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the right atrium is the ﬁrst chamber aﬀected, followed closely
by the left atrium. Second, as the pericardial pressure progressively increases, the right ventricle free wall starts to collapse
during diastole. Due to its higher intracavitary pressure, the left
ventricle is the last chamber aﬀected by the rising pericardial
pressures. Only late in the tamponade progression, the interventricular septum shifts toward the left ventricle, impairing
its ﬁlling and also the systolic function. However, even with
a large pericardial eﬀusion, a left ventricular free wall collapse
is uncommon (6).
In 1991, Kisanuki et al (8) indicated that large pleural effusions can also be responsible for the clinical and
echocardiographic signs of tamponade despite the traditional
link between cardiac tamponade and accumulation of ﬂuid in
the pericardial space. Experimental evidence in canine models
corroborated the clinical experience, when euvolemic canines
developed cardiac tamponade regardless of whether it was induced by intrapericardial or intrapleural ﬂuid infusion (6). Right
ventricular diastolic collapse was observed in both groups, and
its onset occurred at a similar intrapericardial pressure. During intrapleural ﬂuid infusion, intrapleural and intrapericardial
pressures rose in the same manner (6). Subsequently, other case
reports demonstrated the development of clinical echocardiographic and Doppler ultrasound signs of cardiac tamponade
in patients with pleural eﬀusions and otherwise insigniﬁcant
pericardial eﬀusions; drainage of pleural ﬂuid in these patients
resulted in hemodynamic improvement (6-9). As in our report, the tamponade physiology resolution after pleural eﬀusion drainage strongly suggests a direct and signiﬁcant eﬀect
of concomitant large pleural eﬀusions in addition to mild to
moderate pericardial eﬀusions in causing tamponade as a severe
hemodynamic complication.
Pericardial ﬂuid analysis in a myxedema coma patient
usually demonstrates a high protein and cholesterol content;
however, that study is not routinely part of the immediate
diagnostic workup (10). As it requires invasive procedures
and has no evident implications in initial management of
myxedema coma, a diagnostic pericardial tap is reserved for
patients who do not respond to standard treatment with thyroid hormone replacement when an alternative diagnosis is
considered (2, 10). In the reported case, the patient's pres-

July 2017

entation was compatible with myxedema coma and a therapeutic pericardiocentesis was planned for the only purpose
of relieving the cardiac tamponade and the hemodynamic
compromise. As the cardiac eﬀusion promptly resolved after
the initial pleural tap and no pericardial eﬀusion was noted
in the subsequent echocardiogram performed 12 hours later,
no aggressive eﬀorts to drain and sample the pericardial ﬂuid
were deemed necessary.
In summary, although a rare consequence of severe hypothyroidism, cardiac tamponade is a life-threatening condition. Cardiac tamponade may occur secondary to high intrapericardial
pressure generated by signiﬁcant pleural eﬀusions despite being
usually linked with the presence of moderate to large pericardial
eﬀusion. As illustrated by our report, in patients presenting with
both pleural and pericardial eﬀusions, thoracentesis is probably the safest initial procedure to perform and might result in
complete recovery of hemodynamic status.
1.

Salomo LH, Laursen AH, Reiter N, Feldt-Rasmussen U. Myxoedema
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2. Majid-Moosa A, Schussler JM, Mora A. Myxedema coma with cardiac
tamponade and severe cardiomyopathy. Proc (Bayl Univ Med Cent)
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3. Lin CT, Liu CJ, Lin TK, Chen CW, Chen BC, Lin CL. Myxedema
associated with cardiac tamponade. Jpn Heart J 2003;44(3):447-450.
4. Arvan S. Pericardial tamponade in a patient with treated myxedema. Arch
Intern Med 1983;143(10):1983-1984.
5. Vaska K, Wann LS, Sagar K, Klopfenstein HS. Pleural eﬀusion as a cause
of right ventricular diastolic collapse. Circulation 1992;86(2):609-617.
6. Klopfenstein HS, Wann LS. Can pleural eﬀusions cause tamponade-like
eﬀects? Echocardiography 1994;11(5):489-492.
7. Saito Y, Donohue A, Attai S, Vahdat A, Brar R, Handapangoda I,
Chandraratna PA. The syndrome of cardiac tamponade with "small"
pericardial eﬀusion. Echocardiography 2008;25(3):321-327.
8. Kisanuki A, Shono H, Kiyonaga K, Kawataki M, Otsuji Y, Minagoe S,
Nakao S, Nomoto K, Tanaka H. Two-dimensional echocardiographic
demonstration of left ventricular diastolic collapse due to compression
by pleural eﬀusion. Am Heart J 1991;122(4 Pt 1):1173-1175.
9. Traylor JJ, Chan K, Wong I, Roxas JN, Chandraratna PA. Large pleural
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Thoracentesis-reverting cardiac tamponade physiology in a patient with myxedema coma and large pleural effusion

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https://doi.org/10.1136/bcr-2013-203223 https://doi.org/10.1136/bcr-2013-203223

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