Hamostaseologie 2019; 39(01): 020-027
DOI: 10.1055/s-0039-1677853
Review Article
Georg Thieme Verlag KG Stuttgart · New York

Trauma-Induced Coagulopathy

Sirak Petros
1   Medical ICU, University Hospital, Leipzig, Germany
2   Division of Hemostaseology, University Hospital, Medical Clinic 1, Leipzig, Germany
› Author Affiliations
Further Information

Publication History

26 September 2018

23 December 2018

Publication Date:
31 January 2019 (online)

Abstract

Trauma-induced coagulopathy (TIC) is a heterogeneous entity that contributes to a significant morbidity and mortality following trauma. The activated protein C system, endotheliopathy and platelet dysfunction have been implicated in the pathogenesis of TIC, although there are still controversies on the exact pathogenesis. TIC can be modified by hypoperfusion, acidosis, hypothermia, haemodilution, underlying disease conditions, pre-injury medications as well as genetic predispositions. Current definition of this syndrome is based on laboratory abnormalities that do not easily allow a distinction between adaptive and maladaptive changes of the haemostatic system. The management of the coagulopathy in the early phase of trauma focuses on the treatment of bleeding. The improving quality in the early damage control following trauma has led to a marked reduction in morbidity and mortality. In the later phase, hypercoagulopathy and inflammation contribute to organ dysfunction, venous thromboembolism and poor outcome. Despite considerable advances in trauma management, TIC remains a diagnostic and therapeutic challenge both in the early and late phases of trauma. This review mainly focuses on the pathogenesis of TIC, with a very short discussion on diagnostic and therapeutic principles.

Zusammenfassung

Trauma-induzierte Koagulopathie ist eine heterogene Entität, die zu einer signifikanten Morbidität und Mortalität nach Trauma beiträgt. Das aktivierte Protein C System, Endotheliopathie und Plättchendysfunktion wurden in der Pathogenese der Trauma-induzierten Koagulopathie diskutiert. Dennoch gibt es weiterhin Kontroversen über die Pathogenese. Trauma-induzierte Koagulopathie kann durch Hypoperfusion, Azidose, Hypothermie, bereits vorliegende Erkrankungen, Vormedikation und genetische Prädisposition weiter modifiziert werden. Die aktuelle Definition dieses Syndroms basiert auf abnorme Laborparameter, die eine Unterscheidung zwischen adaptiven und maldaptiven hemostatischen Veränderungen nicht ohne weiteres erlauben. Die Behandlung der Koagulopathie in der Frühphase fokussiert auf die Therapie der Blutung. Die Qualitätssteigerungen in der Frühbehandlung nach Trauma haben zur erheblichen Senkung der Morbidität und Mortalität beigetragen. In der Spätphase tragen Hyperkoagulopathie und Inflammation in der Entstehung der Organdysfunktion und der venösen Thromboembolie und zu einer schlechten Prognose bei. Trotz den erheblichen Fortschritten im Trauma-Management stellt die Trauma-induzierte Koagulopathie nach wie vor sowohl in der Früh- als auch Spätphase eine diagnostische und therapeutische Herausforderung dar. Diese Übersicht fokussiert hauptsächlich auf die Pathogenese der Trauma-induzierten Koagulopathie, mit einer sehr kurzen Diskussion über diagnostische und therapeutische Prinzipien.

 
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