Intracerebral hemorrhage related to non–vitamin-K antagonist oral anticoagulants (NOACs) is associated with a high risk of mortality and frequently involves hematoma expansion, according to a study published online ahead of print December 14, 2015, in JAMA Neurology.
The characteristics and natural history of acute-phase NOAC-associated ICH “are largely unknown,” and there are no prospective data concerning hematoma expansion or the effectiveness of prothrombin complex concentrate in limiting that expansion by reversing anticoagulation. Nevertheless, current recommendations suggest that clinicians consider administering prothrombin complex concentrate to this patient population, said Jan C. Purrucker, MD, neurology intern at Heidelberg University in Germany, and his associates.
To characterize the clinical and radiologic course, management, and outcome of NOAC-associated ICH in routine clinical practice, Dr. Purrucker and associates performed the ICH substudy of the Registry of Acute Stroke Under New Oral Anticoagulants (RASUNOA). This is a prospective registry involving 38 neurology departments with certified stroke units across Germany. For their substudy, the investigators examined 61 adults with a mean age of 76 (range, 46 to 97) who were taking NOACs (ie, apixaban, dabigatran etexilate, or rivaroxaban) and had moderate to severe neurologic deficit and a median hematoma volume of 10.8 mL at presentation. Thirty-five of these patients (57%) were treated with prothrombin complex concentrate.
The mortality rate was 16% (10 patients) during the acute inpatient stay and 28% (17 patients) at three months. Overall, 65% of the survivors had an unfavorable outcome. Substantial hematoma expansion, defined as a 33% or greater relative increase or a 6-mL or greater absolute increase in ICH volume, occurred in 38% of patients. “This proportion was within the range reported for vitamin-K antagonist–associated intracerebral hemorrhage (36% to 56%) and is higher, compared with that related to ICH in patients not receiving anticoagulation (12% to 26%),” said the investigators.
Larger hematoma volume at baseline (odds ratio [OR], 2.37) and intraventricular extension at baseline (OR, 8.13) strongly correlated with adverse outcomes. In contrast, prothrombin complex concentrate failed to limit lesion expansion or avert adverse outcomes. This failure might result from the fact that patients given the treatment tended to have more severe initial neurologic deficits and more unfavorable hematoma location than did those who were not given prothrombin complex concentrate. “Our study design, the limited sample size, and the potential for confounding by indication do not allow any [firm] conclusions regarding a potential association between prothrombin complex concentrate treatment and outcome,” the authors concluded.
—Mary Ann Moon