O'Keeffe Fergus, Cervoni Isolde, Ganau Mario, Prisco Lara
University of Oxford, Oxford, UK.
The Kennedy Institute of Rheumatology, University of Oxford, Oxford, UK.
Intensive Care Med Exp. 2025 Sep 1;13(1):90. doi: 10.1186/s40635-025-00795-z.
Delirium is a frequent and serious complication of critical illness, yet its pathophysiological mechanisms remain incompletely understood. Serum biomarkers offer a potential avenue for improved diagnosis, risk stratification, and mechanistic insight. This systematic review synthesises evidence from 28 studies evaluating 54 serum biomarkers in relation to delirium among critically ill adult patients. Biomarkers were categorised by mechanistic pathway, including central nervous system (CNS) injury, immune activation, hormonal dysregulation, neurotransmission, coagulation, and amino acid metabolism. Among CNS injury markers, S100β and neurofilament light chain (NfL) demonstrated the most consistent associations with delirium presence and severity, supporting a role for astrocytic and axonal injury in delirium pathogenesis. Inflammatory markers such as interleukin-6 (IL-6), C-reactive protein (CRP), and tumour necrosis factor-alpha (TNF-α) were frequently studied but showed variable associations, reflecting the complex and non-specific nature of systemic inflammation. Hormonal biomarkers, including cortisol and prolactin, showed preliminary promise, while neurotransmitter-related biomarkers yielded inconsistent results, challenging canonical hypotheses. A major limitation in the literature was the lack of standardisation in delirium assessment, sampling timelines, and adjustment for confounding variables. Only a minority of studies incorporated temporal profiling or longitudinal outcomes, and replication across cohorts was limited. Heterogeneity in ICU populations further reduced generalisability. This review proposes a new conceptual framework of mechanistic endotyping, integrating multimodal biomarker profiling with clinical phenotyping to define biologically distinct subtypes of delirium. Such an approach may support precision medicine strategies by aligning therapeutic interventions with underlying pathophysiology. Future biomarker research should prioritise longitudinal sampling, harmonised protocols, and integration with EEG, imaging, and cognitive outcomes. Despite early promise, serum biomarkers for ICU delirium remain investigational and require further validation before clinical application.
谵妄是危重症常见且严重的并发症,但其病理生理机制仍未完全明确。血清生物标志物为改善诊断、风险分层及深入了解发病机制提供了一条潜在途径。本系统综述综合了28项研究的证据,这些研究评估了54种血清生物标志物与成年危重症患者谵妄的关系。生物标志物按作用机制途径分类,包括中枢神经系统(CNS)损伤、免疫激活、激素失调、神经传递、凝血及氨基酸代谢。在CNS损伤标志物中,S100β和神经丝轻链(NfL)与谵妄的存在及严重程度表现出最一致的关联,支持星形细胞和轴突损伤在谵妄发病机制中的作用。白细胞介素-6(IL-6)、C反应蛋白(CRP)和肿瘤坏死因子-α(TNF-α)等炎症标志物虽常被研究,但关联结果不一,反映出全身炎症的复杂性和非特异性。包括皮质醇和催乳素在内的激素生物标志物显示出初步前景,而与神经递质相关的生物标志物结果不一致,对传统假说提出了挑战。文献中的一个主要局限是谵妄评估、采样时间线及混杂变量调整缺乏标准化。仅有少数研究纳入了时间特征分析或纵向结局,且不同队列间的重复性有限。重症监护病房(ICU)人群的异质性进一步降低了研究结果的普遍性。本综述提出了一个新的作用机制内分型概念框架,将多模式生物标志物分析与临床表型分析相结合,以定义生物学上不同的谵妄亚型。这种方法可通过使治疗干预与潜在病理生理学相匹配来支持精准医学策略。未来生物标志物研究应优先考虑纵向采样、统一方案以及与脑电图、影像学和认知结局相结合。尽管血清生物标志物早期显示出前景,但ICU谵妄的血清生物标志物仍处于研究阶段,在临床应用前需要进一步验证。