Association of early dexmedetomidine exposure with brain injury biomarker levels following moderate - severe traumatic brain injury: A TRACK-TBI study

• Published in: Journal of clinical neuroscience 2024-08, Vol.126, p.338-347
• Main Authors: Wongsripuemtet, Pattrapun, Ohnuma, Tetsu, Temkin, Nancy, Barber, Jason, Komisarow, Jordan, Manley, Geoffrey T., Hatfield, Jordan, Treggiari, Miriam, Colton, Katharine, Sasannejad, Cina, Chaikittisilpa, Nophanan, Ivins-O’Keefe, Kelly, Grandhi, Ramesh, Laskowitz, Daniel, Mathew, Joseph P., Hernandez, Adrian, James, Michael L., Raghunathan, Karthik, Miller, Joseph, Vavilala, Monica, Krishnamoorthy, Vijay
• Format: Article
• Language: English
• Subjects: Biomarkers; Critical Care; Dexmedetomidine; Sedation; Traumatic brain injury
• ISSN: 0967-5868; 1532-2653; 1532-2653
• DOI: 10.1016/j.jocn.2024.07.003

•14.5 % of the moderate-to-severe traumatic brain injury patients were exposed to early dexmedetomidine.•There was no significant association between early dexmedetomidine exposure and day 3 biomarkers.•Dexmedetomidine might be a safe choice for ICU sedation. Traumatic brain injury (TBI) triggers autonomic dysfunction and inflammatory response that can result in secondary brain injuries. Dexmedetomidine is an alpha-2 agonist that may modulate autonomic function and inflammation and has been increasingly used as a sedative agent for critically ill TBI patients. We aimed to investigate the association between early dexmedetomidine exposure and blood-based biomarker levels in moderate-to-severe TBI (msTBI). We conducted a retrospective cohort study using data from the Transforming Clinical Research and Knowledge in Traumatic Brain Injury Study (TRACK-TBI), which enrolled acute TBI patients prospectively across 18 United States Level 1 trauma centers between 2014–2018. Our study population focused on adults with msTBI defined by Glasgow Coma Scale score 3–12 after resuscitation, who required mechanical ventilation and sedation within the first 48 h of ICU admission. The study’s exposure was early dexmedetomidine utilization (within the first 48 h of admission). Primary outcome included brain injury biomarker levels measured from circulating blood on day 3 following injury, including glial fibrillary acidic protein (GFAP), ubiquitin C-terminal hydrolase-L1 (UCH-L1), neuron-specific enolase (NSE), S100 calcium-binding protein B (S100B) and the inflammatory biomarker C-reactive protein (CRP). Secondary outcomes assessed biomarker levels on days 5 and 14. Linear mixed-effects regression modelling of the log-transformed response variable was used to analyze the association of early dexmedetomidine exposure with brain injury biomarker levels. Among the 352 TRACK-TBI subjects that met inclusion criteria, 50 (14.2 %) were exposed to early dexmedetomidine, predominantly male (78 %), white (81 %), and non-Hispanic (81 %), with mean age of 39.8 years. Motor vehicle collisions (27 %) and falls (22 %) were common causes of injury. No significant associations were found between early dexmedetomidine exposure with day 3 brain injury biomarker levels (GFAP, ratio = 1.46, 95 % confidence interval [0.90, 2.34], P = 0.12; UCH-L1; ratio = 1.17 [0.89, 1.53], P = 0.26; NSE, ratio = 1.19 [0.92, 1.53], P = 0.19; S100B, ratio = 1.01 [0.95, 1.06], P = 0.82; hs-CRP, ratio = 1.29 [0.91,