Trauma-induced coagulopathy

Ernest E. Moore* (Corresponding Author), Hunter B. Moore, Lucy Z. Kornblith, Matthew D. Neal, Maureane Hoffman, Nicola Mutch, Herbert Schöchl, Beverley J. Hunt, Angela Sauaia

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

244 Citations (Scopus)
13 Downloads (Pure)

Abstract

Uncontrolled hemorrhage is a major preventable cause of death in trauma, the latter accounting for 9% of global deaths. There is no agreed definition of trauma-induced coagulopathy (TIC), the term is used to describe abnormal coagulation attributable to trauma. Early TIC occurs within 6 hours of injury and is characterized by hypocoagulability resulting in bleeding; whereas late TIC represents a hypercoagulable state associated with thromboembolic events and multiple organ failure. Research into pathophysiological mechanisms have recognized that acute blood loss, metabolic acidosis, endothelial activation, immune system of activation, platelet activation, and traumatic brain injury account for the diverse phenotypes of TIC. Multiple haemostatic abnormalities have been described including fibrinogen depletion, inadequate thrombin
generation, platelet dysfunction, dysregulated fibrinolysis, and endothelial dysfunction resulting in various phenotypes.Diagnosis is made by detecting abnormalities in viscoelastic haemostatic assays (VHA) or coagulation screening especially prolonged prothrombin times. Management priorities are controlling blood loss and reversing shock with balanced ratios of blood products; alongside prehospital tranexamic acid in long transport or austere environments. There is no international agreement on the composition of initial blood components for presumed TIC. For those who survive, there are high rates of morbidity especially in those with traumatic brain injury, which dominates short and long term quality of life and functional outcome.
Original languageEnglish
Article number30
Number of pages23
JournalNature reviews. Disease primers
Volume7
DOIs
Publication statusPublished - 29 Apr 2021

Bibliographical note

Acknowledgements
E.E.M. and A.S. appreciate the generous support from the National Institutes of Health for their inflammation and coagulation research over the past 35 years (NIGMS: 1-6 P50 GM49222, 1-6 T32 GM08315, 1-2 U54 GM 62119, RM1 GM 131968 and NHLBI: UM1 HL120877). H.B.M. acknowledges the generous support from the National Institutes of Health (NHBLI: K99HL1518870) L.Z.K. acknowledges the generous support from the National Institutes of Health for her platelet biology research (NIGMS: K23GM130892-01). M.D.N. acknowledges the generous support by the National Institutes of Health (NIGMS: R35 GM119526 and NHLBI R01 HL141080).

Author Correction: Trauma-induced coagulopathy (Nature Reviews Disease Primers, (2021), 7, 1, (30), 10.1038/s41572-021-00264-3)

Keywords

  • Circulation
  • Trauma

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