key: cord-285395-vybruu3o authors: Polat, Veli; Bostancı, Güngör İlayda title: Sudden death due to acute pulmonary embolism in a young woman with COVID-19 date: 2020-05-11 journal: J Thromb Thrombolysis DOI: 10.1007/s11239-020-02132-5 sha: doc_id: 285395 cord_uid: vybruu3o Coronavirus disease 2019 (COVID-19) is an infectious disease that primarily affects the respiratory system, but it may cause cardiovascular complications such as thromboembolism. Rarely, pulmonary embolism may be encountered in patients with severe COVID-19 infection, especially in intensive care units. An asymptomatic young case of COVID-19 presenting with sudden death due to acute massive pulmonary embolism has not been previously described. We report a 41-year-old woman presented to emergency department with sudden death during physical activity. She had only history of diabetes mellitus and she was asymptomatic until sudden death. CT pulmonary angiography and chest CT scans revealed acute massive embolism and typical imaging findings of COVID-19 pneumonia, respectively. Interestingly, the patient had no symptoms or signs of infection and also had no risk factors for thromboembolism. COVID-19 infection appears to induce venous thromboembolism, especially pulmonary embolism. The case is remarkable in terms of showing how insidious and life-threatening COVID-19 infection can be. Coronavirus disease 2019 (COVID-19) is a clinical syndrome caused by infection with the novel coronavirus called severe acute respiratory syndrome coronavirus 2. COVID-19 is an infectious disease that primarily affects the respiratory system, but it can also cause other complications, such as cardiovascular problems. Although the symptoms of COVID-19 may resemble the symptoms of pulmonary embolism (PE), in some cases, PE may accompany COVID-19 [1] . Lately, cases of acute PE associated with severe COVID-19 infection have been reported. These reported cases are generally in the elderly group and there is no robust risk factor to explain acute PE [2] [3] [4] [5] . We report a case of acute massive PE, resulting in sudden death associated with COVID-19. A 41-year-old woman presented to the emergency department with sudden death during physical activity. She had no known history of disease other than diabetes mellitus and she had no history of medication usage including oral contraceptives except insulin. According to the information received from the patient's relatives, she was asymptomatic until sudden death. Spontaneous circulation was achieved in the patient after 20 min of successful cardiopulmonary resuscitation. Since she had no spontaneous breathing, she was intubated, and mechanical ventilation was initiated. Laboratory tests displayed slightly elevated C-reactive protein level of 14 mg/L, leukocytosis of 14.010/mm 3 , modest increased troponin I level of 45 pg/mL and elevated d-dimer level of 7.29 µg/mL. She was afebrile but her nasopharyngeal swab reverse transcription polymerase chain reaction test was positive for SARS-CoV-2. Her measured blood gas values were 52.8 mmHg for partial oxygen pressure and 84.3 mmHg for partial carbon dioxide pressure. Straight after these tests, her 12-lead electrocardiogram was obtained and it revealed sinus tachycardia, ST elevation in V 1 ≥ 1 mV and in a VR ≥ 1 mV, Qr in V 1 , prominent S wave in lead I. An immediate hand-held echocardiogram showed right ventricular systolic dysfunction, enlargement in the right heart chambers and moderate tricuspid regurgitation. In computed tomography (CT) pulmonary angiography, the diagnosis of acute massive pulmonary embolism was made after detecting that the right and left pulmonary arteries were partially obliterated with thrombus ( Fig. 1) . Simultaneous chest CT scan determined peripheral ground-glass opacities in bilateral lung parenchyma with consolidation in the left upper lobe (Fig. 2) . The chest CT scan findings of the patient were typical for COVID-19 pneumonia [6, 7] . She had no known risk factor for venous thromboembolism. In addition, thrombus was not detected in the bilateral lower extremity venous Doppler examination. She was promptly treated with intravenous tissue plasminogen activator (100 mg/2 h) and subcutaneous enoxaparin (1 mg/kg twice a day). She had a sudden cardiac arrest within the 4 h of the thrombolytic therapy. Unfortunately, despite early cardiopulmonary resuscitation in the intensive care unit, spontaneous circulation was not achieved, and she was declared dead. COVID-19 may lead to arterial and venous thromboembolic events by either inducing excessive systemic inflammatory response, procoagulant activity, immobilization, and hypoxia, or causing disseminated intravascular coagulation [3, 8, 9] . A few cases and trials of acute PE associated with COVID-19 infection have recently been reported [2, 3, 5, 10]. To the best of our knowledge, this is the first reported case of COVID-19 infection, which was presented with acute massive PE without any symptoms of COVID-19 infection. This case suggests that sudden, unexpected deaths outside of hospital may also be associated with COVID-19 infection during the pandemic period. COVID-19 pneumonia was detected in addition to massive PE during chest CT imaging, which was planned according to electrocardiogram and echocardiographic findings compatible with pulmonary embolism. Viral infections may induce coagulopathy by affecting coagulation cascade, fibrinolysis and primary hemostasis. Particularly, respiratory tract viral infections are known to raise the risk of deep venous thrombosis and PE. In severe acute respiratory syndrome caused by coronaviruses between 2003 and 2004, the occurrence of pulmonary infarction has been reported due to damage in small and medium-sized pulmonary vessels, deep vein thrombosis, diffuse intravascular coagulation and pulmonary thromboembolism [11] . COVID-19 infection appears to trigger venous thromboembolism, especially PE, even without underlying risk factor. It should be kept in mind that patients who are admitted to the hospital with a clinical picture of PE without signs and symptoms of infection during pandemic may also have COVID-19 infection. This case also emphasizes the importance of anticoagulant therapy in the prevention of thromboembolic complications in COVID-19 patients. Furthermore, in the case of sudden clinical deterioration, hypoxia, hemodynamic deterioration or cardiac arrest in COVID-19 patient during the follow-up, acute PE should be considered even if the patient is receiving anticoagulant therapy. 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