Jawad T Ali1, Mitchell J Daley2, Nina Vadiei3, Zachary Enright4, Joseph Nguyen5, Sadia Ali6, Jayson D Aydelotte7, Pedro G Teixeira8, Thomas B Coopwood9, Carlos Vr Brown10. 1. Department of Trauma Services, University Medical Center Brackenridge, United States; Department of Surgery, Dell Medical School at the University of Texas at Austin, United States. Electronic address: jtali@seton.org. 2. Department of Pharmaceutical Services, University Medical Center Brackenridge, United States; College of Pharmacy, University of Texas at Austin, United States. Electronic address: mjdaley@seton.org. 3. Department of Pharmaceutical Services, University Medical Center Brackenridge, United States; College of Pharmacy, University of Texas at Austin, United States. Electronic address: nvadiei@seton.org. 4. Department of Pharmaceutical Services, University Medical Center Brackenridge, United States; College of Pharmacy, University of Texas at Austin, United States. Electronic address: zme07a@acu.edu. 5. Department of Pharmaceutical Services, University Medical Center Brackenridge, United States; College of Pharmacy, University of Texas at Austin, United States. Electronic address: josephn5833@gmail.com. 6. Department of Trauma Services, University Medical Center Brackenridge, United States. Electronic address: Sali@seton.org. 7. Department of Trauma Services, University Medical Center Brackenridge, United States; Department of Surgery, Dell Medical School at the University of Texas at Austin, United States. Electronic address: jdaydelotte@seton.org. 8. Department of Trauma Services, University Medical Center Brackenridge, United States; Department of Surgery, Dell Medical School at the University of Texas at Austin, United States. Electronic address: pgteixeira@seton.org. 9. Department of Trauma Services, University Medical Center Brackenridge, United States; Department of Surgery, Dell Medical School at the University of Texas at Austin, United States. Electronic address: tbcoopwoodjr@seton.org. 10. Department of Trauma Services, University Medical Center Brackenridge, United States; Department of Surgery, Dell Medical School at the University of Texas at Austin, United States. Electronic address: cvrbrown@seton.org.
Abstract
PURPOSE: Thromboelastography (TEG) has been recommended to characterize post-traumatic coagulopathy, yet no study has evaluated the impact of pre-injury anticoagulation (AC) on TEG variables. We hypothesized patients on pre-injury AC have a greater incidence of coagulopathy on TEG compared to those without AC. METHODS: This retrospective chart review evaluated all trauma patients admitted to an urban, level one trauma center from February 2011 to September 2014 who received a TEG within the first 24h. Patients were classified as receiving pre-injury AC or no AC if their documented medications prior to admission included warfarin, dabigatran, or anti-Xa (aXa) inhibitors (apixaban or rivaroxaban). The presence of coagulopathy on TEG or conventional assays was defined by exceeding local laboratory reference standards. RESULTS: A total of 54 patients were included (AC, n=27 [warfarin n=13, dabigatran n=6, aXa inhibitor n=8] vs. no AC, n=27). Baseline characteristics were similar between groups, including age (72±13years vs. 72±15; p=0.85), male gender (70% vs. 74%; p=0.76) and blunt mechanism of injury (100% vs. 100%; p=1). There was no difference in the number of patients determined to have coagulopathy on TEG (no AC 11% vs. AC 15%; p=0.99). Conventional tests, including the international normalized ratio (INR) and activated partial thromboplastin time (aPTT), identified coagulopathy in a high proportion of anti-coagulated patients (no AC 22% vs. AC 85%; p<0.01). CONCLUSION: TEG has limited clinical utility to evaluate the presence of pre-injury AC. Traditional markers of drug induced coagulopathy should guide reversal decisions.
PURPOSE: Thromboelastography (TEG) has been recommended to characterize post-traumatic coagulopathy, yet no study has evaluated the impact of pre-injury anticoagulation (AC) on TEG variables. We hypothesized patients on pre-injury AC have a greater incidence of coagulopathy on TEG compared to those without AC. METHODS: This retrospective chart review evaluated all traumapatients admitted to an urban, level one trauma center from February 2011 to September 2014 who received a TEG within the first 24h. Patients were classified as receiving pre-injury AC or no AC if their documented medications prior to admission included warfarin, dabigatran, or anti-Xa (aXa) inhibitors (apixaban or rivaroxaban). The presence of coagulopathy on TEG or conventional assays was defined by exceeding local laboratory reference standards. RESULTS: A total of 54 patients were included (AC, n=27 [warfarin n=13, dabigatran n=6, aXa inhibitor n=8] vs. no AC, n=27). Baseline characteristics were similar between groups, including age (72±13years vs. 72±15; p=0.85), male gender (70% vs. 74%; p=0.76) and blunt mechanism of injury (100% vs. 100%; p=1). There was no difference in the number of patients determined to have coagulopathy on TEG (no AC 11% vs. AC 15%; p=0.99). Conventional tests, including the international normalized ratio (INR) and activated partial thromboplastin time (aPTT), identified coagulopathy in a high proportion of anti-coagulated patients (no AC 22% vs. AC 85%; p<0.01). CONCLUSION: TEG has limited clinical utility to evaluate the presence of pre-injury AC. Traditional markers of drug induced coagulopathy should guide reversal decisions.
Authors: Leslie M Kobayashi; Alexandra Brito; Galinos Barmparas; Patrick Bosarge; Carlos V Brown; Marko Bukur; Matthew M Carrick; Richard D Catalano; Jan Holly-Nicolas; Kenji Inaba; Stephen Kaminski; Amanda L Klein; Tammy Kopelman; Eric J Ley; Ericca M Martinez; Forrest O Moore; Jason Murry; Raminder Nirula; Douglas Paul; Jacob Quick; Omar Rivera; Martin Schreiber; Raul Coimbra Journal: Trauma Surg Acute Care Open Date: 2018-10-15