# Multimodal characterization of flow-induced thrombus initiation and growth in extracorporeal membrane oxygenation

**Authors:** Frida Nilsson, Benedikt Sochor, Sara Henriksson, Stephan V. Roth, Lars Mikael Broman, Lisa Prahl Wittberg

PMC · DOI: 10.1038/s41598-026-40177-3 · Scientific Reports · 2026-02-18

## TL;DR

This study combines multiple techniques to understand how blood clots form in ECMO devices, which could improve device design and patient care.

## Contribution

A novel multiscale methodology combining CFD, USAXS, and SEM to analyze thrombus formation in ECMO circuits.

## Key findings

- USAXS revealed fibrin density and alignment in thrombus scaffold structures.
- CFD identified high thrombotic potential regions in ECMO circuits.
- SEM showed cellular morphology and surface fibrin structure of thrombi.

## Abstract

In cases of severe cardiopulmonary failure, extracorporeal membrane oxygenation (ECMO) may be temporarily used as a life-saving support for cardiac and/or lung function. Operating under non-physiological flow conditions, characterized by elevated shear rates and stagnant flow zones, there is an increased risk of inducing thrombosis, bleeding and hemolysis. Pinpointing the underlying mechanism triggering the onset of thrombus formation may aid development of device design, as well as management of anti-coagulation, benefiting patient outcome. Here we present a combined methodology enabling a multiscale understanding of thrombus development. Two thrombi collected from different ECMO circuits were analyzed by computational fluid dynamics (CFD), ultra small angle X-ray scattering (USAXS) and scanning electron microscopy (SEM). USAXS quantified the density and bulk alignment of fibrin, building the thrombus scaffold structure. SEM provided information on cellular morphology and surface fibrin structure, and CFD identified regions in the ECMO circuit with high thrombotic potential. Together, this combined approach was able to link local flow conditions and the structural growth of thrombi in ECMO circuits.

## Full-text entities

- **Genes:** VWF (von Willebrand factor) [NCBI Gene 7450] {aka F8VWF, VWD}
- **Diseases:** hemolysis (MESH:D006461), cardiac or respiratory failure (MESH:D012131), bleeding (MESH:D006470), fatigue (MESH:D005221), hypercoagulability (MESH:D019851), cardiopulmonary failure (MESH:D051437), inflammation (MESH:D007249), ML (MESH:D015433), thromboembolism (MESH:D013923), coagulation (MESH:D001778), thrombocytopenia (MESH:D013921), cytotoxic (MESH:D064420), Thrombus (MESH:D013927), blood damage (MESH:D006402)
- **Chemicals:** platinum (MESH:D010984), sodium chloride (MESH:D012965), Phosphate (MESH:D010710), Glutaraldehyde (MESH:D005976), heparin (MESH:D006493), carbon dioxide (MESH:D002245), EMCO (-)
- **Species:** Sus scrofa (pig, species) [taxon 9823], Rattus norvegicus (brown rat, species) [taxon 10116], Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12920996/full.md

## References

5 references — full list in the complete paper: https://tomesphere.com/paper/PMC12920996/full.md

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Source: https://tomesphere.com/paper/PMC12920996