Respiratory disease, and treatment / thematic poster session COVID-19 outcome-based pathology reveals the birth of fibrosing interstitial pneumonitis

RATIONALE: Fibrosing interstitial pneumonitis can be the common end result to many different lung diseases, including chronic viral inflammations, as COVID-19. Some SARS-CoV-2 infected patients develop the acute respiratory distress syndrome. This condition is histopathologically known as diffuse alveolar damage which may be followed by a proliferative phase. Whereas COVID-19 has showed a longer disease outcome until clinical cure or death compared to other chronic infections, our hypothesis is that COVID-19 patients tend to develop a more prominently proliferative phase, even those who progress to death, with an exacerbated fibroblast and myofibroblast proliferation. METHODS: Minimally invasive autopsy(MIA) was performed on 47 confirmed COVID- 19 patients for lung samples. Clinical, demographic, mechanical ventilation parameters and radiological data were collected by electronic medical record. A detailed histomorphological analysis by two pulmonary pathologists was performed by HE2) Better lung outcome - a progressive increase in PaO2/FiO2 ratio and low complacency levels, usual pattern of elastic and collagen fibers and SMA+ cells, but sudden death due to acute pulmonary thromboembolism. Moreover, SARS-CoV-2 viral genome was detected in all lung tissue collected(47), with a mean of 3,403,775 and 90,683,263 copies/mg for N2 and E genes respectively. CONCLUSIONS: The fibrotic septal thickening is related to poor lung outcome by progressive decline in PaO2/FiO2 ratio and late death. This pathophysiological process may be an important sequel in pos- COVID19 patients to trigger a fibrosing interstitial pneumonitis. Further investigations with larger studies are warranted. .