The preventive effect of dexmedetomidine on paroxysmal sympathetic hyperactivity in severe traumatic brain injury patients who have undergone surgery: a retrospective study.

Qilin Tang,Junfeng Feng,Qing Mao,Xiang Wu,Hongpeng Li,Weiji Weng,Jiyao Jiang,Guoyi Gao

doi:10.7717/peerj.2986

Abstract

BackgroundParoxysmal sympathetic hyperactivity (PSH) results and aggravates in secondary brain injury, which seriously affects the prognosis of severe traumatic brain injury patients. Although several studies have focused on the treatment of PSH, few have concentrated on its prevention.MethodsNinety post-operation (post-op) severe traumatic brain injury (sTBI) patients admitted from October 2014 to April 2016 were chosen to participate in this study. Fifty of the post-op sTBI patients were sedated with dexmedetomidine and were referred as the “dexmedetomidine group” (admitted from May 2015 to April 2016). The other 40 patients (admitted from October 2014 to May 2015) received other sedations and were referred as the “control group.” The two groups were then compared based on their PSH scores and the scores and ratios of those patients who met the criteria of “probable,” “possible” and “unlikely” using the PSH assessment measure (PSH-AM) designed by Baguley et al. (2014). The durations of the neurosurgery intensive care unit (NICU) and hospital stays and the Glasgow outcome scale (GOS) values for the two groups were also compared to evaluate the therapeutic effects and the patients’ prognosis.ResultsThe overall PSH score for the dexmedetomidine group was 5.26 ± 4.66, compared with 8.58 ± 8.09 for the control group. The difference between the two groups’ PSH scores was significant (P = 0.017). The score of the patients who met the criterion of “probable” was 18.33 ± 1.53 in the dexmedetomidine group and 22.63 ± 2.97 in the control group, and the difference was statistically significant (P = 0.045). The ratio of patients who were classified as “unlikely” between the two groups was statistically significant (P = 0.028); that is, 42 (84%) in the dexmedetomidine group and 25 (62.5%) in the control group. The differences in NICU, hospital stays and GOS values between the two groups were not significant.ConclusionDexmedetomidine has a preventive effect on PSH in sTBI patients who have undergone surgery.

Highlights

Sympathetic activity after stress is the body’s necessary protective response, but sympathetic overactivity following acute brain injury fosters hemodynamic instability and contributes to secondary brain damage, which severely affects the prognosis (Baguley et al, 2006; Hinson & Sheth, 2012; Lv et al, 2011)
We report that dexmedetomidine may have a preventive effect on Paroxysmal sympathetic hyperactivity (PSH) in postoperative patients who have suffered severe traumatic brain injury
The patients in the dexmedetomidine group were sedated for a period of 5.46 ± 2.82 days, compared with 6.08 ± 2.95 in the control group (p = 0.317)

Summary

Introduction

Sympathetic activity after stress is the body’s necessary protective response, but sympathetic overactivity following acute brain injury fosters hemodynamic instability and contributes to secondary brain damage, which severely affects the prognosis (Baguley et al, 2006; Hinson & Sheth, 2012; Lv et al, 2011). PSH episodes can last for several minutes to hours and may recur multiple times during the day (Blackman et al, 2004) Unstable conditions such as high blood pressure or fever, can result in and aggravate secondary brain injury, which is considered to be one of the main causes of unfavorable prognosis (Baguley, 2008a; Baguley et al, 2007a; Fernandez-Ortega et al, 2012; Fernandez-Ortega et al, 2006; Greer et al, 2008). The score of the patients who met the criterion of ‘‘probable’’ was 18.33 ± 1.53 in the dexmedetomidine group and 22.63 ± 2.97 in the control group, and the difference was statistically significant (P = 0.045). Dexmedetomidine has a preventive effect on PSH in sTBI patients who have undergone surgery

Methods

Results

Conclusion