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Ann Biomed Eng. 2018 Aug;46(8):1173-1182. doi: 10.1007/s10439-018-2031-9. Epub 2018 Apr 19.

Computational Model for Hyperfibrinolytic Onset of Acute Traumatic Coagulopathy.

Author information

1
Department of Mechanical Engineering, University of California Santa Barbara, Santa Barbara, CA, 93106, USA. tiebo@ucsb.edu.
2
Department of Computer Science, University of California Santa Barbara, Santa Barbara, CA, 93106, USA.
3
Department of Biochemistry, University of Vermont, Colchester, VT, USA.
4
Department of Surgery, Denver Health and Hospital Authority, 777 Bannock St, Denver, CO, 80204, USA.
5
Department of Mechanical Engineering, University of California Santa Barbara, Santa Barbara, CA, 93106, USA.

Abstract

The onset of acute traumatic coagulopathy in trauma patients exacerbates hemorrhaging and dramatically increases mortality. The disease is characterized by increased localized bleeding, and the mechanism for its onset is not yet known. We propose that the fibrinolytic response, specifically the release of tissue-plasminogen activator (t-PA), within vessels of different sizes leads to a variable susceptibility to local coagulopathy through hyperfibrinolysis which can explain many of the clinical observations in the early stages from severely injured coagulopathic patients. We use a partial differential equation model to examine the consequences of vessel geometry and extent of injury on fibrinolysis profiles. In addition, we simulate the efficacy of tranexamic acid treatment on coagulopathy initiated through endothelial t-PA release, and are able to reproduce the time-sensitive nature of the efficacy of this treatment as observed in clinical studies.

KEYWORDS:

Coagulopathy; Computational medicine; Fibrinolysis; Partial differential equations; Tissue-plasminogen activator; Tranexamic acid; Trauma

PMID:
29675813
DOI:
10.1007/s10439-018-2031-9

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