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429Thorax 1991;46:429-432
Asbestos induced pericardial effusion andconstrictive
pericarditis
D Davies, M I J Andrews, J S P Jones
City Hospital,Nottingham NG5 1PBD DaviesJ S P JonesSt Mary's
Hospital,Portsmouth P03 6ADM I J AndrewsReprint requests
to:Professor JonesAccepted 21 February 1991
AbstractThe number of disorders attributable toasbestos exposure
has increasedgradually over the years. The latest to berecorded is
pericardial effusion and con-strictive pericarditis, and three
cases arereported here. A man with bilateralpleural thickening and
plaquesdeveloped acute pericarditis and aneffusion and was treated
by pericardi-ectomy. Two men died from constrictivepericarditis
associated with bilateralpleural effusions and diffuse pleural
thick-ening. The pericardium showed non-specific fibrous
thickening. All had beenoccupationally exposed to asbestos. Inthe
fatal cases the lungs containedamphibole fibres, in keeping with
amodest degree of occupational exposure.Asbestos produces
progressive fibrosis ofthe pericardium that is similar to
diffusepleural thickening and may be fatal.Both conditions may
develop afterrelatively short or light exposure.
The association between asbestos exposureand diffuse lung
fibrosis was established by1930 but the recognition of other
disorderscaused by asbestos came slowly. The associa-tion with lung
cancer was recognised by 1955and with mesothelioma in 1960. At
about thesame time the association between asbestosexposure and
hyaline pleural plaques was de-scribed'2 and soon afterwards
asbestosinduced pleural effusions were reported,3 someof which
cleared while others left considerablepleural thickening. Diffuse
pleural thickeningwithout preceding effusions45 was recognisedand
bilateral diffuse pleural thickening becamea prescribed disease in
1985. Another variantis visceral pleural plaque formation; this
tendsto cause rounded atelectasis, which mimics atumour.6
Calcified plaques are sometimes seen on theheart border. Nearly
all are in the mediastinalpleura, though occasional plaques occur
inthe parietal pericardium.7 A few asbestosassociated primary
mesotheliomas of thepericardium have been reported.89
Pleuralmesotheliomas often invade the pericardiumand may cause
constrictive pericarditis. Twocases of asbestos associated
non-malignantconstrictive pericarditis have been pub-lished.'°0 We
present a further three.
Case reportsPATIENT IIn November 1983 a man of 43 was admitted
tohospital with precordial pain of 12 hours'duration. No
abnormality was found by clinicalexamination but he had
neutrophilia and araised erythrocyte sedimentation rate.
Theelectrocardiogram showed changes of acutepericarditis. Serial
cardiac enzymes were nor-Mal. Radiographs showed diffuse
bilateral
~~~~pleural thickening, calcified plaques, and anormal heart
shadow. The pain eased and hewas discharged after three days with a
diagnosisof pericarditis of undetermined cause.
Fresh precordial pain led to his readmission amonth later. He
was febrile, the venous pres-sure in the neck was 3 cm and he had
apericardial rub. The chest radiograph showedan enlarged cardiac
shadow and--unchangedpleural shadowing (fig 1).
Echocardiographyshowed a moderate effusion.The tuberculin skin test
and blood culture
gave negative results. Concentrations ofcardiac enzymes, serum
electrolytes, glucose,and complement were normal. Autoantibodiesand
antibodies against viruses, psittacosis, andcoxiella were not
found. The antistreptolysin
Figure I Chest radiograph from case 1 showing an enlarged
cardiac shadow, calcified titre was normal and viruses were not
isolatedplaques and diffuse bilateral pleural thickening. from
throat swabs or stools.
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Davies, Andrews, Jones
A thoracotomy was carried out. Pleuralplaques were present in
the parietal layer of thelower chest wall and diaphragm. There
wasalso diffuse fibrous thickening ofthe pleura andpericardium. A
partial pericardiectomy wascarried out.
Histologically the pleural plaques showedcharacteristic bundles
of collagen arranged in a"basket weave" pattern. The
thickenedpericardium and pleura showed a similarbasket weave
pattern with hyalinisation andmoderate lymphocytic infiltration. In
addition,the pericardium showed a fibrinous exudate onits surface
(fig 2). Examination of the veryscanty peripheral fragments of lung
tissue thatwere adherent to the thickened pleura showedoccasional
asbestos bodies of classicalappearance but no asbestosis. The
patientmade a good recovery and there has been noprogression of the
pleural thickening.Occupational history Heavy exposure toasbestos
of unknown type had occurred fromthe age of 18 to 20, when he
worked as a lagger.
PATIENT 2In 1982 a man aged 64 years complained ofdizziness and
was found to be hypertensive. Noother abnormality was detected and
anelectrocardiogram was normal. A chestradiograph showed calcified
plaques on bothdiaphragms. His blood pressure was controlledwith
hydrochlorothiazide and triamterene.
In January 1984 he developed chest tight-ness, a dry cough, and
shortness of breath.When seen in hospital he had
tachycardia,slightly enlarged liver and normal blood pres-sure. An
electrocardiogram showed low voltageand T wave inversion in leads
1, 2, 3, AVF, andV 4-6. The chest radiograph showed a largeheart
and clear lung fields. Liver function testsgave abnormal results.
He was considered tohave had a myocardial infarction with
secon-
Figure 2 Microscopicappearance of the visceralpericardium (case
1)showing hyalinised "basketweave" thickening, with azone of
lymphocytesadjacent to themyocardium and afibrinous exudate on
thesurface.
dary congestion ofthe liver. Hypotensive drugswere
discontinued.He was readmitted to hospital in June 1984
because of increased shortness of breath. Hehad distended neck
veins, a large liver, oedemaup to the thighs, and a large right
pleuraleffusion. An echocardiogram was considered toshow congestive
cardiomyopathy. Aspirationofthe pleural effusion produced 2 litres
of strawcoloured pleural fluid, which formed a clotcontaining
lymphocytes and mesothelial cells.The oedema decreased with
diuretic treatment.Over the next year he remained short of
breathbut with little oedema. In 1985 he became moreoedematous and
the liver was enlarged to 5 cmdespite large doses of diuretics. In
October hehad gross oedema, distended neck veins, andbilateral
pleural rubs. A chest radiographshowed a large effusion on the
right and amoderate effusion on the left. Repeated aspira-tions
ofthe effusion on the right produced bloodstained fluid with a high
protein content con-taining red cells, lymphocytes, and a
fewmesothelial cells. Pleural biopsy specimensshowed dense fibrous
tissue only. He continuedto deteriorate, with increased shortness
ofbreath, gross neck vein distension, and largebilateral pleural
effusions, and he died inJanuary 1986.Necropsy showed a rigid,
constrictive
pericardium resulting from dense hyalinethickening of both
visceral and parietal layers(fig 3). The former was up to 0-2 cm in
diameterand the latter up to 0 5 cm. Microscopically,the
pericardium varied from acellular collagen-ous areas to cellular
fibroblastic tissue accom-panied by a non-specific inflammatory
reaction(fig 4). Fibrin was present on the surface. Noevidence of
neoplasm was seen. The pleuralcavities contained 800 ml of blood
stainedeffusion on the right side and a similar 700 mleffusion on
the left. Calcified hyalinised pleuralplaques were present on the
diaphragmaticpleurae of both sides. The right lung showed
Figure 3 Hyaline thickening of visceral and parietallayers
ofpericardium, which have become partially fusedtogether (case
2).
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Asbestos induced pericardial effusion and constrictive
pericarditis
Figure 4 Microscopicappearance of thethickened pericaridum(case
2) showingcollagenous bundles ofvarying
cellularity.Myocardialfibres at loweredge ofphotograph.
Figure 5 Diffuse fibrousthickening of visceralpleura (case
2).
diffuse thickening of the visceral pleura up to0-2 cm in
diameter (fig 5). The parietal pleurashowed hyaline thickening up
to 1 cm. The leftlung showed a lesser degree of diffuse
fibrousthickening and a fibrinous deposit on the vis-ceral pleural
surface. No evidence of pleuralneoplasm was present and the
microscopicappearances were similar to those of thepericardium.
Microscopic examination of the
lung tissue showed a minor degree of asbestosiswith patchy
interstitial fibrosis, and asbestosbodies ofclassical appearance.
Mineral analysisof lung tissue at the Medical Research Councilunit
at Penarth, using electron microscopy andenergy dispersive x ray
analysis, showed 3-6million fibres ofcrocidolite and 22 million
fibresof amosite per gram of dry lung.Occupational history In his
youth this patienthad served in the Merchant Navy and at theend of
the war he became a marine engine fitter,working in a naval
dockyard. He had beenexposed to asbestos intermittently over
manyyears until his retirement in 1982.
PATIENT 3In July 1976 a man aged 43 years complainedof weight
loss and shortness of breath.Radiographs showed extensive pleural
thicken-ing over the periphery and base of the rightlung and a
large left pleural effusion, which wasfound to be blood stained. He
remained unwelland short of breath. He gradually developedsigns of
right heart failure and the amount ofpleural shadowing increased on
both sides. Hedied from heart failure in 1980 at the age of
47years.Necropsy showed severe pericardial restric-
tion with fusion of the visceral and parietallayers to form a
diffuse dense fibrous encap-sulation of the heart up to 0 9 cm
across. Thepleurashoweddiffuse fibrous thickening consis-ting of
white compact hyalinised connectivetissue up to 4 cm in diameter.
In places thevisceral and parietal layers of the pleura werefused,
while in others a haemorrhagic effusionwas present in the pleural
space. Micro-scopically the pericardial and pleural tissueswere of
similar appearance, showing densehyaline thickening of acellular
collagenousmaterial (fig 6). Capillary blood vessels werepresent,
but there was no evidence of activeinflammation. No neoplasm was
present. Thelung tissue showed no evidence of asbestosis-that is,
no generalised fibrosis and only scantyasbestos bodies were
detected by light micro-scopy. Mineral analysis ofthe lung tissue
by theMRC Unit, Penarth, using electron micro-scopy and energy
dispersive x ray analysis'2showed: 2-5 million fibres of
crocidolite, 0 9million fibres ofamosite, and 14-2 million fibresof
chrysolite per gram of dry lung.Occupational history In 1963 and
1964 thepatient worked alongside a man who mixed anasbestos
compound while casting lead grids. In1971 he spent several months
making carbatteries. For this he melted bitumen in a largemixer and
tipped in bags of asbestos and mica,which were then stirred in. The
mixture wasthen poured into moulds.
DiscussionThe three men had been occupationallyexposed to
asbestos, but by comparison withlife long insulation workers, for
example, theirexposure was not heavy. The asbestos contentof the
lungs in two of the cases is in keepingwith a relatively modest
degree of occupationalexposure to amphibole fibres. Patient 1
had
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Davies, Andrews, Jones
Figure 6 Acellular collagen showing "basket weave" pattern on
pleural surface, withidentical appearance on pericardial surface
(case 3).
heavy exposure for two years to asbestos ofunknown type. The
exposure in patient 2 wasspread over 25 years or more, but it
wasprobably very intermittent. Patient 3 had fairlylight exposure
for about two years and heavyexposure for less than a year, the
latter almostcertainly to crocidolite. It is well recognisedthat
relatively light exposures to amphiboleasbestos may produce benign
pleural fibrosis.'3Asbestosis requires heavier exposures.
All three patients had asbestos inducedpleural effusions and
diffuse pleural fibrosis.Patient 1 developed acute pericarditis
super-imposed on bilateral diffuse pleural thickeningof unknown
duration, which had not changedduring five years of subsequent
observation.The pericardial effusion appeared 23 years afterhis
last exposure to asbestos. This is muchlonger than the usual
interval for asbestosinduced pleural effusions. The
pericarditisbecame fibrinous, and considerable fibrousthickening
developed over six weeks. He wouldprobably have developed
progressive constric-tive pericarditis but for the
pericardiectomy.We believe that patient 2 began with a
pericardial effusion, and the only precedingasbestos related
condition was parietal pleuralplaques. The fluid decreased quickly
and hedeveloped a unilateral pleural effusion some fivemonths
later. The extensive oedema and livercongestion at that time
indicates that thepericardial constriction was well
advanced.Bilateral pleural effusions developed 10 monthsafter the
onset of illness and persisted until thepatient died from
constrictive pericardialdisease. The minor degree of asbestosis
foundat necropsy did not contribute materially to his
death. The interval from first exposure toasbestos to the
development of pericardial andpleural effusions was again
long-almost 40years-but the interval after hig-4at exposurewas
probably fairly short. The time sequence incase 3 is less clear.
The patient had establisheddiffuse pleural thickening on the right
side at thetime when the left pleural effusion was detected.Whether
he ever had a pericardial effusion orwhether the pericardial
thickening developedon its own is unknown. Probably an effusion
waspresent at some stage. The interval between thelast asbestos
exposure and the onset of thepleural effusion was fairly typical at
five years.
It has been suggested that the structureslining the body
cavities-pleura, peritoneum,pericardium, and tunica vaginalis
testis-havean identical disease pattern in response tocommon
causative agents. " Asbestos inducedmalignant mesothelioma is such
an example.These three cases of diffuse pericardial
fibrosis,arising in patients who had been exposed toasbestos, are
presented in support of this thesis.They illustrate the way in
which the peri-cardium has produced a pathological
responseidentical to that of the pleura.
We thank Mr W E Morgan for permission to publish the
detailsabout patient 1 and Dr D Colin-Jones for the details
aboutpatient 2; Dr T C Williams and Dr R M Whittington, HMCoroner,
for permission to publish the details about patient 3;Professor F D
Pooley, Dr A R Gibbs, and Mr D M Griffiths forthe mineral analyses;
Mr Keith Miller for his technical expertise,and Mrs Valerie Bolton
for the preparation of the manuscript.
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