| ||||||||||||||
|
|
|||||||||||||
Department of Anesthesiology University of Washington School of Medicine Seattle, WA 98108
In their recent article, Habre et al. (1) found that asthmatic children tracheally intubated during sevoflurane anesthesia administration experienced a mean 17% increase in respiratory system resistance. They concluded that "one should be cautious when using sevoflurane for endotracheal intubation in asthmatic children." We question whether this conclusion is warranted because 1) there is no control group, and 2) a 17% increase in resistance is minimal and unlikely to be of clinical consequence.
Endotracheal intubation is a significant stimulus to airway constriction, especially in patients with hyperreactive airways. If Habre et al. had studied a control group whose tracheas had been intubated after thiopental, propofol, or even halothane induction of anesthesia, they might have found a much larger increase in resistance. In a group of asthmatics tracheally intubated after propofol induction, we found a mean increase in respiratory resistance of 300%400% (2). Hence, an increase of only 17% after deep sevoflurane anesthesia administration leads us to conclude that sevoflurane is most likely an excellent anesthetic for the induction of an asthmatic patient.
We also disagree with their statement that their study is at odds with our finding that 1.1 minimum alveolar concentration sevoflurane decreases resistance after intubation (3). We studied the ability of sevoflurane to decrease resistance after intubation under thiopental anesthesia. The study of Habre et al. examined the result of intubation under deep sevoflurane anesthesia, but did not compare it to any other anesthetic. Had they used a control group, they might have found that sevoflurane was an effective anesthetic in preventing a large increase in resistancea result that would be in line with our findings.
References
Paediatric Anaesthesia Unit Geneva Childrens Hospital Geneva, Switzerland Division of Clinical Sciences Institute for Child Health Research Department of Paediatrics University of Western Australia Perth, Australia
We would like to point out the difficulties of including a control group such as intubating the tracheas of asthmatic children during thiopental administration alone as suggested. We have previously demonstrated that sevoflurane prevented a methacholine-induced increase in lung resistance in an animal model (1), and therefore, we were able to proceed to the clinical investigation of sevoflurane as a sole anesthetic for tracheal intubation in asthmatic children. Furthermore, we measured total respiratory system resistance (Rrs) during the same conditions (spontaneous ventilation and end-tidal concentration of sevoflurane) before and after tracheal intubation, and therefore, we can reliably compare the effect of tracheal intubation on Rrs in children with and without asthma.
Rooke et al. (2) have shown that after tracheal intubation during thiopental administration in adults without asthma, sevoflurane decreased Rrs effectively after 10 min of exposure at 1.1 minimum alveolar concentration. In children without asthma, tracheal intubation during sevoflurane administration did not induce an increase in Rrs, but even a mild decrease of 4%. However, in children with mild to moderate asthma without symptoms before the procedure, tracheal intubation resulted in an increase in Rrs (approximately 18%), which was statistically significant but didnt reach our definition of clinical significance as designed in the study to be 25%. Thus, our conclusion was not to contraindicate sevoflurane in asthmatic children, but we caution the use of the drug, especially in children with less stable asthma in whom the increase in Rrs would have been more intense.
References
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|