Effect of stellate ganglion block on brain hemodynamics and the inflammatory response in moderate and severe traumatic brain injury: a pilot study

医学 脑血流 脑灌注压 创伤性脑损伤 血流动力学 麻醉 大脑中动脉 颅内压 血压 经颅多普勒 心脏病学 内科学 缺血 精神科
作者
Ivan Kostadinov,Jernej Avsenik,Joško Osredkar,Aleš Jerin,Primož Gradišek
出处
期刊:Regional Anesthesia and Pain Medicine [BMJ]
卷期号:51 (6): 687-694 被引量:10
标识
DOI:10.1136/rapm-2024-106185
摘要

INTRODUCTION: Traumatic brain injury (TBI) is often associated with reduced cerebral blood flow and an increased inflammatory response, leading to secondary brain damage. Stellate ganglion block (SGB) has been shown to improve cerebral hemodynamics in non-TBI, but its effects in TBI are still unclear. OBJECTIVE: This prospective pilot study investigates the effects of SGB on cerebral hemodynamics and neuroinflammatory responses in patients with moderate to severe TBI with the aim of evaluating its potential as a therapeutic intervention. METHODS: A prospective, single-center observational study was conducted in 20 patients with moderate to severe TBI. SGB was performed ipsilateral to the most severely affected hemisphere using an ultrasound-guided lateral approach at the level of C6 with 8 mL 0.5% levobupivacaine. The primary outcome was the change in blood flow velocity in the ipsilateral middle cerebral artery as measured by transcranial color-coded duplex ultrasonography before and after the procedure. Secondary outcomes included changes in (a) the diameter of the basal arteries of the brain as measured by computed angiography tomography; (b) cerebral blood flow, volume and time to peak as measured by computed perfusion tomography; (c) cerebral perfusion pressure, intracranial pressure and brain oxygenation. The changes in the biomarkers of inflammation and brain injury interleukin 6, neuron-specific enolase, protein S100B and glial fibrillar acidic protein measured at baseline, 12 hours and 24 hours after SGB were defined as tertiary outcomes. RESULTS: SGB significantly reduced blood flow velocity in the middle cerebral artery, increased the diameter of the large basal cerebral arteries, improved cerebral blood flow and volume in certain brain regions on the ipsilateral side. Inflammatory markers such as IL-6 and S100B decreased significantly within 24 hours. The intracranial pressure decreased, the cerebral perfusion pressure and the oxygen supply to the brain tissue improved after SGB. No adverse events were observed. CONCLUSION: SGB modulates cerebral hemodynamics and lowers intracranial pressure in patients with TBI, demonstrating its potential as a neuroprotective intervention. While these results highlight the therapeutic potential of SGB, further randomized controlled trials are needed to determine its optimal use and short-term and long-term benefits in the treatment of TBI. TRIAL REGISTRATION NUMBER: NCT04208477.
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