Case Presentation: A 76-year-old Hispanic male with a past medical history of well-controlled hypertension, Pre-diabetes, class 3 obesity, unprovoked Deep vein thrombosis (DVT) progressing to pulmonary embolism (PE) diagnosed 6 months ago, treated with apixaban, presented to the ED with 2 weeks history of progressively worsening dyspnea, dry cough and orthopnea. Denies any chest pain, fever, rhinorrhea, chills, myalgias, nausea, vomiting, weight loss, appetite change. Transthoracic echocardiography (TTE) done 6 months ago showed preserved ejection fraction, aortic valve stenosis, and no pericardial effusion. Vitals signs on presentation were unremarkable. Chest exam was within normal limits. On cardiac exam, friction rub was noted with ejection systolic murmur, Jugular venous distension (JVD) was absent on admission. EKG with normal sinus rhythm with nonspecific ST and T wave abnormality. The initial investigation included complete cell count, comprehensive metabolic panel, coagulation panel, and cardiac troponin all of which were unremarkable. D-dimer was 1,352ng/ml and Covid-19 PCR was positive. CT pulmonary Angiogram (Fig. 1) showed small pericardial effusion and left-sided pleural effusion, no PE was seen. The patient was admitted for close monitoring. Subsequently, he developed positive JVD and tachycardia within 48 hours of admission. Repeat TEE showed moderate circumferential pericardial effusion with signs of impending tamponade including a respiratory variation of the mitral valve and the mild inward mid-diastolic motion of the free Right ventricular wall. Emergent IR-guided pericardiocentesis was performed that confirmed gross blood in pericardial effusion i.e, hemopericardium resulting in significant clinical improvement in our patient.

Discussion: Only a few cases have been reported to date with pericardial effusions/tamponade in COVID-19. There are several hypotheses of the pathogenesis of pericardial effusion in COVID-19 patients such as the indirect effect of cytokine production, activation of ACE 2 signaling pathway, and severe hypoxia leading to myocardial stress injury. However, the presence of the direct effect of COVID-19 in pericardial effusion still seems to be unknown. One observation noted during the literature review is that significant pericardial effusion leading to tamponade occurs mostly as a late complication of Covid -19 disease which was also evident in our case. Autoimmune, infectious, and malignancy work-up was negative for our patient. Fluid analyses were significant for 40k RBC, 1.9k WBC with neutrophilic predominance, LDH of 1011, and total protein of 5.8 which favors an exudative effusion just concurrent with most of the previously published case reports. We believe that it remains a diagnosis of exclusion at this point as limited availability to run PCR tests on pericardial fluid detecting the virus.

Conclusions: In the absence of malignancy and autoimmune disease, COVID-19 is the most likely cause of this patient’s hemorrhagic pericardial effusion. Although the patient was on apixaban for the last six months, the symptoms of cardiac tamponade only started after the patient tested positive for COVID-19. With the limitation of data and guidelines on the pathogenesis and prevention of cardiac tamponade in COVID-19 as well as the detection of new variants such as Delta and Omicron, physicians may expect rare presentations of the disease.