gms | German Medical Science

Deutscher Kongress für Orthopädie und Unfallchirurgie
73. Jahrestagung der Deutschen Gesellschaft für Unfallchirurgie
95. Tagung der Deutschen Gesellschaft für Orthopädie und Orthopädische Chirurgie
50. Tagung des Berufsverbandes der Fachärzte für Orthopädie und Unfallchirurgie

21. - 24.10.2009, Berlin

Early prediction of late onset sepsis in multi trauma patients by analysis of neutrophil activation

Meeting Abstract

  • K. Groeneveld - UMC Utrecht, Utrecht, Netherlands
  • B. L. Warren - University of Stellenbosch, Cape Town, South Africa
  • A. Serafin - University of Stellenbosch, Cape Town, South Africa
  • L. Koenderman - UMC Utrecht, Utrecht, Netherlands
  • L. P. H. Leenen - UMC Utrecht, Utrecht, Netherlands

Deutscher Kongress für Orthopädie und Unfallchirurgie. 73. Jahrestagung der Deutschen Gesellschaft für Unfallchirurgie, 95. Tagung der Deutschen Gesellschaft für Orthopädie und Orthopädische Chirurgie, 50. Tagung des Berufsverbandes der Fachärzte für Orthopädie. Berlin, 21.-24.10.2009. Düsseldorf: German Medical Science GMS Publishing House; 2009. DocWI17-1237

DOI: 10.3205/09dkou156, URN: urn:nbn:de:0183-09dkou1564

Published: October 15, 2009

© 2009 Groeneveld et al.
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Outline

Text

Problem: Systemic activation of the innate immune system attracts functional neutrophils into damaged tissues. Dysfunctional neutrophils stay behind in the circulation. This causes a paralyzed innate immune system and increased susceptibility to late onset sepsis.

Method: In this prospective, observational study, we sampled blood of adult multi trauma patients (ISS>16) within twelve hours after the trauma, unless known with immunodeficiency or use of immunosuppressive drugs. Blood samples were analyzed for neutrophil activation by determining expression of activation markers with flowcytometry. Patients stayed in follow-up until they were discharged.

Results and conclusions: Severely injured patients are at risk to develop postoperative sepsis and non-septic inflammatory complications. These complications occur in a biphasic fashion and peak shortly after trauma as a result of the sustained injury (SIRS) and after about a week during the compensatory anti-inflammatory response syndrome (CARS). This latter condition is often associated with late-onset sepsis (>5 days). Unfortunately no validated scoring systems are available to identify individual patients with a high risk for the development of these late inflammatory conditions. Also determination of inflammatory mediators, such as cytokines and chemokines, have not provided an adequate differentiation. Activation of cells of the innate immune system forms the final step in the inflammatory response and are therefore essential is the development of inflammatory complications.

The activation status of the innate immune system at a certain moment in time can be determined by analysis of the expression activation markers on neutrophils in peripheral blood. In previous studies our research group showed that a combination of these receptors, combined in a "priming score", reflected the inflammatory status of individual patients.

In total 73 patients were included and 24 patients developed a sepsis. The median Injury Severity Score of septic patients was 30 compared to an ISS of 25 in other patients. Eleven patients died. Within twelve hours after trauma, blood neutrophils showed a significantly lower activity in active FcγRII (745,0 vs 133,5, p 0,012) and fMLP induced active FcγRII (3546,7 vs 1249,6, p0,003) in patients who develop a sepsis 3–14 days later. Considering that circulating cells were measured, this finding points at a paralysis of the innate immune system. In addition, at admission, neutrophils show decreased FcγRIIIB expression (381,7 vs 119,2, p0,000), which is indicative for recruitment of immature neutrophils.

Multi trauma caused a decreased activation status and less excitable of systemic neutrophils within twelve hours after trauma. This decreased status leads to a dysfunctional innate immune system and made patients susceptible to late onset sepsis. Determination of active FcγRII and fMLP induced active FcγRII can predict the development of late onset sepsis.