癫痫样活动与毒性代谢性脑病预后的关系。

Patrick M Chen, Sophie Schuurmans Stekhoven, Adnan Haider, Jin Jing, Wendong Ge, Eric S Rosenthal, M Brandon Westover, Sahar F Zafar
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引用次数: 0

摘要

癫痫样异常(EAs)特异性毒性代谢性脑病(TME)的临床意义尚不清楚。目的:量化TME患者的EA负担及其与神经系统预后的关系。设计背景和参与者:这是一项回顾性研究。TME和EA(阳性)患者队列的年龄、序贯器官衰竭评估评分、急性生理和慢性健康评估II (APACHE-II)评分与没有EA(对照组)的TME患者队列相匹配。单因素分析比较了ea阳性患者和对照组。对基础疾病病因进行多变量逻辑回归校正,以检验出院时EA负担与神经系统预后不良概率(修正Rankin评分[mRS] 4-6)之间的关系。2012年至2019年期间,连续入住住院楼层或icu,在单个中心接受连续脑电图(cEEG)监测。纳入标准为:1)诊断为TME的患者,2)年龄大于18岁,3)脑电图≥16小时。排除急性脑损伤和心脏骤停患者。主要结局和指标:以mRS (mRS 4-6)定义的神经系统预后差。结果:纳入116例患者,其中58例有EA, 58例对照组无EA,年龄和APACHE-II评分进行匹配。中位年龄为66岁(Q1-Q3, 57-75),中位APACHE II评分为18分(Q1-Q3, 13-22)。总体队列出院死亡率为22%,70%的患者神经系统预后不良。EA负担峰值定义为EA患病率最高的12小时记录窗口。在校正了Charlson合并症指数和初次诊断的多变量分析中,ea的存在与不良预后相关(优势比3.89;CI [1.05-14.2], p = 0.041)。峰值EA负担从0%增加到100%,使不良出院神经预后的可能性增加30%。结论和相关性:EA负担的增加与TME患者较差的出院结果相关。未来的研究需要确定短期抗癫痫药物治疗是否能改善潜在代谢紊乱的结果。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Association of Epileptiform Activity With Outcomes in Toxic-Metabolic Encephalopathy.

The clinical significance of epileptiform abnormalities (EAs) specific to toxic-metabolic encephalopathy (TME) is unknown.

Objectives: To quantify EA burden in patients with TME and its association with neurologic outcomes.

Design setting and participant: This is a retrospective study. A cohort of patients with TME and EA (positive) were age, Sequential Organ Failure Assessment Score, Acute Physiology and Chronic Health Evaluation II (APACHE-II) score matched to a cohort of TME patients without EA (control). Univariate analysis compared EA-positive patients against controls. Multivariable logistical regression adjusting for underlying disease etiology was performed to examine the relationship between EA burden and probability of poor neurologic outcome (modified Rankin Score [mRS] 4-6) at discharge. Consecutive admissions to inpatient floors or ICUs that underwent continuous electroencephalography (cEEG) monitoring at a single center between 2012 and 2019. Inclusion criteria were 1) patients with TME diagnosis, 2) age greater than 18 years, and 3) greater than or equal to 16 hours of cEEG. Patients with acute brain injury and cardiac arrest were excluded.

Main outcomes and measures: Poor neurologic outcome defined by mRS (mRS 4-6).

Results: One hundred sixteen patients were included, 58 with EA and 58 controls without EA, where matching was performed on age and APACHE-II score. The median age was 66 (Q1-Q3, 57-75) and median APACHE II score was 18 (Q1-Q3, 13-22). Overall cohort discharge mortality was 22% and 70% had a poor neurologic outcome. Peak EA burden was defined as the 12-hour window of recording with the highest prevalence of EAs. In multivariable analysis adjusted for Charlson Comorbidity Index and primary diagnosis, presence of EAs was associated with poor outcome (odds ratio 3.89; CI [1.05-14.2], p = 0.041). Increase in peak EA burden from 0% to 100% increased probability of poor discharge neurologic outcome by 30%.

Conclusions and relevance: Increasing burden of EA is associated with worse discharge outcomes in patients with TME. Future studies are needed to determine whether short-term treatment with anti-seizure medications while medically treating the underlying metabolic derangement improves outcomes.

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