Trauma-associated hyperfibrinolysis

H. Schöchl; W. Voelckel; M. Maegele; C. Solomon

doi:10.5482/ha-1178

Hämostaseologie, Table of Contents

Hamostaseologie 2012; 32(01): 22-27
DOI: 10.5482/ha-1178

Review

Schattauer GmbH

Trauma-associated hyperfibrinolysis

Trauma-assoziierte Hyperfibrinolyse

Authors

H. Schöchl

¹Ludwig Boltzmann Institute for Experimental and Clinical Traumatology, Vienna, Austria

²Department of Anaesthesiology and Intensive Care Medicine, AUVA Trauma Centre, Salzburg, Austria
W. Voelckel

²Department of Anaesthesiology and Intensive Care Medicine, AUVA Trauma Centre, Salzburg, Austria
M. Maegele

³Department of Trauma and Orthopedic Surgery, University of Witten/Herdecke, Cologne-Merheim Medical Center (CMMC), Cologne, Germany
C. Solomon

⁴Department of Anaesthesiology, Intensive Care and Perioperative Medicine, Salzburg University, Hospital SALK, Salzburg, Austria

Abstract

Summary

Trauma-induced coagulopathy (TIC) has been considered for a long time as being due to depletion of coagulation factors secondary to blood loss, dilution and consumption. Dysfunction of the remaining coagulation factors due to hypothermia and acidosis is assumed to additionally contribute to TIC. Recent data suggest that hyperfibrinolysis (HF) represents an additional important confounder to the disturbed coagulation process. Severe shock and major tissue trauma are the main drivers of this HF. The incidence of HF is still speculative. According to visco-elastic testing of trauma patients upon emergency room admission, HF is present in approximately 2.5–7% of all trauma patients. However, visco-elastic tests provide information on severe forms of HF only. Occult HF seems to be much more common but diagnosis is still challenging. Results from a recent randomized, placebo-controlled trial suggest that the early treatment of trauma patients with tranexamic acid may result in a significant reduction of trauma-associated mortality.

Zusammenfassung

Bislang wurden Trauma-induzierte Gerinnungsstörungen häufig als Kombination aus Verlust und Dysfunktion von Gerinnungsfaktoren verstanden. Azidose und Hypothermie bedingen eine weitere Funktionseinschränkung der verbleibenden Gerinnungsfaktoren. Neue Daten lagen nahe, dass Hyperfibrinolyse den Gerinnungsprozess zusätzlich beeinträchtigt. Als wesentliche Ursachen für profibrinolytische Prozesse werden die Kombination aus schockbedingter Hypoperfusion und substanziellem Gewebetrauma vermutet. Die wahre Inzidenz der Hyperfibrinolyse nach Trauma ist nach wie vor unklar. Anhand thromboelastometrischer/thrombelasto- graphischer Befunde bei Aufnahme im Schockraum wird gemutmaßt, dass 2.5–7% der Schwerverletzten betroffen sind. Viskoelastische Testverfahren erlauben allerdings nur die Diagnose ausgeprägter HF-Formen. Okkulte Hyperfibrinolysen treten vermutlich wesentlich häufiger auf und sind nach wie vor schwierig zu detektieren.Aktuelle Daten einer großen multizentrischen, multinationalen, randomisierten Doppelbildstudie legen nahe, dass die Mortalität von Traumapatienten durch den frühen Einsatz von Tranexamsäure signifikant gesenkt werden kann.

Keywords

Hyperfibrinolysis - trauma - ROTEM - TEG - tranexamic acid

Schlüsselwörter

Hyperfibrinolyse - Trauma - ROTEM→ - TEG→ - Tranexamsäure

Full Text

References

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