Damage control resuscitation

Contents

Concept of Damage Control

Damage control resuscitation (DCR) is a military-derived, evidence-based approach to managing traumatic haemorrhage. It differs fundamentally from traditional resuscitation by prioritising haemostasis over normalisation of physiology.

Traditional vs Damage Control Paradigm

Traditional Damage Control
Large-volume crystalloid → restore BP Minimal crystalloid; blood products first
Normalise BP Permissive hypotension (SBP 80–90)
Surgery to repair all injuries Abbreviated surgery: haemostasis + contamination control only
ATLS protocol DCR integrated with damage control surgery (DCS)

The Lethal Triad

The lethal triad (or "bloody vicious cycle") describes the interaction of three factors that amplify each other and worsen haemorrhagic death:

  1. Hypothermia: impairs enzyme function → clotting factor activity falls (enzymatic reactions slow at lower temperatures); platelet dysfunction; acidosis worsens
  2. Acidosis: H⁺ ions inhibit coagulation cascade directly; thrombin generation falls; vasodilation worsens haemodynamic compromise
  3. Coagulopathy: dilution (crystalloid resuscitation), consumption (DIC), fibrinolysis, factor dysfunction

Key point: large-volume crystalloid resuscitation accelerates all three — it dilutes clotting factors (and the heat they carry), worsens acidosis (hyperchloraemia), and contributes to hypothermia through cold solutions. DCR aims to break this cycle by avoiding crystalloid and replacing directly with blood products.

Trauma-Induced Coagulopathy (TIC)

Coagulopathy in trauma is not simply dilutional — it is an early, intrinsic response to severe injury:

  • Tissue injury + hypoperfusion → activation of protein C → consumption of factors V and VIII; fibrinolysis
  • ~25% of severely injured patients have evidence of coagulopathy on arrival before any resuscitation
  • TIC is independent of and precedes the dilutional coagulopathy from crystalloid

Permissive Hypotension

Permissive hypotension (also: "hypotensive resuscitation") accepts a lower-than-normal MAP/SBP during active haemorrhage to avoid disrupting clot formation:

  • Target SBP: 80–90 mmHg in haemorrhagic shock before definitive haemostasis
  • Rationale: raising BP to normal before haemostasis disrupts forming clots ("popping the clot"), dilutes coagulation factors, and drives continued haemorrhage from injured vessels
  • Evidence: ATLS demonstrated reduced mortality when avoiding aggressive fluid resuscitation before haemostasis in penetrating trauma

Exceptions to Permissive Hypotension

Traumatic Brain Injury (TBI): absolute contraindication to permissive hypotension

  • Injured brain requires higher CPP (CPP = MAP − ICP)
  • TBI patients: target SBP ≥100 mmHg (or MAP ≥80 mmHg); lower MAP → secondary brain injury
  • In combined trauma (TBI + haemorrhage): target SBP 90–100 mmHg (compromise)

Spinal cord injury: similarly, hypotension → secondary cord ischaemia; maintain MAP ≥85 mmHg

Elderly / chronic hypertension: normal BP of 80–90 mmHg may represent relative hypotension; individualise

Haemostatic Resuscitation

Blood Product Ratios

Empirical ratio of 1:1:1 (red cells : plasma : platelets) derived from military experience (Borgman, 2007) and supported by the PROPPR trial:

PROPPR Trial (Holcomb, JAMA 2015):

  • RCT in severely injured patients requiring massive transfusion
  • 1:1:1 (FFP:platelets:RBC) vs 1:1:2 ratio
  • Result: 1:1:1 ratio significantly reduced 24-hour mortality (12.7% vs 17.0%), achieved haemostasis faster, and reduced early death from haemorrhage; no increase in complications
  • Conclusion: 1:1:1 ratio is the standard for massive haemorrhage resuscitation

Massive Haemorrhage Protocol (MHP)

  • Activate MHP when: significant haemorrhage with haemodynamic compromise; >10 units RBC anticipated in 24h
  • Triggers delivery of pre-packaged blood product packs (e.g., 6 RBC + 6 FFP + 1 pool platelets) in sequence
  • Minimises crystalloid: only use crystalloid to maintain IV access until blood products available

Fibrinogen

  • First factor to fall in haemorrhagic coagulopathy
  • Target fibrinogen >1.5–2.0 g/L
  • Replace with: cryoprecipitate (2 pools, each containing ~1 g fibrinogen in 100–150 mL) or fibrinogen concentrate (Haemocomplettan/RiaSTAP — more concentrated, faster, no viral risk, but no blood bank stock — expensive)

Calcium

  • Citrate in blood products chelates ionised calcium → hypocalcaemia with massive transfusion
  • Give calcium chloride 10% 5–10 mL or calcium gluconate 10% 20 mL IV after each 4 units of blood products; monitor ionised Ca²⁺ — target >1.1 mmol/L

Avoid Crystalloid

  • Normal saline and Hartmann's do not restore haemostasis — they dilute clotting factors, lower ionised Ca²⁺, cause hyperchloraemia (normal saline), and worsen acidosis
  • If fluid needed urgently before blood available: maximum 1L crystalloid; switch to blood products as soon as available

Tranexamic Acid (TXA)

TXA is a synthetic lysine analogue that inhibits fibrinolysis — it blocks binding of plasminogen to fibrin, preventing conversion to plasmin and consequent fibrin degradation.

CRASH-2 Trial (Shakur, Lancet 2010)

  • RCT, n=20,211 adults with significant trauma and risk of haemorrhage
  • TXA 1 g IV over 10 min → 1 g IV over 8 hours vs placebo
  • Result: TXA significantly reduced risk of death from haemorrhage (5.7% vs 7.2%, RR 0.81) with no increase in vascular occlusive events
  • Critically: TXA given within 3 hours of injury → mortality reduction; TXA given after 3 hours → no benefit and possible harm (trend to increased haemorrhagic death after 3 hours — paradoxical fibrinolysis as late fibrinolytic rebound possible)

WOMAN Trial (CRASH-3 collaborators, Lancet 2017)

  • TXA in postpartum haemorrhage — see massive haemorrhage page

Current Practice

  • TXA 1 g IV as soon as possible (within 3 hours of injury) for all traumatic haemorrhage or suspected significant haemorrhage; repeat 1 g IV over 8 hours
  • Pre-hospital TXA: recommended in UK pre-hospital guidelines for significant trauma; given by HEMS/paramedics
  • Do not give TXA after 3 hours from injury

Fibrinolysis in Trauma

  • CRASH-2 subgroup: if given >3 hours, trend to harm — fibrinolysis at later stages may be a protective mechanism preventing thrombosis in injured vessels
  • ROTEM can identify hyperfibrinolysis (↓ clot lysis resistance) — targeted TXA

ROTEM/TEG-Guided Therapy

Viscoelastic haemostatic assays (VHA) — ROTEM (rotational thromboelastometry) and TEG (thromboelastography) — measure whole-blood clotting in real time:

What VHA Measures

  • EXTEM/INTEM: clot initiation (CT), clot formation (CFT), maximum clot firmness (MCF), lysis (LI30, ML)
  • FIBTEM: MCF reflects fibrinogen-mediated clot contribution (fibrin clot, no platelet contribution)
  • APTEM: adds aprotinin — if clot improves vs EXTEM, confirms fibrinolysis component

ROTEM-Guided DCR Algorithm

  1. FIBTEM MCF <10 mm → fibrinogen deficiency → cryoprecipitate or fibrinogen concentrate
  2. EXTEM MCF <50 mm (normal FIBTEM) → platelet deficiency → platelet transfusion
  3. EXTEM CT prolonged → factor deficiency → FFP or PCC
  4. LI30 >15% (early lysis) → fibrinolysis → TXA
  5. HIT pattern or specific factor issues → targeted therapy

VHA-guided resuscitation reduces over-transfusion of FFP and platelets, reduces exposure to blood products, and may improve outcomes — adopted in many major trauma centres.

See also massive haemorrhage and transfusion and TRIC journal club.

Damage Control Surgery

DCR is delivered alongside damage control surgery (DCS) — an abbreviated surgical approach:

Phase 1: Emergency Surgery (Haemostasis)

  • Surgical control of haemorrhage: packing, vessel ligation, temporary shunts
  • Contamination control: bowel spillage controlled; temporary closure
  • NOT definitive repair — organs left damaged but bleeding controlled
  • Time in theatre: target <60–90 minutes
  • Abdominal packing + temporary closure with negative pressure dressing

Phase 2: ICU Resuscitation

  • Correct hypothermia (warm blankets, warm IV fluids, warming mattress)
  • Correct coagulopathy (blood products, guided by ROTEM)
  • Correct acidosis (usually self-corrects with resuscitation and haemostasis)
  • Wean vasopressors; organ support

Phase 3: Definitive Surgery

  • Performed once physiology restored (temperature >36°C, pH >7.35, normalised coagulation, lactate normalising)
  • Bowel anastomosis, definitive vascular repair, closure

Viva Questions

1. Explain the rationale for permissive hypotension in traumatic haemorrhage and when it is contraindicated.

In traumatic haemorrhage before surgical haemostasis, the bleeding site has a partially formed clot under local hydrostatic pressure. Aggressively restoring normal blood pressure before controlling haemorrhage mechanically disrupts this clot ("pops the clot"), drives further haemorrhage from the injured vessel, dilutes clotting factors (if achieved with crystalloid), and accelerates the development of the lethal triad (hypothermia, acidosis, coagulopathy). Permissive hypotension (target SBP 80–90 mmHg) accepts below-normal perfusion pressure to preserve the forming clot until surgical or interventional haemostasis can be achieved. Evidence supports this strategy in penetrating trauma; evidence in blunt trauma is less strong but the physiological rationale applies. Absolute contraindications: traumatic brain injury (requires adequate CPP to prevent secondary brain injury — target SBP ≥100 mmHg); spinal cord injury (hypotension → cord ischaemia — target MAP ≥85 mmHg); the presence of TBI fundamentally changes the resuscitation target. Elderly patients and those with chronic hypertension may not tolerate SBP 80–90 mmHg as their organs are conditioned to higher perfusion pressure — individualise accordingly.

2. What did the CRASH-2 trial show about tranexamic acid in trauma, and why does timing matter?

CRASH-2 (Shakur, Lancet 2010) was an RCT of 20,211 adult trauma patients at risk of significant haemorrhage. TXA 1 g IV over 10 minutes followed by 1 g over 8 hours significantly reduced risk of death from haemorrhage (5.7% vs 7.2%) compared to placebo, with no increase in thrombotic complications. This result was consistent across subgroups and was highly statistically significant. The critical timing finding: patients treated within 1 hour of injury had the greatest benefit; those treated at 1–3 hours had smaller but statistically significant benefit; those treated after 3 hours had no benefit and there was a non-significant trend to harm (increased haemorrhagic death). The most likely explanation: TXA inhibits fibrinolysis. In early trauma, hyperfibrinolysis contributes to TIC and haemorrhage — inhibiting it is beneficial. After 3 hours, fibrinolysis may shift from a harmful to a physiologically important process (limiting thrombosis in injured and repaired vessels); inhibiting late fibrinolysis may paradoxically worsen outcomes. The practical implication: TXA must be given within 3 hours of injury (and ideally within 1 hour). It is now part of pre-hospital trauma protocols in the UK.

3. Compare haemostatic resuscitation using 1:1:1 blood product ratios with traditional crystalloid resuscitation. What is the evidence?

Traditional ATLS taught aggressive crystalloid resuscitation (2L crystalloid followed by blood) — this approach accelerates the lethal triad: crystalloid dilutes clotting factors (coagulopathy), is given cold (hypothermia), and causes hyperchloraemia and acidosis (0.9% NaCl). It also provides no haemostatic activity. Haemostatic resuscitation replaces crystalloid with balanced blood components: RBCs (carry O₂), FFP (replaces clotting factors), and platelets, in a 1:1:1 empirical ratio. The PROPPR trial (Holcomb, JAMA 2015) randomised 680 severely injured patients to 1:1:1 vs 1:1:2 (lower plasma:platelet ratio). The 1:1:1 ratio significantly reduced 24-hour mortality (12.7% vs 17.0%), achieved haemostasis faster, and reduced early haemorrhagic death. No increase in complications. PROPPR also confirmed the importance of early platelet administration — historically platelets were given late. The current approach: activate major haemorrhage protocol immediately; give blood products in 1:1:1 ratio; minimise crystalloid (maximum 1L); give TXA within 3 hours; use ROTEM for targeted component therapy to avoid over-transfusion; see TRIC journal club for transfusion threshold evidence after haemostasis is achieved.