By Dr. Ling Zang, MD
Please refer to
Indication: stroke prevention in atrial fibrillation
Mechanism of action: reversible, competitive, direct thrombin inhibitor (downstream from other anticoagulants)
- Half time: 13 hours in patients with normal renal function (Cr clearance > 80%), up to 28 hours in those with renal function impairment (Cr clearance < 30%)
- Peak effect: 2-3 hours
- Excretion: renal
Why it is preferred over Coumadin:
- more predictable pharmacokinetics
- no CYP450 interaction
- one dose for all patients
- no monitoring
- Similar to – if not better than – Coumadin in stroke prevention as an outcome
How to measure the anticoagulation effect of Dabigatran?
- Thrombin time – very sensitive, but not standardized
- aPTT – sensitive, but underestimates level of anticoagulation at high doses
- INR – not useful as it only cause mild elevation even at high doses
Which agents could be used to reverse Dabigatran?
- Vit K – allows synthesis of clotting factors, upstream from Dabigatran, won’t work.
- FFP – contains all clotting factors, including thrombin. Consider using.
- PCC – contains some factors and some thrombin. Consider using.
- Factor VIIa – can directly activate thrombin. Considering using.
At 2 hours, about 62% of Dabigatran will be removed.
Approach to a bleeding patient on Dabigatran
- Assess the severity of bleeding
- Determine timing of last dose of Dabigatran to see if patient is being anticoagulated by it
- Hemorrhage control
- Draw aPTT and TT. If normal, it is unlikely that the patient has significant anticoagulation
- Consider FFP, Factor VIIa, and dialysis. If last dose is within 2 hours, give activated charcoal.