V Hofer1,2, H Wrigge1, A Wienke3, G Hofmann4,5, P Hilbert-Carius6. 1. Klinik für Anästhesiologie, Intensiv‑, Notfallmedizin und Schmerztherapie, Bergmannstrost BG-Klinikum Halle (Saale), Merseburgerstr. 165, 06112, Halle (Saale), Deutschland. 2. Klinik für Anästhesiologie, Universitätsklinik Regensburg, Regensburg, Deutschland. 3. Institut für Medizinische Epidemiologie, Biometrie und Informatik, Martin-Luther-Universität Halle-Wittenberg, Halle (Saale), Deutschland. 4. Klinik für Unfall- und Wiederherstellungschirurgie, Bergmannstrost BG-Klinikum Halle (Saale), Halle (Saale), Deutschland. 5. Klinik für Unfall‑, Hand- und Wiederherstellungschirurgie Universitätsklinikum, Friedrich Schiller Universität Jena, Jena, Deutschland. 6. Klinik für Anästhesiologie, Intensiv‑, Notfallmedizin und Schmerztherapie, Bergmannstrost BG-Klinikum Halle (Saale), Merseburgerstr. 165, 06112, Halle (Saale), Deutschland. peter.hilbert@bergmannstrost.de.
Abstract
BACKGROUND: Plasmatic coagulation disorders in trauma patients are common and their management is subject to current guidelines. Less evidence exists for platelet function. Although it is known that several trauma-associated factors have a negative influence on platelet function, routine monitoring has not yet become established. METHODS: A retrospective single center study was carried out at a German level 1 trauma center from 2010 to 2016. In all patients fulfilling the requirements for the German Trauma Society (DGU) Traumaregister® who were admitted directly from the scene of the incident, platelet function was analyzed using the Platelet Function Analyzer (PFA 100®) with adenosine diphosphate (ADP) and epinephrine as activation factors. After exclusion of patients with intake of long-term anticoagulant and antiaggregant medication, possible influencing factors of a reduced platelet function were identified. RESULTS: The results from 310 patients (44.0 ± 14.7 years, 76% male, Injury Severity Score, ISS 28.4 ± 14.2 points) were available. A delayed platelet activation was found in 25.5% using ADP and 31% using epinephrine. Laboratory parameters indicated a greater blood loss. Prolonged closure times were associated with an increased transfusion rate of packed red blood cell concentrates and a higher mortality rate. Logistic regression revealed hemoglobin (Hb) and fibrinogen levels at admission to be independent predictors for a decreased platelet activation in the assay with ADP (p < 0.001, Cohen's f = 0.61) and with epinephrine (p < 0.001, f = 0.42). CONCLUSION: Approximately one quarter to one third of primarily admitted trauma patients without long-term anticoagulation medication showed a delayed platelet activation in the PFA-100 test. By considering all trauma patients an even higher rate can be expected. The Hb and fibrinogen levels at admission can be helpful to estimate platelet disorders. The development of platelet assays to guide the resuscitation of individual patients seems to be absolutely necessary. The contribution of platelet disorders to trauma-induced coagulopathy is not sufficiently understood. Regarding the importance assigned to platelet transfusion or administration of desmopressin, these aspects should be the subject of further research.
BACKGROUND: Plasmatic coagulation disorders in traumapatients are common and their management is subject to current guidelines. Less evidence exists for platelet function. Although it is known that several trauma-associated factors have a negative influence on platelet function, routine monitoring has not yet become established. METHODS: A retrospective single center study was carried out at a German level 1 trauma center from 2010 to 2016. In all patients fulfilling the requirements for the German Trauma Society (DGU) Traumaregister® who were admitted directly from the scene of the incident, platelet function was analyzed using the Platelet Function Analyzer (PFA 100®) with adenosine diphosphate (ADP) and epinephrine as activation factors. After exclusion of patients with intake of long-term anticoagulant and antiaggregant medication, possible influencing factors of a reduced platelet function were identified. RESULTS: The results from 310 patients (44.0 ± 14.7 years, 76% male, Injury Severity Score, ISS 28.4 ± 14.2 points) were available. A delayed platelet activation was found in 25.5% using ADP and 31% using epinephrine. Laboratory parameters indicated a greater blood loss. Prolonged closure times were associated with an increased transfusion rate of packed red blood cell concentrates and a higher mortality rate. Logistic regression revealed hemoglobin (Hb) and fibrinogen levels at admission to be independent predictors for a decreased platelet activation in the assay with ADP (p < 0.001, Cohen's f = 0.61) and with epinephrine (p < 0.001, f = 0.42). CONCLUSION: Approximately one quarter to one third of primarily admitted traumapatients without long-term anticoagulation medication showed a delayed platelet activation in the PFA-100 test. By considering all traumapatients an even higher rate can be expected. The Hb and fibrinogen levels at admission can be helpful to estimate platelet disorders. The development of platelet assays to guide the resuscitation of individual patients seems to be absolutely necessary. The contribution of platelet disorders to trauma-induced coagulopathy is not sufficiently understood. Regarding the importance assigned to platelet transfusion or administration of desmopressin, these aspects should be the subject of further research.
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