Abstract
BackgroundAutoptic pulmonary findings have been described in severe COVID-19 patients, but evidence regarding the correlation between clinical picture and lung histopathologic patterns is still weak.MethodsThis was a retrospective cohort observational study conducted at the referral center for infectious diseases in northern Italy. Full lung autoptic findings and clinical data of patients who died from COVID-19 were analyzed. Lung histopathologic patterns were scored according to the extent of tissue damage. To consider coexisting histopathologic patterns, hierarchical clustering of histopathologic findings was applied.ResultsWhole pulmonary examination was available in 75 out of 92 full autopsies. Forty-eight hospitalized patients (64%), 44 from ICU and four from the medical ward, had complete clinical data. The histopathologic patterns had a time-dependent distribution with considerable overlap among patterns. Duration of positive-pressure ventilation (p < 0.0001), mean positive end-expiratory pressure (PEEP) (p = 0.007), worst serum albumin (p = 0.017), interleukin 6 (p = 0.047), and kidney SOFA (p = 0.001) differed among histopathologic clusters. The amount of PEEP for long-lasting ventilatory treatment was associated with the cluster showing the largest areas of early and late proliferative diffuse alveolar damage. No pharmacologic interventions or comorbidities affected the lung histopathology.ConclusionsOur study draws a comprehensive link between the clinical and pulmonary histopathologic findings in a large cohort of COVID-19 patients. These results highlight that the positive end-expiratory pressures and the duration of the ventilatory treatment correlate with lung histopathologic patterns, providing new clues to the knowledge of the pathophysiology of severe SARS-CoV-2 pneumonia.
Highlights
SARS-CoV-2 infection causes a systemic disease, namely coronavirus 2019 disease (COVID-19), with multiple organ involvement [1,2,3]
Autoptic findings usually reveal variable degrees of diffuse alveolar damage (DAD): Acute-phase DAD usually shows exudative features with interstitial widening, formation of intra-alveolar edema, thickened alveolar septa, and perivascular lymphoplasmacytic infiltration, while in late-phase DAD proliferative features prevail with pneumocyte hyperplasia inducing interstitial thickening and collapsed alveoli, which may develop into organizing patterns, with marked fibroblastic proliferation and fibrosis, sometimes even leading to squamous metaplasia [4,5,6,7,8]
Even though the DAD pattern is not found exclusively in COVID-19, exudative or proliferative DAD development is a key pathophysiological mechanism in lung injury induced by SARS-CoV-2
Summary
SARS-CoV-2 infection causes a systemic disease, namely coronavirus 2019 disease (COVID-19), with multiple organ involvement [1,2,3]. Autoptic findings usually reveal variable degrees of diffuse alveolar damage (DAD): Acute-phase DAD (during the first week after the pulmonary injury) usually shows exudative features with interstitial widening, formation of intra-alveolar edema, thickened alveolar septa, and perivascular lymphoplasmacytic infiltration, while in late-phase (one to several weeks) DAD proliferative features prevail with pneumocyte hyperplasia inducing interstitial thickening and collapsed alveoli, which may develop into organizing patterns (weeks to months), with marked fibroblastic proliferation and fibrosis, sometimes even leading to squamous metaplasia [4,5,6,7,8]. Even though the DAD pattern is not found exclusively in COVID-19, exudative or proliferative DAD development is a key pathophysiological mechanism in lung injury induced by SARS-CoV-2. Autoptic pulmonary findings have been described in severe COVID-19 patients, but evidence regarding the correlation between clinical picture and lung histopathologic patterns is still weak
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