gms | German Medical Science

83rd Annual Meeting of the German Society of Oto-Rhino-Laryngology, Head and Neck Surgery

German Society of Oto-Rhino-Laryngology, Head and Neck Surgery

16.05. - 20.05.2012, Mainz

What is „Adult Supraglottic Obstruction“? Supraglottoplasty acc. to Schedler – An Update to Hyoidpharyngoplasty

Meeting Abstract

Search Medline for

  • corresponding author presenting/speaker Michael G. J. Schedler - Germanamerican Hospital Ramstein, Ramstein, Germany
  • Ilya Botev - Germanamerican Hospital Ramstein, Ramstein, Germany
  • Benjamin Ernst - Universitätsklinik, Frankfurt, Germany

German Society of Oto-Rhino-Laryngology, Head and Neck Surgery. 83rd Annual Meeting of the German Society of Oto-Rhino-Laryngology, Head and Neck Surgery. Mainz, 16.-20.05.2012. Düsseldorf: German Medical Science GMS Publishing House; 2012. Doc12hno67

doi: 10.3205/12hno67, urn:nbn:de:0183-12hno672

Published: July 23, 2012

© 2012 Schedler et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.



Adult form of supraglottic obstruction (SGO) is a largely unknown and scarcely described airway disease [1]. Still it seems to be not quite uncommon in apnea patients. In our series of 2416 consecutive, videodocumented somnoscopies, we found about 35% incidence of SGO [2]. What is SGO? We see 3 different obstruction types. Our classification of obstruction level comprises Level I: Base of tongue (hyoid based pharyngeal obstruction or "retracted hyoid"), Level II: Epiglottis (e.g. large, flat,omega shaped,"floppy") and Level III: Arytenoid region (hyperplasia of arytenoid mucosa, arymucosal aspiration phenomenon) [1], [2]. Level I and II are anterior, and Level III posterior supraglottic obstructions. In our experience Level I plays a major role not only in OSA, but also in dysphagia, globus sensation, intubation problems (Cormack/Lehane III/IV) and unability to expose larynx via straight endoscopy (Microlaryngoscopy). Level I and II SGO may predispose for a condition, we named "supine position based apnea (asphyxia)" (SPBA), meaning unability to ly in supine position and breath normally, especially in deep sleep. SBPA can be present at 2 distinct anatomic levels: Level I – base of tongue, Level II – epiglottis and in severe cases even be combined. Obstructions at Levels II and III may be regarded as "adult acquired Laryngomalacia" (AAL)[1]. These anatomic varieties are not rare and could be detected in about one third of our series of suspected apnea patients. In our recent evaluation of 2416 videodocumented somnoscopies in suspected apnea patients we counted 30% incidence of Level I and II , and 4–5% of Level III SGO [1], [2]. Still these conditions are almost undetectable in medical literature, and if, mostly in newborns [3], [4], [5], [6], [7], [8], [9], [10], [11], [12], [13], [14], [15], [16], [17], [18], [19], [20], [21], [22].

We refer to SBPA level I as "hyoid based pharyngeal stenosis/obstruction" (HBPS) and level II as adult form of laryngomalacia, in typical case caused by overly large, overhanging and/or "floppy epiglottis". In the ideal setting both conditions can be treated by N-CPAP ventilation, while unfortunately Level I and especially Level II obstructions with deflected epiglottis are in our series a major cause for N-CPAP non-compliance or intolerance [1], [2]. Regarding this group of non compliant patients, a differential indication, regarding obstruction level and morbidity, had to be implemented. We found, a resection of hyoid corpus and pre-epiglottic adipose tissue, followed by a "dead space suture" (Hyoidpharyngoplasty-HPP) to be very help-full in Level I obstructions, i.e. resolving compliance problems and enabling tolerance to N-CPAP ventilation [1], [2]. In Level II obstruction a Laser partial resection of epiglottis (LEPR) proved to be effective. In patients having both conditions, as well HPP as laser assisted epiglottis partial resection , had to be performed. We named this 2 stage procedure, with a time interval of at least 6–8 weeks, supraglottoplasty (SGP). Usually LEPR was performed first and HPP was second stage. In cases, where not even the epiglottis could be exposed by straight microlaryngoscopy ,resection of hyoid corpus (HPP) had to be performed first. In some of these cases the narrowness of pharyngeal lumen would actually mask the "floppy" condition of epiglottis, since it would somehow "lean" against the posterior pharyngeal wall and thus not show the full amount of laxity it indeed already had. In this case a one stage supraglottoplasty, HPP and LEPR in one session, had to be carried out. By Oct 2011 we had performed LEPR N=149, HPP N=117 and SGP N=12, 1 of which as one stage procedure, presented here. 2 other one stage SGP had been performed after deadline of this publication and will be reported later.

A 23 years old male with a BMI of 28,6 and midgrade adenotonsillar hyperplasia suffering from OSA with AHI 35/h and average SA-O2 of 94%, minimal SA-O2 72%, was operated for SGO Level I, base of tongue. We performed HPP since epiglottis appeared to be stabile. During routinely performed post op somnoscopy at end of surgical procedure, a floppy epiglottis, with severe deflection and aspiration phenomenon of epiglottis was noted. We decided to perform additional LEPR, for supraglottoplasty in one stage procedure. Extubation and post op course was uneventful and without major problems. Mild dysphagia was the only post op complication and major improvement of airway patency noted already in recovery room immediately after surgical procedure. Further post op course was smooth without major complaints and patient could be released from inpatient treatment after 3 days. 8 weeks post op, persisting adenotonsilar hyperplasia, but otherwise normally configured airway could be documented in somnoscopic evaluation. Sleep study showed improvement of AHI from 35/h to 7/h, average SA-O2 94% to 97% and minimal SA-O2 of 72% versus 80% post op. Patient experienced normalisation of sleep quality and QOL parameters.

As well HPP, as SGP proved to be safe procedures. In 110 out of 117 cases of HPP and all SGP cases we noted an instant improvement of airway patency, accompanied by only mild to moderate dysphagia from 5 days to 4 weeks post op, except N=3 up to 6 weeks [2]. Tube feeding wasn't needed at any time of post op course. In 3 out of 117 HPP cases, we had to perform SGP (additional LEPR) in a time interval of less than one week, because of developping airway problems on Level II. In presented case epiglottal collapse was so massive, that LEPR had to carried out in same surgical session (1 stage SGP). In 2 other cases instability of epiglottis had not been evident in routinely – immediately post op (during extubation) – executed somnoscopy. These cases of delayed second procedure (executed on day 3 and 5 post op) proved to be difficult to handle. Especially inserting and positioning straight endoscope (Weerda's spreading laryngoscope) was impaired. Both cases could be resolved successfully without tracheostomy and tube feeding, showing good airway patency after completion SGP. Both individuals had extremely narrow, retracted mandible, hindering exposition of larynx. We recommend to try to perform LEPR first, if ever possible. Patients with small chin and prognathia should be considered risk cases for HPP and straight endoscopic exposition of larynx be verified before attempting surgery. If epiglottis could not be exposed and therefore HPP needed to be carried out first, a critical reevaluation of surgical indication should be considered. If still indicated, one stage SGP seems to be the better choice.


Schedler MGJ, Bodlaj R. Anatomic variants of epiglottis and their significance for supraglottic obstruction in OSA - do we have a surgical treatment option? In: 81st Annual Meeting of the German Society of Oto-Rhino-Laryngology, Head and Neck Surgery; 2010.
Schedler MGJ, Bodlaj R, Christoph D. Hyoidpharyngoplasty – a surgical approach to supraglottic obstruction in hyoid based pharyngeal stenosis. In: 82st Annual Meeting of the German society of Oto-Rhino-Laryngology, Head and Neck Surgery; 2011.
Belmont JR, Grundfast K. Congenital laryngeal stridor (laryngomalacia): etiologic factors and associated disorders. Ann Otol Rhinol Laryngol. 1984;93:430-437.
Holinger LD, Konior RJ. Surgical management of severe laryngomalacia. Laryngoscope. 1989;99:136-142.
Zalzal GH, Anon JB, Cotton RT. Epiglottoplasty for the treatment of laryngomalacia. Ann Otol Rhinol Laryngol. 1987;96:72-76.
Jackson C, Jackson C. Diseases and injuries of the larynx Congenital laryngeal stridor (laryngomalacia): etiologic factors and associated disorders. New York: MacMillan; 1942. p. 63-9.
Belmont JR, Grundfast K. Congenital laryngeal stridor (laryngomalacia): etiologic factors and associated disorders. Ann Otol Rhinol Laryngol. 1984;93(5 Pt 1):430-7.
McClurg FLD, Evans DA. Laser laryngoplasty for laryngomalacia. Laryngoscope. 1994;104:247-252.
Roger G, Denoyelle F, Triglia JM, Garabedian EN. Severe laryngomalacia; surgical indications and results in 115 patients. Laryngoscope. 1995;105:1111-7.
Olney DR, Greinwald JH, Smith RJH, Bauman NM. Laryngomalacia and its treatment. Laryngoscope. 1999;109:1770-5
Kelly SM, Gray SD. Unilateral endoscopic supraglottoplasty for severe laryngomalacia. Arch Otolaryngol Head Neck Surg. 1995;121:1351-4.
Toynton SC, SaundersMW, Bailey CM. Aryepiglottoplasty for laryngomalacia: 100 consecutive cases. J Laryngol Otol. 2001;115:35-8.
Loke D, Ghosh S, Panarese A, Bull PD. Endoscopic division of the ary-epiglottic folds in severe laryngomalacia. Int J Pediatr Otorhinolaryngol. 2001;60:59-63.
Werner JA, Lippert BM, Dunne AA, Ankermann T, Folz BJ, Seyberth H. Epiglottopexy for the treatment of severe laryngomalacia. Eur Arch Otorhinolaryngol. 2002;259:459-64
Manning SC, Inglis AF, Mouzakes J, Carron J, Perkins JA. Laryngeal anatomic differences in pediatric patients with severe laryngomalacia. Arch Otolaryngol Head Neck Surg. 2005;131:340-3.
Thompson DM. Abnormal sensorimotor integrative function of the larynx in congenital laryngomalacia: a new theory of etiology. Laryngoscope. 2007;117:1-33.
Giannoni C, Sulek M, Friedman EM, et al. Gastroesophageal reflux association with laryngomalacia:a prospective study. Int J Pediatr Otorhinolaryngol. 1998;43:11-20.
Richter GT, Thompson DM. The surgical management of laryngomalacia. Otolaryngol Clin North Am. 2008;41(5):837-64, vii.
Polonovski JM, Contencin P, Francois M, et al. Aryepiglottic fold excision for the treatment of severe laryngomalacia. Ann Otol Rhinol Laryngol. 1990;99:625-7.
Zalzal GH, Collins WO. Microdebrider-assisted supraglottoplasty. Int J Pediatr Otorhinolaryngol. 2005;69(3):305-9.
Whymark AD, Clement WA, Kubba H, et al. Laser epiglottopexy for laryngomalacia:10 years' experience in the west of Scotland. Arch Otolaryngol Head Neck Surg. 2006;132:978-82.
Mukerji S, Pine H. Current Concepts in Diagnosis and Management of Laryngomalacia: Grand Rounds Presentation. UTMB, Dept of Otolaryngology; 2009.