• Neurocritical care · Apr 2014

    Observational Study

    Subarachnoid Extension of Primary Intracerebral Hemorrhage is Associated with Fevers.

    • James C Guth, Alexander J Nemeth, Neil F Rosenberg, Adam R Kosteva, Rebecca M Bauer, Eric M Liotta, Shyam Prabhakaran, Andrew M Naidech, and Matthew B Maas.
    • Department of Neurology, Northwestern University, 710 N Lake Shore Drive, 11th Floor, Chicago, IL, 60611, USA, james.guth@northwestern.edu.
    • Neurocrit Care. 2014 Apr 1;20(2):187-92.

    BackgroundExtension of hemorrhage into the subarachnoid space in primary intracerebral hemorrhage (ICH) has recently been associated with poor outcomes, although the mechanisms underlying that association are uncertain. The objectives of this study are to confirm the association between fever and poor outcomes after ICH, and to determine whether subarachnoid hemorrhage extension (SAHE) is associated with fevers.MethodsPatients with primary ICH were enrolled into a prospective registry between December 2006 and July 2012. SAHE was identified on imaging by blinded expert reviewers. Patient temperature was recorded hourly, and we defined febrile as any recorded temperature >38 °C within the first 14 days. Regression models were developed to test whether fever was associated with poor outcome and whether the occurrence of SAHE was a predictor of fever.ResultsOf the 235 patients studied, 39.7 % had SAHE and 58 % had fever. Fever was associated with higher modified Rankin scores at 3 months (odds ratio, OR 1.8 [1.04-3.12], p = 0.04) after adjustment for ICH score. SAHE was a predictor of fevers (OR 1.82 [95 % confidence interval 1.02-3.24], p = 0.04) after adjustment for ICH score, and remained significant after adjustment for other confounders like pneumonia identified in the univariate analysis.ConclusionsOur data confirm the deleterious effect of fever on the outcome of patients with ICH and show that SAHE is an independent predictor of fever after ICH. SAHE may provoke dysfunctional thermoregulation similar to what is observed after aneurysmal subarachnoid hemorrhage, creating mechanistic pathway between SAHE and poor functional outcomes.

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