London, United Kingdom 2013 2 Interesting and challenging cases Successful treatment of Rivaroxaban-associated intracerebral hemorrhage with prothrombin complex concentrate M. Schmid-Burgk1, S.S. Fischer2, E. Schmid3, T. Steiner4, H. Bäzner5 Klinikum Stuttgart, Neurozentrum, Neurologische Klinik, Stuttgart, GERMANY1, Klinikum Stuttgart, Neurozentrum, Neurologische Klinik, Stuttgart, GERMANY2, Klinikum Stuttgart, Neu-rozentrum, Neurologische Klinik, Stuttgart, GERMANY3, Klinikum Frankfurt Hoechst, Klinik für Neurologie, Frankfurt, GERMANY4, Klinikum Stuttgart, Neurozentrum, Neurologische Klinik, Stuttgart, GERMANY55 Background: Novel anticoagulants including dabigatran, rivaroxaban and apixaban carry a lower risk of hemorrhagic stroke and intracranial hemorrhage compared to warfarin. However, in rare cas-es of severe bleeding complications, there is no antidote to novel anticoagulants. Therefore success-ful emergency management strategies have not yet been established. Methods: We report a 71-year-old patient who presented to our emergency stroke service with som-nolence, headache, dysarthria, diplopia and right-sided hemiplegia since the same morning. The patient was treated with Rivaroxaban 20mg for atrial fibrillation. Despite triple antihypertensive therapy, at admission his systolic blood pressure was 230 mmHg. Both magnetic resonance imag-ing (MRI) and computed tomography (CT) showed a left thalamic hemorrhage with intraventricu-lar hemorrhage and perifocal oedema, extending to the mesencephalon and left cerebral peduncle. Although the patient assured, that he didn’t take Rivaroxaban in the morning of the admission, his factor Anti-Xa activity was nevertheless at 2.98 IU/ml, indicating a significant treatment effect. Im-mediate decision was made to treat with prothrombin complex concentrate (Beriplex P/N®, CSL Behring, Marburg, Germany) at a dosage of 30 units per kg body weight. Results: Within 8 hours the Anti-Xa activity was reduced to 1.52 IU/ml and to 0.41 IU/ml 14 hours later. Hypertension was successfully treated by intravenous application of Urapidil and Nitroglycer-ine. Patients’ clinical symptoms remained stable. Two CTs on the same day showed no hemorrhage growth. The patient could be discharged to a rehabilitation centre 14 days later. During the whole course of hospitalization the patient remained in sinus rhythm, and low molecular weight heparine was given at a dose of 3000 IU of Certoparin/day. Conclusion: This case report supports a possible role of prothrombin complex concentrate in the emergency treatment of Rivaroxaban-associated intracranial hemorrhage. E-Poster Session Red Cerebrovasc Dis 2013; 35 (suppl 3)1-854 267 1 Interesting and challenging cases HaNDL or stroke: thrombolysis or lumbar puncture? M. Guillan1, A. DeFelipe-Mimbrera2, A. Alonso-Canovas3, M.C. Matute4, I. Hernandez-Medrano5, N. García-Barragán6, J. Masjuan7 Hospital Universitario Ramón y Cajal, madrid, SPAIN1, Hospital Universitario Ramón y Cajal, Madrid, SPAIN2, Hospital Universitario Ramón y Cajal, Madrid, SPAIN3, Hospital Universitario Ramón y Cajal, Madrid, SPAIN4, Hospital Ramón y Cajal, Madrid, SPAIN5, Hospital Universitario Ramón y Cajal, Madrid, SPAIN6, Hospital Universitario Ramon y Cajal, Madrid, SPAIN7 Background: The syndrome of transient Headache and Neurological Deficits with cerebrospinal flu-id Lymphocytosis (HaNDL) can present as sudden onset of focal neurological deficits, hence clinical and radiologically indistinguishable from an ischemic stroke. Its diagnosis requires a lumbar punc-ture (LP), which contraindicates further intravenous thrombolytic therapy (IV-tPA). Methods: We retrospectively analysed all patients who were referred to the Stroke Unit of our tertia-ry university hospital as a Stroke Code, resulting in a final diagnosis of HaNDL from January 2010 to January 2013. Results: We identified 8 cases, 6 women, with a mean age of 26 years (range 15-51). Clinical onset consisted of motor aphasia (1), global aphasia (1) and global aphasia with hemiparesis (5) or hemi-anesthesia (1). All patients had headache, lasting 6-18 hours; none had history of migraine. Cranial CT was normal in all. Perfusion CT was performed in 6, showing diffuse left hemispheric hypoper-fusion in 2, focal left frontal-parietal hypoperfusion in 1 and normality in the remaining 3. CT an-giography was abnormal in 1 case (left frontal asymmetry). 5 were initially diagnosed of stroke and treated uneventfully with IV-tPA, being 24 hours control MRI normal. LP was performed after the second episode of focal deficit (3) or after 24 hours of IV-tPA (5), showing in all cases pleocyto-sis (range 17-176 cells/mm3), hyperproteinorrhachia (range 0.6-1.6 g/l) and normal glycorrhachia (range 48-67 mg/dl). In all cases neurological deficit and headache resolved within 24 hours. Pa-tients were asymptomatic between episodes and after remission (duration <4 months, mean of 6 epi-sodes/ patient). Conclusions: HaNDL may mimic acute stroke; furthermore multimodal CT scans can provide mis-leading results. Hence it poses a diagnostic and therapeutic challenge for the neurologist. E-Poster Terminals 6
Karger_ESC London_2013
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