Postmortem Lung Biopsy in a Sample of COVID-19 Patients in Iraq

Abstract

Background: The entire world was affected by the outbreak of novel coronavirus 2 (SARS-CoV-2), which influenced daily life worldwide and affected the medical, social, and economic prospects of all nations. This virus occurs clinically in four variants: asymptomatic; mild upper respiratory tract infection (URTI); anosmia and/ or ageusia as the only symptoms; and severe systemic disease, such as bilateral interstitial pneumonia. Approximately 20% of the population develops the severe course associated with cytokine release syndrome (CRS). Those who develop lung injury and dyspnea have higher mortality. An autopsy can reveal the pathogenesis and determine the cause of death. Objectives: To understand the pathophysiological changes in lung tissue in COVID-19-affected individuals. Patients and Methods: This is a case series of post-mortem lung histopathology examinations of deceased COVID-19-positive patients. Samples were collected from postmortem models acquired from six diseased individuals who tested positive for SARS-CoV-2 by reverse transcriptase polymerase chain (PCR) reaction and subsequently passed away in the tertiary hospital between July and September 2020 because of COVID-19. Their slides and paraffin-embedded blocks of lung biopsies, as well as their reports, were collected and sent to two pathologists for further evaluation of COVID-19-related changes in the lungs. Results: Only two of the six patients confirmed features of diffuse alveolar injury with hyaline layer and fibrin thrombi in pulmonary arteries, small vessel congestion, and pulmonary infarction. Two patients demonstrated diffuse alveolar fibrosis (organizing pneumonia), severe inflammation, and foci of squamous metaplasia, in addition to the deposition of carbon particles. One case had diffuse pulmonary fibrosis with pulmonary artery thrombosis without an inflammatory background. In another case, there were atypical large cells, ischemic necrosis, and severe inflammation with macrophages and pneumocyte hyperplasia inside the alveoli. Conclusion: the thromboembolic events suggest a role for COVID-19-induced coagulopathy. Molecular mechanisms and clinical features of COVID -19 should be studied. Atypical alterations need to be investigated to confirm their relation to COVID-19 infection.