Efficacy of continuous stellate ganglion block for prevention of cerebral vasospasm following interventional treatment of intracranial aneurysms
10.3760/cma.j.issn.0254-1416.2017.01.009
- VernacularTitle:连续星状神经节阻滞预防颅内动脉瘤介入术后患者脑血管痉挛的效果
- Author:
Xu WANG
;
Shen QU
;
Ding WAN
;
Xinli NI
- Keywords:
Stellate ganglion;
Nerve block;
Vasospasm,intracranial;
Intracranial aneurysm
- From:
Chinese Journal of Anesthesiology
2017;37(1):43-46
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the efficacy of continuous stellate ganglion block (SGB) for prevention of cerebral vasospasm (CVS) following interventional treatment of intracranial aneurysms.Methods Forty patients of both sexes with ruptured intracranial aneurysm,aged 20-60 yr,of American Society of Anesthesiologists physical status Ⅱ or Ⅲ,with Hunt-Hess grade Ⅰ-Ⅲ,scheduled for elective interventional treatment of intracranial aneurysms,were divided into 2 groups (n =20 each) using a random number table:control group (C group) and continuous SGB group (SGB group).After induction of anesthesia,patients received ipsilateral continuous SGB with 0.25％ ropivacaine 6-8 ml followed by continuous infusion of 0.2％ ropivacaine 2 ml/h for 3 days in group SGB.Transcranial Doppler ultrasound was used to measure the blood flow in bilateral middle cerebral arteries and internal carotid arteries within 3 days after operation,and the development of CVS was assessed.Before operation and at 2 and 6 h and 1 and 3 days after operation,blood samples were collected from the internal jugular vein for determination of plasma melatonin (MT) and endothelin-1 (ET-1) concentrations by enzyme-linked immunosorbent assay.Results Compared with group C,the incidence of CVS (5％) was significantly decreased,and the plasma ET-1 concentration was decreased at 2 and 6 h and 1 and 3 days after operation (P ＜ 0.05),and no significant change was found in plasma MT concentrations at each time point in group SGB (P＞0.05).Conclusion Continuous SGB can effectively prevent the development of CVS following interventional treatment of intracranial aneurysms,and the mechanism may be related to inhibited release of ET-1 from vascular endothelial cells,but not related to MT.
