A reply

This is the authors' abstract. We don't add key points for this paper.

We thank Drs Bosley, McSwiney, McGuire and Lee for their interest in our study. The apparatus used to administer the local anesthetic was a glass atomiser with adjustable tip (DV-15-RD, Sunrise Medical, Montreal, Canada). Oxygen (10 l.min−1), used to deliver the drug, was taken from the anesthesia machine’s auxiliary oxygen supply via plastic tubing that connected the atomiser to the oxygen source. A hole was cut in the tubing, just proximal to the atomiser, so that it could be periodically plugged by a digit and so provide ‘on/off’ control of drug delivery. Patients were positioned in the supine ‘sniffing’ position with the nares clamped. They were exhorted to take large, vital capacity breaths with their tongue protruding. Atomisation continued through both inspiration and expiration; lidocaine mist was directed posteriorly during inspiration and the hard and soft palate and tongue were ‘painted’ during expiration. Atomisation can therefore take advantage of the entire phase of respiration. The doses selected were based on our prior clinical experience in the morbidly obese when it is essential to achieve first-rate airway topicalisation while avoiding excessive sedation, and from the literature concerned with non-obese patients topicalised using a variety of methods. Intractable cough, bronchospasm, laryngospasm, and aspiration with ensuing impaired gas exchange are potential complications of inadequate airway anaesthesia. This can be especially disastrous in morbidly obese patients because of their limited physiological reserve. We remain convinced that it is imperative to ensure optimal airway anesthesia prior to airway manipulation in this unusual patient population. For a variety of reasons it is difficult to predict lidocaine serum concentration following airway topicalisation using this technique. Drug absorption will depend on the quantity of local anaesthetic inhaled, exhaled and swallowed. This relates to both the pharmacokinetic properties of atomised lidocaine as well as the ‘art’ of topicalization (for example the respiratory rate, breath holding, coughing, deep versus shallow breathing, etc.) that is not easily controlled on a patient to patient basis. It is also difficult to quantify how lidocaine will be distributed in the metabolically inert fat. Although useful as a guide, the British Thoracic Society recommendation to limit dose of local anaesthetic to 8.2 mg.kg−1 does not take into consideration the method of topicalisation (that is, atomisation as the sole method), nor size of patient [1]. Because loss of consciousness was produced immediately after securing the airway, there was only a short period of time to observe clinical toxicity. This period occurred prior to peak plasma lidocaine concentration and so, conceivably, we missed the opportunity to observe clinical signs of drug toxicity. There were no ECG changes consistent with lidocaine toxicity. The study referred to by Drs McGuire and Lee regarding lidocaine plasma levels peaking at 20–30 min did not involve atomisation delivery of local anaesthetic [2]. Tolerance to airway instrumentation was not statistically different between the two groups, although there was a trend towards improved tolerance in the 4% cohort. Despite this, we believe acceptable intubating conditions are achieved with 2% lidocaine and gagging in this cohort was minimal. Unfortunately, the simplicity of our tolerance scale (0 = no response; 1 = some gagging; 2 = intolerable) did not allow this to be apparent. Using this simple scale helped to eliminate the subjectivity of ‘patient tolerance’ assessment but, unfortunately, did not distinguish between mild, moderate, and severe gagging.