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ICU TopicsHaematology / trauma

ICU · Haematology / trauma

Massive Transfusion & Trauma Coagulopathy — The Lethal Triad, TXA & 1:1:1

Also known as Massive transfusion · MTP · Trauma coagulopathy · Acute traumatic coagulopathy · ATC · Lethal triad · Tranexamic acid · TXA · CRASH-2 · PROPPR · Hyperfibrinolysis · TEG · ROTEM

The trauma coagulopathy has the two components: the acute traumatic coagulopathy (ATC — the early, the injury-driven, the protein-C activation, the hyperfibrinolysis) and the dilutional coagulopathy (the massive RBC without the factors or the platelets). The lethal triad — the acidosis (the clotting-factor dysfunction), the hypothermia (the platelet and the enzyme dysfunction), and the coagulopathy — the vicious the cycle. The massive transfusion protocol (MTP) — the 1 to 1 to 1 (RBC to the plasma to the platelets), PROPPR no mortality difference but the fewer the exsanguination. The tranexamic acid (TXA) — the CRASH-2, the 1 g plus the 1 g within 3 h (the beyond the 3 h the harmful). The calcium (the citrate the chelation — the under 0.90 the severe, the double the mortality). The fibrinogen (the first the factor to the fall — the under 1.5 g per L the treat). The viscoelastic (the TEG the ROTEM — the LY30 the hyperfibrinolysis, the FIBTEM the fibrinogen).

high28 referencesUpdated 2 Sept 202636 min readSource-verified · Sept 2026

Checked against its sources on 2 Sept 2026

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Trauma coagulopathy is an endogenous auto-anticoagulation, not a dilution. The acute traumatic coagulopathy (ATC) develops within minutes of severe injury — driven by the protein-C pathway and acute hyperfibrinolysis — before any fluid is given; roughly one in three severely injured patients arrives already coagulopathic, and the dilutional component layers on top once resuscitation starts. The lethal triad (acidosis, hypothermia, coagulopathy) accelerates the bleed. Resuscitate with damage control — permissive hypotension until haemorrhage control (Bickell; Tran meta-analysis) with the non-negotiable TBI exception (one hypotensive episode doubles severe-TBI mortality), 1:1:1 products (PROPPR: no mortality difference, fewer exsanguination deaths), TXA 1 g over 10 min then 1 g over 8 h within 3 h (CRASH-2; harmful beyond 3 h), minimise crystalloid, damage control surgery — replace calcium (citrate chelation), treat a fibrinogen under 1.5 g/L, and let TEG/ROTEM guide the rest.[7][8][9][12][1][2][3][21][22][18]

Meet the patient

A 24-year-old motorcyclist lands in the trauma bay 45 minutes after a high-speed collision — pale, agitated, GCS 14, HR 132, BP 74/40, a tense abdomen with a positive FAST, an open femur, a clinically unstable pelvis. He has already had a litre of warmed crystalloid, and the registrar is reaching for a second bolus to push the pressure back to normal.[1]

The first gas shows pH 7.18, lactate 6.8, INR 1.8, fibrinogen 1.3, ionised calcium 0.85, temperature 35.1°C — the full lethal triad, before a single unit of blood has been given. The one question that decides his next hour is the one every trauma coagulopathy stem turns on: is this dilution, or is it the body's own auto-anticoagulation? Get it right and permissive hypotension, 1:1:1, early TXA, and calcium all fall into place. Get it wrong and you chase a number with crystalloid while he exsanguinates.[7][9]

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References28ShowHide
  1. [1]Holcomb JB, Tilley BC, Baraniuk S, et al. Transfusion of plasma, platelets, and red blood cells in a 1:1:1 vs a 1:1:2 ratio and mortality in patients with severe trauma: the PROPPR randomized clinical trial JAMA, 2015.PMID 25647203
  2. [2]Shakur H, Roberts I, Bautista R, et al. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2): a randomised, placebo-controlled trial Lancet, 2010.PMID 20554319
  3. [3]Roberts I, Shakur H, Afolabi A, et al. The importance of early treatment with tranexamic acid in bleeding trauma patients: an exploratory analysis of the CRASH-2 randomised controlled trial Lancet, 2011.PMID 21439633
  4. [4]CRASH-3 trial collaborators Effects of tranexamic acid on death, disability, vascular occlusive events and other morbidities in patients with acute traumatic brain injury (CRASH-3): a randomised, placebo-controlled trial Lancet, 2019.PMID 31623894
  5. [5]Morrison JJ, Dubose JJ, Rasmussen TE, Midwinter MJ Military Application of Tranexamic Acid in Trauma Emergency Resuscitation (MATTERs) Study Arch Surg, 2012.PMID 22006852
  6. [6]Gruen RL, Mitra B, Bernard SA, et al. Prehospital Tranexamic Acid for Severe Trauma N Engl J Med, 2023.PMID 37314244
  7. [7]Brohi K, Cohen MJ, Ganter MT, et al. Acute traumatic coagulopathy: initiated by hypoperfusion: modulated through the protein C pathway? Ann Surg, 2007.PMID 17457176
  8. [8]Cohen MJ, Call M, Nelson M, et al. Critical role of activated protein C in early coagulopathy and later organ failure, infection and death in trauma patients Ann Surg, 2012.PMID 22133894
  9. [9]Rossaint R, Afshari A, Bouillon B, et al. The European guideline on management of major bleeding and coagulopathy following trauma: sixth edition Crit Care, 2023.PMID 36859355
  10. [10]Santiago R, Slocum G, Riggi G Resuscitating massive transfusion knowledge: An update for the pharmacist Am J Health Syst Pharm, 2025.PMID 40580496
  11. [11]Cannon JW, Khan MA, Raja AS, et al. Damage control resuscitation in patients with severe traumatic hemorrhage: A practice management guideline from the Eastern Association for the Surgery of Trauma J Trauma Acute Care Surg, 2017.PMID 28225743
  12. [12]Bickell WH, Wall MJ Jr, Pepe PE, et al. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries N Engl J Med, 1994.PMID 7935634
  13. [13]Tran A, Yates JM, Lau A, et al. Permissive hypotension versus conventional resuscitation strategies in adult trauma patients with hemorrhagic shock: A systematic review and meta-analysis of randomized controlled trials J Trauma Acute Care Surg, 2018.PMID 29370058
  14. [14]Chesnut RM, Marshall SB, Piek J, et al. Early and late systemic hypotension as a frequent and fundamental source of cerebral ischemia following severe brain injury in the Traumatic Coma Data Bank Acta Neurochir Suppl, 1993.PMID 8310858
  15. [15]Fuller G, Hasler RM, Mealing N, et al. The association between admission systolic blood pressure and mortality in significant traumatic brain injury: a multi-centre cohort study Injury, 2014.PMID 24206920
  16. [16]Nunez TC, Voskresensky IV, Dossett LA, Shinall R, Dutton WD, Cotton BA Early prediction of massive transfusion in trauma: simple as ABC (assessment of blood consumption)? J Trauma, 2009.PMID 19204506
  17. [17]Takahashi K, Yamakawa K, Siletz AE, et al. Hyperfibrinolysis: a crucial phenotypic abnormality of posttraumatic fibrinolytic dysfunction Res Pract Thromb Haemost, 2024.PMID 39430866
  18. [18]Baksaas-Aasen K, Gall LS, Stensballe J, et al. Viscoelastic haemostatic assay augmented protocols for major trauma haemorrhage (ITACTIC): a randomized, controlled trial Intensive Care Med, 2021.PMID 33048195
  19. [19]Davenport R, Curry N, Fox EE, et al. Early and Empirical High-Dose Cryoprecipitate for Hemorrhage After Traumatic Injury: The CRYOSTAT-2 Randomized Clinical Trial JAMA, 2023.PMID 37824155
  20. [20]Winearls J, Wullschleger M, Wake E, et al. Fibrinogen Early In Severe Trauma studY (FEISTY): results from an Australian multicentre randomised controlled pilot trial Crit Care Resusc, 2021.PMID 38046391
  21. [21]Meizoso JP, Moore EE, Pieracci FM, et al. Role of Fibrinogen in Trauma-Induced Coagulopathy J Am Coll Surg, 2022.PMID 35290265
  22. [22]Giancarelli A, Birrer KL, Alban RF, et al. Hypocalcemia in trauma patients receiving massive transfusion J Surg Res, 2016.PMID 27083965
  23. [23]Raza S, Ali Baig M, Chang C, et al. A prospective study on red blood cell transfusion related hyperkalemia in critically ill patients J Clin Med Res, 2015.PMID 25883703
  24. [24]Steiner T, Poli S, Griebe M, et al. Fresh frozen plasma versus prothrombin complex concentrate in patients with intracranial haemorrhage related to vitamin K antagonists (INCH): a randomised trial Lancet Neurol, 2016.PMID 27302126
  25. [25]Pollack CV Jr, Reilly PA, Eikelboom J, et al. Idarucizumab for Dabigatran Reversal N Engl J Med, 2015.PMID 26095746
  26. [26]Lacroix J, Hébert PC, Fergusson DA, et al. Age of transfused blood in critically ill adults N Engl J Med, 2015.PMID 25853745
  27. [27]Cooper DJ, McQuilten ZK, Nichol A, et al. Age of Red Cells for Transfusion and Outcomes in Critically Ill Adults N Engl J Med, 2017.PMID 28952891
  28. [28]Johansson PI, Vigstedt M, Curry NS, et al. Trauma induced coagulopathy is limited to only one out of four shock induced endotheliopathy (SHINE) phenotypes among moderate-severely injured trauma patients: an exploratory analysis Scand J Trauma Resusc Emerg Med, 2024.PMID 39160625

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