Shrinking pleuritis with atelectasis - Thoraxthis lesion shrinking pleuritis with atelectasis. In...

Thorax 1982;37:252-258

Shrinking pleuritis with atelectasisL DERNEVIK, P GATZINSKY, E HULTMAN, K SELIN, G WILLIAM-OLSSON,L ZETTERGREN

From the Departments of Thoracic and Cardiovascular Surgery, X-ray andPathology, University of Gdteborg,Sahlgrenska sjukhuset, Giiteborg, Sweden

ABSTRACT During a 10-year period 28 patients with shrinking pleuritis with atelectasis (SPA) were

observed and operated upon. This lesion has been given different names in the literature, for instancerounded atelectasis, pleuroma, pulmonary pseudotumour, and lung folding. All patients except

two were operated upon because of a diagnosis of pulmonary tumour. However, at operation no

tumour was found. The aetiology and pathogenesis of SPA are discussed on the basis of X-ray,operative, and histopathological findings.

In 1966 Blesovsky' described three patients who wereoperated upon because of suspected pulmonarytumour. At operation no tumour was found but athick fibrous membrane covered part of the lung.The underlying parenchyma was atelectatic butwhen the membrane was stripped off, the lungexpanded completely and looked normal. Similarcases were described by Hanke2 in 1971 andKretzschmar3 in 1975. They collected seven andfive cases respectively and called the lesion roundedatelectasis. Other reports have since been pub-lished.4-10 The diagnosis in the reported cases wasmade by X-ray and was not always verified byoperation or histopathological examination. Radio-logically, the lesion is characterised by a roundedor lobulated mass under the visceral pleura withadjacent pleural thickening and with vessels andbronchi curling into it like a "comet tail" (figs 1-3).In many cases the radiological findings are suf-ficiently typical to allow the diagnosis to be madewith confidence. The aim of this paper is to presenta series of patients with this lesion, which we havecalled shrinking pleuritis with atelectasis (SPA),and to discuss its aetiology and pathogenesis.

Patients

During the years 1970-80, 26 patients were operatedupon at the Department of Thoracic and Cardio-vascular Surgery at Sahlgrenska Hospital in Gothen-burg because of suspected pulmonary malignancy.At operation, however, no tumour was present.

Address for reprint requests: L Demevik, Department ofThoracic and Cardiovascular Surgery, Sahlgrenska sjukhuset,413 45 Goteborg, Sweden.

Only atelectatic lung tissue was found, covered by athick fibrotic visceral pleura. In two other patientsa similar lesion was discovered at operation forhiatal hernia. The series thus comprises 28 patients.All patients except one were male. The age distribu-tion is given in fig 4 and the locations of the lesionsare summarised in table 1.

Fourteen patients were asymptomatic. In 12 aradiographic opacity was found during a routine

Fig 1 Lateral tomogram demonstrating the typicalfeatures of shrinking pleuritis with atelectasis-asharply defined mass with vessels curling into its borderand adjacent pleural thickening.

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253Shrinking pleuritis with atelectasis

Fig 2 Chestradiograph showing acyst-like lesion in theright lung. Sanmepatient as fig 1.

Table I Location of shrinking pleuritis withatelectasis

Location Number

Left upper lobe 3 (2 in lingulaRight middle lobe 3Left lower lobe 8Right lower lobe 14

health check and two were found during operationfor hiatal hernia. The remaining patients had variouspulmonary symptoms. Cough was found in eightpatients and was usually non-productive. Twopatients presented with haemoptysis and two withfatigue and dyspnoea. The duration of symptomsbefore operation usually varied from two to sixmonths but three patients had had symptoms fortwo or three years. Twenty-five patients weresmokers. Eighteen of them had a history of occupa-tional exposure to asbestos. In addition three non-smoking patients were exposed to asbestos. Othersubstances, such as chemicals, textile fibres, glassfibres, silicone, and stone dust, were found onlyoccasionally (fig 5). No patient had a history oftuberculosis.

Preoperative chest radiographs were re-examined

in all patients except one, with special reference tosigns of rounded atelectasis as described by Hankeand Kretzschmar6 and Schneider et al.7 Antero-posterior and lateral views and in 12 cases lateraltomograms, were available.

Results

The three most typical radiological signs of SPAare a rounded parenchymal lesion, pleural plaques,and "comet tail" (table 2). In 17 cases all threesigns were present, in five cases one or two signscould be recognised, and in six cases none of themwere present. Two of the latter patients were operatedupon for hiatal hernia, three had diffuse pulmonaryinfiltration, and one had lower lobe atelectasis.

Eighteen patients were referred for operationimmediately after investigations at the lung clinic.In eight patients the lesions were observed from twoto 44 months before operation (mean 11 months).In most cases no radiographic change was notedduring the observation period. In one case, however,a change in the lesion was demonstrated. Thispatient was a 62-year-old shipyard worker withmassive exposure to asbestos. He was also a heavysmoker. The patient was examined as part of a



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Dernevik, Gatzinsky, Hultman, Selin, William-Oisson, Zettergren

Fig 3 Same patientas figs and 2 10months later. The

lesion has beconmecompact and roundsimulating a lungtumour.

Table 2 Features indicating shrinking pleuritis with

atelectasisNumber

3

2

35-39 40-44 45-49Age (years)

Fig 4 Distribution ofpatients according to age.

routine health examination and had no symptoms.The radiograph showed marked pleural thickeningand a cyst-like lesion in the middle lobe (fig 2).There were wide vessels curling into the lower

pole of the lesion. The findings did not suggest a

Number ofpatients

Rouaded lesion 21Pleural plaques 18"Comet tail" 18

tumour. A new radiograph taken two months latershowed a dense oblong opacity. The vessels had thesame appearance as before. A further radiograph(fig 3), eight months after the second one, showedthe lesion to be compact and round. In view of thepossibility of tumour the patient was referred foroperation. This revealed a folding of the lung in themiddle lobe, together with several pleural plaques.There was no pleural fluid and the process wascompletely localised.

Cytological examination of sputum, broncho-scopy, and mediastinoscopy were performed asstandard investigations in all patients in whom a

tumour was suspected. One patient had a falsepositive cytological finding (Papanicolau class IV)but in all other patients these investigations were

negative. Lung function tests (VC, FEV %, andFEVj) were performed in all patients. Two had

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atelectatic part of the lung could be expanded andNumber the normal appearance was restored. In one case a

large atelectatic part of the lower lobe could not be25 expanded after decortication and lobectomy was

performed.

HISTOPATHOLOGYMicroscopic examination of the material from seven

20 - of the patients showed fibrous thickening of thevisceral pleura in all cases. The connective tissue wasalmost acellular and in two cases partly hyalinised.In one of these cases the pleural lesion had theappearance of a pleural plaque (fig 6). In most cases

15 a slight or moderate infiltration of inflammatorycells was noted in the pleura. In four cases, numerousfibrous fascicles were seen reaching from the thick-ened pleura down into the pulmonary parenchymaperpendicular to the surface (fig 7). They showed a

10 parallel arrangement and followed pre-existingfibrous septa and fissures. The parenchyma underthe thickened pleura was in all cases atelectatic.Slight interstitial fibrosis and scattered lymphocytes

Asbestos Smoking OtherKX

OPERATIVE FINDINGS AND TREATMENT ;The standard procedure was decortication and thiswas performed in 27 patients. At operation the lung,was usually free from adhesions to the chest wall g' .and acute pleurisy was never found. Twenty of thepatients had plaques on the parietal pleura, oftenclose to theparenchy mallesion.Thisconsisted of asubpleural palpable mass covered With a localisedgreyish-white coating. It was usually limited to angarea about the size of the palm of the hand but inw

threecases it co veredthe whole lobe. The surround-ing pulmonary tissue was sometimes emphysema-

At decortication it was found that the coating . M g ! lconsisted of several layers of fibrous tissue causing Fig 6 Visceral pleural plaque consisting of almostfolding and atelectasis of the underlying lung tissue. acellular hyalinised collagenous connective tissue.When all the layers of the coating were removed, the H and E x 30.

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Fig 7 Fibrous fascicles are seen reaching from thethickened pleura (top left) into the atelectatic pulmonaryparenchyma. The tissue is infiltrated by inflammatorycells. H and E x 30.

and plasma cells were seen. The pulmonary vesselswere sclerotic (fig 8). In two cases corpora amylaceawere noted in the alveoli, in one of them in greatnumbers. In the boundary between the fibroticpleura and the parenchyma carbon pigment with a

varying admixture of small, double refringentparticles (silica) was observed. In four cases asbestosbodies were noted, both in the pigmented area anddeeper in the parenchyma. The asbestos bodies were

numerous in one of these cases and sparse in two.In the fourth case asbestos bodies were found onlyoccasionally. Particles of silica and carbon were alsopresent deeper in the lung parenchyma.

FOLLOW-UP

There were no operative deaths and the postoperativecourse was uneventful in all patients except one whosustained a small myocardial infarction. Follow-upchest radiographs were obtained from 17 patients

at intervals ranging from four to 37 months (mean18 months). No recurrences have been observed.

Discussion

The aetiology and pathogenesis of SPA are stillnot clear. Hanke2 suggested that the changes werecaused by the mechanical influence of a pleuraleffusion. However, few patients in published reportshave actually been shown to have had a pleuraleffusion before the discovery of the parenchymallesion. We have observed pleural fluid beforeoperation in only four out of 14 patients withsymptoms. In three of these patients the effusionwas found on the same side as the atelectasis and inone patient on the contralateral side. The quantityof fluid was only small. In none of the patientswithout symptoms was any effusion observed on theradiograph or at operation.

In our opinion, this lesion starts as a local processin the visceral pleura. It seems that the main aetio-

I4

40.

,i4's

thick-walled vessel.s. H and E x 70.

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Shrinking pleuritis with atelectasis

Fig 9 A case with very localised pleural shrinkage compressing the underlying lung. To the right a parietalplaque is seen on the diaphragm.

logical factor is the irritant effect of asbestos, aloneor in combination with other irritants, such assilica or smoking. This irritation causes a localreaction with formation of a thick pleural fibroticcoating over a limited area of the lung. Subsequentshrinkage of this coating leads to folding of thelung surface. It seems that the development of newlayers of the coating proceeds in parallel withshrinkage of the older ones. The result of thispleural shrinkage is the development of atelectasis ofthe underlying pulmonary parenchyma. The per-pendicular septa noted on microscopical examinationmay also shrink, giving the collapsed area a roundedform. The fibrous coating on the visceral pleuramay be aetiologically analogous to the parietalpleural plaque. This theory is supported by theirvery frequent coexistence and the fact that thevisceral coating in two cases had a plaque-likeappearance (fig 9). For these reasons we have calledthis lesion shrinking pleuritis with atelectasis.

In one patient we observed pathological changesin the lung which we believe to be a very earlystage of this lesion. This was a 61-year-old manwith a history of asbestos exposure many yearsearlier who had a thoracotomy because of hiatal

hernia. On the costal surface of the left lower lobethere was a localised greyish-white fibrotic coatingwith a similar appearance to that of patients withSPA. There was no pleural fluid. Slight folding ofthe lobe was seen when the fibrous coating on thelung surface had been dissected away and it wasapparent that some shrinkage of the lung tissue hadalready occurred. When the coating was removed thelung parenchyma beneath it expanded completely.At biopsy asbestos bodies were found in the pul-monary parenchyma while the coating itself showednon-specific inflammation. This observation seemsto contradict the earlier theory that the lesionstarts with copious amounts of fluid folding thelung.The diagnosis of SPA can be made from the

typical radiographic appearance in many cases.In some cases, however, this is not possible. In 11of the patients in this series, including the hiatalhernia patients, the radiographic features were nottypical. In some of these the diagnosis could probablyhave been made with oblique views and tomogramsif we had been more aware of the existence of thiscondition at the time. Nowadays computed tom-ography may be of assistance in diagnosis.

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There are no published data concerning lungfunction in patients suffering from SPA. The testsof lung function in our patients gave somewhatsurprising results. Vital capacity and forced expira-tory volume were normal in all patients except two.Even in three patients in whom the atelectasisoccupied a large part of a lobe, normal values werefound. There may thus be a functional derangementof ventilation which cannot be detected by spiro-metry.At present there is no generally accepted policy

on the management of SPA. We consider that inpatients in whom the diagnosis can be made withcertainty the interference with lung function is tootrivial to justify operation. However, these patientsshould be followed up regularly because very littleis known about the natural history of the conditionand no long-term observations appear to have beenpublished. When the diagnosis of SPA is not certainthe patient requires operation. Decortication is thenan adequate procedure. The postoperative follow-up showed satisfactory results with this simpleprocedure in our patients. In really advanced cases,when the normal appearance of the atelectatic

part cannot be restored, a limited resection isjustified.

ReferencesBlesovsky A. The folded lung. Br J Dis Chest 1966;60:

19-22.2 Hanke R. Rundatelektasen (Kugel- und Walzenatelek-

tasen). Roefo 1971 ;114:164-83.3 Kretzschmar R. Ober atelaktatische Pseudotumoren der

Lunge. Roefo 1975;122:19-29.4 Benard Y, Mandard JC, Evrard C, Lemenager J. Opacite

ronde pseudotumorale par atelectasie (A proposd'une observation). Rev Fr Mal Respir 1973;1:1171-7.

5 Brune J, Bosly A, Bory R, Perinetti M, Wiesendanger T,Galy P. Condensations parencymateuses pulmonairesarrondies post-pleuretiques mecanisme physiopatholo-gique. Lyon Medical 1974;231:605-9.

6 Hanke R, Kretzschmar R. Round atelectasis. Seminarsin roentgenology 1980;15:2, 174-182.

Schneider HJ, Felson B, Gonzalez LL. Rounded atelec-tasis. AJR 1980;134:225-32.

Sinner WN. Pleuroma-a cancer-mimicking atelectaticpseudotumor of the lung. Roefo 1980;133:578-85.

Hillerdal G, Hemmingsson A. Pulmonary pseudotumoursand asbestos. Acta Radiol (Diagn) (Stockh) 1980;21:615-20.

10 Payne CR, Jaques P, Kerr IH. Lung folding simulatingperipheral pulmonary neoplasm (Blesovsky's syndrome).Thorax 1980;35:936-40.

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