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Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model
Published on: June 18, 2021
Electroencephalographic Response to Sodium Nitrite May Predict Delayed Cerebral Ischemia After Severe Subarachnoid
Payashi S Garry1, Matthew J Rowland, Martyn Ezra
11Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, United Kingdom. 2Neurosciences Intensive Care Unit, Neurosciences, Orthopaedics, Trauma and Specialist Surgery, Oxford University Hospitals NHS Trust, John Radcliffe Hospital, Oxford, United Kingdom. 3Department of Clinical Health Care, Oxford Brookes University, Oxford, United Kingdom. 4School of Psychology and Clinical Language Sciences, University of Reading, Reading, United Kingdom. 5Department of Anaesthesia, University of Auckland, Waikato Hospital, Hamilton, New Zealand.
Objectives:
Aneurysmal subarachnoid hemorrhage often leads to death and poor clinical outcome. Injury occurring during the first 72 hours is termed "early brain injury," with disruption of the nitric oxide pathway playing an important pathophysiologic role in its development. Quantitative electroencephalographic variables, such as α/δ frequency ratio, are surrogate markers of cerebral ischemia. This study assessed the quantitative electroencephalographic response to a cerebral nitric oxide donor (intravenous sodium nitrite) to explore whether this correlates with the eventual development of delayed cerebral ischemia.
Design:
Unblinded pilot study testing response to drug intervention.
Setting:
Neuroscience ICU, John Radcliffe Hospital, Oxford, United Kingdom.
Patients:
Fourteen World Federation of Neurosurgeons grades 3, 4, and 5 patients (mean age, 52.8 yr [range, 41-69 yr]; 11 women).
Interventions:
IV sodium nitrite (10 microg/kg/min) for 1 hour.
Measurements And Main Results:
Continuous electroencephalographic recording for 2 hours. The alpha/delta frequency ratio was measured before and during IV sodium nitrite infusion. Seven of 14 patients developed delayed cerebral ischemia. There was a +30% to +118% (range) increase in the alpha/delta frequency ratio in patients who did not develop delayed cerebral ischemia (p < 0.0001) but an overall decrease in the alpha/delta frequency ratio in those patients who did develop delayed cerebral ischemia (range, +11% to -31%) (p = 0.006, multivariate analysis accounting for major confounds).
Conclusions:
Administration of sodium nitrite after severe subarachnoid hemorrhage differentially influences quantitative electroencephalographic variables depending on the patient's susceptibility to development of delayed cerebral ischemia. With further validation in a larger sample size, this response may be developed as a tool for risk stratification after aneurysmal subarachnoid hemorrhage.
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