Article Type : Case Report
Authors : Woei WS
Keywords : COVID-19; Pericardial effusion; Tamponade; Tuberculosis; Pericarditis; Case report
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.
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.
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 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 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.
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.
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].
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 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.