0007-1285-37-437-344

1964, Brit. J. Radiol, 37, 344-357

P. Lesley Bidstrup

SUMMARY1. 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 theiroccupations are discussed.

3. The fact that a few men have survived and been ableto work for more than five years following operation indi-cates that routine radiology, combined with strict medicalsupervision of persons at risk, is of value in the diagnosisof lung cancer as an industrial disease.

REFERENCESGWYNNE 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 bronchitisContributed to the symposium on "Industrial pulmonary disease" at the Annual Congress of The BritishInstitute 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 CibaGuest Committee on chronic pulmonary emphysemaand related conditions clearly defined the clinicalstate of chronic bronchitis as chronic or recurrentcough with expectoration which is not attributableto conditions excluded from chronic non-specificlung disease. The words "chronic" or "recurrent"may be defined as "occurring" on most days for atleast three months in the year during at least twoyears. Infection is frequently but not necessarilypresent. The same report also precisely lays downthe definitions, classification and terminology forthe associated reversible and irreversible obstructivelung disease and emphysema.

Unfortunately no such easy radiological definitionexists and to describe specific radiological changes inchronic bronchitis and emphysema has been recog-nised as a most difficult task for nearly a quarter of acentury. Stuart Harris and Hanley in 1957 statedthat there are no radiological appearances which canbe used in a positive diagnostic sense and they con-sider that the main value of radiography is toexclude other lung diseases which may present asimilar clinical picture. Nevertheless, it is rare tofind a radiologist who will frankly admit that hecannot recognise the chest radiograph of a chronicbronchitic. In it he sees a variation from the normaldifficult to describe and inconstant in appearance.

Numerous attempts have been made to explainthese changes more precisely and for many years atheory of peribronchial thickening was in voguewhich was thought to give rise to a more dense lungpattern than normal. Alternatively, it was thought

that this pattern may be due to hyperaemia of thearterioles of the bronchial arteries in the walls ofthe bronchi.

Very strong evidence to the contrary was providedby the exhaustive work of Simon and Reid (1958)who showed that the bronchial thickening and hy-peraemia which occurred was of such dimensions asto be invisible on the normal radiograph.

In 1953 Simon and Galbraith examined the plainradiographs of 857 patients with a clinical diagnosisof chronic bronchitis and were unable to detect anychanges in the intra-pulmonary vascular patternapart from those attributable to emphysema. In 41per cent of these cases they saw no radiological ab-normality and throughout the series they saw nogeneralised abnormal shadowing which might cor-respond to the larger bronchi or to peribronchialstructures lying in juxtaposition to the vascularshadows.

These observations may not be so true in thefuture when with a greater use of a multiline grid ofthe Schmit type and short exposures in the regionof 3 jjus, structures of the order of 0-3 mm can beseen.

Perhaps the most valuable contribution by Simonat that time was the recognition and detailed des-cription of the specific bronchographic changes oc-curring in chronic bronchitis. Leopold and Seal in1961 described a further type of peripheral poolthought to be due to the opaque medium lying in thespace created by areas of centrilobular emphysema.

Diffuse interstitial reticulation has been observedby Lodge (1946), Simon (1958), Kerley (1962) and

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others to occur in the lower zones in some cases, butdoubt exists as to whether or not this finding is infact related to the Hamman-Rich syndrome.

Thus it is currently accepted that whereas thebronchographic changes in chronic bronchitis maybe regarded as characteristic the diagnosis on theplain radiograph depends on the recognition of thepresence of the concurrent emphysema.

This paper is based on the material passing througha 1,000-bedded peripheral general hospital, partacute and part geriatric, situated in south-westLancashire, one of the areas in which there is a highincidence of the disease. The material has been col-lected from and includes the winter of 1957-58.

The hospital has for many years filled the role ofa local district hospital and has provided an oppor-tunity for studying the radiological behaviour of thedisease for periods of a decade or more.

Other patients have been radiographed in con-nection with a therapeutic trial conducted by anindustrial medical officer in the same area.

In both instances the material is, of course, highlyselective, the hospital usually being concerned withsevere exacerbation of the advanced case. In the caseof the factory, the trial was conducted on knownchronic bronchitics with a bad sickness record.Nevertheless, due to the high incidence of the dis-ease in the area, the ordinary hospital intake for non-related conditions has provided material for thestudy and integration of the radiology in the quies-cent phase of the disease, and has also providedchest radiographs of a similar age and environmentalgroup in which there is no clinical evidence ofbronchitis and emphysema.

The clinical diagnosis was supported in mostinstances by pulmonary function tests, electrocardio-grams and vector electrocardiograms, sputum ex-aminations and blood counts, and in some instancescardiac catheterisation.

For various reasons the radiological investigationhas been restricted to postero-anterior and lateralradiographs of the chest in various stages of thedisease. In those cases where clinical or radiologicalevidence pointed to the presence of pulmonaryarterial hypertension, tomograms were taken of theright hilum and lung fields in the supine positionusing a Philips Danatome and a multisection cas-sette. Occasional bronchograms and pulmonaryangiograms have been done where it was felt neces-sary to confirm or supplement evidence supplied bythe plain radiographs.

In cases where films were not available prior tohospital admission every effort was made to obtaina further radiograph of the patient during a period of

maximum clinical recovery, usually in the followingsummer. These films were used for comparativepurposes to assess the changes occurring during ex-acerbations or any progressive deterioration. Forreference the film is termed the "summer" or "quies-cent" film.

FACTORS INFLUENCING THE RADIOGRAPHAt an early stage it became apparent that there

were many factors which influenced the appearancesof the radiograph and these have been summarised asfollows:(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 poly-

cythaemia.Some of these factors are variants associated with

the disease under review, others are extraneousfactors. The changes due to ischaemic heart disease,systemic hypertension, fibroid tuberculosis, pneumo-coniosis, chronic renal disease and other concur-rent diseases must be recognised and discounted.

Similarly, recognising the known influences ofpolycythaemia on the pulmonary vascular pattern,blood counts were taken of the cases. Although amild polycythaemia was demonstrated in a numberof cases, in no instance was this thought to be suffi-cient to influence the radiograph.

The physical build of the patient and the presenceof deformities of the thoracic cage will determine theshape and volume of the thorax. This in time mayinfluence the clinical course of the disease or maymodify the radiological appearances. Alternatively,the shape and volume of the thorax may be the resultof chronic bronchitis and emphysema.

The effects of gross congenital deformities of theribs, kyphoscoliosis and other severe abnormalitiesare well recognised and I do not wish to refer tothese in detail.

Perhaps of more pertinent interest are the possibleeffects of what may be regarded as the normal varia-tions in the physical characteristics of individuals.

In a tall thin hyposthenic patient emphysematouschanges in the lung fields may either be simulated orexaggerated due to an early increase in the verticaldiameter of the chest which does not occur so readily

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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 zonesand 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 normalconfiguration. 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 contouris tall, narrow and vertical from an early stage.

Conversely, in the sthenic patient the relativelyhigh diaphragm tends to mask the radiologicalchanges of emphysema for a longer period if viewedsolely in the postero-anterior projection. The in-crease in the volume of the thoracic cage in thesecases initially occurs in the antero-posterior dia-meter with exaggerated anterior bowing of the stern-um and an increasing kyphos. To a lesser extentthere is an increase in the transverse diameter of thebase. The heart does not readily assume the char-acteristic narrow vertical silhouette but it doesdiminish in size and this feature of a small heart ina large chest in a sthenic individual may be regardedas a diagnostic pointer in these cases.

The height/weight/thoracic volume ratio also ap-pears to be of significance. For a similar height andweight one patient will have a large volume chest andanother a smaller than normal volume thorax. Al-though this aspect of the subject is still underinvestigation the patient with the small volumethorax appears to be more prone to develop chronicinfective lung disease, whereas in patients with alarge volume thorax the dominant characteristic isa progressive emphysema.

Obesity is of great importance and in the extremecan 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 intimatelybound up w7ith the features of the disease that theywill be discussed under the appropriate headings.

RADIOLOGICAL APPEARANCES

If the influence of these many variants is recog-nised then the radiographs of patients suffering fromchronic bronchitis and emphysema can be seen tofall into fairly well defined categories. In the major-ity of cases the radiographs also bear some relationto the severity of the disease and a progressive de-terioration can be demonstrated. For conveniencethe appearances may be described under two head-ings; those occurring in simple uncomplicated casesof chronic bronchitis and emphysema and those occur-ring incases in which a significant degree of pul-monary arterial hypertension with or withoutcongestive cardiac failure has developed. In the firstcategory the radiographs may be divided into fourfairly clearly defined although overlapping groups.

A. SIMPLE UNCOMPLICATED CASESGroup 1

Those cases in which there is irrefutable clinical

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evidence of chronic bronchitis but the chest radio-graph shows little evident variation from the normal.

Group 2Those cases in which the radiological finding is

one of widespread diffuse emphysema.

Group 3Those cases in which there is a mixture of chronic

inflammatory change in the lung fields interspersedwith areas of radiologically normal or hyperaemiclung and areas of emphysema.

Group 4Those cases in which there are extensive chronic

inflammatory changes in the lung fields, and theseare the dominant features of the radiograph.

GROUP 1Great emphasis has always been given to the dis-

parity between the clinical state of the patient andthe appearances of the chest film.

It is reasonable to suppose that in early andmoderate cases in which chronic bronchitis, that isan excessive secretion of mucus with infective epi-sodes, is the major pathology, with little in the wayof concurrent emphysema and structural damage tothe lung, then a chest radiograph must of necessityappear normal in a quiescent phase.

The anomaly of the respiratory cripple with anapparently normal chest film remains a problem.However, reports are appearing in the literature ofsuch patients with little radiological change butmarked changes in the lung function tests (Fletcher,Hugh-Jones, McNichol and Pride, 1963). Thus itmay be that a normal chest radiograph in the pre-sence of a severe respiratory disability is not in facta radiological failure but of great diagnostic andprognostic significance indicating disturbed alveolarventilation and gas tensions rather than destructionof the lung.

It is perhaps of significance that in a group of 48patients all classified as known chronic bronchiticswho were radiographed in connection with a thera-peutic clinical trial I was unable to recognise anydefinite abnormality in the lung fields in seven of thecases.

Three of these chests were in all respects normal.One had normal lung fields but evidence of ischae-mic heart disease. The other four had large volumechests relative to the height and weight of the patientand a cardio-thoracic ratio of less than 0-4. Therewas, however, no obvious change in the vascularpattern of the lung fields.

It may well be that these large volume chests withrelatively small hearts and normally distributed vas-culature in patients with respiratory symptoms re-present the stage of dilatation of the distal air spacesprior to the development of centrilobular destruction(Fig. 2).

GROUP 2Although these cases fulfil the clinical criteria for

chronic bronchitis, progressive breathlessness isusually the main complaint and the infective epi-sodes and exacerbations are not so frequent and notso marked as in the other groups. The main radio-logical finding is one of widespread diffuse emphy-sema, which is more evenly distributed than in thefollowing groups. Recognisable inflammatory sha-dowing plays little part in the composition of thefilms (Figs. 3A and 3B).

It is evident that a considerable discrepancy existsbetween the radiological diagnosis of emphysemaand subsequent pathological findings. Nevertheless,

FIG. 2.Male, aged 59 years. Postero-anterior chest film showing alarge volume thorax. The diaphragm is below the anteriorend of the 7th rib and the heart and mediastinum are com-pressed. A lateral view confirmed the expanded thorax. Thevascular pattern of the lung fields is normally distributedand there is plenty of background filling. Tomogramsshowed normal vessels. The patient suffers severe disabilitywith 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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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.

if the radiological criteria are strictly applied then itis a fair assumption that a radiological diagnosis ofemphysema is likely to be confirmed pathologically,whereas the absence of radiological evidence ofemphysema on the plain film does not necessarilyexclude its presence.

The radiological changes occurring in this groupof cases may be summarised under the followingheadings.

(a) Changes due to the influence of the increased lungvolume and rigidity on the adjacent structures

The thoracic wall is expanded, first in one andthen in all diameters. The diaphragm is depressedand restricted in movement. The mediastinum iscompressed, producing a thin mediastinal shadow inwhich the aortic knuckle is prominent and the maindivisions of the pulmonary arteries are clearlyvisible. The cardiac silhouette is tall, thin andnarrow.

(b) Changes in the vascularity of the lung fieldsThe lung fields are diffusely hypertranslucent and

oligaemic due to narrowing of the peripheral lung

vessels and diminution in the degree of backgroundfilling.

The distribution of the vasculature is even, dis-counting the variations due to the volumetric changesin the thorax, and there is not the same degree oflocal distortion of vessels which is seen in the follow-ing group. Bullae are normally absent.

The work of Laws and Heard (1962) stresses theimportance of the alterations in the pulmonaryvasculature in the radiological diagnosis of emphy-sema and I am in agreement that these are probablythe ultimate diagnostic criteria.

(c) Change in the heart sizeThere is usually a progressive diminution in the

size of the heart as the degree of emphysema pro-gresses. This is thought to be the result of threefactors:(1) the descent of the diaphragm which elongates

the heart;(2) the increase of the intrathoracic pressure;(3) a diminished right heart blood flow.

The heart size tends to remain constant, otherthan in periods of infective exacerbation when some

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enlargement occurs, until with the onset of conges-tive heart failure, with or without associated pulmon-ary arterial hypertension, the heart again enlarges,sometimes dramatically.

GROUP 3These are cases in which there is an uneven

distribution throughout the lung fields of emphy-sema, inflammatory changes, areas of normal lungtissue and areas of overfilled lung tissue.

The effect of these elements on the radiograph isto produce a disruption of the normal lung patternof very varying degree depending on the preponder-ance of one or other component (Fig. 4).

This is by far the most common finding in chronicbronchitis. A slowly progressive deterioration occursmanifest by a diminution of the amount of recog-nisable lung tissue and an increase in the extent anddegree of the abnormal elements.

FIG. 4.An example of the type of radiological change occurring inGroup 3. The patient has suffered from chronic bronchitisfor over ten years. The radiograph shows a large volumechest with emphysema of the left apex and the left lowerzone. Areas of chronic inflammatory shadowing are presentin 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 4In these cases the extensive chronic inflammatory

changes in the lung fields are the dominant featuresof the radiograph.

The changes are usually of two types, both ofwhich may be present in the same patient.(1) Frank bronchiectatic areas.(2) Chronic inflammatory shadowing disseminatedand dispersed between the emphysematous areas.This shadowing is usually hard, discrete and nodu-lar. The changes vary little over long periods ir-respective of the clinical condition of the patient.(Figs. 5A and 5B).

Chronic inflammatory shadowing may also takethe form of areas of fibrosis which produce bizarreappearances and distortion of the lung.

BEHAVIOUR DURING AN ACUTE CHEST ILLNESS OREXACERBATION

This is recognised clinically by a deteriorationin the clinical condition of the patient, the presenceof purulent or mucopurulent sputum and an increasein such symptoms as cough and dyspnoea. Pyrexiamay be present.

The first three groups show essentially similarradiological behaviour as assessed against the quies-cent or summer film. The following changes havebeen observed.

1. One or more areas of consolidation and de-aeration of segmental or greater distribution. Morerarely, the shadowing is more widespread and is of abronchopneumonic character. The areas of con-solidation frequently recur over the years in the samesite leading eventually to frank bronchiectasis. Lobu-lar collapse was seen only infrequently. Radiologicalresolution is variable. The lesion may resolve pro-gressively over two to three weeks or alternativelyresidual shadowing may persist for many monthsand possibly still be present on the "summer" film.Of a series of 126 patients admitted during thewinter of 1958-59, 40 showed this type of change.

2. Changes in the vascular pattern of the lungfields with or without associated evidence of pulmon-ary oedema. These changes consist of: (a) a lack ofdefinition of the intrapulmonary vessels which mayoccur locally in one zone or diffusely throughout thelung fields; or (b) an increase in the vascular patternof the lung fields which is a true increase in both thesize and number of the vessels visualised. This isusually unevenly distributed and may occur to agreater extent in one area than in another or berestricted to one area (Figs. 6A and 6B).

The changes are most marked in those areas leastaffected by the emphysema, where a pulmonary

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-v.

FIG. 5. (A) Postero-anterior film of a chronic bronchitic patient of many years standing. Over thepast five years the patient has had repeated infective episodes with inflammatory shadowing in bothlower and middle zones. Less resolution occurred with each infection until the present stage hadbeen reached when little change occurred in the appearances of the chest over long periods. Broncho-grams 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 thelung fields, particularly in those areas where the emphysema is less marked.

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vascular pattern is still visible. Emphysematous bul-lae and the extent of the gross lung damage may oftenbe recognised more easily during an exacerbationwhen these areas appear translucent and featurelessin an otherwise hyperaemic and infected lung.

Alternatively, emphysema recognised in the quies-cent film is sometimes masked in an exacerbationdue to the easy distensibility of the pulmonary vascu-lar bed and the presence of superimposed inflam-matory changes.

The lung pattern may be disorganised, unusuallylarge vessels appearing in the periphery of the lungfield.

Where the changes are extreme, a miliary type ofmottling is present, generally or locally, due in partto the number of vessels seen "end on" and possiblyin part to miliary pulmonary oedema (Fig. 7). Frankintra-alveolar pulmonary oedema is occasionallyobserved.

There is usually a small or moderate increase inthe size of the heart and the hilar vessels. There maybe associated bronchospasm with distension of thethoracic cage.

With adequate treatment these changes resolvequite quickly over a period of days, although the

FIG. 7.Known chronic bronchitic in an exacerbation showingmiliary mottling throughout the lung fields. The "summer"

film of this patient is shown in Fig. 4.

clinical state may lag behind the radiological re-covery.

Fifty-three patients in the series showed this typeof radiological pattern. In none of these cases wrasthere any evidence at the time or subsequently ofleft ventricular failure.

3. Seventeen cases presented with a pleural effu-sion usually unilateral and of no appreciable specificcharacteristics.

4. Superimposed on the above changes in a num-ber of the more advanced cases there was moredefinite evidence of a transient pulmonary arterialhypertension, manifest by right heart enlargementand significant increase in the size of the pulmonaryartery and its main branches.

5. The 16 cases not included in the above figuresare unclassifiable for one reason or another—usuallydue to technical faults or concomitant disease.

It has been observed that the patients tend to be-have in a similar manner in each episode, i.e. if theyshow opacities in the lung fields in one exacerbationthey will tend to do so in the next exacerbation.

The fourth group of cases in which there is exten-sive chronic inflammatory shadowing do not showsuch a marked radiological change in the lung fieldsduring an exacerbation due to the already extensiveshadowing. In some cases the exacerbation may bereflected in the size of the cardiac outline, however,which enlarges.

BEHAVIOUR OVER A LONG PERIODThis is very variable. In those cases where the

disease becomes manifest following an acute chestinfection in a previously healthy adult, deteriorationrapidly takes place over a few years with increasingemphysema and repeated infections. The patientsuccumbs after a relatively short period either as aresult of infection or following the onset of corpulmonale.

The more usual picture is one of slow deteriora-tion over the years (many patients give a history of20 to 25 years), with either the infective element oremphysema becoming the dominant chest character-istic. In the absence of a fatal intercurrent infection,pulmonary arterial hypertension develops with epi-sodes of cardiac failure. Nevertheless, the patientmay live for many years in this state.

Finally, there is a group of patients in whom thedisease appears to remain static both clinically andradiologically for a decade or more. In these cases itis difficult on occasion to distinguish between thefirst and the last radiograph.

B. COMPLICATED CASESApart from complications due to diseases common

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to the age group such as systematic hypertension,ischaemic heart disease and chronic renal disease,many cases of chronic bronchitis admitted to hospi-tal show clinical and radiological evidence of pul-monary arterial hypertension.

PULMONARY ARTERIAL HYPERTENSIONA series of patients has been studied who had

clinical evidence of pulmonary arterial hypertensionand vector cardiographic evidence of right ventri-cular hypertrophy. In a proportion of these cases thepulmonary arterial hypertension was confirmed bycardiac catheterisation, and this aspect of the in-vestigation will form the basis of a future communi-cation.

In view of the well-established relationship be-tween pulmonary arterial hypertension and enlarge-ment of the proximal divisions of the pulmonaryarteries, tomograms were done of the right hilum ofthese patients in the supine position and arrestedinspiration in an endeavour to study the changes indetail. A Philips Danatome was used in conjunctionwith a multisection cassette.

Radiological changes attributable to hypertensionin the lesser circulation were observed in two formsduring the series:

1. Transient pulmonary hypertensionConsistent with the findings of Mounsey, Ritz-

mann and Selverstone (1952) a transient form ofpulmonary arterial hypertension occurs in cases ofchronic bronchitis which have no demonstrablechronic cor pulmonale and show the following radio-logical changes:(a) The heart enlarges and the pulmonary conus

becomes more prominent.(b) The main pulmonary arteries enlarge as do their

proximal divisions.(c) The periphery of the lung field tends to remain

oligaemic in those cases where there is diffuseemphysema, but where the emphysema is moreunevenly distributed the lung fields may showareas of hyperaemia and of oligaemia inter-spersed.

(d) Fluoroscopy shows the heart to be thrustful andactive. There is an increased systolic expansionand opacification of the proximal divisions of thepulmonary arteries.

A feature of the condition is the rapidity withwhich the changes resolve and the chest radiographreverts to its basic state.

2. Chronic cor pulmonaleA series of 34 cases was studied in which there

was clinical evidence of chronic cor pulmonale andvector cardiographic evidence of right ventricularhypertrophy.

Although in this group the clinical findings wereapproximately the same in all the cases and werebasically those of cyanosis, dyspnoea, oedema andvarying degrees of carbon dioxide narcosis, radio-logically the group showed a number of varyingfeatures.(a) The size and shape of the heart. It was soonappreciated that comparable degrees of cor pulmon-ale in a similar clinical state could be present asso-ciated with either an enlarged heart or with a smallheart.

The cardio-thoracic ratio in the series varied from0-33 to 0-59. The majority of cases (19) had a cardio-thoracic ratio less than 0-45, whilst in nine cases thecardio-thoracic ratio was greater than 0-5.

Variation in size also occurred in the individualcase during the various stages of exacerbation andrecovery, the heart enlarging during a period ofclinical deterioration whether or not this was asso-ciated with peripheral oedema.

The shape of the heart shows an undue pre-ponderance of the ventricular mass relative to theheart as a whole, the mass being situated anteriorlyin the region of the right ventricle. In the absence ofsevere concurrent disease the left ventricle is normalin size or small.

The pulmonary conus may be a prominent featureof the radiograph during the whole of the period ofobservation or may become apparent during a periodof clinical deterioration, diminishing in size on thepatient's recovery. This variation occurs indepen-dently of any variation in the size of the pulmonaryarteries, which tends to remain fairly constant, oncethe state of cor pulmonale is established. The mainpulmonary arteries are not invariably symmetricallyincreased in size and the branches of the right andleft pulmonary arteries may not all show the samedegree of enlargement. The appearances probablyreflect the uneven distribution of the chronic bron-chitis and emphysema resulting in varying degreesof destruction of the vascular bed.

The right atrium may show a moderate degree ofenlargement and in these cases there is fullness ofthe superior vena cava and of the azygos vein.

In the absence of atheroma or systemic hyper-tension the aorta was small and no selective enlarge-ment was noted of the left auricle in any of the cases.

In comparable degrees of failure fluoroscopy re-vealed either a thrustful active heart with an asso-ciated increase in the haemodynamics of the rightoutflow tract, the exaggerated systolic opacification

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and expansion of the arteries extending well out intothe lung fields, or a quiet poorly contracting heartwith little ventricular thrust. A number of theselatter showed an exaggerated inspiratory increase incardiac volume on all borders similar to that des-cribed by Munk and Lederer (1954) in obstructivelaryngo-tracheitis in infants.(b) The pulmonary vessels. Tomograms of the pul-monary vessels divided a series of 38 cases into threefairly clearly defined groups.

1. In the first group, consisting of 17 cases, thereis a considerable enlargement of the main pulmonaryarteries and their proximal divisions. There is thenrapid attenuation of these vessels into small intra-pulmonary vessels which may be tortuous and dis-torted.

Occasionally these changes become so markedthat the intrapulmonary vessels have a "nipped-off"appearance adjacent to the hilum and numeroussmall abnormal vessels appear in the lung fields.Fluoroscopy in these cases shows the main pulmo-nary arteries to be still pulsatile.

The penetration of the vessels to the periphery ofthe lung is poor although it is possible to recogniseabnormal sub-pleural vessels in some cases. Thepulmonary veins are small.

These cases are usually associated with small ornormal-sized hearts only five out of the 17 havingcardio-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 thesegive rise to large, tortuous florid vessels extendingfar out into the lung fields, and then attenuating intosmall twigs which do not reach the periphery of thelung.

These large vessels are usually clear-cut in arelatively translucent lung field with little back-ground filling but in three out of the ten cases

FIG. 8.Established chronic bronchitis for 30 years. The clinicalstate is now one of chronic cor pulmonale with episodes ofcongestive cardiac failure. Vector electrocardiogram showedright ventricular preponderance.(A) Postero-anterior chest film taken in a period of clinicalremission. The heart is enlarged as is the main pulmonaryartery and its right and left branches. The normal lungarborisations have largely disappeared except for a numberof vessels adjacent to the hila. The rest of the lung fieldsare either oligaemic or show excessive background filling.The aorta is small.(B) A composite tracing of the tomograms shows greatdisruption of the vessels in the outer two-thirds of the lungfields. Both the arteries and veins are small and irregular indistribution, shape and size. The upper and lower lobes areapproximately equally affected.

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FIG. 9.A respiratory cripple with a history of chronic bronchitissince childhood. The patient is in a state of chronic corpulmonale with attacks of congestive cardiac failure. Thefilms were taken in a period of clinical remission. Vectorelectrocardiogram 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 thesechanges to be fairly evenly distributed throughout the lung

field.

numerous small abnormal vessels could also berecognised in the lung field similar to the vesselsseen in some of the cases in the first group.

The pulmonary veins in both the upper and lowerlobes are enlarged.

In eight out of the ten cases the cardiothoracicratio was significantly in excess of 0-5. Fluoroscopymay show the heart to be quiet or alternatively thrust-ful 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 featurescommon to both the above groups in different partsof the lung field. The pulmonary arteries and theirprimary divisions are enlarged in all cases. Some ofthe 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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1

A FIG. 10. B

Case of advanced pulmonary hypertension due to chronic bronchitis and emphysema. Vector electro-cardiograms showed right ventricular preponderance.

(A) Postero-anterior chest film showing cardiac enlargement with slight prominence of the pulmon-ary 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 arelative paucity of the small terminal branches.

the same lobe in different cases in the series. Pulsa-tion is retained in those portions of the vessels proxi-mal 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 smallwhere the arteries are small.

DISCUSSIONIt has not been possible as yet to correlate the

differing pulmonary vascularity with any clearlydefined clinical syndromes, all the patients showingsimilar clinical features. The appearances in the firstgroup are in conformity with the generally acceptedreaction of a vascular tree to a chronic hypertension,namely a destruction and obliteration of the vascularbed with thickening of the arterial walls, narrowingof the lumen and finally obliteration of the arteries.

Tomograms following prolonged administrationof oxygen showed no appreciable change in theappearances and similarly repeated tomograms overthe period of survival perhaps amounting to three tofour years again showed no material alteration.

The second group is more difficult to explain,

particularly in those cases in which there is a poorcardiac thrust at rest. Recent cases have shown nochange in the tomographic appearances followingexercise although a marked increase in the pulmon-ary tension and heart rate occurred.

In both the above groups the paucity of smallperipheral vessels and the presence of abnormalsmall vessels suggests that the normal vascular bedis largely destroyed.

The third group of cases may demonstrate theshunting of blood away from underventilated areasof the lung by means of arteriolar spasm stimulatedby disturbed alveolar gas tensions. This process ispresumably reversible in the early stages but isfollowed by organic obliteration with the develop-ment of hyperkinetic increased blood flow throughthe less damaged areas in an attempt at compensa-tion.

Although the role of thrombo-embolism has notbeen fully assessed we have found no major emboliin the cases coming to post-mortem.

It is apparent that many varied appearances arefound when groups of patients suffering fromchronic bronchitis are X-rayed. It is likely that a

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number of conditions are included under this titlewhich will no doubt be more clearly defined in thefuture.

The work of Ogilvie (1959), Platts, Hammond andStuart Harris (1960) and Fletcher et al. (1963) indi-

cates that these subdivisions are becoming recog-nised and explored. It may be that a radiologicalsurvey will prove to be an easy method of classifi-cation in addition to excluding other forms of pul-monary disease.

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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 hilarvessels.

(B) A composite tracing of the tomograms in this case shows that it is the upper lobe vessels which are small and partiallyobliterated, whereas the middle and lower lobe vessels are enlarged.

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

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

SUMMARY1. A number of factors influencing the appearances of

the radiograph in cases of chronic bronchitis and emphy-sema are discussed.

2. In simple uncomplicated cases of chronic bronchitisthe radiographs fall into four fairly clearly defined groups.The radiological appearances of these groups are described.

3. Changes occurring in the radiograph during acuteexacerbation of cases of chronic bronchitis are described.

4. The behaviour of the radiological appearances over along period are discussed.

5. The radiological findings are described in cases ofchronic bronchitis complicated by congestive cardiac failureand pulmonary arterial hypertension.

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

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.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

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

STUART HARRIS, C. H., and HANLEY, T., 1957, ChronicBronchitis, Emphysema and Cor Pulmonale (Wright, Bristol).

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