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Dexmedetomidine for endovascular neurosurgery


Perioperative managements for endovascular neurosurgery require some considerations such as minimizing hemodynamic changes and especially avoiding blood pressure elevation accompanying extubation, immobilizing the trunk and lower limbs until bleeding from the site of femoral artery sheath removal has stopped, and monitoring patients in the ICU for at least 12 hours to notice neurological deterioration promptly. The aim of this study was to assess the usefulness of dexmedetomidine as a postoperative sedative drug for endovascular neurosurgery.


The study included 182 patients with endovascular neurosurgery admitted to the ICU in 2006. The authors evaluated the postoperative sedative state and hemodynamics with the Richmond Agitation Sedation Scale (RASS) [1], heart rate (HR) and mean arterial pressure (MAP). To examine the time-dependent changes of the RASS, MAP and HR, data were collected from medical records, including at the start and end of dexmedetomidine infusion and at the time of extubation.


The surgical indications in patients with endovascular neurosurgery were unruptured cerebral aneurism (57%), sub-arachnoid hemorrhage (20%), arteriovenous malformation (5%), arteriovenous fistula (3%) and others (15%). One hundred and eighteen patients (85.3%) received dexmedetomidine. The RASS showed patients with dexmedetomidine experienced RASS -1 to -3 states, which was arousable with verbal stimulation. There were no dexmedetomidine-induced HR and MAP deteriorations; furthermore, dexmedetomidine prevented the blood pressure elevation accompanying extubation. The overall morbidity and mortality rates relating to endovascular neurosurgery were 1.6% and 0.54%, respectively.


Application of sedative drugs for the postoperative management for neurovascular disease may be controversial; however, the use of dexmedetomidine facilitates postoperative management of endovascular neurosurgery. Compared with the reported endovascular neurosurgery morbidity (3.7–5%) and mortality (1.1–1.5%), our morbidity and mortality rate showed that dexmedetomidine did not cause neurological deteriorations.


  1. Ely EW, Truman B, Shintani A, et al.: JAMA. 2003, 289: 2983-2991. 10.1001/jama.289.22.2983

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Kase, Y., Obata, T. Dexmedetomidine for endovascular neurosurgery. Crit Care 12 (Suppl 2), P277 (2008).

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