gms | German Medical Science

Deutscher Kongress für Orthopädie und Unfallchirurgie (DKOU 2017)

24.10. - 27.10.2017, Berlin

Microparticle Phenotype Profile of Severely Injured Trauma Patients and their Procoagulant Activity under in vitro simulated Lethal Triad Conditions

Meeting Abstract

  • presenting/speaker Michael Caspers - Institut für Forschung in der operativen Medizin, Universität Witten/Herdecke, Klinik für Unfallchirurgie, Orthopädie, Sporttraumatologie, Köln, Germany
  • Nadine Schäfer - Institut für Forschung in der Operativen Medizin, Universität Witten/Herdecke, Experimentelle Forschung, Köln, Germany
  • Matthias Fröhlich - Kliniken der Stadt Köln gGmbH, Klinikum Köln-Meerheim, Klinik für Unfallchirurgie, Orthopädie u. Sporttraumatologie, Köln, Germany
  • Bertil Bouillon - Kliniken der Stadt Köln gGmbH, Klinikum Köln-Merheim, Klinik für Unfallchirurgie, Orthopädie u. Sporttraumatologie, Lehrstuhl der Privaten Universität Witten/Herdecke, Köln, Germany
  • Manuel Mutschler - Kliniken der Stadt Köln gGmbH, Klinikum Köln-Merheim, Klinik für Unfallchirurgie, Orthopädie u. Sporttraumatologie, Lehrstuhl der Privaten Universität Witten/Herdecke, Köln, Germany
  • Marc Maegele - Kliniken der Stadt Köln gGmbH, Klinikum Köln-Meerheim, Klinik für Unfallchirurgie, Orthopädie u. Sporttraumatologie, Köln, Germany

Deutscher Kongress für Orthopädie und Unfallchirurgie (DKOU 2017). Berlin, 24.-27.10.2017. Düsseldorf: German Medical Science GMS Publishing House; 2017. DocGR19-1315

doi: 10.3205/17dkou542, urn:nbn:de:0183-17dkou5421

Veröffentlicht: 23. Oktober 2017

© 2017 Caspers et al.
Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). Lizenz-Angaben siehe http://creativecommons.org/licenses/by/4.0/.


Gliederung

Text

Objectives: Trauma-induced coagulopathy (TIC) is an endogenous entity comprising all components of haemostasis that follows rapidly to tissue injury, hypoperfusion and haemorrhagic shock. Following a major trauma, microparticles (MP) of 0.1 - 0.9 µm in size are known to be released in large quantities from different cell types (platelets: PDMP; endothelial: EDMP; monocytes: MDMP) having functions at the conjunction of cellular and plasmatic coagulation.

The present study aimed to perform a phenotypic MP profiling after major trauma and to elucidate specific procoagulative receptors on MP surface. Subsequently, coagulative capacity of trauma-derived MPs was tested using an in vitro lethal triad simulation assay.

Methods: For MP isolation, blood samples from 10 trauma patients (mean ISS >16) were included. For phenotyping, samples were pooled, extracted and concentrated by using an ultracentrifuge protocol to achieve a highly pure MP trauma phenotype sample. Specific cell surface markers were measured by flow cytometry. Our MP trauma phenotype profile was subsequently added in high (2931 PDMP/µl) and low (29.3 PDMP/µl) concentration to an in vitro lethal triad assay simulating coagulopathy, hypothermia and acidosis. Following, a comprehensive coagulation function analysis was performed including a standard coagulation analysis, ROTEM, ROTEG PlateletMapping and expression of CD62P on platelets surface by flow cytometry.

Results and Conclusion: Within our MPs trauma phenotype profile, PDMP were found as predominant (56 %) followed by EDMP (33%) and MDMP (11%). EDMP characterized by CD144, CD62E and Annexin were determined most frequent but as well EDMP expressing CD62P. In addition, Tissue Factor (TF, CD142) expression was measured on all MP entities (EDMP 63%, PDMP 30%, MDMP 7%). Within our lethal triad simulation assay, the addition of low and high concentrated MP did not cause any significant alteration in standard coagulation assay, coagulation initiation, clot kinetics or clot stability. Concerning platelet function, addition of high concentrated MP increased platelet function significantly and a similar effect was observed when investigating P-selectin expression on platelet surface.

Our results indicate that MP derived from trauma patients have specific procoagulant activity at least in part mediated via activity increase in platelets resulting in an improved contribution of platelets to clot formation under condition of lethal triad. There are indications that expression of selectins and TF on MP surfaces are involved in this activation process, but there is a necessity to investigate this pathway and MP-platelet interaction in more detail. From a functional point of view, our data could not provide evidence that MP in the given concentrations can influence clot kinetics or clot firmness significantly.