CT Image Segmentation for Inflamed and Fibrotic Lungs Using a Multi-Resolution Convolutional Neural Network (preprint)

The purpose of this study was to develop a fully-automated segmentation algorithm, robust to various density enhancing lung abnormalities, to facilitate rapid quantitative analysis of computed tomography images. A polymorphic training approach is proposed, in which both specifically labeled left and right lungs of humans with COPD, and nonspecifically labeled lungs of animals with acute lung injury, were incorporated into training a single neural network. The resulting network is intended for predicting left and right lung regions in humans with or without diffuse opacification and consolidation. Performance of the proposed lung segmentation algorithm was extensively evaluated on CT scans of subjects with COPD, confirmed COVID-19, lung cancer, and IPF, despite no labeled training data of the latter three diseases. Lobar segmentations were obtained using the left and right lung segmentation as input to the LobeNet algorithm. Regional lobar analysis was performed using hierarchical clustering to identify radiographic subtypes of COVID-19. The proposed lung segmentation algorithm was quantitatively evaluated using semi-automated and manually-corrected segmentations in 87 COVID-19 CT images, achieving an average symmetric surface distance of $0.495 \pm 0.309$ mm and Dice coefficient of $0.985 \pm 0.011$. Hierarchical clustering identified four radiographical phenotypes of COVID-19 based on lobar fractions of consolidated and poorly aerated tissue. Lower left and lower right lobes were consistently more afflicted with poor aeration and consolidation. However, the most severe cases demonstrated involvement of all lobes. The polymorphic training approach was able to accurately segment COVID-19 cases with diffuse consolidation without requiring COVID-19 cases for training.

Can Hyperperfusion of Nonaerated Lung Explain COVID-19 Hypoxia? (preprint)

Early stages of the novel coronavirus disease (COVID-19) have been associated with ‘silent hypoxia’ and poor oxygenation despite relatively small fractions of afflicted lung. Although it has been speculated that such paradoxical findings may be explained by impairment of hypoxic pulmonary vasoconstriction in infected lungs regions, no studies have confirmed this hypothesis nor determined whether such extreme degrees of perfusion redistribution are physiologically plausible. Here, we present a mathematical model which provides evidence that the extreme amount of pulmonary shunt observed in patients with early COVID-19 is not plausible without hyperperfusion of the relatively small fraction of injured lung, with three-fold increases in regional perfusion to afflicted regions. Although underlying perfusion heterogeneity (e.g., due to gravity or pulmonary emboli) exacerbated existing shunt in the model, the reported severity of hypoxia in early COVID-19 patients could not be replicated without considerable reduction of vascular resistance in nonoxygenated regions.