Trauma-Induced Coagulopathy (TIC)

Definition:

Trauma-induced coagulopathy (TIC) is a complex disorder of hemostasis that occurs in trauma patients due to severe injury, shock, tissue hypoperfusion, and massive transfusion. It leads to uncontrolled bleeding and increased mortality.


Types of Trauma-Induced Coagulopathy:

  1. Acute Traumatic Coagulopathy (ATC):
    • Develops within minutes of injury due to shock and hypoperfusion.
    • Endothelial injury causes excess activation of protein C, leading to fibrinolysis and anticoagulation.
    • Strongly associated with poor outcomes.
  1. Resuscitation-Induced Coagulopathy (RIC):
    • Occurs secondary to excessive fluid resuscitation, causing dilutional coagulopathy.
    • Massive transfusion of PRBCs without clotting factors can lead to deficiency of coagulation factors.
  1. Consumptive Coagulopathy (DIC-like Syndrome):
    • Disseminated intravascular coagulation (DIC) features in severe trauma, sepsis, or multi-organ failure.
    • Uncontrolled clotting leads to platelet and coagulation factor depletion, causing widespread bleeding.


Pathophysiology of TIC:

  1. Tissue Hypoperfusion & Shock:
    • Leads to endothelial activation → release of protein C → degradation of factors Va & VIIIa → impaired clot formation.
    • Also causes hyperfibrinolysis (excessive clot breakdown).
  1. Endothelial Dysfunction & Glycocalyx Disruption:
    • Trauma damages the endothelial glycocalyx, exposing subendothelial tissue, which activates platelets and coagulation factors.
    • However, excessive fibrinolysis and platelet dysfunction impair clot formation.
  1. Hyperfibrinolysis:
    • Overactivation of plasminogen to plasmin leads to excessive clot breakdown.
    • Seen in massive bleeding trauma patients.
  1. Hypothermia, Acidosis, & Hemodilution (“Lethal Triad”)
    • Hypothermia (<34°C): Impairs enzyme activity of coagulation cascade.
    • Acidosis (pH <7.2): Inhibits thrombin generation and platelet function.
    • Hemodilution: Large-volume crystalloid infusion leads to dilution of clotting factors.


Diagnosis of TIC:

Laboratory Findings:

  • Prolonged PT & aPTT (↓ clotting factors).
  • Low fibrinogen (<1.5 g/L).
  • Increased D-dimer (suggests hyperfibrinolysis).
  • Low platelet count (<50 × 10⁹/L).
  • Low ionized calcium (<1.0 mmol/L) (citrate toxicity from transfusion).
  • Thromboelastography (TEG) / ROTEM: Identifies coagulation defects in real-time (e.g., hyperfibrinolysis, factor deficiency).


Management of Trauma-Induced Coagulopathy:

1. Damage Control Resuscitation (DCR):

  • Permissive Hypotension (SBP 80–90 mmHg) to limit ongoing bleeding until hemorrhage control is achieved.
  • Avoid excessive crystalloid use (>1.5L) to prevent dilutional coagulopathy.


2. Balanced Blood Component Therapy (1:1:1 Strategy)

  • Packed Red Blood Cells (PRBC): Fresh Frozen Plasma (FFP): Platelets in a 1:1:1 ratio.
  • Fibrinogen replacement: Cryoprecipitate or fibrinogen concentrate if fibrinogen <1.5 g/L.


3. Antifibrinolytics (Tranexamic Acid – TXA):

  • TXA 1g IV over 10 minutes, followed by 1g infusion over 8 hours.
  • Effective if given within 3 hours of injury (reduces mortality by 20%).
  • Avoid TXA if DIC or hypercoagulability is suspected.


4. Correction of Metabolic Disturbances:

  • Maintain normothermia (>35°C) → Warm fluids, forced-air warmers.
  • Correct acidosis (pH >7.2) → Reduce excessive saline, use buffered solutions.
  • Maintain ionized calcium (>1.0 mmol/L) → Give Calcium chloride 10mL IV per 4 units of PRBCs.


5. Hemostatic Adjuncts:

  • Prothrombin Complex Concentrate (PCC) for rapid factor replacement.
  • Recombinant Factor VIIa (rFVIIa) only in refractory cases due to thrombosis risk.