Pulmonary artery thrombosis in COVID-19 patients

Arising in China in the winter of 2019, COVID-19 (caused by the SARS-CoV-2 virus) has caused a global pandemic and severely stressed medical systems across the world. Although knowledge about this novel coronavirus is still emerging, the most common reason for hospitalization of COVID-19 patients is severe respiratory distress.1 COVID-19 has been accurately described as the cause for a proinflammatory and hypercoagulable state with marked elevations seen in Lactate Dehydrogenase, Ferritin, Creactive protein, D-Dimer, and Interleukin levels.2 The inflammatory response, including production of inflammatory cells and cytokines, induces a procoagulant effect and diffuse endothelial damage that predisposes thrombotic vascular lesions and Disseminated Intravascular Coagulation (DIC).3 D-Dimer is related to the severity of the disease and an increased value is associated with the worst. prognosis. Retrospective studies demonstrated that patients admitted to Intensive Care Unit (ICU) had an elevated D Dimer value and, in this setting, some Authors recommended a therapeutic heparin doses for the patients with higher values.4 A recent ICU observation reported an increased risk of Pulmonary Embolism (PE) in COVID-19 compared to the historical control group even in patients that had undergone the Low Molecular Weight Heparin (LMWH) prophylaxis.5 We evaluated 138 patients with COVID 19 admitted to our Institution between March 2020 and May 2020. All patients were COVID 19 positive according to clinical diagnostic criteria reverse-transcription---polymerase chain-reaction (RT-PCR) and Chest Thoracic tomography. On admission, most of them were haemodynamically stable (78%) and febrile (87%). During hospitalization, some developed progressive respiratory failure and received oxygen supplementation (41%). Four of them were started on Continuous Positive Airways Pressure (CPAP) but two died because of worsening Respiratory Failure. All patients were treated with hydroxycloroquine (400 mg/day), darunavir/ritonavir (800/100 mg/day) and enoxaparin (4000 UI/day). Some patients (26 pts) received additional therapy with IL-6 and IL-1 antagonist (20%). Every three days after their hospitalization, laboratory exams with