SummaryIntroductionCognitive 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.MethodsWe 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.ResultsOf 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.DiscussionThe 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.

中文翻译：

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危重症后神经认知功能障碍的机制：系统评价


摘要简介认知障碍是全球一个重大的医疗保健问题，其患病率预计将影响全球超过 1.5 亿人。无论表现如何，危重病的幸存者都经常受到长期神经认知功能障碍的影响，但对其机制知之甚少。本综述的目的是综合有关危重疾病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途径。方法我们对 1974 年 1 月 1 日至 2023 年 7 月 15 日期间发表的研究的文献进行了系统检索。我们纳入了涉及因任何病因而患有危重症的成年患者的出版物，这些出版物评估了疾病恢复后认知障碍，并探讨了或调查了潜在的潜在致病机制。使用 Newcastle-Ottawa 量表评估单个研究的质量和偏倚风险。结果在 7658 篇综述参考文献中，选择了 37 项研究，涉及 4344 名患者。大多数研究是单中心研究，样本量为 < 100 名患者。长期认知障碍患者的比例从 13% 到 100% 不等。探讨了各种各样的理论机制，其中生物标志物和神经影像学使用最频繁。许多研究报告了所研究的机制与认知能力下降之间的关联;其中一些机制与其他形式的长期神经退行性疾病有关。急性疾病期间炎性细胞因子水平升高和恢复后神经影像学上白质高信号是最常见的关联。讨论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。涉及其他神经退行性疾病的机制表明，这可能代表了相同过程的加速版本。需要大规模的研究来进一步阐明危重疾病幸存者这一重大问题的原因。