General
- Acute traumatic coagulopathy develops in over one third of patients with isolated TBI, (Epstein et al., 2014).
Due to
- Release of large amounts of tissue factor, altered protein C homeostasis, and platelet dysfunction.
Both extremes can occur
Hypocoagulable
- Reversing anticoagulants NICE
- Over 16
- Use prothrombin complex concentrate immediately in adults (16 or over) with major trauma who have active bleeding and need emergency reversal of a vitamin K antagonist.
- Consult a haematologist immediately
- Who have active bleeding and need reversal of any anticoagulant agent other than a vitamin K antagonist.
- Under 16
- Consult a haematologist immediately for advice
- Who have active bleeding and need reversal of any anticoagulant agent other than a vitamin K antagonist.
- Do not reverse anticoagulation in patients who do not have active or suspected bleeding.
- Do not use plasma to reverse a vitamin K antagonist in patients with major trauma.
Hypercoagulable
- DVT prophylaxis
- Head injury with an Abbreviated Injury Score of ≥3 was an independent predictor of VTE in trauma patients
- Numbers
- TBI has been associated with
- 54% incidence of deep venous thrombosis without prophylactic treatment
- 25% incidence in patients with isolated TBI treated with sequential compression devices.
- Ekeh: DVT occurred in 1/3 of moderate and severe TBI patients with isolated head injuries,
- Having a lower incidence than those patients with concomitant extracranial injuries.
- Reiff: 3-4x increase in the DVT risk in TBI despite use of mechanical and chemoprophylaxis
- Predictors of DVT
- Age
- Subarachnoid haemorrhage
- Injury Severity Score >15
- Extremity injury
- VTE risk increases with TBI severity.
- Mechanism
- Primary brain injury
- Prolonged periods of immobilization
- Focal motor deficits.
- Outcome
- DVT if not treatment can result in potentially debilitating or fatal pulmonary embolism.
- Management
- Pharmacological VTE prophylaxis + mechanical compression boots better than mechanical prophylaxis alone.
- However, there is an increased risk for expansion of intracranial haemorrhage
- Abdel- Aziz 2015: chemoprophylaxis should be started after
- 72 h in patients at medium or high risk of haematoma expansion,
- 48 h in those with low risk of haematoma expansion and absence of expansion.
Tranexamic acid
- Head injury + GCS score =< 12 + not thought to have active extracranial bleeding
- Dosage
- > 16: 2 g IV bolus
- < 16: 15 mg/kg to 30 mg/kg (up to a maximum of 2 g) IV bolus
- NICE: Give TXA within 2 hours of the injury, in the pre-hospital or hospital setting and before imaging
- CRASH 3: (Head injury + GCS score =< 12 + not thought to have active extracranial bleeding)
- Support use of tranexamic acid,
- Given within three hours of injury
- Reduces mortality in bleeding trauma patients without increasing adverse events in mild to moderate head injury
- Head injury, and suspected or confirmed extracranial bleeding NICE
- IV TXA as soon as possible in patients with major trauma and active or suspected active bleeding.
- Do not use IV TXA more than 3 hours after injury in patients with major trauma unless there is evidence of hyperfibrinolysis.
Diagnosis of disseminated intravascular coagulation (DIC)
- Low platelet count
- Prolonged PT
- Elevated fibrin degradation products
- Reduced fibrinogen level
When to restart anticoagulation when patient was on it pre injury
- No consensus yet (King 2020)
Coagulopathy in TBI
- TBI induced coagulopathy
- Platelet inhibitors
- P2Y12
- Anticox
- IIb IIIa
- Anticoagulants
- Heparin
- Factor Xa
- Direct thrombin inhibitors
- Vit K
- Youmans for list ofdrugs
- 9 doses to be stopped for dagibatran
- 3 doses for apixaban, edoxaban,
- Worse complication in warfarin
- See Savioli 2020
- Summary of key outcomes
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