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As an aerosol and droplets generating procedure, tracheostomy increases contamination risks for health workers in the coronavirus disease context.To preserve the health care system capacity and to limit virus crosstransmission, protecting caregivers against coronavirus infection is of critical importance. We report the use of external fixator equipment to set up a physical interface between the patient's neck and the caregiver performing a tracheostomy in COVID-19 patients. Once the metal frame set in place, it is wrapped with a single-use clear and sterile cover for surgical C-arm. This installation is simple, easy, and fast to achieve and can be carried out with inexpensive material available in every hospital. This physical interface is an additional safety measure that prevents the direct projection of secretions or droplets. It should, of course, only be considered as a complement to strict compliance with barrier precautions and personal protective equipment.

Coronavirus disease 2019 (COVID-19) is a new pandemic acute respiratory disease caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)11-3. We provide here a longitudinal analysis of immune responses, including immune cell phenotyping and assessments of the soluble factors present in the blood and broncho-alveolar lavage fluid (BALF) of patients at various stages of COVID-19 severity: paucisymptomatic, pneumonia and acute respiratory distress syndrome (ARDS). While we confirm a lymphopenia associated with COVID-19 severity4-7, we report an increase in expression of the NKG2A and PD-1 inhibitory receptors on T and natural killer (NK) cells, as well as an increase in CD39 expression on NK cells, suggesting that therapeutic blocking antibodies targeting these molecules already used for cancer immunotherapy8 could be repurposed as first line of defense to promote SARS-CoV-2 clearance. In addition, the C5a anaphylatoxin and its receptor C5aR1 (CD88) play a key role in the initiation and maintenance of inflammatory responses, by recruiting neutrophils and monocytes to the lungs9,10. We report an increase in soluble C5a levels proportional to COVID-19 severity and high levels of C5aR1 expression in blood and BALF myeloid cells, indicating a potential role of the C5a-C5aR1 axis in the pathophysiology of ARDS. Avdoralimab is a clinical-stage anti-C5aR1 therapeutic monoclonal antibody (mAb) that prevents C5a-mediated myeloid cell recruitment and activation. We propose the use of this antibody to limit myeloid cell infiltration in the lung and to prevent the excessive lung inflammation associated with ARDS in COVID-19 patients.

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