Li Weiqing, Shi Qin, Bai Ronghua, Zeng Jingzheng, Lin Lu, Dai Xuemei, Huang Qingqing, Gong Gu
Department of Anesthesiology, The General Hospital of Western Theater Command, Chengdu, Sichuan 610083, P.R. China.
Mol Med Rep. 2025 Aug;32(2). doi: 10.3892/mmr.2025.13585. Epub 2025 Jun 6.
Postoperative delirium (POD) is a common postoperative complication, characterized by acute, transient and fluctuating declines in consciousness and attention, with an incidence that increases with age. POD is associated with various adverse postoperative outcomes, including prolonged hospital stays, higher medical costs and increased morbidity and mortality rates. Moreover, it has been suggested that POD, as an early manifestation of postoperative cognitive impairment, may serve as a precursor to long‑term cognitive dysfunction. Given its considerable clinical impact, the prevention and management of POD are of critical importance. However, the mechanisms underlying POD remain insufficiently understood. Current hypotheses primarily implicate neuroinflammation, oxidative stress, neurotransmitter dysregulation and pathological protein changes, such as β‑amyloid deposition and tau hyperphosphorylation. Disruptions in the sleep‑wake cycle, electroencephalographic burst suppression, the microbiota‑gut‑brain axis, the olfactory‑brain axis and genetic susceptibility to delirium may also contribute to POD occurrence. Multiple signaling pathways are involved in POD, including the Wnt/β‑catenin, PI3K/AKT, brain‑derived neurotrophic factor/tropomyosin receptor kinase B, toll‑like receptor and NF‑κB pathways. These findings not only elucidate potential mechanisms but also highlight essential therapeutic targets and theoretical foundations for clinical management. However, due to the complexity and multifactorial nature of the pathogenesis of POD, no comprehensive or widely accepted clinical measures have yet been established for its prevention and treatment. Both non‑pharmacological and pharmacological interventions have a role in POD prevention and treatment. Non‑pharmacological strategies are currently prioritized, such as cognitive training, the Hospital Elder Life Program and comprehensive geriatric assessment. Pharmacological interventions include dexmedetomidine, melatonin and non‑steroidal anti‑inflammatory drugs, with intranasal insulin emerging as a promising preventive approach. Additionally, anesthesia management strategies, including depth of anesthesia monitoring, blood pressure regulation and multimodal postoperative analgesia, have also been recognized as effective measures for reducing the risk of POD. The present review provides a comprehensive overview of the pathogenesis of POD, relevant signaling pathways and available preventive and therapeutic strategies. By deepening the understanding of POD, the present review aims to offer practical guidance for clinicians in optimizing prevention and management approaches.
术后谵妄(POD)是一种常见的术后并发症,其特征为意识和注意力急性、短暂且波动的下降,发病率随年龄增长而增加。POD与多种不良术后结局相关,包括住院时间延长、医疗费用增加以及发病率和死亡率上升。此外,有人提出POD作为术后认知障碍的早期表现,可能是长期认知功能障碍的先兆。鉴于其相当大的临床影响,POD的预防和管理至关重要。然而,POD的潜在机制仍未得到充分理解。目前的假说主要涉及神经炎症、氧化应激、神经递质失调和病理性蛋白质变化,如β-淀粉样蛋白沉积和tau蛋白过度磷酸化。睡眠-觉醒周期紊乱、脑电图爆发抑制、微生物群-肠道-脑轴、嗅觉-脑轴以及谵妄的遗传易感性也可能导致POD的发生。多种信号通路参与了POD,包括Wnt/β-连环蛋白、PI3K/AKT、脑源性神经营养因子/原肌球蛋白受体激酶B、Toll样受体和NF-κB通路。这些发现不仅阐明了潜在机制,还突出了临床管理的重要治疗靶点和理论基础。然而,由于POD发病机制的复杂性和多因素性质,尚未建立全面或被广泛接受的预防和治疗临床措施。非药物和药物干预在POD的预防和治疗中均发挥作用。目前优先采用非药物策略,如认知训练、医院老年生活计划和综合老年评估。药物干预包括右美托咪定、褪黑素和非甾体抗炎药,鼻内胰岛素正成为一种有前景的预防方法。此外,麻醉管理策略,包括麻醉深度监测、血压调节和多模式术后镇痛,也被认为是降低POD风险的有效措施。本综述全面概述了POD的发病机制、相关信号通路以及可用的预防和治疗策略。通过加深对POD的理解,本综述旨在为临床医生优化预防和管理方法提供实用指导。