Hamostaseologie 2011; 31(01): 15-20
DOI: 10.5482/ha-1148
Review
Schattauer GmbH

Haemostasis management of massive bleeding

Hämostase-Management bei massivem Blutverlust
B. Pötzsch
1   Institute of Experimental Haematology and Transfusion Medicine , University Hospital, Rheinische Friedrich Wilhelms University Bonn, Germany
,
V. Ivaskevicius
1   Institute of Experimental Haematology and Transfusion Medicine , University Hospital, Rheinische Friedrich Wilhelms University Bonn, Germany
› Author Affiliations
Further Information

Publication History

Publication Date:
27 December 2017 (online)

Summary

Trauma-induced coagulopathy (TIC) is a frequent complication of severely injured patients. The etiology of TIC is complex. Contributing factors include overwhelming generation of thrombin and activated protein C, consumption of coagulation factors and platelets, hyperfibrinolysis, and dilution of clotting factors through administration of fluids. In addition, hypothermia and shock-associated metabolic acidosis augment the clotting dysfunctions. The occurrence of TIC has been shown to be an independent risk factor for death after trauma warranting aggressive treatment. On admission to the emergency room patients with massive blood loss should be employed on basis of clinical and diagnostic variables to identify patients at high risk of coagulopathy. Patients at high risk should be treated with tranexamic acid (1 g bolus followed by 1 g/8 h), and critical factor and platelet deficiencies should be corrected by transfusion of factor concentrates and platelet concentrates. In addition, plasma should be administered in a 1 : 1 ratio with red cells. The use of recombinant factor VIIa should be considered if major bleeding persists despite best-practive use of blood products.

Zusammenfassung

Die Trauma-induzierte Koagulopathie (TIK) ist eine häufig auftretende Komplikation bei Patienten mit schweren Verletzungen. Zu den auslösende Ursachen werden eine unkontrollierte Thrombinbildung, eine überschießende Aktivierung des Protein-C-Systems, der Verbrauch von Gerinnungsfaktoren, die Entwicklung einer Hyperfibrinolyse, und das Auftreten einer Verdünnungskoagulopathie gerechnet. Hypothermie und eine metabolische Azidose verstärken die Gerinnungsstörung. Das Auftreten einer TIK erhöht die Mortalität von Traumapatienten. Dies rechtfertigt einen aggressiven Therapieansatz. Nach Ankunft im Schockraum sollte das TIK-Risiko bewertet werden. Patienten mit einem hohen Risiko sollten sofort einen Tranexamsäurebolus von 1 g gefolgt von 1 g/8 h erhalten. Ein klinischrelevanter Mangel an Gerinnungsfaktoren und Thrombozyten sollte durch die Gabe von Faktorenkonzentraten und Thrombozytenkonzentraten ausgeglichen werden. Gleichzeitig sollte Plasma im Verhältnis 1 : 1 zu Erythro- zytenkonzentraten verabreicht werden. Bei fortbestehender Blutung trotz optimierter Substitutionstherapie ist die Gabe von rekombinantem aktiviertem Faktor VII eine Therapieoption.

 
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