Garry Payashi S, Rowland Matthew J, Ezra Martyn, Herigstad Mari, Hayen Anja, Sleigh Jamie W, Westbrook Jon, Warnaby Catherine E, Pattinson Kyle T S
1Nuffield 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.
Crit Care Med. 2016 Nov;44(11):e1067-e1073. doi: 10.1097/CCM.0000000000001950.
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.
Unblinded pilot study testing response to drug intervention.
Neuroscience ICU, John Radcliffe Hospital, Oxford, United Kingdom.
Fourteen World Federation of Neurosurgeons grades 3, 4, and 5 patients (mean age, 52.8 yr [range, 41-69 yr]; 11 women).
IV sodium nitrite (10 μg/kg/min) for 1 hour.
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).
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.
动脉瘤性蛛网膜下腔出血常导致死亡和不良临床结局。在最初72小时内发生的损伤被称为“早期脑损伤”，一氧化氮途径的破坏在其发展过程中起着重要的病理生理作用。定量脑电图变量，如α/δ频率比，是脑缺血的替代标志物。本研究评估了对脑一氧化氮供体（静脉注射亚硝酸钠）的定量脑电图反应，以探讨这是否与迟发性脑缺血的最终发展相关。
测试对药物干预反应的非盲先导研究。
英国牛津约翰拉德克利夫医院神经科学重症监护病房。
14例世界神经外科医生联合会3、4和5级患者（平均年龄52.8岁[范围41 - 69岁]；11名女性）。
静脉注射亚硝酸钠（10μg/kg/分钟），持续1小时。
连续脑电图记录2小时。在静脉注射亚硝酸钠期间及之前测量α/δ频率比。14例患者中有7例发生迟发性脑缺血。未发生迟发性脑缺血的患者中，α/δ频率比增加了30%至118%（范围）（p < 0.0001），但发生迟发性脑缺血的患者中，α/δ频率比总体下降（范围为11%至 - 31%）（p = 0.006，多变量分析考虑了主要混杂因素）。
严重蛛网膜下腔出血后给予亚硝酸钠对定量脑电图变量的影响因患者发生迟发性脑缺血的易感性而异。经过更大样本量的进一步验证后，这种反应可能会被开发为动脉瘤性蛛网膜下腔出血后风险分层的工具。
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