key: cord-0867104-p7iraa2k authors: Derveni, Vaia; Kaniaris, Evangelos; Toumpanakis, Dimitris; Potamianou, Efstathia; Ioannidou, Ilianna; Theodoulou, Danai; Kyriakoudi, Anna; Kyriakopoulou, Magda; Pontikis, Konstantinos; Daganou, Maria title: Acute Life-threatening Cardiac Tamponade in a Mechanically Ventilated Patient with COVID-19 Pneumonia date: 2020-07-02 journal: IDCases DOI: 10.1016/j.idcr.2020.e00898 sha: 37fef26e8118ef4d9b40bc947576eefb5e4cfef8 doc_id: 867104 cord_uid: p7iraa2k Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has recently evolved as a pandemic disease. Although the respiratory system is predominantly affected, cardiovascular complications have been frequently identified, including acute myocarditis, myocardial infarction, acute heart failure, arrhythmias and venous thromboembolic events. Pericardial disease has been rarely reported. We present a case of acute life-threatening cardiac tamponade caused by a small pericardial effusion in a mechanically ventilated patient with severe COVID-19 associated pneumonia. The patient presented acute circulatory collapse with hemodynamic features of cardiogenic or obstructive shock. Bedside echocardiography permitted prompt diagnosis and life-saving pericardiocentesis. Further investigation revealed no other apparent cause of pericardial effusion except for SARS-CoV-2 infection. Cardiac tamponade may complicate COVID-19 and should be included in the differential diagnosis of acute hemodynamic deterioration in mechanically ventilated COVID-19 patients. COVID-19 caused by SARS-CoV-2 has evolved as a pandemic disease affecting predominantly the respiratory system. In Europe, 5-10% of hospitalized patients with COVID-19 require admission to the Intensive Care Unit (ICU) mostly because of severe hypoxemic respiratory failure [1] . Cardiovascular complications including acute myocarditis, myocardial infarction, acute heart failure with cardiomyopathy, arrhythmias and venous thromboembolic events are frequently associated with COVID-19 [2] . As many pathophysiologic and clinical aspects of this newly recognized entity are still unknown, reports of atypical presentations and unusual complications of COVID-19 are of particular interest. In this context, we report a case of acute cardiac tamponade manifesting as obstructive shock in a mechanically ventilated patient with severe COVID-19 associated pneumonia. Abnormal laboratory tests included mild leukocytosis with low lymphocyte count (800/μL) and elevated C-reactive protein (24.77mg/dL; RR <0.5 mg/dL), ferritin (2279ng/mL; RR 11-307 ng/mL), interleukin-6 (52pg/mL; RR <5pg/mL) and d-dimer levels However, on the sixth day he developed septic shock and multi-organ failure caused by multi-drug resistant Acinetobacter baumanii and died. Pericardial effusion has been reported in 4.55% out of 2738 COVID-19 patients in a meta-analysis of chest computed tomography imaging findings [3] . Critically ill patients had higher incidence of pericardial effusion compared to less severely ill [4] . However, clinically significant pericardial disease is rare. To our knowledge, only three cases of cardiac tamponade have been reported so far [5, 6, 7] . One in a 47-yearold woman with a past history of myopericarditis, the second in a 67-year-old woman with a history of non-ischemic cardiomyopathy, and the third in a 59-year-old man six weeks after coronary artery bypass surgery. All three patients had pre-existing cardiac disease and none was on mechanical ventilation. In our case cardiac tamponade was caused by a small localized pericardial effusion and presented as life-threatening obstructive shock. It is well known that rapid accumulation of as little as 150mL of fluid may lead to marked increase in pericardial pressure and this can be accentuated by inflammatory stiffening of the pericardium [8] . Positive pressure ventilation may exaggerate the hemodynamic consequences of pericardial effusion through transmission of high positive intra-thoracic pressures to the pericardial space and may thus further compromise cardiac filling [9] . TTE permits prompt diagnosis and immediate bedside pericardiocentesis in acute life-threatening cases of cardiac tamponade [10] . Viral pericarditis is a common cause of pericardial effusion and may occasionally be complicated by cardiac tamponade. Although in most cases viral etiology is presumed by exclusion of other causes, definite diagnosis requires molecular testing of pericardial fluid and/or tissue [10] . Our patient's fluid RT-PCR for SARS-CoV-2 was J o u r n a l P r e -p r o o f negative. In only one reported case pericardial fluid tested positive, albeit for a single target gene [7] . However, RT-PCR testing has several false negative results, necessitating repeat testing after 24-48 hours in clinically suspected patients [11] . Moreover, it has been hypothesized that mechanisms other than direct virus invasion may be implicated in the pathogenesis of cardiovascular involvement in COVID-19 patients, such as auto-immune type reactions through molecular mimicry or excessive recruitment of the immune system leading to a "cytokine storm" and exaggerated systemic inflammatory response [6, 10] . Our patient's high levels of serum inflammatory markers advocate the latter mechanism as a plausible pathogenetic scenario. In conclusion, pericardial effusion causing cardiac tamponade may complicate severe COVID-19. Mechanical ventilation may exaggerate hemodynamic consequences leading to life-threatening shock necessitating prompt bedside therapeutic pericardiocentesis. VD and AK performed TTE and pericardiocentesis, DT, MK and KP contributed to data acquisition, EK, EP, II, DT prepared the draft, MD wrote the final manuscript as a corresponding author. All authors read and approved the final manuscript. Funding This report did not receive any specific grant from funding agencies in the public, commercial or not-for-profit sectors Written informed consent for publication of this case report and any accompanying images was obtained from the patient's next of kin. A copy of the written consent is available for review by the Editor-in-Chief of this journal Authors declare no conflict of interest. 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