Haemostatic Resuscitation

Haemostatic Resuscitation in Trauma: Targets and Justification

Definition and Overview

Haemostatic resuscitation is a damage control strategy that aims to restore physiological blood coagulation while simultaneously addressing tissue perfusion during the early phase of trauma management. This approach evolved from the recognition that traditional large-volume crystalloid resuscitation contributes to the lethal triad of hypothermia, acidosis, and coagulopathy in severe trauma patients.

Primary Targets

1. Blood Component Therapy Ratios

• Target: Balanced transfusion with plasma:platelets:RBCs ratio approximating 1:1:1 or 1:1:2

• Justification: Mimics whole blood composition, addresses all components of the coagulation system simultaneously, and has been associated with improved survival in observational studies (PROPPR trial demonstrated reduced exsanguination deaths)

2. Fibrinogen Replacement

• Target: Maintain fibrinogen levels >1.5-2.0 g/L (using cryoprecipitate or fibrinogen concentrate)

• Justification: Fibrinogen is often the first coagulation factor to reach critical levels in trauma, and adequate levels are essential for clot formation and stability

3. Platelet Count and Function

• Target: Maintain platelet count >50×10⁹/L (>100×10⁹/L for TBI)

• Justification: Platelets provide the cellular framework for coagulation and are essential for clot formation, particularly in neurological injuries

4. Coagulation Factors

• Target: Prothrombin time/INR <1.5, APTT <40 seconds

• Justification: Ensures adequate coagulation factor activity for proper clot formation

5. Permissive Hypotension

• Target: Systolic BP 80-90 mmHg (or MAP 50-60 mmHg) in hemorrhagic shock without TBI

• Justification: Limits hydrostatic pressure on forming clots, reduces blood loss until definitive hemorrhage control is achieved

6. Damage Control Resuscitation Adjuncts

• Target: Early TXA administration (<3 hours), targeted temperature management, ionized calcium >1.0 mmol/L

• Justification: TXA reduces fibrinolysis; normothermia preserves enzyme function in coagulation cascade; calcium is essential for multiple steps in coagulation

Monitoring and Guidance

Viscoelastic Haemostatic Assays (VHA)

• Target: Utilize TEG/ROTEM to guide product replacement

• Justification: Provides real-time assessment of clot formation, strength, and lysis; allows targeted therapy for specific coagulation defects rather than empiric treatment

Pathophysiological Justification

1. Trauma-Induced Coagulopathy (TIC): Up to 25-35% of severely injured trauma patients present with coagulopathy before receiving any fluid therapy, associated with 4-fold increased mortality.

2. Endotheliopathy of Trauma: Damage to endothelium from tissue injury, shock, and inflammation results in dysregulated coagulation and compromised vascular integrity.

3. Iatrogenic Factors: Traditional large-volume crystalloid resuscitation causes hemodilution of coagulation factors, hypothermia, and metabolic acidosis, further impairing coagulation.

4. Fibrinolysis: Hyperfibrinolysis (accelerated clot breakdown) occurs in 5-15% of severely injured patients and carries mortality rates of 70-90%.

Outcome Benefits

• Reduction in mortality (estimated 15-20% relative risk reduction in exsanguination deaths)

• Decreased total blood product usage

• Reduced incidence of multiple organ failure

• Lower rates of abdominal compartment syndrome

• Shorter ICU and hospital length of stay

• Improved survival among patients requiring massive transfusion

Haemostatic resuscitation represents a paradigm shift from treating shock with crystalloids to early blood product administration aimed at restoring both tissue perfusion and coagulation function simultaneously, addressing both the cause and consequences of hemorrhagic shock in trauma.