Trauma-Induced Coagulopathy

Trauma induced coagulopathy is an abnormality of coagulation after injury, appearing within minutes of severe trauma and shock, before significant resuscitation. It is characterised by a prolonged prothrombin time (INR over 1.2 to 1.5), low fibrinogen, impaired clot strength and hyperfibrinolysis.

Epidemiology. It occurs in about 25 to 35% of severely injured patients on arrival and is associated with a three to four fold increase in mortality and transfusion requirement.

Risk factors. Severe tissue injury, shock (base deficit 6 mmol/L or more), head injury, acidosis, hypothermia, haemodilution and pre-existing anticoagulant therapy.

Pathophysiology. Tissue injury and shock activate protein C, which inactivates factors Va and VIIIa and promotes fibrinolysis by inhibiting plasminogen activator inhibitor-1. Endothelial glycocalyx shedding, platelet dysfunction, fibrinogen consumption and tissue plasminogen activator release cause hyperfibrinolysis. Resuscitation, hypothermia and acidosis add dilution and impaired enzyme function.

Presentation is diffuse bleeding from wounds, puncture sites and surgical areas that persists after surgical control, with shock out of proportion to visible loss.

Red flags.

• Prothrombin time or INR prolonged on arrival.
• Fibrinogen under 1.5 g/L, or clot strength weakened on viscoelastic testing.
• Base deficit over 6 mmol/L or temperature under 35 °C.

Viscoelastic testing (clot time, clot firmness, lysis at 30 minutes) allows early treatment. Laboratory tests: prothrombin time, activated partial thromboplastin time, Clauss fibrinogen, platelet count, D-dimer, arterial gas with lactate, base deficit and ionised calcium. Take an anticoagulant history.

Differential diagnosis. Dilutional coagulopathy, disseminated intravascular coagulation, anticoagulant effect, liver disease and hypothermic coagulopathy.

Control haemorrhage first. Surgical or radiological control, with damage control surgery.

Tranexamic acid. 1 g IV over 10 minutes within 3 hours of injury (as early as possible), then 1 g over 8 hours. Avoid late use after 3 hours, since harm is possible.

Blood components. Early balanced resuscitation with red cells, plasma and platelets (1 to 1 to 1), or whole blood. Limit crystalloid to 1 L.

Fibrinogen. Cryoprecipitate 2 pools or fibrinogen concentrate 3 to 4 g IV for fibrinogen under 1.5 g/L, or low clot firmness.

Prothrombin complex concentrate. 25 units/kg (maximum 2500 units) for delayed clotting that persists after plasma, or for anticoagulant reversal, with attention to thrombosis risk.

Platelets. Transfuse to over 50 x 10^9/L (over 100 x 10^9/L in head injury).

Calcium. Calcium gluconate 10% 20 mL IV after each 4 units to keep ionised calcium over 1.1 mmol/L.

Maintain physiology. Active warming above 36 °C, correct acidosis by restoring perfusion, and avoid hypocalcaemia.

Anticoagulated patients. Warfarin: prothrombin complex concentrate 25 to 50 units/kg with vitamin K 10 mg IV. Dabigatran: idarucizumab 5 g IV. Factor Xa inhibitors: prothrombin complex concentrate 50 units/kg (maximum 5000 units) or the specific reversal agent.

Monitoring. Viscoelastic test or laboratory coagulation every 30 to 60 minutes during massive bleeding, platelets, fibrinogen, calcium, temperature and lactate.

Referral and escalation. Trauma team leader, haematology and blood bank. Move early to theatre or interventional radiology.

Special groups. In head injury, higher platelet targets and early tranexamic acid. In pregnancy, fibrinogen over 2.0 g/L. In children, tranexamic acid 15 mg/kg IV (maximum 1 g) then 2 mg/kg/h.