Role of Anesthetics and Their Adjuvants in Neurovascular Protection in Secondary Brain Injury after Aneurysmal Subarachnoid Hemorrhage

Abstract

Aneurysmal rupture accounts for the majority of subarachnoid hemorrhage and is responsible for most cerebrovascular deaths with high mortality and morbidity. Initial hemorrhage severity and secondary brain injury due to early brain injury and delayed cerebral ischemia are the major determinants of outcomes after aneurysmal subarachnoid hemorrhage. Several therapies have been explored to prevent these secondary brain injury processes after aneurysmal subarachnoid hemorrhage with limited clinical success. Experimental and clinical studies have shown a neuroprotective role of certain anesthetics in cerebrovascular disorders including aneurysmal subarachnoid hemorrhage. The vast majority of aneurysmal subarachnoid hemorrhage patients require general anesthesia for surgical or endovascular repair of their aneurysm. Given the potential impact certain anesthetics have on secondary brain injury after SAH, appropriate selection of anesthetics may prove impactful on overall outcome of these patients. This narrative review focuses on the available evidence of anesthetics and their adjuvants in neurovascular protection in aneurysmal subarachnoid hemorrhage and discusses current impact on clinical care and future investigative directions.

Cerebrospinal fluid metabolic profiling reveals divergent modulation of pentose phosphate pathway by midazolam, propofol and dexmedetomidine in patients with subarachnoid hemorrhage: a cohort study

“…Midazolam, propofol and dexmedetomidine are the most used sedatives [ 6 , 8 , 9 ]. Previous studies have demonstrated that sedatives might play roles in altering the outcome of the brain-injured patients; however, the influences of different agents are divergent [ 10 ]. Low dose dexmedetomidine, rather than no use, is significantly associated with higher rate of favorable outcome in poor-grade SAH patients [ 10 , 11 ].…”

“…Previous studies have demonstrated that sedatives might play roles in altering the outcome of the brain-injured patients; however, the influences of different agents are divergent [ 10 ]. Low dose dexmedetomidine, rather than no use, is significantly associated with higher rate of favorable outcome in poor-grade SAH patients [ 10 , 11 ]. Dexmedetomidine also exerts brain protective effect in patients with intracranial aneurysm [ 12 ].…”

“…Levels of glial and neuronal injury markers are preserved in dexmedetomidine-treated patients while these markers significantly increased in patients treated with normal saline [ 12 ]. Meanwhile, most experimental and clinical studies also demonstrate the beneficial effect of propofol on secondary brain injury after SAH [ 10 ]. Propofol significantly reduces cerebral edema and improves neurological outcome of SAH rats [ 10 ].…”

“…Meanwhile, most experimental and clinical studies also demonstrate the beneficial effect of propofol on secondary brain injury after SAH [ 10 ]. Propofol significantly reduces cerebral edema and improves neurological outcome of SAH rats [ 10 ]. And the cognitive function is better in propofol-treated SAH patients undergoing intracranial aneurysm clipping [ 10 , 13 ].…”

“…Propofol significantly reduces cerebral edema and improves neurological outcome of SAH rats [ 10 ]. And the cognitive function is better in propofol-treated SAH patients undergoing intracranial aneurysm clipping [ 10 , 13 ]. Interestingly, on the contrary, another clinical study describes that the administration of propofol might be the detrimental [ 14 ].…”