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

Andrew M Naidech*, J. Drescher, Paul C Tamul, Ali Shaibani, H. H. Batjer, M. J. Alberts

*Corresponding author for this work

Research output: Contribution to journalArticle

39 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)1340-1344
Number of pages5
JournalJournal of Neurology, Neurosurgery and Psychiatry
Volume77
Issue number12
DOIs
StatePublished - Dec 1 2006

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Cerebral Infarction
Subarachnoid Hemorrhage
Angiography
Intracranial Vasospasm
Odds Ratio
Brain Edema
Tomography
Confidence Intervals
Arteries
Nervous System

ASJC Scopus subject areas

  • Surgery
  • Clinical Neurology
  • Psychiatry and Mental health

Cite this

@article{a1e18114001e432ca1a1073bcc0040a4,
title = "Acute physiological derangement is associated with early radiographic cerebral infarction after subarachnoid haemorrhage",
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.",
author = "Naidech, {Andrew M} and J. Drescher and Tamul, {Paul C} and Ali Shaibani and Batjer, {H. H.} and Alberts, {M. J.}",
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Acute physiological derangement is associated with early radiographic cerebral infarction after subarachnoid haemorrhage. / Naidech, Andrew M; Drescher, J.; Tamul, Paul C; Shaibani, Ali; Batjer, H. H.; Alberts, M. J.

In: Journal of Neurology, Neurosurgery and Psychiatry, Vol. 77, No. 12, 01.12.2006, p. 1340-1344.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Acute physiological derangement is associated with early radiographic cerebral infarction after subarachnoid haemorrhage

AU - Naidech, Andrew M

AU - Drescher, J.

AU - Tamul, Paul C

AU - Shaibani, Ali

AU - Batjer, H. H.

AU - Alberts, M. J.

PY - 2006/12/1

Y1 - 2006/12/1

N2 - 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.

AB - 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.

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