Mechanism of emergence agitation induced by sevoflurane anesthesia

This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http:// creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. CC Sevoflurane is an inhalational anesthetic used widely as a pediatric or outpatient anesthesia due to its excellent hemo­ dynamic stability and low blood solubility, which allows rapid induction and emergence from general anesthesia, as well as control of the depth of anesthesia. However, when sevoflurane is used alone it is associated with a higher incidence of emergence agitation in children. The rapid removal of residual anesthetics due to low blood solubility of sevoflurane has been suggested to cause emergence agitation in some patients [1,2]. In addition, a variety of other explanations have been proposed for the etiology of emergence agitation. These include the lack of a young child's ability to adapt to sudden changes due to an unfamiliar environment after awakening, immature neurological development, anxiety from being separated from their parents, increased pain sensation and sympathetic hyperactivation [2,3]. Emergence agitation is characterized by self­limiting aggre­ ssive agitation that develops in the early phase of awakening from anesthesia at the end of surgery. Emergence agitation can be dangerous to patients, particularly to young children. Patients suffering from emergence agitation may harm themselves and dislodge drains or catheters, which affects the results of surgery. They may inflict a bodily injury on their care­givers or cause a paranoiac accident, which makes the management and monitoring of patients at the post anesthesia care unit difficult [4]. There have been many attempts to reduce the incidence of emergence agitation but the etiology and preventive treatments of emergence agitation are still unclear. Some studies have reported that midazolam which acts on its target effect site GABA A , reduces emergence agitation [5,6], and its antagonist, flumazenil reverses this effect [7]. However, the mechanism is still not clear, and it is not known whether sevoflurane and midazolam interact at the GABA A receptor level. Most GABA A receptors consist of two α subunits, two β subunits and a γ subunit. The γ2 subunits of GABA A receptor exist as a long type (γ2L) and a short type (γ2S), generated by alternative splicing of RNA. The most common pattern for GABA A receptor is α1β2γ2 type, which accounts for 43% of all GABA A receptors [8]. This implies that the diversity …