A case report is presented of pleural mesothelioma with simultaneous development of benign effusive-constrictive pericarditis

Gerstenhaber, B.

Weir, N. A.

English

PubMed

Weir, Nargues A., MD

Gerstenhaber, Brett, MD

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Advanced Lung Disease and Lung Transplantation
Articles Advanced Lung Disease and Lung Transplantation
2001
A Case of Pleural Mesothelioma with Effusive-
Constrictive Pericarditis
Nargues A. Weir MD
Inova Fairfax Hospital, nargues.weir@inova.org
Brett Gerstenhaber MD
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Recommended Citation
Weir NA, Gerstenhaber B. (2001). A case of pleural mesothelioma with effusive-constrictive pericarditis. Yale Journal of Biology and
Medicine, 74(3);159-63.
YALE JOURNAL OF BIOLOGY AND MEDICINE 74 (2001), pp. 159-163.
Copyright @)2001. All rights reserved.
CASE REPORT
A Case of Pleural Mesothelioma with
Effusive-Constrictive Pericarditis
Nargues A. Weira and Brett Gerstenhaber
Division of Pulmonary and Critical Care, Department of Medicine,
Yale School of Medicine, New Haven, Connecticut
INTRODUCTION
Mesothelioma infrequently causes
pericardial constriction and rarely sympto-
matic pericardial tamponade. Most com-
monly, a primary pleural malignancy will
extend locally, but primary involvement of
pericardium is also well-recognized. How-
ever, pericardial fibrosis in conjunction
with pleural mesothelioma has not been
described before in the literature. We
report a case of pleural mesothelioma with
simultaneous development of benign effu-
sive-constrictive pericarditis.
CASE REPORT
S.H., a 76-year-old man, presented for
consultation after the incidental finding of
a pleural effusion. In preparation for a hip
replacement, a chest radiograph was per-
formed revealing a moderate sized left-
sided effusion. He denied any history of
pneumonia, bronchitis, asthma, tuberculo-
sis, cough, hemoptysis, weight loss,
orthopnea, or paroxysmal nocturnal dysp-
nea. His past medical history was signifi-
cant for a left carotid endarterectomy,
peripheral vascular disease, and bilateral
knee replacements. Medications included
chlorthalidone and occasional alprazolam.
He denied allergies to any medications.
Social history was significant for a remote
history of smoking (40 pack years) and
moderate daily alcohol consumption. He
was a retired telephone installer and
denied any known exposure to occupation-
al inhalants. His family history was signif-
icant for two siblings dying from cancer
(patient did not know the primary sources)
and one sibling dying from a myocardial
infarction.
Physical examination revealed a well-
nourished, afebrile man with a pulse of 94,
blood pressure of 150/90 mmHg, and a res-
piratory rate of 14 breaths per minute. The
head and neck examination were normal,
most notably for the absence of neck vein
distention and lymphadenopathy. Dull
breath sounds were heard over the left lung
base with decreased tactile fremitus and
absent egophony. The remainder of the car-
diopulmonary examination was otherwise
a To whom all correspondence should be addressed: Nargues A. Weir, M.D., Division of Pul-
monary and Critical Care, Department of Medicine, Yale School of Medicine, 333 Cedar
Street, LCI 105, P.O. Box 208057. Tel.: 203-281-7037. E-mail: narguesnscottweir@ msn.com.
b Abbreviations: CT, computed tomography.
Received: Received: February 1, 2001; Accepted: April 18, 2001.
159
160 Weir and Gerstenhaber: Pleural mesothelioma and constrictive pericarditis
unremarkable. The abdominal, extremity
and neurological examinations were also
unremarkable.
Laboratory evaluations revealed a
white blood cell count of 8.10 K/ul, with
58 percent granulocytes, 33 percent lym-
phocytes, and 5 percent monocytes.
Hemoglobin was 13.8 g/dl, and the platelet
count was 520 KIul. Hematologic indices
were significant for a mean corpuscular
volume of 94 fl, red blood cell distribution
width of 15.2 percent, and a sedimentation
rate of 66 mm/hr. Coagulation, urinalysis
and chemistry studies were normal, with
the exception of an alkaline phosphatase
of 100 U/l (reference range 36-92). Thy-
roid studies were also within normal
ranges. Electrocardiogram showed a nor-
mal sinus rhythm, normal intervals and
axis, with an inverted T wave in lead III,
which was unchanged from prior studies.
A chest radiograph showed enlargement of
the cardiac silhouette, bilateral pleural
effusions left considerably larger than the
right, and pleural thickening. A persantine
thallium scan showed a small inferobasilar
defect without ischemia.
At thoracentesis of the left chest, 500
ml of serosanguinous fluid were removed;
analysis of the fluid demonstrated 2,100
RBC's, 5,100 white blood cells (80 per-
cent lymphocytes, 12 percent granulo-
cytes), lactate dehydrogenase of 307 U/l
(fluid/serum ratio of 1.88), protein 4.5 g/dl
(fluid/serum ratio of 0.625), and glucose
111 mg/dl. Gram stain and acid fast smear
were negative, and cultures failed to grow
any organisms. Cytopathology was nega-
tive for malignant cells. A computed
tomogram of the chest was obtained
which revealed pleural thickening and cal-
cification without any masses or signifi-
cant adenopathy. The patient again denied
any history of exposure to asbestos, but
_ w ^ * ' - ** 8 * . ^ . . , & X . u , . . , _1~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~....
Figure 1. Left pleural thickening with a rounded pleural mass suggestive of a pleur-
al malignancy. Calcifications within the pleura indicate prior exposure to asbestos. Peri-
cardial thickening and effusion are also noted.
Weir and Gerstenhaber: Pleural mesothelioma and constrictive pericarditis 161
nevertheless was felt to most likely have
had a benign asbestos-related effusion
given the pleural abnormalities on the
computed tomography (CT)a scan.
S.H. was followed serially with phys-
ical examination and chest radiographs.
The pleural effusions did not reaccumulate
and he remained asymptomatic. Two years
later, he was admitted to hospital for new
onset atrial fibrillation with liver enzyme
abnormalities. He now reported dyspnea
on exertion, peripheral edema, and weight
loss. A repeat chest CT scan (Figure 1) at
that time showed a new right-sided pleural
effusion with a moderate sized pericardial
effusion. Physical examination was now
remarkable for an irregular pulse of 60,
blood pressure of 110/60 mmHg, respira-
tory rate of 22 breaths per minute, distend-
ed neck veins without Kussmaul's sign,
distant heart sounds without a diastolic
knock, hepatomegaly without ascites, and
moderate pedal edema. Electrocardiogram
now showed diffuse nonspecific T wave
abnormalities with diminished voltage.
Echocardiogram demonstrated the pericar-
dial effusion without right heart compro-
mise. Both visceral and parietal pericardi-
um were thickened with fibrinous strand-
ing, and a thick pericardial peel adherent
to the surface of the epicardium was noted.
The patient's dyspnea improved with
diuresis, anticoagulation, and rate control.
A right and left heart catheterization
revealed elevated pressures in all cham-
bers and equalization of diastolic pres-
sures. A coronary arteriogram showed
minimal three-vessel disease with pre-
served left ventricular systolic function.
With the diagnosis of constrictive
pericarditis and persistence of pleural effu-
sions, there was rising concern for
mesothelioma of the pleura and pericardi-
um. An open video-assisted thoracoscopy
and pericardial biopsy were performed,
with creation of a pericardial window. The
pathologic evaluation of the parietal pleu-
ra was consistent with malignant mesothe-
lioma, but the pericardial tissue showed
only chronic inflammation and fibrosis.
The pericardial fluid was bloody, and cyto-
logic examinations demonstrated reactive
mesothelial cells without malignant fea-
tures. Concomitant biopsies of the peri-
toneum and diaphragm also failed to show
malignancy.
Clinically, S.H. continued to deterio-
rate steadily. Treatment with chemothera-
py and/or radiation was declined, and S.H.
died three weeks later of respiratory insuf-
ficiency.
DISCUSSION
Mesothelioma is a well recognized
malignancy of mesodermal tissue. It com-
monly affects the pleura and peritoneum,
and less commonly the pericardium. The
association between asbestos exposure
and mesothelioma was first alluded to in
the 1940s. Later observations of the high-
er incidence of mesothelioma in workers
exposed to asbestos solidified this associ-
ation. A rising incidence of this malignan-
cy is now seen due to the latent develop-
ment of the disease after exposures 20 to
40 years ago. The most common reaction
to asbestos is pleural plaque formation
seen 20 years or longer after exposure [1].
Pleural effusions are seen less commonly.
The effusions are typically exudative and
bloody [2]. A similar response may occur
in the pericardium. The latter reaction was
first noted in the 1950s, when Beck's pro-
cedure was performed for myocardial
revascularization. The operation entailed
opening the pericardial sac, scoring the
epicardial layer and sprinkling asbestos
onto the epicardium in hopes of generat-
ing collateral circulation. A fibrotic reac-
tion then ensued, occasionally creating a
constrictive pericardium [3, 4]. More
recently, several cases of occupational
asbestos exposure have been described
that have also resulted in constrictive peri-
carditis [5, 6]. Our patient had a bloody
162 Weir and Gerstenhaber: Pleural mesothelioma and constrictive pericarditis
pleural effusion in the setting of calcified
pleural plaques, thrombocytosis, and an
elevated sedimentation rate. Initially, his
history, physical examinations, radi-
ographs and laboratory results of the
pleural fluid ruled out other plausible
causes of exudative effusion. He was diag-
nosed with a benign asbestos-related effu-
sion, and for two years, he showed no fur-
ther evidence of pleural disease. Subse-
quently, he developed dyspnea and failure
to thrive. He demonstrated recurrent
pleural effusions, and malignancy was
confirmed by an open biopsy. He eventu-
ally died from constrictive pericarditis
which was surprisingly not of malignant
etiology.
The finding of pericardial constriction
and cardiac tamponade has previously
been described in case reports of patients
with pleural mesothelioma [7]. However,
those reports have always shown the con-
striction due to local invasion from the
pleural primary malignancy, not from
benign fibrosis of the pericardium itself.
Asbestos-induced involvement simultane-
ously of the pleura and pericardium is fre-
quently due to either an effusive-constric-
tive reaction [6] or due to mesothelioma
with local extension [8]. Mesothelioma
usually develops within the pleura and
grows contiguously, although hematoge-
nous and lymphatic metastases are possi-
ble. It is unusual to see, however, a
mesothelioma and benign fibrotic reaction
together (although mesotheliomas can be
associated with an intense desmoplastic
reaction).
Our patient had clear evidence of
pleural mesothelioma on biopsy, with a
likely related benign effusive-constrictive
pericarditis. Even though an autopsy was
not performed, the open biopsy of the peri-
cardium with sampling of all related tis-
sues and fluid failed to offer an alternate
explanation. Cultures of the tissue and
fluid failed to demonstrate an infectious
etiology for the fibrosis. It is conceivable
that the pericardium was invaded by the
mesothelioma, and the fibrosis seen in the
biopsied tissue was due to a local desmo-
plastic reaction to malignant invasion. Per-
haps autopsy would have proven this.
However, the pericardial biopsies showed
chronic inflammation, and the parietal
pleura showed an epithelial mesothelioma
without fibrotic reaction. The only case
reported in the literature that is similar to
ours was by Yilling and co-workers in
1982. They described a case of primary
pericardial mesothelioma with benign
reactive fibrosis of the pleura [9].
A review of several series of patients
with pleural mesothelioma also failed to
reveal any mixed reactions to asbestos as
described in our patient. Roberts reviewed
32 cases of pleural mesothelioma in 1976.
Involvement of the heart occurred in six
percent of their series, specifically pericar-
dial and epicardial involvement by tumor
without benign fibrosis [10]. Chahinian
and co-workers in 1982 published a
prospective evaluation of 69 patients with
mesothelioma [11]. The pericardium was
replaced by tumor in 12 percent, and the
heart was invaded in 4 percent of their
patients. None had benign fibrotic involve-
ment. Ruffie and co-workers in 1989
reviewed 332 patients with pleural
mesothelioma [12]. In their series, 49 per-
cent of patients had pericardial involve-
ment at autopsy, and 5 percent died from
pericardial constriction or tamponade. The
pericardial involvement, however, was not
described as a fibrotic or benign process.
Two other series of 140 and 180 patients,
respectively, with pleural mesothelioma
did not find pericardial involvement [13,
14].
The pericardium can rarely be the pri-
mary source of mesothelioma. Although
several cases have described this subtype
of mesothelioma [15, 7], the incidence is
likely lower than case reports would have
us believe given the definition of a true pri-
mary pericardial mesothelioma, as
Weir and Gerstenhaber: Pleural mesothelioma and constrictive pericarditis 163
described by Anderson and Hansen in
1974 [16]. In conclusion, we report a
unique case of asbestos-related bloody
pleural effusions with later development of
pleural mesothelioma. The patient's death,
however, was due to a benign effusive-
constrictive pericarditis, more likely than
not caused by asbestos.
ACKNOWLEDGEMENT: We would like to
thank Dr Richard A. Matthayfor his assistance
in completing this paper
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A Case of Pleural Mesothelioma with Effusive-Constrictive Pericarditis

A 77-year-old man with progressive dyspnea on exertion.

Asbestos induced pericardial effusion and constrictive pericarditis. Thorax 46:429-432,

Asbestos-related lung disease. In: Fishman's Pulmonary Diseases and Disorders.

Chronic constrictive pericarditis associated with asbestosis.

Constrictive pericarditis late after the Beck operation.

Diffuse malignant mesothelioma of the pleura in Ontario and Quebec: a retrospective study of 332 patients.

Distant visceral metastases in pleural mesothelioma.

Malignant epithelial mesothelioma presenting as cardiac tamponade.

Malignant mesothelioma arising after direct application of asbestos and fiber glass to the pericardium.

Malignant mesothelioma of the pleura: clinical aspects and symptomatic treatment.

Malignant mesothelioma: prognostic variables in a registry of 180 patients, the Dana-Farber Cancer Institute and the Brigham andWomen's Hospital experience over two decades,

Pericardial constriction caused by primary mesothelioma.

Pericardial mesothelioma. Chest 81:520-523,

Prevalence and incidence of benign asbestos pleural effusion in a working population.

https://www.inovaideas.org/cgi/viewcontent.cgi?article=1018&amp;context=lung_articles

A case of pleural mesothelioma with effusive-constrictive pericarditis.

A case of pleural mesothelioma with effusive-constrictive pericarditis.

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