Satoshi Gando1,2, Atsushi Shiraishi3, Takeshi Wada2, Kazuma Yamakawa4, Seitaro Fujishima5, Daizoh Saitoh6, Shigeki Kushimoto7, Hiroshi Ogura8, Toshikazu Abe9,10, Yasuhiro Otomo11. 1. Department of Acute and Critical Care Medicine, Sapporo Higashi Tokushukai Hospital, Sapporo, Japan. 2. Division of Acute and Critical Care Medicine, Department of Anesthesiology and Critical Care Medicine, Hokkaido University Graduate School of Medicine, Sapporo, Japan. 3. Emergency and Trauma Center, Kameda Medical Center, Kameda, Japan. 4. Division of Trauma and Surgical Critical Care, Osaka General Medical Center, Osaka, Japan. 5. Center for General Medicine Education, Keio University School of Medicine, Tokyo, Japan. 6. Division of Traumatology, Research Institute, National Defense Medical College, Tokorozawa, Japan. 7. Division of Emergency and Critical Care Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan. 8. Department of Traumatology and Acute Critical Medicine, Osaka University Graduate School of Medicine, Osaka, Japan. 9. Department of General Medicine, Juntendo University, Tokyo, Japan. 10. Health Services Research and Development Center, University of Tsukuba, Tsukuba, Japan. 11. Trauma and Acute Critical Care Center, Medical Hospital, Tokyo Medical and Dental University, Tokyo, Japan.
Abstract
BACKGROUND: Trauma-induced coagulopathy (TIC) may progress to disseminated intravascular coagulation (DIC) due to dysregulated inflammatory and coagulofibrinolytic responses to trauma. OBJECTIVES: We explored how DIC and TIC elicit the same coagulofibrinolytic changes which lead to massive transfusion. METHODS: Severely injured trauma patients with an injury severity score ≥ 16 were prospectively included. Platelet counts, global markers of coagulation and fibrinolysis and specific markers of thrombin and plasmin generation, anticoagulation, endothelial injury, and inhibition of fibrinolysis were measured at presentation to the emergency department (0 hour) and 3 hour after arrival. The patients were subdivided into those with and without DIC and those with and without TIC using the 0-hour data. Time courses of specific markers and the frequency of massive transfusion were evaluated. The association of various variables with DIC development was also confirmed. RESULTS: Two hundred and seventy-six patients were eligible for the analyses. The severity of injury (odds ratio; 1.038, P = .022) and thrombin generation (odds ratio; 1.014, P = .024) were associated with the development of DIC. Both DIC and TIC patients showed increased thrombin generation, insufficient anticoagulation controls, endothelial injury and increased fibrinolysis followed by elevated plasminogen activator inhibitor-1 levels at 0 and 3 hours. The frequency of massive transfusion was higher in both DIC (33.6% vs 7.9%, P < .001) and TIC (50.0% vs 13.3%, P < .001) patients than in those without DIC or TIC, respectively. CONCLUSIONS: Disseminated intravascular coagulation and TIC evoked the same coagulofibrinolytic responses in severely injured trauma patients immediately after trauma and needed massive transfusion.
BACKGROUND:Trauma-induced coagulopathy (TIC) may progress to disseminated intravascular coagulation (DIC) due to dysregulated inflammatory and coagulofibrinolytic responses to trauma. OBJECTIVES: We explored how DIC and TIC elicit the same coagulofibrinolytic changes which lead to massive transfusion. METHODS: Severely injured traumapatients with an injury severity score ≥ 16 were prospectively included. Platelet counts, global markers of coagulation and fibrinolysis and specific markers of thrombin and plasmin generation, anticoagulation, endothelial injury, and inhibition of fibrinolysis were measured at presentation to the emergency department (0 hour) and 3 hour after arrival. The patients were subdivided into those with and without DIC and those with and without TIC using the 0-hour data. Time courses of specific markers and the frequency of massive transfusion were evaluated. The association of various variables with DIC development was also confirmed. RESULTS: Two hundred and seventy-six patients were eligible for the analyses. The severity of injury (odds ratio; 1.038, P = .022) and thrombin generation (odds ratio; 1.014, P = .024) were associated with the development of DIC. Both DIC and TIC patients showed increased thrombin generation, insufficient anticoagulation controls, endothelial injury and increased fibrinolysis followed by elevated plasminogen activator inhibitor-1 levels at 0 and 3 hours. The frequency of massive transfusion was higher in both DIC (33.6% vs 7.9%, P < .001) and TIC (50.0% vs 13.3%, P < .001) patients than in those without DIC or TIC, respectively. CONCLUSIONS:Disseminated intravascular coagulation and TIC evoked the same coagulofibrinolytic responses in severely injured traumapatients immediately after trauma and needed massive transfusion.
Authors: Alexander P Morton; Jamie B Hadley; Arsen Ghasabyan; Marguerite R Kelher; Ernest E Moore; Shaun Bevers; Monika Dzieciatkowska; Kirk C Hansen; Mitchell S Cohen; Anirban Banerjee; Christopher C Silliman Journal: J Trauma Acute Care Surg Date: 2022-01-01 Impact factor: 3.697
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Authors: Joseph D Krocker; Kyung Hyun Lee; Hanne H Henriksen; Yao-Wei Willa Wang; Erwin M Schoof; Sigurdur T Karvelsson; Óttar Rolfsson; Pär I Johansson; Claudia Pedroza; Charles E Wade Journal: Int J Mol Sci Date: 2022-06-01 Impact factor: 6.208