围术期脑保护的研究进展PPT课件.pptxVIP

围术期脑保护的研究进展解轶 2012年3月现状尽管近年麻醉技术及监测手段不断进步，但是术中与术后神经损伤仍是最严重的并发症。目前尚无足够的临床证据制订的官方指南，其主要原因是脑缺血机制错综复杂。对脑缺血高风险患者不仅要避免不利因素的影响，而且要积极采取措施来保护神经系统功能稳定。在一些特殊的外科手术中应用各种手段来提高脑组织对缺血缺氧的耐受力，减少缺血缺氧所导致的神经细胞死亡和神经功能受损，已成为围术期脑保护迫切需要解决的重大课题。1 生理性的脑保护1． 1 选择性脑降温1． 2 控制血糖1． 3 控制血压和保证氧供1. 4 血红蛋白浓度1． 1 选择性脑降温选择性脑降温是指在离头部较近处加强热量散发，使颅内温度低于躯体温度，可以避免全身低温所带来的不利影响，同时又能有效地改善缺血缺氧性脑损伤。脑保护机制不仅与降低脑代谢率有关，还涉及抑制缺血缺氧诱发的“瀑布式反应”的进展，如抑制谷氨酸释放、减少自由基生成、抑制凋亡、保护血脑屏障等，并且可为其他治疗措施延长治疗时间窗。The National Acute Brain Injury Study: Hypothermia II was a randomized multicenter trial in which 97 patients with moderate-to-severe TBI received either normothermia or total-body hypothermia to 33°C for 48 hours. The primary outcome measure was the rate of poor outcome (ie, GOS showing severe disability, vegetative state, or death). 1． 2 控制血糖大量研究证实，围术期控制血糖有助于改善患者神经功能预后。在一些危重和心脏手术患者中，严格控制围术期的血糖水平可以降低脑缺血发病率和病死率。围术期持续高血糖可增加缺血性脑损伤的范围，使得临床结局更差。McGirt 的研究发现，血糖＞ 11． 11 mmol /L ( 无论患者是否患有糖尿病) 可使颈动脉内膜剥脱术围术期脑卒中发生率增高。但是严格的血糖控制( 4． 44～ 6． 11 mmol /L) 可能会增加低血糖的风险。 Sui reported data from 43,933 men who underwent a comprehensive preventative medical between 1971 and 2002 （were free of myocardial infarction, stroke, cancer, or known diabetes mellitus）They were followed until either stroke, death, or the study end date (December 31, 2004) occurred. BG concentrations were stratified into 3 groups: (1) normal (80 to 109 mg/dL); (2) impaired (110 to 125 mg/dL); and (3) diabetes mellitus (=126 mg/dL). Nonfatal stroke rate was 10.3, 11.8, and 18.0 per 10,000 person-years in the 3 groups (P=0.002). Fatal stroke, with stroke rates of 2.1, 3.4, and 4.0 per 10,000 person-years (P=0.008). For fasting plasma glucose concentrations 110 mg/dL, each 10 mg/dL increase in serum glucose concentration was associated with a 6% greater risk of fatal stroke events (P=0.05) and an 8% increase in nonfatal stroke events (P0.05). A prospective study of fasting plasma glucose and risk of stroke in asymptomatic men. Mayo Clin Proc. 2011;86:1042–1049.Kamouchi utilized data