Dataset Information

Tracking the time course of pathological patterns of lung injury in severe COVID-19.

ABSTRACT:

Background

Pulmonary involvement in COVID-19 is characterized pathologically by diffuse alveolar damage (DAD) and thrombosis, leading to the clinical picture of Acute Respiratory Distress Syndrome. The direct action of SARS-CoV-2 in lung cells and the dysregulated immuno-coagulative pathways activated in ARDS influence pulmonary involvement in severe COVID, that might be modulated by disease duration and individual factors. In this study we assessed the proportions of different lung pathology patterns in severe COVID-19 patients along the disease evolution and individual characteristics.

Methods

We analysed lung tissue from 41 COVID-19 patients that died in the period March-June 2020 and were submitted to a minimally invasive autopsy. Eight pulmonary regions were sampled. Pulmonary pathologists analysed the H&E stained slides, performing semiquantitative scores on the following parameters: exudative, intermediate or advanced DAD, bronchopneumonia, alveolar haemorrhage, infarct (%), arteriolar (number) or capillary thrombosis (yes/no). Histopathological data were correlated with demographic-clinical variables and periods of symptoms-hospital stay.

Results

Patient´s age varied from 22 to 88 years (18f/23 m), with hospital admission varying from 0 to 40 days. All patients had different proportions of DAD in their biopsies. Ninety percent of the patients presented pulmonary microthrombosis. The proportion of exudative DAD was higher in the period 0-8 days of hospital admission till death, whereas advanced DAD was higher after 17 days of hospital admission. In the group of patients that died within eight days of hospital admission, elderly patients had less proportion of the exudative pattern and increased proportions of the intermediate patterns. Obese patients had lower proportion of advanced DAD pattern in their biopsies, and lower than patients with overweight. Clustering analysis showed that patterns of vascular lesions (microthrombosis, infarction) clustered together, but not the other patterns. The vascular pattern was not influenced by demographic or clinical parameters, including time of disease progression.

Conclusion

Patients with severe COVID-19 present different proportions of DAD patterns over time, with advanced DAD being more prevalent after 17 days, which seems to be influenced by age and weight. Vascular involvement is present in a large proportion of patients, occurs early in disease progression, and does not change over time.

SUBMITTER: Mauad T

PROVIDER: S-EPMC7844838 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:OBJECTIVES:To examine the potentially modifiable drivers that injure and heal the "baby lung" of acute respiratory distress syndrome and describe a rational clinical approach to favor benefit. DATA SOURCES:Published experimental studies and clinical papers that address varied aspects of ventilator-induced lung injury pathogenesis and its consequences. STUDY SELECTION:Published information relevant to the novel hypothesis of progressive lung vulnerability and to the biophysical responses of lung injury and repair. DATA EXTRACTION:None. DATA SYNTHESIS:In acute respiratory distress syndrome, the reduced size and capacity for gas exchange of the functioning "baby lung" imply loss of ventilatory capability that dwindles in proportion to severity of lung injury. Concentrating the entire ventilation workload and increasing perfusion to these already overtaxed units accentuates their potential for progressive injury. Unlike static airspace pressures, which, in theory, apply universally to aerated structures of all dimensions, the components of tidal inflation that relate to power (which include frequency and flow) progressively intensify their tissue-stressing effects on parenchyma and microvasculature as the ventilated compartment shrinks further, especially during the first phase of the evolving injury. This "ventilator-induced lung injury vortex" of the shrinking baby lung is opposed by reactive, adaptive, and reparative processes. In this context, relatively little attention has been paid to the evolving interactions between lung injury and response and to the timing of interventions that worsen, limit or reverse a potentially accelerating ventilator-induced lung injury process. Although universal and modifiable drivers hold the potential to progressively injure the functional lung units of acute respiratory distress syndrome in a positive feedback cycle, measures can be taken to interrupt that process and encourage growth and healing of the "baby lung" of severe acute respiratory distress syndrome.