Behandlung der traumainduzierten Koagulopathie – Was ist die Evidenz?

Zusammenfassung

Das zunehmende Verständnis des Phänomens der traumainduzierten Koagulopathie hat zu einer Erweiterung der Therapiestrategien bei der akuten Versorgung polytraumatisierter Patienten geführt. Der Artikel gibt einen Überblick über die aktuellen Empfehlungen zur Therapie basierend auf einer Übersicht der aktuellen Literatur mit besonderer Berücksichtigung der gültigen Leitlinien. Die traumainduzierte Koagulopathie ist ein eigenständiges hochakutes multifaktorielles Krankheitsbild mit signifikantem Einfluss auf die Mortalität schwerstverletzter Patienten. Maßgeblich verantwortlich für das Auftreten und die Ausprägung scheint neben dem Gewebetrauma eine schockbedingte Gewebsminderperfusion zu sein. Verstärkt wird die Koagulopathie durch begleitende Faktoren wie Hypothermie oder Dilution. Diagnose und Therapie einer traumainduzierten Koagulopathie müssen so früh wie möglich beginnen. Standardgerinnungslaborparameter sind bei der Diagnosefindung nur eingeschränkt hilfreich. Die Therapie erfolgt nach dem Konzept der Damage-Control-Resuscitation. Die Substitution großer Mengen an Volumen sollte vermieden und ein mittlerer arterieller Druck von 65mmHg (unter Berücksichtigung der Kontraindikationen!) angestrebt werden. Ein spezifisches Massivtransfusionsprotokoll sollte eingeführt und fortgesetzt werden. Eine Azidose sollte vermieden und durch adäquate Therapie des Schocks behandelt werden. Ein Auskühlen des Patienten sollte durch aktives Wärmemanagement verhindert oder therapiert werden. Eine Hypokalzämie<0,9mmol/l sollte vermieden und kann therapiert werden. Bei massiver Blutung kann eine Transfusion mit Erythrozyten ab einem Hb von 10g/dl(6,2mmol/l) begonnen werden.Wird die Gerinnungstherapie bei Massivtransfusionen mit FFP durchgeführt, sollte ein Verhältnis von FFP zu EK im Bereich von 1:2 bis 1:1 angestrebt werden. Zur Behandlung einer Hyperfibrinolyse nach schwerem Trauma sollte frühzeitig der Einsatz von Tranexamsäureerwogen werden. Bei signifikanter Blutung sollte eine Substitution von Fibrinogen ab einer Konzentration von 1,5g/l(4,41μmol/l)erfolgen. Prothrombinkomplexpräparate können bei fortbestehender schwerer Blutung oder antikoagulatorischer Vormedikation hilfreich sein. Die Indikation zur Thrombozytentransfusion kann bei akuter Blutung ab 100000/μl erfolgen. Bei diffus blutenden Patienten mit V.a.Thombozytopathie kann ein Therapieversuch mit Desmopressin in Erwägung gezogen werden.Wenn eine Faktor XIII(FXIII)-Messung nicht zeitnah möglich ist, kann bei schweren akuten Blutungen eine FXIII-Blindgabe erwogen werden.Bei massiver persistierender Blutung kann, nach Ausschöpfung sämtlicher Therapieoptionen und Schaffung optimaler Rahmenbedingungen, im Einzelfall die Applikation vonrekombinantem aktiviertem Faktor VII (rFVIIa) außerhalb der Zulassungsindikation erwogen werden.

Abstract:

The increasing understanding of trauma-induced coagulopathy has led to an expansion of treatment strategies in the acute management of trauma patients. The aim of this manuscript is to give a summary of current recommendations for the treatment of trauma-induced coagulopathy based on current literature and valid guidelines. Thetrauma-induced coagulopathyis an independentacutemultifactorial diseasewith significantimpact on the mortalityof severelyinjured patients. Largely responsible for the occurrence and severity of trauma-induced coagulopathy seems to be tissue trauma and shock-induced hypoperfusion. Coagulopathy is amplified by accompanying factors such as hypothermia or dilution. Diagnosis and therapy of deranged coagulation should start as soon as possible. Routinely tested coagulation parameters are of limited use to confirm diagnosis. Therapy follows the concept of "damage control resuscitation". Infusion of large volumes should be avoided and a mean arterial pressure of 65mmHg (in consideration of contraindications!) may be aimed.A specific protocol for massive transfusion should be introduced and continued.Acidaemia should be prevented and treated by appropriate shock therapy.Loss of body temperature should be prevented and treated. Hypocalcaemia <0.9 mmol/l should be avoided and may be treated. For actively bleeding patients, packed red blood cells (pRBC) may be given at haemoglobin<10g/dl(0,62mmol/l). If massive transfusion is performed using fresh frozen plasma (FFP), a ratio of FFP to pRBC of 1:2 to 1:1 should be achieved.For treatment of hyperfibrinolysis after severe trauma the use of tranexamic acid should be considered at an early stage. Fibrinogen should be substituted at levels <1,5g/l (4,41μmol/l). Prothrombin complex concentrates may be helpfull for treatment of diffuse bleeding or anticoagulativemedikation. In acute bleeding, platelets may be transfused at a platet count <100000/μl. For diffuse bleeding or thrombocytopathic patients desmopressin might be a therapeutic option.If a factor XIII (FXIII) measurement is not promptly available, a factor XIII blind-dose should be considered in severe ongoing bleeding. The use of recombinant activated coagulation factor VII (rFVIIa) be considered if major bleeding persists despite standard attempts to control bleeding and best practice use of blood components.

Kernaussagen

• Die traumainduzierte Koagulopathie (TIC) ist ein eigenständiges hochakutes multifaktorielles Krankheitsbild mit signifikantem Einfluss auf die Mortalität schwerstverletzter Patienten.

• Die Pathophysiologie der akuten TIC basiert auf dem aktuellen zellbasierten Modell der Gerinnung mit der Gewebefaktor(TF)-exprimierenden Zelle im Mittelpunkt.

• Zentrale Ursache der TIC scheint eine Verletzung des Endothels in Kombination mit einer relevanten systemischen Hypoperfusion („Schock“) zu sein.

• Hauptverantwortlich für Auftreten und Ausprägung einer TIC sind im Wesentlichen die Faktoren Gewebeverletzung, Minderperfusion / Schock, Verdünnung /Verlust, Hypothermie, Azidose und Inflammation.

• Der entscheidende Faktor für ein adäquates Management der akuten Gerinnungsstörung nach schwerem Trauma ist die frühzeitige Diagnose.

• Die Therapie der TIC erfolgt nach dem Konzept der Damage-Control-Resuscitation und beinhaltet die permissive Hypotension, den Ausgleich von Azidose, Hypokalzämie und Hypothermie sowie die Transfusion von Blutprodukten und die Gabe gerinnungsaktiver Präparate.

• Entscheidend ist eine adäquate Schocktherapie als Kombination aus Volumenersatz und Gerinnungsoptimierung zur Verhinderung eines Multiorganversagens.

• Ein spezifisches Massivtransfusionsprotokoll führt zu einer früheren und schnelleren Transfusion mit hohem FFP/ EK-Verhältnis und daher zu einer signifikanten Reduktion der Mortalität polytraumatisierter Patienten.

Schlüsselwörter:

Trauma - Blutung - Koagulopathie - Massivtransfusion - Gerinnungstherapie

Key words:

trauma - bleeding - coagulopathy,massive transfusion - coagulation therapy

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