Andonovic Mark, Morrison Holly, Allingham William, Adam Robert, Shaw Martin, Quasim Tara, McPeake Joanne, Quinn Terence
Academic Unit of Anaesthesia, Critical Care and Perioperative Medicine, University of Glasgow, Glasgow, UK.
Department of Anaesthesia, NHS Lanarkshire, Glasgow, UK.
Anaesthesia. 2025 Feb;80(2):188-196. doi: 10.1111/anae.16494. Epub 2024 Dec 12.
Cognitive impairment is a significant healthcare problem globally and its prevalence is projected to affect over 150 million people worldwide. Survivors of critical illness are impacted frequently by long-term neurocognitive dysfunction regardless of presenting illness, but the mechanisms are poorly understood. The goal of this review was to synthesise the existing evidence regarding potential mechanisms underlying neurocognitive dysfunction following critical illness in order to guide potential avenues for future research.
We performed a systematic search of the literature for studies published between 1 January 1974 and 15 July 2023. We included publications involving adult patients with critical illness due to any aetiology that assessed for cognitive impairment following recovery from illness, and explored or investigated potential underlying causative mechanisms. The quality and risk of bias of the individual studies was assessed using the Newcastle-Ottawa scale.
Of the 7658 reviewed references, 37 studies comprising 4344 patients were selected for inclusion. Most studies were single centre with sample sizes of < 100 patients. The proportion of patients with long-term cognitive impairment ranged from 13% to 100%. A wide variety of theoretical mechanisms were explored, with biomarkers and neuroimaging utilised most frequently. Many studies reported associations between investigated mechanisms and reduced cognition; several of these mechanisms have been implicated in other forms of long-term neurodegenerative conditions. Increased levels of inflammatory cytokines during acute illness and white matter hyperintensities on neuroimaging following recovery were the associations reported most commonly.
The underlying pathophysiology of neurocognitive decline after critical illness is not yet understood fully. The mechanisms implicated in other neurodegenerative conditions suggest that this may represent an accelerated version of the same processes. Large scale studies are required to further elucidate the cause of this significant problem for survivors of critical illness.
认知障碍是全球范围内一个重大的医疗保健问题，预计其患病率将影响全球超过1.5亿人。危重症幸存者经常受到长期神经认知功能障碍的影响，无论其当前疾病如何，但相关机制尚不清楚。本综述的目的是综合关于危重症后神经认知功能障碍潜在机制的现有证据，以指导未来研究的潜在方向。
我们对1974年1月1日至2023年7月15日期间发表的研究进行了系统的文献检索。我们纳入了涉及因任何病因导致危重症的成年患者的出版物，这些研究评估了患者从疾病中康复后的认知障碍，并探索或研究了潜在的潜在致病机制。使用纽卡斯尔-渥太华量表评估个体研究的质量和偏倚风险。
在7658篇综述参考文献中，选择了37项研究，共4344例患者纳入。大多数研究为单中心研究，样本量小于100例患者。长期认知障碍患者的比例从13%到100%不等。探索了多种理论机制，其中生物标志物和神经影像学应用最为频繁。许多研究报告了所研究的机制与认知功能下降之间的关联；其中一些机制与其他形式的长期神经退行性疾病有关。急性疾病期间炎症细胞因子水平升高以及康复后神经影像学上的白质高信号是最常报告的关联。
危重症后神经认知功能下降的潜在病理生理学尚未完全了解。其他神经退行性疾病中涉及的机制表明，这可能代表了相同过程的加速版本。需要大规模研究来进一步阐明这个对危重症幸存者来说重大问题的原因。
