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Lookup NU author(s): Dr Barbara Gregson, Patrick Mitchell
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Objective: Subarachnoid haemorrhage (SAH) may present with coma and this is known to be associated with aneurysmal origin and blood load. Aneurysmal origin is associated with increased blood load and existing data do not allow us to determine if the association between coma and aneurysmal SAH is wholly due to blood load or if aneurysmal origin has an additional independent effect. The objective of our study is to find if an aneurysmal origin is a predictor of acute onset of coma independent of blood load.Methods: A series of consecutive patients with spontaneous SAH were divided into two groups: aneurysmal (aSAH) and non-aneurysmal - angiographically negative SAH (naSAH). Blood load was quantified so that the effect of aneurysmal origin could be resolved from the effect of the amount of blood spilled. Non-parametric regression was used to relate blood load to coma and poor outcome rates for aneurysmal bleeds.Results: We analysed a total of 421 patients presenting during the period 2009-2011. Ninety aneurysmal cases presented with coma, seventy immediately in the early phase and seven shortly after rebleeding. None of the naSAH cases presented with immediate coma and 1 developed delayed coma. Delayed coma was associated with acute hydrocephalus in both groups. Aneurysmal origin was found to be an independent determinant of immediate coma (p = 0.02) and poor outcome (p < 0.001).Conclusion: Immediate coma and poor outcome in SAH are associated with an aneurysmal origin and do not characterize naSAH. (C) 2013 Elsevier B.V. All rights reserved.
Author(s): Tsermoulas G, Flett L, Gregson B, Mitchell P
Publication type: Article
Publication status: Published
Journal: Clinical Neurology and Neurosurgery
Year: 2013
Volume: 115
Issue: 8
Pages: 1362-1365
Print publication date: 01/08/2013
Online publication date: 14/01/2013
Acceptance date: 23/12/2012
ISSN (print): 0303-8467
ISSN (electronic): 1872-6968
Publisher: Elsevier BV
URL: http://dx.doi.org/10.1016/j.clineuro.2012.12.019
DOI: 10.1016/j.clineuro.2012.12.019
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