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 a higher mortality. An autopsy can reveal the pathogenesis and determine the cause of death.
Objectives: to understand the pathophysiological changes that occur in lung tissue in COVID-19 affected individuals and specify the cause of death.
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 were 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 as a result of COVID-19. Their slides and paraffin embedded blocks regarding lung biopsies, together with their reports, were obtained and submitted for assessment by two pathologists (specialist and consultant) for further assessment of lung changes caused by COVID-19.
Results: Only 2 of the 6 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. One case showed intra-alveolar atypical large cells, ischemic necrosis, and severe inflammation with intra-alveolar macrophages and pneumocyte hyperplasia.