What We Learned From COVID 19? Trying to find best approach from pathophysiology to treatment. (preprint)

ABSTRACT

Introduction: The outbreak of the novel coronavirus 2019 (COVID-19) caused a pandemic that led to death of more than 3 million people globally. COVID-19 may yield a variety of clinical pictures, differing from pneumonitis to Acute Respiratory Distress Syndrome (ARDS) along with vascular damage in the lung tissue, which is named as endotheliitis, To date, no specific treatment was approved by any authority for the prevention or treatment of COVID-19. Materials and Methods: Here, we presented our experience on COVID-19 with evaluating 11,190 COVID-19 patients by presenting the manifestations of endotheliitis in skin, lung, and brain tissues according to different phases of COVID-19. In our perspective, distinctive manifestations in each COVID-19 patient, including non-respiratory conditions in the acute phase and the emerging risk of long-lasting complications, suggest that COVID-19 has an endotheliitis-centred thrombo-inflammatory pathophysiology. Accordingly, our treatment strategy was adopted to prevent both respiratory and vascular distresses, which are categorized according to extent of endotheliitis. (Group A no or mild pulmonary involvement, Group B moderate pulmonary involvement with clinical risk of deterioration, Group C severe pulmonary involvement and respiratory failure). Potential pathophysiological mechanisms contributing to endotheliitis includes cytokine storm and toxic plasma, thromboinflammation and systemic microangiopathy. Results: A total of 11.190 COVID-19 patients that were diagnosed and treated in Samsun VM Medicalpark Hospital, Turkey, between March 2020 and April 2021 were retrospectively evaluated. The mean age was 59.2 years and male to female ratio was 5507/5683. Among these patients, 1896 (16.9%) individuals were hospitalized. While 1220 (64.3%) of the inpatients were hospitalized within the first 10 days after the diagnosis, 676 (35.7%) of them were hospitalized 10 days after their diagnosis. The number of patients who did not respond to group A and B treatments and developed hypoxemic respiratory failure (Group C) was 520 (27.4%). Among hospitalized patients, 146 (7.7%) individuals needed ventilator support (non-invasive/invasive mechanical ventilation) and were followed in the intensive care unit, and 43 (2.2%) patients died. In conclusion; Endotheliitis can also explain the mechanism behind the respiratory failure in COVID-19, and the difference of COVID-19 related ARDS from ARDS seen in other critical conditions. Hence, daily evaluation of momentary changes in clinical, laboratory and radiological findings of patients and deciding appropriate pathophysiological treatment would help to reduce the mortality rate of COVID-19.