Trauma-Induced Coagulopathy
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Direct answer
One in four severely injured patients arrives coagulopathic before any fluid has been given — that endogenous phenomenon, driven by shock and tissue injury (protein C activation, endothelial glycocalyx disruption, hyperfibrinolysis), is trauma-induced coagulopathy (TIC), and it is an independent predictor of death. It is not the old dilutional story of too much crystalloid: even the freshly injured, untransfused patient bleeds abnormally when shock and tissue hypoperfusion are severe. Management therefore runs on three rails — mechanical haemorrhage control, haemostatic resuscitation with balanced blood components guided by viscoelastic testing (ROTEM/TEG), and pharmacological correction with tranexamic acid, fibrinogen and calcium — while simultaneously treating the amplifiers of the lethal diamond: hypothermia, acidosis, hypocalcaemia and dilution.
What you must remember
- TIC is early and endogenous: present on arrival in roughly a quarter of patients with severe trauma and shock, associated with a several-fold increase in mortality; conventional tests (INR, APTT) are prolonged without prior anticoagulant exposure or dilution.
- Mechanisms: activation of the protein C pathway consuming factors Va and VIIIa, endothelial glycocalyx shedding with autopheparinisation, platelet dysfunction, hyperfibrinolysis, plus consumption at wound sites.
- The lethal triad becomes a diamond: hypothermia (below 35 degrees C impairs enzyme kinetics of coagulation), acidosis (pH below about 7.2), coagulopathy, and hypocalcaemia from citrate in massive transfusion — keep ionised calcium above about 1.1 mmol/L.
- Tranexamic acid inhibits hyperfibrinolysis: 1 g bolus plus 1 g over 8 hours, within 3 hours of injury (CRASH-2); CRASH-3 supported use in mild-to-moderate traumatic brain injury within the same window.
- Fibrinogen is the first factor to reach critical levels (target commonly above 1.5–2 g/L in bleeding trauma): replace with cryoprecipitate or fibrinogen concentrate; on ROTEM, FIBTEM A5 or A10 guides dosing.
- Viscoelastic testing (ROTEM/TEG) beats conventional assays in trauma because it reports clot initiation, strength and lysis within minutes on whole blood, reflecting the real hypocoagulable or hyperfibrinolytic state.
- Prevention is the best treatment: minimise crystalloid (dilution), keep the patient warm (warmed fluids, forced-air warmers, warm theatre), control haemorrhage early, and treat acidosis with perfusion rather than bicarbonate.
- Recognise the lethal pattern clinically: diffuse ooze from puncture sites and raw surfaces, bleeding disproportionate to injury, in a cold, acidotic patient — the phenotype of "medical bleeding" joining surgical bleeding.
How to work through it
A 30-year-old with a ruptured spleen and a pelvic fracture arrives cold (34.2 degrees C), acidotic (pH 7.14, base deficit -10) and hypotensive. Bloods drawn before any transfusion show an INR of 1.6 and an APTT ratio of 1.5 — no anticoagulants, no fluids yet: this is endogenous TIC, and the label itself changes management. The team activates the massive transfusion protocol (balanced 1:1:1 components rather than red cells alone), gives tranexamic acid inside the 3-hour window, pushes calcium chloride alongside the second cooler of blood, covers the patient with a forced-air warmer and warms all fluids. A ROTEM run in the theatre side room shows prolonged clotting time and a low FIBTEM amplitude: cryoprecipitate is given for fibrinogen, further plasma follows, and the trace normalises over the next hour while the surgeon packs the pelvis and removes the spleen. The lesson in the sequence: the coagulopathy was treated in parallel with the operation, not after it — because once the diamond closes (cold, acidotic, empty of factors, calcium-chelated), no surgical knot holds.
Where students slip
Two outdated models cost marks. First, "dilutional coagulopathy from fluids" as the whole story — correct as a contributor, wrong as the cause; the endogenous, shock-driven mechanism is the modern answer, and citing protein C activation or autopheparinisation from glycocalyx shedding marks a well-read candidate. Second, "correct the INR with fresh frozen plasma to a target of 1.5" recited as a lone strategy — viscoelastic-guided, ratio-based component therapy plus fibrinogen early is the contemporary standard. A third slip is temperature: candidates check the theatre table for warmth but forget the emergency department and CT scanner, where most cooling happens; and a fourth is calcium, omitted entirely from many answers despite being a formal corner of the lethal diamond.
Frequently asked questions
Why is trauma-induced coagulopathy called endogenous?
Because it appears in a quarter of severely injured patients before crystalloid or blood has been given, driven by shock and tissue injury through protein C activation, endothelial glycocalyx shedding and hyperfibrinolysis.
Which factor falls first in traumatic bleeding?
Fibrinogen, reaching critical levels early; replacement with cryoprecipitate or fibrinogen concentrate guided by levels or FIBTEM amplitude is prioritised in current guidance.
Why is ionised calcium monitored during massive transfusion?
Citrate in stored blood chelates calcium, producing hypocalcaemic myocardial depression and coagulopathy — the fourth arm of the "lethal diamond" — so calcium is replaced prophylactically during ongoing transfusion.
What advantage does ROTEM or TEG hold over INR and APTT in trauma?
Whole-blood viscoelastic testing reports the speed, strength and stability of the clot within minutes, detecting hyperfibrinolysis and guiding component and factor therapy in real time, whereas plasma assays are slower and miss platelet and fibrinolytic components.
How does hypothermia worsen traumatic bleeding?
Below about 35 degrees C the enzyme reactions of the coagulation cascade slow measurably (functionally equivalent to a factor deficiency), platelet function falls, and fibrinolysis increases — warming the patient is a coagulation intervention.