Paroxysmal Sympathetic Hyperactivity in Moderate-to-Severe Traumatic Brain Injury and the Role of Beta-Blockers: A Scoping Review

Introduction. Most cases of paroxysmal sympathetic hyperactivity (PSH) result from traumatic brain injury (TBI). Little is known about its pathophysiology and treatment, and several neuroprotective drugs are used including beta-blockers. The aim of our study is to collate existing evidence of the role of beta-blockers in the treatment of PSH. Methods. We searched MEDLINE, ResearchGate, and Google Scholar, for keywords related to PSH and the role of beta-blockers in moderate-to-severe TBI on September 23, 2020. Two authors blindly screened the articles found with Rayyan. Both resolved their conflicts by mutual consent. If no solution was found, a third author was consulted. Simple descriptive data analysis was performed and the results were presented both in a narrative and tabular form. Results. Of the 19 items found, 10 met the criteria for inclusion. 50% were systematic reviews without meta-analysis, 40% were observational studies, and 10% were experimental studies. Propranolol was the main beta-blocker found in 80% of the studies and was the only molecule used in the treatment of paroxysmal sympathetic hyperactivity in 40% of the included studies. Only two studies evaluated and showed a significant association between beta-blockers and mortality rate (5.1% vs. 10.8%; P = 0.03 ), (3% vs. 15%; P = 0.002 ), respectively. Conclusion. Propranolol is the beta-blocker that has been shown to be effective in reducing the length of stay and mortality rate in moderate-severe traumatic brain injury patients with PSH. However, further studies are needed to precisely define the terms and conditions of its use.

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P88 Paroxysmal sympathetic storm and the role of beta-blockers in traumatic brain injury: a scoping review protocol

BJS Open ◽

10.1093/bjsopen/zrab032.087 ◽

2021 ◽

Vol 5 (Supplement_1) ◽

Author(s):

Stéphane Nguembu ◽

Marco Meloni ◽

Geneviève Endalle ◽

Hugues Dokponou ◽

Olaoluwa Ezekiel Dada ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Length Of Stay ◽

Glasgow Coma Scale ◽

Scoping Review ◽

Beta Blockers ◽

Clinical Signs ◽

Sympathetic Hyperactivity ◽

Paroxysmal Sympathetic Hyperactivity

Abstract Introduction Most cases of paroxysmal sympathetic hyperactivity (PSH) result from traumatic brain injury (TBI). Little is known about its pathophysiology and treatment, and several neuroprotective drugs are used including beta-blockers. The aim of our study is to collate existing evidence of the role of beta-blockers in the treatment of PSH. Method We will search MEDLINE, Web of Science, EMBASE, Cochrane, and Google Scholar. The search terms used will cover the following terms: “paroxysmal sympathetic hyperactivity”, “traumatic brain injury” and “beta-blockers.”: No language or geographical restrictions will be applied. Two independent co-authors will screen the titles and abstracts of each article following predefined inclusion and exclusion criteria. If there is a conflict the two reviewers will find a consensus and if they cannot a third co-author will decide. Using a pre-designed and pre-piloted data extraction form, data from each included citation will be collected (authors identification, study type, TBI severity, type of beta-blockers used, dosage of the drug, clinical signs of PSH, Glasgow Coma Scale, Glasgow Outcome Scale, mortality, morbidity and length of stay). Simple descriptive data analyses will be performed and the results will be presented both in a narrative and tabular form. Results The effectiveness of beta-blockers in post-TBI PHS will be evaluated through clinical signs of PHS(increased heart rate, respiratory rate, temperature, blood pressure, and sweating), Glasgow Coma Scale, and Glasgow Outcome Scale. mortality, morbidity and length of stay. Conclusion At the end of this scoping review we will design a systematic review with metaanalysis if there are a reasonable number of studies otherwise we will design a randomized controlled trial.

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Paroxysmal sympathetic hyperactivity and the role of beta-blockers in moderate/severe traumatic brain injury: a scoping review protocol

10.14293/s2199-1006.1.sor-.ppebgar.v1 ◽

2020 ◽

Author(s):

Stephane Nguembu

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Length Of Stay ◽

Glasgow Coma Scale ◽

Scoping Review ◽

Beta Blockers ◽

Clinical Signs ◽

Sympathetic Hyperactivity ◽

Paroxysmal Sympathetic Hyperactivity

INTRODUCTION Most cases of paroxysmal sympathetic hyperactivity (PSH) result from traumatic brain injury (TBI). Little is known about its pathophysiology and treatment, and several neuroprotective drugs are used including beta-blockers. Our study aims to collate existing evidence of the role of beta-blockers in the treatment of PSH. METHOD We will search MEDLINE, Web of Science, EMBASE, Cochrane, and Google Scholar. The search terms used will cover the following terms: paroxysmal sympathetic hyperactivity, traumatic brain injury and beta-blockers. No language or geographical restrictions will be applied. Two independent co-authors will screen the titles and abstracts of each article following predefined inclusion and exclusion criteria. If there is a conflict the two reviewers will find a consensus and if they cannot a third co-author will decide. Using a pre-designed and pre-piloted data extraction form, data from each included citation will be collected ( authors identification, study type, TBI severity, type of beta-blockers used, the dosage of the drug, clinical signs of PSH, Glasgow Coma Scale, Glasgow Outcome Scale , mortality , morbidity and length of stay). Simple descriptive data analyses will be performed and the results will be presented both in a narrative and tabular form. RESULTS The effectiveness of beta-blockers in post-TBI PHS will be evaluated through clinical signs of PHS(increased heart rate, respiratory rate, temperature, blood pressure, and sweating), Glasgow Coma Scale, and Glasgow Outcome Scale.. mortality, morbidity and length of stay. CONCLUSION At the end of this scoping review, we will design a systematic review with metaanalysis if there are a reasonable number of studies otherwise we will design a randomized controlled trial.

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Peer Review #1 of "The preventive effect of dexmedetomidine on paroxysmal sympathetic hyperactivity in severe traumatic brain injury patients who have undergone surgery: a retrospective study (v0.1)"

10.7287/peerj.2986v0.1/reviews/1 ◽

2017 ◽

Keyword(s):

Traumatic Brain Injury ◽

Retrospective Study ◽

Brain Injury ◽

Peer Review ◽

Severe Traumatic Brain Injury ◽

Preventive Effect ◽

Sympathetic Hyperactivity ◽

Paroxysmal Sympathetic Hyperactivity

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

PeerJ ◽

10.7717/peerj.2986 ◽

2017 ◽

Vol 5 ◽

pp. e2986 ◽

Cited By ~ 8

Author(s):

Qilin Tang ◽

Xiang Wu ◽

Weiji Weng ◽

Hongpeng Li ◽

Junfeng Feng ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Severe Traumatic Brain Injury ◽

Control Group ◽

Therapeutic Effects ◽

Preventive Effect ◽

Sympathetic Hyperactivity ◽

Paroxysmal Sympathetic Hyperactivity ◽

Hospital Stays ◽

The Difference

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.

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