The actual Coronavirus Disease (COVID 19) pandemic is due to Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a member of the coronavirus family. Besides the respiratory involvement, COVID 19 patients frequently develop a pro-coagulative state caused by virus-induced endothelial dysfunction, cytokine storm and complement cascade hyperactivation. It is common to observe diffuse microvascular thrombi in multiple organs, mostly in pulmonary microvessels. Thrombotic risk seems to be directly related to disease severity and worsens patients' prognosis. Therefore, the correct understanding of the mechanisms underlying COVID-19 induced prothrombotic state can lead to a thorough assessment of the possible management strategies. Hence, we review the pathogenesis and therapy of COVID 19-related thrombosis disease, focusing on the available evidence on the possible treatment strategies and proposing an algorithm for the anticoagulation strategy based on disease severity. Keywords COVID-19 • SARS-CoV-2 • Thrombosis • Anticoagulation Highlights • SARS-CoV-2 induced complement hyperactivation, endothelial dysfunction and cytokine storm have a prothrombotic effect. • COVID 19 patients develop a pro-coagulative state directly related to disease severity. • In COVID 19 critical patients, thrombotic lesions in pulmunary microvessels have a prevalence twice higher than critical non-COVID 19 patients. • Anticoagulant treatment is associated with lower mortality. Hence, we propose an algorithm for the anticoagulation strategy based on disease severity.

Latest evidences from literature suggest that SARS-CoV-2 disease 2019 (COVID-19) is commonly complicated with coagulopathy and that disseminated intravascular coagulation is present in the majority of deceased patients. Particularly, conventional coagulation parameters appear to be significantly altered in patients with poor prognosis. A wide-ranging cross- talk between coagulative haemostasis and inflammation, as well as the activation of coagulation cascade during viral infections, are well established. Another important evidence which may explain coagulation disorders in COVID-19 is the increase of thrombus formation under conditions of hypoxia. Despite the exact pathophysiological mechanism of coronavirus-induced thromboembolism needs to be further investigated, this finding suggests that it is good practice to assess the risk of thrombosis in COVID-19 patients to improvethe clinical management in terms of anticoagulation therapy. Anticoagulants, mainly low-molecular-weight heparin (LMWH), should be tailored in patients meeting sepsis induced coagulopathy (SIC) criteria or with markedly elevated D-dimer. In this context, further studies are needed to optimise the decision making in therapeutic approach.

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Background Respiratory viral infections, such as COVID-19, predispose patients to co-infections leading to increased morbidity and mortality. A. baumannii poses as a serious threat to hospital facilities because of its ability to persist in the environment and acquire multi-drug resistance. The aim of this study was to quantify the extent of A. baumannii cross-infection and identify any gene clonality between isolates in SARS-CoV-2 patients. Methods Bacterial isolates of A. baumannii found in patients with SARS-CoV-2 admitted to the main Intensive Care Unit (ICU) of the Umberto I Teaching Hospital of Rome were collected between March 2020 and February 2021. Isolates were typed by pulsed-field electrophoresis to analyse their homology relationships. Results Overall, 196 SARS-CoV-2 patients were admitted to the ICU. They were mainly male (N = 138) and aged 63 years on average. Of these, 122 died, and 74 were discharged. A total of 157 strains of A. baumannii were isolated from 74 patients (38%), who had a higher mean hospital stay than patients in whom the bacterial strain had not been isolated (24.6 vs. 12.2 days). The genotypic analysis of 120 isolates revealed two main patterns (A and F) and a few subtypes, especially A8 (43%), A4 (29%), and A11 (10%). Clone A8 was found mainly between October 2020 and February 2021, clone A4 in April-December 2020 and January-February 2021, and A11 in December 2020 and January 2021. The strains were susceptible to colistin only, were isolated mostly from tracheobronchial aspirates (41%) or rectal swabs (35%) and accounted for 56 healthcare-associated infections (33% of which sustained by A4, 38% by A8, and 9% by A11). Conclusions The isolation of A. baumannii from patients with COVID-19 highlighted the importance of monitoring co-infections caused by this pathogen, which frequently shows a multi-drug resistant profile that may lengthen the hospital stay. It is essential to implement preventive measures to contain these infections. Key messages A. baumanni is a pathogen that needs to be monitored because it may lengthen the hospital stay of SARS-CoV-2 patients. In critically ill patients, the continued growth of multidrug-resistant organisms shows the importance of preventing these infections.