Impact of Oral Anticoagulation and Adenosine Diphosphate Inhibitor Therapies on Short-term Outcome of Traumatic Brain Injury.


Journal

Neurology
ISSN: 1526-632X
Titre abrégé: Neurology
Pays: United States
ID NLM: 0401060

Informations de publication

Date de publication:
13 Sep 2022
Historique:
received: 22 11 2021
accepted: 22 04 2022
pubmed: 29 6 2022
medline: 15 9 2022
entrez: 28 6 2022
Statut: ppublish

Résumé

Usage of oral anticoagulants (OACs) or adenosine diphosphate inhibitors (ADPi) is known to increase the risk of bleeding. We aimed to investigate the impact of OAC and ADPi therapies on short-term outcomes after traumatic brain injury (TBI). All adult patients hospitalized for TBI in Finland during 2005-2018 were retrospectively studied using a combination of national registries. Usage of pharmacy-purchased OACs and ADPi at the time of TBI was analyzed with the pill-counting method (Social Insurance Institution of Finland). The primary outcome was 30-day case-fatality (Finnish Cause of Death Registry). The secondary outcomes were acute neurosurgical operation (ANO) and admission duration (Finnish Care Register for Health Care). Baseline characteristics were adjusted with multivariable regression, including age, sex, comorbidities, skull or facial fracture, OAC/ADPi treatment, initial admission location, and the year of TBI admission. The study population included 57,056 persons (mean age 66 years) of whom 0.9% used direct OACs (DOACs), 7.1% vitamin K antagonists (VKA), and 2.3% ADPi. Patients with VKAs had higher case-fatality than patients without OAC (15.4% vs 7.1%; adjusted hazard ratio [aHR] 1.35, CI 1.23-1.48; Preinjury use of VKA is associated with increases in short-term mortality and in need for ANOs after TBI. DOACs are associated with lower fatality than VKAs after TBI. ADPi were not independently associated with the outcomes studied. These results point to relative safety of DOACs or ADPi in patients at risk of head trauma and encourage to choose DOACs when oral anticoagulation is required. This study provides Class II evidence that among adults with TBI, mortality was significantly increased in those using VKAs but not in those using DOACs or ADPi.

Sections du résumé

BACKGROUND AND OBJECTIVES
Usage of oral anticoagulants (OACs) or adenosine diphosphate inhibitors (ADPi) is known to increase the risk of bleeding. We aimed to investigate the impact of OAC and ADPi therapies on short-term outcomes after traumatic brain injury (TBI).
METHODS
All adult patients hospitalized for TBI in Finland during 2005-2018 were retrospectively studied using a combination of national registries. Usage of pharmacy-purchased OACs and ADPi at the time of TBI was analyzed with the pill-counting method (Social Insurance Institution of Finland). The primary outcome was 30-day case-fatality (Finnish Cause of Death Registry). The secondary outcomes were acute neurosurgical operation (ANO) and admission duration (Finnish Care Register for Health Care). Baseline characteristics were adjusted with multivariable regression, including age, sex, comorbidities, skull or facial fracture, OAC/ADPi treatment, initial admission location, and the year of TBI admission.
RESULTS
The study population included 57,056 persons (mean age 66 years) of whom 0.9% used direct OACs (DOACs), 7.1% vitamin K antagonists (VKA), and 2.3% ADPi. Patients with VKAs had higher case-fatality than patients without OAC (15.4% vs 7.1%; adjusted hazard ratio [aHR] 1.35, CI 1.23-1.48;
DISCUSSION
Preinjury use of VKA is associated with increases in short-term mortality and in need for ANOs after TBI. DOACs are associated with lower fatality than VKAs after TBI. ADPi were not independently associated with the outcomes studied. These results point to relative safety of DOACs or ADPi in patients at risk of head trauma and encourage to choose DOACs when oral anticoagulation is required.
CLASSIFICATION OF EVIDENCE
This study provides Class II evidence that among adults with TBI, mortality was significantly increased in those using VKAs but not in those using DOACs or ADPi.

Identifiants

pubmed: 35764401
pii: WNL.0000000000200834
doi: 10.1212/WNL.0000000000200834
doi:

Substances chimiques

Anticoagulants 0
Vitamin K 12001-79-5
Adenosine Diphosphate 61D2G4IYVH

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e1122-e1130

Informations de copyright

© 2022 American Academy of Neurology.

Auteurs

Jussi P Posti (JP)

From the Neurocenter (J.P.P.), Department of Neurosurgery and Turku Brain Injury Center; Neurocenter (J.O.R.), Department of Neurology, Turku University Hospital and University of Turku; Clinical Neurosciences (J.O.T.S.), University of Turku; Department of Neurology (J.O.T.S.), North Karelia Central Hospital, Siun sote, Joensuu; Department of Neurosurgery (T.M.L.), Tampere University Hospital and Tampere University; Clinical Research Center (P.R.), Turku University Hospital and University of Turku; Heart Centre and Center for Population Health Research (V.K.), Turku University Hospital and University of Turku; Research Center of Applied and Preventive Cardiovascular Medicine (V.K.), University of Turku; Administrative Center (V.K.), Hospital District of Southwest Finland, Turku; and Department of Public Health (V.K.), Faculty of Medicine, University of Helsinki, Finland. jussi.posti@utu.fi.

Jori O Ruuskanen (JO)

From the Neurocenter (J.P.P.), Department of Neurosurgery and Turku Brain Injury Center; Neurocenter (J.O.R.), Department of Neurology, Turku University Hospital and University of Turku; Clinical Neurosciences (J.O.T.S.), University of Turku; Department of Neurology (J.O.T.S.), North Karelia Central Hospital, Siun sote, Joensuu; Department of Neurosurgery (T.M.L.), Tampere University Hospital and Tampere University; Clinical Research Center (P.R.), Turku University Hospital and University of Turku; Heart Centre and Center for Population Health Research (V.K.), Turku University Hospital and University of Turku; Research Center of Applied and Preventive Cardiovascular Medicine (V.K.), University of Turku; Administrative Center (V.K.), Hospital District of Southwest Finland, Turku; and Department of Public Health (V.K.), Faculty of Medicine, University of Helsinki, Finland.

Jussi O T Sipilä (JOT)

From the Neurocenter (J.P.P.), Department of Neurosurgery and Turku Brain Injury Center; Neurocenter (J.O.R.), Department of Neurology, Turku University Hospital and University of Turku; Clinical Neurosciences (J.O.T.S.), University of Turku; Department of Neurology (J.O.T.S.), North Karelia Central Hospital, Siun sote, Joensuu; Department of Neurosurgery (T.M.L.), Tampere University Hospital and Tampere University; Clinical Research Center (P.R.), Turku University Hospital and University of Turku; Heart Centre and Center for Population Health Research (V.K.), Turku University Hospital and University of Turku; Research Center of Applied and Preventive Cardiovascular Medicine (V.K.), University of Turku; Administrative Center (V.K.), Hospital District of Southwest Finland, Turku; and Department of Public Health (V.K.), Faculty of Medicine, University of Helsinki, Finland.

Teemu M Luoto (TM)

From the Neurocenter (J.P.P.), Department of Neurosurgery and Turku Brain Injury Center; Neurocenter (J.O.R.), Department of Neurology, Turku University Hospital and University of Turku; Clinical Neurosciences (J.O.T.S.), University of Turku; Department of Neurology (J.O.T.S.), North Karelia Central Hospital, Siun sote, Joensuu; Department of Neurosurgery (T.M.L.), Tampere University Hospital and Tampere University; Clinical Research Center (P.R.), Turku University Hospital and University of Turku; Heart Centre and Center for Population Health Research (V.K.), Turku University Hospital and University of Turku; Research Center of Applied and Preventive Cardiovascular Medicine (V.K.), University of Turku; Administrative Center (V.K.), Hospital District of Southwest Finland, Turku; and Department of Public Health (V.K.), Faculty of Medicine, University of Helsinki, Finland.

Päivi Rautava (P)

From the Neurocenter (J.P.P.), Department of Neurosurgery and Turku Brain Injury Center; Neurocenter (J.O.R.), Department of Neurology, Turku University Hospital and University of Turku; Clinical Neurosciences (J.O.T.S.), University of Turku; Department of Neurology (J.O.T.S.), North Karelia Central Hospital, Siun sote, Joensuu; Department of Neurosurgery (T.M.L.), Tampere University Hospital and Tampere University; Clinical Research Center (P.R.), Turku University Hospital and University of Turku; Heart Centre and Center for Population Health Research (V.K.), Turku University Hospital and University of Turku; Research Center of Applied and Preventive Cardiovascular Medicine (V.K.), University of Turku; Administrative Center (V.K.), Hospital District of Southwest Finland, Turku; and Department of Public Health (V.K.), Faculty of Medicine, University of Helsinki, Finland.

Ville Kytö (V)

From the Neurocenter (J.P.P.), Department of Neurosurgery and Turku Brain Injury Center; Neurocenter (J.O.R.), Department of Neurology, Turku University Hospital and University of Turku; Clinical Neurosciences (J.O.T.S.), University of Turku; Department of Neurology (J.O.T.S.), North Karelia Central Hospital, Siun sote, Joensuu; Department of Neurosurgery (T.M.L.), Tampere University Hospital and Tampere University; Clinical Research Center (P.R.), Turku University Hospital and University of Turku; Heart Centre and Center for Population Health Research (V.K.), Turku University Hospital and University of Turku; Research Center of Applied and Preventive Cardiovascular Medicine (V.K.), University of Turku; Administrative Center (V.K.), Hospital District of Southwest Finland, Turku; and Department of Public Health (V.K.), Faculty of Medicine, University of Helsinki, Finland.

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