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Journal article

EEG response to sodium nitrite may predict delayed cerebral ischaemia after severe subarachnoid haemorrhage

Abstract:
Objective: Aneurysmal subarachnoid haemorrhage (SAH) often leads to death and poor clinical outcome. Injury occurring during the first 72 hours is termed early brain injury (EBI), with disruption of the nitric oxide (NO) pathway playing an important pathophysiological role in its development. Quantitative electroencephalography (qEEG) parameters such as alpha/delta frequency ratio (ADR) are surrogate markers of cerebral ischaemia. This study assessed the qEEG response to a cerebral NO donor (intravenous sodium nitrite) to explore whether this correlates with the eventual development of delayed cerebral ischaemia (DCI).
Design: Unblinded pilot study testing response to drug intervention.
Setting: Neurosciences Intensive Care Unit (NICU), John Radcliffe Hospital, Oxford, UK
Patients: 14 World Federation of Neurosurgeons grades 3, 4 and 5 patients (mean age 52.8; range 41-69; 11 female).
Interventions: IV sodium nitrite 10 mcg/kg/min for one hour.
Measurements and Main Results: Continuous EEG recording for two hours. The ADR was measured before and during intravenous sodium nitrite infusion. Seven out of fourteen patients developed DCI. There was a +30% to +118% (range) increase in ADR in patients who did not develop DCI (p<0.0001) but an overall decrease in ADR in those patients who did develop DCI (range +11% to -31%) (p=0.006, multivariate analysis accounting for major confounds).
Conclusions: Administration of sodium nitrite after severe SAH differentially influences qEEG parameters depending on the patient’s susceptibility to development of DCI. With further validation in a larger sample size, this response may be developed as a tool for risk stratification after aneurysmal SAH.
Publication status:
Published
Peer review status:
Peer reviewed

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Publisher copy:
10.1097/CCM.0000000000001950

Authors

More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Clinical Neurosciences
Role:
Author
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Clinical Neurosciences
Role:
Author
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Clinical Neurosciences
Role:
Author
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Clinical Neurosciences
Role:
Author
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Clinical Neurosciences
Role:
Author



Publisher:
Lippincott, Williams and Wilkins
Journal:
Critical Care Medicine More from this journal
Volume:
44
Issue:
11
Pages:
e1067-e1073
Publication date:
2016-11-01
Acceptance date:
2016-03-25
DOI:
ISSN:
0090-3493


Keywords:
Pubs id:
pubs:612174
UUID:
uuid:f22cb86d-7b84-4854-906e-02a738056932
Local pid:
pubs:612174
Source identifiers:
612174
Deposit date:
2016-03-30
ARK identifier:

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