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Traumatic brain injury with associated intracranial bleeding is an emergency requiring diag‐ nostic and supportive measures directed at limiting subsequent morbidity and mortality. If this intracranial bleeding is discovered in a patient that is anticoagulated, further aggressive steps are indicated to reverse the effects of the anticoagulant and limit further bleeding. Hematoma or bleeding volume & growth does correlate with various outcome measures [1-3]. Following spontaneous ICH, hematoma expansion on follow-up neuroimaging is not‐ ed in as much as 26% of cases [1]. Particularly in anticoagulated patients, such hematoma expansion is associated with poor outcomes [4]. Hemostatic therapy with agents directed at trying to reverse the effects of the anticoagulant have been shown to potentially be effective in reducing hematoma expansion in such patients [5,6]. Failing to correct a high INR, for ex‐ ample, may be associated with higher mortality [7]. Therefore, prompt recognition of this condition and taking immediate action is important in treating traumatic intracranial hem‐ orrhage. There are more options than ever for providing systemic anticoagulation to pa‐ tients. These different agents work in different ways and have different pharmacokinetics and pharmacodyanmics. Published data supporting specific strategies for reversing the ef‐ fects of these agents is limited, particularly for novel anticoagulants. However, the pharma‐ cology and mechanism of action of some anticoagulant therapies (outlined in Figure 1 & Table 1) have led to at least initial studies that can provide some guidance.

Immediate Treatment of the Anticoagulated Patient with Traumatic Intracranial Hemorrhage