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EM TopicsDamage control resuscitation

EM · Damage control resuscitation

Damage control resuscitation in trauma

Also known as DCR · Haemostatic resuscitation · Trauma haemorrhage resuscitation · Permissive hypotension

Damage control resuscitation — the lethal triad of trauma (hypothermia, acidosis, coagulopathy), the permissive hypotension principle (SBP 80 to 90 until the bleeding is controlled), the haemostatic resuscitation with a balanced blood-product ratio (1:1:1), the tranexamic acid within 3 hours (the CRASH-2 trial), the calcium replacement, the damage-control surgery (control the bleeding, control the contamination, temporary closure), and the massive haemorrhage protocol. ACEM-primary, globally tagged.

high13 referencesUpdated 26 July 202625 min readSource-verified · Sept 2026

Checked against its sources on 2 Sept 2026

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Target exams

ACEMFRCEMABEMFRCPCCCFPEMEBEEM

Red flags

  • The lethal triad of trauma — hypothermia, acidosis and coagulopathy — each feeds the other and spirals to an irreversible death if not broken
  • Do NOT resuscitate to a normal blood pressure in the actively bleeding trauma patient — permissive hypotension (SBP 80 to 90) preserves the clot until the bleeding is surgically controlled
  • Minimise the crystalloid — large volumes of saline dilute the clotting factors, worsen the acidosis, and drop the temperature
  • Tranexamic acid 1 g intravenously within 3 hours of the injury reduces the mortality from traumatic haemorrhage (the CRASH-2 trial) — after 3 hours it may be harmful
  • The massive transfusion causes a hypocalcaemia from the citrate — give calcium chloride or calcium gluconate
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Related topics

  • The primary survey (ABCDE) — the trauma assessment framework
  • Major trauma resuscitation — the team-based systematic approach
  • Burn management in the emergency department
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Your progress

Saved on this device.

Target exams

ACEMFRCEMABEMFRCPCCCFPEMEBEEM

Red flags

  • The lethal triad of trauma — hypothermia, acidosis and coagulopathy — each feeds the other and spirals to an irreversible death if not broken
  • Do NOT resuscitate to a normal blood pressure in the actively bleeding trauma patient — permissive hypotension (SBP 80 to 90) preserves the clot until the bleeding is surgically controlled
  • Minimise the crystalloid — large volumes of saline dilute the clotting factors, worsen the acidosis, and drop the temperature
  • Tranexamic acid 1 g intravenously within 3 hours of the injury reduces the mortality from traumatic haemorrhage (the CRASH-2 trial) — after 3 hours it may be harmful
  • The massive transfusion causes a hypocalcaemia from the citrate — give calcium chloride or calcium gluconate
The one-line answer

Damage control resuscitation recognises that the bleeding trauma patient dies of a lethal triad — hypothermia, acidosis and coagulopathy, each feeding the other in a spiral to death — and that the resuscitation must target haemostasis, not the blood pressure. Four pillars applied together and early break the spiral: permissive hypotension (SBP 80–90 until the bleeding is surgically controlled), haemostatic resuscitation (1:1:1 blood products, minimal crystalloid), damage-control surgery (control the bleeding and the contamination, temporary closure), and pharmacology — above all tranexamic acid 1 g IV as early as possible, within 3 hours of the injury.[1] [3]

Meet the patient

A 24-year-old motorcyclist rolls into the trauma bay 20 minutes after a high-speed crash — pale, diaphoretic, confused (GCS 13), BP 74/48, HR 138. He has a deformed pelvis, an open tibial fracture bleeding externally, a tense distended abdomen, a FAST positive in the right upper quadrant, lactate 7.8, INR 1.8, core temperature 34.6 °C. There is no head injury.[1]

The question this patient forces on you at 3 a.m. is the question every major haemorrhage forces: do I resuscitate him to a normal blood pressure, or do I let him run low until the bleeding is surgically controlled? The wrong answer restarts a spiral that kills him within the hour. Hold that question, and the four pillars below are its answer.[2]

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References13ShowHide
  1. [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. [2]Indorewala Y, Nasef Y, Jayagopi K, et al. Permissive hypotension in adult trauma: A systematic review of outcomes across clinical settings, injury type, and resuscitation strategies Am J Emerg Med, 2026.PMID 42030689
  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]Morrison JJ, Dubose JJ, Rasmussen TE, Midwinter MJ. Military Application of Tranexamic Acid in Trauma Emergency Resuscitation (MATTERs) Study Arch Surg, 2012.PMID 22006852
  5. [5]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
  6. [6]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
  7. [7]Rowell SE, Meier EN, McKnight B, et al. Effect of out-of-hospital tranexamic acid vs placebo on 6-month functional neurologic outcomes in patients with moderate or severe traumatic brain injury: a randomized clinical trial JAMA, 2020.PMID 32897344
  8. [8]Spaite DW, Hu C, Bobrow BJ, et al. Optimal out-of-hospital blood pressure in major traumatic brain injury: a challenge to the current understanding of hypotension Ann Emerg Med, 2022.PMID 35339285
  9. [9]Gonzalez E, Moore EE, Moore HB, et al. Goal-directed hemostatic resuscitation of trauma-induced coagulopathy: a pragmatic randomized clinical trial comparing a viscoelastic assay to conventional coagulation assays Ann Surg, 2016.PMID 26720428
  10. [10]Ho KM, Leonard AD. Concentration-dependent effect of hypocalcaemia on mortality of patients with critical bleeding requiring massive transfusion: a cohort study Anaesth Intensive Care, 2011.PMID 21375089
  11. [11]Chowdhury AH, Cox EF, Francis ST, Lobo DN. A randomized, controlled, double-blind crossover study on the effects of 2-L infusions of 0.9% saline and plasma-lyte 148 on renal blood flow velocity and renal cortical tissue perfusion in healthy volunteers Ann Surg, 2012.PMID 22580944
  12. [12]Alghanem H, Liu NC, Gupta A, et al. Ratios of calcium to citrate administration in blood transfusion for traumatic hemorrhage: a retrospective cohort study Transfusion, 2024.PMID 39351914
  13. [13]Brohi K, Cohen MJ, Ganter MT, et al. Acute coagulopathy of trauma: hypoperfusion induces systemic anticoagulation and hyperfibrinolysis J Trauma, 2008.PMID 18469643
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Related topics

  • The primary survey (ABCDE) — the trauma assessment framework
  • Major trauma resuscitation — the team-based systematic approach
  • Burn management in the emergency department