Baylor University Medical Center Proceedings July 2017 - 296

Figure 2. Additional diagnostic imaging. (a) Plethoric inferior vena cava without respiratory variation, which is supportive of tamponade physiology, and (b) respiratory
variation >25% in mitral inflow with pulse wave Doppler. (c, d) Point-of-care echocardiography, subcostal long-axis view, showing (c) right atrium collapse during
systole and (d) normal appearance on diastole.

had a portable chest radiograph and a limited transthoracic
echocardiogram showing large pericardial eﬀusion and large,
left-sided pleural eﬀusion (Figure 1). Obstructive shock secondary to cardiac tamponade was considered and reiterated
by the echocardiogram ﬁndings of a plethoric inferior vena
cava without respiratory variation in its diameter of 2.63 cm
(Figure 2a), respiratory variation higher than 25% in mitral
valve inﬂow using pulse wave Doppler (Figure 2b), and a right
atrium collapse during systole and normal appearance during
diastole (Figure 2c, 2d).
As the lung transthoracic ultrasound signaled a pleural effusion of 1.4 L by Balik's formula, and considering the patient's
large body habitus, it was decided to proceed with a thoracostomy tube placement (pigtail catheter). After the pleural
ﬂuid drainage, the patient's hemodynamic status improved dramatically, and the vasopressors were stopped. A second chest
radiograph (Figure 3a) and a comprehensive transthoracic
echocardiogram by the cardiology team (Figure 3b, 3c) were
performed; both demonstrated the nearly complete resolution
of both the pleural and pericardial eﬀusions. Pericardiocentesis
was deemed no longer necessary.
DISCUSSION
Our report illustrates a severe case of hypothyroidism presenting with myxedema coma. This condition is a medical
emergency that, despite aggressive treatment, still carries a high

mortality rate (1, 2). It can occur either as a natural progression
of hypothyroidism or be precipitated by a number of events
including acute illness, metabolic disturbances, use of opiates
or hypnotics, trauma, or cold exposure (2).
As seen in our patient, hypothermia and obtundation are
common presentations of myxedema coma. Diastolic hypertension associated with a narrowed pulse pressure is its most
described hemodynamic ﬁnding, and it can progress to hypotension once the cardiac output is reduced (2). The occurrence
of pericardial and pleural eﬀusions can be as prevalent as 80%
when myxedema coma is present (2). The increased capillary
permeability and the impaired lymphatic drainage participate
in the ongoing accumulation of ﬂuid into body cavities, raising
intrathoracic pressure and progressively restricting cardiac ﬁlling
(3). The slow onset of ﬂuid accumulation and the ability of the
pericardium to distend are possible explanations for the rare occurrence of tamponade physiology in hypothyroid patients, even
when moderate or large pericardial eﬀusions are present (3, 4).
Cardiac tamponade is caused by increased pericardial pressure leading to cardiac chamber compression and collapse. Its
presentation can range from mild hemodynamic ﬁndings to
obstructive shock and death (5-7). During the development of
cardiac tamponade, a sequence of external compression of the
cardiac chambers is usually seen. First, the atria are aﬀected by
the transmural pressure elevation, and their free wall begins to
collapse during systole. Due to its low intracavitary pressure,

Figure 3. Imaging after treatment. (a) Chest radiograph performed after thoracostomy tube placement. (b, c) Formal echocardiography exam performed under
Mayo Clinic format (opposite probe marker orientation) with subcostal long-axis views that show no pericardial effusion and no right atrium collapse during systole.
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