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Woei WS (2021). Pericardial Tamponade in COVID-19: A Case Report. SunText Rev Case Rep Image 2(2): 124.
1
SunText Review of Case Reports & Images Open Access
ISSN: 2766-4589 Case Report
Volume 2:2
Pericardial Tamponade in COVID-19: A Case
Report
Woei WS*
Department of Cardiology, Tan Tock Seng Hospital, Singapore
*Corresponding author: Woei WS, Department of Cardiology, Tan Tock Seng Hospital, 11
Jalan Tan Tock Seng, Singapore; E-mail: shiun_woei_wong@ttsh.com.sg
Abstract
Background: Tuberculous pericarditis is a rare manifestation of tuberculosis infection. COVID-19 pandemic poses a challenge in
detecting uncommon disease. Pericardial effusion with tamponade has been described with COVID-19 but the association with
tuberculosis is not yet known.
Case summary: A 47-year-old man was admitted with symptoms of COVID-19 infection. Rapid progression of cardiomegaly on
radiograph with clinical deterioration were suggestive of pericardial tamponade. Urgent pericardiocentesis revealed hemoserous fluid,
elevated adenosine deaminase and positive TB PCR. He was started on anti-tuberculous therapy and Remdesivir with marked
improvement of symptoms. Repeat echocardiogram and CT Thorax showed resolution of pericardial fluid and patient was discharged
well.
Discussion: This case highlights the difficulty in detecting a concomitant rare but important disease. The development of massive
pericardial tamponade acutely is not pathognomonic for COVID-19, and a careful diagnostic process involving multi-modality
imaging, occurred to arrive at a diagnosis of tuberculosis.
Keywords: COVID-19; Pericardial effusion; Tamponade; Tuberculosis; Pericarditis; Case report
Introduction
Tuberculous pericarditis is rare and associated with significant
morbidity and mortality [1]. We present the case of a patient
admitted with symptoms of COVID-19 infection that developed
pericardial tamponade subsequently. Urgent pericardiocentesis
revealed evidence of tuberculous pericarditis and he was
appropriately managed.
Case Presentation
A 47 year old gentleman presented with productive cough,
pleuritic chest pain and fever for two days. Physical examination
revealed a febrile, generally ill appearing gentleman. He had a
regular pulse, S1/S2 were normal without murmurs or rub. Lung
examinations revealed left basal crepitations. Vital signs were
blood pressure 130/83 mmHg, heart rate 104 beats/min, oxygen
saturation 97% on room air, respiratory rate 16/min, and
temperature 38oC. Chest radiograph showed left lower zone
retrocardiac opacities and he was transferred to the isolation ward.
SARS-CoV-2 PCR came back positive from his nasopharyngeal
swab. The patient did not have any significant medical history. He
denied travel but he was in close contact with a colleague with
COVID-19. He came from a TB endemic area (Figure 1).
On day 3 of hospitalization he deteriorated requiring 4L nasal
cannula to achieve SpO2 94%. His BP was 125/80mmHg, his rate
rate 110 beats/min and he had tachypnea 20/min. There was no
evidence of heart failure or tamponade. Electrocardiogram (ECG)
showed sinus tachycardia with normal QRS complexes. High
sensitive troponin I was 4 ng/ml (normal values: <14 ng/ml).
There was absolute monocytosis (0.92 x 109/L) and elevated C-
reactive protein (CRP) at 134.7 mg/L (normal values < 5 mg/L).
A repeat chest radiograph showed marked increased in heart size.
He was started on active drug remdesivir as a part of an ongoing
trial (Figures 2 and 3).
Subsequent ECG revealed persistent sinus tachycardia and no
evolution of ST-T wave changes. Labs were remarkable for
Received date: 10 July 2021; Accepted date: 12 July
2021; Published date: 17 July 2021
Citation: Woei WS (2021). Pericardial Tamponade in
COVID-19: A Case Report. SunText Rev Case Rep
Image 2(2): 124.
DOI: https://doi.org/10.51737/2766-4589.2021.024
Copyright: © 2021 Woei WS. This is an open-access
article distributed under the terms of the Creative
Commons Attribution License, which permits
unrestricted use, distribution, and reproduction in any
medium, provided the original author and source are
credited.
Woei, SunText Rev Case Rep Image (2021), 2:2
Citation:
Woei WS (2021). Pericardial Tamponade in COVID-19: A Case Report. SunText Rev Case Rep Image 2(2): 124.
monocytosis (1.02 x 109/L). Liver function tests and coagulation
panel were normal. Arterial blood gas showed acute respiratory
alkalosis with pH 7.48, pCO2 39, pO2 68, Bicarbonate of 29 on 3L
nasal cannula. Lactate was raised at 2.7 mmol/L (normal value <
2 mmol/L).
Figure 1: Chest radiograph showed left retrocardiac opacities. Cardiac silhouette appears normal.
Figure 2: ECG: sinus tachycardia with normal QRS complexes.
Transthoracic echocardiogram demonstrated hyperdynamic left
ventricle with LVEF of 65%. There was right atrial collapse,
diastolic collapse of right ventricle, 3.5 cm of pericardial effusion
and plethoric inferior vfiena cava of 2.2 cm with < 50%
variation.The effusion was noted to be complex with fibrin
deposits adhering to the myocardium. The transmitral flow
variation was 30% and transtricuspid variation was 50%. The
patient was transferred to the intensive care unit. The patient
developed sinus tachycardia (range up to 130 beats per minute)
with concomitant febrile episodes of 39oC. Pericardiocentesis was
performed in view of persistent tachycardia and rapid
accumulation of pericardial effusion. The procedure was done
under echocardiographic guidance. Pericardiocentesis yielded 900
mL of hemoserous fluid [fluid lactate dehydrogenase (LDH)
2,253 IU/L, fluid/serum LDH > 0.6]. Cytology was negative for
malignancy. Adenovirus PCR, Enterovirus PCR and SARS-CoV-
2 PCR were negative. Acid fast bacilli was detected and TB PCR
was positive. Fluid microscopy revealed predominantly nucleated
cells (8,513 cells/uL) with 91% lymphocytes. Adenosine
deaminase for pericardial fluid was significantly elevated at
Woei, SunText Rev Case Rep Image (2021), 2:2
Citation:
Woei WS (2021). Pericardial Tamponade in COVID-19: A Case Report. SunText Rev Case Rep Image 2(2): 124.
44U/L (normal value < 20U/L). Retroviral screen was negative.
The immediate resolution of tachycardia (heart rate reduced to
80-90 beats per minute) signifies the hemodynamic improvement
gained from relieving the tamponade. The pericardial effusion
was highly diagnostic of tuberculous pericarditis in the absence of
coagulopathy, malignancy and autoimmune etiologies. He was
commenced on rifampicin, isoniazid, ethambutol and
pyrazinamide. Subsequent echocardiogram showed resolution of
effusion with marked improvement of symptoms. A follow up CT
Thorax revealed left lung lower lobe collapse-consolidation, small
pleural effusion with marked reduction in pericardial effusion
(Figure 4).
Figure 3: Chest radiograph showed persistent opacities over left
retrocardiac region. Interval increased in cardiomegaly.
Figure 4: CT Thorax showed left lower lobe collapse-consolidation with
small pleural effusion. Minimal pericardial effusion.
He was discharged after 2 weeks into anti-tuberculous therapy.
Subsequently, he was reviewed during follow up (4 weeks post
discharge) with resolution of pericardial effusion and residual left
retrocardiac consolidation on chest X-ray.
Discussion
Ever since the first cases of pneumonia of unknown origin were
described in Wuhan, China in January 2020, COVID-19 has
rapidly spread worldwide resulting in a public health emergency.
Complications described in the Intensive Care Unit (ICU) include
shock, Acute Respiratory Distress Syndrome (ARDS),
arrhythmias and acute cardiac injury.2 Case reports of cardiac
involvement including Acute ST-Elevation Myocardial infarction,
myocarditis, stress cardiomyopathy and arrhythmias have also
been reported [2-5].
While viral infections such as Epstein-Barr virus, Parvovirus B19
and Coxsackievirus are known to cause pericarditis and
pericardial effusion, little is known about the pericardial
complications of COVID-19 and their pathophysiology [6]. The
fibrinoid appearance of pericardial effusion has been strongly
associated with pericardial inflammation, as in the case of
tuberculoid, bacterial or malignant pericardial effusion [7,8]. This
could also be postulated to be due to increased viral expression in
the heart via angiotensin-converting enzyme 2 (ACE2) as the
entry receptor, resulting in an inflammatory response, although
more studies are required to substantiate this [9]. The appearance
of fibrin, lymphocyte rich, elevated adenosine deaminase level
with detection of acid fast bacilli and positive TB PCR in the
pericardial fluid is pathognomonic of tuberculous involvement
[1,11]. There is a possibility that COVID-19 infection induced an
inflammatory response that serves as a nidus for TB reactivation
in this patient. In addition, this may explain the rapid progression
of pericardial tamponade as TB normally runs an indolent course.
TB pericarditis is closely linked to constrictive pericarditis with
significant morbidity and mortality.1 Follow-up is required to
detect the development of constrictive pericarditis. Treatment
with steroids may shorten the time to resolution of symptoms,
such as tachycardia and restriction of activity. However, this was
not shown to reduce mortality or retard the progression to
irreversible constrictive pericarditis [12].
Case series from Italy reported 20 patients with active TB who
developed COVID-19 infection subsequently, but none was
associated with pericarditis or tamponade [13].
Conclusion
In conclusion, TB pericarditis is a rare manifestation of rapid
development of massive pericardial effusion. The presence of TB
pericarditis, and consequently its risk, may not be easily identified
in the face of COVID-19 pandemic. Thus, a low threshold to use
serial echocardiography and dedicated imaging modalities,
including CT may be appropriate, particularly in young patient
Woei, SunText Rev Case Rep Image (2021), 2:2
Citation:
Woei WS (2021). Pericardial Tamponade in COVID-19: A Case Report. SunText Rev Case Rep Image 2(2): 124.
who deteriorate at an alarming speed. Noteworthy, to the best of
our knowledge, the current case comprises the first case of
concurrent tuberculous pericarditis with tamponade in COVID-
19.
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