Der Anaesthesist

, 58:1010

Gerinnungsmanagement bei der Polytraumaversorgung

Notfallmedizin

Zusammenfassung

In den letzten Jahren konnte ein verbessertes Verständnis traumaassoziierter Gerinnungsstörungen (traumainduzierte Koagulopathie) durch eine Reihe neuer wissenschaftlicher Erkenntnisse erreicht werden. Neben dem Gewebetrauma scheinen auch Schock und Minderperfusion für die Entwicklung einer Koagulopathie maßgeblich verantwortlich zu sein. Hypoperfusion kann über eine Endothelaktivierung zur Hyperfibrinolyse führen. Additive Effekte wie Hypothermie und Acidose verstärken diese Gerinnungsstörung. Standardgerinnungstests wie Quick-Test und die Bestimmung der aktivierten partiellen Thromboplastinzeit (aPTT) werden zwar häufig zu Therapieentscheidungen herangezogen, sind aber mit Nachteilen behaftet. Die Thrombelastometrie/-graphie scheint den Routinegerinnungtests überlegen zu sein. Da die Prophylaxe der traumainduzierten Koagulopathie einfacher als die Therapie ist, ist eine antizipierende Vorgehensweise notwendig. Während die pathophysiologischen und pharmakologischen Zusammenhänge der geschilderten Therapieoptionen schlüssig sind, fehlt jedoch für die meisten eine evidenzbasierte Bestätigung durch randomisierte, kontrollierte Studien. Zu dem notärztlichen und anästhesiologischen Konzept der „damage control resuscitation“ gehören die Begrenzung der Infusion von kristalloidem und kolloidalem Volumenersatz auf einen mittleren arteriellen Druck (MAP) von ≥65 mmHg (höher bei Schädel-Hirn-Trauma), ein aktives Wärmemanagement, die Verhinderung bzw. der Ausgleich einer Acidose auf einen pH>7,2 bzw. ein „base excess“ (BE)≤−6 mmol/l sowie die frühzeitige und ausreichende Gabe von gerinnungsaktiven Medikamenten. Da Erythrozyten auch einen beträchtlichen Anteil am Gerinnungsprozess haben, sollten bei massiver, nichtgestillter Blutung Hämoglobin- (Hb-)Werte um 6,2 mmol/l (10 g/dl) bzw. ein Hämatokrit (HKT) um 30% angestrebt werden. Ein Fibrinogenmangel entwickelt sich bei schweren Polytraumen früh und muss adäquat ausgeglichen werden. Wenn eine Gerinnungstherapie mit gefrorenem Frischplasma (GFP) durchgeführt wird, müssen ausreichende Mengen (20–30 ml/kgKG) verabreicht werden, um die Gerinnungsfaktoren entsprechend anzuheben. Prothrombinkomplexpräparate (PPSB) können bei schweren Blutungen zur Optimierung der Thrombingenerierung hilfreich sein. Da eine Hyperfibrinolyse nach schwerem Trauma häufiger ist als bislang angenommen, sollte insbesondere bei kreislaufinstabilen Patienten an den Einsatz eines Antifibrinolytikums gedacht werden. Die Thrombozytenzahl sollten bei blutenden Polytraumata 100.000/µl nicht unterschreiten. Bei thrombopathischer, diffuser Blutung kann die Infusion von Desmopressin (DDAVP) indiziert sein. Rekombinanter aktivierter Faktor VII stellt eine Therapieoption dar, allerdings nur bei strenger Indikationsstellung und wenn oben genannte Maßnahmen zur Optimierung der Gerinnungssituation ergriffen wurden.

Schlüsselwörter

Koagulopathie Trauma Therapie Diagnose Massivtransfusion 

Coagulation management in the treatment of multiple trauma

Abstract

In recent years a new understanding of trauma-associated hemorrhaging and trauma-induced coagulopathy has been achieved. This coagulopathy is multifactorial with the predominant mechanisms being tissue trauma, shock and hypoperfusion which can lead to hyperfibrinolysis by activation of the endothelium. Routinely tested coagulation parameters, such as prothrombin time and partial thromboplastin time, are frequently employed for decision making but remain problematic as they do not give any information on clot stability, lysis or platelet function. Thrombelastometry seems to be a useful alternative. A pro-active anticipatory approach is required for a successful outcome to be achieved as rescue correction is more difficult than prevention. While the pathophysiological conception of causal relationship of the mentioned therapeutic options is conclusive, an evidence-based validation by randomized controlled studies is mostly lacking. The emergency and anesthesiological concept of damage control resuscitation consists of limiting volume therapy with crystalloids and colloids to reach a mean arterial pressure ≥65 mmHg (higher for head injuries), active (re-)warming management, the prevention of a pH≤7.2 and a base excess (BE) ≤−6 mmol/l. The early and sufficient application of hemostatic drugs is essential. Because erythrocytes play a substantial role in the coagulation process, hemoglobin (Hb) values of around 6,2 mmol/l (10 g/dl) and/or a hematocrit of 30% should be strived for when massive non-arrested hemorrhaging occurs. After severe multiple trauma a fibrinogen deficit develops and must be adequately compensated. If coagulation therapy is carried out using fresh frozen plasma sufficient quantities (20–30 ml/kgBW) must be administered to correspondingly raise the coagulation factors. Prothrombin complex concentrates can be helpful to optimize thrombin generation during severe hemorrhaging. Because hyperfibrinolysis occurs more often than previously assumed during severe trauma, an anti-fibrinolytic therapy should be used especially for patients with an instable circulation. The platelet count should not go below 100,000/µl when hemorrhaging occurs after multiple trauma. For thrombocytopathic patients with diffuse bleeding desmopressin (DDAVP) is a therapeutic option and the “off label” use of recombinant activated factor VIIa (rFVIIa) remains an option for individual situations with stringent indications and when the above named measures to optimize the coagulation situation have been taken.

Keywords

Coagulopathy Trauma Therapy Diagnosis Massive Transfusion 

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Copyright information

© Springer Medizin Verlag 2009

Authors and Affiliations

  1. 1.Klinik für Anästhesiologie und Operative Intensivmedizin Universitätsklinikum Köln KölnDeutschland
  2. 2.Abt. für Anästhesiologie und IntensivmedizinAUVA Unfallkrankenhaus SalzburgSalzburgÖsterreich

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