|Posted by gulseth.michael on April 25, 2017 at 12:25 AM|
I keep running into a lack of understanding of the effects of DOACs on traditional labs. I want to summarize, and keep this simple:
Dabigatran will modestly prolong aPTT at therapeutic and high levels. If normal, patient could still have therapeutic levels. Best lab to confirm low dabigatran levels for many is thrombin time. If the thrombin time is measurable or normal, patient likely has very low dabigatran levels.
Rivaroxaban typically causes a significant prolongation of pt/INR; degree of this will vary based on reagent. A normal pt/INR likely confirms low levels of rivaroxaban. If you work at a hospital using anti-Xa heparin levels, a measureable heparin level also likely indicates low levels of rivaroxaban.
Apixaban typically causes a prolongation of pt/INR; but not as much as rivaroxaban. A normal pt/INR likely confirms low levels of apixaban.
So, there it is in a nutshell. Current practice gaps/errors I see:
1. People giving vitamin K for high INRs due to rivaroxaban/apixaban to “reverse” them. I chuckle a little every time I see this.
2. Not recognizing the value of drawing labs to guide therapy in reversal, procedural situations, and guiding agent transitions. We need to step up and educate our colleagues on these issues.
As always, thank you for the great care you provide your patients.
Michael P. Gulseth, Pharm. D., BCPS, FASHP