Department of Anesthesiology and Intensive Care Medicine, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Sahlgrenska University Hospital, Gothenburg, Sweden.
Department of Physiology and Pharmacology, Section of Anesthesiology and Intensive Care Medicine, Karolinska Institutet, Stockholm, Sweden.
Br J Anaesth. 2021 Feb;126(2):467-476. doi: 10.1016/j.bja.2020.09.043. Epub 2020 Nov 9.
Postoperative neurocognitive decline is a frequent complication in adult patients undergoing major surgery with increased risk for morbidity and mortality. The mechanisms behind cognitive decline after anaesthesia and surgery are not known. We studied the association between CSF and blood biomarkers of neuronal injury or brain amyloidosis and long-term changes in neurocognitive function.
In patients undergoing major orthopaedic surgery (knee or hip replacement), blood and CSF samples were obtained before surgery and then at 4, 8, 24, 32, and 48 h after skin incision through an indwelling spinal catheter. CSF and blood concentrations of total tau (T-tau), neurofilament light, neurone-specific enolase and amyloid β (Aβ1-42) were measured. Neurocognitive function was assessed using the International Study of Postoperative Cognitive Dysfunction (ISPOCD) test battery 1-2 weeks before surgery, at discharge from the hospital (2-5 days after surgery), and at 3 months after surgery.
CSF and blood concentrations of T-tau, neurone-specific enolase, and Aβ1-42 increased after surgery. A similar increase in serum neurofilament light was seen with no overall changes in CSF concentrations. There were no differences between patients having a poor or good late postoperative neurocognitive outcome with respect to these biomarkers of neuronal injury and Aβ1-42.
The findings of the present explorative study showed that major orthopaedic surgery causes a release of CSF markers of neural injury and brain amyloidosis, suggesting neuronal damage or stress. We were unable to detect an association between the magnitude of biomarker changes and long-term postoperative neurocognitive dysfunction.
术后神经认知功能下降是接受大手术的成年患者的常见并发症,增加发病率和死亡率的风险。麻醉和手术后认知能力下降的机制尚不清楚。我们研究了脑脊液(CSF)和血液中神经元损伤或脑淀粉样蛋白生物标志物与神经认知功能长期变化之间的关系。
在接受大骨科手术(膝关节或髋关节置换术)的患者中,通过留置的脊髓导管在术前以及皮肤切口后 4、8、24、32 和 48 小时时采集血液和 CSF 样本。测量 CSF 和血液中总 tau(T-tau)、神经丝轻链、神经元特异性烯醇化酶和淀粉样蛋白β(Aβ1-42)的浓度。在手术前 1-2 周、出院时(手术后 2-5 天)和手术后 3 个月使用国际术后认知功能研究(ISPOCD)测试套件评估神经认知功能。
手术后 CSF 和血液中的 T-tau、神经元特异性烯醇化酶和 Aβ1-42 浓度增加。血清神经丝轻链也出现类似增加,但 CSF 浓度没有总体变化。在神经元损伤和 Aβ1-42 的这些生物标志物方面,术后神经认知结局较差或较好的患者之间没有差异。
本探索性研究的结果表明,大骨科手术会引起 CSF 中神经损伤和脑淀粉样蛋白的标志物释放,提示存在神经元损伤或应激。我们未能检测到生物标志物变化幅度与长期术后神经认知功能障碍之间的关联。