Massive Transfusion Protocol Activation in Trauma
Activate the massive transfusion protocol immediately when a trauma patient remains hypotensive, tachycardic, or shows signs of ongoing hemorrhagic shock after receiving 2 L of isotonic crystalloid, and manage with balanced blood product resuscitation in a 1:1:1 ratio while simultaneously achieving hemorrhage control. 1, 2
Clear Triggers for MTP Activation
The decision to activate MTP should be based on physiologic indicators rather than waiting for laboratory confirmation:
- Persistent hemodynamic instability after 2 L crystalloid (systolic BP <90 mmHg, tachycardia, poor peripheral perfusion) is the primary trigger 1, 2
- Elevated lactate ≥4 mmol/L indicates severe tissue hypoperfusion and predicts need for aggressive blood product resuscitation 2
- Significant metabolic acidosis (base deficit) serves as a sensitive marker of shock severity 1, 2
- Ongoing uncontrolled bleeding with clinical evidence of hemorrhagic shock 1, 3
- Elevated shock index (heart rate/systolic BP) reflects inadequate perfusion 2
Immediate Management Algorithm
Step 1: Hemorrhage Control (Simultaneous with Resuscitation)
- Achieve rapid hemorrhage control through direct pressure, tourniquets, hemostatic dressings, or emergent surgical intervention 2, 4
- Do not delay MTP activation while attempting prolonged hemorrhage control measures 2
Step 2: Blood Product Administration
- Transfuse in 1:1:1 ratio of packed red blood cells:fresh frozen plasma:platelets 2, 3, 5
- Begin early FFP administration at 10-15 mL/kg to prevent dilutional coagulopathy 2
- Maintain platelet count ≥75 × 10⁹/L throughout resuscitation 2
- Target hemoglobin 70-90 g/L during active resuscitation 2
Step 3: Adjunctive Pharmacotherapy
- Administer tranexamic acid with loading dose of 15 mg/kg (maximum 1 g) within 3 hours of injury for patients at risk of massive hemorrhage 6
- Give fibrinogen concentrate for documented low fibrinogen or established coagulopathy (>15 mL/kg FFP) 2, 3
Step 4: Monitoring Parameters
- Serial lactate and base deficit measurements to assess response to resuscitation 1, 2
- Viscoelastic testing (if available) to guide component therapy 3
- Coagulation parameters including PT, aPTT, fibrinogen, and platelet count 2
Critical Pitfalls to Avoid
- Never use hemoglobin level alone as transfusion trigger in hemorrhagic shock—this ignores the dynamic physiology 2
- Avoid excessive crystalloid administration beyond the initial 2 L, as volumes >2-3 L worsen dilutional coagulopathy (incidence >40% with >2000 mL, >50% with >3000 mL, >70% with >4000 mL) 7, 2
- Do not delay blood products while continuing crystalloid resuscitation 7, 2
- Transition immediately to blood products after 2 L crystalloid if shock persists 1, 2
Special Considerations for Traumatic Brain Injury
If the patient has concurrent traumatic brain injury or intracranial hemorrhage, the approach differs critically:
- Permissive hypotension is contraindicated—maintain mean arterial pressure ≥80 mmHg to ensure adequate cerebral perfusion pressure 7, 2
- Avoid hypotonic solutions (Ringer's lactate) as they worsen cerebral edema 7, 2
- Use 0.9% saline for initial crystalloid, limiting to 1-1.5 L before transitioning to blood products 7
- Initiate vasopressor therapy (norepinephrine preferred) if hypotension persists despite adequate fluid resuscitation 7
Permissive Hypotension Strategy (Non-TBI Patients)
For penetrating torso trauma without head or spinal injury:
- Target systolic BP 80-90 mmHg until hemorrhage control is achieved 8, 2
- This approach minimizes ongoing blood loss while maintaining minimal organ perfusion 4
- Abandon permissive hypotension immediately once definitive hemorrhage control is achieved 4
Timing and Logistics
- Blood products should be immediately available in the trauma bay when the patient arrives—faster delivery correlates with better outcomes 5
- Standardized MTP activation reduces waste and improves execution speed 9, 5
- Damage control resuscitation principles include limited crystalloid, balanced blood products, prevention of hypothermia, and rapid bleeding control 4, 5