DOI: 10.31038/OHT.2020113

Keywords

Airway volume, Obstructive sleep apnea, Pcrit, Uvulopalatopharyngoplasty.

Editorial

Obstructive sleep apnea (OSA) syndrome is a highly prevalent disease, with an estimated prevalence of approximately4%in men and 2%in women [1]. It isassociated with significant morbidity and mortality that increases with age and its prevalence peaks at approximately 55 years of age in men [2]. Therefore, effective treatment of patients with OSA is critical.Unfortunately,treatments that bypass the airway, or simply open the pharyngeal airway are either morbid or unsuccessful, respectively. Uvulopalatopharyngoplasty (UPPP), since Fujita et al[3] first described as a surgical procedure in 1981, has been developed as a surgical approach for treating adultswith OSA, with the aim of opening (dilating) the pharyngeal airway. It stillremains the most common surgical procedure performed to treatadults with OSA, with an overall success rate of approximately 40% in unselected patients [4, 5]. Therefore, OSA surgeonsdo not favor UPPPas a treatment of choice for all patients with OSA.UPPP could be effective, in appropriately selected patients, such as those with hypertrophic large tonsils, webbing of the posterior pillars, elongated and thickened uvulas, redundant pharyngeal folds and a normal tongue with a retro-displaced soft palate(“favorable” anatomic structures).OSA is characterized by upper airway collapse and/or occlusion during sleep, which mainly affects the middle pharyngeal area especially velopharyngeal and glossopharyngeal portions.Patients with OSA tend to have a more narrow middle pharyngeal space, smaller middle pharyngeal airway volume [6], that is characterized with the anatomical imbalance between the large volume of upper airway contents(i.e., tonsils and surrounding soft-tissues) andsmall volume of container (i.e., craniofacial bony structures)(Anatomical balance theory) [7] .This means if patients have a large volume of soft tissue content and/or small container volume, the residual pharyngeal air space mightresultin crowding and stuffing,which may cause airway occlusion during sleep. In applying this theory to sleep surgery, OSA surgeons often try to reduce the soft tissue contents and/or dilate the bony container surrounding the pharyngeal airway, which should increase airway volumeand enlarge the pharyngeal airway. UPPP is designed to resect large hypertrophic tonsils, removing the redundant excessive distal palatal tissue. It will dilate the airway lumenat the level ofvelopharyngeal area,which is expected to increaseupper airway volume.It is not clear, however, why UPPP does not always increaseupper airway volume as the OSA surgeon anticipates.Recently, the changes in velopharyngeal and glossopharyngeal airway morphology and volume after UPPP were examined in adult patients with OSA and bilateral large tonsils by three-dimensional computed tomography [8]. In this paper, morphology of the glossopharyngeal airway was compared before and after UPPP. In their three cases, patients’ apnea-hypopnea indices and daytime sleepiness had improved dramatically after UPPP, but interestingly enough,they found that the glossopharyngeal airway clearly dilated after UPPP, although the volume changes in the velopharyngeal and glossopharyngeal airways were negligible.

Just imagine two 250ml coca-cola or pepsi bottles, one is made of plastic and the other is made of aluminum. Consider their characteristics: is the crushability (collapsibility) of those two bottles equal? As we imagined, even if the size of two empty coca-cola or pepsicontainersis the same, the plastic bottle is crushable and aluminum can might be quite stiff.Even a plastic bottle of 500ml would be easy to be dent, whereas an aluminum can of similar or even smaller size would be hard to crush or collapse. Thus, the ultimate size of the airway impacts less on the success of surgery than the change in its mechanical properties (stiffness or collapsibility). It is worth recalling that OSA is characterized by upper airway collapse and/or occlusion during respiration and sleep,which is not static but dynamic phenomenon. Treating OSA is complicated,of course. Dilating of the upper airway might be necessary yet insufficient to open the upper airway. To be sure, dilating a small airway might be an important treatment component of therapy, but it might not be the main goal of therapy. Even if the airway becomes wide and dilated post-operatively, if it is still soft and collapsible (and easy to dent), the airway will dynamically collapse and/or occlude very easily during sleep.In a similar vein,just imagine a rubber band,whenstretched (dilated), it will become stiff or even rigid and less collapsible. It is possible that when we dilate (stretch) the patient’s pharyngeal airway with a UPPP procedure, it could become less collapsible. But anatomic factors (i.e., small airway) may not be the only reason a patient has OSA. Instead, a dynamicphenomenon (i.e., respiration and sleep),airway characteristics (i.e., not easy to dent), airway stiffness (collapsibility) must be also considered in evaluating the airway and the potential effects of surgery. It is likely that airway dilation (with a concomitant increase in volume) is not our primary surgical goal. Our goal must be to stabilize the upper airway (i.e., make it uncrushable: not easy to dent) against dynamiccollapse that threatens its patency in patients with OSA.Whereas investigators have identified both anatomic and neuromuscular control factors that increase pharyngeal collapsibility during sleep in patients with OSA [9], a physiologic basis for measuring pharyngeal collapsibility (critical pressure: Pcrit) would be useful to evaluate in patientswith OSA; the collapsibility of individuals with varying levels of pharyngeal airway obstruction during sleep could be examined before surgery; and the relationship between changes in pharyngeal collapsibility and changes in the severity of OSA before and after UPPP could be elucidated [10]. Evaluation of Pcritpre-operatively for individualpatients with OSA before surgery, might help predict success in treating a patient. Despite the potential utility of Pcrit measurement, Pcrit cannot be easily measured, especially in the outpatient clinic or in the hospital ward. Such measurements should be facilitated in the outpatient clinic or in the hospital ward for individual OSA patients before and after surgery, as if it were simply a blood pressure measurement.Recently, a simple, novel non-invasive streamlined approach for measuring Pcritwas published [11]. Additional research to extend this approach to Pcrit measurements in prospective UPPP patients is warranted.

References

1. Young T, Palta M, Dempsey J, Skatrud J, Weber S et al. (1993)The occurrence of sleep- disordered breathing among middle-agedadu lts.N Engl J Med 328: 1230-1235. [crossref]
2. Bixler EO, Vgontzas AN, Ten Have T, Tyson K, Kales A (1998) Effects of age on sleep apnea in men: I. Prevalence and severity.Am J Respir Crit Care Med157: 144-1488. [crossref]
3. Fujita S, Conway W, Zorick F, Roth T (1981) Surgical correction of anatomic abnormalities in obstructive sleep apnea syndrome: uvulopalatopharyngoplasty.Otolaryngol Head Neck Surg89: 923-934. [crossref]
4. Sher AE, Schechtman KB, Piccirillo JF.(1996) The efficacy of surgical modifications of the upper airway in adults with obstructive sleep apnea syndrome. Sleep.19: 156-177. [crossref]
5. Senior BA, Rosenthal L, Lumley A, Gerhardstein R, Day R (2000)Efficacy of uvulopalatopharyngoplasty in unselectedpatients with mild obstructive sleep apnea.Otolaryngol Head Neck Surg123: 179-182. [crossref]
6. Schwab RJ, Pasirstein M, Pierson R, Mackley A, Hachadoorian R et al. (2003) Identification of upperairway anatomic risk factors for obstructive sleep apnea with volumetric magnetic resonance imaging.Am J Respir Crit Care Med168: 522-530. [crossref]
7. Watanabe T, Isono S, Tanaka A, Tanzawa H, Nishino T (2002) Contribution of body habitus and craniofacial characteristics to segmental closing pressures of the passive pharynx in patients with sleep-disordered breathing. Am J Respir Crit Care Med 165: 260-265. [crossref]
8. Nishimura Y, Fujii N, Yamamoto T, Hamed MA, Nishimura M et al. (2016)Volumes of Velopharyngeal and Glossopharyngeal Airway Were Not Changed afterUvulopalatopharyngoplasty: Report of Three Cases.Case Rep Otolaryngol. [crossref]
9. Patil SP, Schneider H, Schwartz AR, Smith PL (2007) Adult obstructive sleep apnea: pathophysiology and diagnosis.Chest132:325-37. [crossref]
10. Schwartz AR, Schubert N, Rothman W, Godley F, Marsh Bet al. (1992) Effect of uvulopalatopharyngoplasty on upper airway collapsibility in obstructive sleep apnea.Am Rev Respir Dis 145: 527-532. [crossref]
11. Nishimura Y, Arias RS, Pho H, Pham LV, Curado TF et al. (2018)A Novel Non-invasive Approach for Measuring Upper Airway Collapsibility in Mice.Front Neurol9. [crossref]