Radiation damage to thoracic tissuesthoracic cage is relatively uncommon. Rib frac-tures are its...

$: Radiation damage to thoracic tissuesthoracic cage is relatively uncommon. Rib frac-tures are its mostfrequent manifestation and their symptom is pain. Their presence in one or several$
Thorax (1963), 18, 371

Radiation damage to thoracic tissuesA. G. W. WHITFIELD,' W. H. BOND, AND P. B. KUNKLER2

From the Departments of Medicine and Radiotherapy, United Birmingham Hospitals,University of Birmingham

Radiotherapy to the thorax in conventional dosageappears to be capable of causing damage to any ofthe tissues in the thoracic wall or within thethoracic cavity. Since the earliest days of x-raytreatment radiation changes in the skin have beensuch an everyday problem that they scarcelywarrant discussion here except to note that withthe advent of new radiotherapeutic techniques theyare becoming less frequent and less severe.

THE THORACIC WALL, SHOULDER GIRDLE, ANDBREASTS

Radiation damage to the bony structure of thethoracic cage is relatively uncommon. Rib frac-tures are its most frequent manifestation and theirsymptom is pain. Their presence in one or severalribs is confirmed by careful scrutiny of the chestradiograph (Fig. 1). They must, of course, bedifferentiated from pathological fractures resultingfrom metastases, but if they occur after radio-therapy to the thorax the great probability is thatthey are attributable to it. Expansion of the boneis never seen, the fractures usually occur in theanterior axillary line, and surprising though it isthey unite well and pain soon abates (Fig. 2). Theyusually follow radiotherapy for breast cancer butmay be a sequel to x-ray treatment for otherthoracic disorders. Some concomitant radiationdamage to the lung is commonly evident. Age doesnot appear to be a factor in their causation as wehave seen them in early adult life. They have beenpreviously described by Fike (1932), Freid andGoldberg (1940), Eggs (1941), Leach, Farrow,Foote, and Wawro (1942), Blumenfeld and Thomas(1945), Braun and Frik (1954), Koldr and Vrabec(1957), and Baudisch (1960). Kolar and Vrabec(1957) and Baudisch (1960) have also reportedradiation fractures of the clavicle after post-mastectomy radiotherapy for breast cancer, andBorgstrom and Gynning (1957) described osteo-porotic vertebral collapse after intense rotation1 Paper given at the Tenth International Congress of Radiology inMontreal, 19622 Presetit address: Radiotherapy Department, United CardiffHospitals

roentgen therapy for cancer of the oesophagus,but we have not encountered these lesions.

After mastectomy and radiotherapy for breastcancer the shoulder not uncommonly becomesfixed or relatively so, and in such cases osteo-porotic changes may be seen in the humerus andscapula (Fig. 3). To what extent such processesstem directly from radiation and how much theyare attributable to disuse one cannot be certainbut the latter is probably an important influence.

Other types of bony lesion are occasionally seen.Two examples are shown in Figures 4 and 5a.Figure 4 shows the shoulder of an old lady who,after radiotherapy for breast cancer, developedshoulder pain attributable to necrosis of the headof the humerus. Figure 5a is from a woman whoat the age of 10 was given radiotherapy for whatat thoracotomy was thought to be an inoperablemalignant lung tumour. No biopsy was taken.Thereafter the scapula failed to grow to its normalsize and the breast was also affected (Fig. Sb).When at the age of 30 she gave birth to a childthere was no lactatory response on the damagedside. Mammary hypoplasia following radiotherapyin childhood has been reported previously (Rube,1954; Kolaf, Vrabec, and Bek, 1957; Gros andKeiling, 1958).

THE LUNGS

The lungs are the most vulnerable of the tissueswithin the thorax, and radiation damage is stillrelatively common after x-ray treatment for breastcancer, though it occurs much less frequently thanin the early days of radiotherapy. This is particu-larly so after wide-field irradiation for malignantlymphomas or lung secondaries. Six cases, two of'them fatal, have recently been reported afterradioactive iodine therapy for carcinoma of thethyroid with pulmonary metastases (Rall, Alpers,Lewallen, Sonenberg, Berman, and Rawson, 1957)but we have not encountered radiation lungdamage arising in this way. In a series of 49 caseswhich we have studied, 25 followed routine post-mastectomy radiotherapy for breast cancer, 11

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FIG. 1. Female, aged 40. Fractured sixth and seventh ribsafter post-mastectomy radiotherapy for breast cancer.Some radiation damage to the right lung is evident.

FIG. 2. Female, aged 27. Soundly united fracture of leftsecond rib six months after radiotherapy through media-stinal fields for Hodgkin's disease involving mediastinallymph nodes. Radiation fibrosis of the lung is also present.

FIG. 3. Female, aged 49. Fixation of left shoulder with

osteop,orosis of humei-us and scapula after mastectomy and

radiotherapy for breast cancer. Severe radiation damage to

the lef lung is also showi,,

FIG. 4. Female, aged 84. Necrosis of head of humerusafter radiotherapy for breast cancer. Radiation fibrosis ofthe lung is also evident.



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Radiation damage to thoracic tissues

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FIG. 6

DYSPNOEA

COUGH

DOOR STOPOBSTRUCTION -TO INSPIRATION

FIG. 5a. Female. Failure of right scapula to grow to itsnormal size following radiotherapy in childhood for amalignant lung tumour. Radiation fibrosis of lung alsopresent.

FIG. 5b. Same patient as in Fig. 5a, showing mammaryhypoplasia on treated side.

FIG. 6. Interval between conclusion of radiotherapy andonset ofsymptoms of radiation pneumonia.

FIG. 7. Symptoms in patients with radiation lung damage.

RIB FRACTURES o

OESOPHAGEAL -

NONE

FIG. 7

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A. G. W. Whitfield, W. H. Bond. and P. B. Kunlkler

occurred after chest baths for lung secondaries ormalignant lymphomas, two followed therapydirected to the whole of one side of the thorax,six occurred after treatment limited to the media-stinum, and the remaining five followed treatmentthrough limited fields for carcinoma of thebronchus or oesophagus. Where radiotherapy wasunilateral, the lung damage was limited to thetreated side in all but one case, whereas when bothlungs had been treated all save one sufferedbilateral damage. It was usually strikingly limitedto the area irradiated.

SYMPTOMS AND PHYSICAL SIGNS The intervalbetween the conclusion of x-ray treatment and thedevelopment of symptoms attributable to radia-tion pneumonia varied from 1 to 16 weeks witha peak incidence at one month (Fig. 6). Sixpatients had no symptoms (Fig. 7) and their lungdamage was slight and was only revealed byroutine follow-up radiography of the chest. Inthe remainder dyspnoea was the dominant symp-tom. At first only evident on exercise, it increasedrapidly and in severe cases became obvious atrest. In those who survived it gradually diminishedover a period of weeks but only exceptionally wasa normal exercise tolerance ever restored. A 'doorstop' obstruction to full inspiration is evident insevere cases and was a striking feature of four ofthe patients studied. Half the patients had a dryirritating cough aggravated by exercise or deepbreathing. In some this symptom was onlypresent in the pneumonia stage, but in many itpersisted in lesser degree indefinitely. Sputum wasunusual both during the pneumonia stage andwhen fibrosis had supervened, no doubt becausethe upper lobes are most commonly affected.

Fractured ribs were noted in four patients. Theygave rise to severe pain, but in the absence of suchlesions radiation pneumonitis is strikingly pain-less. Oesophageal symptoms were sometimes pre-sent but not commonly at the same time as thedyspnoea and cough of acute radiation pneu-monia. The dysphagia of radiation oesophagitishas usually subsided before the symptoms ofpneumonia develop, and when sometimes theintrathoracic fibrosis produces an hiatus hernia,the lung damage has progressed to the fibroticstage. Pyrexia was unusual, only occurring in twoof the group studied.

Conventional physical examination of the chestwas usually negative in the pneumonia stage butin severe unilateral cases subsequent fibrosis gaverise to tracheal and mediastinal shift and to somealteration in the breath sounds and dullness topercussion over the affected lung. Some of our

patients were left with a tendency to recurrentbronchitis and pleurisy but only one was bronchi-ectatic. During the pneumonia stage the sedi-mentation rate was usually considerably raisedbut the only haematological abnormality we havefound was a slight polymorphonuclear leuco-cytosis in three of our most severe cases.

RESPIRATORY FUNCTION TESTS Respiratory functiontests were only occasionally performed but showeda uniform pattern of abnormality. There wvas adiminution in all divisions of lung volume, but theratio of the various divisions to total capacity wasnot significantly altered from normal. The maxi-mum breathing capacity was likewise markedlyreduced. The arterial oxygen saturation was nor-mal at rest but severe cases showed desaturationon exercise, while the carbon dioxide content wasnormal or low at rest and on exercise. Similarfindings have been reported by Leach (1943b),Baldwin, Cournand, and Richards (1949), Stone,Schwartz, and Green (1956). Rodman, Karr, andClose (1960), and Cooper, Guerrant, Harden, andTeates (1961). We have not examined the carbonmonoxide diffusing capacity in any of our patientsbut such abnormal physiology as we and othershave found indicates the presence of alveolo-capillary block, and the histopathological featuresimmediately confirm that such must be thedominant functional defect.

PROGNOSIS Seven of our 49 patients, all withsevere bilateral damage, died as a result of alveolo-capillary block. The remaining 42 survived or diedfrom other causes. In only two of these did thelungs revert to normal, the remainder showingvarying degrees of residual fibrosis and disability.In fatal cases deterioration can be extremelyrapid: three of our patients died within days ofthe onset of serious dyspnoea.

PATHOLOGY Four of our patients with radiationlung damage came to necropsy and the findingshave been reported elsewhere (Whitfield, Lanni-gan, and Bond, 1954; Whitfield, Bond, and Arnott,1956; Whitfield and Bond, 1959). In the gross thelungs are firm, rubbery, and airless, and on thesurface depressed scars may be evident. Histo-logically, the striking feature is loss of alveolarspace. This is due first to thickening of the alveolarwalls which show lymphocytic infiltration, fibrosis,and thickening and fragmentation of the elastictissue ; secondly to swelling of the alveolar liningcells ; thirdly to the presence within the alveoliand alveolar ducts of hyaline membrane, organiz-ing exudate, desquamated cells, and macrophages.

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some of which contain lipoid material; andfourthly to the collapse of some alveoli. Anincrease in the fibrous tissue around bronchi andlarge vessels is also seen.

RADIOLOGY The development of dyspnoea and drycough a month or so after radiotherapy to thethorax strongly suggests the presence of radiationlung damage: the tendency to spontaneous im-provement together with the respiratory functiontest pattern of alveolo-capillary block providegood supporting evidence. The usual diagnosticdifficulty is that of differentiating radiation pneu-monia from neoplastic involvement of the lungs(Whitfield et al., 1956), and here the chest radio-graph is of paramount importance: indeed thediagnosis cannot be made with certainty withoutit. In the pneumonia stage the appearances afterirradiation for breast cancer are those of upperlobe consolidation though the abnormality is notanatomically lobar in distribution, while afterwide-field irradiation of the thorax the radio-graphic pattern is that of oedema (Fig. 8). In thecourse of a few weeks the lung shadowing beginsto clear, and evidence of fibrosis with pleural and

pericardial tenting (Fig. 9) and, in unilateral cases,mediastinal shift (Fig. 10) becomes apparent.Radiological improvement continues for someyears but complete radiographic resolution is ex-ceptional and only occurred in two of our patients.The lung damage as shown on the chest radio-graph is usually strictly limited to the areairradiated, and this, together with the tendency tospontaneous clinical and radiographic improve-ment, strongly favours a diagnosis of radiationdamage as opposed to neoplastic involvement.

TREATMENT When there is such a striking tendencyto spontaneous improvement it is difficult to assessthe value of therapy. Steroids have been widelyemployed and are probably of limited use (Whit-field et al., 1956; Rubin, Andrews, Paton, andFlick, 1958; Douglas, 1959; Lougheed andMaguire, 1960; Rodman et al., 1960), though theoccasional slight relapse when steroids are pre-maturely withdrawn certainly suggests that theyare of some benefit (Cosgriff and Kligerman,1951 ; Bluestein and Roemer, 1953; Whitfield,Bond, and Arnott, 1954). Other writers have re-ported no improvement (Stone et al., 1956;

FIG. 8. Acute radiation pneumonia after chest baths for mediastinal Hodgkinl'sdisease. Appearances are those ofpulmonary oedema.

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FIG. 9. Radiation pneumonitis showing evidence ofprogression to fibrosis.

FIG. 1O. Unilateral fibrosis after irradiation for breast cancer.



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Lichtenstein, 1960) or no more than would havebeen expected to occur spontaneously followingtheir use (Chu, Nickson, and Uzel, 1956).Nine of our 49 patients were given steroids, and

of these five showed marked improvement thoughall were left with some residual fibrosis. Threedied from radiation lung damage but two of thesewere inadequately treated and the third died with-in two days of starting treatment. One patient withchronic fibrosis of six years' standing showed noimprovement after four months' treatment withprednisone (Whitfield, 1959). Our present beliefis that steroids should be given for three monthsto all patients whose lungs have not progressed tothe stage of fibrosis. Even so it seems likely thatsometimes the degree of lung damage is so greatthat death is inevitable whatever is done. The onlyother treatment that can be offered is rest duringthe acute phase, oxygen, sedatives to allay cough,and antibiotic cover to prevent secondary infec-tion. Bergmann and Graham (1951) performedpneumonectomy in two patients with severe uni-lateral disease, and this procedure was consideredin one of our patients who had bronchiectasis in aseverely fibrotic lung. However, her psychologicalinstability and the improvement that followedconservative measures made us decide not toproceed with surgical treatment.

PROPHYLAXIS Prevention of radiation lungdamage is of course more important than itstreatment. It may well be that some people aremore sensitive to the harmful effects of radiationthan others, but if this is so it is impossible toidentify such subjects in advance of treatment.Age and arterial degenerative change do notappear to be relevant factors, but thin people doseem more liable to radiation lung damage thanthose of greater body weight (Desjardins, 1932;Whitfield et al., 1956). Rubin et al. (1958) andStone et al. (1956) are of the opinion that thedominant influences in radiation lung damage aretotal dosage, rate of administration, and the per-centage of the total lung volume irradiated, whileGish, Coates, DuSault, and Doub (1959) con-sidered that the risk is reduced if treatment isprotracted in time. Our own experience stronglysupports these opinions. Evans (1960) has recentlyinvestigated a series of patients with carcinomaof the bronchus on these lines and found that ifthe maximum tumour dose did not exceed 5500 r,if the field was not more than 150 cm.2 and thetreatment was spread over 60 days, only minimalradiation damage to the lung ensued. It isobvious therefore that wide-field therapy is onlyjustifiable when it is the sole possible weapon of

palliation or hope of cure, as for example inseminoma or chorion epithelioma lung secon-daries. In addition dosage should not be unneces-sarily high and treatment should be as protectedas is reasonable.

In view of the possible therapeutic response tosteroids in radiation lung damage we gave sixpatients, undergoing wide-field thoracic irradia-tion, prophylactic cortisone in a dose of 75-100mg. daily during and for three months after radio-therapy. Of these, one died from radiation lungdamage while still taking 50 mg. cortisone dailyand another developed a small area of radiationpneumonia which cleared completely while takinga similar dose (Whitfield and Bond, 1959). Otherworkers (Chu et al., 1956) have had similarlydisappointing results, but Friedenberg and Ruben-feld (1954) reported a series of patients in whomsteroids appeared to afford some protection againstradiation lung damage, and this certainly seemedto be so in respect of the rats studied by Moss,Haddy, and Sweany (1960). Animal experiments(Boys and Harris, 1943) have suggested that anti-coagulant cover of thoracic radiotherapy mayreduce the danger of radiation lung damage, andthe work of Macht and Perlberg (1950) indicatedthat this was so in humans. We therefore gavephenindione to eight patients in whom wide-fieldthoracic irradiation was necessary, but of thesethree developed radiation pneumonia and one diedfrom radiation damage to the heart.

THE HEART

The incidence and exact nature of radiationreactions in the heart are less clearly defined thanis radiation lung damage. We have studied 27patients clinically, radiologically, and electro-cardiographically before, during, and after radio-therapy to the thorax, and of these 12 developedT wave changes in the electrocardiogram. Twoof the 12 died suddenly, apparently from cardiacarrest, and in one of these dyspnoea and galloprhythm were evident for a few hours before death.In the other, necropsy showed no naked-eye orhistological abnormality of the heart or coronaryarteries and no cause for sudden death. Anotherof the 12 patients died from radiation damageto the lungs, and the heart showed no macroscopicor microscopic abnormality at necropsy despitethe presence of electrocardiographic changesduring life. The remaining nine had no cardiacsymptoms and no objective cardiac abnormalities,and the electrocardiographic changes disappearedwithin a year or less.

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TABLE ILESIONS FOR WHICH THORACIC RADIOTI

GIVENWith SubsequentNew E.C.G.Abnormality

Carcinoma of breast 6Carcinoma of bronchus 3Carcinoma of oesophagusCervico-thoracic

reticulosesLung secondaries 0

TABLE IIMEAN AGE IN RELATION TO ELECTROCAFABNORMALITY FOLLOWING RADIOTHER

THORAX

Patients showing subsequent new electro-cardiographic abnormality

Patients showing no electrocardiographicchange

TABLE IIIPREVIOUS CARDIOVASCULAR STATUS INELECTROCARDIOGRAPHIC ABNORMALITY

RADIOTHERAPY TO THORA)With SubsequentNew E.C.G.Abnormality

NormalHypertensionCoronary artery diseaseRheumatic heart disease

and cardiac failure

2

0

The primary disease of the 27 patcovered the usual range of conditiorradiotherapy to the thorax is comi

(Table I), and neither age (Table:existing cardiac disease (Table III) srelated to the subsequent developmercardiographic changes or to death. Irtreated for carcinoma of the oesophsix patients given post-mastectomyfor breast cancer through opposed a

and a single parasternal field, T wa

was only seen in leads V.-V3. Inchest baths and in two treated throand posterior 15 x 15 cm. fields forthe bronchus, it occurred in most12 leads.The development of transient T v

in the electrocardiogram after radiotithorax has been reported by o

(Gloriozov, 1949; Whitfield and KtCatterall, 1960; Catterall and Evans,and Wedgwood, 1960; Vaeth, FeigMerrill, 1961) but their exact siuncertain. Some have suggested thatdirect radiation damage to the(Whitfield and Kunkler, 1957;Evans, 1960) and, though the ti

appearance accords with this hypothesis, there isHIERAPY WAS certainly no histopathological evidence to support

it. On the contrary, much of the published workChange suggests that the myocardium is relatively

insensitive to radiation. Certainly in animals very6 high dosage is necessary to produce recognizable41 myocardial damage (Davis, 1924; Hartman,2 Bolliger, Doub, and Smith, 1927; Warthin and2 Pohle, 1927, 1929; Werthemann, 1930; Leach and

Sugiura, 1941, 1942) and the necropsy on thepatient of Ross (1932) indicates that the same is

RDIOGRAPHIC true for humans. She reported a patient in whom*APY TO THE a 2 mg. radium needle remained in the heartMean Age (yr.) muscle for three years: such myocardial damage

as was evident on examination of the heart after50 7 death was ischaemic in nature and resulted from411 narrowing of the lumina of smaller arterioles

presumably due to radiation. The electrocardio-graphic changes seen in humans after radiotherapyto the thorax occur too soon to be explicable on

rFOLLOWING this basis, and the histology of the myocardiumin our fatal cases has shown no abnormality of

Without the arteries or arterioles. Pearson (1958) reportedSubsequentE.C.G. Change two cases of myocardial infarction six months

after x-ray treatment to the thorax, but this may2 well have been co-incidental as radiation does not2

usually produce changes in arteries as large as1 the main coronary arteries.The work of Senderoff, Kahn, Peck, and

ients studied Baronofsky (1960) and of Senderoff, Kaneko.ns for which Beck, and Baronofsky (1961) has shown thatmonly given radiotherapy to the dog's thorax in comparableII) nor pre- dosage to that used in humans does not produceeemed to be any histologically identifiable myocardial injury.nt of electro- It tends to improve the blood supply to thea one patient myocardium, and any T wave changes that mayagus, and in develop occur equally frequently in dogs that haveradiotherapy not been irradiated. The T wave changes that areixillary fields seen in humans after radiotherapy are not howeverive inversion seen in normal people and must indicate someU three given pathological change usually, if not always, mild,)ugh anterior symptomless, transitory, and fully recoverablecarcinoma of without treatment.or all of the Leach (1943a), Blumenfeld and Thomas (1945).

Hurst (1959), Jones and Wedgwood (1960), andvave changes Connolly (1962) have all reported constrictiveherapy to the pericarditis after radiotherapy to the thorax.)ther writers Freid and Goldberg (1940) also described pern-inkler, 1957; carditis in 8 of 18 patients with radiation lung1960; Jones damage, and Vaeth et al. (1961) noted pericarditis

enbaum, and in 2 of 20 patients receiving x-ray treatment tognificance is the thorax. The T wave changes in the electro-they indicate cardiogram could therefore be due to pericarditis,myocardium but in our patients pericardial friction was never

-atterall and heard, and there was no clinical or radiologicalme of their evidence of pericardial effusion or of the

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subsequent development of constrictive peri-carditis.Both of our patients who died suddenly showed

increasing electrocardiographic abnormality duringthe days preceding death. In only one of these two

was a necropsy obtained and the heart andcoronary arteries were normal in the gross andmicroscopically, and no cause for sudden deathwas found. Although we are not sure that eitherdeath was related to radiation, we think thatelectrocardiographic changes after radiotherapy tothe thorax may not always be unimportant or

recoverable.THE AORTA

We have not seen any damage to the aorta as a

result of radiation but Thomas and Forbus (1959)reported a case in which, in addition to bilateralradiation pneumonia, there was localized necrosisof all layers of the aortic wall. Attempts at healingthrough proliferative connective tissue were

evident, and fragments of thrombus which hadformed at the site of injury had caused splenicand renal infarcts.

THE OESOPHAGUS

Previous writers have reported radiation stricturesof the oesophagus (Seaman and Ackerman, 1957;Freid, 1948). We have seen seven patients withapparently non-malignant oesophageal stricturesdeveloping after radiotherapy to the thorax,larynx or thyroid. They appeared wholly fibrouson oesophagoscopy and biopsy showed no

evidence of malignancy. We therefore made a

diagnosis of radiation stricture but the subsequentcourse has shown that the stricture was in factmalignant in all seven patients. We think radiationstricture of the oesophagus must be very rare ifit ever occurs. In patients who have sustainedvery gross radiation lung damage, oesophagealnarrowing has not been evident radiologicallythough some distortion from extra-oesophagealfibrosis and hiatus hernia has sometimes been seen.

SUMMARY

Of all the thoracic tissues the lungs are the mostvulnerable to radiation damage. The risk isincreased when large areas of lung are irradiated,the total dosage is high, and the course of treat-ment is given quickly. Forty-nine cases afterirradiation of the thorax for breast cancer, malig-nant lymphomas, lung secondaries, and oeso-

phageal and bronchial cancer are reported. Seven

2E

of the 49, all with severe bilateral damage, diedfrom it. Steroids may be of some therapeuticvalue but their prophylactic use appears ineffectiveas does that of anticoagulants.Thoracic irradiation may cause constrictive peri-

carditis or be followed by transitory T wave

changes in the electrocardiogram. The significanceof the latter is uncertain. They are usually unasso-

ciated with cardiac symptoms or objective cardiacabnormality and disappear within a year or less.Twelve of 27 patients studied showed suchchanges, and sudden death occurred in two.The most frequent manifestation of radiation

damage to the bony structure of the thorax isfractured ribs. It usually follows post-mastectomyradiotherapy. Other less common bony lesionsattributable to radiation are described.Thoracic irradiation of females in childhood

may result in mammary hypoplasia and absenceof lactation.

Radiation stricture of the oesophagus was

suspected in seven patients but the diagnosis was

disproved in each instance: we think the conditionmust be rare.

We are greatly indebted to the consultant staff ofthe United Birmingham Hospitals for allowing us tostudy patients under their care, to Mr. T. F. Dee forreproduction of the figures, and to Miss J. Rutledgefor help with the electrocardiograms.

REFERENCES

Baldwin, E. deF., Cournand, A., and Richards, D. W. (1949). Pul-monaryinsufficiency. II. A study ofthirty-nine cases ofpulmonaryfibrosis. Medicine, Baltimore, 28, 1.

Baudisch, E. (1960). Beitrag zu den Strahlenschaden der Rippen undSchlusselbeine bei Brustkrebs-Patienten. Strahlentherapie, 113,312.

Bergmann, M., and Graham, E. A. (1951). Pneumonectomy for severeirradiation damage of the lung. J. thorac. Surg., 22, 549.

Bluestein, S. G., and Roemer, J. (1953). The treatment of radiationpneumonitis with cortisone. J. med. Soc. N.J., 50, 106.

Blumenfeld, H., and Thomas, S. F. (1945). Chlronic massive peri-cardial effusion following roentgen therapy for carcinoma of thebreast; with a case report. Radiology, 44, 335.

Borgstrnm, K. E., and Gynning, I. (1957). Roentgenographic changesin the lungs and vertebrae following intense rotation roentgentherapy of esophageal cancer. Acta radiol. (Stockh.), 47, 281.

Boys, F., and Harris, I. D. (1943). The effect of heparinization onexperimental post-irradiation tissue changes in the lung. Amer. J.Roentgenol., 50, 1.

Braun, H., and Frik, W. (1954). Rippenschadigung nach Rontgen-bestrahlung. Strahlentherapie, 94, 234.

Catterall, M. (1960). The effect of radiation upon the heart. Brit. J.Radiol., 33, 159.and Evans, W. (1960). Myocardial injury from therapeuticirradiation. B-it. Heart J., 22, 168.

Chu, F. C. H., Nickson, J. J., and Uzel, A. R. (1956). The effect ofACTH and cortisone on radiation pneumonitis. Amer. J. Roent-genol., 75, 530.

Connolly, D. C. (1962). Personal communication.Cooper, G., Guerrant, J. L., Harden, A. G., and Teates, D. (1961).

Some consequences of pulmonary irradiation. Amer. J. Roent-genol., 85, 865.

Cosgriff, S. W., and Kligerman, M. M. (1951). Use of ACTH andcortisone in the treatment ofpost-irradiation pulmonary reaction.Radiology, 57, 536.

Davis, K. S. (1924). Intrathoracic changes following X-ray treatment:a clinical and experimental study. Ibid., 3, 301.

Desjardins, A. U. (1932). Action of Roentgen rays and radium on theheart and lungs. Amer. J. Roentgenol., 28, 699.

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Douglas, A. C. (1959). Treatment of radiation pneumonitis withprednisolone. Brit. J. Dis. Chest, 53, 346.

Eggs, F. (1941). Osteoradionekrose der Rippen nach Rontgen-bestrahlung des Mammakarzinoms. Strahlentherapie, 70, 315.

Evans, J. C. (1960). Time-dose relationship of radiation; fibrosis oflung. Radiology, 74, 104.

Fike, R. H. (1932). The occurrence of Roentgen pleuropneumonitisin treatment of breast cancer. Amer. J. Roentgenol., 27, 509.

Freid, J. R. (1948). Roentgen treatment of cancer of the esophagus.Ibid., 59, 551.

-and Goldberg, H. (1940). Post-irradiation changes in the lungsand thorax. Ibid., 43, 877.

Friedenberg, R. M., and Rubenfeld, S. (1954). The role of cortisonein preventing pulmonary fibrosis following irradiation. Ibid., 72,271.

Gish, J. R., Coates, E. O., DuSault, L. A., and Doub, H. P. (1959).Pulmonary radiation reaction: A vital capacity and time-dosestudy. Radiology, 73, 679.

Gloriozov, B. N. (1949). Effect of Roentgenotherapy on heart;electrocardiogram in patients with esophageal cancer duringRoentgenotherapy according to Dillon method. Klin. Med.(Mosk.) (in Russian), No. 12, 27, p. 60.

Gros, C. M., and Keiling, R. (1958). Aplasie d'un sein apres roent-gentherapie profonde pour un sarcome mediastinal. J. Radiol.Electrol., 39, 636.

Hartman, F. W., Bolliger, A., Doub, H. P., and Smith, F. J. (1927).Heart lesions produced by the deep x-ray: an experimental andclinical study. Bull. Johns Hopk. Hosp., 41, 36.

Hurst, D. W. (1959). Radiation fibrosis of pericardium, with cardiactamponade: case report with post-mortem studies and reviewof literature. Canad. med. Ass. J., 81, 377.

Jones, A., and Wedgwood, J. (1960). Effects of radiations on theheart. Brit. J. Radiol., 33, 138.

Kolat, J., and Vrabec, R. (1957). t'ber Knochenschaden beimRontgengeschwur. Strahlentherapie, 102, 112.-- and Bek, V. (1957). Entwicklungsstorungen der weiblichen

Brust nach Rontgenbestrahlung im Kindesalter. Ibid., 104, 596.Leach, J. E. (1943a). Effect of Roentgen therapy on the heart. Arch.

intern. Med., 72, 715.(1943b). Abnormal pulmonary physiology as a result of chronicirradiation pleuropulmonitis. Amer. J. Roentgenol., 50, 772.Farrow, J. H., Foote, F. W., and Wawro, N. W. (1942). Fibrosisof the lung following roentgen irradiation for cancer of the breast.Ibid., 47, 740.and Sugiura, K. (1941). The effect of high voltage roentgen rayson the heart of adult rats. Ibid., 45, 414.- (1942). Late effect of high voltage roentgen rays on heartof adult rats. Ibid., 48, 81.

Lichtenstein, H. (1960). X-ray diagnosis of radiation injuries of thelung. Dis. Chest, 38, 294.

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- Kaneko, M., Beck, A. R., and Baronofsky, I. D. (1961). Theeffects of cardiac irradiation upon the normal canine heart. Ibid.,86, 740.

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Warthin, A. S., and Pohle, E. A. (1927). The effect of roentgen rayson the heart. 1. The microscopic changes in the heart muscle ofrats and rabbits following a single exposure. J. Amer. med. Ass.,89, 1825.-(1929). The effect of roentgen rays on the heart. It. Themicroscopic changes in the heart muscle of rats and of rabbitsfollowing a series of exposures. Arch. intern. Med., 43, 15.

Werthemann, A. (1930). Experimentelle Rontgenschadigungen desHerzmuskels. Strahlentherapie, 38, 702.

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(1956). Radiation reactions in the lung. Quart. J.Afed., 25, 67.and Kunkler, P. B. (1957). Radiation reactions in the heart.Brit. Heart J., 19, 53.Lannigan, R., and Bond. W. H. (1954). Fatal post-radiationpneumonitis. Lancet, 2, 117.

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