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Editorials: Editorial

Anesthesia, Sleep, and Nasendoscopy

Hillman, David R., MD

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doi: 10.1213/ANE.0000000000000379
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Drug-induced “sleep” nasendoscopy (DISE) is performed regularly by otorhinolaryngologists to assess the site and nature of collapse in the upper airway under sedation as part of preoperative workup for pharyngeal surgery in patients with obstructive sleep apnea.1 It is a procedure founded on the principle that upper airway behavior during sleep- and drug-induced sedation are similar. There is plenty of evidence to suggest this is so, provided that sedation is deep, that is, sufficient to induce sleep-like loss of consciousness.2 Crossing the divide from consciousness to unconsciousness during sedation or sleep is associated with a sharp reduction in upper airway muscle activation and increase in its collapsibility.3,4 This state provides favorable conditions for obstruction in individuals with vulnerable upper airways, such as those with obstructive sleep apnea.

In this issue of Anesthesia & Analgesia, Atkins et al.5 describe an elegant DISE dosing strategy to quickly and systematically induce sedation to a point at which pharyngeal obstruction is noted by the attending otolaryngologist, who has an endoscope in place to observe the pharynx from the start of the procedure. This is a useful contribution because delays in this sequence increase the potential for hypoxia and/or intervention by the anesthesiologist to secure the airway before otorhinolaryngological assessment, potentially complicating, compromising, and prolonging the procedure.

This is all very well, but there are a few loose ends to be considered that relate to the rationale for DISE itself, and to events beyond the onset of obstruction, which was the end point of the study by Atkins et al.5 Although there is likely to be a general relationship between upper airway collapsibility during sleep and under deep sedation, it is not known how representative the assessment is of nature and site of collapse under drug-induced circumstances of natural sleep. Upper airway collapsibility is influenced by other factors apart from degree of muscle activation, including body posture, mouth opening, neck flexion/extension, and lung volume.6 Sleep is not a homogenous state because it occurs in a variety of postures and consists of a number of stages with variable ventilatory drive and muscle activation. Hence, upper airway behavior during sleep may vary quite markedly from the carefully contrived circumstances of DISE. These relationships deserve further pursuit.

The end point of the study by Atkins et al.5 was the onset of obstruction. By that point, all being well, the otorhinolaryngologist will have conducted an expeditious assessment of the upper airway during evolution of obstruction to help guide subsequent surgical decision making. A question posed by the study is “having smoothly reached this obstructive end point, what then?” This bears directly on a fundamental difference between sleep- and drug-induced sedation and responses to obstruction in the two states. Sleep is a state of rousable unconsciousness, with arousal an important protective response to threatened asphyxia. Not so, of course, with deep sedation, where recovery of consciousness relies on elimination of the drug, and until this occurs, upper airway obstruction requires active management. Hence, the sequence described by Atkins et al.5 is just part of the picture. Airway management after the completion of endoscopy no doubt involves interventions that the authors were careful to circumvent before their “onset of obstruction” end point. An approach that matches the elegance of procedures to that point would be desirable. Perhaps, to borrow further from anesthesiology and sleep medicine common ground, this could involve the application of continuous positive airway pressure until consciousness returns.

Nevertheless, Atkins et al.5 present an elegant anesthetic dosing strategy for DISE to ensure the end point of otolaryngological investigation is reached expeditiously and, in so doing, provide favorable preconditions for an orderly emergence.

DISCLOSURES

Name: David R. Hillman, MD.

Contribution: This author is sole author of this editorial.

Attestation: David R. Hillman has approved the final manuscript.

This manuscript was handled by: Peter S. A. Glass, MB ChB.

REFERENCES

1. Kezirian EJ, Hohenhorst W, de Vries N. Drug-induced sleep endoscopy: the VOTE classification. Eur Arch Otorhinolaryngol. 2011;268:1233–6
2. Eastwood PR, Szollosi I, Platt PR, Hillman DR. Comparison of upper airway collapse during general anaesthesia and sleep. Lancet. 2002;359:1207–9
3. Hillman DR, Walsh JH, Maddison KJ, Platt PR, Kirk ness JP, Noffsinger WJ, Eastwood PR. Evolution of changes in upper airway collapsibility during slow induc tion of anesthesia with propofol. Anesthesiology. 2009;111:63–71
4. Wilkinson V, Malhotra A, Nicholas CL, Worsnop C, Jordan AS, Butler JE, Saboisky JP, Gandevia SC, White DP, Trinder J. Discharge patterns of human genio glossus motor units during sleep onset. Sleep. 2008;31:525–33
5. Atkins JH, Mandel JE, Rosanova G. Safety and efficacy of drug-induced sleep endoscopy using a probability ramp propofol infusion system in patients with severe obstructive sleep apnea. Anesth Analg. 2014
6. White DP. Pathogenesis of obstructive and central sleep apnea. Am J Respir Crit Care Med. 2005;172:1363–70
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