Three cases of spontaneous intracerebral hemorrhage on rivaroxaban

Debata, Ayumi; Tateishi, Yohei; Hamabe, Jumpei; Horie, Nobutaka; Izumo, Tsuyoshi; Hayashi, Kentarō; Kamada, Kensaku; Matsuo, Takayuki; Nagata, Isamu; Tsujino, Akira

doi:10.3995/jstroke.37.41

Cited by 3 publications

(1 citation statement)

References 16 publications

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“…The advantage of NOACs is probably that they do not inhibit the production of factor VII and prothrombin [ 18 – 19 , 21 – 22 , 25 ], the key factors in the blood coagulation cascade, and they inhibit the coagulation activities of factor Xa and thrombin in a reversible manner, unlike warfarin. Another suggested reason is the loss of anticoagulant action of NOACs at blood trough concentrations, so that the intracranial hemostatic mechanism becomes normal temporarily.…”

Section: Discussionmentioning

confidence: 99%

Characteristics of Symptomatic Intracranial Hemorrhage in Patients Receiving Non-Vitamin K Antagonist Oral Anticoagulant Therapy

2015

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ObjectivesThe first non-vitamin K antagonist oral anticoagulant (NOAC) introduced to the market in Japan was dabigatran in March 2011, and three more NOACs, rivaroxaban, apixaban, and edoxaban, have since become available. Randomized controlled trials of NOACs have revealed that intracranial hemorrhage (ICH) occurs less frequently with NOACs compared with warfarin. However, the absolute incidence of ICH associated with NOACs has increased with greater use of these anticoagulants, and we wanted to explore the incidence, clinical characteristics, and treatment course of patients with NOACs-associated ICH.MethodsWe retrospectively analyzed the characteristics of symptomatic ICH patients receiving NOACs between March 2011 and September 2014.ResultsICH occurred in 6 patients (5 men, 1 woman; mean ± SD age, 72.8 ± 3.2 years). Mean time to onset was 146.2 ± 111.5 days after starting NOACs. Five patients received rivaroxaban and 1 patient received apixaban. None received dabigatran or edoxaban. Notably, no hematoma expansion was observed within 24 h of onset in the absence of infusion of fresh frozen plasma, activated prothrombin complex concentrate, recombinant activated factor VIIa or hemodialysis. When NOAC therapy was initiated, mean HAS-BLED and PANWARDS scores were 1.5 ± 0.5 and 39.5 ± 7.7, respectively. Mean systolic blood pressure was 137.8 ± 15.9 mmHg within 1 month before spontaneous ICH onset.ConclusionSix symptomatic ICHs occurred early in NOAC therapy but hematoma volume was small and did not expand in the absence of infusion of reversal agents or hemodialysis. The occurrence of ICH during NOAC therapy is possible even when there is acceptable mean systolic blood pressure control (137.8 ± 15.9 mmHg) and HAS-BLED score ≤ 2. Even stricter blood pressure lowering and control within the acceptable range may be advisable to prevent ICH during NOAC therapy.

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Section: Discussionmentioning

confidence: 99%

Characteristics of Symptomatic Intracranial Hemorrhage in Patients Receiving Non-Vitamin K Antagonist Oral Anticoagulant Therapy

2015

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Intracranial Bleeding

Yasaka¹

2016

Treatment of Non-Vitamin K Antagonist Oral Anticoagulants

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New Insights into Nonvitamin K Antagonist Oral Anticoagulants' Reversal of Intracerebral Hemorrhage

Yasaka¹

2015

New Insights in Intracerebral Hemorrhage

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The nonvitamin K antagonist oral anticoagulants (NOACs) dabigatran, rivaroxaban, apixaban, and edoxaban are associated with an equal or lower incidence of stroke and systemic embolism and a much lower incidence of intracranial hemorrhage and hemorrhagic stroke than warfarin is, without the need for routine laboratory monitoring. However, reversal strategies are not currently established in the case of NOAC-related hemorrhagic stroke. In emergency situations, well-defined management for NOAC-related hemorrhagic stroke may improve clinical outcomes. Thus, in this chapter, general measures initially required to prevent the expansion of intracerebral hematomas, charcoal administration to reduce NOAC absorption from the gastrointestinal tract, application of hemodialysis to remove dabigatran, and coagulation factor therapy including 4-factor prothrombin complex concentrate and recombinant activated factor VII are reviewed. The specific reversal agents idarucizumab, which is a monoclonal antibody against dabigatran; andexanet alfa, a recombinant human factor Xa decoy for Xa inhibitors; and PER977, a small synthetic molecule for reversal of both Xa and thrombin inhibitors, are currently under development. These agents will facilitate the clinical management of NOAC-associated hemorrhagic stroke and other severe bleeding.

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Three cases of spontaneous intracerebral hemorrhage on rivaroxaban

Cited by 3 publications

References 16 publications

Characteristics of Symptomatic Intracranial Hemorrhage in Patients Receiving Non-Vitamin K Antagonist Oral Anticoagulant Therapy

Characteristics of Symptomatic Intracranial Hemorrhage in Patients Receiving Non-Vitamin K Antagonist Oral Anticoagulant Therapy

Intracranial Bleeding

New Insights into Nonvitamin K Antagonist Oral Anticoagulants' Reversal of Intracerebral Hemorrhage

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