Tranexamic acid administration in the field does not affect admission thromboelastography after traumatic brain injury.
Abbreviated Injury Scale
Adolescent
Adult
Antifibrinolytic Agents
/ administration & dosage
Blood Coagulation
/ drug effects
Blood Coagulation Disorders
Brain Injuries, Traumatic
/ blood
Female
Fibrin Fibrinogen Degradation Products
/ analysis
Fibrinolysin
/ analysis
Fibrinolysis
/ drug effects
Humans
Infusions, Intravenous
Injections, Intravenous
Male
Middle Aged
Thrombelastography
/ statistics & numerical data
Time-to-Treatment
Tranexamic Acid
/ administration & dosage
Treatment Outcome
Young Adult
alpha-2-Antiplasmin
/ analysis
Journal
The journal of trauma and acute care surgery
ISSN: 2163-0763
Titre abrégé: J Trauma Acute Care Surg
Pays: United States
ID NLM: 101570622
Informations de publication
Date de publication:
11 2020
11 2020
Historique:
entrez:
26
10
2020
pubmed:
27
10
2020
medline:
3
2
2021
Statut:
ppublish
Résumé
No Food and Drug Administration-approved medication improves outcomes following traumatic brain injury (TBI). A forthcoming clinical trial that evaluated the effects of two prehospital tranexamic acid (TXA) dosing strategies compared with placebo demonstrated no differences in thromboelastography (TEG) values. We proposed to explore the impact of TXA on markers of coagulation and fibrinolysis in patients with moderate to severe TBI. Data were extracted from a placebo-controlled clinical trial in which patients 15 years or older with TBI (Glasgow Coma Scale, 3-12) and systolic blood pressure of ≥90 mm Hg were randomized prehospital to receive placebo bolus/placebo infusion (placebo), 1 g of TXA bolus/1 g of TXA infusion (bolus maintenance), or 2 g of TXA bolus/placebo infusion (bolus only). Thromboelastography was performed, and coagulation measures including prothrombin time, activated partial thromboplastin time, international ratio, fibrinogen, D-dimer, plasmin-antiplasmin (PAP), thrombin antithrombin, tissue plasminogen activator, and plasminogen activator inhibitor 1 were quantified at admission and 6 hours later. Of 966 patients receiving study drug, 700 had laboratory tests drawn at admission and 6 hours later. There were no statistically significant differences in TEG values, including LY30, between groups (p > 0.05). No differences between prothrombin time, activated partial thromboplastin time, international ratio, fibrinogen, thrombin antithrombin, tissue plasminogen activator, and plasminogen activator inhibitor 1 were demonstrated across treatment groups. Concentrations of D-dimer in TXA treatment groups were less than placebo at 6 hours (p < 0.001). Concentrations of PAP in TXA treatment groups were less than placebo on admission (p < 0.001) and 6 hours (p = 0.02). No differences in D-dimer and PAP were observed between bolus maintenance and bolus only. While D-dimer and PAP levels reflect a lower degree of fibrinolysis following prehospital administration of TXA when compared with placebo in a large prehospital trial of patients with TBI, TEG obtained on admission and 6 hours later did not demonstrate any differences in fibrinolysis between the two TXA dosing regimens and placebo. Diagnostic test, level III.
Sections du résumé
BACKGROUND
No Food and Drug Administration-approved medication improves outcomes following traumatic brain injury (TBI). A forthcoming clinical trial that evaluated the effects of two prehospital tranexamic acid (TXA) dosing strategies compared with placebo demonstrated no differences in thromboelastography (TEG) values. We proposed to explore the impact of TXA on markers of coagulation and fibrinolysis in patients with moderate to severe TBI.
METHODS
Data were extracted from a placebo-controlled clinical trial in which patients 15 years or older with TBI (Glasgow Coma Scale, 3-12) and systolic blood pressure of ≥90 mm Hg were randomized prehospital to receive placebo bolus/placebo infusion (placebo), 1 g of TXA bolus/1 g of TXA infusion (bolus maintenance), or 2 g of TXA bolus/placebo infusion (bolus only). Thromboelastography was performed, and coagulation measures including prothrombin time, activated partial thromboplastin time, international ratio, fibrinogen, D-dimer, plasmin-antiplasmin (PAP), thrombin antithrombin, tissue plasminogen activator, and plasminogen activator inhibitor 1 were quantified at admission and 6 hours later.
RESULTS
Of 966 patients receiving study drug, 700 had laboratory tests drawn at admission and 6 hours later. There were no statistically significant differences in TEG values, including LY30, between groups (p > 0.05). No differences between prothrombin time, activated partial thromboplastin time, international ratio, fibrinogen, thrombin antithrombin, tissue plasminogen activator, and plasminogen activator inhibitor 1 were demonstrated across treatment groups. Concentrations of D-dimer in TXA treatment groups were less than placebo at 6 hours (p < 0.001). Concentrations of PAP in TXA treatment groups were less than placebo on admission (p < 0.001) and 6 hours (p = 0.02). No differences in D-dimer and PAP were observed between bolus maintenance and bolus only.
CONCLUSION
While D-dimer and PAP levels reflect a lower degree of fibrinolysis following prehospital administration of TXA when compared with placebo in a large prehospital trial of patients with TBI, TEG obtained on admission and 6 hours later did not demonstrate any differences in fibrinolysis between the two TXA dosing regimens and placebo.
LEVEL OF EVIDENCE
Diagnostic test, level III.
Identifiants
pubmed: 33105308
doi: 10.1097/TA.0000000000002932
pii: 01586154-202011000-00009
pmc: PMC7878849
mid: NIHMS1622831
doi:
Substances chimiques
Antifibrinolytic Agents
0
Fibrin Fibrinogen Degradation Products
0
SERPINF2 protein, human
0
alpha-2-Antiplasmin
0
fibrin fragment D
0
Tranexamic Acid
6T84R30KC1
Fibrinolysin
EC 3.4.21.7
Types de publication
Clinical Trial, Phase II
Journal Article
Multicenter Study
Randomized Controlled Trial
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
900-907Subventions
Organisme : NHLBI NIH HHS
ID : L30 HL138880
Pays : United States
Organisme : NHLBI NIH HHS
ID : U01 HL077866
Pays : United States
Organisme : NHLBI NIH HHS
ID : U01 HL077871
Pays : United States
Organisme : NHLBI NIH HHS
ID : U01 HL077887
Pays : United States
Organisme : NHLBI NIH HHS
ID : U01 HL077863
Pays : United States
Organisme : NHLBI NIH HHS
ID : U01 HL077873
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL126585
Pays : United States
Organisme : NHLBI NIH HHS
ID : U01 HL077881
Pays : United States
Références
Semin Thromb Hemost. 2017 Mar;43(2):135-142
pubmed: 28052305
J Thromb Haemost. 2015 Jun;13 Suppl 1:S98-105
pubmed: 26149056
PLoS One. 2015 Dec 14;10(12):e0145012
pubmed: 26658824
Arch Surg. 2012 Feb;147(2):113-9
pubmed: 22006852
J Thromb Haemost. 2013 Feb;11(2):307-14
pubmed: 23176206
Blood. 2015 Apr 16;125(16):2558-67
pubmed: 25673638
J Trauma Acute Care Surg. 2014 Dec;77(6):811-7; discussion 817
pubmed: 25051384
Eur J Trauma Emerg Surg. 2018 Feb;44(1):35-44
pubmed: 28918481
J Trauma Acute Care Surg. 2017 Jun;82(6):1080-1086
pubmed: 28328682
J Trauma Acute Care Surg. 2015 Jun;78(6 Suppl 1):S65-9
pubmed: 26002266
J Cell Physiol. 2019 Nov;234(11):19121-19129
pubmed: 30941770
J Trauma Acute Care Surg. 2017 Feb;82(2):293-301
pubmed: 27779595
Pflugers Arch. 2007 Jun;454(3):345-59
pubmed: 17256154
Shock. 2013 Feb;39(2):121-6
pubmed: 23222525
Lancet. 2010 Jul 3;376(9734):23-32
pubmed: 20554319
Health Technol Assess. 2012;16(13):iii-xii, 1-54
pubmed: 22417901
J Trauma Acute Care Surg. 2013 Dec;75(6):961-7; discussion 967
pubmed: 24256667
J Trauma Acute Care Surg. 2012 Jul;73(1):60-6
pubmed: 22743373
Lancet. 2019 Nov 9;394(10210):1713-1723
pubmed: 31623894
Semin Thromb Hemost. 2013 Nov;39(8):896-901
pubmed: 24114009
J Am Coll Surg. 2016 Apr;222(4):347-55
pubmed: 26920989
J Trauma Acute Care Surg. 2018 Jan;84(1):75-80
pubmed: 29040203