gms | German Medical Science

Since 1999 we performed more than 3000 sleep-endoscopies.Our investigation comprises 2416 consecutive, video-documented somnoscopies, using standardized technique (Propofol induced sleep) and equipment (Pentax EPM 3000/3300 and EB 1530, 1580 and 1830 video-endoscopes) performed in Ramstein from Jan 2001 to Nov 2010 . We found in patients intolerant to N-CPAP supraglottic obstruction at epiglottis level as main cause of intolerance. Especially large, flat or paradoxically curved epiglottis and/or pharyngeal stenosis at Hyoid level ("Hyoid based pharyngeal obstruction/stenosis") are predisposing to N-CPAP intolerance and also to Cormack/Lehane III and IV intubation problems, including CVCI. Supraglottic obstruction in adult persons is only scarcely described in medical literature and no standardized classification available. In contrast to congenital supraglottic obstruction, i.e. Laryngomalacia, which had been described and classified by different authors (e.g. Holinger 1984, Shradda 1989).

Anatomic changes as found in our research may be respected as "adult acquired Laryngomalacia (AAL)" and share many characteristics with congenital form. Based on Shradda's modification of Holinger classification of congenital Laryngomalacia, we developed as well a descriptive model (nomenclature) of anatomic epiglottis variants (Type A,B,C,D,E,F), as a new extended classification of supraglottic obstruction, comprising all kinds of adult forms of Laryngomalacia (anterior, posterior, lateral, combined). We also defined grading classification, based on severity and expression of clinical signs of obstruction. In our patient collective microlaryngoscopic partial resection of epiglottis by CO2-Laser and/or partial resection of hyoid proofed to be effective to enable N-CPAP ventilation, not possible before. In our still limited group of 106 operated patients about 80% abandoned N-CPAP even though tolerating it better than before. Currently we are reevaluating the outcome of this subgroup regarding RDI and SAO2 levels pre- and post-op.

Basic research on airway physics guided us to a possible etiology of supraglottic obstruction. The "Venturi effect" enables the glottis, as narrowest part of airway, to accelerate air flow maximally to maintain sufficient breathing capacity.The glottis is, in contrast to supraglottis, perfectly constructed for this purpose. If supraglottis defines narrowest part of airway, an increased pressure gradient between windpipe(lower airway) and short-pipe(upper airway) will result,which again will predispose for airway collapse, especially by forced inspiration through rising CO2 (hyperkapnia) and hypoxia. Our findings indicate pressure gradient changes in the larynx as possible origin of OSA not only at laryngeal but also at pharyngeal level. Our endoscopic documentation suggests also, that complete obstruction with frustraneous thoracic and maximal diaphragm excursions will lead to negative pressure levels in terminal esophagus, which again can cause intrusion of gastric fluids, hence being possible co/etiology of EERD and LPR (laryngopharyngeal reflux) seen in ⅓ of our patients with supraglottic obstruction. This research, since being retrospective, is of limited evidence level, still all our cases and their outcomes are as well clinically as video documented and open for further investigation to all researchers interested in airway medicine.