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Updated: Sep 6, 2025

Lung CT Segmentation to Identify Consolidations and Ground Glass Areas for Quantitative Assesment of SARS-CoV Pneumonia
Published on: December 19, 2020
Acute Pulmonary Embolism in COVID-19: A Potential Connection between Venous Congestion and Thrombus Distribution
Franck Nevesny1, David C Rotzinger2, Alexander W Sauter3
1Department of Vascular and Interventional Radiology, François-Mitterrand University Hospital, 21079 Dijon, France.
Abstract:
Background: Vascular abnormalities, including venous congestion (VC) and pulmonary embolism (PE), have been recognized as frequent COVID-19 imaging patterns and proposed as severity markers. However, the underlying pathophysiological mechanisms remain unclear. In this study, we aimed to characterize the relationship between VC, PE distribution, and alveolar opacities (AO). Methods: This multicenter observational registry (clinicaltrials.gov identifier NCT04824313) included 268 patients diagnosed with SARS-CoV-2 infection and subjected to contrast-enhanced CT between March and June 2020. Acute PE was diagnosed in 61 (22.8%) patients, including 17 females (27.9%), at a mean age of 61.7 ± 14.2 years. Demographic, laboratory, and outcome data were retrieved. We analyzed CT images at the segmental level regarding VC (qualitatively and quantitatively [diameter]), AO (semi-quantitatively as absent, <50%, or >50% involvement), clot location, and distribution related to VC and AO. Segments with vs. without PE were compared. Results: Out of 411 emboli, 82 (20%) were lobar or more proximal and 329 (80%) were segmental or subsegmental. Venous diameters were significantly higher in segments with AO (p = 0.031), unlike arteries (p = 0.138). At the segmental level, 77% of emboli were associated with VC. Overall, PE occurred in 28.2% of segments with AO vs. 21.8% without (p = 0.047). In the absence of VC, however, AO did not affect PE rates (p = 0.94). Conclusions: Vascular changes predominantly affected veins, and most PEs were located in segments with VC. In the absence of VC, AOs were not associated with the PE rate. VC might result from increased flow supported by the hypothesis of pulmonary arteriovenous anastomosis dysregulation as a relevant contributing factor.
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