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Bizhan Aarabi, Dale C. Hesdorffer, Edward S. Ahn, Carla Aresco, Thomas M. Scalea, and Howard M. Eisenberg

with secondary decompression following a primary surgery for evacuation of an intracranial hematoma. Nine of 53 patients with diffuse swelling were excluded from our analysis because they had undergone lobectomy or contusionectomy at the time of decompressive craniectomy. Prehospital Management Prehospital management was completed according to the standards of the Maryland Institute for Emergency Medical Services Systems, which is compatible with the Brain Trauma Foundation Guideline for Prehospital Management of Traumatic Brain Injury. 40 On admission to

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Bizhan Aarabi, Babak Tofighi, Joseph A. Kufera, Jeffrey Hadley, Edward S. Ahn, Carnell Cooper, Jacek M. Malik, Neal J. Naff, Louis Chang, Michael Radley, Ashker Kheder, and Ronald H. Uscinski

critical care and neurosurgical management at 1 of the 9 trauma centers; 74 (38.5%) survived acute care and were discharged to have traumatic brain injury (TBI) rehabilitation. Thirty of 74 patients (40.5%) underwent neurosurgical management. Overall, 712 (91%) of the 786 patients in this series eventually died. Of the 69 patients who were admitted to the STC, 46 (66.7%) died; 21 were dead on arrival; and 25 died during their acute care. Of the 23 patients discharged, 6 were lost to follow-up and 17 had a follow-up of at least 3 months (mean 40.6, range 3–136 months

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Anthony A. Figaji, A. Graham Fieggen, and Jonathan C. Peter

, and would support a similar trial in children. Although Taylor et al. 3 reported modest benefit in the craniectomy group in their trial, their surgical approach was relatively conservative. The results of a more aggressive surgical approach would be interesting. References 1 Figaji AA , Fieggen AG , Peter JC : Early decompressive craniotomy in children with severe traumatic brain injury . Childs Nerv Syst 19 : 666 – 673 , 2003 2 Hatashita S , Koike J , Sonokawa T , Ishii S : Cerebral edema associated with craniectomy and arterial

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Uttam K. Bodanapally, Kathirkamanathan Shanmuganathan, Alexis R. Boscak, Paul M. Jaffray, Giulia Van der Byl, Ashis K. Roy, David Dreizin, Thorsten R. Fleiter, Stuart E. Mirvis, Jaroslaw Krejza, and Bizhan Aarabi

I ntracranial arterial injuries in penetrating traumatic brain injury (PTBI) are caused by direct impact, by transfer of kinetic energy from the projectiles with resultant shock wave and cavitation, or by both means. 15 As a result, arteries can be damaged even in the absence of direct contact with the projectile. Bone fracture fragments and missile fragments can form secondary projectiles that can cause additional damage. 7 The true incidence of intracranial arterial injury after PTBI remains largely unknown; because of significant mortality associated

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Oral Presentations

2010 AANS Annual Meeting Philadelphia, Pennsylvania May 1–5, 2010

, Rene Sanchez-Meija , MD , Nicolas Phan , MD , J. Claude Hemphill III , MD , Christine Martin , RN, MS , and Geoffrey T. Manley , MD, PhD (San Francisco, CA) 8 2010 113 2 A415 A415 This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose. 2010 Introduction: Cerebral autoregulation may be altered after traumatic brain injury (TBI) and autoregulation status may influence cerebral perfusion pressure (CPP) goals. We evaluated the