DexSAH: A Systematic Review and Meta-analysis of Dexmedetomidine in Aneurysmal Subarachnoid Hemorrhage

Dexmedetomidine is increasingly used for sedation in aneurysmal subarachnoid hemorrhage (aSAH), but its effects on functional recovery, delayed cerebral ischemia (DCI), vasospasm, and biological markers of secondary brain injury remain uncertain. We systematically reviewed randomized and observational evidence while preserving the distinction between treatment effects and nonrandomized associations.

We searched databases for studies evaluating dexmedetomidine in patients with aSAH or related subarachnoid hemorrhage populations. Randomized controlled trials were synthesized separately from prospective and retrospective observational studies. The primary outcome was favorable functional outcome. Secondary outcomes included DCI, vasospasm-related outcomes, and biochemical markers of neuronal injury, metabolic stress, sympathetic activation, and inflammation.

Three randomized trials comprising 431 participants contributed to the meta-analysis. Dexmedetomidine was not significantly associated with favorable functional outcome compared with control treatment (RR, 1.20; 95% CI, 0.96-1.50; I² = 45%). DCI (RR, 0.84; 95% CI, 0.54-1.30; I² = 0%) and vasospasm-related outcomes (RR, 0.91; 95% CI, 0.65-1.27; I² = 0%) were also not significantly reduced. Randomized biomarker evidence demonstrated lower concentrations of neuronal injury, metabolic stress, sympathetic activation, and inflammatory markers with dexmedetomidine, although outcomes were predominantly derived from individual studies. Observational evidence was heterogeneous. Large database studies associated dexmedetomidine exposure with lower in-hospital mortality, while one cohort suggested increased respiratory complications. Prospective studies suggested preserved cerebral autoregulation and altered cerebral metabolic pathways.

Randomized evidence does not establish that dexmedetomidine improves functional outcome or prevents DCI or vasospasm after aSAH. Favorable biological signals and observational mortality associations support further investigation but do not establish causal neuroprotective benefits.