Time-Dependent Association of Preinjury Anticoagulation on Traumatic Brain Injury-Induced Coagulopathy: A Retrospective, Multicenter Cohort Study.


Journal

Neurosurgery
ISSN: 1524-4040
Titre abrégé: Neurosurgery
Pays: United States
ID NLM: 7802914

Informations de publication

Date de publication:
24 Oct 2024
Historique:
received: 03 04 2024
accepted: 26 08 2024
medline: 25 10 2024
pubmed: 25 10 2024
entrez: 24 10 2024
Statut: aheadofprint

Résumé

The impact of preinjury anticoagulation on coagulation parameters over time after traumatic brain injury (TBI) has remained unclear. Based on the hypothesis that preinjury anticoagulation significantly influences the progression and persistence of TBI-induced coagulopathy, we retrospectively examined the association of preinjury anticoagulation with various coagulation parameters during the first 24 hours postinjury in 5 periods. Data from the Japanese registry of patients with TBI aged ≥65 years admitted between 2019 and 2021 were used. Time since injury was classified into 5 categories through a graphical analysis of coagulation parameters. We examined the association between preinjury anticoagulation and the platelet count, prothrombin time-international normalized ratio (PT-INR), activated partial thromboplastin time (APTT), D-dimer level, and fibrinogen level during each period by analysis of covariance using 10 clinical factors as confounding factors. Data from 545 patients and 795 blood tests were analyzed. The patients' mean age was 78.9 years, and 87 (16%) received anticoagulation therapy. The preinjury anticoagulation group had significantly greater Rotterdam computed tomography scores and poorer outcomes at discharge than the control group, with significantly lower D-dimer levels and higher fibrinogen levels. Analysis of covariance revealed significant associations between the D-dimer level and preinjury anticoagulation within 2 to 24 hours postinjury, APTT and preinjury anticoagulation within 1 to 24 hours, and PT-INR and preinjury anticoagulation throughout all periods up to 24 hours postinjury. Despite more severe TBI signs and poorer outcomes, the preinjury anticoagulation group had significantly lower D-dimer levels, especially within 2 to 24 hours postinjury. Thus, D-dimer levels during this period may not reliably represent TBI severity in patients receiving anticoagulation therapy before injury. Preinjury anticoagulation was also associated with an elevated PT-INR and prolonged APTT from early to 24 hours postinjury, highlighting the importance of aggressive anticoagulant reversal early after injury.

Sections du résumé

BACKGROUND AND OBJECTIVES OBJECTIVE
The impact of preinjury anticoagulation on coagulation parameters over time after traumatic brain injury (TBI) has remained unclear. Based on the hypothesis that preinjury anticoagulation significantly influences the progression and persistence of TBI-induced coagulopathy, we retrospectively examined the association of preinjury anticoagulation with various coagulation parameters during the first 24 hours postinjury in 5 periods.
METHODS METHODS
Data from the Japanese registry of patients with TBI aged ≥65 years admitted between 2019 and 2021 were used. Time since injury was classified into 5 categories through a graphical analysis of coagulation parameters. We examined the association between preinjury anticoagulation and the platelet count, prothrombin time-international normalized ratio (PT-INR), activated partial thromboplastin time (APTT), D-dimer level, and fibrinogen level during each period by analysis of covariance using 10 clinical factors as confounding factors.
RESULTS RESULTS
Data from 545 patients and 795 blood tests were analyzed. The patients' mean age was 78.9 years, and 87 (16%) received anticoagulation therapy. The preinjury anticoagulation group had significantly greater Rotterdam computed tomography scores and poorer outcomes at discharge than the control group, with significantly lower D-dimer levels and higher fibrinogen levels. Analysis of covariance revealed significant associations between the D-dimer level and preinjury anticoagulation within 2 to 24 hours postinjury, APTT and preinjury anticoagulation within 1 to 24 hours, and PT-INR and preinjury anticoagulation throughout all periods up to 24 hours postinjury.
CONCLUSION CONCLUSIONS
Despite more severe TBI signs and poorer outcomes, the preinjury anticoagulation group had significantly lower D-dimer levels, especially within 2 to 24 hours postinjury. Thus, D-dimer levels during this period may not reliably represent TBI severity in patients receiving anticoagulation therapy before injury. Preinjury anticoagulation was also associated with an elevated PT-INR and prolonged APTT from early to 24 hours postinjury, highlighting the importance of aggressive anticoagulant reversal early after injury.

Identifiants

pubmed: 39446739
doi: 10.1227/neu.0000000000003238
pii: 00006123-990000000-01405
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Japan Society for the Promotion of Science, CSL Behring
ID : 21K18079

Informations de copyright

Copyright © 2024 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the Congress of Neurological Surgeons.

Références

Nguyen RK, Rizor JH, Damiani MP, et al. The impact of anticoagulation on trauma outcomes: an national trauma data bank study. Am Surg. 2020;86(7):773-781.
Grandhi R, Harrison G, Voronovich Z, et al. Preinjury warfarin, but not antiplatelet medications, increases mortality in elderly traumatic brain injury patients. J Trauma Acute Care Surg. 2015;78(3):614-621.
Nederpelt CJ, van der Aalst SJM, Rosenthal MG, et al. Consequences of pre-injury utilization of direct oral anticoagulants in patients with traumatic brain injury: a systematic review and meta-analysis. J Trauma Acute Care Surg. 2020;88(1):186-194.
Hecht JP, LaDuke ZJ, Cain-Nielsen AH, Hemmila MR, Wahl WL. Effect of preinjury oral anticoagulants on outcomes following traumatic brain injury from falls in older adults. Pharmacotherapy. 2020;40(7):604-613.
Markou M, Pleger B, Grozinger M, et al. Intake of NOAC is associated with hematoma expansion of intracerebral hematomas after traumatic brain injury. Eur J Trauma Emerg Surg. 2021;47(2):565-571.
Bohm JK, Guting H, Thorn S, et al. Global characterisation of coagulopathy in isolated traumatic brain injury (iTBI): a CENTER-TBI analysis. Neurocrit Care. 2021;35(1):184-196.
Suehiro E, Shiomi N, Yatsushige H, et al. The current status of reversal therapy in Japan for elderly patients with head injury treated with antithrombotic agents: a prospective multicenter observational study. Heliyon. 2024;10(3):e25193.
Nakae R, Takayama Y, Kuwamoto K, Naoe Y, Sato H, Yokota H. Time course of coagulation and fibrinolytic parameters in patients with traumatic brain injury. J Neurotrauma. 2016;33(7):688-695.
von Elm E, Altman DG, Egger M, et al. The Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) statement: guidelines for reporting observational studies. J Clin Epidemiol. 2008;61(4):344-349.
Jadhav A, Pramod D, Ramanathan K. Comparison of performance of data imputation methods for numeric dataset. Appl Artif Intell. 2019;33(10):913-933.
Yeo IK. A new family of power transformations to improve normality or symmetry. Biometrika. 2000;87(4):954-959.
Pedregosa F, Varoquaux G, Gramfort A, et al. Scikit-learn: machine learning in python. J Mach Learn Res. 2011;12:2825-2830.
Juratli TA, Zang B, Litz RJ, et al. Early hemorrhagic progression of traumatic brain contusions: frequency, correlation with coagulation disorders, and patient outcome: a prospective study. J Neurotrauma. 2014;31(17):1521-1527.
Stein ShermanC, Smith DH. Coagulopathy in traumatic brain injury. Neurocrit Care. 2004;1(4):479-488.
Moore EE, Moore HB, Kornblith LZ, et al. Trauma-induced coagulopathy. Nat Rev Dis Primers. 2021;7(1):30.
Halpern CH, Reilly PM, Turtz AR, Stein SC. Traumatic coagulopathy: the effect of brain injury. J Neurotrauma. 2008;25(8):997-1001.
Gando S, Shiraishi A, Wada T, et al. Effects of tranexamic acid on coagulofibrinolytic markers during the early stage of severe trauma: a propensity score-matched analysis. Medicine (Baltimore). 2022;101(32):e29711.
Fletcher-Sandersjoo A, Thelin EP, Maegele M, Svensson M, Bellander BM. Time course of hemostatic disruptions after traumatic brain injury: a systematic review of the literature. Neurocrit Care. 2021;34(2):635-656.
Fair KA, Farrell DH, McCully BH, et al. Fibrinolytic activation in patients with progressive intracranial hemorrhage after traumatic brain injury. J Neurotrauma. 2021;38(8):960-966.
Pahatouridis D, Alexiou GA, Zigouris A, Mihos E, Drosos D, Voulgaris S. Coagulopathy in moderate head injury. The role of early administration of low molecular weight heparin. Brain Inj. 2010;24(10):1189-1192.
Adcock DM, Gosselin RC. The danger of relying on the APTT and PT in patients on DOAC therapy, a potential patient safety issue. Int J Lab Hematol. 2017;39(Suppl 1):37-40.
Samuelson BT, Cuker A, Siegal DM, Crowther M, Garcia DA. Laboratory assessment of the anticoagulant activity of direct oral anticoagulants: a systematic review. Chest. 2017;151(1):127-138.
Kockelmann F, Maegele M. Acute haemostatic depletion and failure in patients with traumatic brain injury (TBI): pathophysiological and clinical considerations. J Clin Med. 2023;12(8):2809.
Filipow N, Main E, Tanriver G, et al. Exploring flexible polynomial regression as a method to align routine clinical outcomes with daily data capture through remote technologies. BMC Med Res Methodol. 2023;23(1):114.
Nakae R, Yokobori S, Takayama Y, et al. A retrospective study of the effect of fibrinogen levels during fresh frozen plasma transfusion in patients with traumatic brain injury. Acta Neurochir (Wien). 2019;161(9):1943-1953.

Auteurs

Kazuya Matsuo (K)

Department of Neurosurgery, Hyogo Emergency Medical Center and Kobe Red Cross Hospital, Kobe, Hyogo, Japan.
Department of Neurosurgery, Kobe University Graduate School of Medicine, Kobe, Hyogo, Japan.

Hideo Aihara (H)

Department of Neurosurgery, Hyogo Prefectural Kakogawa Medical Center, Kakogawa, Hyogo, Japan.
Current Affiliation: Department of Neurosurgery, Hyogo Prefectural Harima-Himeji General Medical Center, Himeji, Japan.

Eiichi Suehiro (E)

Department of Neurosurgery, International University of Health and Welfare, School of Medicine, Narita, Chiba, Japan.

Naoto Shiomi (N)

Department of Critical and Intensive Care Medicine, Emergency Medical Care Center, Saiseikai Shiga Hospital, Ritto, Shiga, Japan.

Hiroshi Yatsushige (H)

Department of Neurosurgery, National Hospital Organization Disaster Medical Center, Tachikawa, Tokyo, Japan.

Shin Hirota (S)

Department of Neurosurgery, Tsuchiura Kyodo General Hospital, Tsuchiura, Ibaraki, Japan.

Shu Hasegawa (S)

Department of Neurosurgery, Kumamoto Red Cross Hospital, Kumamoto, Kumamoto, Japan.

Hiroshi Karibe (H)

Department of Neurosurgery, Sendai City Hospital, Sendai, Miyagi, Japan.

Akihiro Miyata (A)

Department of Neurosurgery, Chiba Emergency Medical Center, Chiba, Chiba, Japan.

Kenya Kawakita (K)

Department of Emergency and Critical Care Medicine, Emergency Medical Center, Kagawa University Hospital, Kita-gun, Kagawa, Japan.

Kohei Haji (K)

Department of Neurosurgery, Yamaguchi University School of Medicine, Ube, Yamaguchi, Japan.

Shoji Yokobori (S)

Department of Emergency and Critical Care Medicine, Graduate School of Medicine, Nippon Medical School, Bunkyo-ku, Tokyo, Japan.

Motoki Inaji (M)

Department of Neurosurgery, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo, Japan.

Takeshi Maeda (T)

Department of Neurological Surgery, Nihon University School of Medicine, Itabashi-ku, Tokyo, Japan.

Takahiro Onuki (T)

Department of Emergency Medicine, Teikyo University School of Medicine, Itabashi-ku, Tokyo, Japan.

Kotaro Oshio (K)

Department of Neurosurgery, St. Marianna University School of Medicine, Kawasaki, Kanagawa, Japan.

Nobukazu Komoribayashi (N)

Department of Neurosurgery, Iwate Prefectural Advanced Critical Care and Emergency Center, Iwate Medical University, Yahaba, Iwate, Japan.

Michiyasu Suzuki (M)

Department of Neurosurgery, Yamaguchi University School of Medicine, Ube, Yamaguchi, Japan.

Classifications MeSH