Pulmonary fibrosis secondary to COVID-19: a narrative review

Pathophysiology and mechanism of long COVID: a comprehensive review

“…Concerning the latter, the suggested mechanism consisted of organ injury that complicated acute disease, possibly provoking persistent symptoms. The reported organ injuries were: stroke [ 46 , 52 , 55 ], myocardial infarction and fibrosis [ 41 , 43 , 49 , 51 , 55 , 57 , 59 ], acute encephalitis [ 43 , 50 ], neuromuscular disorders [ 40 , 41 , 43 , 46 , 48 , 56 ], renal failure [ 41 , 43 , 60 , 61 ], and hepatobiliary damages [ 43 , 44 ]. The other articles reported on endocrine disorders that were unrelated to organ damage, while including hypotheses on new-onset diabetes [ 62 ] and thyroid disorders [ 63 ].…”

“…Lung fibrosis is a potential long-term complication of COVID-19. Eight articles addressed the mechanisms leading to lung fibrosis, which generally occurs following severe respiratory inflammation and injury [ 32 , 41 , 43 , 47 , 53 , 54 , 57 , 59 ]. One of them emphasized that prolonged exposure to supplemental oxygen in most severe cases could lead to an increased oxidative stress within the lungs, thereby contributing in maintaining the inflammatory status while favouring the activation of fibrotic pathways [ 59 ].…”

“…Eight articles addressed the mechanisms leading to lung fibrosis, which generally occurs following severe respiratory inflammation and injury [ 32 , 41 , 43 , 47 , 53 , 54 , 57 , 59 ]. One of them emphasized that prolonged exposure to supplemental oxygen in most severe cases could lead to an increased oxidative stress within the lungs, thereby contributing in maintaining the inflammatory status while favouring the activation of fibrotic pathways [ 59 ]. Lung fibroproliferative damage was evidenced in autopsy specimens of patients who died from COVID-19 [ 65 , 66 , 70 ] in combination with endothelial damages and angiogenesis.…”

Residual Lung Lesions at 1-year CT after COVID-19

“…Histopathological patterns identified in post-COVID-19 pulmonary fibrosis, even though not fully determined, are presumed to be those of an organizing and fibrotic phase of diffuse alveolar damage (DAD), fibrosing nonspecific interstitial pneumonitis, and organizing pneumonia patterns. CT features being potentially identified in pulmonary fibrosis secondary to COVID-19 pneumonia have been suggested to include the presence of architectural distortion, reticular lesions, traction bronchiolectasis, ground-glass opacity, mosaic attenuation, and honeycombing in consideration of presumed histopathologic patterns ( 4 ). But according to the study by Pan et al ( 1 ), the CT features seen at one-year follow-up studies were those of fibrotic-like linear or multifocal reticular and/or cystic lesions.…”

Pseudo-honeycombing in a patient with coronavirus disease 2019 pneumonia

“…Recent studies have documented the development of fibrosis, both histologically and radiologically, during the evolution of Covid-19 pneumonia 1 , 2 . Although pulmonary fibrosis occurs late (after Covid-19) in most cases, some reports show that it can appear in the early stages of the disease 3 .…”