Cervical Ganglion Sympathectomy to Treat Cerebral Vasospasm in Subarachnoid Hemorrhage

The Impact of Inotropes and Vasopressors on Cerebral Oxygenation in Patients with Traumatic Brain Injury and Subarachnoid Hemorrhage: A Narrative Review

“…Nerve fibers emerge from the superior cervical ganglion to join the carotid nerve (which accompanies the internal carotid artery and its branches). In contrast, others from the stellate ganglion accompany the vertebral and basilar arteries and their branches up to the posterior cerebral arteries, where these join the innervation from the internal carotid artery [16][17][18]. Sympathetic innervations release adrenergic mediators that enhance sympathetic tone, a vital component of cerebral autoregulation.…”

“…Moreover, while it is generally understood that catecholamines typically cannot easily penetrate the BBB to enter the brain, except at circumventricular sites where the BBB is absent or less effective [23], experimental evidence suggests paradoxical effects of vasopressors in the context of an acute brain injury, including increases in cerebral blood flow and the cerebral metabolic rate of oxygen, in the setting of BBB disruption [24][25][26]. Similarly, autonomic dysfunction, in particular of the parasympathetic system, which can develop after TBI and SAH, could impair the system's ability to mitigate cerebral vessel vasoconstriction [13,18]. Other factors, such as the potential concurrent use of sedatives and anesthetics in TBI and SAH patients, could alter cerebral vasoreactivity.…”

“…Recently, PbtO 2 was utilized to measure tissue oxygenation during CPP adjustments in a study conducted by Kovacs et al [70], which aimed to assess the CPP threshold that correlates with sufficient PbtO 2 levels in brain-injured patients (the target was >20 mmHg). In total, 53 patients with heterogeneous types of ABI (TBI, SAH or ICH) received an infusion of norepinephrine to reach increases in CPP of at least 10 mmHg, 10-15 min each, at two different steps above the baseline, from 73 (70)(71)(72)(73)(74)(75)(76) to 83 (80)(81)(82)(83)(84)(85)(86) and to 92 (90)(91)(92)(93)(94)(95)(96), with a progressive PbtO 2 increase from 20 (17)(18)(19)(20)(21)(22)(23) to 22 (20)(21)(22)(23)(24) and 24 (22-26), respectively. Focusing on CPP, they concluded that PbtO 2 monitoring indicated the need for higher CPP targets than recommended to prevent tissue hypoxia.…”