd-Luke, London).
SIMON, G., and GALBRAITH, H. J. B., 1953, Lancet, 2,

850.
SIMON, G., and REID, L., 1958, in Recent Trends in

REFERENCES

Chronic Bronchitis (ed. N. C. Oswald) (Lloyd-Luke,

London).

FLETCHER, C. M., HUGH-JONES, P., MCNICHOL, M. W.,

and PRIDE, X. B., 1963, Quart. J. Med., 32, 33.

Bronchitis, Emphysema and Cor Pulmonale (Wright, Bristol).

STUART HARRIS, C. H., and HANLEY, T., 1957, Chronic

357