It is a more specific and reliable reversal agent than fresh frozen plasma.8 2. Vitamin K is a cofactor for hepatic production of factors II, VII, IX, and X. Onset of effect depends on the route of administration (intravenous versus oral), and the dose given should be predicated on the presence of active bleeding, the maintenance dose of the VKA, the magnitude of INR elevation, and the desired range into which to reduce the INR.7,9 11 A 10-mg intravenous dose is recommended for life- threatening bleeding when there is no concern for restarting the VKA within the next week. 3. Idarucizumab (two, 2.5-mg bolus infusions no more than 15 minutes apart) is indicated to reverse the effect of dabigatran when clinically indicated.1,5 Andexanet alfa (bolus and 2-hour infusion, with the dose dependent on the timing of exposure and the individual agent) is used to reverse the effect of the oral anti-Xa agents. Experience with these agents Prothrombin complex concen- trate (or its activated form) has also been used with direct oral anticoagulant related bleeding. 4. A systematic review of the effectiveness and safety of administering vitamin K to patients receiving VKA therapy with an INR between 4.5 and 10.0 and without bleeding indicated a nonsignificant increased risk of mortality and thromboembolism with vitamin K administration, with only moderate certainty of the evidence. Patients receiving vitamin K had a nonsignificant increase in the likelihood of reaching goal INR, with very low certainty of the evidence. The findings suggested that patients on VKA therapy who have an INR between 4.5 and 10.0 and are not bleeding are not likely to benefit from routine vitamin K administration in addition to temporary VKA cessation.13 11.5. 