Anaes · Trauma and massive haemorrhage
Trauma and massive haemorrhage
Also known as Damage control resuscitation · Massive transfusion protocol · Permissive hypotension · Haemostatic resuscitation · Trauma-induced coagulopathy · The lethal triad · Damage control surgery · Tranexamic acid in trauma · Viscoelastic testing in trauma
Trauma and massive haemorrhage is the prototypical time-critical anaesthetic emergency and the commonest cause of preventable trauma death is uncontrolled haemorrhage. The modern response is damage control resuscitation — the integration of permissive hypotension (systolic 80 to 90 mmHg until haemostasis), haemostatic resuscitation with blood products in a 1:1:1 ratio rather than crystalloid, early tranexamic acid (1 g IV within 3 hours, CRASH-2), the activated massive transfusion protocol, damage control surgery (control bleeding, pack, temporary closure, ICU, definitive surgery when stable), and the active prevention of the lethal triad of acidosis, hypothermia and coagulopathy. The anaesthetist is central to the trauma team — the airway with cervical-spine precautions, the breathing, the circulation with haemorrhage control, and the coagulation.
Checked against its sources on 14 Oct 2026
Practise this topic
On this page
Study tools
Your progress
Saved on this device.
Target exams
Red flags
- Uncontrolled haemorrhage is the leading cause of PREVENTABLE trauma death, and the lethal triad of acidosis, hypothermia and coagulopathy is the self-perpetuating death spiral. The young fit patient compensates until a third of the blood volume is gone — a normal pulse and blood pressure do NOT exclude major blood loss. Trust the mechanism, the continuing losses, the rising lactate, the worsening base excess and the clinical trajectory, never the first set of vital signs.
- Permissive hypotension (systolic 80 to 90 mmHg, or a mean arterial pressure of 65 mmHg) is maintained UNTIL SURGICAL HAEMOSTASIS to reduce clot disruption and ongoing blood loss. It is CONTRAINDICATED in the traumatic brain injury (the cerebral perfusion pressure must be defended), the spinal cord injury, and the elderly or cardiovascularly-compromised patient.
- Tranexamic acid 1 g IV over 10 minutes then 1 g over 8 hours reduces all-cause mortality and bleeding death when given within 3 hours of injury (CRASH-2). After 3 hours it increases mortality. Give it EARLY — ideally pre-hospital or the moment haemorrhage is recognised.
- Resuscitate with BLOOD PRODUCTS not crystalloid. Crystalloid dilutes clotting factors and platelets, causes acidosis, and induces the lethal triad. The empirical ratio is 1:1:1 packed red cells to fresh frozen plasma to platelets, fine-tuned by viscoelastic testing. Give calcium — the citrate in transfused products chelates it and hypocalcaemia worsens coagulation, contractility and vascular tone.
- The trauma airway is high-risk: the cervical spine is at risk, the stomach is full, there is blood and debris, and there may be a head injury. A rapid sequence induction with manual in-line stabilisation, videolaryngoscopy and a front-of-neck backup is standard. The patient with a combined TBI is intubated EARLY and kept normoxic and normocapnic.
Meet the patient
A young motorcyclist arrives in the resuscitation bay after a high-speed collision. He is pale, clammy, confused, he is tachycardic and hypotensive with a rigid abdomen. Two large-bore cannulae go in, the massive transfusion protocol is called, the pelvic binder goes on, and the theatre is warned. (Vignette; teaching framing — broad DCR principles per Spahn fifth-edition guidance.)[3] The registrar reaches for a litre of crystalloid. That is the first mistake. (Teaching vignette.)
The questions that decide whether this man lives are the questions that decide every trauma haemorrhage: where is he bleeding, and can we stop it? Resuscitation without haemorrhage control is futile — the 11th-edition ATLS answer is exsanguinating-haemorrhage control first (x-ABCDE), with damage control resuscitation, permissive hypotension, limited crystalloids, and early transfusion. [6][6]
References10ShowHide
- [1]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
- [2]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
- [3]Spahn DR, Bouillon B, Cerny V, et al. The European guideline on management of major bleeding and coagulopathy following trauma: fifth edition Crit Care, 2019.PMID 30917843
- [4]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
- [5]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
- [6]Ramasamy A Advanced trauma life support 2025: A brief review of updates. Injury, 2026.PMID 41671886
- [7]Langeron O, Birenbaum A, Amour J Airway management in trauma. Minerva Anestesiol, 2009.PMID 19412149
- [8]Dupanovic M, Fox H, Kovac A Management of the airway in multitrauma. Curr Opin Anaesthesiol, 2010.PMID 20042974
- [9]Roberts DJ, Leigh-Smith S, Faris PD, et al. Clinical Presentation of Patients With Tension Pneumothorax: A Systematic Review. Ann Surg, 2015.PMID 25563887
- [10]Galvagno SM Jr, Nahmias JT, Young DA Advanced Trauma Life Support(R) Update 2019: Management and Applications for Adults and Special Populations. Anesthesiol Clin, 2019.PMID 30711226