Abstract
We read with interest recent correspondence concerning postoperative nausea and vomiting (PONV) following 8% sevoflurane anaesthesia (Anaesthesia 2000; 55: 189–91). Various explanations were proposed for the observed increase in PONV including the administration of supplemental opioids, and/or a dose-related sevoflurane effect. There is little evidence, if any, to support the latter. In their paper, Dashfield and colleagues use high concentrations of sevoflurane yet report an extremely low incidence of nausea (10%) [1]. It is important to note that Dashfield and colleagues used a nonrebreathing system in their study and thus did not expose the sevoflurane to soda lime. Conversely, Smith and Thwaites used low-flow anaesthesia with CO2 absorption and reported an incidence of 30% [2]. In a study similar to that of Dashfield and co-workers, Philip reports that following sevoflurane induction and maintenance, 78% of patients experienced some nausea. This study maintained anaesthesia using sevoflurane at low fresh gas flows (2 l.min−1). No opioids were administered [3]. Fredman and co-workers also report an extremely high incidence of nausea (56%) following a lower dose of sevoflurane for induction of anaesthesia and maintenance of anaesthesia using low fresh gas flows [4]. We propose an additional cause of PONV following sevoflurane anaesthesia. It is known that sevoflurane can be degraded to formaldehyde when passed through partially exhausted soda lime [5]. Rather than the absolute dose of sevoflurane delivered, an additional factor in PONV may be the administration of sevoflurane through a rebreathing system that contains a strong alkali. Inhalation of formaldehyde, even in minute quantities, will provoke significant nausea and vomiting often for up to 48 h [6]. We believe that when examining the occurrence of nausea following sevoflurane anaesthesia, it is of fundamental importance to know whether or not sevoflurane has been delivered using a rebreathing system. Our own work (in progress) shows that formaldehyde concentrations of four times the MEL (maximum exposure limit) are readily achieved in vitro by simply passing 6–8% sevoflurane over dry soda lime. As a result, we would suggest that degradation of sevoflurane to formaldehyde by CO2 absorbents that contain either KOH or NaOH be considered as an additional factor contributing to PONV after sevoflurane anaesthesia.
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