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London, United Kingdom 2013 Poster Session Blue Cerebrovasc Dis 2013; 35 (suppl 3)1-854 809 875 Intracerebral/subarachnoid haemorrhage and venous diseases Clinical predictors of pituitary dysfunction after subarachnoid haemorrhage L. Khajeh1, K Blijdorp2, M.H. Heijenbrok-Kal3, H.J.G. van den Berg-Emons4, S.J.C.M.M. Neg-gers5, G.M. Ribbers6, D.W.J. Dippel7, F. van Kooten8 Erasmus university medical center, Rotterdam, THE NETHERLANDS1, Erasmus university medical center, Rotterdam, THE NETHERLANDS2, Erasmus university medical center and Rijn-dam Rehabilitation Center, Rotterdam, THE NETHERLANDS3, Erasmus university medical center and Rijndam Rehabilitation Center, Rotterdam, THE NETHERLANDS4, Erasmus university med-ical center, Rotterdam, THE NETHERLANDS5, Erasmus university medical center and Rijndam Rehabilitation Center, Rotterdam, THE NETHERLANDS6, Erasmus university medical center, Rot-terdam, THE NETHERLANDS7, Erasmus university medical center, Rotterdam, THE NETHER-LANDS8 Background Pituitary dysfunction (PD) after aneurysmal subarachnloid haemorrhage (SAH) has been reported in a few case series. The cause of PD after SAH is unknown. Our aim was to describe the occurrence of hypopituitarism shortly after SAH and to identify clinical risk factors for development of PD after SAH. Methods This study was a single center prospective cohort study. We asked consecutive patients with aneu-rysmal SAH who survived the acute phase of SAH to participate. We excluded patients with pre-vious PD or any medical condition that might interfere with the assessment of endocrine function. We collected clinical parameters of all patients. A team of endocrinologists performed a fasting state endocrine evaluation, including dynamic test for growth hormone function. We compared clinical characteristics of SAH patients between endocrine deficient and non-deficient patients using stan-dard statistical methods. Results We included 84 patients with a mean age of 55.8 (SD 11.9), of which 28 (33%) were men, 32 (42%) had hypertension (HT), 19 (23%) had hydrocephalus (HC) on admittance and, 12 (14%) developed HC and 14 (15.5%) developed delayed cerebral ischemia (DCI). The mean time elapsed to endo-crine evaluation was 32 days (SD 32). Thirty-three patients (38.8%) had PD in one or more axes. These consisted of gonadotropin deficiency in 29 (34.1%), growth hormone deficiency in 6 (7.1%), thyroid stimulating hormone deficiency in 2 (2.4%) and corticotrophin deficiency in 1 (1.2%). PD was associated with HT (p< 0.028), HC(p< 0.026) and DCI (p<0.035). In a multivariable analysis adjusting for age, sex, HT and DCI, HC remained associated with PD (OR 2.81, p<0.028) Conclusion A large proportion of patients has PD after SAH. Hydrocephalus is independently associated with pituitary dysfunction. It remains unclear whether pituitary dysfunction is a permanent or temporary phenomenon. We are currently conducting a long-term follow-up study to answer this question. 876 Intracerebral/subarachnoid haemorrhage and venous diseases Effects of Intraventricular Fibrinolysis on Cerebral Perfusion and Metabolism after Severe Intraventricular Hemorrhage. J.B. Kuramatsu1, S. Gerner2, S. Staykov3, I. Eyüpoglu4, S.P. Kloska5, S. Schwab6, H.B. Huttner7 Department of Neurology, University Hospital Erlangen-Nuremberg, Erlangen, GERMA-NY1, Department of Neurology, University Hospital Erlangen-Nuremberg, Erlangen, GERMA-NY2, Department of Neurology, University Hospital Erlangen-Nuremberg, Erlangen, GERMANY3, Departmernt of Neurosurgery, University Hospital Erlangen-Nuremberg, Erlangen, GERMANY4, Department of Neuroradiology, University Hospital Erlangen-Nuremberg, Erlangen, GERMANY5, Department of Neurology, University Hospital Erlangen-Nuremberg, Erlangen, GERMANY6, De-partment of Neurology, University Hospital Erlangen-Nuremberg, Erlangen, GERMANY7 INTRODUCTION: Intraventricular hemorrhage(IVH) is an established predictor of poorer out-come in subarachnoid- and intracerebral- hemorrhage. Though, limited knowledge exists regarding the pathophysiologic mechanisms that may lead to cerebral injury and poorer outcome. This is the first report presenting in vivo data on cerebral blood flow and brain tissue metabolism during the occurrence of IVH and after intraventricular fibrinolysis (IVF). METHODS: A 78-year-old wom-an with severe subarachnoid hemorrhage(SAH), Hunt&Hess grade 3, modified Fisher Scale 4, was admitted to our neuro-critical-care unit. Within the first 24 hours an extraventricular drainage was placed and a left-sided MCA aneurysm was coiled. After obtaining informed consent, the patient received invasive multimodal neuromonitoring, consisting of a cerebral blood flow (CBF)- and mi-crodialysis- probe placed into ipsilateral frontal white matter. RESULTS: Within 8 hours after probe placement we observed a significant drop of CBF (CBF≤20 ml/100g/min) and increased L/P-ra-tio without significant changes in cerebral perfusion- or intracranial-pressure. Imaging revealed a re-hemorrhage into the ventricular system with blockage of the foramina of Monro and acute hydro-cephalus. Consequently, therapeutic IVF was undertaken with 1 mg of rtPA which lead to sufficient clot resolution. After IVF we documented profound changes (ΔCBF>20 ml/100g/min) in CBF and microdialysis parameters (L/P ratio:R^2=.739) leading to normalization of cerebral perfusion and metabolism. CONCLUSIONS: This is the first report on IVH and its potential mechanisms that may contribute to secondary injury in the human brain. A decrease of cerebral blood flow and disturbance of cerebral metabolism was documented during the occurrence of IVH, supporting existing hypoth-eses of global impairment. Moreover, we could document profound treatment effects of IVF leading to a restored CBF and a stable aerobic metabolism in the investigated brain tissue.


Karger_ESC London_2013
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