Dear Sir, We appreciate the opportunity to comment on the Letter to the Editor concerning “Dabigatran and Stanford type A dissection: not a lethal coincidence” by Marchetti et al.[1] They refer to a female patient with a Stanford type A dissection and therapeutic dabigatran anticoagulation. In our original case report,[2] the patient died due to uncontrolled bleeding in the context of therapeutic plasma levels of dabigatran even after multiple exchange transfusions and more than 24 h after the last oral dabigatran intake. Marchetti et al.'s patient had a favourable outcome with a change in management in that they treated the patient pre-operatively with haemodialysis and only operated when the dabigatran plasma concentration decreased below 100 ng/ml. We proposed this procedure to avoid exsanguination due to severe coagulopathy at high dabigatran plasma concentration, but never had the chance to test the efficacy of this by ourselves. Interestingly, dabigatran plasma levels also started to increase due to redistribution after stopping the haemodialyis, as we had observed,[2] and also Chang et al[3] had described. Therefore, continuous haemodialysis is necessary to maintain dabigatran clearance and stable plasma levels. At a dabigatran plasma concentration of 100 ng/ml, Marchetti et al. used FEIBA to improve blood coagulation. However, FEIBA is neither designed nor sufficiently tested in the context of dabigatran-induced coagulopathy, and the coagulation boost can be lethal during extracorporeal circulation, which jeopardizes indication and timing of its application. Moreover, in a very similar case FEIBA neither normalized clinical bleeding nor corrected altered coagulation measurements in conjunction with high dabigatran plasma levels.[4] Fortunately, idarucizumab[5] has been approved by the FDA[6] and the EMA,[7] and we should have this antidote available early in 2016. Until then and probably even beyond the introduction of idarucizumab, timing of “emergency” interventions in relation to the last intake of dabigatran and the patient's renal function will be very important.
Dabigatran anticoagulation and Stanford type A aortic dissection: not a lethal coincidence / Marchetti, Gabriello; Giuliani, Enrico; Urbinati, Stefano; Barbieri, Alberto. - In: ACTA ANAESTHESIOLOGICA SCANDINAVICA. - ISSN 1399-6576. - 60:4(2016), pp. 544-544. [10.1111/aas.12658]
Dabigatran anticoagulation and Stanford type A aortic dissection: not a lethal coincidence.
GIULIANI, Enrico;BARBIERI, Alberto
2016
Abstract
Dear Sir, We appreciate the opportunity to comment on the Letter to the Editor concerning “Dabigatran and Stanford type A dissection: not a lethal coincidence” by Marchetti et al.[1] They refer to a female patient with a Stanford type A dissection and therapeutic dabigatran anticoagulation. In our original case report,[2] the patient died due to uncontrolled bleeding in the context of therapeutic plasma levels of dabigatran even after multiple exchange transfusions and more than 24 h after the last oral dabigatran intake. Marchetti et al.'s patient had a favourable outcome with a change in management in that they treated the patient pre-operatively with haemodialysis and only operated when the dabigatran plasma concentration decreased below 100 ng/ml. We proposed this procedure to avoid exsanguination due to severe coagulopathy at high dabigatran plasma concentration, but never had the chance to test the efficacy of this by ourselves. Interestingly, dabigatran plasma levels also started to increase due to redistribution after stopping the haemodialyis, as we had observed,[2] and also Chang et al[3] had described. Therefore, continuous haemodialysis is necessary to maintain dabigatran clearance and stable plasma levels. At a dabigatran plasma concentration of 100 ng/ml, Marchetti et al. used FEIBA to improve blood coagulation. However, FEIBA is neither designed nor sufficiently tested in the context of dabigatran-induced coagulopathy, and the coagulation boost can be lethal during extracorporeal circulation, which jeopardizes indication and timing of its application. Moreover, in a very similar case FEIBA neither normalized clinical bleeding nor corrected altered coagulation measurements in conjunction with high dabigatran plasma levels.[4] Fortunately, idarucizumab[5] has been approved by the FDA[6] and the EMA,[7] and we should have this antidote available early in 2016. Until then and probably even beyond the introduction of idarucizumab, timing of “emergency” interventions in relation to the last intake of dabigatran and the patient's renal function will be very important.File | Dimensione | Formato | |
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