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J Neurol Neurosurg Psychiatry 2006;77:1340-1344 doi:10.1136/jnnp.2006.089748
  • Paper

Acute physiological derangement is associated with early radiographic cerebral infarction after subarachnoid haemorrhage

  1. A M Naidech1,
  2. J Drescher2,
  3. P Tamul1,
  4. A Shaibani1,
  5. H H Batjer1,
  6. M J Alberts1
  1. 1Northwestern University, Chicago, Illinois, USA
  2. 2University of Chicago, Chicago
  1. Correspondence to:
 A M Naidech
 Department of Neurology, Northwestern University, 710 N Lake Shore Drive, Chicago, IL 60611, USA; a-naidech{at}northwestern.edu
  • Received 30 January 2006
  • Accepted 23 June 2006
  • Revised 21 June 2006
  • Published Online First 4 July 2006

Abstract

Background: Cerebral infarction after aneurysmal subarachnoid haemorrhage (SAH) is presumed to be due to cerebral vasospasm, defined as arterial lumen narrowing from days 3 to 14.

Methods: We reviewed the computed tomography scans of 103 patients with aneurysmal SAH for radiographic cerebral infarction and controlled for other predictors of outcome. A blinded neuroradiologist reviewed the angiograms. Cerebral infarction from vasospasm was judged to be unlikely if it was visible on computed tomography within 2 calendar days of SAH or if angiography showed no vasospasm in a referable vessel, or both.

Results: Cerebral infarction occurred in 29 (28%) of 103 patients with SAH. 18 patients had cerebral infarction that was unlikely to be due to vasospasm because it was visible on computed tomography by day 2 (6 (33%)) or because angiography showed no vasospasm in a referable artery (7 (39%)), or both (5 (28%)). In a multivariate model, cerebral infarction was significantly related to World Federation of Neurologic Surgeons grade (odds ratio (OR) 1.5/grade, 95% confidence interval (CI) 1.1 to 2.01, p = 0.006) and SAH-Physiologic Derangement Score (PDS) >2 (OR 3.7, 95% CI 1.4 to 9.8, p = 0.01) on admission. Global cerebral oedema (OR 4.3, 95% CI 1.5 to 12.5, p = 0.007) predicted cerebral infarction. Patients with cerebral infarction detectable by day 2 had a higher SAH-PDS than patients with later cerebral infarction (p = 0.025).

Conclusions: : Many cerebral infarctions after SAH are unlikely to be caused by vasospasm because they occur too soon after SAH or because angiography shows no vasospasm in a referable artery, or both. Physiological derangement and cerebral oedema may be worthwhile targets for intervention to decrease the occurrence and clinical impact of cerebral infarction after SAH.

Footnotes

  • Published Online First 4 July 2006

  • This research was funded departmentally.

  • Competing interests: None.

  • The Northwestern University Institutional Review Board approved the project.

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