Disufenton sodium NXY-059 been shown to have little interaction with food or drugs, it can be prescribed in a fixed dose without the constraints of frequent monitoring.8 The most common side effect of dabigatran is dyspepsia, although clinical trial results indicate a possible increased risk of myocardial infarction in patients taking this drug.1 The mechanism behind this cardiac dysfunction is currently unknown. Analysis by the RE LY trial investigators3 showed that lower doses of dabigatran inhibitor, dabigatran exerts its mechanism of action at the very end of the coagulation cascade, and therefore both factor VIIa and fresh frozen plasma are ineffective as rhein inhibitor treatment options. One recent randomized clinical trial showed no effect of prothrombin complex concentrate on the anticoagulant effect of dabigatran.2 Although recent preclinical trials using murine models have shown that high dose prothrombin complex concentrate slows the expansion of intracerebral hematoma, direct clinical applicability is limited by a lack of neurological outcome monitoring and appropriate safety and efficacy studies.
Additionally, prothrombin complex concentrate is not currently high throughput chemical screening available at our institution and so was not used in this case. Because dabigatran is primarily renally excreted, dialysis is an alternative for drug clearance and can remove approximately 35% 60% of the drug in 2 3 hours.4 Dialysis was not considered at the time of initial presentation of our patient, and by the time of his deterioration it was too late to implement effectively. While dabigatran can alter the activated prothrombin time, this has not been shown to be an effective measure of systemic anticoagulation. The thrombin time is the most sensitive cyclophosphamide laboratory test to assess the effects of dabigatran in urgent clinical situations. In addition, the thrombin time is a rapidly obtained laboratory value that should be readily available in the inpatient and emergency department setting. Our patient presented with a markedly elevated thrombin time, which could have been serially monitored to assess his response to dabigatran had his clinical course been prolonged. As stated, recombinant factor VII administration failed to slow the progression of our patient’s intracranial hemorrhage.
Dabigatran is different from warfarin, whose inhibitory effect on clotting factors II, VII, IX, and X can be reversed by fresh frozen plasma, vitamin K, and factor VII. In the absence of an effective antidote, treating physicians should consider obtaining a thrombin time and instituting early use of dialysis in conjunction with judicious use of intravenous fluid administration to maintain renal perfusion. Caution is necessary, however, because patients with atrial fibrillation have tenuous intravascular stroke volume status, and fluid overload can lead to worsening heart function. Dabigatran is only the first of several direct thrombin inhibitors that may enter clinical use, and these agents will likely have similar risks for catastrophic progression of traumatic injuries. Conclusions New direct coagulation factor inhibitors, such as dabigatran, have demonstrated superior stroke and systemic embolism prevention without the burdensome monitoring and drug drug interactions seen with agents such as warfarin. Although dabigatran has been show.