key: cord-286293-f5qg7vcz authors: Ullah, Waqas; Saeed, Rehan; Sarwar, Usman; Patel, Rajesh; Fischman, David L. title: COVID-19 complicated by Acute Pulmonary Embolism and Right-Sided Heart Failure date: 2020-04-17 journal: JACC Case Rep DOI: 10.1016/j.jaccas.2020.04.008 sha: doc_id: 286293 cord_uid: f5qg7vcz Abstract A patient with Coronavirus Disease-2019 (COVID-19) developed sudden shortness of breath and hypoxia. She was diagnosed with a massive pulmonary embolism (PE) complicated by right sided heart failure, which was successfully managed conservatively. This marks the first report of COVID-19 induced PE in association with acute heart failure. The patient was febrile (100.2F°) and tachycardic with a heart rate of 120 beats per minute. Her arterial oxygen saturation (SaO 2 ) was 97% on 2 liters of supplemental oxygen. Physical examination demonstrated coarse crackles in the bilateral lower lung fields. Her past medical history included hypertension and diabetes mellitus. The differential diagnosis included community acquired pneumonia, atypical pneumonia and COVID-19. Laboratory investigation revealed leukopenia (2.6 K/uL), elevated lactate dehydrogenase (LDH) of 812 U/L, C-reactive protein of 56 mg/L and a d-dimer level of 1280 ng/mL. A rapid influenza test was negative. The electrocardiogram (EKG) was unremarkable. (Figure 1 ) Computed tomography (CT) of the chest revealed bilateral interstitial densities consistent with an infectious or inflammatory process and no evidence of pulmonary embolism. (Figure 2a ) She was started on intravenous fluids, prophylactic dose of enoxaparin and broad-spectrum antibiotics including vancomycin, levaquin and cefepime due to high suspicion for pneumonia. She was also tested for COVID-19. The following day her real-time fluorescence polymerase chain reaction for SARS-CoV-2 returned positive. Her symptoms improved with supportive measures, antibiotics were discontinued and a plan was made to discharge her home to self-quarantine. However, prior to discharge she developed sudden severe dyspnea while walking in her room. She was noted to be hypoxic with her SaO 2 dropping to 83% with a resultant oxygen requirement of 6 liters by nasal The patient was started on therapeutic enoxaparin and was closely monitored for hemodynamic instability. She declined to take hydroxychloroquine, recommended for management for COVID-19. She remained hemodynamically stable and was transitioned to oral anticoagulant therapy (apixaban) with plans to continue anticoagulation for 6 months. The novel CoronaVirus Disease 2019 (COVID-19) outbreak is an unprecedented global public health challenge. Since the end of December 2019, when the first cases of novel Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) were detected in Wuhan, China, the disease has spread exponentially. [1] On January 30, 2020, the World Health Organization (WHO) declared the disease caused by the novel coronavirus (COVID-19) a public health emergency of international concern (PHEIC) later officially upgrading it as a global pandemic. As of April 2, 2020, more than 980,000 confirmed cases from over 177 countries and more than 50,000 deaths have been documented worldwide. The projected United States (US) death toll is greater than 240,000 with an estimated total burden of more than 1 million COVID-19 cases. In approximately 88% of cases, fever is the most common presentation, followed by cough (68%), vomiting (5%) and diarrhea (3.8%). [2] In up to 15% of patients, the natural course of the disease is complicated by severe interstitial pneumonia, which can lead to acute respiratory distress syndrome (ARDS), multi-organ failure including acute kidney injury, disseminated intravascular coagulation and death. [2] To our knowledge, there have been no reported cases of COVID-19 complicated by massive pulmonary embolism and right-sided heart failure. During the SARS-CoV-1 epidemic of 2014, the reported incidence of deep venous thrombosis and pulmonary embolism in affected patients was about 20% and 11%, respectively. [3] So far, there has been no concrete data on the overall incidence of thrombosis in patients with SARS-CoV-2 infection. [3] It is, however, estimated that about 50% of these patients have elevated ddimer levels during disease progression which is directly associated with the risk of increased thrombosis and poor prognosis of the disease. [2, 5] Multivariable regression showed increased odds of in-hospital death associated with d-dimer greater than 1 μg/mL (18·42, 2·64-128·55; p=0·0033). [4] A higher risk of vessel thrombosis has been correlated with the severity of the disease and multiorgan involvement, leading support to the argument of therapeutic anticoagulation of COVID-19 patients with elevated d-dimer levels. [5] The proposed mechanisms for COVID-19 induced thrombosis include a disease-specific hypercoagulable state, cytokine-mediated diffuse microvascular damage and in some cases reactive thrombocytosis. [6] The risk of thrombosis and pulmonary embolism can further be compounded by obesity, advanced age, and hospitalization related immobilization. In the present case, the patient had elevated CRP and d-dimer levels with no other risk factor for pulmonary embolism, indicating COVID-19 related hypercoagulable state as possible etiology for thrombosis in the pulmonary vasculature. Patient remained asymptomatic with no further episodes of breathlessness or hypoxia at 1-week follow-up. She remains on apixaban with plans to follow up with a Hematologist in 1 month. As patients with COVID-19 are admitted for treatment and isolation, it is imperative to follow prophylactic measures for avoiding venous thromboembolism. Sudden deterioration in respiratory status not explained by significant radiological changes in the lung fields, and especially in conjunction with high titers of d-dimers should raise suspicion for pulmonary embolism. More studies are needed to determine the utility of therapeutic doses of anticoagulation in high-risk patients with COVID-19. • To be able to make a differential diagnosis of pulmonary embolism in patients with COVID-19 with sudden onset of dyspnea and hypoxemia. • To understand the potential role of early anticoagulation in high-risk patients with COVID-19. A novel coronavirus from patients with pneumonia in China Clinical characteristics of coronavirus disease 2019 in China Analysis of deaths during the severe acute respiratory syndrome (SARS) epidemic in Singapore: challenges in determining a SARS diagnosis Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study Anticoagulant treatment is associated with decreased mortality in severe coronavirus disease 2019 patients with coagulopathy Characteristics, causes, diagnosis and treatment of coagulation dysfunction in patients with COVID-19. Zhonghua xue ye xue za zhi= Zhonghua xueyexue zazhi Axial unenhanced chest CT scan obtained on day 1 after the onset of symptoms shows bilateral areas of ground-glass interstitial opacities. b, CT pulmonary angiography demonstrates multiple bilateral filling defects involving lobar, segmental, branches of the pulmonary artery (yellow arrow) and linear saddle pulmonary embolus Figure 3a: Parasternal short-axis view of the heart showing a dilated right ventricle (red arrow). b, Doppler echocardiographic view of severe tricuspid regurgitation