The free access does not apply to institutional or commercial use.
Information:
claudia.boehm@schattauer.de
![]() |
|
H. Schöchl (1, 2), W. Voelckel (2), M. Maegele (3), C. Solomon (4)
(1) Ludwig Boltzmann Institute for Experimental and Clinical Traumatology, Vienna, Austria; (2) Department of Anaesthesiology and Intensive Care Medicine, AUVA Trauma Centre, Salzburg, Austria; (3) Department of Trauma and Orthopedic Surgery, University of Witten/Herdecke, Cologne-Merheim Medical Center (CMMC), Cologne, Germany; (4) Department of Anaesthesiology, Intensive Care and Perioperative Medicine, Salzburg University, Hospital SALK, Salzburg, Austria
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.
Trauma, TEG, ROTEM, hyperfibrinolysis, tranexamic acid
| 1. | ||
P. Innerhofer Hämostaseologie 2006 26 6: 3-14 | ||
| 2. | ||
T. Lang1,2, M. von Depka2 Hämostaseologie 2006 26 6: 21-29 | ||
| 3. | ||
P. Innerhofer Hämostaseologie 2006 26 6: 3-14 | ||