Surgical Management of Sleep Apnea and Snoring

____________________________________________________ SURGICAL MANAGEMENT OF SLEEP APNEA AND SNORING SURGICAL MANAGEM...

Author: David J. Terris | Richard L. Goode

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SURGICAL MANAGEMENT OF SLEEP APNEA AND SNORING

SURGICAL MANAGEMENT OF SLEEP APNEA AND SNORING edited by

David J.Terris Medical College of Georgia Augusta, Georgia, U.S.A. Richard L.Goode Stanford University School of Medicine Stanford, California, U.S.A.

Boca Raton London New York Singapore

Published in 2005 by Taylor & Francis Group 6000 Broken Sound Parkway NW, Suite 300 Boca Raton, FL 33487–2742 This edition published in the Taylor & Francis e-Library, 2006. “ To purchase your own copy of this or any of Taylor & Francis or Routledge’s collection of thousands of eBooks please go to www.eBookstore.tandf.co.uk.” © 2005 by Taylor & Francis Group, LLC No claim to original U.S. Government works ISBN 0-203-02690-X Master e-book ISBN

International Standard Book Number-10: 0-8247-5910-9 (Print Edition) (Hardcover) International Standard Book Number-13: 978-0-8247-5910-0 (Print Edition) (Hardcover) This book contains information obtained from authentic and highly regarded sources. Reprinted material is quoted with permission, and sources are indicated. A wide variety of references are listed. Reasonable efforts have been made to publish reliable data and information, but the author and the publisher cannot assume responsibility for the validity of all materials or for the consequences of their use. No part of this book may be reprinted, reproduced, transmitted, or utilized in any form by any electronic, mechanical, or other means, now known or hereafter invented, including photocopying, microfilming, and recording, or in any information storage or retrieval system, without written permission from the publishers. For permission to photocopy or use material electronically from this work, please access www.copyright.com (http://www.copyright.com/) or contact the Copyright Clearance Center, Inc. (CCC) 222 Rosewood Drive, Danvers, MA 01923, 978-750-8400. CCC is a not-for-profit organization that provides licenses and registration for a variety of users. For organizations that have been granted a photocopy license by the CCC, a separate system of payment has been arranged. Trademark Notice: Product or corporate names may be trademarks or registered trademarks, and are used only for identification and explanation without intent to infringe. Library of Congress Cataloging-in-Publication Data Catalog record is available from the Library of Congress

Taylor & Francis Group is the Academic Division of T&F Informa plc. Visit the Taylor & Francis Web site at http://www.taylorandfrancis.com

Preface The young field of sleep-disordered breathing continues to mature, with regard to both diagnostic accuracy and treatment alternatives. Besides the nonsurgical management having evolved considerably over the past decade, procedural options have also changed, justifying a fresh and comprehensive review of this surgical discipline. Leading practitioners of surgical treatment of sleep-disordered breathing have spent a considerable amount of time in detailing thought-provoking and educative coverage of a multitude of time-honored and new procedures in this text, with emphasis on the latest path-breaking discoveries and glimpses into what the future may hold. The atlas-like figures will make this a helpful reference for anyone embarking upon novel procedures. The expert review of the diagnostic tools and nonsurgical treatment will serve to fortify the knowledge base requisite for practitioners managing patients with sleep disorders. Finally, the thought-provoking chapters on evidence-based medicine and the “ideal procedure” should stimulate individuals to join the growing army of investigators who together will answer many of the remaining questions in this field. David J.Terris Richard L.Goode

Contents Preface

iv

Contributors

ix

1. Upper Airway Surgical Anatomy 2. The Anatomy of Sleep Disordered Breathing: An Evolutionary Perspective Terence M.Davidson 3. Physiology of Sleep Disordered Breathing B.Tucker Woodson and Chris Yang 4. Maintenance of Wakefulness Yau Hong Goh and Kheng Ann Lim 5. Polysomnography Judy L.Chang and Clete A.Kushida 6. Home Sleep Testing Terence M.Davidson 7. Video Sleep Nasendoscopy V.J.Abdullah and C.A.van Hasselt 8. Special Diagnostic Studies in Sleep Apnea Mike Yao and Pamela H.Nguyen 9. Clinical Staging for Sleep Disordered Breathing: A Guide to Diagnosis, Treatment, and Prognosis Michael Friedman and Hani Ibrahim 10. Continuous Positive Airway Pressure in Obstructive Sleep Apnea Syndrome Susmita Chowdhuri and Jed Black 11. Nonsurgical Management: Oral Appliances James E.Eckhart 12. Patient Selection for Surgery Samuel A.Mickelson 13. Anesthesia Management for Sleep Apnea Surgery Terry Stephen Vitez 14. Nasal Surgery for Sleep Apnea Patients Richard L.Goode 15. Uvulopalatopharyngoplasty Richard L.Goode

1 28

53 79 93 109 172 185 214

225

240 267 278 286 303

16. Surgery of the Palate and Oropharynx: Laser-Assisted Techniques Regina Paloyan Walker 17. Temperature-Controlled Radiofrequency Palatoplasty Lionel M.Nelson 18. Coblation Techniques for Sleep Disordered Breathing Luc G.Morris and Kelvin C.Lee 19. Cautery-Assisted Palatal Stiffening Operation Eric A.Mair 20. Transpalatal Advancement Pharyngoplasty B.Tucker Woodson 21. Injection Snoreplasty Scott E.Brietzke and Eric A.Mair 22. Skeletal Techniques: Mandible Robert J.Troell 23. Skeletal Techniques: Hypopharynx Robert J.Troell 24. Skeletal Techniques: Mandible and Maxilla Kasey K.Li 25. Radiofrequency Tissue Volume Reduction of the Tongue Samuel A.Mickelson 26. Tracheotomy Vincent D.Eusterman and Wayne J.Harsha 27. Surgery for Pediatric Sleep Apnea David H.Darrow 28. Surgery for the Upper Airway Resistance Syndrome James Newman References

316

29. Electrical Stimulation for Sleep Disordered Breathing David W.Eisele, Alan R.Schwartz, and Philip L.Smith 30. Temperature-Controlled Radiofrequency Tonsil Reduction Lionel M.Nelson 31. Harmonic Scalpel in Tonsillectomy Ashkan Monfared and David J.Terris 32. Post-operative Management of Obstructive Sleep Apnea Patients Edgar F.Fincher and David J.Terris 33. Avoidance of Complications in Sleep Apnea Patients Samuel A.Mickelson 34. Failure Analysis in Sleep Apnea Surgery K.Christopher McMains and David J.Terris

514

330 341 365 374 387 394 433 443 454 462 480 504

526 538 548 556 569

35. The Ideal Procedure for Snoring and Obstructive Sleep Apnea Richard L.Goode Index

584 590

Contributors V.J.Abdullah Division of Otolaryngology, Department of Surgery, Prince of Wales Hospital, Chinese University of Hong Kong, Shatin, Hong Kong Brian J.Baumgartner Department of Otolaryngology—Head and Neck Surgery, Madigan Army Medical Center, Fort Lewis, Washington, U.S.A. Jed Black Standard Sleep Disorders Center, Stanford University, Palo Alto, California, U.S.A. Scott E.Brietzke Department of Otolaryngology, Walter Reed Army Medical Center, Washington, D.C., U.S.A. Judy L.Chang Stanford University Center of Excellence for Sleep Disorders, Stanford, California, U.S.A. Susmita Chowdhuri Division of Pulmonary/Critical Care and Sleep Medicine, Department of Medicine, John D.Dingell Veterans Affairs Medical Center, Wayne State University School of Medicine, Detroit, Michigan, U.S.A. David H.Darrow Departments of Otolaryngology and Pediatrics, Eastern Virginia Medical School, Children’s Hospital of The King’s Daughters, Norfolk, Virginia, U.S.A. Terence M.Davidson Division of Otolaryngology—Head and Neck Surgery, University of California at San Diego and VA San Diego Health Care System, San Diego, California, U.S.A. James E.Eckhart Manhattan Beach, California, U.S.A. David W.Eisele Department of Otolaryngology—Head and Neck Surgery, University of California, San Francisco, California, U.S.A. Vincent D.Eusterman Department of Otolaryngology—Head and Neck Surgery, Madigan Army Medical Center, Fort Lewis, Washington, U.S.A. Edgar F.Fincher Department of Otolaryngology, Medical College of Georgia, Augusta, Georgia, U.S.A. Michael Friedman Department of Otolaryngology and Bronchoesophagology, RushPresbyterian-St. Luke’s Medical Center, and Division of Otolaryngology, Advocate Illinois Masonic Medical Center, Chicago, Illinois, U.S.A. Yau Hong Goh Mount Elizabeth Medical Centre and Department of Otolaryngology, Singapore General Hospital, Singapore Richard L.Goode Department of Otolaryngology—Head and Neck Surgery, Stanford University Medical Center, Stanford, California, U.S.A. Wayne J.Harsha Department of Otolaryngology—Head and Neck Surgery, Madigan Army Medical Center, Fort Lewis, Washington, U.S.A. Hani Ibrahim Department of Otolaryngology and Bronchoesophagology, RushPresbyterian-St. Luke’s Medical Center, and Division of Otolaryngology, Advocate Illinois Masonic Medical Center, Chicago, Illinois, U.S.A. Clete A.Kushida Stanford University Center of Excellence for Sleep Disorders, Stanford, California, U.S.A.

Kelvin C.Lee Department of Otolaryngology, New York University School of Medicine, New York, New York, U.S.A. Kasey K.Li Sleep Disorders Clinic and Research Center, Stanford University Medical Center, Stanford, California, U.S.A. Kheng Ann Lim Mount Elizabeth Medical Centre, Singapore Eric A.Mair Department of Otolaryngology, Wilford Hall USAF Medical Center, San Antonio, Texas, U.S.A. K.Christopher McMains Department of Otolaryngology—Head and Neck Surgery, Medical College of Georgia, Augusta, Georgia, U.S.A. Samuel A.Mickelson The Atlanta Snoring & Sleep Disorders Institute, Advanced Ear, Nose & Throat Associates, Atlanta, Georgia, U.S.A. Ashkan Monfared Department of Otolaryngology—Head and Neck Surgery, Stanford University Medical Center, Stanford, California, U.S.A. Luc G.Morris Department of Otolaryngology, New York University School of Medicine, New York, New York, U.S.A. Lionel M.Nelson Department of Surgery, Stanford University School of Medicine, Stanford, California, U.S.A. James Newman Division of Otolaryngology—Head and Neck Surgery, Stanford University Medical Center, Stanford, California, U.S.A. Pamela H.Nguyen Department of Radiology, Mercy Hospital and Medical Center, Chicago, Illinois, U.S.A. Alan R.Schwartz Division of Pulmonary and Critical Care Medicine, Johns Hopkins Sleep Disorders Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, U.S.A. Philip L.Smith Division of Pulmonary and Critical Care Medicine, Johns Hopkins Sleep Disorders Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, U.S.A. David J.Terris Department of Otolaryngology—Head and Neck Surgery, Medical College of Georgia, Augusta, Georgia, U.S.A. Robert J.Troell Beauty By Design, Las Vegas, Nevada, U.S.A. C.A. van Hasselt Division of Otolaryngology, Department of Surgery, Prince of Wales Hospital, Chinese University of Hong Kong, Shatin, Hong Kong Terry Stephen Vitez San Jose, California, U.S.A. Regina Paloyan Walker Loyola University Medical Center, Maywood, Illinois, and Hinsdale Hospital, Hinsdale, Illinois, U.S.A. B.Tucker Woodson Department of Otolaryngology and Communication Sciences, Medical College of Wisconsin, Milwaukee, Wisconsin, U.S.A. Chris Yang Department of Otolaryngology and Communication Sciences, Medical College of Wisconsin, Milwaukee, Wisconsin, U.S.A. Mike Yao Department of Otolaryngology/Head and Neck Surgery, University of Illinois at Chicago, Chicago, Illinois, U.S.A.

1 Upper Airway Surgical Anatomy Vincent D.Eusterman and Brian J.Baumgartner Department of Otolaryngology—Head and Neck Surgery, Madigan Army Medical Center, Fort Lewls, Washington, U.S.A. 1. INTRODUCTION Obstructive sleep disordered breathing (OSDB) results from anatomical upper airway abnormalities and changes in neural activation mechanisms intrinsic to sleep causing hypotonia of the pharyngeal dilator muscles (1). Surgical correction of the obstruction requires accurate identification of the obstructive process and a thorough knowledge of the anatomy and function of the site to allow the surgeon to create a physiologic airway when medical therapy has failed. The purpose of this chapter is to discuss the anatomy of these structures as they relate to surgical treatment of upper airway obstruction during sleep. As our knowledge of the anatomic and physiologic functions of the upper airway expands, so will the treatment options to produce minimally invasive procedures to obtain functional and long-lasting results. 2. NASAL AIRWAY The primary function of the nasal passages is to work as a resistor. By matching impedance of the upper and lower airways, the nasal passages control breathing frequency and expiratory length (2). The pertinent parts of nasal airway anatomy are the nasal valves, lateral nasal walls, nasal septum, and nasal mucosa. The nasal valve is the narrowest portion of the nasal passage and is composed of an internal and an external portion (Fig. 1). The internal valve is the primary nasal airflow regulator in leptorrhine (Caucasian) noses (3). In contrast, the inferior turbinates are the primary nasal airflow regulators in platyrrhine (Asian and African) noses (3). The internal nasal valve is the area between the caudal end of the upper lateral cartilage and the septal cartilage. The posteroinferior limit is the anterior part of the inferior turbinate and the soft tissue at the pyriform aperture. The angle between the caudal end of the upper lateral cartilage and the septal cartilage is the valve angle. This angle is normally 10–15° in the leptorrhine nose and is more obtuse in platyrrhine noses. The external valve comprises the mobile alar wall and cutaneous skeletal support (Fig. 1). It is described as the region caudal to the internal valve,

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Figure 1 Internal and external nasal valve. (Modified from Ref. 3.) bounded laterally by the nasal alae containing fibro-fatty tissue and bony pyriform aperture, medially by the septum and columella, and inferiorly by the nasal floor. Both internal and external valves function as Starling resistors. The transmural pressure increases at these narrow sites according to the Bernoulli principle leading to collapse and a decrease in airflow. Weak valves deform at low transmural pressure and lead to premature collapse and airway obstruction. The lateral nasal wall contains the inferior, middle, superior, and, if present, a supreme turbinate (Fig. 2). These tissue ridges are composed of scrolls of bone covered with a thick mucous membrane. The bony portions of the middle and superior turbinates are extensions of the ethmoid bone. The inferior turbinate is an independent bone which articulates with the nasal surface of the maxilla, the perpendicular plate of the palatine bone, and the ethmoid and lacrimal bones. The main bulk of the inferior turbinate is the lamina propria, which is built of loose connective tissue and superficially harbors an inflammatory cell infiltrate (Fig. 3). The medial mucosal layer (MML) is thicker than the bone and the lateral mucosa. There are more glands and goblet cells in the lateral mucosa layer (LML). The extent of venous sinusoids varies significantly, with the greatest difference in the inferior mucosa layer (IML). Decreased proportion of glands and an increase in venous sinusoids are associated with advanced age. The cancellous central bony layer is made of interwoven trabeculae and houses the major arterial supply of the turbinate. Both MML and IML are ideal targets for surgical reduction in cases of obstruction caused by turbinate dysfunction. The superior turbinate has a thinner and less vascular mucosa and is the only turbinate to contain olfactory epithelium, housing the olfactory nerve sensory cells in its mucous membrane. Turbinate enlargement produced by “overstimulation” of the parasympathetic system or “understimulation” by the sympathetic innervation can produce obstruction. Resistance or turbulence produced by

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the turbinate optimizes air contact with the mucous membrane and produces a sensation of normal airflow. If it is too high or too low, a sensation of obstruction may occur. The “nasal cycle” is a cyclic alteration of constriction and dilation of the inferior turbinate and occurs approximately every 3–6hr. Abnormalities in cycling, vasoconstrictive medications, infections, allergic disease, and compensatory hypertrophy may

Figure 2 Lateral nasal wall with inferior, middle, and superior turbinates. (Adapted from Ref. 3.)

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Figure 3 Inferior turbinate, thick MML, vascular IML, thin LML, and central artery (A). (Adapted from Ref. 5.)

Figure 4 Components of the nasal septum, membranous, cartilaginous,

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and bony portions made up of the perpendicular plate of the ethmoid and vomer bones. (Adapted from Ref. 3.) cause anatomic obstruction. Concha bullosa is turbinate enlargement caused by the pneumatization of the turbinate portion of the anterior ethmoid bone. Concha bullosa often refers to aeration of the middle turbinate but can occur in the superior and inferior turbinate and can be a source of nasal airway obstruction. The nasal septum divides the nasal cavity in the midline and consists of membranous, cartilaginous, and bony portions (Fig. 4). The membranous septum is a skin-covered membrane extending from the columella to the caudal edge of the quadrangular cartilage. The cartilaginous and bony septal portions are covered by perichondrium and periosteum, respectively. A thin mucous membrane covers these layers. The cartilaginous septum is wider at its base, at its junction with the upper lateral cartilages, and at the anterior septal body. The septal body corresponds to a widened area of septal cartilage just anterior to the middle turbinate (1). The major bony portion of the septum is formed by the perpendicular plate of the ethmoid bone (superiorly) and the vomer (inferiorly). The perpendicular plate of the ethmoid makes up a portion of the anterior skull base. Surgical manipulation of this bone during septoplasty can fracture the cribiform plate and cause cerebral spinal fluid leakage. The vomer articulates with the palatine and maxillary bones inferiorly and clivis posteriorly (Fig. 4). The nasal spine of the frontal bone and the nasal crest of the maxillary and palatine bones also provide a small contribution to the bony septum (Fig. 4). General sensory innervation to the nasal mucosa is primarily by the trigeminal nerve (V1, V2) and the greater petrosal branch of the facial nerve. The nasal septum is supplied anteriorly by the nasopalatine nerve (V2) and the anterior ethmoidal nerve (V1) and posteroinferiorly by the nasal branches of the greater palatine nerve (V2). The lateral nasal wall is supplied by the nasal branch of the maxillary nerve (V2), the greater palatine (V2), and anterior ethmoidal nerves (V1). Blood supply to the nasal cavity is by the internal and external carotid artery systems. The sphenopalatine branch of the internal maxillary artery supplies the posterior nose and can be a significant source of postoperative bleeding in turbinate surgery. This branch exits the pterygopalatine fossa through the sphenopalatine foramen and one to three branches course within the inferior turbinate (Fig. 3). The anterosuperior nose is supplied by the anterior and posterior ethmoid arteries from the internal carotid by the ophthalmic artery. Retraction of these vessels into the orbit during nasal surgery can produce intraorbital hemorrhage. The nasal vestibule is supplied by branches of the facial artery. The septum is supplied by the anterior and posterior ethmoidal arteries, greater palatine artery, sphenopalatine branches, as well as the septal branch of the superior labial artery from the facial artery. These vessels anastomose in the anterior septal cartilage mucosa as Kiesselbach’s plexus.

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3. ORAL AIRWAY 3.1 Tongue The tongue is divided into oral tongue (anterior two-thirds) and pharyngeal tongue (posterior one-third) by the sulcus terminalis. This sulcus is a V-shaped groove behind the circumvallate papillae. The apex of the V is posterior and represents the foramen cecum. The oral tongue surface is covered by filiform, fungiform, and circumvallate papillae. Papillae are replaced on the pharyngeal tongue surface by lingual tonsils. The lingual tonsil is the inferior portion of Waldeyer’s ring and is made up of discrete lymphoid tissue masses with overlying lenticular papillae (6). Hypertrophy of lingual and palatine tonsils and adenoid tissues is common and often significant. These anatomic obstructions of the oral and nasal airways require careful evaluation during the patients work-up for OSDB. The tongue muscle consists of intrinsic and extrinsic muscles. The four intrinsic muscles are located entirely within the tongue and are divided by a median fibrous septum fixed to the hyoid bone (Fig. 5). The intrinsic muscles consist of superior

Figure 5 Genioglossus and hyoid bone on median section. (Modified from Grant’s Atlas of Anatomy, 10th ed. Baltimore, MD: Williams and Wilkins, 1999.)

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and inferior longitudinal muscles and, to a lesser extent, the transverse and vertical muscles. The longitudinal muscles modify the shape of the tongue during speaking and swallowing. The transverse muscles narrow and elongate the tongue whereas the vertical muscles flatten and broaden the tongue. Four extrinsic muscles, the genioglossus, hyoglossus, styloglossus, and palatoglossus, attach outside the tongue (Table 1). The larger genioglossus and hyoglossus extend into the tongue from the sublingual region while the styloglossus and palatoglossus enter the tongue superiorly and laterally (Fig. 6) The genioglossus protrudes and depresses the tongue. It originates on the lingual surface of the anterior mandible at the superior genial tubercle just above the geniohyoid muscle attachment (Figs. 5 and 6). This tubercle can be palpated and serves as an important landmark in tongue advancement surgery for avoiding incisor root damage and preserving muscle attachment. The distance from the genial tubercle superior border to the central root apex can be less than 5mm (8). The genioglossus opens the retroglossal air space and is considered the most important muscle in keeping the upper airway patent. Contraction is phasic with inspiration; this activity decreases with sleep, becomes almost non-existent during rapid eye movement sleep, ceases in patients with obstructive sleep apnea (OSA) at the onset of an apnea, and increases at the termination of an obstruction (9). Mechanoreceptors control genioglossus activity and are critical in maintaining upper airway patency in patients with OSDB. Overworking of the genioglossus during the day can result in both muscle hypertrophy with airway impingement and loss of muscle contraction (10). The hyoglossus muscle (Fig. 6) arises from the lateral body and greater horn of the hyoid, travels vertically, and passes lateral to the posterior portion of the genioglossus. It courses between the styloglossus laterally and the inferior longitudinal muscle medially to insert into the side of the tongue. It depresses and retracts the tongue. Surgical advancement of the hyoidhyoglossus complex can advance the tongue base to open the posterior airway space (PAS). The styloglossus extends from the styloid process and ligament to insert on the side and inferior aspect of the tongue (Fig. 6). Its action is to pull the tongue upward and backward. The palatoglossus travels from the palatine aponeurosis inferiorly toward the tonsil and forms the palatoglossal arch (anterior pillar). It inserts into the side of the tongue and is responsible for elevating the posterior tongue (Table 1). Mathur (11) suggests that a similar mechanoreceptor reflex that activates the genioglossus activates the palatoglossus muscle to dilate the pharynx under negative upper airway pressure. The mylohyoid and digastric muscles are associated with tongue position and movement (Fig. 6). The mylohyoid muscle extends from the mylohyoid line on the mandibular inner surface to the midline where posterior fibers insert onto the hyoid bone and anterior fibers meet contralateral mylohyoid fibers at the median raphe. It elevates the hyoid bone and consequently the floor of the mouth and tongue base. The geniohyoid muscle and tongue musculature lie above the mylohyoid muscle and the anterior belly of the digastric muscle and a portion of the submandibular gland lie below. The digastric muscle consists of anterior and posterior bellies. From its origin on the medial mastoid process, the posterior belly travels toward the hyoid bone. Its fibers transition into a tendon that then pierces the stylohyoid muscle, passes through the hyoid fascial sling, and continues anteriorly as the anterior belly. The digastric muscles, and likely the mylohyoid and geniohyoid muscles, aid in mouth opening. Because these muscles are attached to the

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mandible and hyoid, they play a role in opening the PAS with mandibular advancement surgery.

Table 1 Extrinsic Tongue Muscles Muscle

Origin

Insertion

Innervation

Action

Genioglossus* Upper part of Ventral surface of CN XII mental spine of tongue; anterior mandible surface of body of hyoid bone

Draws forward and posterior part protrudes the apex of the tongue

Palatoglossus* Oral surface of the palatine aponeurosis

Side and dorsum of the tongue

CN XI via the pharyngeal branch of the CN X and pharyngeal plexus.

Elevates posterior part of tongue

Styloglossus

Styloid process and stylohyoid ligament

Side and inferior aspect of tongue

CN XII

Elevation and retraction of the tongue, creating a trough for swallowing

Hyoglossus

Body and greater horn of hyoid bone

Into the inferior side of the tongue

CN XII

Depresses and retracts tongue

Note: The asterisks denote pharyngeal dilators. Source: From Ref. 27.

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Figure 6 Extrinsic tongue muscles, genioglossus, hyoglossus, styloglossus, and palatoglossus, attached to the outside of the tongue. (Modified from Grant’s Atlas of Anatomy, 10th ed. Baltimore, MD: Williams and Wilkins, 1999.) The hyoid bone has no osseous articulation like other species. It is a freely mobile bone that participates in swallowing and phonation (Figs. 5 and 6). In humans it descends in the neck as the oral pharynx elongates. The lengthening of the oral pharynx may be responsible for the laxity at the tongue base that produces obstruction in recumbent sleep (12). This length is measured by the MP-H distance between the mandibular plane (MP) and the hyoid bone (H) on lateral cephalometric films (Fig. 9). The reference range is 11– 19mm. The longer this distance, the higher the possibility of the patient having OSA. The hyoid bone is derived from the second and third arches. The second (hyoid) arch assists in forming the side and front of the neck. From the hyoid cartilage are developed the styloid process, stylohyoid ligament, and lesser cornu of the hyoid bone. The third arch cartilage gives rise to the greater cornu of the hyoid bone. The ventral ends of the second and third arches unite with those of the opposite side to form the body of the hyoid bone and the posterior tongue. The middle constrictor and pharynx attach to the hyoid laterally. During the pharyngeal phase of swallowing, the hyoid (and attached thyroid and cricoid cartilage) is raised by the suprahyoid muscles (mylohyoid, anterior belly digastric,

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geniohyoid, stylohyoid, hyoglossus, genioglossus, styloglossus, and palatoglossus), which elevate the larynx. The infrahyoid muscles (thyrohyoid, omohyoid, and sternohyoid) depress and stabilize the hyoid bone and with the geniohyoid stabilize and dilate the retroepiglottic laryngopharynx by tensing the hyoepiglottic ligament (9). These muscles are phasic with inspiration and factors that affect hyoid position can adversely affect the muscles and cause narrowing of the laryngopharynx. Surgical immobilization of the hyoid bone during suspension procedures may cause dysphagia (13). Blood supply to the tongue is primarily from the two lingual arteries that branch from the external carotid at the level of the greater horn of the hyoid bone (Fig. 6). The lingual artery gives off a suprahyoid branch at the posterior edge of the hyoglossus muscle, passes deep to this muscle, and gives two dorsal lingual branches that supply the pharyngeal tongue and palatine tonsil. Near the anterior hyoglossus muscle border, it divides into the deep lingual and sublingual arteries. The deep lingual artery (s. artery ranine) is in the lateral tongue and can be identified and controlled intraoperatively on the lateral surface of the genioglossus if injured during midline tongue reduction or thermal volumetric reduction. The sublingual artery supplies the sublingual gland and tongue musculature. Motor innervation to both intrinsic and extrinsic tongue musculature, excluding the palatoglossus, is by the hypoglossal nerve (XII) (Fig. 6). The medial branch of the hypoglossal nerve innervates the tongue protruders (genioglossus and geniohyoid). The lateral branch of the hypoglossal nerve innervates the tongue retractors (styloglossus and hyoglossus). Selective electrical stimulation of these nerves can stiffen and dilate the PAS during sleep (14). The lingual nerve (V3) is a branch of the inferior alveolar nerve and supplies general sensory innervation for touch, pain, and temperature sensation to the oral tongue and lingual gingiva. It also contains post-ganglionic special visceral afferents (taste) via the chorda tympani nerve (VII) from the geniculate ganglion and parasympathetic nerves for the submandibular and sublingual glands. The glossopharyngeal nerve (IX) supplies taste and general sensation to the pharyngeal tongue and vallecula. The internal branch of the superior laryngeal nerve (X) supplies sensory fibers to the base of the tongue and epiglottis. Although the circumvallate papillae are part of the oral tongue, they are innervated by the general sensation and taste fibers of the glossopharyngeal nerve (IX). Airway assessment of the anatomic tongue-palate position was described in a preanesthesia airway assessment by Mallampati et al. (15). Fujita (16) and Friedman (17) have described pre-surgical assessments of the palate and tongue base to predict surgical results. The Mallampati test is performed with the patient in the sitting position, head held neutral, mouth wide open, and tongue protruding to the maximum. Class I is visualization of the soft palate, fauces, uvula, anterior and posterior pillars. Class II is visualization of the soft palate, fauces, and uvula. Class III is visualization of the soft palate and the base of the uvula. Class IV is soft palate that is not visible at all. Dempsey and Woodson have found that clinical airway assessments using Mallampati and Mueller tests did not correlate with apnea-hypopnea index (AHI) and body mass index (BMI) (18). Although surgeons do not have a perfect clinical tool for evaluation of the anatomic site of lesion evaluation, imaging studies, sleep endoscopy, and newer methods of airway assessment and classification are ongoing and will, in time, account for more accurate diagnosis and surgical outcomes.

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3.2 Maxilla and Mandible The bony support of the oral airway is provided by the maxilla and mandible. The maxilla develops from membranous bony plates and has five components: the zygo-matic and frontal extensions, the palatine bone, the alveolar processes, and an aerated maxillary sinus. The palatine bones articulate with each other to form the majority of the hard palate. The maxilla articulates with the vomer, lacrimal, sphenoid, and palatine bones. The palate consists of an anterior, bony, hard palate and a posterior, mobile, fibromuscular soft palate. The anterior portion of the hard palate is composed of the maxillary palatine processes and the palatine horizontal plates. Posteriorly, the hard and soft palates are continuous. Posterior to the maxillary central incisor teeth, the incisive canal transmits the nasopalatine nerve and greater palatine artery, which provide sensation and vascularity to the anterior hard palate. The greater palatine foramen is medial to the third molar teeth and transmits the greater palatine nerve and vessels supplying sensation and vascularity to the posterior hard and soft palate. The greater palatine foramen can be used to access the maxillary branch of the trigeminal nerve (V2) in the pterygopalatine fossa with local anesthesia. The posterior hard palate can be surgically reduced or advanced to mobilize the intact soft palate away from the posterior retropalatal pharynx in palatal advancement surgery for OSDB (19). This method retains the natural anatomy and function of the soft palate and uvula. The mandible develops from Meckel’s cartilage and consists of the horizontal body, the tooth-bearing alveolar portion, and two vertical rami that extend superiorly from the mandibular angle (Fig. 8). The mandibular ramus contains the anterior coronoid process and posterior condylar process, which are separated by the mandibular notch. The genial tubercles, which may be fused in the midline, project from the lingual aspect of the mandibular body as superior and inferior mental spines (Fig. 9). The genioglossus and geniohyoid muscles attach to the superior and inferior spines, respectively. The sublingual fovea lies lateral to each genial tubercle and contains a sublingual gland. Posterior to the sublingual fovea is the attachment of the mylohyoid muscle. Just inferior to the genial tubercle is the attachment of the anterior belly of the digastric muscle in the digastric fossa. The mandibular canal containing the inferior alveolar nerve lies posterosuperior to the mylohyoid line. The lingula (Fig. 9) is a sharp bony edge that overhangs the mandibular canal and serves as the inferior surgical landmark for the medial horizontal cut of the bilateral sagittal split osteotomy (BSSO). The lingula-tomandibular-notch distance varies from 10.5 to 15mm (3). The mandibular foramen is 15– 20mm inferior to the mandibular notch. The inferior alveolar nerve is in close association with the mandible for about 4–5mm above the lingula. The horizontal ramus osteotomy is best placed 7.5mm below the mandibular notch (3). The inferior alveolar nerve (V3) descends with the lingual nerve between the medial and lateral pterygoid muscles. Its mylohyoid branch lies in the mylohyoid groove and provides a motor branch to the mylohyoid muscle and anterior belly of the digastric muscle. It then enters the mandibular foramen to innervate mandibular dentition. The inferior alveolar nerve and associated vessels travel through the mandibular canal; it exits through the mental foramen as the mental nerve and vessels. The mental nerve innervates the skin of the lower lip and chin, the lip mucosa, and adjacent gingiva. At the mental foramen, the neurovascular bundle is susceptible to injury during genioglossus muscle advancement

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procedures. The mental foramen is located on the lateral mandibular body at or near the vertical body midline and between the first and second premolar root apices (Fig. 8). It can be posterior to the second premolar in about 24% of cases or anterior to the first premolar in 1–2% of cases (20). The masseter and medial pterygoid muscles attach laterally and medially to the ramus and angle and serve as the blood supply to the proximal mandible, which assists in proximal bone survival in BSSO procedures. The blood supply to the distal mandible is by the inferior alveolar artery. It travels through the mandibular canal and supplies dentition, bone, and the surrounding soft tissue. The mandible is also supplemented anteriorly by vessels in the geniohyoid, genioglossus, and digastric (anterior belly) muscles (21). At the level of the first premolar, the inferior alveolar artery branches into the incisive and mental branches. The incisive branch supplies the anterior teeth and supporting structures. The mental branch joins the inferior labial and submental vessels and supplies the chin. Vessels of the temporal mandibular joint capsule and lateral pterygoid muscle supply the condyle. The temporalis muscle inserts on the coronoid process and provides blood supply to this aspect of the ramus. The dental relationship was described by Angle in 1899 as the relationship of the maxillary and mandibular teeth. In class I occlusion, the mesial buccal cusp of the maxillary first molar contacts the mesial buccal groove of the mandibular first molar. In class II occlusion or retrognathia, the mesial buccal cusp is mesial to the groove and in class III occlusion or prognathic occlusion, the cusp is distal to the groove. The skeletal relationship ultimately determines the soft tissue relationships of the airway; it refers to the position of the maxilla and mandible in relation to the skull base and is measured by the lateral cephalometric radiograph (Fig. 7). The SNA (sella, nasion, subspinale) and SNB (sella, nasion, supramentale) angles determine the relative differences and deficiencies in facial growth. SNA is 82° (greater denotes maxillary hyperplasia, and less, maxillary hypoplasia). SNB is 80° (greater denotes prognathism and less, retrognathism). Mandibular retrognathia is associated with a posterior tongue position and pharyngeal airway obstruction. Riley in 1989 suggested that an SNB <78% should undergo genioglossus advancement to open the PAS. A long MH distance (MPH), mentioned earlier, and a narrow PAS measurement are helpful in determining site of lesion and treatment options (22). In a meta-analysis evaluating retrognathic mandibles, narrow PAS, enlarged tongues and soft palates, inferiorly positioned hyoid bones, and retrognathic maxillas, Miles et al. (23) found that only one cephalometric variable, mandibular body length (Go-Gn: gonion-gnathion), demonstrated a clinically significant association in patients with OSA. Dempsey found that the single most important cephalometric variable in predicting AHI severity was the horizontal dimension of the maxilla. A horizontal distance from the porion vertical to the A point (PV-A: porion verticalsupradentale) or the PV-A distance correlated well with the BMI for an increasing amount of the variance in AHI as the severity of AHI increased (Fig. 7) (18). Cephalometric studies are limited to two dimensions; they are inaccurate for crosssectional or volumetric data and miss soft tissue structures such as the lateral pharyngeal walls or parapharyngeal fat. Schwab and Goldberg (24) describe the usefulness of the CT and MRI scans to provide direct volumetric acquisitions of images of bony support and adipose tissue. Studies by Shepard and Thawley (25) and Trudo et al. (26) have shown the most common site of pharyngeal collapse identified with CT and MRI scans and

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suggest the retropalatal pharynx as the most common site of obstruction and not retroglossal (25,26). These data suggest that patients undergoing UPPP without scanning would predictably have good results while those with retroglossal obstruction may not show improvement.

Figure 7 Lateral cephalometric radiograph: SNA, sella-nasionsubspinale (82±2) where A is the maximal concavity on the anterior surface of the maxilla; SNB, sellanasion-supramentale is the mandibular-cranial base angle (80±2), B is the maximal concavity on the anterior surface of the mandible; mandibular plane (MP) from the gnathion (Gn, most inferior point on the mandibular symphysis) through the gonion (Go, point of the jaw angle intersection between the ramal and mandibular lines); hyoid bone (H) and MH distance (11–19); PAS, posterior airway space (10–16) between the

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posterior tongue dorsum and posterior pharyngeal wall on a line between the gonion and the B point; P, porion is the central point on the upper margin of the external auditory meatus. 4. PHARYNGEAL AIRWAY Based on standard anatomic definitions (Gray’s Anatomy) and others (7,27), the pharyngeal airway is anatomically divided into three regions: the nasopharynx, defined as the area behind the nose and above the soft palate; the oropharynx, defined as the area from the soft palate to the upper border of the epiglottis; and the laryngopharynx, defined as the area from the upper border of the epiglottis to the inferior border of the cricoid cartilage (28). Accurate evaluation of the obstructing airway behind the soft palate and tongue has subdivided the oropharynx into the retropalatal pharynx (or velopharynx) and the retroglossal pharynx, respectively. The obstructing portion behind the epiglottis in the laryngopharynx (or hypopharynx) is referred to as the retroepiglottic pharynx. Consistency in this terminology can accurately localize the anteroposterior site of collapse and will improve data collection, surgical training, and, most importantly, surgical outcome. Pharyngeal patency during wakefulness is attributable to continuous neuromuscular control, which supervises the activity of the dilator capacity of the pharyngeal musculature. Diaphragmatic contraction creates airflow and subatmospheric intra-airway pressure, which narrows the collapsible segments (9). Dilator muscles

Figure 8 Mandible, lateral aspect of body, alveolus, ramus, condyle, and coronoid process.

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stiffen the airway and are discussed later and in Tables 1–3. Pharyngeal patency is a function of the transmural pressure across the pharyngeal wall as well as the compliance of the pharyngeal wall (28). Rowley et al. feel that the intrinsic properties of the airway wall determine retroglossal compliance independent of changes in the neuromuscular activity associated with changes in the sleep state (30). Huang and Williams (31) suggest that rigid tissue is required to maintain airway patency, low tissue

Figure 9 Mandible, lingual aspect, genial tubercles, mylohyoid line, mandibular foramen, and coronoid notch. Table 2 Muscles of the Palate Muscle Tensor veli palatini*

Origin

Insertion

Scaphoid fossa of medial pterygoid plate, spine of sphenoid, and auditory tube cartilage

Tendon around hamulus to insert in the palatine aponeurosis

CN V medial pterygoid n. via otic ganglion

Side of tongue

Elevates posterior part CN XI through pharyngeal branch of tongue and draws of vagus via soft palate into tongue

Palatoglossus* Palatine aponeurosis

Innervation

Action Tenses soft palate and opens mouth of auditory tube during swallowing and yawning

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pharyngeal plexus Palatopharyngeus*

Posterior boarder hard palate and palatine aponeurosis

Lateral wall of pharynx and posterior boarder thyroid cartilage

CN XI through pharyngeal branch of vagus via pharyngeal plexus

Musculus uvulae

Posterior nasal spine and palatine aponeurosis

Mucosa of uvula

CN XI through Shortens uvula and pharyngeal branch pulls it superiorly of vagus via pharyngeal plexus

Levator veli palatini

Cartilage of Palatine auditory tube and aponeurosis petrous part of the temporal bone

Tenses soft palate and pulls walls of pharynx superoanteriorly and medially during swallowing

CN XI through Elevates soft palate pharyngeal branch during swallowing and of vagus via yawning pharyngeal plexus

Note: The asterisks denote pharyngeal dilators. Source: From Ref. 27.

Table 3 Pharyngeal Muscles Muscle

Origin

Insertion

Innervation

Action

Stylopharyngeus*

Medial styloid process of temporal bone

Posterior and superior boarders of thyroid cartilage with palatopharyngeus

CN IX

Dilate retropalatal oropharynx at rim of soft palate

Salpingopharyngeus

Inferior cartilaginous portion of auditory tube

Blends with palatopharyngeus

Cranial root of XI via pharyngeal br. of X and pharyngeal plexus

Elevates (shortens and widens) pharynx

Palatopharyngeus

Posterior portion of hard palate and palatine aponeurosis

Posterior boarder of lamina of thyroid cartilage and side of pharynx and esophagus

Cranial root of XI via pharyngeal br. of X and pharyngeal plexus

Elevates (shortens and widens) pharynx

Superior constrictor

PtergoMedian raphe of mandibular raphe, pharynx and tubercle of ptergoid plate, the occipital bone ptergoid hamulus, mandible

Cranial root of XI via pharyngeal br. of X and pharyngeal plexus

Constricts pharyngeal wall during swallowing

Middle constrictor

Greater and lesser Median raphe of horn hyoid bone pharynx

Cranial root of XI via pharyngeal br. of X and pharyngeal plexus

Constricts pharyngeal wall during swallowing

Inferior constrictor

Oblique line thyroid lamina

Median raphe of pharynx

Cranial root of XI Constricts via pharyngeal br. of pharyngeal

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X and pharyngeal plexus and recurrent laryngeal

wall during swallowing

Note: The asterisk denotes pharyngeal dilator. Source: From Ref. 27.

(structural) stiffness will cause initial narrowing, and the Bernoulli effect will lower effective stiffness. Neuromuscular function reaction to negative pressure is delayed during sleep and is powerless to stop the airway from collapsing. The adult human is the only mammal that suffers from OSA because the oropharyngeal complex lacks support; in other mammals the tip of the uvula touches the tip of the epiglottis and the hyoid bone supports this segment by its articulation with the cervical spine (32). The anatomic or structural changes within each pharyngeal segment are affected by neuronal tone and by the position of the patient (33). Studies suggest that the male predisposition to pharyngeal collapse is anatomically based, primarily as a result of the increased length of the vulnerable airway as well as increased soft palate size (12). 4.1 Nasopharynx The nasopharynx is posterior to the nasal cavity beginning at the paired posterior nasal choanae just superior to the soft palate. The roof and posterior wall of the nasopharynx form a continuous surface that lies inferior to the body of the sphenoid bone and the basilar part of the occipital bone. The pharyngeal tonsil (adenoid) is in the mucous membrane of the roof and posterior wall of the nasopharynx and is often the site of obstruction in adenoid hyperplasia. The lateral wall of the nasopharynx contains the auditory tube and cartilage, the tensor and levator palate, and salpingopharyngeus muscles. Posterior to the auditory tube and salpingopharyngeal fold is the pharyngeal recess. 4.2 Oropharynx The oropharynx extends from the soft palate to the tip of the epiglottis and is bounded laterally by the palatoglossal and palatopharyngeal arches. The collapsible segment posterior to the soft palate is referred to as the retropalatal pharynx. Inferior to that, the collapsible tongue base segment of the oropharynx, which is posterior to the tongue from the tip of the uvula to the tip of the epiglottis, is the retroglossal pharynx. The soft palate is connected to the hard palate by a tensor aponeurosis of connective tissue, which extends posterior-inferiorly from the margin of the hard palate. It serves as a point of attachment for much of the soft palate musculature and is continuous with the lateral pharyngobasilar fascia and tensor veli palatine muscle tendons (Fig. 10) The soft palate contains five muscles, four paired slings and one midline muscle, listed in Table 2. The palatopharyngeus muscle (posterior pillar) is the most superficial of the soft palate musculature and has anterior and posterior extensions that blend with the musculus uvula and levator veli palatini (Fig. 10). The palatopharyngeus originates on the hard palate and palatine aponeurosis and inserts into the lateral pharyngeal wall. During swallowing, it tenses the soft palate and pulls the pharyngeal walls superiorly, anteriorly, and medially.

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The uvular muscle (musculus uvulae) lies just deep to the posterior (upper) layer of the palatopharyngeus muscle (Fig. 10). It extends inferiorly in the soft palate midline and pulls the uvula superiorly and anteriorly. The palatoglossus muscle (anterior pillar) originates from the palatine aponeurosis and inserts into the side of the tongue. It draws the posterior tongue and soft palate together. It is a soft palate muscle because it receives vagus innervation like other soft palate musculature, and will be discussed in the section on external tongue musculature. The tensor veli palatini muscle originates from the lateral wall of the Eustachian tube cartilage, sphenoid spine, and scaphoid fossa of the medial pterygoid plate. As it passes inferiorly, it

Figure 10 Diagram of the aponeuroticomuscular structure of the soft palate in longitudinal section above and muscles of the soft palate from below. (From Hollinshead WH. Anatomy for Surgeons: Volume 1, The Head and Neck. 2nd ed. Hagerston, MD: Harper and Row, 1968:386.) hooks around the pteygoid hamulus and inserts into the palatine aponeurosis. The tensor veli palatini opens the Eustachian tube as well as tenses and retracts the soft palate away from the posterior pharyngeal wall (Table 2). The decrease in tonic activity of the tensor palatini during sleep correlates with increased upper airway resistance (9). The levator veli palatini muscle originates on the inferior surface of the petrous temporal bone and inferomedial Eustachian tube cartilage, travels inferoanteriorly between the musculus

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uvula and palatopharyngeus, and inserts into the soft palate. It contributes to soft palate bulk, opens the Eustachian tube, and retracts the soft palate to bring it in contact with the posterior pharyngeal wall. Together the levator palatini and palatopharyngeus work with the superior constrictor to close the retropalatal pharynx, an event important in speech and swallowing (Table 2). Motor innervation to the soft palate is by the branches of the ascending pharyngeal plexus (X); however, the tensor veli palatini muscle associated with the Eustachian tube, is innervated by a branch of the mandibular nerve (V3). The blood supply to the palate is primarily from the descending palatine artery, a branch of the maxillary artery. The greater palatine artery branches from the descending palatine artery, then travels with the greater palatine nerve anteriorly on the junction of the hard palate and alveolar process. It enters the incisive canal and ultimately anastamoses with septal branches of the sphenopalatine artery in the nasal cavity. The lesser palatine arteries anastomose with the ascending pharyngeal (palatine branch), facial (ascending palatine branch) and dorsal lingual (tonsillar branch) arteries on the soft palate. These accessory vessels are an important source of blood supply to the palate in maxillary advancement surgery, when the greater palatine vessels are sectioned in the posterior cuts of the Lefort osteotomy. Pharyngeal lymphatic tissue predominates in an incomplete ring located in the pharyngeal (adenoid), tubal, palatine, and lingual tonsil regions known as Waldeyer’s ring (Fig. 11). The palatine tonsils are located in the fossa between the palatoglossal and palatopharyngeal arches. The pharyngobasilar fascia overlies the palatopharyngeus and superior constrictor muscles to create the tonsil bed. The dominant tonsillar blood supply is the tonsillar branch of the facial artery (Figs. 12 and 13). It travels through the superior constrictor muscle and enters the inferior tonsillar pole. Additional palatine tonsil blood supply includes tonsil branches of the ascending and descending palatine, lingual, and ascending pharyngeal arteries. The glossopharyngeal, vagus, and pharyngeal plexus branches innervate the tonsils and pharyngeal arch (Fig. 13). 4.3 Laryngopharynx The laryngopharynx or hypopharynx lies posterior to the larynx (Fig. 11) and extends from the tip of the epiglottis and pharyngoepiglottic folds to the inferior border of the cricoid cartilage, where it narrows and becomes continuous with the eso- phagus. The segment capable of collapsing is referred to as the retroepiglottic pharynx, which lies just posterior to the epiglottis. Posteriorly, the laryngopharynx is related to the bodies of C4–6 vertebrae. Its posterior and lateral walls are formed by the middle and inferior constrictor muscles. Anterior movement of the hyoid bone by muscle pull or by surgical intervention will dilate the retroepiglottic pharynx through traction on the hyoepiglottic ligament (Fig. 5).

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Figure 11 Interior of the pharynx, side view. (Modified from Grant’s Atlas of Anatomy, 10th ed. Baltimore, MD: Williams and Wilkins, 1999.)

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Figure 12 Interior of the pharynx dissected, side view. (Modified Grant’s Atlas of Anatomy, 10th ed. Baltimore, MD: Williams and Wilkins, 1999.) 4.4 The Pharynx The respiratory and alimentary passages become common in the middle part of the pharynx where the collapsing nature of the alimentary portion potentially compromises the respiratory passage during sleep, specifically, anterior obstruction from the palate (retropalatal), tongue (retroglossal), and epiglottis (retroepiglottic) and lateral pharyngeal wall collapse. Anatomically, the pharynx lies in front of the cervical vertebral column and prevertebral fascia and behind the nasal cavity, oral cavity, and larynx (Figs. 11 and 12). This fibromuscular tube has deficiencies in the walls at the nasal choanae, the oral cavity (oropharyngeal isthmus), and the laryngeal inlet. The lateral walls are complete except for the Eustachian tube openings in the nasopharynx. The mucosa of the nasopharynx is purely respiratory having respiratory

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Figure 13 Interior of the pharynx deep dissection, side view. (Modified from Grant’s Atlas of Anatomy, 10th ed. Baltimore, MD: Williams and Wilkins, 1999.) epithelium, the oropharynx mucosa is both respiratory and alimentary, and the laryngopharynx is alimentary having stratified squamous epithelium. Outside the mucosa is the pharyngobasilar fascia, which is the submucosa of the pharyngeal wall and is visible superiorly since there is no muscular layer external to it (Fig. 12). This fascia separates the epithelium from the pharyngeal constrictor muscles. The constrictor muscles are surrounded by a thin buccopharyngeal fascia, which allows the pharynx expansion and mobility and contains the pharyngeal plexus of nerves (7). The muscular wall of the pharynx is composed of two layers of three muscles each. The external layer is composed of circular constrictor muscles (superior, middle, and inferior), which contract serially to push a bolus down to the esophagus. The internal layer is composed of longitudinal muscles (palatopharyngeus, stylopharyngeus, and salpingopharyngeus), which elevate and dilate the pharynx to accommodate a bolus during swallowing (Figs. 12 and 13). The superior constrictor has a continuous anterior attachment to the medial pterygoid plate, pterygoid hamulus, pterygomandibular raphe, and posterior end of the mylohyoid line. From here it sweeps posteriorly to attach in the midline to the pharyngeal tubercle of the occipital bone (skull base) superiorly and to the pharyngeal raphe inferiorly. The

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middle constrictor has a relatively smaller anterior attachment from the lower portion of the stylohyoid ligament and lesser and greater cornu of the hyoid bone. It fans posteriorly to attach at the pharyngeal raphe enclosing the superior constrictor above and extending to the level of the larynx below. The stylopharyngeus muscle and glossopharyngeal nerve pass through the gap between the superior and middle constrictors. The inferior constrictor arises from the oblique line on the lamina of the thyroid and cricoid cartilage. The fibers arch upward overlapping the middle constrictor; inferior fibers from the cricoid cartilage run horizontally and constitute the cricopharyngeus muscle. The three constrictors are supplied by the branches of the pharyngeal plexus IX, X, IX (cranial root), and sympathetic plexus. The cricopharyngeus muscle is supplied by the external branch of the superior laryngeal nerve (X). The action of the pharyngeal constrictors is elevation and compression of the pharynx (7). The pharyngeus muscles (stylo-, salpingo, and palatopharyngeus) dilate the pharynx and elevate the larynx in phonation and swallowing (Table 3). The stylopharyngeus muscle arises from the medial aspect of the styloid process and descends close to the superior pharyngeal constrictor and passes through the gap between the superior constrictor and middle constrictor muscles before attaching to the posterior boarder of the thyroid cartilage. It elevates the larynx and pharynx and is supplied by the glossopharyngeal nerve (IX). The salpingopharyngeus muscle arises from the cartilage of the Eustachian tube, descending inside the superior constrictor muscle to attach like the stylopharyngeus to the thyroid cartilage. It lies within the muscular wall of the pharynx, adding an additional fold to the pharynx below the Eustachian tube. The salpingopharyngeus elevates the larynx and pharynx and opens the Eusta-chian tube. It is innervated by the pharyngeal plexus. The palatopharyngeus muscle originates from the palatine aponerosis and inserts on the posterior pharyngeal wall and thyroid cartilage. It elevates the larynx and pharynx while depressing the palate and is innervated by the pharyngeal plexus. The most important dilator of the pharynx is the genioglossus muscle and, to a minor extent, the tensor veli palatini (Tables 1 and 2). The tensor palatini may require palatopharyngeal muscle coordinated activation to adequately influence upper airway collapse (34). The geniohyoid and sternohyoid muscles are considered as dilators of the pharynx. The infrahyoid muscles (thyrohyoid, omohyoid, and sternohyoid) work in conjunction with the geniohyoid at the hyoid bone to enlarge the retroepiglottic laryngopharynx by tensing the hyoepiglottic ligament. According to Benumof (9), “The inspiratory patency of the retropalatal, retroglossal, and retroepiglottic pharynx is caused by contraction of the tensor palatini, the genioglossus, and the hyoid bone muscles, respectively.” Sources for anatomic obstruction of pharyngeal airway include inflammatory disorders that cause diffuse enlargement of lymphatic tissues, hypertrophy of tongue and pharyngeal muscles, extra-pharyngeal fat compression, and structural deformities. Neoplastic disease (benign and malignant), metabolic and traumatic abnormalities are rare and should be considered in the evaluation of the obstructed airway. Patients with craniofacial abnormalities and sleep apnea compared with normal controls have small retroposed mandibles, narrow PAS, enlarged tongues and soft palates, inferiorly positioned hyoid bones, and retroposition of their maxillas (24,26,36). Patients with mandibular retrognathia (SNB <74°) and morbid obesity (BMI >33kg/m2) are poor candidates for UPPP because it will not address the underlying process involving the

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lateral walls and retroglossal pharynx (37). Lymphoid hypertrophy causing airway obstruction may result in mouth breathing and deformities of the hard palate and upper maxillary dentition. The palatine tonsils cause obstruction of the lateral pharynx and displacement of palatoglossus and palatopharyngeus muscles. Lingual tonsil hypertrophy can obstruct the retroglossal and retroepiglottic airway in the midline. Both palatine and lingual tonsil hypertrophy respond well to a variety of surgical options (38). The lateral nasopharynx may have wall enlargement from tubal elevations (tori tubarii) from superior and posterior cartilaginous projections. In addition, muscle hypertrophy and lateral wall fold enlargement by the salpingopharyngeus muscle and palatopharyngeus muscles within the muscular wall may decrease the lateral airway space below the tubal elevations (Figs. 11–13). “The deposition of fat in the pharynx of OSA patients appears to be predominantly into the lateral walls of the pharynx and the volume of fat in the lateral pharyngeal walls correlates well with the severity of OSA. The converse is also true; weight loss improves the pharyngeal and glottic function of OSA patients. Fat deposition in the lateral walls not only narrows the airway but also changes the shape of the pharynx in obese patients from a long transverse (lateral) ellipse to a short transverse and long anterior-posterior axis. Pharyngeal dilator muscles that increase the upper airway size are located anterior to the pharynx and are less efficient with a long anteriorposterior elliptical axis” (9). The pharynx is innervated through the pharyngeal plexus. The pharyngeal plexus is a group of fine, ramifying nerve fibers on the posterior aspect of the pharynx which lie over the middle constrictor muscles. Motor innervation is derived from the vagus nerve (X), which supplies efferent motor fibers from the cranial part of the accessory nerve which originate within the nucleus ambiguous and supply the pharyngeal constrictor muscles, levator palate, salpingopharyngeus, palatopharyngeus, and palatoglossus (all striated muscles derived from brachial arches). The exceptions are stylo-pharyngeus supplied by the glossopharyngeal nerve (IX) and the tensor veli palatini by the trigeminal nerve (V3) (7). The vagus also supplies parasympathetic motor to the glands of the mucosa. Recent studies indicate that the glossopharyngeal nerve also supplies the levator veli palatini, pharyngeal constrictors, and cricopharyngeus muscles via its inputs to the pharyngeal plexus. Glossopharyngeal nerve activity has dilatory effects on the pharyngeal airway (14). Kuna (39) showed that stimulation of the glossopharyngeal nerve resulted in a greater increase in the lateral diameter of the retropalatal and oropharyngeal levels, whereas stimulation of the pharyngeal branch of the vagus decreased the retropalatal and retroglossal airways. Surgical treatment of the lateral wall to reduce soft tissue volume or increase tissue stiffening could potentially injure the glossopharyngeal nerve and potentially affect the dilator function of the stylopharyngeus muscle, possibly injuring the stylopharyngeus directly (Fig. 13). Sensory innervation of the pharynx is by the vagus nerve (X) from afferent general somatic fibers originating in the sensory nucleus of the trigeminal nerve via the maxillary nerve (pterygopalatine ganglion) to the nasopharynx. The glossopharyngeal nerve (IX) supplies afferent fibers from the pharyngeal mucosa of the mucous membrane below the nasopharynx. Sympathetic fibers from the superior cervical ganglion supply the blood vessels and are responsible for vasoconstriction within the pharynx. The blood supply of the pharynx is by multiple sources, most are branches of the external carotid artery and include the ascending pharyngeal, ascending palatine, facial,

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lingual, laryngeal, and superior and inferior thyroid arteries. Venous plexuses on the external surface of the larynx drain into the internal jugular vein. Lymph from the pharynx passes to the retropharyngeal lymph nodes and drains to the deep cervical nodes. The carotid and facial arteries are lateral to the middle and inferior constrictor muscles of the oropharynx and laryngopharynx (Fig. 13). These vessels would also be at risk of injury in surgical procedures treating the lateral pharynx at this level. Currently, surgical treatment of the obstructing pharynx is limited to “anterior wall therapy,” treating the soft palate, advancing the tongue and hyoid bone, and advancing the maxilla and mandible. Superior and lateral wall therapy is limited to adenoid and tonsil removal. The lateral pharynx probably plays a significant role in some cases of OSDB; however, this potential is not easily quantified or often studied by current methods. Although a consideration for surgical therapy, one should proceed with caution as the potential to damage the pharyngeal dilator nerves and muscles and carotid artery is significant. For this reason and the fact that the posterior pharyngeal wall is not at this time an option for airway enlargement therapy, continuous positive airway pressure and surgical procedures to treat anteroposterior collapse of the palate, tongue, and epiglottis will continue as standard therapy for OSDB. Surgeons are encouraged to use universal nomenclature for naming the obstructing pharyngeal segments in their studies to improve research and surgical outcome. We must continue to pursue accurate site of lesion testing to identify the obstructing level(s) that accurately depict the obstructing segment during sleep. By understanding the anatomy and physiologic mechanisms which support the open upper airway during sleep, we can better expand our role in the diagnosis and management of OSDB and continue to pursue surgical treatment procedures that produce safe, functional, and lasting results. REFERENCES 1. Horner RL. The neuropharmacology of upper airway motor control in the awake and asleep states: implications for obstructive sleep apnoea. Respir Res 2001; 2:286–294. 2. Mirza N, Lanza DC. The nasal airway and obstructed breathing during sleep. Otolaryn Clin North Am 1999; 32(2):243–262. 3. Janfaza P, Montgomery WW, Salman SD. Surgical Anatomy of the Head and Neck. Philadelphia, PA: Williams & Wilkins, 2001:259–272. 4. Kern EB. Rhinomanometry. Otolaryn Clin North Am 1973; 6:863. 5. Berger G, Balum-Azim M, Ophir D. The normal inferior turbinate: histomorphometric analysis and clinical implications. Laryngoscope 2003; 113(7):1192–1198. 6. Paff GH. Anatomy of the head and neck. Philadelphia, PA: W.B. Saunders Company, 1973:179. 7. Moore KL, Dalley AF. Clinically Oriented Anatomy. 4th ed. 4th. Philadelphia, PA: Lippincott Williams & Wilkins, 1999:1049–1059. 8. Mintz SM, Ettinger AC, Geist JR. Anatomic relationship of the genial tubercles to the dentition as determined by cross sectional tomography. J Oral Maxillofac Surg 1995; 53:1324. 9. Benumof JL. Obstructive sleep apnea in the adult obese patient: implications for airway management. Anesthesiol Clin North Am 2002; 20(4):789–811. 10. Yang C, Woodson BT. Upper airway physiology and obstructive sleep-disordered breathing. Otolaryngol Clin North Am 2003; 36(3):409–421. 11. Mathur R, Mortimer IL, Jan MA, Douglas NJ. Effect of breathing pressure and posture on palatoglosal and genioglossal tone. Clin Sci (Colch.) 1995; 89:441–445.

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12. Malhotra A, Huang Y, Fogel RB, et al. The male predisposition to pharyngeal collapse importance of airway length. Am J Respir Crit Care Med 2002; 166:1388–1395. 13. Li KK, Riley RW, Powell NB, Troell R, Guilleminault C. Overview of phase I surgery for obstructive sleep apnea syndrome. Ear Nose Throat J 1999; 78(11):836, 837, 841–845. 14. Kuna S, Remmers JE. Anatomy and physiology of upper airway obstruction. In: In: Principles and Practice of Sleep Medicine. 3rd ed. 3rd. Philadelphia, PA: W.B. Saunders Company, 2000:840–858. 15. Mallampati SR, Gatt SP, Gugino LD, Desai SP, et al. A clinical sign to predict difficult tracheal intubation: a prospective study. Can Anaesth Soc J 1985; 32(4):429–434. 16. Fujita S. Obstructive sleep apnea syndrome: pathophysiology, upper airway evaluation and surgical treatment. Ear Nose Throat J 1993; 72(1):67–72, 75–76. 17. Friedman M, Ibrahim H, Bass L. Clinical staging for sleep-disordered breathing. Otolaryngol Head Neck Surg 2002; 127(1):13–21. 18. Dempsey JA, Skatrud JB, Jacques AJ, et al. Anatomic determinants of sleep-disordered breathing across the spectrum of clinical and nonclinical male subjects. Chest 2002; 122:840– 851. 19. Woodson BT, Toohill RJ. Transpalatal advancement pharyngoplasty for obstructive sleep apnea. Laryngoscope 1993; 103(3):269–276. 20. Tebo HG, Telford IR. An analysis of the relative positions of the mental foramina. Anat Res 1950; 106:254 (abstract). 21. Castelli W. Vascular architecture of the human adult mandible. J Dent Res 1963; 42:786. 22. Riley R, Powell N, Guilleminault C. Inferior mandibular osteotomy and hyoid myotomy suspension for obstructive sleep apnea: a review of 555 patients. J Oral Maxillofac Surg 1989; 47:159–164. 23. Miles PG, Vig PS, Weyant RJ, et al. Craniofacial structure and obstructive sleep apnea syndrome—a qualitative analysis and meta-analysis of the literature. Am J Orthod Dentofacial Orthop 1996; 109:163–172. 24. Schwab RJ, Goldberg AN. Upper airway assessment: radiographic and other imaging techniques. Otolaryngol Clin North Am 1998; 31(6):931–968. 25. Shepard JW, Thawley SE. Evaluation of the upper airway by computerized tomography in patients undergoing uvulopalatopharyngoplasty for obstructive sleep apnea. Am Rev Respir Dis 1989; 140(3):711–716. 26. Trudo FJ, Gefter WB, Welch KC, et al. State-related changes in upper airway caliber and surrounding soft-tissue structures in normal subjects. Am J Respir Crit Care Med 1998; 158(4):1259–1270. 27. Williams PL, Warwick R, eds. Gray’s Anatomy. 37th ed. London: Churchill Livingston, 1989:1323–1330. 28. Rama AN, Tekwani SH, Kushida CA. Sites of obstruction in obstructive sleep apnea. Chest 2002; 122:1139–1147. 29. Badr MS. Pathogenesis of obstructive sleep apnea. Prog Cardiovasc Dis 1999; 41:323–330. 30. Rowley JA, Sanders CS, Zahn BR, Badr MS. Effect of REM sleep on retroglossal crosssectional area and compliance in normal subjects. J Appl Physiol 2001; 91:239–248. 31. Haung L, Williams JE. Neuromechanical interaction in human snoring and upper airway obstruction. J Appl Physiol 1999; 86(6):1759–1763. 32. Barsh CI. The origin of pharyngeal obstruction during sleep. Sleep Breath 1999; 3(1): 17–21. 33. Isono S, Tanaka A, Nishino T. Lateral position decreases collapsibility of the passive pharynx in patients with obstructive sleep apnea. Anesthesiology 2002; 97(4):780–785. 34. McWhorter AJ, Rowley JA, Eisele DW, et al. The effect of tensor veli palatini stimulation on upper airway patency. Arch Otolaryngol Head Neck Surg 1999; 125:937–940. 35. Yu X, Fujimoto K, Urushibata K, Matsuzawa Y, Kubo K. Cephalometric analysis in obese and nonobese patients with obstructive sleep apnea syndrome. Chest 2003; 124(1):212–218.

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36. Watanabe T, Isono S, Tanaka A, et al. Contribution of body habitus and craniofacial characteristics to segmental closing pressures of the passive pharynx in patients with sleepdisordered breathing. Am J Respir Crit Care Med 2002; 165(2):260–515. 37. Riley RW, Powell NB, Guilleminault C. Maxillary, mandibular, and hyoid advancement for treatment of obstructive sleep apnea: a review of 40 patients. J Oral Maxillofac Surg 1990; 48:20–22. 38. Suzuki K, Kawakatsu K, Hattori C, et al. Application of lingual tonsillectomy to sleep apnea syndrome involving lingual tonsils. Acta Otolaryngol Suppl 2003; 550:65–71. 39. Kuna ST. Effects of pharyngeal muscle activation on airway size and configuration. Am J Respir Crit Care Med 2001; 164:1236–1241.

2 The Anatomy of Sleep Disordered Breathing: An Evolutionary Perspective Terence M.Davidson Division of Otolaryngology—Head and Neck Surgery, University of California at San Diego and VA San Diego Health Care System, San Diego, California, U.S.A. Nothing in biology makes sense except in the light of evolution. —Theodosius Dobzhansky

1. INTRODUCTION Anatomy is the foundation on which the house of surgery is designed and built. Sleep disordered breathing (SDB) is an anatomic abnormality. In spite of our physical examinations, surgical procedures, and clinical studies, we have failed to fully define the anatomy of SDB and find a simple, successful operation to correct this morbid, mortal condition. It is possible that an evolutionary viewpoint answers the question of why anatomically modern Homo sapiens (H. sapiens) experience this disease and brings perspective to the anatomy. To elucidate the evolutionary concept, this chapter will describe the anatomic changes that have occurred in man’s evolution from our closest living primate relative, the chimpanzee, to modern man. The anatomic changes discussed herein are well described in the literature and are listed in Table 1. Table 2 describes several key terms. There are multiple theories on the cause of these modifications in man’s anatomy, including bipedalism, binocular vision, and expansion of the brain. A fourth view, possibly the most important, is that the changes were driven by man’s development of an upper respiratory tract to facilitate speech. Man is arguably the only animal that experiences SDB (2,3). Man is inarguably the only animal with complex speech. Man is also the only animal with a true oropharynx, the principal site of SDB. In order to speak and articulate vowels, the supralaryngeal vocal cord tract (SVT) requires a horizontal ratio (pharynx to lips) equal to the vertical ratio (vocal cords to pharynx) or SVTH:SVTV=1:1 (4,5). The SVT begins at the glottis, and

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Table 1 Anatomic Requirements and SVT Changes for Modern Speech Requirements

Changes

1:1 ratio SVTV to SVTH

Klinorynchy, laryngeal descent

Buccal speech

Laryngeal descent, shortened soft palate, loss of epiglottic-soft palate lock-up

Narrow, distensible, angulated SVT

Klinorynchy, anterior migration of foramen magnum, oropharyngeal tongue, acute craniobase angulation

Source: From Ref. 1.

includes the oropharynx and oral cavity. Figure 1 shows the 1:1 ratio in man, as compared to Pan troglodytes, the common chimpanzee. The 1:1 SVT required descent of the larynx and shortening of the face. As the larynx was left unprotected in the new, elongated oropharynx, the tongue, which is flat in most animals and generally restricted to the oral cavity, became rounded and rotated posteriorly into the oropharynx. This facilitates speech and protects the larynx during swallowing, but when man falls asleep and the muscles relax, the tongue falls into the oropharynx and obstructs the airway. Sleep apnea then ensues (6). Figure 2 is a drawing of the midsaggital section of the head of a goat, Capra hircus. Note the long mouth, small flat tongue, and high larynx. Figure 3(a) is an MRI of an adult H. sapiens. Note the short face, the large oropharyngeal tongue and the low larynx as compared to C. hircus. Figure 3(b) is a midsagittal MRI of the upper respiratory tract of an intubated, prone Rhesus monkey, Macaca mulatto, with the head extended. Comparisons to H. sapiens and C. hircus show the marked changes that have occurred to H. sapiens. This chapter will describe the upper aero-digestive tract of modern mammals using the common chimpanzee, our closest relative, review the anatomic evolutionary changes from chimpanzee to modern man, and last, explore current scientific work showing that these changes are more pronounced in those with increasing SDB severity. 2. ANATOMY P. troglodytes, the common chimpanzee, is an obligate nose breather. Air passes through the nose to the nasopharynx. The larynx sits high, adjacent to C2. The

Table 2 Key Terms Primates: Diverse order of mammals ranging from lemurs to humans. Man belongs to the family Pongidae, which includes the great apes, the genera Pongo (orangutans), Pan (chimpanzees), Gorilla (gorillas) and Homo (man) Homo sapiens (abbreviated H. sapiens): Genus and species of man. Anatomically modern man (abbreviated H. sapiens) separates this group from various taxa of “archaic” H. sapiens

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Pan troglodytes (abbreviated P. troglodytes): The common chimpanzee Supra vocal cord tract (abbreviated SVT): The voice passage from vocal cords to oral lips including the supraglottis, oropharynx, and oral cavity. The vertical segment, SVTV, extends from the vocal cords to the top of the oropharynx. The horizontal segment, SVTH, extends from the oropharynx to the lips Source: From Ref. 1.

Figure 1 Ratios of distances from incisor to pharynx and pharynx to larynx in H. sapiens and P. troglodytes. The 1:1 SVTV to SVTH ratio is shown on the left. For comparison, the same ratio for the common chimpanzee is shown on the right. (From Ref. 1.) epiglottis locks behind the long soft palate. The oropharynx, meaning soft palate to hyoid, is essentially nonexistent, so air passes from the nasopharynx directly into the larynx, i.e., it does not pass through an oropharynx. The mandible and maxilla are long and robust, primarily to hold the teeth. Using the formula of incisors (I), canine (C), premolars (P), and molars (M), nonhominid primates have 44 teeth designated: Maxilla

3I-1C-4P-3M = 44

Mandible

3I-1C-4P-3M

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Figure 2 Midsagittal view of C. hircus. Note the high position of the larynx relative to the descended position in man, the relationship of epiglottis to soft palate (epiglottic-soft palate lock-up), the facial projection, the long maxilla and mandible, the length of the sphenoid bone, the obtuse craniobase angle, the long palate to foramen magnum distance, and the small, flat tongue, which resides exclusively in the oral cavity. (From Ref. 7.) The tongue of nonhominid, modern mammals, primates included, is long, flat, and confined to the oral cavity. The tongue’s primary function is to bolus food to the hypopharynx for swallowing. The soft palate is long and drapes like a curtain in front of the epiglottis. Food is therefore shuttled under the soft palate, around the epiglottis, and directly into the hypopharynx, which is large in diameter. Prehominid mammals can typically breathe

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Figure 3 (Facing page) Midsagittal MRI of H. sapiens and Macaca mulatta. (a) T1 midsagittal MRI of an

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adult male H. sapiens. Note in comparison to Figs. 2 and 3(b), the narrow oropharynx, the short face, the low-lying larynx adjacent to the bottom of C4, and the large globular tongue. A portion of the tongue falls in the oropharynx. (b) T1 midsagittal MRI of the upper respiratory tract of a Rhesus monkey, M. mulatta. The anesthetized patient is sternal recumbent and the endotracheal catheter is placed transorally. As the animal is anesthetized, the head is extended. Compared to Fig. 3(a), note the long soft palate, the craniobase extension, the wide oropharynx, the high larynx with vocal cords adjacent to the bottom of C1, and the relatively small, flat tongue confined to the oral cavity. As the animal is intubated, the epiglottis has been pressed anteriorly, but in the nonintubated patient, would lock behind the soft palate. If one defines the superior end of the oropharynx as beginning at the level of the posterior end of the soft palate, then the upper and lower boundaries of the oropharynx essentially overlap and there is no oropharynx. Conversely, if one defines the oropharynx as beginning at the posterior border of the hard palate, then an oropharynx exists, but as can be seen, is quite wide. (Courtesy of Erik Wisner, D.V.M., University of California, Davis, School of Veterinary Medicine.)

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and swallow at the same time, advantageous both for respiration and for olfaction. As previously mentioned, the larynx is high, typically adjacent to C1–C2. Aspiration of food is uncommon. In H. sapiens, the nose is intended as the primary respiratory tract. However, humans with anatomic and inflammatory nasal problems use the oral cavity to assist in respiration. Most humans use their oral cavity for respiration during heavy exertion. Many suffer partial to total nasal obstruction when asleep and the oral cavity becomes a major part of the upper respiratory tract. Man’s nasopharynx is held open, as it is in animals, by a bony skeleton including the pterygoid bones laterally, the basisphenoid above, and the occipital bone and cervical spine posteriorly. Air must pass from the nasopharynx through the oropharynx to the laryngeal introitus. The oropharynx is a floppy, distensible tube and is partially supported by bone. This area can be filled with soft tissue including the tonsils, tongue, and soft palate. The top of the oropharynx is variably defined as beginning at the posterior hard palate or at the posterior soft palate. The bottom of the oropharynx is at the level of the hyoid. The valleculae lie at the level of the hyoid and may be used to define the inferior border of the oropharynx when viewed from above by direct or endoscopic inspection. The larynx is low, lying at the level of the bottom of C4. Once air enters the larynx, the respiratory tube is well supported by cartilage. Sleep apnea is a disorder almost exclusively of the oropharynx. This 2–3cm portion of the pharynx is the only piece of the respiratory tract not fully supported by skeleton. Man is really the only animal with an oropharynx. Other modern mammals have an oropharynx in theory, but in most animals, the distal nasopharynx connects directly to the proximal laryngopharynx (hypopharynx), so the oropharynx for all intents and purposes is a nonexistent structure. Even if one argues that the oropharynx extends from hard palate to hyoid and is an existing portion of the pharynx in animals, it is wide and short, and as the epiglottis protrudes superiorly, the respiratory tract is fully protected from the digestive tract and from the collapse of the surrounding soft tissue during sleep. While man’s oropharynx is easily distended, such as when exhaling against pursed lips, it is easily collapsed, as readily seen during a Mueller maneuver. As for deglutition, man’s oral cavity is short, barely holding 32 teeth, which are designated: Maxilla

2I-1C-2P-3M = 32

Mandible

2I-1C-2P-3M

This includes the wisdom teeth, i.e., the third molars, for which there is often little room. Man’s teeth are also significantly smaller than the teeth of similar-sized animals (8). They are reportedly 10% smaller than those in a similar-sized primate (9). There is little to no room for the four third molars and orthodontists often have the four premolars extracted to make room for orthodonture. This would leave man with 24 teeth designated: Maxilla

2I-1C-1P-2M = 24

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Mandible

35

2I-1C-1P-2M

Other mammals do not have impacted molars, even though they have more teeth, all of which are larger. In some humans, the oral cavity is particularly short in an anterior posterior direction and narrow in a coronal dimension. The soft palate is short compared to other animals. The oropharynx transcends a distance of 2–3cm. Food is bolused from the oral cavity to the oropharynx. During deglutition, food passes directly over the laryngeal introitus before passing into the hypopharynx. One hundred and forty-five years ago, Charles Darwin noted “…the strange fact that every particle of food and drink we swallow has to pass over the orifice of the trachea with some risk of falling into the lungs” (10). To protect the airway, the supraglottis must close and the oropharyngeal tongue must press the bolus through the oropharynx, over the larynx, and into the hypopharynx. It is unclear whether the epiglottis plays any role in deglutition as its resection rarely results in aspiration in contrast to the aspiration difficulties which occur following oropharyngeal tongue resection or supraglottectomy. In summary, the upper respiratory tract in nonhominid mammals is well supported throughout its length and clearly separated from the alimentary tract. The two tracts cross at the level of the epiglottis, but as the epiglottis sits high and locks behind the soft palate, and as the soft palate is long, food passes on either side of the airway. In man, the respiratory and alimentary tracts must share the floppy oropharynx. At one moment the oropharynx serves the respiratory tract and at another moment the oropharynx serves the alimentary tract. 3. EVOLUTIONARY ANATOMIC CHANGES Seen from an evolutionary perspective, the anatomy of man’s upper respiratory tract is particularly interesting. The driving force for recent evolutionary nonhominid change is the positive selection for speech (11). The changes seen are predicated on the fact that in order to pronounce vowels, the supralaryngeal vocal cord tract requires that SVTH:SVTV=1:1 (4,5). Conversely, other theories for recent evolutionary change, i.e., bigger brain, binocular vision, or bipedalism, would not have required the changes described in this chapter. There are several ways to view evolutionary change. The first is to choose some distant relative and examine the evolved differences. Man’s closest living relative is P. troglodytes, the common chimpanzee. This of course assumes that our mutually common ancestor, approximately 5 million years ago, looked more like P. troglodytes than H. sapiens. A second perspective is to assume that ontogeny recapitulates phylogeny or that development from embryo to adult in some manner reflects our phylogenetic development. This approach has been taught and held to be true by scientific students of evolution. A third way to view evolution is to examine fossils of more recent ancestors and to deduce from their skeletons what changes have occurred most recently.

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A fourth viewpoint is examination of the spectrum of variation in modern man to determine whether there is a correlation with anatomic changes, in this case, a correlation of anatomic change with increasing apnea-hypopnea index (AHI). All four approaches will be used to describe the evolutionary changes of the SVT that predispose man to SDB. 3.1 Klinorynchy Klinorynchy is the rotation of the splanchnocranium under the neurocranium (2). Figure 4 is an artist’s depiction of the evolution from P. troglodytes to

Figure 4 Klinorynchy as demonstrated by the evolution from P. troglodytes to H. sapiens. The lower right figure is a midsagittal view of P. troglodytes. The upper left figure is a midsagittal view of H. sapiens, with the tongue drawn in the awake position with the tongue base pulled forward. The upper right figure shows the splanchnocranium of

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P. troglodytes combined with the neurocranium of H. sapiens. The lower left shows the neurocranium of P. troglodytes combined with the splanchnocranium of H. sapiens. The key changes have not been driven by the expansion of the neurocranium over the midface, but rather the retrusion of modern man’s mid- and lower faces. (From Ref. 1.)

Figure 5 Side view of skulls of primates, showing progressive

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shortening of the muzzle, downward bending of the face below the eyes and forward growth of the chin. A. Eocene lemuroid; B. Old World monkey; C. Female chimpanzee, D. Man. (B and C after Elliot.) (From Ref. 12.)* H. sapiens. One might think the frontal lobes of the brain increased in size and pushed the forehead over the face. While the brain did expand anteriorly, the majority of the change comes from shortening of the maxillary bones, palatine bones, ethmoid bones, and mandible. Numerous sources document this shortening of the splanchnocranium (4,12). Figure 5, from the anthropology book, Our Face from Fish to Man, originally printed in 1929, shows klinorynchy from lemur to man. The change in dentition from 44 teeth in P. troglodytes to 32 teeth in H. sapiens further documents the shortening of the facial bones, specifically those bones surrounding the oral cavity, namely maxillary, palatine, and mandibular bones. *Originally printed in 1929. The author has made every effort to trace the copyright holders for this figure. If there is a copyright holder that has been inadvertently overlooked, the author will be pleased to make the necessary arrangements at the first opportunity.

Figure 6 Maxillae of P. troglodytes, Homo erectus, and H. sapiens. The

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maxilla of H. sapiens is short and wide. The teeth are crowded. The shortening of the maxilla is depicted in the lateral views. The arrows on the figure’s right depict the anterior rim of the foramen magnum and serve as a reference point for the posterior pharynx. Note the narrowing of the pharynx as depicted by the distance from the posterior maxilla to the anterior foramen magnum. (From Ref. 9.) 3.2 Anterior Migration of the Foramen Magnum The second change that shortened the SVTH was the anterior migration of the foramen magnum and the cervical spine. This is shown in Fig. 6. Examination of primate skulls shows that the foramen magnum is located more anteriorly the closer one gets to modern man (13). While one could opine that this helped balance the forward enlarging cranium and favored bipedalism, one can also opine that this further shortened the horizontal segment of the SVT, thereby improving speech. Keep in mind that the further the larynx descends, the longer the oropharynx extends, the more the respiratory and alimentary tracts overlap, and the more at risk is man of aspiration and asphyxiation. 3.3 Laryngeal Descent and Loss of Epiglottic-Soft Palate Lock-Up The next and perhaps most important change that occurred in man’s anatomy is laryngeal descent. Negus describes descent of the larynx in the classic text, The Comparative Anatomy and Physiology of the Larynx. Negus writes that the larynx and epiglottis in all animals reside superior to the oropharynx (please note that if the larynx resides superior to the oropharynx, there is no oropharynx). In many mammals, including dolphins, bears, and dogs, the larynx sits at the skull base. The monkey’s larynx is between the skull base and the first cervical vertebra. The cat and the squirrel have the lowest-lying larynx, which resides at the top of the first cervical vertebra (14). Only man has a descended larynx, which is located between the third and fourth

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Figure 7 The epiglottic-soft palate relationship and the descent of the larynx. (a) In the dog, Canis familiaris, the tongue resides exclusively in the oral cavity, the epiglottis and soft palate are locked up, and the larynx resides high in the neck. (b) In the common chimpanzee, P. troglodytes, the tongue resides exclusively in the oral cavity, the epiglottic-soft palate relationship persists, and the larynx is high. (c) In the infant H. sapiens, the epiglottic-soft palate lock-up persists (ontogeny recapitulates phylogeny), the larynx is high, and the tongue is primarily in the oral cavity. As the

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juvenile matures, the larynx descends and the tongue falls into the pharynx. (d) In the adult H. sapiens, the epiglottic-soft palate lock-up is lost. The larynx is descended. The tongue protrudes into the pharynx. (From Ref. 1.) cervical vertebrae in the human newborn and is located at the bottom of the fourth cervical vertebrae in the human adult. Figure 7(a–d) shows these relationships in the dog, the chimpanzee, the infant human, and the adult human. Negus’ view of the evolution of speech is summarized as follows. As primates assumed an upright position, they began to rely more on vision than on olfaction. This permitted the degeneration of the sense of smell and liberated the soft palate (14). The degeneration of the sense of smell liberated the soft palate from the necessity of contact with the epiglottis and allowed a gap to be interposed between the two. After separation had occurred, it became easy for laryngeal sounds to escape from the mouth and for the oral cavity, lips, and oral tongue to form vowel and consonant sounds, i.e., buccal speech. Primates and other modern mammals have a long soft palate to direct food rostrally, around the epiglottis, and toward the hypopharynx and cervical esophagus. In man, the soft palate is shortened. The uvula is in fact the remnant of the previously longer soft palate. As the palate shortened and the larynx descended, the epiglottic-soft palate lockup was lost. This allowed man to readily expire through the mouth and achieve buccal speech, clearly an important part of today’s speech, for it allows the oral cavity, tongue, cheeks, and lips to assist in articulation. Without buccal speech, we would be speaking through our noses. This does not explain the wide variation in soft palate length, thickness, and lateral attachment. The anatomic variations of the soft palate need to be further investigated. Figure 8(a,b) shows the epiglottis and soft palate as viewed from the posterior pharynx in the human infant and the human adult. Note the loss of the epiglottic-soft palate lock-up in the adult. Dorsal displacement of the soft palate (DDSP) in race horses is a further indication of how the epiglottis sticks up behind the soft palate (15–17) in most mammals. In the sprinting race horse, the soft palate will occasionally flip over the epiglottis and get stuck behind it. As the soft palate now flops on top of the larynx, the horse develops inspiratory stridor. This condition prevents the animal from completing the race and, in the absence of surgical correction, from further competition.

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Figure 8 Epiglottis-soft palate lock-up as viewed from the posterior pharynx. (a) In the human infant, the epiglottis overlaps the soft palate and food is diverted laterally around the epiglottis. Alimentation and respiration can occur concurrently. In animals, there is no uvula and the soft palate hangs like a curtain, further separating the alimentary and respiratory tracts. (b) In the human adult, the larynx is descended, the soft palate is shortened, and the epiglottic-soft palate lock-up is lost. While food theoretically channels around the larynx, there is a constant risk of aspiration. As Charles Darwin (10) wrote, “…every particle of food and drink which we swallow has to pass over the orifice of the trachea,

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with some risk of falling into the lungs, notwithstanding the beautiful contrivance by which the glottis is closed.” (From Ref. 1.) DDSP is confirmation that the normal anatomy is a larynx and airway well separated from the soft palate and oral cavity. This is accomplished by the airway protruding superiorly in an otherwise wide pharynx. 3.4 Oropharyngeal Tongue The oropharyngeal tongue of H. sapiens is well described in anatomy books and scientific literature. Crelin (13) notes that man is the only animal whose tongue resides partially in the pharynx. In all other animals, including the nonhuman primates, the tongue resides exclusively in the oral cavity. Negus (14) opines that the tongue is primarily designed for mastication and that a smaller, shorter tongue would suffice for this purpose. The human oral cavity is far smaller than that of a similar-sized nonhominid primate, yet the tongue remains approximately the same volume. It is likely that the tongue fills the oropharynx for two reasons. First, an oropharyngeal tongue is required to protect the descended larynx from aspiration and asphyxiation. Second, the oropharyngeal tongue is an important part of modulating speech and pronunciation of vowels and consonants, not to speak of pitch. Resection of the oropharyngeal tongue for cancer invariably results in dysphagia, dysarthria, and aspiration. 3.5 Craniobase Angulation Craniobase angulation, depicted in Fig. 9, is the relationship between the maxilla, ethmoid, sphenoid, and basioccipital bones. This creates a bend in the SVT. Craniobase angulation occurs early in the development of H. sapiens. Flexion is seen in H. sapiens, whereas extension is seen in nonhominid primates. In man, the cranial base flexes 8–16° postnatally. In P. troglodytes 15–28° degree flexions are seen postnatally (19). Craniobase angulation could certainly assist in downward gaze, such as that used when working with one’s hands, but just like the bend in a wind instrument, craniobase angulation helps to modulate speech.

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Figure 9 Differences in the orientation of the skull on the first two cervical vertebrae. Comparison of a bipedal (left) and a quadrupedal primate (right). (From Ref. 18.) 4. ONTOGENY RECAPITULATES PHYLOGENY All of the described anatomic changes focus on the evoution from P. troglodytes to H. sapiens. The same anatomic changes are seen in the ontogenetic development of the newborn to adult human. The newborn larynx is high. It lies between C3 and C4. It is readily viewed transorally. The pharynx is short and wide in an anterior posterior dimension. Newborns are obligate nose breathers. Newborns can drink and breathe concurrently, which implies an intact epiglottic-soft palate lock-up. This ability is not seen in adults, albeit attempted at one time or another by most beer drinkers. The pharynx of newborns is relatively wide, as readily seen in physical examination. Crelin (13) writes that the base of the newborn and young H. sapiens skull is similar in proportion to that of the adult chimpanzee and other nonhominid primates. So, in fact, the human newborn upper respiratory and alimentary tracts are much like the same tracts of the adult P. troglodytes. In the absence of congenital deformity, it is not surprising that infants and young children do not suffer from sleep apnea. Snoring and sleep apnea are seen in up to 10% of children as they develop. However, unlike the human adult, human preadolescents with snoring and sleep apnea can be cured by tonsillectomy in 90% of the cases.

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5. FOSSIL RECORDS Looking at a much shorter time frame, one can trace the fossil records of nonhominid skulls from archaic to modern species. Lieberman et al. (20) compare nonhominid skulls from the Pleistocene to recent human fossils, concluding that in H. sapiens …crania are uniquely characterized by two general structural autapomorphies [unique features]: facial retraction and neurocranial globularity. Morphometric analysis of the ontogeny of these autapomorphies indicates that the developmental changes that led to modern human cranial form derive from a combination of shifts in modern human cranial base angle, cranial fossae length and width and facial length. Similar observations for laryngeal descent and the oropharyngeal tongue do not exist as these are soft tissues and are not measurable in fossil records. 6. STUDIES ON ANATOMIC CORRELATIONS WITH SDB A series of scientific studies examine anatomic variables of the upper aerodigestive tract that correlate with severity of SDB. Cephalometrics has been used extensively to explore skeletal anatomy and SDB. While the “golden” cephalometric measurement has not been found, the evolutionary changes described in this chapter have been seen in many cephalometric SDB publications. These are summarized in Table 3. The UCSD Head and Neck Surgery Sleep Clinic performed cephalometric examinations on a consecutive series of patients undergoing sleep testing for symptoms of SDB. Figure 10 is the graph of hyoid to mandibular plane (H to MP) vs. AHI with a P value of <0.01. Figure 11 is the graph of menton to gonion (B to

Table 3 Cephalometric Studies Study

OSA vs.

Laryngeal

Craniobase

Sample

control

descent

angulation (%)

description

klinorynchy

(mm)

(%) Guilleminault et al. (21)

MP-H >20 vs. 12

60 patients: 30 OSA, 30 control

Jamieson et al. SNB 79 vs. 80 (22)

MP-H 27 vs. 16 N-S-Ba 1–9 vs. 132

196 patients separated by sex: 155 OSA (142 M, 13 F), 41 control (29 M, 20 F)

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De-Berry Borowiecki et al. (23) Strelzow et al. (24)

46

Go-H 41 vs. 34; A- Gn 67 vs. 62; A-B 42 patients: 30 OSA S-H 129 vs. 116 43 vs. 36; ANS-B 53 (27 M, 3 F), 12 control vs. 46; A-N 69 vs. (10 M, 2 F) 64; B-N 110 vs. 99 Go-Gn 71 vs. 75

Go-H 39 vs. 35; N-B 105 vs. 102 S-H 130 vs. 119

102 Caucasian male patients: 90 OSA, 12 control

Partinen et al. (25)

MP-H >125, correlates with increased RDI

157 OSA patients (143 M, 14 F) correlated cephalometric data with RDI

Lyberg (26,27)

H-Frankfort N-S-Ba 126 vs. 127 horizontal 106 vs. 133 vs. 96; Hmandibular line 27 vs. 17

35 male patients: 25 OSA, 10 control

Lowe et al. (28) Tangugsorn et al. (29)

Mandibular plane 105 patients: 80 OSA angle 36 vs. 32; facial (71 M, 9F), 25 control heights 133 vs. 127 (18 M, 7F) H-MP severe 27.8, nonsevere 24.2, control 17.1

FH-NSL control 6.76, nonsevere 8.71, severe 8.01; NSLOPT control 90.8, nonsevere 96.15, severe 100.36

136 Caucasian male patients: 49 severe OSA, 51 nonsevere OSA, 36 control

Battagel et al. (30)

Go-B 69 vs. 70 H-MP or MP-H N-S-Ba 126 vs. 127 vs. 73 26 vs. 23 vs. 22 vs. 133

Finkelstein et al. (31)

MP-H 25 vs. 17 N-S-Ba 130 vs. 132

160 patients: 100 OSA (86 M, 14F), 60 control (30 M, 30 F)

Hans et al. (32)

MP-H 25 vs. 17 N-S-Ba 129 vs. 129

Phase I—120 patients: 60 nonapneic, 60 apneic (85 M, 35 F); phase II—66 patients: 47 nonapneic, 19 apneic (43 M, 23 F)

Ito et al. (33)

MP-H 26 vs. 9

90 patients: 60 (? M/F ratio) OSA, 30 control (Japanese males, 13 nonobese OSA used for patients in this table)

Dempsey et al.

N-S-Ba 134 vs. 129

115 Caucasian male patients: 24 without snoring, 46 simple snoring, 45 OSA

Horizontal dimension 204 male patients: 142

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(34)

47

of the maxilla: portion vertical to supradentale; P-VA 88 vs. 102

nonclinical, 62 OSA

Note: RDI, respiratory disturbance index.

Figure 10 Scatter plot of measurement of hyoid to mandibular plane (H to MP) vs. AHI with a P value of <0.001. Go) vs. AHI with a P value >0.05. These findings support the hypothesis that facial shortening and laryngeal descent correlate with SDB. A particularly interesting cephalometric study examined the role of pharyngeal length in SDB. Upright and supine cephalograms were taken in control, mild, moderate, and severe male SDB patients. Oropharyngeal length and width were measured. The authors concluded that pharyngeal length increases with SDB severity. This is most apparent in the supine position (35). Similar results have been reported when examining cephalometrics and pharyngeal critical closing pressure (Pcrit): Sforza (36). Our results show that both pharyngeal soft tissue abnormalities and the lower position of the hyoid bone affect Pcrit in obstructive sleep apnea (OSA) patients, suggesting that an anatomic narrowing contributes to the upper airway collapsibility.

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Figure 11 Scatter plot of measurement of menton to gonion (B to Go) vs. AHI with a P value <0.001. Magnetic resonance imaging (MRI) has been another tool used to examine the upper respiratory tract. Malhotra et al. (37) studied the SVT of normal male and female humans using MRI. They defined the pharyngeal length and the distance from the hard palate to the base of the epiglottis. The study concluded that the average pharyngeal length was approximately 76mm in men and 58mm in women. When compared with women, men had increased pharyngeal airway length, increased soft palate area… The average male airway was substantially more collapsible than the average female airway based purely on anatomic features, with differences in airway length being the most important variable. Although it is not discussed in this chapter, it is likely that the male voice drove the selection for change. Women are attracted to the deep male voice, so the male voice has positive selection advantage for reproduction. A low-pitched, loud voice is also advantageous for hunting and battle, again strong selective advantages. Males have lower-pitched voices, so the evolutionary anatomic changes are greater in males than they are in females. SDB, a consequence of the anatomic evolution, is more prevalent in males than in females (38). It is therefore no surprise that the male oropharynx (described as the pharynx in the Malhotra et al. study) is longer in men than in women. Other MRI studies describe collapse of the oropharynx during OSA. Retropalatal and retrolingual collapse is seen (39,40). Oropharyngeal wall thickening is also noted (41). These studies support the hypothesis that the oropharynx is the anatomic site of SDB. If all the proposed anatomic changes evolved to facilitate speech and caused SDB, why was there no negative selection pressure preventing the changes? SDB does not

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manifest in humans until the fourth and fifth decades of life, which is beyond man’s procreative peak and until the last century, beyond man’s life expectancy. Therefore, the negative selection pressures of SDB were not operant. There is a neural component to speech and upper respiratory tract function. This must also be important to SDB. Lieberman’s (42) paper, “On the Nature and Evolution of the Neural Bases of Human Language,” is an excellent review. This review also goes into greater depth on speech and the anatomy of the SVT. While it is clear that the SVT 1:1 ratio is important to speech, minor changes in the SVT anatomy in an individual who has already developed language does not appear to make a difference in their voice. Maxillomandibular advancement is an example of this. 7. CONCLUSION Man’s upper respiratory tract anatomy evolved to facilitate speech. These changes resulted in an anatomy that predisposed man to SDB. The primary anatomic site of SDB is the oropharynx, a floppy segment of the pharynx where the respiratory and alimentary tracts cross and share a common passage. Veterinary anatomists only recently describe an oropharynx in other mammals, but if it exists, it is short and wide, and with the possible exception of bracycephalic dogs, does not result in SDB Hendricks (3). There are other sites where respiratory air flow can be restricted. Examples are nasal and nasopharyngeal obstructions, which can be the sole obstruction or can increase the negative pressures in the oropharynx, causing collapse during inspiration. The epiglottis may be another site. The SVT of H. sapiens has absolutely no redeeming feature other than facilitating speech. The small oral cavity contains 12 fewer teeth than our ancestors. Man is the only animal with impacted third molars. If infected, prior to antibiotics and dental extraction, this could lead to early death. The oropharyngeal tongue is not required for bolus formation and swallowing. It clearly contributes to SDB and probably is the main soft tissue obstruction in SDB. The long, narrow, floppy oropharynx is unique to man. It is the junction and crossover of the respiratory and alimentary tracts. The descended larynx has no value except to achieve a 1:1 ratio of the SVT. The descended larynx at the bottom of the long, floppy, narrow oropharynx places man at risk of aspiration, asphyxiation, and sleep apnea. If surgeons wish to improve SDB, they must focus their attention on enlarging or stiffening the pharynx and reducing intrusion by the surrounding soft tissues, including tonsils, soft palate, oropharyngeal tongue, floppy lateral pharyngeal walls, and possibly epiglottis. ACKNOWLEDGMENT This work was supported by a grant from ResMed and The Farrell Fund of the San Diego Foundation.

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REFERENCES 1. Davidson TM. The great leap forward: the anatomic basis for the acquisition of speech and obstructive sleep apnea. Sleep Med 2003; 4:185–194. 2. Barsh LI. The origin of pharyngeal obstruction during sleep. Sleep Breath 1999; 3:17–21. 3. Hendricks JC, Kline LR, Kovalski RJ, O’Brien JA, Morrison AR, Pack AI. The English bulldog: a natural model of sleep-disordered breathing. Am Physiol Soc 1987; 63:1344–1350. 4. Lieberman DE, McCarthy RC, Hiiemae KM, Palmer JB. Ontogeny of postnatal hyoid and larynx descent in humans. Arch Oral Biol 2001; 46:117–128. 5. Lieberman PEve Spoke. 47–48. New York: WW Norton and Company, 1988:139–141. 6. Noble H. Comparative functional anatomy of temporomandibular joint. Oral Sci Rev 1973; 3:3– 28. 7. McCracken TO, Kainer RA, Spurgeon TLSpurgeon’s Color Atlas of Large Animal Anatomy: The Essentials. Philadelphia, PA: Lippincott Williams and Wilkins, 1999:83. 8. Roberts D. The etiology of the temporomandibular joint dysfunction syndrome. Am J Orthod 1974; 66:498–515. 9. Miles AEW. The evolution of dentitions in the more recent ancestors of man. Proc R Soc Med 1972; 65:396–399. 10. Darwin COn the Origin of Species. Cambridge, MA: Harvard University Press, 1964:191. 11. Diamond JThe Third Chimpanzee: The Evolution and Future of the Human Animal. New York: Harper Collins Publishers, 1992:21, 23, 32–56. 12. Gregory WKOur Face from Fish To Man. New York: Hafner Press, 1963:59. 13. Crelin ESThe Human Vocal Tract: Anatomy, Function, Development and Evolution. New York: Vantage Press, Inc., 1987:97, 220, 223–224. 14. Negus VE The Comparative Anatomy and Physiology of the Larynx. New York: Grune and Stratton, Inc., 1949:21, 187. 15. Ducharme NG, Hackett RP, Woodie JB, Dykes N, Erb HN, Mitchell LM, Soderholm LV. Investigations into the role of the thyrohyoid muscles in the pathogenesis of dorsal displacement of the soft palate in horses. Equine Vet J 2003; 35(3):258–263. 16. Parente EJ, Martin BB, Tulleners EP, Ross MW. Dorsal displacement of the soft palate in 92 horses during high-speed treadmill examination (1993–1998). Vet Surg 2002; 31(6):507–512. 17. Franklin SH, Naylor JR, Lane JG. The effect of tongue-tie in horses with dorsal displacement of the soft palate. Equine Vet J Suppl 2002; Sep(34):430–433. 18. Ankle-Simons F Primate Anatomy: An Introduction. 2nd ed.. San Diego, CA: Academic Press, 2000:255. 19. Lieberman D, McCarthy RC. The ontogeny of cranial base angulation in humans and chimpanzees and its implications for reconstructing pharyngeal dimensions. J Hum Evol 1999; 36:487–517. 20. Lieberman D, McBratney BM, Krovitz G. The evolution of cranial form in Homo sapiens. Proc Natl Acad Sci USA 2002; 3:1134–1139. 21. Guilleminault C, Riley R, Powell N. Obstructive sleep apnea and abnormal cephalometric measurements: implications for treatment. Chest 1984; 86(5):793–794. 22. Jamieson A, Guilleminault C, Partinen M, Quera-Salva M. Obstructive sleep apneic patients have craniomandibular abnormalities. Sleep 1986; 9(9):469–77. 23. De-Berry Borowicki B, Kukwa A, Blanks RHI. Cephalometric analysis for diagnosis and treatment of obstructive sleep apnea. Laryngoscope 1988; 98:226–234. 24. Strelzow VV, Blanks RHI, Basile A, Strelzow AE. Cephalometric airway analysis in obstructive sleep apnea syndrome. Lanryngoscope 1988; 98(11):1149–1158. 25. Partinen M, Guilleminault C, Quera-Salva M, Jamieson A. Obstructive sleep apnea and cephalometric roentgenograms, the role of anatomic upper airway abnormalities in the definition of abnormal breathing during sleep. Chest 1988; 93(6):1199–1205.

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26. Lyberg T. Cephalometric analysis in patients with obstructive sleep apnoea syndrome: I. Skeletal morphology. J Laryngol Otol 1989; 103:287–292. 27. Lyberg T. Cephalometric analysis in patients with obstructive sleep apnoea syndrome: II. Soft tissue morphology. J Laryngol Otol 1989; 103:293–297. 28. Lowe AA, Fleetham JA, Adachi S, Ryan CF. Cephalometric and computed tomographic predictors of obstructive sleep apnea severity. Am J Orthod Dentofacial Orthop 1995; 106(6):589–595. 29. Tangugsorn V, Krogstad O, Espeland L, Lyberg T. Obstructive sleep apnoea: multiple comparisons of cephalometric variables of obese and non-obese patients. J Craniomaxillofac Surg 2000; 28:204–212. 30. Battagel JM, Johal A, Kotecha B. A cephalometric comparison of subjects with snoring and obstructive sleep apnoea. Eur J Orthod 2000; 22:353–365. 31. Finkelstein Y, Wexler D, Horowitz E, Berger G, Nachmani A, Shapiro-Feinberg M, Ophir D. Frontal and lateral cephalometry in patients with sleep disordered breathing. Laryngoscope 2001; 111:634–641. 32. Hans MG, Nelson S, Pracharktam N, Baek SJ, Strohl K, Redline S. Subgrouping persons with snoring and/or apnea by using anthropometric and cephalometric measures. Sleep Breath 2001; 5(2):79–91. 33. Ito D, Akashiba T, Yamamoto H, Kosaka N, Horie T. Craniofacial abnormalities in Japanese patients with severe obstructive sleep apnoea syndrome. Respirology 2001; 6:157–161. 34. Dempsey J, Skatrud JB, Jacques A, Ewanowski SJ, Woodson T, Hanson P, Goodman B. Anatomic determinants of sleep disordered breathing across the spectrum of clinical and nonclinical male subjects. Chest 2002; 122(3):840–851. 35. Pae E-K, Lowe AA, Fleetham JA. A role of pharyngeal length in obstructive sleep apnea patients. Am J Orthod Dentofacial Orthop 1997; 111:12–17. 36. Sforza E, Bacon W, Weiss T, Thibault A, Petiau C, Krieger J. Upper airway collapsibility and cephalometric variables in patients with obstructive sleep apnea. Am J Respir Crit Care Med 2000; 161:347–352. 37. Malhotra A, Huang Y, Fogel RB, Pillar G, Edwards JK, Kikinis R, Loring SH, White DP. The male predisposition to pharyngeal collapse: importance of airway length. Am J Respir Crit Care Med 2002; 166:1388–1395. 38. Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med 1993; 328(17):1230–1235. 39. Ciscar MA, Juan G, Martinez V, Ramon M, Lloret T, Minguez J, Armengot M, Marin J, Basterra J. Magnetic resonance imaging of the pharynx in OSA patients and health subjects. Eur Respir J 2002; 17(1):79–86. 40. Trudo FJ, Gefter WB, Welch KC, Gupta KB, Maislin G, Schwab RJ. State-related changes in upper airway caliber and surrounding soft tissue structures in normal subjects. Am J Respir Crit Care Med 1998; 158:1259–1270. 41. Schwab RJ. Properties of tissues surrounding the upper airway. Sleep 1996; 19(10):S170– S174. 42. Lieberman P. On the nature and evolution of the neural bases of human language. Yearb Phys Anthropol 2002; 45:36–62.

3 Physiology of Sleep Disordered Breathing B.Tucker Woodson and Chris Yang Department of Otolaryngology and Communication Sciences, Medical College of Wisconsin, Milwaukee, Wisconsin, U.S.A. 1. INTRODUCTION The human upper airway is challenged with the difficult task of maintaining ventilation while simultaneously serving other functions including alimentation, phonation, and speech. In some individuals the upper airway becomes the limiting factor in respiratory gas exchange of oxygen and toxic carbon dioxide. The upper airway’s contribution to sleep disordered breathing represents a broad continuum of disorders. The spectrum can range from intermittent snoring and partial obstruction of the airway, to complete obstruction causing frequent, overt apneic events associated with significant medical morbidity and mortality. Most of the pathophysiologic processes for each are similar, differing in degree, not in nature. Although the most of the discussion presented in this chapter regards the pathophysiology of airway obstruction in adults, the principles also apply to the pediatric airway. Our current understanding of upper airway collapse indicates that multiple elements contribute to obstruction, but that the major cause is that anatomic and structural abnormalities interact with normal physiologic mechanisms (1). Obstruction and collapse during sleep is a complex phenomenon. Physiologic factors contributing to collapse may include alterations in neuromuscular tone, ventilatory control and periodicity, vascular tone, surface tension forces, arousal thresholds, and expiratory positive pressure. Structural variables include the craniofacial framework and anatomic soft tissue mass. It is exceptional to find patients whose obstructive sleep apnea (OSA) is caused by a single factor. Rather, the disease processes that instigate this disorder are multi-faceted abnormalities, which may or may not be individually pathologic. The pathology of OSA is rooted in multiple factors which often act additively and synergistically to cause upper airway compromise. One of the biggest challenges we face today lies in identifying and precisely evaluating the multitude of these variables to develop better treatments. The frequent number of unsatisfactory medical and surgical treatments for OSA illustrates the need for further progress in this area. Future research will enable us to treat beyond our current boundaries. To accomplish this, knowledge of these factors, both individually and collectively, is essential.

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1.1 Concepts of Airway Collapse Historically, two basic schools of thought existed to describe the genesis of airway collapse, “active” vs. “passive” mechanisms. Weitzman et al. (2), in 1978, proposed the active theory. They noted that there was spasmodic closure of the lateral pharyngeal walls and closure of the velopharynx timed at the end of expiration, immediately preceding the subsequent inspiration. Endoscopic observation of the velopharynx demonstrated “spasmodic” sphincteric closure, which was maintained for the duration of inspiration. Brief airway openings occurred intermittently during early expiration or following arousals. It was speculated that the mechanism of velopharyngeal closure was “apparently by active muscle contraction.” Closure also occurred inferior to the level of the velopharynx at the level of the tongue base and supraglottis. This closure was not observed to occur with expiration, but instead occurred during subsequent inspiratory efforts. The concept that active muscular contraction contributed to sleep related airway obstruction has not been widely accepted as the primary mechanism for airway closure in sleep apnea and snoring. In humans, electromyographic studies of pharyngeal constrictors have not documented expiratory muscle activity occurring with airway closure (3). Although, these human studies argue against a simple contraction of constrictor muscles to actively close the airway, recent animal studies performed during sleep while creating a prolonged expiration (i.e., central apnea) demonstrate a potential alternative mechanism. During early expiration, inhibition of both pharyngeal dilators and constrictor muscles is observed (4). However, subsequent recovery of muscle activity in later expiration is unequal with dilator muscles having less activity compared to constrictor muscles. This difference creates a relative imbalance in favor of forces that may contribute toward airway collapse. The imbalance is greater during wake than during sleep, raising the possibility, yet untested, that muscle imbalance may occur during arousal and not during sleep. Although muscle imbalance may exist in humans, studies have not identified constrictor activation or dilator inhibition prior to or following apnea. Although data are insufficient to totally exclude Weitzman’s idea that active muscle forces may contribute to collapse, subsequent models do not require active mechanisms. The currently most advocated concept of airway collapse focuses on passive mechanisms and the crucial role of the interaction of the dilating activity of pharyngeal muscles, the bulk of the tongue, and negative intraluminal pressures with inspiration. Sauerland and Harper (5) observed in 1978 that with the onset of non-rapid eye movement (NREM) sleep, apnea subjects lost both phasic and tonic muscular tongue activity. These findings contrasted with the results of several adult subjects who snored. Genioglossus activity was augmented in adults who snored during inspiration with the onset of NREM sleep. Normal individuals who did not snore were not observed to have significant electromyographic activity in the genioglossus muscle during wakefulness or NREM sleep. This suggested that muscle activity was important in maintaining stability but that loss of muscle activity alone was inadequate to create airway closure. They speculated that in patients with “particular conditions…such as a large tongue” displacement of the tongue and associated structures occurs with a loss of muscle activity. If the upper airway collapsed beyond a “critical point” in these patients, then a combination of both collapse and negative inspiratory airway pressures could result in airway obstruction. During inspiration, the airway was sucked closed due to an imbalance of muscle tone and negative inspiratory pressure.

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2. STATIC AND DYNAMIC FORCES When conceptualizing the upper airway, it is often very easy to oversimplify the many complex interactions. Classically, collapse of the upper airway has been thought to occur during inspiration when negative inspiratory pressure and airflow predominate. However, collapse is not limited to inspiration and also occurs during expiration. Critical events occur during expiration. It is when passive collapse and static characteristics predominate that the majority of structural collapse occurs. Although biologically the hypoxemia and arousal of sleep disordered breathing is an inspiratory disease, it is mechanically a disorder of expiration. Dividing various forces into static and dynamic components helps in better conceptualizing what determines the size of the upper airway (6). Static determinants of the airway can be thought of as the intrinsic pharyngeal characteristics such as craniofacial framework and upper airway soft tissue mass. Major dynamic forces include phasic neuromuscular tone and airflow (7,8). Other dynamic components may include surface tension forces which increase collapse and impede opening, vascular compliance, which may alter upper airway size, and segmental interactions of the upper airway during inspiration and expiration (9–11). All forces have multiple complex physiologic levels of control, many of which are yet to be adequately described. 2.1 Neuromuscular Tone Neuromuscular tone is the primary determinant of upper airway dilation during wake and sleep and is under complex regulation. In OSA, muscle tone is increased during wake compared to non-apneic “normals.” Augmented muscle activity in OSA patients is reduced during sleep (Fig. 1). The nature of the mechanisms that underlie these changes remains incompletely understood and they involve both the central and the peripheral nervous systems, muscle and tissue changes, among other factors. Muscle tone is determined by central respiratory neurons that affect both the diaphragm and the upper airway muscles via the phrenic and hypoglossal nerves. Central respiratory neurons are affected by multiple stimuli including sleep state (wake, NREM, and REM sleep), ventilation (hypercarbia and hypoxia), and upper airway mechanoreceptors. Upper airway muscle activity may be both phasic and tonic. Phasic activity is linked to the ventilation cycle. The effects of sleep/wake state on different upper airway muscles are non-uniform (12). In many postural and upper airway muscles, tonic muscle activity decreases progressively with depth of sleep, with a part of this activity maintained during NREM (but not phasic REM) sleep (Fig. 2). In contrast, for many upper airway muscles (such as the genioglossus, ala nasi, stylopharyngeus, styloglossus) phasic muscle tone is lost during sleep. A loss of inspiratory phasic activity occurs acutely at transitions from sleep to wake. The combined loss of tonic upper airway and compensatory phasic upper airway muscle activities creates airway instability.

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Figure 1 Changes in pharyngeal upper airway muscle tone in patients with OSA and normal subjects (lower panel). Sleep onset (arrow) is associated with decrease in tonic muscle tone in both groups. Awake to sleep transitions are associated with loss of phasic muscle tone until CNS activation associated with apneas occurs (vertical lines). A pictorial representation of integrated EMG activity (upper panel) is provided. The etiology of phasic upper muscle activity is twofold, and critical in understanding neuromuscular control of the upper airway. Independent central nervous system (CNS) and peripheral nervous system mechanoreceptors contribute. Central mechanisms preactivate upper airway muscles during inspiration. The resulting upper airway muscle activity stabilizes the upper airway when negative inspiratory forces are generated by the diaphragm (13). This activity is independent of upper airway mechanoreceptors. Upper airway pre-activation, but not diaphragm activity, is suppressed by various sedative medications including alcohol and benzodiazepam medications. These drugs favor an imbalance of upper airway collapsing forces over dilating forces, and may worsen upper airway obstruction. The second mechanism driving phasic upper airway muscle activity is upper airway mechanoreceptors (14,15). Receptors primarily located at the level of the epiglottis are sensitive to negative airway pressure. Stimulation activates the upper airway muscles.

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These reflexes are present in both OSA and non-apneic individuals. In non-apneic individuals, the reflex is not active during resting breathing during

Figure 2 A sleep related decrease in muscle tone and its associated increase in upper airway resistance with differing levels of NREM sleep. (Modified from Tangle, et al. J Appl Physiol 1991; 70:2574–2581)

Figure 3 Pattern of collapse as a function of the ventilatory cycle in both OSA and normal subjects. The presence of phasic upper airway muscle activity contributes to significant variability in OSA patients. This activity in fluctuations and airway

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size is not present in normal individuals. wakefulness. During augmented breathing (such as during exercise), this reflex mechanism may be activated. In OSA patients, this reflex likely mediates the increased upper airway muscle activity present during wakefulness. Acutely following the transition from wake to sleep, changes in the brainstem occur and this reflex is lost (16). When this occurs in subjects without sleep disordered breathing, airway stability is not critically affected. However, in OSA upper airway collapse is augmented. In non-apneic, anatomically “normal” individuals, the combined effects of loss of expiratory phasic upper airway muscle tone and tonic muscle tone during sleep are not sufficient to cause significant flow limitation. This contrasts with individuals with abnormal upper airway anatomy. In this group, loss of phasic muscle tone and decreased muscle tone during sleep, results in upper airway obstruction. Because the loss of muscle tone is greatest at end expiration, collapse is maximal at end expiration on nonobstructed breaths (Fig. 3) (17). Because this collapse is not dependent on negative forces within the airway, it is referred to as static collapse. Collapse during obstructed breaths may be further augmented in two ways by dynamic forces. During some breaths, static collapse of the upper airway results in a minimal airway diameter that exceeds the minimal protective threshold at end expiration, inspiratory forces then dynamically close and obstruct the airway (18). During other breaths, static collapse causes complete airway closure, the subsequent inspiratory effort then occurs with a closed airway and results in no flow. In both types of closure, the associated increased work of breathing during obstruction causes mechanical stress. Lower airway mechanoreceptors then mediate, in turn, CNS activation. Depending on the patient host factors and severity of the event, this results in brainstem (autonomic blood pressure or heart rate change) or cortical (EEG) arousal, muscle activation, airway opening, and resumption of ventilation. Decreased airflow results in asphyxia. Increased work of breathing and mechanoreceptor stimulation results in CNS arousal and sleep fragmentation. These contribute to the medical and pschophysiologic manifestations of OSA. 2.2 Other Effects of Sleep on the Upper Airway Both REM and NREM sleep are associated with multiple physiologic changes compared to wakefulness (19). With the onset of sleep, the control of ventilation by the CNS is altered in several ways. The CNS drive to neurons that contribute to tonic upper airway muscle tone is reduced. The factors which normally stimulate ventilation (hypoxia and hypercapnia) are also altered by sleep. Hypoxic ventilatory drive is reduced in NREM and markedly decreased in REM sleep. Hypercapneic drive is also reduced in NREM and REM sleep. Hypoventilation (leading to both hypoxia and hypercarbia) may occur if other physiologic mechanisms are not activated. During NREM sleep, ventilation is primarily under chemical control (primarily via carbon dioxide). Fragmented NREM sleep may significantly affect ventilation. The mechanisms are complex and involve oscillations in chemical ventilatory control during sleep and changes in CO2 (Fig. 4). Arousals and brief awakenings serve to rapidly increase the brainstem’s CO2 sensitivity. Activation of central respiratory neurons may cause ventilatory overshoots

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(increased drive) followed by ventilatory undershoots (decreased drive) with the rapid resumption of sleep. If the decrease in carbon dioxide levels is below a critical hypocapneic ventilatory threshold, ventilatory undershoots result in central apneas or central hypopneas. Alternatively, reductions in ventilatory drive may not create a central apnea but may cause a periodic breathing pattern with oscillating decreases and increases in respiratory muscles activity. Oscillations in muscle activity to the diaphragm and upper airway muscles are not uniform with some muscles such as the genioglossus more susceptible to loss of ventilatory drive. Furthermore, in patients with sleep disordered breathing where upper airway muscle drive is crucial in maintaining airway size, even a small loss of upper airway drive may result in airway obstruction. Periodic ventilation therefore contributes to upper airway obstruction. As noted previously, mechanoreceptor mediated increases in upper airway muscle tone have been noted to be critical in maintaining upper airway patency in patients with OSA. Mechanoreceptors are known to serve a role in reflex mediated compensatory pharyngeal dilator muscle activity when exposed to collapsing negative inspiratory forces. Their importance is greater in patients with OSA than

Figure 4 The interaction of small upper airways, increased resistance (with associated increase carbon dioxide), and the effects of sleep on muscle tone. Changes in sleep state and the associated changes in central ventilatory control augment normal physiologic reflexes, which result in decreased central respiratory drive and worsening of upper airway obstruction. (See text for details.)

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in normal patients as they must compensate for their poor anatomy. This has been demonstrated in laboratory-based studies that show that both peak and phasic genioglossus EMG activities are significantly higher in OSA patients than in normal controls during wakefulness. The stimulatory effect of negative inspiratory pressure can be ameliorated when continuous positive airway pressure (CPAP) is applied. When CPAP is applied to OSA patients during wakefulness, there is a marked decrease in genioglossus EMG activity, whereas normal subjects display essentially no change (20). Furthermore, waking muscle tone decreases following application of topical oropharyngeal anesthesia (21). The importance of these receptors during sleep is demonstrated by the worsening of obstruction in snorers who have oropharyngeal topical anesthesia during sleep. This suggests that mechanoreceptor mediated neuromuscular compensation reflexes may be critical in OSA, but not necessarily in normal, subjects. Mechanoreceptors also play a significant role in the arousal response in OSA (22). Reopening of the upper airway during obstructive events is associated with increase in upper airway muscle tone to levels above baseline activity. This increase requires arousal, awakenings, and change in the sleep state. As the work of breathing increases as a result of increased hypercapneic ventilatory drive, increased mechanoreceptor stimulation occurs as apnea progresses. Increased mechanoreceptor stimulation resulting from arousal induced increase in CO2 sensitivity ultimately leads to activation of upper airway muscles resulting in reopening of the upper airway. Hence, it is mechanoreceptor stimulation that is the primary mediator of cortical arousal and changes in sleep state. Abnormalities of the upper airway mechanoreceptor mediators are implicated in the pathophysiology of OSA. Some of these abnormalities may be acquired and include evidence of decreases in pharyngeal sensitivity and evidence of pharyngeal nerve damage. These are speculated as possibly resulting from the vibratory trauma of snoring. Histopathologic studies have demonstrated evidence of both muscle bundle hypertrophy and muscle fiber degeneration and damage (23). The etiology of these changes may include eccentric contraction during stretch as well as from motor neuron damage (24). Lengthening or stretching during muscular contraction (eccentric contraction) results in muscle fiber damage and hypertrophy. Immunohistopathologic changes in muscle fiber types are also consistent with muscle denervation and reinervation (25). Electron microscopy and other studies have demonstrated motor neuron damage in OSA. The ultimate result is potential muscle damage and hypertrophy. Hypertrophy may further contribute to an impingement on airway size while muscle damage may decrease muscle elastance, strength of contraction, and force of dilation (26). 3. STRUCTURE Physiologic variables are important contributors to apnea, however, by far the most significant abnormality that can predispose one to developing OSA are structural abnormalities (27,28). Current evidence supports the axiom that abnormal upper air-way structure is the fundamental abnormality in OSA. Structural factors may affect airway size, compliance, and shape. Each of these contributes to airway collapse and flow limitation during sleep. Airway shape has received little rigorous evaluation; however,

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abnormalities of both size and compliance (collapsibility) have been associated with the presence and severity of OSA (Fig. 5).

Figure 5 Differences in airway collapsibility are associated with different levels of sleep disordered breathing. Critical airway closing pressure (Pcrit) measures airway stability and collapse. Individuals with apnea require positive pressure to maintain stability. Normal individuals have stable airways that require the application of negative pressure to close the airway. Although the epicenter of the abnormality lies within the pharynx, no single morphologic abnormality defines the disorder (Fig. 6). The three major structural determinates of OSA include obesity, soft tissue, and skeletal structure (29). Differences in structural abnormalities exist depending on ethnicity, gender, obesity, and age (30–34). In children adenotonsillar hypertrophy is a predominant, although not unique, cause (35). Craniofacial structural abnormalities also are present in childhood (36). Adenotonsilar hypertrophy may compromise preferentially airways structurally predisposed to obstruction. In adults, no single structural abnormality has been identified with this disorder and the presence of multiple anatomic abberations is common. Isolated anatomic pathologies in adults are uncommon. Instead, the anatomy in patients with sleep disordered breathing is disproportionate, with both soft tissue and skeletal structure contributing to an underlying anatomic vulnerability. When combined with the normal

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physiologic changes associated with sleep, airway obstruction occurs. The site of obstruction is variable (Fig. 6). Obesity has

Figure 6 Patterns of manometric upper airway collapse are depicted. The retropalatal segment is the most common single segment of obstruction but most subjects demonstrate a mixed pattern of collapse and obstruction. important associations with OSA. Obesity increases the risk and severity of OSA and the severity of hypoxemia during sleep. It is unclear which of the multiple mechanisms may contribute to the association of obesity with OSA. Although fat distribution around the neck and airway may compromise the airway, additional factors include alterations in metabolic control, changes in lung volume, and other soft tissue changes may contribute (33,37–39). 3.1 Craniofacial Characteristics The skeletal and cartilage framework are the supporting foundation for the soft tissues which ultimately determine airway size and compliance. Abnormalities of the framework result in a small and unstable upper airway that is vulnerable to collapse. Given the variable nature of the human facial structure, identifying any single facial structural abnormality is unlikely. Instead, a constellation of abnormalities have been consistently observed (Fig. 7). When comparing OSA from normal non-snoring controls, craniofacial variables associated with OSA include increased distance of the hyoid bone from the mandibular plane, a decreased mandibular and maxillary projection, a downward and posterior rotation “dolicocephalic” of facial development (in contrast to anterior growth), increased vertical length of the upper airway, and increased cervical angulation. The hyoid position is consistently identified as an important association in sleep disordered breathing, serving as a central anchorage

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Figure 7 Common lateral cephalometric x-ray abnormalities associated with OSA are depicted: an inferior placed hyoid (A), increased length and width of the soft palate (B), increased apposition of the tongue and palate in repose (C), and decreased projection of the maxilla and mandible (D). for the tongue muscles that partly determines the position of the tongue, a marker of tongue mass, with a more inferiorly positioned hyoid associated with increased tongue size, and a marker of the contribution of the hypopharynx to the overall pharyngeal dimensions. A major problem of studies assessing the relationship of cephalometric structure to OSA risk is that most lack appropriate control groups. Control subjects may be of a different age, weight and gender, and “normal” is often based only on clinical assessment and not on polysomnographic documentation. A study of middle-aged employees of the state of Wisconsin, evaluated facial structure and obesity (Wisconsin Cohort of Sleep

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Disordered Breathing) and identified major contributors to both the risk and the severity of OSA (29). Overall two-thirds of the variability of the apnea-hypopnea index was explained by facial structure and obesity. In subjects with lower body mass index, the major contributor was facial structure. The most important component identified was decreased projection of the maxilla. Given the known central role of the maxilla in craniofacial development this suggests that OSA is primarily a disorder of maxillary not mandibular development. The pharyngeal airway is clearly critical in contributing to sleep disordered breathing. In many aspects, the human upper airway is unique among mammals (40). In other mammals the larynx is positioned near the skull base creating a physiologically separate respiratory and alimentary pathway. In the most extreme form, the whales have developed an epiglottic remnant that extends superiorly and is rotated caudally to form the blowhole. The intimate relationship of the larynx to the skull base results in a highly stable upper airway that is independent of upper airway muscle tone. The process of laryngeal descent in humans, which may have facilitated the development of speech (klinoraphy), however, resulted in the creation of a soft tissue supraglottic airway that often requires muscle tone to maintain stability. This change occurs with aging (Fig. 8). Major modifications in the position and function of the tongue and larynx are present in adult humans. Whereas, in most mammals the tongue is located within the oral cavity, in humans, the posterior tongue resides in the pharynx and makes up the wall of the anterior hypopharynx. The laryngeal location in the neck increases airway length and airway instability. Length is increased both in males and in subjects with OSA (41,42). Ultimately,

Figure 8 Differences in upper airway length between infants (left) and adults (right). In infants, the tongue compromises a shorter segment of the pharyngeal airway and the larynx may reside at the level of the second cervical vertebrae. In nonapneic adults, the larynx may reside at the fourth

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cervical vertebrae and studies demonstrate a more inferior position in patients with obstructive sleep apnea. physiologic fluctuations in muscle tone of the tongue and other pharyngeal muscles increase the risk of upper airway obstruction. 3.2 Nose Nasal obstruction may contribute to the presence and severity of OSA (43). Nasal blockage may: (1) reduce nasal afferent reflexes which help to maintain muscular tone, (2) augment the tendency for mouth opening which destabilizes the lower pharyngeal airway (by posterior rotation, vertical opening, and inferior displacement of the hyoid), and (3) increase upstream airway resistance increasing downstream airway collapse (44). A multitude of pathologies cause nasal obstruction and warrant appropriate evaluation. 3.3 Body/Jaw Position/Gravity Body position alters airway size and collapsibility. The upper airway changes following movements from sitting to supine as well as lateral decubitus to supine (45). Tissue mass, change in lung volume, tracheal tug, and vascular volume may contribute to the changes observed. Studies directed at identifying the effects of gravity in non-apneic subjects during parabolic flight have demonstrated that the lower pharynx and retroepiglottic airway are affected more than other segments by gravity (46). The upper pharynx and upper tongue base are not altered. In apneic subjects, the isolated effects of gravity have not been evaluated. It is speculated that in apneics with a more unstable upper airway, gravity contributes to obstruction in the lower pharynx, and affects all segments depending on the mass of the tissues involved. The lateral body position provides a more stable upper airway configuration than the supine position. 3.4 Pharyngeal Soft Tissues In adults no single soft tissue structure contributes to OSA. The relative contribution of soft tissue size differs among individuals and particularly between ethnic groups (47). Current genetic research associates abnormalities in soft tissues to African-American populations with skeletal abnormalities more common in Caucasians and Asian populations (48,49). The size as well as the position of the tongue are important considerations in OSA. In the supine position, the tongue projects posteriorly and is counteracted by the tone of the genioglossal muscle. MRI volumetric studies have identified tongue size as a major predictor of OSA. Another soft tissue upper airway abnormality is the lateral pharyngeal wall (50). The lateral wall is composed of muscle, blood vessels, and fat. Anatomically these structures are highly vascular and the effectiveness of low CPAP pressures (5–15cm H2O) suggests that venous blood volume may contribute significantly to the abnormal lateral wall size observed (Fig. 9) (51). The soft palate occupies significantly more of the upper pharyngeal space and has overall increased dimension than in the normal individual. The

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cross-sectional shape of the airway in apneics tends to be more elliptical rather than more circular. The elliptical shape increases the surface area of the airway and frictional resistance compared to a more circular conduit. Additionally, an airway with a long axis in an anterior-posterior direction (in the mid-sagittal plane) will be less affected by contraction of major airway dilators such as the genioglossus muscle. Apnea is more severe when airways are elliptically shaped with the long axis in the mid-sagittal plane. Given this knowledge, we still

Figure 9 Collapsibility of the lateral pharyngeal wall is depicted at differing levels of nasal CPAP pressure. Anterior-posterior dimensions are minimally affected by CPAP. The lateral walls are affected by small amounts of pressure consistent with high compliance. The etiology of this high compliance is speculative but may be due to venous blood volume. have only a minimal understanding of the contribution of the lateral wall to OSA. The lateral walls are highly compliant and are the main structures that are impacted and altered by nasal CPAP. Other mechanisms contributing to passive narrowing may include tissue surface adhesive forces (52). Increased surface tissue adhesion contributes to airway collapse, and lubricants decrease airway collapse. An additional study shows upper airway pressure flow characteristics during NREM sleep demonstrate a hysteresis. At the same

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pressure, flow is decreased in late inspiration point compared to early inspiration. This phenomenon suggests that surface adhesive forces contribute to collapse. Lung volume has significant effects on pharyngeal upper airway size. The dependence of pharyngeal airway size on lung volume occurs during wakefulness and sleep (53). In general, increased lung volume increases pharyngeal size and decreased lung volume contributes to pharyngeal collapse. Postulated mechanisms of this association have included reflex activation of upper airway dilator muscles or the mechanical effects of tracheal and thoracic traction. The most likely effect is via direct mechanical interactions. Thoracic traction markedly influences pharyngeal size and patency. The mechanism of this effect is mediated through the mediastinum, intrathoracic pressures, and the trachea. Commonly, referred to as “tracheal tug”, this has been shown to contribute to pharyngeal patency independent of neuromuscular activity or upper airway muscle support (Fig. 10). It is postulated that passive tracheal traction alters pharyngeal collapsibility by increasing longitudinal tension and stability on the pharyngeal wall (54,55). Blood volume changes in the head and neck may affect upper airway size. In human subjects, pharyngeal upper airway size may be altered by changes in leg elevation (56). This effect is mediated presumably through changes in central venous blood volume. As noted previously, nasal CPAP changes most the highly compliant and

Figure 10 Effects of tracheal tug and longitudinal tension on the airway. Inferior displacement of the trachea and/or hyoid bone increases longitudinal tension of the pharyngeal airway and decreases collapsibility. vascular lateral pharyngeal walls. This association raises the enticing possibility that blood volume changes may contribute to airway collapse in sleep. Expiratory obstruction and flow limitation are common in adults who snore and OSA patients (57). This is in contrast to normal subjects who fail to demonstrate induced expiratory flow limitation. Expiratory airway obstruction results in expiratory positive airway pressure (auto-PEEP). This both increases the work of breathing and decreases upper airway stability (58). Studies of both non-apneic and apneic individuals

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demonstrate that during both wakefulness and sleep, positive expiratory intraluminal pressure dilates the airway (59,60). Woodson (61) suggested the novel hypothesis that in patients with OSA who have lower pharyngeal and tongue base levels of obstruction, this obstruction decreases the effect of positive expiratory pressures on dilating rostrally located retropalatal segments (Fig. 11) (11). This loss

Figure 11 Behavior of multi-element model of the pharynx is depicted for expiration. Without lower pharyngeal obstruction (left) positive pressure contributes to stability of both lower and upper pharyngeal segments. With lower pharyngeal obstruction (right), positive expiratory pressure (+) is not transmitted to the upper pharyngeal segments. Cross-sectional airway size in the retropalatal segment (lower) collapses more on obstructed (solid line) than on non-obstructed (dotted line) breaths. of dilating forces decreases retropalatal size and predisposes the upper airway to obstruction on subsequent inspiratory breaths. Our understanding of airway collapse during expiration is inadequate. It is known that airway size and ventilation are observed to decrease progressively during expiration in the breaths prior to apnea (Fig. 12) (61). In OSA subjects, at the onset of expiration in non-obstructed breaths, the cross-sectional area increases. The airway then collapses

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during the latter half of expiration. This pattern of expiratory collapse begins several breaths before the actual apnea. Collapse becomes significant when a critical decrease in airway size is reached. At this critical threshold value, the collapsing forces of negative inspiratory pressure, Bernoulli forces, and surface adhesive forces combine to create airway closure. Though inspiration is important in causing closure, it is only one element in the process. Cross-sectional airway size during inspiration only decreases when airway size and other flow limiting characteristics predispose the airway to collapse. Even in severe OSA, it is only the inspiratory breath immediately preceding apnea that demonstrates any abnormality. Inspiratory collapse is a secondary phenomenom. Primary collapse is an expiratory phenomenon. Airway shape is critical in airway collapse and contributes to the distribution of frictional and streamlined flow in the airway. Circular tubes are more efficient than those that are flat (62). How shape determines surgical outcomes is unknown but likely significant. Early observations of airway shape focused on the role of muscle action on the upper airway and were compiled on patient populations of severe OSA with obesity where marked lateral wall collapse resulted in sagitally oriented airways (63). With changes in the nature of OSA, sagittally oriented airways are now clinically uncommon. Regardless, airway shape is likely a critical feature of collapse airflow limitation and surface adhesive forces.

Figure 12 Progressive expiratory collapse of the upper airway preceding apnea. Flow and pressure (upper two panels) are minimally changed (upper panel). Cross-sectional airway size and end expiration (arrows) progressively

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decrease preceding apnea. Note that the airway size at the peak of inspiration is essentially unchanged prior to apneic events. 4. BALANCE OF FORCES AND STARLING RESISTOR The multitude of anatomic and physiologic processes so far described only begin to touch on the true complexity of the upper airway. Integrating these and other factors into a manageable concept is difficult. One method that allows this integration is the concept of “balance of forces.” Dynamic upper airway collapse may be further understood by applying the concept of the “Starling resistor” which describes flow in collapsible tubes. At any instant in time, upper airway size is determined by the combined contributions of multiple structural and physiologic variables. The balance of forces model allows an accurate description of how multiple variables alter upper airway size (Fig. 13). Airway size is determined by both dilating and collapsing forces. Dilating forces include; upper airway muscle tone, mechanical force of the airway wall struoture, and positive intraluminal airway pressure. Collapsing forces include; tissue mass, surface adhesive forces, and negative intraluminal pressures. The resulting difference in these forces is the distending force which acts on the wall of the upper airway. When the distending force increases, the airway size increases; when it decreases, the airway size decreases. The distending force of the upper airway is the transmural pressure (Ptm) of the airway. The equation Ptm=Pout−Pin defines transmural pressure, where Pout represents the sum of the dilating upper airway forces and Pin represents the sum of the collapsing forces. Another, more clinically relevant, means to conceive of the forces that act on the upper airway is by considering the skeletal airway structure as a constant and describe the dynamic forces as being either tissue pressures or luminal pressures (Ptm=Ptissue−Pluminal). Tissue pressure includes the forces from tissue mass, tissue elastance, surface tension, and neuromuscular dilating and collapsing forces. Luminal pressures include the segmental airway pressure (Pairway) and pressures relating to airflow (Pflow). As noted above, airway pressures may be dilating (if positive such as with expiration or with the application of external

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Figure 13 The principle of the balance of forces. Transmural forces (Ptm) on the upper airway are depicted. As Ptm increases, the airway enlarges; as Ptm decreases the airway collapses. Ptm is described by the basic equation Ptm=Pout−Pin. Ptm may also be described as the difference between tissue forces (Ptissue) and luminal (Pluminal) or airway forces (i.e., Ptm=Ptissue−Pluminal). (See text for details.) positive airway pressures) or collapsing (such as during inspiration). Studies have been able to replicate a syndrome identical to OSA in non-OSA subjects by applying negative pressures to the upper airway during sleep. Although seemingly esoteric, such a model (Ptm=Pluminal−Ptissue) provides a means of quantifying upper airway collapse. The compliance (dA/dP) of the upper airway represents the tendency of the upper airway to collapse during respiration. Airway compliance can be calculated allowing measurement of the intrinsic collapsibility of the upper airway. The effects of airflow on decreasing luminal pressures are determined by its velocity and are described by Bernoulli’s equation. If airflow velocity is 0, (Pluminal=Pairway+0) and if neuromuscular tone is held constant (Ptissue=k), then the measured airway pressure represents the distending or transmural pressure of the upper airway (Ptm=Pairway−k). This measured pressure combined with measures of upper airway size allows calculation of airway compliance (dA/dP) independent of physiologic influences. Airway pressure can be measured and manipulated (such as with nasal CPAP) to assess changes in airway size and compliance.

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4.1 Starling Resistor The Starling resistor concept describes flow in collapsible tubes, which serves as an ideal model for the upper airway (Fig. 14). In the human upper airway, the collapsible tube is the supraglottis and pharynx. Upstream pressure is ambient pressure and downstream pressure is pleural pressure. During wakefulness, low negative pleural pressures (i.e., 5cm H2O) combined with a large upper airway (the result of multiple balance of forces) result in unimpeded flow. During sleep, changes occur in the balance of forces, and distinct clinical populations occur. In non-apneic non-snoring patients, a structurally larger upper airway remains patent. In snorers and

Figure 14 Characteristics of a Starling resistor. In the model a basin with two attached rigid tubes is spanned by a collapsible segment (upper left). Behavior of an ideal Starling resistor is depicted for differing conditions of upstream pressure (Pus). The pressure difference (i.e., transmural pressure=Pin−Pout=Ptm) across the airway determines the nature of flow. In the upper right, fluid fills the basin such that the pressure outside the tube (Pout) is greater than the pressure inside (PinPout), the

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tube is patent and flow occurs. In the lower right figure, flow increases by more positive upstream pressures and unchanged downstream pressures. apneic subjects, a structurally small upper airway results in a cascade of pathologic events. The Starling resistor concept builds upon Poiseuille’s law, which describes flow in noncollapsible tubes. Poiseuille’s law states that V=P1–P2/R, where V is the flow, P1 is the pressure upstream, and P2 is the pressure downstream. The resistance component (R) is determined by the length of the tube (L), fluid viscosity (η), and radius (r) of the tube (R= resistance=8ηL/πr4). Since viscosity and length are constant, changes in resistance are primarily related to changes in the area of the tube. Since area is unchanged in a rigid tube, flow in a non-collapsible airway depends significantly on pressure across the tube (P1−P2=driving pressure). This contrasts to a collapsible, Starling resistor airway where flow may be independent of driving pressure. In a Starling resistor, resistance is variable and resistance and flow are primarily determined by airway size. Airway size is determined by the surrounding forces that act on the airway. In a simple collapsible tube (i.e., a tube with a wall without intrinsic structural forces that is often modeled with a penrose drain placed between two rigid tubes) the airway size determinant forces are primarily the upstream and downstream airway pressures and flow. Three basic clinical patterns can be observed which include normal breathing, snoring, and obstruction. Likewise, three possible conditions of flow across a collapsible upper airway exist and may include unimpeded flow, flutter, and obstruction. These three conditions are determined by the balance of three groups of pressures exerted on the upper airway. These are the downstream pressure (Pds or negative inspiratory pressure), the upstream pressure (Pus or ambient pressure), and the transmural pressure (Ptm). For the condition of unimpeded flow, transmural pressure is greater than both downstream and upstream pressures (Ptm>Pus>Pds). Because transmural pressure is greater than other pressures, airway collapse does not occur and airway size and resistance are not altered. This contrasts with the condition of obstruction where transmural pressures are less than both downstream and upstream pressures (Pus>Pds>Ptm). With a negative transmural pressure, airway size is 0 and no flow occurs. When transmural pressure is less than upstream pressure but greater than downstream pressure (Pus>Ptm>Pds), the condition of flutter occurs. A choke point or narrowing of the airway occurs in the segment of the collapsible upper airway that is exposed to negative transmural pressure. In this segment airway size decreases (in an ideal Starling resistor, the resultant airway size is 0). When the airway is closed, there is no flow and the segment becomes exposed to upstream pressure, which dilates the upper airway. However, when flow occurs, this segment is again exposed to downstream pressure, which acts to collapse this segment. Repeating this cycle results in the choke point being exposed to alternating upstream or downstream pressures depending on the presence of flow in the airway. The result is flutter. Due to these characteristics, flow in a collapsible tube in patients at risk of OSA is not determined by the difference between upstream and downstream pressures (driving pressure) but rather by the difference between upstream pressures and the pressures surrounding the collapsible segment (22). In a structurally patent airway, the pressure

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difference across the collapsible tube wall is of minimal importance; however, in an airway that is more vulnerable to collapse these forces may become a major determinant of airway cross-sectional area and therefore resistance to air flow. 5. CONCLUSION Upper airway competence involves complex interactions between anatomy and physiology. For most, OSA is an abnormality of a structurally small and abnormally collapsible upper airway interacting with physiologic mechanisms. So far, simplistic models have hampered progress in this field. Thus, successful medical and surgical treatment of OSA continues to be elusive for too many patients. Great strides remain to be seen but the possibility of major advances is within reach. REFERENCES 1. Ayappa I, Rapoport DM. The upper airway in sleep physiology of the pharynx. Sleep Med Rev 2003; 7:9–34. 2. Weitzman ED, Pollak CP, Borowiecki BB, Shprintzen R, Rakoff S. The hypersomniasleep apnea syndrome: site and mechanism of upper airway obstruction. In: Guilleminault C, Dements WC, eds. Sleep Apnea Syndromes. Kroc Foundation Series. Vol. 11. New York: Alan R Liss Inc., 1978:Ch 15. 3. Guilleminault C, Hill M, Simmons FB, et al. Passive constriction of the upper airway during central apneas: fiberoptic and EMG investigations. Respir Physiol 1997; 108:11–22. 4. Feroah T, Forster HV, Pan L, et al. Effect of slow wave and REM sleep on thyropharyngeus and stylopharyngeus activity during induced central apneas. Respir Physiol 2001; 124:129–140. 5. Sauerland EK, Harper RM. The human tongue during sleep: electromyographic activity of the genioglossus muscle. Exp Neurol 1976; 51:160–170. 6. Remmers JE, deGroot WJ, Sauerland EK, Anch AM. Pathogenesis of upper airway occlusion during sleep. J Appl Physiol 1978; 44:931–938. 7. Malhotra A, Pillar G, Fogel RB, et al. Pharyngeal pressure and flow effects on genioglossus activation in normal subjects. Am J Respir Crit Care Med 2002; 165:71–77. 8. Fogel R, Malhotra A, Pillar G, et al. Genioglossal activation in patients with obstructive sleep apnea versus control subjects—mechanisms of muscle control. Am J Respir Crit Care Med 2001; 164:2025–2030. 9. Jokic R, Klimaszewski A, Mink J, Fitzpatrick M. Surface tension forces in sleep apnea: the role of a soft tissue lubricant—a randomized double-blind, placebo-controlled trial. Am J Respir Crit Care Med 1998; 157:1522–1525. 10. Shepard J, Pevernagie D, Stanson A, et al. Effects of changes in central venous pressure on upper airway size in patients with obstructive sleep apnea. Am J Respir Crit Care Med 1996; 153:250–254. 11. Woodson BT. Expiratory pharyngeal airway obstruction during sleep: a multiple element model. Laryngoscope. 2003; 113(9):1450–1459. 12. Series F. Upper airway muscles awake and asleep. Sleep Med Rev 2002; 6:195–212. 13. Strohl KP, Hensley MJ, Hallet M, Saunders NA, Ingram RH. Activation of upper airway muscles before onset of inspiration in normal humans. J Appl Physiol 1983; 53: 87–98. 14. Malhotra A, Pillar G, Fogel RB, et al. Pharyngeal pressure and flow effects on genioglossus activation in normal subjects. Am J Respir Crit Care Med 2002; 165:71–77.

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15. Mezzanote WS, Tangle DJ, White DP. Influence of sleep onset on upper-airway muscle activity in apnea patients versus normal controls. Am Rev Respir Crit Care Med 1996; 153:1880–1887. 16. Mezzanote WS, Tangle DJ, White DP. Waking genioglossal electromyogram in sleep apnea patients versus normal controls (a neuromuscular compensation mechanism). J Clin Invest 1992; 89:1571–1579. 17. Schwab RJ, Gefter WB, Hoffman EA, Gupta KB, Pack AI. Dynamic upper airway imaging during respiration in normal subjects and patients with sleep disordered breathing. Am Rev Respir Dis 1993; 148:1385–1400. 18. Tuck S, Remmers J. Mechanical properties of the passive pharynx in Vietnamese potbellied pigs. II. Dynamics. J Appl Physiol 2002; 92:2236–2244. 19. Dempsey J, Smith C, Harms C, Chow C, Saupe K. Sleep and breathing state of the art review: sleep-induced breathing instability. Sleep 1996; 19(3):236–247. 20. Deegan PC, Nolan P, Carey M, McNicholas WT. Effects of positive airway pressure on upper airway dilator muscle activity and ventilatory timing. J Appl Physiol 1996; 81(1):470–479. 21. Liistro G, Stanescu D, Veriter C, Rodenstein D, D’Odemont J. Upper airway anesthesia induces airflow limitation in awake humans. Am Rev Respir Dis 1992; 146:581–585. 22. Kimoff RJ, Cheong TH, Olha AE, et al. Mechanisms of apnea termination in obstructive sleep apnea: role of chemoreceptor and mechanoreceptor stimuli. Am J Respir Crit Care Med 1994; 149:707–714. 23. Woodson BT, Garancis JC, Toohill RJ. Histopathologic changes in snoring and obstructive sleep apnea syndrome. Laryngoscope 1991; 1010:1318–1322. 24. Petrof BJ, Pack AI, Kelly, Eby J, Hendricks JC. Pharyngeal myopathy of loaded upper airway in dogs with sleep apnea. J Appl Physiol 1994; 76(4): 1746–1752. 25. Friberg D. Heavy snorer’s disease: a progressive local neuropathy. Acta Otolaryngol 1999; 119(8):925–933. 26. Sériès F, Cote C, St Pierre S. Dysfunctional mechanical coupling of upper airway tissues in sleep apnea syndrome. Am J Respir Crit Care Med 1999; 159(5 Pt 1):1551–1555. 27. Isono S, Remmers J, Tanaka A, et al. Anatomy of the pharynx in patients with obstructive sleep apnea and in normal subjects. J Appl Physiol 1997; 82:1319–1326. 28. Galvin JR, Rooholamini SA, Standford W. Obstructive sleep apnea: diagnosis with ultrafast CT. Radiology 1989; 171:775–778. 29. Dempsy JA, Skatrud JB, Jacques AJ, Ewanowski SJ, Woodson T, Hanson PR, Goodman B, Young T. Anatomical determinates of sleep disordered breathing across the spectrum of clinical and non-clinical subjects. Chest 2002; 122:840–851. 30. Lyberg T, Krogstad O, Djupesland G. Cephalometric analysis in patients with obstructive sleep apnea syndrome: skeletal morphology. J Laryngol Otol 1989; 103:287–292. 31. Lyberg T, Krogstad O, Djupesland G. Cephalometric analysis in patients with obstructive sleep apnoea syndrome: soft tissue morphology. J Laryngol Otol 1989; 103:293–297. 32. Pracharktam N, Hans MG, Strohl KP, et al. Upright and supine cephalometric evaluation of obstructive sleep apnea syndrome and snoring subjects. Angle Orthod 1994; 64:63–74. 33. Mortimore I, Marshall I, Wraith P, et al. Neck and total body fat deposition in nonobese and obese patients with obstructive sleep apnea compared with that in control subjects. Am J Respir Crit Care Med 1998; 157:280–283. 34. Will MJ, Ester MS, Ramirez SG, Tiner BD, McAnear JT, Epstein L. Comparison of cephalometric analysis with ethnicity in obstructive sleep apnea syndrome. Sleep 1995; 18:873– 875. 35. Aren R, McDonough JM, Costarino AT, Mahboubi S, et al. Magnetic resonance imaging of the upper airway structure of children with obstructive sleep apnea syndrome. Am J Resp Crit Care Med 2001; 164:698–703. 36. Zucconi M, Caprioglio A, Calori G, Ferini-Stambi, Oldani A, et al. Craniofacial modifications in children with habitual snoring and obstructive sleep apnoea: a case control study. Eur Respir J 1999; 13:411–17.

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37. Do K, Ferreyra H, Healy J, et al. Does tongue size differ between patients with and without sleep-disordered breathing? Laryngoscope 2000; 110:1552–1550. 38. Bradley T, Brown I, Grossman R, et al. Pharyngeal size in snorers, nonsnorers, and patients with obstructive sleep apnea. N Engl J Med 1986; 315:1327–1331. 39. Kryger M, Felipe L, Holder D, et al. The sleep deprivation syndrome of the obese patient—a problem of periodic nocturnal upper airway obstruction. Am J Med 1974; 56:531–539. 40. Lieberman DE, McCarthy RC. The ontogeny of cranial base angulation in humans and chimpanzees and its implications for reconstructing pharyngeal dimensions. J Hum Evol 1999; 36:487–517. 41. Malhotra A, Huang Y, Gogel R, et al. The male predisposition to pharyngeal collapse: importance of airway length. Am J Respir Crit Care Med 2002; 166:1388–1395. 42. Pae EK, Lowe AA, Fleetham, JA. A role of pharyngeal length in obstructive sleep apnea patients. Am J Orthod Dentofacial Orthop 1997; 111:12–17. 43. Young T, Finn L, Kim H. Nasal obstruction as a risk factor for sleep-disordered breathing. Allergy Clin Immunol 1997; 99:757–762. 44. Meurice J, Marc I, Carrier G, Sériès F. Effects of mouth opening on upper airway collapsibility in normal sleeping subjects. Am J Respir Crit Care Med 1996; 153:255–259. 45. Martin S, Marshall I, Douglas N. The effect of posture on airway caliber with the sleepapnea/hypopnea syndrome. Am J Respir Crit Care Med 1995; 152:721–724. 46. Beaumont M, Fodil R, Isabey D, Lofaso F, Touchard D, Harf A, Louis B. Gravity effects on upper airway area and lung volumes during parabolic flight. J Appl Physiol 1998; 84(5):1639– 1645. 47. Schwab RJ, Gefter WB, Hoffman EA, Gupta KB, Pack AI. Dynamic upper airway imaging during respiration in normal subjects and patients with sleep disordered breathing. Am Rev Respir Dis 1993; 148:1385–1400. 48. Redline S, Tishler PV, Hans MG, et al. Differences in sleep disordered breathing in African Americans and Caucasians. Am J Respir Crit Care Med 1997; 155:186–192. 49. Schwab RJ, Parirstein M, Pierson R, Mackley A, et al. Identification of upper airway anatomic risk factors for obstructive sleep apnea with volumetric magnetic resonance imaging. Am J Respir Crit Care Med 2003; 168(5):522–530. 50. Schwab RJ, Gupta KB, Gefter WB, Metzger LJ, Hoffman EA, Pack AI. Upper airway and soft tissue anatomy in normal subjects and patients with sleep-disordered breathing. Significance of the lateral pharyngeal walls. Am J Respir Crit Care Med 1995; 152: 1673–1689. 51. Kuna ST, Deepak GB, Ryckman C. Effect of nasal airway positive pressure on upper airway size and configuration. Am Rev Respir Dis 1988; 138:969–975. 52. Van der Touw T, Crawford ABH, Wheatley JR. Effects of a synthetic lung surfactant on pharyngeal patency in awake human subjects. J Appl Physiol 1997; 79:78–85. 53. Series F, Marc I. Influence of lung volume dependence of upper airway resistance during continuous negative airway pressure. J Appl Physiol 1994; 77:840–844. 54. Van de Graaff W. Thoracic traction on the trachea: mechanisms and magnitude. J Appl Physiol 1991; 70(3):1328–1336. 55. Rowley JA, Permutt S, Willey S, et al. Effect of tracheal and tongue displacement on upper airway airflow dynamics. J Appl Physiol 1996; 80:2171–2178. 56. Shepard J, Pevernagie D, Stanson A, et al. Effects of changes in central venous pressure on upper airway size in patients with obstructive sleep apnea. Am J Respir Crit Care Med 1996; 153:250–254. 57. Stanescu D, Kostinavev S, Sonna A, Liistro G, Veriter CI. Expiratory flow limitation during sleep in heavy snorers and obstructive sleep apnea patients. Eur Respir J 1996; 9:2116. 58. Lofasa F, Lorino AM, Fodil R, et al. Heavy snoring with upper airway resistance syndrome may induce positive end-expiratory pressure. J Appl Physiol 1998; 85:860.

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59. Badr SM, Dawak A, Skatrud JB, Morrell MJ, Zahn BR, Babcock MA. Effect of induced hypocapnic hypopnea on upper airway patency in humans during NREM sleep. Respir Physiol 1997; 110:33–45. 60. Rowley JA, Sannders CS, Zahn BR, Badr SM. Effect of REM sleep on retroglossal crosssectional area and compliance in normal subjects. J Appl Physiol 2001; 91(1):239–248. 61. Morrell MJ, Arabi Y, Zahn B, Badr MS. Progressive retropalatal narrowing preceding obstructive apnea. Am J Respir Crit Care Med 1998; 158:1974–1981. 62. Leiter JC. Upper airway shape. Is it important in the pathogenesis of obstructive sleep apnea? Am J Respir Crit Care Med 1996; 153:894–898. 63. Rodenstein DO, Dooms G, Thomas Y, Liistro G, Stanesco DC, Culle C, Aubert-Tulkens G. Pharyngeal shape and dimensions in healthy subjects, snorers, and patients with obstructive sleep apnoea. Thorax 1990; 45:723–727.

4 Maintenance of Wakefulness Yau Hong Goh Mount Elizabeth Medical Centre and Department of Otolaryngology, Singapore General Hospital, Singapore Kheng Ann Lim Mount Elizabeth Medical Centre, Singapore 1. INTRODUCTION Why do we sleep? We sleep to stay awake is perhaps a succinct, albeit overly simplistic, response. Defined as a transient state of altered consciousness and perceptual disengagement from our environment, sleep unlike coma is an active process involving a host of complex interactions between many cortical, brainstem, diencephalic, and forebrain structures. During this ‘rest’ state, the cerebral metabolism and oxygen consumption within the brain remain significant. Any disorder that interferes with this intriguing cerebral event during sleep will therefore disrupt the proper execution of this necessary and vital state of our existence. Although the function of sleep is largely unknown, one observation is evident—that good sleep is critical to the level of our state of wakefulness. The biggest clue to how important a properly executed sleep is to our daytime function is derived mainly from our studies on the clinical effects of sleep disorders as well as experimental studies on sleep deprivation. In recent years research in the neurophysiological and neuro-chemical aspects of sleep has also yielded new and exciting data on the biochemical events in the brain during sleep and awake states. This microlevel information has opened up a vast frontier that can potentially allow us to employ biochemical tools to manipulate these two states of vigilance. Although much has been learned from the multitude of studies over the past several decades, the answer to why we sleep remains elusive. It is not difficult, on the other hand, to explain why we stay awake. At the most basic level, we stay awake to feed, to protect ourselves from harm, and to reproduce to ensure the continuity of our species. We achieve these primary objectives by farming, hunting, working, guarding our territory, interacting with others, raising children, and engaging in activities that will perpetuate our existence. The disengagement we experience from our environment and the cessation of the aforementioned activities during sleep therefore presents us with potential physical risks. Any detriment in our level of wakefulness may disrupt our ability to carry out our daily routine or even predisposes us to significant risks, as seen when one falls asleep while driving. The phenomenon of sleep is also associated with profound physiological alterations. Under normal circumstances, these physiological changes in the various human systemic functions during sleep occur without any serious consequences. In pathologic states,

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however, changes that ensue in any of our systemic functions may present serious physiological risks with consequences that affect the qualitative and quantitative aspects of our sleep and daytime function (1–3). 2. THE CIRCADIAN PACEMAKER The maintenance of wakefulness involves a sophisticated system of feedback mechanism from the visceral, somatic, and special sensory organs, as well as integration of information in specialized areas within the cerebral cortex and the brainstem. The suprachiasmatic nucleus (SCN) of the anterior hypothalamus has been identified as the pacemaker of our circadian rhythm and principal regulator of our hour-to-hour state of vigilance. The SCN functions primarily as the dominant pacemaker that controls many other closely linked systems, mainly via efferents to nearby hypothalamic structures as well as via humoral agents (4,5). It is this biological clock that determines the neurobehavioral variables, such as feeling alert or tired, we experience at different times of our day and night. Non-circadian factors such as noise, light, and temperature have been shown to influence and alter the intrinsic rhythmicity of this pacemaker. Failure to execute the neuro-physiological processes that are intrinsic to sleep appears to result in the failure to initiate and facilitate the physiological events necessary to maintain wakefulness in the day. In humans, the circadian pacemaker maintains our state of wakefulness for an average 16hr and induces us into sleep for about 7–8hr over a 24hr daily cycle. Increasing the length of wakefulness, as in sleep deprivation, increases the duration of subsequent restorative sleep. Maintaining wakefulness beyond our circadian limit will consequently result in the waning of our level of alertness and increases the degree of sleepiness. In a typical 24-hr sleep and wake biological time frame, maximum sleepiness typically occurs in the middle of the night during sleep. When the process of nocturnal sleep is hindered, neurobehavioural manifestation of irritability, lethargy, sleepiness, and impaired mental function emerges at the time of maximum biological sleepiness (2– 6a.m.). Similar symptoms are also experienced if significant physiological sleepiness is allowed to intrude into one’s wake realm during the day, such as after a night without sleep. 3. WAKEFULNESS AND SLEEPINESS We all know what it is like to be sleepy or awake. But how best should wakefulness or sleepiness be defined is highly debatable. Is an extremely sleepy person also not so awake, or another alert person not so sleepy? Whether sleepiness and wakefulness are opposites in the same linear scale or overlapping variables in a multi-dimensional one is a controversial issue. It is however logical to view sleepiness and wakefulness as different sides of the same coin and to regard them as different “states” existing simultaneously in a reciprocating manner. The extent to which one feels sleepy or awake is an important measure of one’s state of vigilance. In practice, however, the level of one’s state of

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wakefulness is not measured directly but instead reciprocally quantified by measuring one’s level of sleepiness. 3.1 What Is Sleepiness? Sleepiness can be viewed as a basic physiological need state like hunger or thirst that is vital to human survival. Deprivation of sleep causes sleepiness, and as eating and drinking satisfy hunger or thirst, sleeping reverses sleepiness. Under normal circumstances, severe sleep-deprived states do not occur as normal homeostatic and behavioral regulation (like eating and drinking reverse hunger and thirst) modulate conditions to facilitate sleeping before severe deprivation states develop. The neurological substrates of sleepiness and the specific nature of this physiological need state have yet to be ascertained. There are essentially two important clinical aspects, objective and subjective, to sleepiness. Slowing down of the alpha rhythm in the EEG as seen in multiple sleep latency tests (MSLT), performance tasks tests, particularly those related to vigilance, is objective evidence of sleepiness while thoughts, sensations, and emotions that are associated with sleep deprivation are the subjective components of sleepiness. 3.1.1 Subjective Sleepiness When examining the nature of subjective sleepiness, three important issues must be highlighted. First, there exists an intrinsic biphasic pattern of objective sleep tendency in every human being, with two troughs of alertness (one between 2 and 6a.m. and the other between 2 and 6p.m.) (6). How sleepy one is depends therefore on when one’s sleepiness is being evaluated. Second, although sleep-deprived patients may present with an increased tendency to fall asleep at inappropriate times, many may not at all complain of sleepiness. These patients often complain of non-specific symptoms of decreased wakefulness such as fatigue, lethargy, irritability, inability to concentrate at work, and loss of a sense of wellbeing. Also, when sleepiness is most intense, these patients may become less aware of the subjective aspects of sleepiness and so may fall asleep without warning. These episodes, called sleep attacks, are commonly experienced when sleep apnea patients are behind the wheel. It is pertinent to emphasize at this juncture that while sleepy patients have impaired levels of wakefulness, not all patients with impaired wakefulness complain of sleepiness. Third, the subjective experience of sleepiness and the behavioral indicators of sleepiness like yawning and head nodding can frequently be suppressed under certain conditions. This sleepy behavior may be reduced or completely suppressed under situations of stress and excitement, high motivation, exercise, and competing needs such as hunger and thirst. Behavioral and subjective indicators thus do not always precisely reflect physiological sleepiness. When physiological sleepiness is most intense, however, the ability to avert overt behavior is markedly reduced. While a physiologically alert person does not experience sleepiness or appear sleepy even in sleep-inducing environment, soporific conditions such as after heavy meals, lazing in cozy rooms, or sitting through a boring lecture will unmask physiological sleepiness.

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Several self-assessment analytic scales have been devised to help clinicians and patients quantify their level of subjective sleepiness. Among the various tools for the measurement of subjective sleepiness, the Stanford Sleepiness Scale (SSS) (7) and the Epworth Sleepiness Scale (ESS) (8) are probably the most validated. Although most study subjects show good correlation between the subjective and the objective assessment of sleepiness (9), it has also been shown that patients’ subjective and objective assessments of sleepiness may not be completely consistent (10,11). The highly subjective nature of subjective sleepiness is indeed a challenging problem for sleep clinicians and researchers. 3.1.2 Objective Sleepiness The majority of the performance tasks used to evaluate the effects of sleep loss are rather insensitive. Currently, only long and monotonous tasks are reliably sensitive in assessing the effects of sleep deprivation with the exception of the 10min visual vigilance task. This test measures task-oriented vigilance lapses (response times ≥500msec) and has been shown to correlate well with sleep loss (12,13). Multiple Sleep Latency Test. MSLT (14) has remained the standard physiological measure of sleepiness. This test, which assesses one’s likelihood of falling asleep, has gained wide acceptance within the field of sleep and sleep disorders as the standard method for quantifying sleepiness (15). Besides being a reliable clinical gauge of sleepiness, MSLT has the further advantage of being able to eliminate the patient’s motivation to stay awake during the test. Although subjects are frequently able, through motivation, to compensate for impaired performance after sleep deprivation, they are highly unlikely to stay awake for long in a darkened room during MSLT. MSLT is an important clinical tool to identify sleep tendency and the maximum risk for patients in their daily environment. 3.2 Symptoms of Impaired Wakefulness Not Related to Sleepiness Apart from complaining of sleepiness, patients with sleep apnea may present with symptoms of fatigue, mood disturbance and loss of the sense of well-being. Although much has been studied on the association between sleep apnea and daytime sleepiness, little is known about the effects of sleep apnea on non-sleepiness-related symptoms. Longitudinal studies of patients with sleep disturbances have shown an increased risk of developing major depression, anxiety disorders, and substance abuse and nicotine dependence (16,17). The antidepressant nature of successful sleep apnea treatment in our clinical practice suggests that sleep disturbance from sleep apnea has profound effects on patients’ mood and behavior. Recognizing the existence of these nonspecific symptoms is necessary when treating obese patients with sleep apnea. These patients frequently require prompt treatment as lingering sleep apnea perpetuates a mental and behavioral state that is a major stumbling block to motivating our patients who are attempting weight reduction. More studies are certainly required to evaluate this neuropsychiatric element of sleep apnea.

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4. OBSTRUCTIVE SLEEP APNEA As in most disorders affecting sleep, impairment in the level of wakefulness is one of the cardinal symptoms of obstructive sleep apnea (OSA). The actual incidence of sleep apnea in the world is unknown and the number of clinically unremarkable patients with occult sleep apnea is speculative. The many patients we frequently encounter in our clinical practice who were discovered to have significant sleep apnea after having been initially investigated for cardiovascular or neurological complaints, for example, suggests that the true incidence of sleep apnea may perhaps be mind-boggling. The problem of sleep apnea is probably grossly under-recognized and under-diagnosed. Several prevalence studies in adult men have estimated prevalence rates of 0.4–24% (18–22) with estimates tending to increase with increasing age. Since the first recognition and description of sleep apnea in 1965 (23,24), crucial clinical and laboratory studies on sleep apnea have added new facets to our understanding of the physiological effects of sleep apnea on humans. The effects of sleep apnea on sleep, the daytime consequences that follow, and the clinical impact of this condition on human life may be far more profound than we can currently fathom. Patients with this condition may present with a variable combination of clinical symptoms affecting both sleep and daytime functions: the former tend to be more specific for sleep apnea while the latter are usually the nonspecific results of abnormal sleep regardless of the cause. To understand the impact of sleep apnea on wakefulness, it would be pertinent to first examine the respiratory physiology during normal sleep, the arousal responses to respiratory alterations during sleep, the effects of sleep apnea on sleep architecture, and the effect of sleep fragmentation on wakefulness. 5. RESPIRATORY PHYSIOLOGY DURING NORMAL SLEEP Breathing during the awake state is regulated by a cluster of complex interrelated factors that include 1. Voluntary and behavioral factors 2. Mechanical signals from lung, airway, and chest receptors 3. Chemical factors such as low oxygen or high carbon dioxide levels and acidosis. During sleep, however, several important alterations in the physiological responses to respiratory stimuli occur. 5.1 Hypoventilation During Sleep In the awake state, both cortical activity and voluntary mental concentration can influence breathing and bring about an increase in both ventilation and ventilatory responses. The loss of the ventilatory drive that is observed during sleep probably reflects the loss of the “wakefulness” drive to ventilation. During rapid eye movement (REM) sleep, the inhibition of both presynaptic and postsynaptic afferent neurons results in an increase in the sensory arousal thresholds to external stimuli and post-synaptic inhibition of motor neurons, which produces postural

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hypotonia characteristic of REM sleep. This combination of decreased sensory and motor functions is believed to account for the significant impairment of ventilatory responses during REM sleep. It is this impaired ventilatory response that permits the development of hypoventilation during sleep. 5.2 Hypoxic and Hypercapnic Ventilatory Response During Sleep Not only is the voluntary control of respiration seen in the awake state lost with the emergence of sleep, the usual ventilatory responses to both low oxygen and high carbon dioxide levels are also blunted (25–28). The marked hypoxemia seen during REM sleep in patients with severe lung and chest disease is due to this phenomenon, which is most depressed during REM sleep. These physiological responses may also be important in the pathogenesis of upper airway obstruction during sleep and are responsible for the patient’s failure to arouse rapidly during apneas or hypopneas. The change in ventilatory sensitivity to external stimuli during sleep therefore predisposes patients with airway problems to develop clinically significant hypoxia and hypercapnia before arousal occurs. 5.3 Increased Airway Resistance and Ventilatory Response During Sleep Besides the blunting of hypoxic and hypercapnic ventilatory responses, sleep also obtunds the ventilatory response to increasing airway resistance. This physiological phenomenon has been shown to be particularly distinct in non-REM (NREM) sleep (29– 32), the phase of sleep when airway resistance typically reaches the maximum (33,34). The effect of increased airflow resistance on ventilation during REM sleep is however not known. 6. AROUSAL RESPONSES TO RESPIRATORY ALTERATIONS DURING SLEEP 6.1 Isocapnic Hypoxia Under normal circumstance, isocapnic hypoxia is a poor stimulus to arousal. Although studies have demonstrated that many subjects are able to remain asleep with oxygen saturation as low as 70% (25,26,35), no difference in arousal threshold has been observed between NREM and REM sleep. Patients with sleep apnea, however, have been shown to exhibit reduced arousal sensitivity to hypoxia during periods of asphyxia (36). 6.2 Hypercapnia Although the level of hypercapnia at which arousal is triggered during sleep is highly variable, laboratory studies have shown that most subjects are awakened before the end tidal carbon dioxide rises by 15mmHg above the level in wakefulness (27,37,38). This response appears to be sensitized by the presence of co-existing hypoxia.

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6.3 Increased Airway Resistance Inspiratory resistance (39) and occlusion of inspiration (40) have been shown to be strong precipitants of sleep arousals. The arousal frequency during control sleep periods is most reduced in stages 3–4 of sleep and remain comparatively lower during slow-wave sleep (SWS) than in REM sleep with increased inspiratory resistance (41,42). Although arousal from REM sleep after airway occlusion is far more rapid than arousal from NREM sleep, patients with OSA tend to have longer apneas during REM sleep (40,43). Why these phenomena occur is still unclear. Whether it is hypoxia, hypercapnia, or increased airway resistance, the final pathway for arousal from sleep appears to be the level of ventilatory effort (44). Awakening from sleep, whatever the cause, leads to an increase in ventilation, just as sleep onset is associated with a decrease in ventilation. In patients with sleep apnea, this arousal response to the increase in airway resistance has been termed respiratory effort-related arousal (RERA) and is an important feature of sleep apnea. Patients with this disorder tend to awaken at relatively reproducible levels of pleural pressure and this arousal may occur without the development of either significant hypoxemia or significant hypercapnia. 7. EFFECTS OF SLEEP APNEA ON SLEEP ARCHITECTURE Sleep apnea (45) is characterized by episodic complete or partial pharyngeal obstruction during sleep. This multilevel disorder is characterized by narrowing at a variable number of pharyngeal locations; the soft palate being the commonest site of collapse and narrowing (46,47). Whether the decrease in the sleep-related pharyngeal neuromuscular activity (48) plays a more dominant role compared with the anatomical narrowing (49–51) of the pharyngeal space is a controversial issue. The extent to which each of these factors comes into play in the pathogenesis of sleep apnea is unknown, although the combined action of these two factors probably plays a significant role in the development of sleep apnea. Decreased upper airway dilator muscle activity (52) and reduction in ventilatory responses to hypercapnia and hypoxia (15) have been shown in 24-hr sleep deprivation studies. Impaired wakefulness therefore depresses arousability to physiological challenges. The result is a vicious cycle of worsening and self-perpetuating breathing disorder during sleep. Depressed physiological responsiveness due to altered wakefulness is clinically significant for patients with sleep apnea and other breathing disorders as they are all exacerbated by sleepiness (52). Sleep disruption triggered by apnea results in the production of more intense and severe pathological apneas. The impact of sleep apnea on sleep architecture can primarily be attributed to tissue vibration during snoring, increase in airway resistance, hypoxia, and hypercapnia. The final outcome of any of these events is arousal (visible or non-visible on the electroencephalogram) and increase in ventilatory effort. This intrinsic survival mechanism leads to fragmentation of sleep. It is this sleep fragmentation and the pathophysiological changes associated with disrupted breathing that are currently believed to account for the symptoms and complications of sleep apnea.

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Other studies have shown that sleep apnea syndromes may be associated with suppression of SWS or REM sleep. Suppression of SWS occurs most commonly in children with sleep apnea while REM suppression is more common in adults with sleep apnea syndromes. Successful treatment of this sleep condition results in SWS or REM rebounds. 8. THE ROLE OF SLEEP FRAGMENTATION ON WAKEFULNESS Increased frequency of arousals causing sleep fragmentation is a common manifestation of a number of sleep disorders as well as medical conditions involving physical pain or discomfort. Sleep apnea, chronic pain from arthitis and neuralgia, rhinosinusitis, for example, may be associated with sleep that is punctuated by frequent, brief arousals of 3– 5sec duration. These arousals are characterized by episodes of EEG speeding or alpha activity with transient increase in skeletal muscle tone. This outburst of subtle EEG arousals is especially important in the diagnosis of upper airway resistance syndrome (53). Nonvisible sleep fragmentation, defined as an increase in heart rate of 4 bpm or blood pressure by 4mmHg without change in EEG in response to sound stimuli has also been shown to be associated with increased sleepiness on MSLT (34,54). Less well studied are EEG arousals that may be associated with other subcortical events not seen in the cortical EEG tracing. This abnormality may account for the increase in both the absolute amount and the proportion of stage 1 sleep with concomitant reduction of stages 3–4 sleep seen in patients with sleep apnea. The association of this event with impaired wakefulness is, however, still not known. Regardless of etiology, sleep arousals generally do not result in shortened sleep but rather in sleep fragmentation. It is this fragmentation that is believed to be an important factor affecting impaired daytime wakefulness. Studies have suggested a strong association between sleep fragmentation and daytime sleepiness (55). Treatment studies also demonstrate a close link between sleep fragmentation and excessive daytime sleepiness. Reduced frequency of arousals from sleep with resultant reduction in the level of sleepiness is commonly seen in patients who are successfully treated for sleep apnea, whereas those who do not subjectively benefit from treatment show no decrease in arousals or sleepiness, despite improved sleeping oxygenation. It must, however, be stressed that lack of fragmented sleep does not exempt one from feeling sleepy. Partial sleep deprivation may occasionally be seen in patients who are unable to sustain sleep from repeated sleep disruption. This is commonly seen in patients with anxiety predispositions or superimposed insomnia. 9. CLINICAL IMPLICATIONS Between the occurrence of pharyngeal closure and the clinical manifestation of impaired wakefulness exist a complex series of physiological events involving several systemic functions within the human body. The key link between the airway trigger and the eventual alteration in the level of the awake state appears to be the extent of sleep

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fragmentation from repeated arousals. While it is well known that patients with impaired wakefulness do not necessarily complain of sleepiness, the relationship between subjective symptoms of disturbed wakefulness and the severity of sleep apnea is less clear. Patients who were deemed to be simple snorers (without symptoms of impaired wakefulness) on clinical grounds have been shown to have significant obstructive sleep apnea of at least moderate severity during polysomnography (25,56,57). While few patients with full-blown clinical symptoms of sleep apnea have minimal apneas or hypopneas, many otherwise asymptomatic snorers (30–50%) have significant sleep apnea (58,59). Patients with altered levels of wakefulness from sleep apnea may not present for treatment in sleep centers but may instead complain of non-specific symptoms of lethargy, depression, cognitive and memory impairment to clinicians in fields such as endocrinology, psychiatry, and neurology. Just how many of these patients with such non-specific complaints actually have underlying sleep apnea is speculative but the true incidence of this sleep disorder is probably grossly under-diagnosed. One explanation why patients with impaired wakefulness can present in such a variable manner is that the clinical manifestation of wakefulness is influenced by a multitude

Table 1 Factors Affecting Wakefulness in Patients with Sleep Apnea Sleep architecture Degree of sleep disturbance (arousal index) Number of sleep arousals (sleep fragmentation) Duration of arousal-free sleep increases restorative effect of sleep Nature of stage-related sleep deprivation Period of disturbance (acute vs. chronic) Recovery/compensatory sleep (length of sleep/naps) Associated sleep disorders (e.g., periodic leg movement, insomnia) Patient’s factor Intrinsic factor, individual sleep quotient Personality/psychosocial makeup Age Sex Associated disease (anxiety, Parkinson’s disease, hypothyroidism, cerebrovascular disease) Daytime environment Working environment/occupation Temperature Light

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Noise Other factors Food/drugs (caffeine, pseudoephedrine, alcohol) Exercise Posture

of factors such as the extent of sleep architecture disruption, patient’s intrinsic factors, as well as environmental and external factors, as listed in Table 1. The ability of sleep apnea patients to overcome their decreased wakefulness during the awake state by consuming caffeine-laden products or compensate by sleeping for a longer duration and taking afternoon naps, for example, makes the measurement of the daytime effects of sleep apnea extremely difficult and challenging. Of special mention are factors such as the age, gender, and personality of our patients, which greatly modify the eventual manifestation of their altered state of wakefulness. An important and extensively discussed issue concerns the association of impaired wakefulness as a consequence of sleep apnea with accidents. Although reports of associations of sleep apnea with road traffic accidents abound in the medical literature (39,60,61), direct epidemiological evidence for a causal role of fatigue in car crash is lacking. There are at present no well-designed observational epidemiological studies to estimate the prevalence of impaired wakefulness in the car-driving population and the level of risk this confers (62). The recent demonstration that driving after sleep deprivation presents risks similar to driving under the influence of alcohol (63–65) has uncovered an entirely new medico-legal aspect to the treatment of sleep apnea patients. The goal in the treatment of any OSA patient is to improve his quality of life by eliminating the cardinal symptoms of this breathing disorder, as well as decreasing his risk of neuro-cardiovascular complications. The restoration of impaired wakefulness in these patients is perhaps the single most rewarding aspect in the treatment of OSA patients. Patients who are successfully treated for OSA often testify to improve-ment in job performance, greater alertness, and a general sense of well-being. However, one of the greatest challenges of a sleep physician lies in identifying OSA patients who present with non-sleepiness-related problems. Our present understanding of the physiological impact of sleep apnea on wakefulness is very much limited to the effects of sleep apnea on sleepiness. Future breakthroughs in our understanding of the non-sleepiness-related problems of impaired wakefulness brought about by sleep apnea may someday uncover new direct associations between sleep apnea and problems related to impaired level of wakefulness, like depression and chronic fatigue, that may not be sleepiness-related. This may change the way we look at neuropsychiatric conditions in the future.

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23. Gastaut H, Tassinari C, Duron B. Etude polygraphique des manifestations episodiques (hypniques et respiratories) du syndrome de Pickwick. Rev Neurol 1965; 112:568–579. 24. Jung R, Kuhlo W. Neurophysiological studies of abnormal night sleep and Pickwickian syndrome. Prog Brain Res 1965; 18:140–159. 25. Berthon-Jones M, Sullivan CE. Ventilatory and arousal responses to hypoxia in sleeping humans. Am Rev Respir Dis 1982; 125:632–639. 26. Douglas NJ, White DP, Weil JV, Pickett CK, Martin RJ, Hudgel DW, Zwillich CW. Hypoxic ventilatory response decreases during sleep in normal men. Am Rev Respir Dis 1982; 125:286– 289. 27. Hedemark LL, Kronenberg RS. Ventilatory and heart rate responses to hypoxia and hypercapnia during sleep in adults. J Appl Physiol 1982; 53:307–312. 28. White DP, Douglas NJ, Pickett CK, Weil JV, Zwillich CW. Hypoxic ventilatory response during sleep in normal post-menopausal women. Am Rev Respir Dis 1982; 126:530–533. 29. Gugger M, Molloy J, Gould GA, Whyte KF, Raab GM, Shapiro CM, Douglas NJ. Ventilatory and arousal responses to added inspiratory resistance during sleep. Am Rev Respir Dis 1989; 140:1301–1307. 30. Hudgel DW, Mulholland M, Hendricks C. Neuromuscular and mechanical responses to inspiratory resistance loading during sleep. J Appl Physiol 1987; 63:603–608. 31. Iber C, Berssenbrugge A, Skatrud JB, Dempsey JA. Ventilatory adaptions to resistive loading during wakefulness and non-REM sleep. J Appl Physiol 1982; 52:607–614. 32. Wiegland L, Zwillich CW, White DP. Sleep and the ventilatory response to resistive loading in normal men. J Appl Physiol 1988; 64:1186–1195. 33. Hudgel DW, Martin RJ, Johnson B, Hill P. Mechanics of the respiratory system and breathing pattern during sleep in normal humans. J Appl Physiol 1984; 56:133–137. 34. Martin SE, Wraith PK, Deary IJ, Douglas NJ. The effect of nonvisible sleep fragmentation on daytime function. Am J Respir Crit Care Med 1997; 155:1596–1601. 35. Gothe B, Goldman MD, Cherniack NS, Mantey P. Effect of progressive hypoxia on breathing during sleep. Am Rev Respir Dis 1982; 126:97–102. 36. Sullivan CE, Issa FG. Pathophysiological mechanisms in obstructive sleep apnea. Sleep 1980; 3:235–246. 37. Birchfield RI, Sieker HO, Heyman A. Alterations in respiratory function during natural sleep. J Lab Clin Med 1959; 54:216–222. 38. Douglas NJ, White DP, Weil JV, Pickett CK, Zwillich CW. Hypercapnicventilatory response in sleeping adults. Am Rev Respir Dis 1982; 126:758–762. 39. Garbarino S, Nobili L, Beelke M, De Carli F, Ferrillo F. The contributing role of sleepiness in highway vehicle accidents. Sleep 2001; 24(2):203–206. 40. Issa FG, Sullivan CE. Arousal and breathing responses to airway occlusion in healthy sleeping adults. J Appl Physiol 1983; 55:1113–1119. 41. Netick A, Dugger WJ, Symmons RA. Ventilatory response to hypercapnia during sleep and wakefulness in cats. J Appl Physiol 1984; 56:1347–1354. 42. Santiago TV, Sinha AK, Edelman NH. Respiratory flow-resistive load compensations during sleep. Am Rev Respir Dis 1981; 123:382–387. 43. Gugger M, Bogershausen S, Schaffler L. Arousal response to added inspiratory resistance during REM and non-REM sleep in normal subjects. Thorax 1993; 48:125–129. 44. Gleeson K, Zwillich CW, White DP. The influence of increasing ventilatory effort on arousal from sleep. Am Rev Respir Dis 1990; 142:295–300. 45. American Academy of Sleep Medicine. Sleep related breathing disorders in adults: recommendations for syndrome definition and measurement techniques in clinical research. Sleep 1999; 22:667–689. 46. Launois SH, Feroah TR, Campbell WN, Issa FG, Morrison D, Whitelaw WA, Isono S, Remmers JE. Site of pharyngeal narrowing predicts outcome of surgery for obstructive sleep apnea. Am Rev Respir Dis 1993; 147:71–94.

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47. Morrison DL, Launois SH, Isono S, Feroah TR, Whitelaw WA, Remmers JE. Pharyngeal narrowing and closing pressures in patients with obstructive sleep apnea. Am Rev Respir Dis 1993; 148:606–611. 48. Leiter JC, Knuth SL, Bartlett D Jr. The effect of sleep deprivation on activity of the genioglossus muscle in man. Am Rev Respir Dis 1985; 132:1242–1245. 49. Guilleminault C, Riley R, Powell N. Obstructive sleep apnea and abnormal cephalometric measurements: implications for treatment. Chest 1984; 86:793–794. 50. Horner RL, Shea SA, McIvor J, Guz A. Pharyngeal size and shape during wakefulness and sleep in patients with obstructive sleep apnea. Q J Med 1989; 72:719–735. 51. Rivlin J, Hoffstein V, Kalbfleish J, McNicholas W, Zamel N, Bryan AC. Upper airway morphology in patients with idiopathic obstructive sleep apnea. Am Rev Respir Dis 1984; 129:355–360. 52. Lopes JM, Tabachnik E, Muller NL, Levison H, Bryan AC. Total airway resistance and respiratory muscle activity during sleep. J Appl Physiol 1983; 54:773–777. 53. Guilleminault C, Stoohs R, Clerk A, Simmons J, Labanowski M. From obstructive sleep apnea syndrome to upper airway resistance syndrome—consistency of daytime sleepiness. Sleep 1992; 15(6 suppl):S13-S16. 54. Hosselet JJ, Norman RG, Ayappa I, Rapoport DM. Detection of flow limitation with nasal cannula/pressure transducer system. Am J Respir Crit Care Med 1998; 157:1461–1467. 55. Stepanski EJ. The effect of sleep fragmentation on daytime function. Sleep 2002; 25(3):268– 276. 56. Goh YH, Choy DKS. Omission of polysomnography in the treatment of snoring: common reasons and medico-legal implications. J Laryngol Otol 2000; 114(7):519–521. 57. Simmons FB, Guilleminault C, Mile LE. A surgical treatment for snoring and obstructive sleep apnea. West J Med 1984; 140(1):43–46. 58. Miles LE, Guilleminault C, Smith LE. Patients who complain only of loud snoring often have significant obstructive sleep apnea. Sleep Res 1983; 12:265. 59. Miles LE, Simmons FB. Evaluation of 190 patients with loud and disruptive snoring. Sleep Res 1984; 13:154. 60. Fuchs BD, McMaster J, Smull G, Getsey J, Chang B, Kozar RA. Underappreciation of sleep disorders as a cause of motor vehicle crashes. Am J Emerg Med 2001; 19(7):575–578. 61. Masa JF, Rubio M, Findley LJ. Habitually sleepy drivers have a high frequency of automobile crashes associated with respiratory disorders during sleep. Am J Respir Crit Care Med 2000; 16(4 Pt 1):1407–1412. 62. Connor J, Whitlock G, Norton R, Jackson R. The role of driver sleepiness in car crashes: a systematic review of epidemiological studies. Accid Anal Prev 2001; 33(1):31–41. 63. Hack MA, Choi SJ, Vijayapalan P, Davies RJ, Stradling JR. Comparison of the effects of sleep deprivation, alcohol and obstructive sleep apnoea (OSA) on simulated steering performance. Respir Med 2001; 95(7):594–601. 64. Powell NB, Schechtman KB, Riley RW, Li K, Troell R, Guilleminault C. The road to danger: the comparative risks of driving while sleepy. Laryngoscope 2001; 111(5): 887–893. 65. Powell NB, Riley RW, Schechtman KB, Blumen MB, Dinges DF, Guilleminault C. A comparative model: reaction time performance in sleep disordered breathing versus alcoholimpaired controls. Laryngoscope 1999; 109(10):1648–1654.

5 Polysomnography Judy L.Chang and Clete A.Kushida Stanford University Center of Excellence for Sleep Disorders, Stanford, California, U.S.A. 1. INTRODUCTION Polysomnography (PSG) is the study of an individual’s sleep using a device capable of measuring the electrical activity of the brain, eyes, chin, and leg muscles. Other measures may include snoring intensity, oronasal airflow, chest and abdominal wall movement, oxygen saturation, heart rate, esophageal pressure, body position, and transcutaneous carbon dioxide (TcCO2). PSG is the chief assessment tool in evaluating disorders of sleep. One of its primary uses is in the evaluation and treatment of sleep disordered breathing (SDB), such as the obstructive sleep apnea syndrome (OSAS). The goal of this chapter is to explain the terms used in PSG, review the indications for PSG, discuss the technical aspects of PSG, describe how sleep stages and breathing abnormalities are scored, and compare portable sleep studies to attended polysomnograms. 2. DEFINITIONS To describe abnormal breathing during sleep, many terms have been used, which are defined as follows. An apnea is cessation or near cessation of respiration for at least 10sec in adults, and 3sec in infants. A hypopnea is airflow reduction lasting at least 10sec. A respiratory effort-related arousal (RERA) is an obstructive event that does not meet the criteria for an apnea or hypopnea, but that results in an arousal from sleep. Apnea-hypopnea index is the total number of apneas and hypopneas per hour of sleep. Respiratory disturbance index typically is the sum of the number of apneas, hypopneas, and RERAs per hour of sleep. The term “obstructive” describes events caused by upper airway obstruction. The term “central” describes events caused by lack of respiratory effort leading to lack of airflow, lasting a minimum of 10sec. “Mixed” events have a combination of central and obstructive qualities. A cardio-respiratory sleep study is a sleep study that requires at least four channels [respiratory effort, airflow, arterial oxygen saturation, and electrocardiogram (ECG) or heart rate] (1,2).

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3. INDICATIONS FOR PSG One of the principal indications for PSG is to diagnose SDB, and for continuous positive airway pressure (CPAP) titration in patients with SDB (1). PSG is also indicated to evaluate patients for OSAS prior to surgical treatment of an abnormal upper airway (1). Follow-up PSG is indicated to assess whether CPAP is still needed at the previously titrated pressure after significant weight loss in patients on CPAP for SDB, to determine whether pressure adjustments are needed in patients previously successfully treated with CPAP who have gained a significant amount of weight and are again symptomatic, and when clinical response is insufficient or when symptoms recur despite a good initial response to CPAP (1). Follow-up PSG is indicated to ensure therapeutic benefit after a good clinical response to oral appliance treatment of OSAS, to ensure a satisfactory response after surgery for OSAS, and to assess treatment result after surgery for OSAS in patients whose symptoms return despite a good initial response to treatment (1). 4. VARIABLES MONITORED DURING SLEEP 4.1 Electroencephalography Electroencephalography (EEG) is used to score sleep onset, the stages of sleep, and arousals. The 10–20 system of electrode placement as developed by Jasper et. al (Fig. 1), with measurements made at intervals of 10% or 20% of the total distance between landmarks on the head. The landmarks are the nasion, inion (external occipital protuberance), left and right preauricular points (3). After the measurements are completed, the patient’s hair is parted, and the scalp cleaned for electrode placement (4). EEG electrodes are attached using small patches of gauze soaked in collodion and dried with compressed air; conducting medium is added through a small hole in the electrodes (4). Referential recording refers to placing one electrode on the site of interest, and the other electrode on an electrically silent area (i.e., the ground). Referential recording of one EEG electrode, either central electrodes C3 or C4, is performed, which is referenced to an electrode on the opposite mastoid or earlobe, giving a C3/A2 or C4/A1 channel (4). However, many laboratories routinely record an occipital EEG (O1/A2 or O2/A1) in addition to the central EEG, to assess sleep onset or arousals (4).

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Figure 1 International (10–20) electrode placement. (From Ref. 3.) 4.2 Electro-oculography Electro-oculography (EOG) is performed to record the phasic eye movements of rapid eye movement (REM), and to record the slow, rolling eye movements of sleep onset (4). EOG is based on the small electropotential difference between the front and back of the eye, with the cornea being positive compared to the retina (4). Right outer canthus (ROC) and left outer canthus (LOC) electrodes are used in EOG recordings, and are offset from the horizontal, one slightly above and the other slightly below the horizontal plane (4). This permits detection of horizontal and vertical eye movements (4). The electrodes are taped to the skin (4). Referential recording of two EOG leads is done, with both outer canthus leads referred to the same preauricular reference (e.g., ROC/A1+LOC/A1) (4). 4.3 Electromyography Surface electromyography (EMG) for muscles beneath the chin is necessary to score REM sleep (4). EMG of the anterior tibialis muscle is used to evaluate patients for periodic limb movements (PLMs) during sleep (4). EMG of the intercostals is used as a measure of respiratory effort (4).

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To record chin EMG, electrodes are taped to the skin overlying the mentalis/ submentalis muscles (4). Three electrodes are placed, even though electrical signals from only two are recorded, to provide redundancy in case of failure or artifacts in one of the electrodes (4). If bruxism is suspected, then one electrode may be placed on the masseter muscle instead. Bipolar recording of EMG is performed (4). Bipolar recording involves connecting both the active and the inactive electrodes to the two inputs of a differential amplifier. 4.4 Electrocardiography A modified V2 lead is used. 4.5 Pulse Oximetry Pulse oximeters use spectrophotoelectrical principles to determine oxygen saturation of arterial blood (SaO2) from a two-wavelength light transmitter and receiver placed on either side of a pulsating arterial bed. The manufacturers recommend placing the device on the ear, nose, or one of the digits. The amplitude of light detected by the receiver is dependent on the magnitude of the change in arterial pulse, the wave-lengths transmitted through the arterial vascular bed, and the SaO2 of the arterial hemoglobin (2). 4.6 Measurement of Obstructive Hypopneas/Apneas The American Academy of Sleep Medicine (AASM) reviewed measurement techniques for breathing parameters in SDB, and recommended that the reference standard be airflow reduction, as detected by pneumotachometer (5). If a pneumotachometer is not used, then two independent techniques are recommended to measure hypopneas, to provide redundancy in case of sensor failure (5). A differential pressure flow transducer is the type of transducer most commonly used with a pneumotachometer (2). Airflow is directed through a cylinder (2). Before exiting the cylinder, air passes through a resistive field, either small parallel tubes or a grill that promotes laminar flow (2). A differential manometer measures the pressure drop across this resistive field (2). With laminar flow, pressure differences are directly proportional to flow (2). Heat is needed to prevent condensation on the resistive element, so calibration should only be performed when the pneumotachograph is heated (2). The flow signal may be electronically or digitally integrated to obtain volume (2). The pneumotachograph is usually connected to a face mask (2). Although this combination is the most accurate way to measure the volume of airflow, it is relatively large and uncomfortable, and thus impractical clinically (2). Alternatively, nasal pressure may be used to detect hypopneas. Changes in nasal pressure during inspiration and expiration reflect changes in inspiratory and expiratory airflow. Flow may be measured by nasal cannula (5). Airflow limitation is inferred when the pressure trace reveals a plateau during inspiration (2). Limitations in the use of nasal pressure/flow to diagnose OSAS include the “non-linear relationship between pressure changes detected at the nostrils and actual airflow, which may result in underestimation of airflow, the occurrence of false positive detection of hypopneas as a result of nasal

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obstruction or mouth breathing, and the feasibility of obtaining an adequate signal in patients with nasal obstruction” (5). Respiratory inductance plethysmography (RIP) is another way to detect breathing abnormalities during sleep. Changes in the cross-sectional area of the chest and abdomen can be electronically measured by determining changes in inductance. Inductance is the opposition to a change of current flow in a conductor. Transducers, which are the physiological equivalent of conductors, are placed around the rib cage and abdomen (2). Changes in lung volumes alter the cross-sectional areas of the chest and abdomen, with a proportional change in the diameter of each transducer. This change directly affects the self-inductance of the transducer (6). RIP detects changes in chest and abdominal volume during inspiration and expiration; when calibrated, the sum of these two signals is a measure of tidal volume. A relative reduction of 50% from baseline in the sum signal of calibrated or uncalibrated RIP is acceptable for a hypopnea (5). Last, an appreciable but less than 50% decrease in the breathing measurement signal can be scored as a hypopnea if it is associated with ≥3% oxygen desaturation or terminates with an arousal. This should not be used as a primary definition of hypopnea, but may be used in equivocal cases when scoring respiratory events. An AASM Task Force recommended that it be used with events detected by nasal pressure, RIP, piezo sensors, strain gauges, thoracic impedance, thermal sensors, and expired CO2 (5). However, an AASM Clinical Practice Review Committee revised the definition of hypopnea as “an abnormal respiratory event lasting at least 10 seconds with at least a 30% reduction in thoracoabdominal movement or airflow as compared to baseline, and with at least a 4% oxygen desaturation” (7). See also the section on obstructive apneas and hypopneas. 4.7 Detection of RERAs An AASM Task Force recommended using esophageal pressure as the reference standard for detecting RERAs (5). Esophageal manometry is also useful in a variety of other situations, including distinguishing obstructive from central respiratory events (8), detecting mild SDB in children (9), and evaluating SDB in thin, female, or adolescent and young adult patients (10,11). One way to measure esophageal pressure is to use a fluid-filled catheter placed within the esophagus, which detects changes in intrathoracic pressure (12). A high-pressure lowflow valve is connected to the esophageal catheter and pressure transducer (Fig. 2). “A pressure infusor (or blood pressure cuff) maintains a pressure of 300mmHg on a saline bag, resulting in a constant drip rate of 3cm3 per hour. The fluid in the catheter transmits the pressure to the transducer and the continuous drip keeps the catheter patent, allowing the measurement of relative changes in esophageal pressure during sleep (12).”

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Figure 2 Fluid-filled catheter system for monitoring esophageal pressure. (Reprinted from Ref. 12.) For more detailed information regarding amplifier calibrations, calibration of the pressure transducer and preparation of the fluid-filled system, catheter preparation, insertion, and connections, patient biocalibrations, indications and contraindications, see the article by Kushida et al. (12). 4.8 Measurement of TcCO2 Measurement of TcCO2 is highly recommended to assess hypoventilation in children who may present without frank apnea but with continuous hypoventilation (13). TcCO2 may be measured either by a silver chloride electrode which measures CO2 that has diffused from the skin through a gas permeable membrane into solution, or by an infrared capnometer that analyzes CO2 in the gaseous phase (14).

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5. TECHNICAL ASPECTS OF RECORDING PSGs A minimum of four channels [one EEG (C3/A2 or C4/A1), two EOG (ROC/ A1+LOC/A1), and one EMG (mentalis/submentalis)] are needed to score sleep stages (15). The minimum channels necessary to evaluate SBD are EEG, EOG, chin EMG, monitoring of respiration (thoracic and abdominal uncalibrated inductive plethysmography, oronasal airflow, pulse oximetry), body position, snoring, and ECG. Anterior tibialis EMG is useful in detecting movement arousals and PLMs (1,11). The recommended paper speed is 10 or 15mm/sec. A minimum gain of 7.5 or 10mm for a 50µV signal for EEG and EOG channels is recommended (15). Chin EMG amplification should be adjusted after the recording has begun so that an acceptable EMG recording is obtained (4). In monitoring nasal pressure, the optimal signal is achieved with a DC amplifier; if an AC amplifier is used, then a long-time constant filter (time constant >5sec) is recommended (16). The esophageal manometer should be calibrated so that a given amount of water pressure corresponds to a particular voltage (e.g., 1V=20cm of water pressure). The filters should be set to allow suitable visualization of a wide range of signals, from slow waves (≤2Hz) to sleep spindles (12–14Hz). In recording EEG and EOG, a high-frequency filter set to 30–35Hz allows essential waveforms to pass through, while filtering out high-frequency (i.e., EMG) interference. A time constant of 0.3sec or shorter (which corresponds to a half-amplitude low-frequency filter of 0.3Hz) is recommended, to ensure adequate coverage of slow-wave activity. For EMG, a low-pass filter setting of 70 or 75Hz [with notch filtering of alternating current interference (60Hz)] is recommended. High-pass filtering at 10Hz (time constant 0.015sec) prevents slow signals from interfering with the EMG tracing. A time constant 0.1sec or longer is recommended for EMG (15). For pulse oximetry, it is recommended to use the least filtering (i.e., the fastest response), because the greater the filtering, the less sensitive the pulse oximeter is to brief, mild hypoxemic episodes (2). For esophageal manometry, a high-frequency filter cutoff of 3Hz is recommended (12). There are, however, circumstances when the default sensitivity, filter, and time constant settings must be adjusted. In the elderly, increasing EEG gain so that a 50 µV pulse gives a pen deflection of 15mm makes the EEG easier to read. In the young, reducing the sensitivity of EEG and EOG channels so that a 50µV pulse gives a pen deflection of 5mm makes the EEG easier to score. When sweat artifact is present, rereferencing or lowering the room temperature usually corrects the artifact; however, if that does not correct it, then changing the low-frequency cutoff to 1Hz (time constant 0.1sec) filters out the artifact (4,15). 6. SCORING SLEEP STAGES 6.1 Background Frequency is measured in cycles per second. Scoring is done in 20–30sec epochs, which corresponds to a single page of chart paper 300mm wide recorded with a chart speed of

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10 or 15mm/sec. Each epoch is scored according to the predominant EEG pattern during that interval, based on tracings obtained from C4/A1 or C3/A2 (4,15). 6.2 Relaxed Wakefulness Alpha activity (8–13Hz) is the predominant rhythm when the patient is relaxed with the eyes closed. It is maximal occipitally, but often also present centrally. It attenuates with eye opening or attention. Relaxed wakefulness appears as a low-voltage, mixedfrequency activity with the eyes open. REMs and eye blinks are typically noted in the EOG, with slow, rolling eye movements often appearing seconds to minutes preceding the EEG change to stage 1 sleep. Relatively high tonic EMG is also present during relaxed wakefulness (4,15). 6.3 NREM Sleep 6.3.1 Stage 1 Sleep Stage 1 sleep is seen as a relatively low-voltage, mixed-frequency (2–7Hz) EEG activity. Vertex sharp waves are common. Slow, rolling eye movements precede the EEG change from wakefulness to stage 1 sleep. The EMG usually reveals low-amplitude activity (4,15). 6.3.2 Stage 2 Sleep Stage 2 sleep is defined as the appearance of sleep spindles and K complexes on a background of relatively low-voltage, mixed-frequency EEG. Sleep spindles are typically 12–14Hz, and by definition, must last at least 0.5sec, such that one can count six or seven distinct waves within the 0.5sec; K complexes have “a well delineated negative sharp wave which is immediately followed by a positive component. The total duration of the complex should exceed 0.5 seconds” (15). The “3min” rule is to default to stage 1 sleep if neither a sleep spindle nor a K complex occurs within a 3min span when the EEG is of relatively low voltage and mixed frequency (4). K complexes may be visible in the EOG. EMG reveals tonically active, lower-amplitude activity compared with wakefulness. 6.3.3 Stages 3 and 4 Sleep Stage 3 sleep is defined as a high-amplitude, slow-wave activity lasting 20–50% of the epoch. Slow waves have a frequency of 2Hz or lower, and an amplitude >75µV from peak to peak (i.e., the difference between the most negative and positive points of the wave) (15). Stage 4 sleep is scored when more than 50% of the epoch is a high-amplitude, slowwave activity.

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6.4 REM Sleep REM sleep is defined as “relatively low voltage, mixed frequency EEG” (15) with episodic REMs and low-amplitude EMG. “Sawtooth” waves may be present (15). A 15sec or longer EMG elevation in REM sleep, even in the absence of an EEG change, requires a stage shift (4). The following two principles, reproduced from Rechtschaffen and Kales (15), are used to score mixtures of REM and sleep spindles: 1. Any section of record contiguous with the REM stage in which the EEG shows relatively low voltage, mixed frequency is scored as stage REM regardless of whether REMs are present, providing EMG is at the stage REM level and there are no intervening movement arousals. 2. An interval of relatively low-voltage, mixed-frequency EEG recorded between two sleep spindles or K complexes is considered stage 2 regardless of the EMG level, if there are no REMs or movement arousals during the interval and if the interval is less than 3min long. 6.5 Movement Time An epoch is scored as movement time when the polygraph record is obscured by movement. When movement arises from sleep, immediately precedes sleep, and lasts at least half the epoch, then the epoch is scored as “movement time.” If the movement is preceded or followed by wakefulness, then it is scored as “wakefulness.” 6.6 Modifications of Scoring Sleep in OSAS Although the Rechtschaffen and Kales (15) criteria are widely accepted for scoring sleep stages, they were created with normal human subjects in mind. Carskadon and Rechtschaffen (4) have modified these criteria to accommodate the more frequent arousals and greater number of body movements commonly found in patients with OSAS: 1. Follow standard guidelines for entry into stage 1 from wakefulness and stage 2 from stage 1. 2. Once stage 2 sleep is scored, continue stage 2 through any arousal that does not result in a transition to wakefulness (more than half the epoch with waking EEG). 3. In REM sleep, ignore EMG elevations that are clearly associated with snoring. 4. In adults, stages 3 and 4 may be combined.

7. SCORING ESOPHAGEAL PRESSURE The change in esophageal pressure (Pes) is measured as a peak-to-trough difference in the waveform on a breath-to-breath basis (17). Obstructive hypopneas and apneas are seen as “‘Pes crescendos’: progressively increasing esophageal pressure” (18). However, RERAs may occur; these are Pes crescendos lasting at least 10sec and resulting in EEG

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arousals in the absence of obstructive hypopneas or apneas. RERAs are associated with a Pes reversal, a rapid return of Pes to baseline after the abnormal respiratory event. There are three other Pes-associated respiratory patterns observed with repetitive transient arousals: “increased Pes without crescendo, terminated by a Pes reversal; one or two breath increases in Pes preceding a Pes reversal; and tachypnea with a normal Pes, abruptly terminated by a normal breath” (18). The rapid increase of esophageal pressure found in RERAs is essential, and helps distinguish an event from a nonphasic increase in pressure that may occur during stages 3 and 4 of NREM sleep. The change in Pes, not the absolute Pes, is significant (5). Esophageal manometry is also useful in distinguishing obstructive from central apneas. Central apneas are characterized by a lack of intrathoracic pressure swing occurring without oronasal airflow and thoraco-abdominal wall movement (12). 8. ABNORMAL RESPIRATORY PATTERNS IN SDB SDB includes OSAS and the upper airway resistance syndrome (UARS) 8.1 Obstructive Apneas and Hypopneas To diagnose OSAS, PSG must demonstrate five or more obstructed breathing events per hour during sleep. This includes obstructive apneas/hypopneas (Fig. 3) and RERAs (5). For clinical purposes, it may not be necessary to distinguish obstructive hypopneas from apneas because they share a common pathophysiology. An obstructive apnea/hypopnea, as defined below by an AASM Task Force (5), must meet criterion 1 or 2, plus criterion 3 as follows: 1. A clear decrease (>50%) from baseline in the amplitude of a valid measure of breathing during sleep. Baseline is defined as the mean amplitude of stable breathing and oxygenation in the 2min preceding onset of the event (in individuals who have a stable breathing pattern during sleep) or the mean amplitude of the three largest breaths in the 2min preceding onset of the event (in individuals without a stable breathing pattern). 2. A clear amplitude reduction of a validated measure of breathing during sleep that does not reach the level indicated by the above criterion but is associated with either an oxygen desaturation of >3% or an arousal. 3. The event lasts 10sec or longer.

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Figure 3 Two-minute recording showing an obstructive apnea/hypopnea. Note the cannula and airflow reduction with associated decrease in oxygen saturation (SpO2). A position paper published by the AASM in 2001 revised the definition of hypopnea as “an abnormal respiratory event lasting at least 10 seconds with at least a 30% reduction in thoracoabdominal movement or airflow as compared to baseline, and with at least a 4% oxygen desaturation” (7). OSAS is associated with disrupted REM sleep (19). For the complete diagnostic criteria for OSAS, please see the reference article (5) by an AASM Task Force. For the purpose of research, apneas and hypopneas may be distinguished. The reference standard is absence of airflow as detected by a pneumotachometer. If that is not feasible, then a thermal sensor, which detects changes in the temperature of nasally and orally expired air, may be used to detect apneas; however, signals from thermal sensors are non-linearly related to actual airflow, so there is overestimation of ventilation. Another way to detect apneas is by measuring CO2 in nasally and orally expired air (5). 8.2 Respiratory Effort-Related Arousals UARS is described as a distinct syndrome (18). RERAs, which may be detected with esophageal manometry, are characteristic of UARS (12). A RERA (Fig. 4) is a sequence of breaths characterized by progressively more negative esophageal pressure, terminated by an abrupt change in pressure to a less negative level and an arousal. By definition, A RERA must last 10sec or longer (5).

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Figure 4 Two-minute recording showing A RERA. Note the crescendo increase in esophageal pressure (Pes) culminating in an arousal. UARS may be simply defined as an arousal index greater than 10 events per hour of sleep, in the presence of excessive daytime sleepiness. Complete diagnostic criteria for UARS are described by Guilleminault et al. (20). 8.3 Flow Limitation Flow limitation is inferred when a plateau appears on the nasal airway pressure trace during inspiration (2). 8.4 Periodic Limb Movement Disorder Periodic limb movement disorder (PLMD) is defined as periodic episodes of repetitive and highly stereotyped limb movements that occur during sleep (21). PLMD (Fig. 5) is often found in association with SDB. 8.5 Problems and Artifacts in Detecting Apnea A thermistor and instruments monitoring expired gases cannot reliably differentiate among a prolonged inspiration, central apnea, and obstructive apnea, so they are usually used with a device sensitive to lung volume or respiratory effort (2). Caution is needed in classifying respiratory activity based on the relation between detection of airflow and respiratory effort, because some patients may have complete

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obstruction on inspiration but small puffs on expiration, which can be detected by a thermistor or CO2 analyzer. These patients may be incorrectly diagnosed as having hypopneas or normal breathing (2). Prolonged cardiogenic oscillations on expired CO2 recording are proof that the upper airway is patent, and that central apneas are present (2).

Figure 5 Two-minute recording showing PLMs. Note the repetitive leg movements in left/ right anterior tibialis (L/RAT) electrodes 9. COMPARISON OF PSGs TO AMBULATORY SLEEP STUDIES 9.1 Classification of Sleep Apnea Evaluation Studies Sleep apnea evaluation studies were divided into four groups by an AASM Task Force (22). These groups include level I, which is standard PSG (minimum of seven parameters, including EEG, EOG, chin EMG, ECG, airflow, respiratory effort, and oxygen saturation). Body position must be documented or objectively measured. Trained personnel must attend the study, and be able to intervene. Leg movement recording (EMG or motion sensor) is desirable but optional. Level II is comprehensive portable PSG (same parameters as level I, but heart rate may be substituted for ECG, and the study may be unattended). Level III is modified portable sleep apnea testing [minimum of four parameters, including ventilation (at least two channels of respiratory movement, or respiratory movement and airflow, heart rate or ECG, and oxygen saturation). Level IV is continuous single- or dual-bioparameter recording (i.e., at least one physiological variable recorded) (22).

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9.2 Advantages and Disadvantages of Portable Studies Advantages of portable studies are that they may be more accessible, convenient, and acceptable to patients, and allow patients to be studied in a familiar environment. In addition, labor, equipment, and operating costs may be cheaper (22). The primary limitation of portable studies is the lack of attended monitoring by a trained technologist. A technologist can correct artifacts and adjust equipment during the recording; enlist patient cooperation; make continuous observations of the patient; intervene to ensure a satisfactory study and the well-being of medically unstable patients; and make provocative or therapeutic interventions like supine positioning, CPAP adjustment, or providing oxygen or resuscitation to the patient (23). 9.3 Indications for Unattended Studies Unattended studies are presently indicated only for patients with severe symptoms of OSAS and when treatment is urgently needed, but an attended study is not available; for patients who cannot be studied in the sleep laboratory; and for follow-up studies when a diagnosis has been made by standard PSG and therapy has begun, but evaluation of the response to therapy is desired (23). 9.4 Recommendations Regarding the Use of Portable Sleep Studies The AASM recommends the following (23): (1) if portable studies are indicated, only level-II and level-III studies are acceptable for the diagnosis and assessment of therapy for OSAS; (2) body position must be documented during recordings to assess the presence of OSAS; and (3) portable sleep apnea devices must record raw data, and stored data must be reproducible. 10. CONCLUSIONS PSG is indicated in the diagnosis and management of sleep disorders, and one of its primary indications is in the evaluation of SDB. Esophageal manometry and transcutaneous CO2 may be helpful in the diagnosis of specific abnormal sleep-related breathing disorders. Last, in some circumstances, portable or unattended sleep studies may be performed as a substitute for PSG. REFERENCES 1. Chesson AL, Ferber RA, Fry JM, Grigg-Damberger M, Hartse KM, Hurwitz TD, Johnson S, Littner M, Kader GA, Rosen G, Sangal RB, Schmidt-Nowara W, Sher A. Practice parameters for the indications for polysomnography and related procedures. Sleep 1997; 20:406–422. 2. Kryger MH. Monitoring respiratory and cardiac function. In: In: Kryger MH, Roth T, Dement WC, eds. Principles and Practice of Sleep Medicine. Philadelphia, PA: W.B. Saunders, 2000:1217–1230.

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3. Courtesy of Polysomnographic Manual, Grass-Telefactor, An Astro-Med Inc. Product Group, West Warwick, RI. 4. Carskadon MA, Rechtschaffen A. Monitoring and staging human sleep. In: In: Kryger MH, Roth T, Dement WC, eds. Principles and Practice of Sleep Medicine. Philadelphia, PA: W.B Saunders Company, 2000:1197–1215. 5. AASM Task Force. Sleep-related breathing disorders in adults: recommendations for syndrome definition and measurement techniques in clinical research. Sleep 1999; 22(5):667–689. 6. Chadha TS, Watson H, Birch S, Jenouri GA, Schneider AW, Cohn MA, Sackner MA. Validation of respiratory inductive plethysmography using different calibration procedures. Am Rev Respir Dis 1982; 124:644–649. 7. Meoli AL, Casey KR, Clark RW, Coleman JA, Fayle RW, Troell RJ, Iber C. Hypopnea in sleepdisordered breathing in adults. Sleep 2001; 24(4):469–470. 8. German W, Vaughn BV. Techniques for monitoring intrathoracic pressure during over-night polysomnography. Am J END Technol 1996; 36:197–208. 9. Guilleminault C, Pelayo R, Leger D, Clerk A, Bocian RCZ. Recognition of sleep-disordered breathing in children. Pediatrics 1996; 98:871–882. 10. Guilleminault C, Stoohs R, Kim Y, Chervin R, Black J, Clerk A. Upper airway sleepdisordered breathing in women. Ann Intern Med 1995; 122:493–501. 11. Guilleminault C, Stoohs R, Clerk A, Simmons J, Labanowski M. Excessive daytime somnolence in women with abnormal respiratory efforts during sleep. Sleep 1993; 16:S137– S138. 12. Kushida CA, Giacomini A, Lee MK, Guilleminault C, Dement WC. Technical protocol for the use of esophageal manometry in the diagnosis of sleep-related breathing disorders. Sleep Med 2002; 3:163–173. 13. Morielli A, Desjardins D, Brouillette RT. Transcutaneous and end-tidal carbon dioxide pressures should be measured during pediatric polysomnography. Am Rev Respir Dis 1993; 148:1599–1604. 14. Clark JS, Votteri B, Ariagno RL, Cheung P, Eichhorn JH, Fallat RJ, Lee SE, Newth CJ, Rotman H, Sue DY. Noninvasive assessment of blood gases. Am Rev Respir Dis 1992; 145:220–232. 15. Rechtschaffen A, Kales A, eds. A Manual of Standardized Terminology, Techniques and Scoring System for Sleep Stages of Human Subjects. Los Angeles: Brain Information Service/Brain Research Institute, UCLA, 1968. 16. Norman RG, Ahmed MM, Walsleben JA, Rapoport DM. Detection of respiratory events during NPSG: nasal cannula/pressure sensor versus thermistor. Sleep 1997; 20:1175–1184. 17. Simmons JH, Giacomini A, Guilleminault C. Routine use of a water-filled catheter for measuring respiration during NPSG studies. An overview of the procedure and clinical utility. Sleep Res 1993; 22:387. 18. Guilleminault C, Chowdhuri S. Upper airway resistance syndrome is a distinct syndrome. Am J Respir Crit Care Med 2000; 161:1412–1416. 19. Sackner MA, Lauda J, Forrest T, Greeneltch D. Periodic sleep apnea: chronic sleep deprivation related to intermittent upper airway obstruction and central nervous system disturbance. Chest 1975; 67:164–171. 20. Guilleminault C, Stoohs R, Clerk A, Cetel M, Maistros P. A cause of excessive daytime sleepiness. The upper airway resistance syndrome. Chest 1993; 104:781–787. 21. American Academy of Sleep Medicine. International Classification of Sleep Disorders, Revised: Diagnostic and Coding Manual. Rochester, MN: American Academy of Sleep Medicine, 2001:65. 22. Ferber R, Millman R, Coppola M, Fleetham J, Murray CF, Iber C, McCall V, NinoMurcia G, Pressman M, Sanders M, Strohl K, Votteri B, Williams A. Portable recording in the assessment of obstructive sleep apnea. Sleep 1994; 17:378–392.

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23. Thorpy M, Chesson A, Ferber R, Kader G, Millman R, Reite M, Smith P, Wooten V. Practice parameters for the use of portable recording in the assessment of obstructive sleep apnea. Sleep 1994; 17:372–377.

6 Home Sleep Testing Terence M.Davidson Division of Otolaryngology—Head and Neck Surgery, University of California at San Diego and VA San Diego Health Care System, San Diego, California, U.S.A 1. INTRODUCTION Sleep disordered breathing (SDB) includes snoring, upper airway resistance syndromes (UARS), mild, moderate, and severe obstructive sleep apnea (OSA), and a myriad of chronic illness-related sleep disorders such as hypoventilation syndromes and Cheyne Stokes breathing. SDB is a common illness affecting 24% of adult males, 9% of adult females, and 10% of children (1). SDB is a morbid, mortal illness (2) causing bedroom disharmony, excessive daytime sleepiness (EDS) (3), poor work performance (4), poor home performance, increased accidents at home, at work, and on the highway (5–9), hypertension (10–14), heart attacks (15,16), heart failure (17), stroke, and death (18,19). SDB contributes to nocturia (20), decreased libido, attention deficit disorder (21,22), asthma (23), gastroesophageal reflux disease (24), stuttering, bruxism (25), nighttime retinal hemorrhage, and eclampsia (26,27). Advanced SDB patients typically present to sleep physicians. They comprise 4% of adult males and 2% of adult females. Snorers, and by this I mean serious snorers, present to otolaryngologists. These snorers are the people with an apnea-hypopnea index (AHI) >5 but <15. This represents 24−4=20% of adult males and 9−2=7% of adult females. The surgeon’ diagnostic challenge is to determine the severity of the illness, the underlying anatomic obstructions, and then decide who requires continuous positive airway pressure (CPAP) and who might benefit from surgical intervention, both for snoring and for OSA. While many experienced sleep physicians and surgeons are quite skilled at predicting SDB severity by the history and physical examination, none of us are good enough to bypass some objective measure, specifically the sleep test (28). 2. RATIONALE FOR SLEEP TESTING What is medically significant SDB? This same question has been asked for hypertension and typically answered by a measure of systolic and diastolic blood pressure.

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Table 1 Sleep Test Measurements Respiration Oxygenation (pulse oximetry) EEG to measure sleep stage and arousals EOG to identify REM Chest and abdominal movement to discern obstructive from central SDB Position sensors, i.e., supine, prone, lateral Leg movements Esophageal pressure ECG to measure cardiac rhythm

The question has been asked for diabetes and typically answered with some measure of blood sugar. The question has been asked for cholesterol, pulmonary function, and liver function and the answer has always been a measure by an objective laboratory test. It is the nature of medicine to find a test to objectively measure the severity of an illness. And so with SDB we measure respiration. Other measurements are often added to augment the respiratory measure and these are listed in Table 1. As we begin to consider objective testing for SDB, let me ask what are we really measuring? What are the consequences of SDB? The first are autonomic neural stimulation (29), elevated blood pressure (11–13), and increased expression of proinflammatory mediators, specifically soluble adhesion molecules (30), leading to hypertension, heart attack, and stroke (15,16,18,19). The second is EDS, leading to feeling poorly, poor work performance, poor home performance, and propensity to accidents at work, at home, and on the road. To begin this discussion, a nighttime abnormality of respiration leads to an arousal from sleep with several physiologic consequences. This is important. Is a respiratory measurement a sufficient objective metric for SDB or do we have to measure the arousal? If the respiratory event is the primary problem and everything else, i.e., arousal, autonomic neural stimulation, hypertension, etc., are consequences, then the multichannel home sleep test is all that is necessary. If not, do we require a measurement of arousals? If so, an EEG is required and polysomnography (PSG) is the required test. There is extensive literature on arousals. Table 2 is an outline of the significance of arousals in sleep. What we learn from Table 2 is that periodic arousals are present in normal sleep for prevention of deep venous thrombosis, prevention of decubitus ulcers, improved circulation, prevention of atelectasis, cyclical autonomic activation, and nighttime vigilance for external dangers. Respiratory obstruction increases the frequency of arousals and increases the physiologic consequences of arousal including sleep interruption with the resultant EDS, increased autonomic activity with the resultant

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hypertension, and increased expression of proinflammatory mediators with the resultant systemic cardiovascular disease. Arousals are an important measure of SDB. However, arousal requires an EEG and is therefore a complex, expensive examination, with limited availability. Respiratory obstruction and arousal lead to movement. Theoretically, actigraphy, the simple, inexpensive measure of movements, should be an excellent measure of SDB. Actigraphy is popular in Scandinavia, but has been poorly received in the United States. Respiratory obstruction leads to a change in blood gases and hence hypoxia should be a good monitor of SDB. Oximetry alone, however, has correlated poorly with PSG and has been neither sensitive nor specific for SDB,

Table 2 Significance of Arousal in Sleep Definition of an arousal from sleep (AASM criteria) Must be asleep for at least 10sec Sudden rises in EEG activity To alpha To a lighter stage of sleep Duration 3–15sec At least 10sec of sleep between arousals Movement component in REM Classification of arousals Etiology Spontaneous Respiratory Limb movement Snore Composition Cortical (EEG) Movement arousal Autonomic Duration Microarousals (<3sec) Arousals (3–15sec) Awakenings (>15sec) Arousal and normal sleep Frequency <12 per hour

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Stage 1 sleep REM sleep Stage 2 sleep Rare in slow wave sleep (SWS) Causes of arousals from sleep Spontaneous Noxious stimuli Sound Touch Pain Hypoxia (<70% SaO2) Hypercapnia (>15mmHg ETCO2) Increased upper airway resistance Arousals in abnormal sleep Insomnia Chronic medical problems Pain Parkinson’s disease Sleep disordered breathing Periodic limb movement during sleep Narcolepsy Parasomnias Somnambulism Sleep terrors Confusional arousal Why do we have arousals? Prevention of deep vein thrombosis Prevention of decubitus tissue damage Improvement of circulation Prevention of atelectasis Cyclical autonomic activation Nighttime vigilance for dangers

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Consequences of frequent arousals Sleep fragmentation Excessive daytime somnolence Cognitive impairment Activation of the sympathetic nervous system Increased expression of proinflammatory mediators Autonomic consequences of arousals Large transient changes in autonomic output Surge in sympathetic nervous output Parasympathetic withdrawal Increase in BP Increase in heart rate Increase in ventilation Arousals in OSA Very common Sleep fragmentation Frequent nocturnal awakenings Excessive daytime somnolence Activation of the autonomic nervous system Contributes to development of hypertension Increased expression of proinflammatory mediators Conclusions Normal sleep is associated with periodic arousals Arousals elicit profound changes in autonomic activity Arousals modulate expression of proinflammatory mediators When arousals are numerous they result in sleep fragmentation and EDS Note: AASM, American Academy of Sleep Medicine. Source: Adapted from a presentation on “Significance of Arousals in Sleep” by Jose Loredo, MD, University of California, San Diego.

particularly the mild to moderate cases and so is not a reliable, objective, specific, sensitive, single measurement of SDB. This leaves the multichannel home sleep test and the PSG. Both use the same respiratory measurements. Both use the same oximetry, chest and abdominal efforts, and position sensors. The multichannel home sleep test is specific and sensitive when

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compared to PSG. It is less expensive, less intrusive, more available, easier to administer, and better accepted by patients. For the following reasons, I therefore recommend the multichannel home sleep test as the best available sleep test for SDB: 1. Abnormality of respiration is the instigating pathogenesis of SDB. Everything else is a consequence and contributes little to the diagnosis of the vast majority of SDB. 2. The multichannel home sleep test is inexpensive, easy to use, and widely available. Conversely, PSG is expensive, difficult to use, and of limited availability. 3. Assuming that PSG is the gold standard, multichannel home sleep tests correlate extremely well and when compared to PSG are highly specific and highly sensitive. 4. Patent acceptance for multichannel home sleep testing is higher than it is for in-house PSG, or in-home, attended PSG, or even in-home, unattended PSG.

3. THE HISTORY As the diagnosis of SDB is based on the history, examination, and the sleep test, a short note on history and examination and how they interplay with the sleep test is included. A full sleep history is complex. For the otolaryngologist, snoring is the premier symptom of SDB. I contend that everyone who snores on a regular basis deserves a sleep workup. EDS (31) strengthens the history. However, EDS is found in those who work too hard, do not sleep enough hours, drink alcoholic beverages, smoke, imbibe too much caffeine, are depressed, have chronic illnesses, etc. Apneic episodes can often be noted, but are not uniformly noted by all with SDB and they are difficult to quantify. Snoring alone is associated with hypertension. I suggest that the entire sleep history boils down to a single question: Do you snore? If the answer is affirmative, a sleep test is indicated. 4. THE EXAMINATION The physical examination is important as certain findings are associated with SDB and are absolutely critical to direct appropriate treatment. My upper respiratory tract sleep examination (quite different in focus from my “normal ENT examination”) is listed in Table 3. The goals of the upper respiratory tract sleep examination are as follows: First, rule out a neoplasm. I have seen patients present with snoring who on examination had otherwise silent pharyngeal pathology, one with a deep lobe parotid tumor, a second a 3cm tongue base epidermoid carcinoma. Second, for some, SDB can be “cured” by anatomic airway repair. Common examples are nasal polyps, 4+ tonsils, a large vallecular cyst, or deformed, floppy epiglottis. Conversely, some are not surgically treatable and will only be successfully treated with CPAP, tracheostomy, or maxillomandibular advancement. These individuals must be recognized and counseled not to look for easy surgical repair.

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Third, CPAP is not an easy treatment. Improving the airway, especially the nasal airway, can facilitate CPAP compliance. The sleep exam identifies these individuals for future reference. Fourth, if the patient has total nasal obstruction, a sleep test with some measure of oral respiration is required or conversely correction of the nasal obstruction should precede the sleep test.

Table 3 Upper Respiratory Tract Sleep Examination Nose 0–IV 0

Postop perfectly straight

I

Straight with normal cartilage/bone at floor <10% obstruction

II

10–50% obstruction worst side

III 50–90% obstruction worst side IV 90–100% obstruction worst side or obstructive nasal polyps Allergic rhinitis—add I. Total not to exceed IV Mallampati I–IV I

Tonsillar pillars and all of uvula

II

Partial uvula and tonsil pillars

II

Base of uvula

IV No uvula Tonsil 0–IV 0

S/P tonsillectomy

I

Inside the pillars

II

Outside the pillars, <25% of airway

III 25% to <75% of airway IV 75% or more of airway Uvula 1

Absent

2

U <50mm2 (5×10mm)

3

50> U <112.5mm2 (7.5×l5mm)

4

112.5> U <200mm2 (10×20mm)

5

200mm2> U

Tongue I–IV by fiberoptic examination (FOE), patient sitting, mouth closed I

Vallecula open

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Vallecula filled with tongue base

III Epiglottis pushed posteriorly IV Epiglottis touching postpharyngeal wall secondary to tongue-base pressure Larynx I–II

Laryngoscopy grade

I

Normal

I

Anterior commissure

II

Any airway obstruction or deformed epiglottis, not covered above

II

Arytenoids

III Epiglottis IV Tongue

Table 3 is a description of the grading system for the upper respiratory tract examination of patients with SDB. The system is designed to localize the site of upper respiratory tract obstruction, to identify the best candidates for surgery, and to direct surgery to the proper anatomic location. The premise of this system is that obstruction occurs at four distinct sites: the nasal cavity, the retropalatal upper pharynx, the base of the tongue/lower pharynx, and, infrequently, the larynx. The grading system is calibrated so that those individuals with grade III and grade IV scores have a high probability of benefiting from surgical repair to the respective area. Those with lower scores may achieve some relief from their non-SDB illnesses, but are not predicted to achieve major benefit for their SDB. Nose The majority of anatomic nasal obstruction occurs in the anterior nasal cavity and typically involves the septum and the nasal valve. When the mucosa is inflamed, the inferior turbinate will contribute. Posterior septal deflections and obstructions may also contribute. Polyps can cause total nasal obstruction. The examiner must determine the site, etiology, and severity of obstruction. Mallampati Mallampati is a grading system developed by an anesthesiologist for identification of patients that will involve a difficult intubation (32). As there is a significant correlation between difficult intubation and SDB, the examination is included in this SDB grading system. Unfortunately, it is not specific in separating the upper and the lower pharynx. It does, however, point toward abnormalities in the pharynx. There are a variety of ways to perform this exam. Some have the patient protrude the tongue, some have the patient say “ahh.” Try having the patient open the mouth with the tongue in repose and say a gentle “ahh.” Tonsil Tonsillar size is a standard grading system for Head and Neck Surgeons. This exam is selfexplanatory. Uvula

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Uvular size has not been previously described. This exam determines the size using area-a measurement that may be difficult to estimate. Nonetheless, this is our best attempt. Tongue Evaluation for the lower pharynx is the most difficult evaluation. The trans-nasal fiber optic exam seems self-explanatory. It is somewhat. arbitrary, but once a person uses it, he/she will develop consistency. This exam is performed with the mouth either closed or gently open if required for respiration. The tongue is in repose. No vocalization is performed. The observation is made with the tip of the endoscope at the base (palatal attachment) of the uvula. The purpose is to assess the size of the base of the tongue and its contribution to pharyngeal obstruction during sleep. There is no question that most examiners have their own preferences and some may have many reasons why this will not work for them. However, several of us have used the grading system for some time and as we use it, we find it increasingly valuable in the evaluation of the upper respiratory tract in patients with SDB. Larynx The larynx exam by fiberoptic or mirror laryngoscopy is included to identify those individuals with significant abnormality of the larynx and the epiglottis. The most common abnormality will be an omega-shaped epiglottis or other congenital abnormality, e.g., a floppy epiglottis. However, occasionally, vocal cord paralysis, tumor, posttraumatic deformity, etc., may be seen. Laryngoscopy Grade The laryngoscopy grade is a system used by anesthesiologists during laryngoscopy to describe the quality of the view at intubation. For this exam, the fiberscope is positioned at the base of the uvula. Grade I laryngoscopy means an excellent view is obtained and the anterior commissure is seen. Grade II means that the vocal cords and arytenoids can be seen but the anterior commissure cannot be seen. Grade III implies that the endolarynx is not visible, but the epiglottis is visible. Grade IV means that the epiglottis cannot be seen and only the base of the tongue is visible. *Cephalametric measurment: spheneoid-nasion-anterior mandible.

Medical vs. surgical decisions are very difficult. SDB is an anatomic illness complicated by age, body mass index (BMI), comorbidities, and patient symptoms. SDB is strongly correlated with BMI, but there are many thin snorers with serious SDB. The disease also progresses with age, so the 30-year-old snorer with an AHI of 5– 10 will almost certainly have an AHI >15–30 by the time they reach 50. Certain physical findings correlate highly with SDB. Those with severe nasal obstruction, i.e., those who are obligate mouth breathers, are likely to snore and are often helped by rhinologic surgery. Lesser degrees of nasal obstruction may affect SDB and may affect CPAP pressure, flow, and compliance. This is not to saythat snorers with nasal obstruction require surgery, but certainly those with nasal polyps and severe obstruction warrant surgical attention. Grades 3 and 4 Mallampati (Table 3) are associated with SDB. The precise meaning of this anatomically, or how to correct it, is unclear. Three- and four-plus tonsils or obstructive nasal pharyngeal tonsils (adenoids) deserve surgical consideration. The retrodisplaced tongue noted at fiberoptic endoscopy is an important physical finding. Short of mandibular advancement surgery, we do not yet have a good operation for the tongue. So tongue retrodisplacement suggests CPAP will be required.

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Occasionally, one will note a floppy epiglottis or an omega or other abnormally shaped epiglottis. This may obstruct the asleep airway and study is required to quantitate epiglottic abnormality and then determine if surgical resection is beneficial. Micrognathia as measured by an SNB on cephalometrics <76° is associated with SDB and if <72°, is a major contributing factor. It remains unclear to me whether the cephalometric radiograph should be a regular part of the sleep examination. 5. THE MULTICHANNEL HOME SLEEP TEST The multichannel home sleep test measures respiration, snore, oximetry, chest and abdominal movement, body position, leg movement, and heart rate. Respiration is measured by a pressure transducer and is recorded via a nasal cannula. An oral thermistor can augment this as a measure of mouth breathing. Snoring is measured by microphone or by the respiratory pressure and by calculating snore as a low-frequency pressure change.

Figure 1 Several respiratory channel recording patterns are shown. Normal is quiet respiration, flow limitation is

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the very beginning of upper airway narrowing. This is seen in UARS. As the airway further narrows, hypopnea is seen. During recovery, respiration with the sigh/ gasp exaggerated is seen. The last is a full apnea with no discernible air movement. A normal individual breathes 10–12 times a minute throughout the night. Apneas and hypopneas can be seen for as short as 5–10sec or as long as 30–40sec. The figure depicts the anatomy of flattening. Flattening is another measure of respiration (33). Flattening, also referred to as inspiratory flow limitation, is a measure of partial upper airway obstruction. The measurement is based on the shape of the inspiratory flow time curve. Flattening is a supplementary measure for respiration and is particularly important for the diagnosis of UARS. Figure 1 depicts the anatomy of respiratory obstruction. Oximetry is based on two light emitting diodes that shine red and infrared light through the tissue (typically finger) sensor. The light detects the fluctuating signal caused by arterial blood pulse. The ratio of the fluctuation of the light signals determines the oxygen saturation content and provides an indirect measurement of oxygen saturation. This is reported as the saturation pressure of oxygen, abbreviated SpO2 Pulse is calculated from the oximeter. Respiratory effort measures obstructive vs. central apneas. Both a thoracic and an abdominal belt are used. Body position indicates patient posture, i.e., prone, supine, right lateral, or left lateral. Actigraphic measurements can be made from the position sensor. As it is assumed that body position changes frequently when awake and less frequently when asleep, the total sleep time (TST), as opposed to the total time in bed, can be estimated.

Table 4 Common Sleep Test Metrics Apnea

A 90% or greater cessation of breathing for 10 or more seconds

Hypopnea

A 50–90% decrease in breathing for 10 or more seconds

Apnea index (AI)

The total number of apneas divided by the TST

Hypopnea index (HI)

The total number of hypopneas divided by the TST

Apnea-hypopnea index (AHI)

The sum of the AI and AHI

Respiratory disturbance index (RDI)

The sum of all respiratory related events as described below

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Obstructive apnea/ hypopnea

An apnea or hypopnea with thoracic and/or abdominal movement

Central apnea/ hypopnea

An apnea or hypopnea with no discernable respiratory effort as measured by thoracic and/or abdominal movements

Mixed apnea

A combination of obstructive and central apnea/ hypopnea

Oxygenation is reported in several ways. The average O2 is an overall measure of oxygen. Oxygen desaturations can be calculated at 2% or 4%. Some believe that an O2 desaturation is necessary for hypopneas to be counted. The LSAT is sometimes used to imply the severity of the desaturations. It is an interesting number, but subject to artifact. Some studies report oxygen desaturations per hour as a correlative measure of AHI. Some studies report respiratory events per hour, combining AHI, flattening, oxygen desaturations, gasps, and sudden heart rate changes as an alternative/correlative measure of AHI.

Limb, typically leg, movements are measured with electromyographic (EMG) leads, affixed to the lower leg. Several common measurements are used to describe the sleep test. These are defined in Table 4. Most multichannel home sleep tests come with autoscoring software and, for the most part, the scoring is accurate. However, whoever interprets the sleep studies should be able to read and manually score the sleep study. The following is an abbreviated tutorial. In the simplest of terms, a respiratory obstruction begins. As in the diving reflex, the heart rate immediately decreases. This is shown in Fig. 2. In response to the autonomic stimulation, blood pressure rises. This is shown in Fig. 3. Within seconds of the initiation of the respiratory obstruction, the level of oxygen falls. This is shown in Fig. 4. Ultimately, be it 10 or 60sec, an arousal occurs and the airway is opened. Typically, one sees a rebound phenomenon and several deep breaths (gasps) are noted, the pulse rises and then falls, the blood pressure normalizes, as does the oxygen. This recurring phenomenon tends to cycle and during deep and rapid eye movement (REM) sleep, is most frequent and severe. During deep and REM sleep clusters of apneas and hypopneas are seen. The most severe oxygen desaturations are noted. The widest swings in respiration, heart rate, and blood pressure are seen. The effects of respiratory obstruction on respiration, SpO2, pulse, and blood pressure are shown in Fig. 5. Sympathetic neural stimulation is not measured by most home sleep tests. The effect has been measured and is shown in Fig. 6. The Itamar Watch-PAT100 home

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Figures 2 and 3 The anatomy of apnea pulse and blood pressure are shown. Typically, upon cessation of breathing, diving reflex physiology is instituted and the pulse slows down. When respiration resumes, the pulse overshoots and then slowly returns to normal. Most people have a decrease in blood pressure during sleep. These individuals are typically described as dippers. Patients with SDB have a nighttime rise in blood pressure. This tracing shows that during an apnea there is autonomic neural stimulation and a rise in blood pressure with slow return to normal upon resumption of normal respiration. sleep machine described later in this chapter uses peripheral arterial tone as a measure of SDB.

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Now look at four case examples using an older sleep machine with a particularly simple, albeit excellent, display. 6. CASE EXAMPLES 6.1 Case 1 The first case is a 23-year-old, second-year medical student who presented himself stating that he was snoring and chronically tired. His girl friend suggested that he may have sleep apnea and in any case, his snoring was so bad that she could no longer sleep near him. He studied every night until midnight. On Mondays, Wednesdays, and Fridays he arose at 6 a.m. On Tuesdays, Thursdays, and Saturdays he arose at 7 a.m. On Sundays, he arose at 8 a.m. He was sleepy and often fell asleep during class. 6.1.1 Examination On examination, the patient appeared to be a normal 23-year-old male with height of 5′7″, a weight of 170lb, and a BMI of 24. ENT exam showed a mildly deviated

Figure 4 Oxygen level as measured by SpO2. Shortly, after cessation of breathing, the blood oxygen level begins to fall. As soon as the patient resumes respiration, the oxygen returns to baseline. While this is seen in the

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expanded tracing, it is more commonly viewed in a condensed tracing as shown in the second figure. The normal oxygenation tracing is seen for a period of 10min. A 10min episode of deep sleep is then shown. This is characterized by desaturations, in this case to an SpO2 of 90. In severe apneas the desaturations can be greater, as is shown in the last portion of the recording with desaturations to 80 and sometimes even lower.

Figure 5 A patient with flattening, decreased breathing, and then apnea. During recovery the respiratory gasping is greater than baseline respiration. The oxygen begins to fall shortly after the onset of apnea and does not return to normal until resolution of the apnea. The pulse also falls during the apnea, it overshoots during recovery and slowly returns to normal. Blood pressure rises during the

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apneic episode and then returns to normal during recovery.

Figure 6 Changes in sympathetic neural activation during obstructive respiratory events. The blood pressure tracing shows one of the effects of sympathetic neural activation. (Courtesy of Dr. Somers, Mayo Clinic.) septum. He had undergone tonsillectomy as a child. His pharynx appeared normal. Transnasal endoscopy showed normal anatomy of the pharynx, nose, and larynx. An overnight sleep study was performed and the results are shown in Fig. 7. 6.1.2 Sleep Study—Case 1 This is a normal sleep study. The oxygen is normal without desaturation. Nasal respiration, as indicated by volume, is also normal. The spikes occur at times when the patient turns over or normally takes a deep breath, and snoring is not evident. There are no significant apneas. There are a few hypopneas measured as is reflected in the AHI on the bottom line. This is a normal sleep study. The student was counseled on better sleep hygiene. Further history revealed that the girl friend was disenchanted with the relationship and used the snoring as an excuse to not have to sleep together. I find this a common ploy and one reason to get a history of snoring from more than a single observer. 6.2 Case 2 The next case is a 48-year-old businessman who presented to the UCSD Head and Neck Surgery Sleep Clinic for an evaluation for sleep apnea. His wife accompanied him and provided much of the history. He is a hard-working, successful professional who has snored for most of his adult life. The wife reports that his snoring has become increasingly louder over time. Also, over the past several years, his wife noted an

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increase in the frequency and duration of apneic episodes. Despite up to 10–12hr of sleep per night, the patient remains sleepy during the day. He falls asleep at meetings and spends his weekends at home napping. Needless to say, his problem is beginning to impair his professional and marital life. 6.2.1 Examination On examination, he had a height of 6′1″ and a weight of 230lb, with a BMI of 30. His upper respiratory exam showed a reasonably patent nasal cavity. On oral exam, he had a Mallampati grade 4 and his tonsils were 2+. His uvula was long and edematous, grade II, and his tongue appeared to fill his entire mouth.

Figure 7 Case 1 sleep study. On transnasal fiber optic exam, the soft palate was indeed retrodisplaced. The base of the tongue was positioned posteriorly. His vallecula was occupied by his tongue. This caused posterior displacement of his epiglottis (grade 3). The distance from the epiglottis to the

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pharynx (the posterior air space) was only millimeters wide. Based on the symptoms of snoring, apneic episodes, and EDS, a multichannel home sleep study was ordered. The results are shown in Fig. 8. 6.2.2 Sleep Study—Case 2 In contrast to case 1 this is an abnormal study. As you can see just by the volume of ink, there is a marked difference between the two studies. Looking at the oxygen channel it is evident that the patient spends the majority of the night with significant desaturations, as much as a third of the evening desaturating below 80%. Looking at the nasal ventilation, this patient holds his breath and then gasps, and hence one sees the wide excursions in the respiratory channel. Snoring is evident throughout the study. Apneas are evident throughout the study and are typically 30–45sec in duration. Apneas and hypopneas accrue in each hour of the study. The apnea index is 45, the AHI is 50, and the lowest oxygen desaturation (LSAT) is officially recorded as 70. This is an abnormal sleep study and represents severe OSA.

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Figure 8 Case 2 sleep study. 6.3 Case 3 Case three is a 30-year-old orthodontist who was accompanied by his wife. He described himself as a very loud snorer. Before his examination, he and his wife had vacationed with another couple in a motor home. After 2 days, the other couple had to leave because of his snoring. When questioned about apneic episodes, his wife thought that they occurred sometimes. When questioned about his sleep behavior, the patient reported going to bed between 9 and 10p.m. and awaking between 6 and 7a.m., with frontal headaches. He reported difficulty arising in the morning, but denied any overt symptoms of daytime sleepiness. 6.3.1 Examination The patient was an average, healthy 30-year-old male in good physical shape; his height was 5′11″, weight was 185lb, and BMI was 26. The ENT exam showed no significant obstructive abnormalities. The nose appeared patent. The tonsils were resected when he was a child. Mallampati was 3. The uvula was edematous, grade II, but the posterior space was not otherwise compromised. A multichannel home sleep study was recommended. The results are shown in Fig. 9.

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Figure 9 Case 3 sleep study. 6.3.2 Sleep Study—Case 3 Reviewing this study shows normal oxygenation through most of the night, but on three or four occasions, probably during REM sleep, some desaturations are noted. Nasal ventilation is not quite normal and during the desaturation periods is more active. Snoring is seen throughout much of the study and is consistent with the patient’s complaint. Apneas and hypopneas accrue. The apnea index is 9, the AHI is 21, and the LSAT is 82. While this patient states that he snores, he is young and somehow not yet affected by daytime sleepiness. However, this is sleep apnea. This causes autonomic stimulation. This causes hypertension. This causes release of adhesion molecules, which will contribute to hypertension, heart attacks, stroke, and early death. This patient should be treated for his sleep apnea. CPAP is recommended. Some would argue that the AHI is only 20 and the patient’s only real problems are snoring. Why not do a snoring surgery and follow the patient. My opinion is that an AHI of 20 is abnormal. This is beginning to cause hypertension and long-term cardiovascular effects. This disease will progress with

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age and weight gain. By age 45, the BMI will be 30, the AHI 45, and hypersomnolence will be present. Early hypertension will be noted. The patient will probably have had at least one motor vehicle accident (MVA). CPAP is the preferred treatment. In addition, if palatal surgery is performed and the patient goes on to develop more advanced sleep apnea, as is predicted and typically seen in this illness, the patient may be placed at risk of mouth leak and a more complicated CPAP therapy. 6.4 Case 4 Case 4 is a 12-year-old boy who presented with loud snoring. His mother had witnessed apneic episodes. When she discussed this with her pediatrician, she was advised to consult with a specialist. Neither he nor his mother noted any other sleep symptoms. 6.4.1 Examination On examination, the patient was a thin, 12-year-old male, 54″ in height and 99.5lb in weight, with a BMI of 24. On examination, the patient had a normal nose. He had 3.5+ tonsils and no other obvious abnormality. The patient was recommended for an overnight sleep study. The results are shown in Fig. 10. 6.4.2 Sleep Study—Case 4 The oxygen recordings are seemingly normal. Nasal ventilations are exaggerated, particularly for a 12-year-old. Snoring is evident, some apneas are seen, hypopneas are seen, the AI is 4, the AHI is 14. This is an abnormal study for a 12-year-old boy and confirms the indications for tonsillectomy and adenoidectomy. This child subsequently underwent a tonsillectomy and adenoidectomy (T&A) and made an uneventful recovery. When seen 1 month following surgery, the mother reported that somehow the child seemed calmer and was noted to be doing better at school. When I asked if there was anything else, she said: “You know, it is interesting that this boy has wet his bed every single night of his life. On the day of the surgery the bed-wetting stopped.” She asked: “Do you think that might be related to the sleep apnea, tonsillectomy, and the adenoidectomy?” The answer, of course, is YES. Enuresis is commonly caused by SDB.

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Figure 10 Case 4 sleep study. A follow-up sleep study was normal. 7. SLEEP MACHINES AVAILABLE TO OTOLARYNGOLOGISTS AND PRIMARY CARE PHYSICIANS There are several multichannel home sleep diagnostic machines available to the medical community. To present, compare, and contrast these, I have asked each company to provide their own information in response to the same questions. Where needed, I have edited to remove unnecessary marketing superlatives (Figs. 11–22).

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7.1 Machine 1 Name: Embletta Company: Medcare Size: 2.0cm by 6.5cm by 12.4cm Weight: 110g Channels: Seven sensors, 14 derived signals Recording capacity: 12hr (16Mb memory) Measurements: Flow/pressure (nasal cannula) Nasal/oral flow (thermistor) Snore (by nasal pressure or by neck vibrations with Piezo element sensor) Thoracic movement (by belt with Piezo element sensor) Oximetry (SpO2 average) Oximetry (SpO2 beat to beat) Pulse rate (oximeter) Body position Activity meter Flow limitation Event (marker) Limb movement (optional)

7.1.1 Dispensing The unit is provided to the patient in the office. The usual instruction time is 20min. The patient uses the unit for a single night and returns the unit the next day. Data are downloaded to a computer and then automatically and/or manually scored and a default or customized report printed. Analysis time is <2min with autoscore, 10–30min with manual review or manual scoring.

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Figure 11 A picture of the Embletta unit on a patient. The Embletta combines the sophisticated ResMed respiratory flow algorithm with Medcare, state-of-the-art Somnologica sleep study software. Because this is a sophisticated machine, it takes some trial and error to learn to dispense and interpret. However, once mastered, this is a robust, sophisticated system. 7.1.2 Diagnosis and Treatment Codes Description

Codes

Snoring

ICD.9

780.5

SDB without hypersomnolence

780.53

SDB with hypersomnolence

780.57

ENT examination

CPT

99203/4

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Fiberoptic laryngoscopy

31575

Sleep diagnosis unattended

95806.52

Oximetry

94762

CPAP titration

94660

7.1.3 Validation References Kiely JL, Delahunty C, Matthews S, McNicholas WT. Comparison of a limited computerized diagnostic system (ResCare Autoset) with polysomnography in the

Figure 12 (a) A standard Embletta study reports (above). (b) A summary graph (See next page).

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diagnosis of obstructive sleep apnoea syndrome. Eur Respir J 1996; 9(11): 2360–2364. Alymow G, Topfer V, El-Sebai MA, El-Kholy MGA, Konietzko N, Teschler H. Comparison of a portable respiratory-only polygram with simultaneous polysomnography. Respiratory and Sleep Medicine. Essen, Germany: Ruhrlandklinik. Bradley PA, Mortimore IL, Douglas NJ. Comparison of polysomnography with ResCare Autoset in the diagnosis of the sleep apnoea/hypopnoea syndrome. Thorax 1995; 50(11):1201–1203. Gugger M. Comparison of ResMed AutoSet (version 3.03) with polysomnography in the diagnosis of the sleep apnoea/hypopnoea syndrome. Eur Respir J 1997; 10(3):587– 591. Fleury B, Rakotonanahary D, Hausser-Hauw C, Lebeau B, Guilleminault C. A laboratory validation study of the diagnostic mode of the Autoset system for sleep-related respiratory disorders. Sleep 1996; 19(6):502–505. Davidson TM, Do KL, Justus S. The use of ENT-prescribed home sleep studies for patients with suspected obstructive sleep apnea. Ear Nose Throat J 1999; 78:754–766.

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Figure 12 (b) (See color insert.) 7.1.4 Additional Information Medcare Buffato NY Tel 716 691–0718. www.medcare.com 7.2 Machine 2 Name: Stardust Sleep Diagnostic Device Company: Respironics, Inc. Size: 11.5cm long, 5.8cm wide, 2cm high Weight: 102g (22lb without 9V battery)

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Channels: Three sensors, eight channels Recording capacity: 10hr (256kb, 0.25mg)

(Note: complete study can easily be e-mailed) 7.2.1 Measurements Three inputs for seven-channel recording:

Figure 13 A picture of the Stardust unit on a patient. 1. Airflow sensor measures breath-rate. 2. Oximeter measures pulse rate and oxygen saturation (SpO2). 3. Effort sensor measures chest or abdominal movement. 4. CPAP pressure can be measured with Respironic CPAP machines. 5. Event marker for manual marking of lights out, bathroom units, etc. 6. Body position monitor. 7.2.2 Dispensing The Stardust is an ultraportable unit worn on the patient’s chest. Three patient sensors are attached to the device. The Stardust study may take place both in the home or as an attended procedure. The data are auto and/or manually scored with automatic and custom report capabilities generated in Microsoft Word format. The device has a real-time view and record capability, which may be used for the attended as well as the unattended in home use. The unit is powered by a 9V battery with easy to learn viewing, scoring, and reporting.

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Stardust uses the Alice® 4 software in a Windows-based application. The unit has preprogrammed default settings that can be adjusted. Manual and autoscore capabilities and default or customized reports are available. Manual scoring takes time to learn, but one material is reliable. 7.2.3 Diagnosis and Treatment Codes Description

Codes

Snoring

ICD.9

780.5

SDB without hypersomnolence

780.53

SDB with hypersomnolence

780.57

ENT examination

CPT

99203/4

Fiberoptic laryngoscopy

31575

Sleep diagnosis unattended

95806

Sleep diagnosis attended

95807

Oximetry

94762

CPAP titration

94660

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Figure 14 (a) A picture of a typical tracing of the Stardust study (above). (See color insert.) (b) A summary graph. 7.2.4 Validation References Ferguson KA, Heighway K, George CFP. Evaluation of the stardust respiratory diagnostic device during polysomnography in suspected obstructive sleep apnea. In: 6th World Congress on Sleep Apnea, Sydney, Mar 2000. 7.2.5 Additional Information Global headquarters: Pittsburgh, PA, USA (412) 731–2100

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Corporate Customer Service (1–800) 345–6443 Respironics, Europe 33–(0) 1–55–60–19–80 Respironics, Asia-Pacific 852–234–342–18 www.respironics.com

Figure 14 (b) (See color insert.)

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Figure 15 A picture of the NovaSom unit on a patient.

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Figure 16 A picture of a typical tracing of the NovaSom on (a) study night 1 (above). (See color insert.) (b) study night 2, and (c) study night 3. (d) Sleep study summary.

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7.3 Machine 3 Name: NovaSom QSG Company: Sleep Solutions, Inc. Size: 10cm by 6.2cm by 2.8cm (patient module) Weight: 113g (patient module) Channels: Three sensors, five derived signals Recording capacity: More than four nights

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Figure 16 (b) (See color insert.) Measurements: Respiratory airflow, oral/nasal combined Snoring, by acoustic microphone Respiratory effort by thoracic belt Oximetry (SpO2 with 1sec resolution) Pulse rate (oximeter)

7.3.1 Dispensing How Does the Service Work? The physician orders the sleep test via phone, fax, or website www.sleepsolutions.com. The NovaSom QSQ is delivered directly to the patient’s home. An instructional packet and video guide the patient through the setup. The patient applies three small comfortable sensors and then pushes the “start” button. Voice prompts guide the patient through the process and alert them if any of the sensors are displaced during the night. After up to three nights of use the patient places the system back in the original shipping box and returns it to Sleep Solutions using a prepaid airway bill. The data are extracted and analyzed, and a summary of the data is prepared and delivered to the referring physician via fax, mail, or Internet. The NovaSom QSG utilizes clinically validated, patented digital signal processing technology to provide a respiratory signal with a linear correlation to actual airflow. This robust signal, along with unique human factors, allows for the reliable self-administration of this device for up to three nights. The resulting sleep data are condensed into a highly readable report that contains all of the data needed for diagnosis of OSA. The NovaSom QSG is the only device cleared by the US Food and Drug Administration (FDA) specifically designed for unattended and unassisted use in the patient’s home and clinically proven to be equivalent to PSG in-the laboratory.

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Figure 16 (c) (See color insert.)

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Figure 16 (d)

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Figure 17 Pictures of the SNAP unit on a patient. 7.3.2 Diagnosis and Treatment Codes Description

Codes

Snoring

ICD.9 780.5

SDB without hypersomnolence

780.53

SDB with hypersomnolence

780.57

ENT examination

CPT

99203/4

Fiberoptic laryngoscopy

31575

Sleep diagnosis unattended

95806 (22 modifiers sleep study; 26 modifiers for interpretation)

Oximetry

94762

CPAP titration

94660

7.3.3 Validation References Pending. 7.3.4 Additional Information Sleep Solutions [email protected] Tel 877 753–3775 www.sleepsolutions.com

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7.4 Machine 4 Name: SNAP Model 6 Company: SNAP Laboratories LLC Size: 17.7cm by 18.8cm by 5.8cm Weight: 1278.6g (2lb 13.1 oz.) Channels: Five sensors, seven derived signals Recording capacity: 8hr

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Figure 18 Pictures of a typical tracing of the SNAP study: (a) apnea analysis, (b) snoring analysis, and (c) oximetry analysis. Measurements:

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Airflow (oro-nasal cannula) Snoring (oro-nasal microphone) Oximetry (SpO2 beat to beat, average) Pulse rate (oximetry) Respiratory effort (belt, piezoelectric sensor) Body position (optional) Limb movement (optional)

149

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Figure 18 (b) 7.4.1 Dispensing The unit is provided to the patient in the physician’s office. The usual instruction time is 10min. After one night of use the patient returns the unit to the physician’s office where a large-capacity disk containing all data is removed from the system and forwarded to

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SNAP Laboratories. At SNAP the data are downloaded to a computer analysis system and automatically and manually analyzed. A report including apnea, objective snoring analysis, and oximetry is generated. Interpretation is performed by medical consultants at SNAP Laboratories or by the referring physician.

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Figure 18 (c) The SNAP system uniquely detects and quantifies sleep apnea using airflow technology that has been shown to be significantly more accurate than traditional thermistors. SNAP provides the only objective method for the acoustic analysis and spectral profiling of snoring. This information is particularly useful for physicians to localize and quantify the source of snoring in the upper airway.

Figure 19 A picture of the WatchPAT100 unit on a patient. 7.4.2 Diagnosis and Treatment Codes Description

Codes

Snoring

ICD.9

780.5

SDB without hypersomnolence

780.53

SDB with hypersomnolence

780.57

ENT examination

CPT

99203/4

Fiberoptic laryngoscopy

31575

Dispensing equipment

99211

Sleep test (built by SNAP)

95806.52

Interpretation

95806.26

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7.4.3 Validation References Weingarten CZ, Raviv G. Evaluation of criteria for uvulopalatoplasty (UPP) patient selection using acoustic analysis of oronasal respiration (SNAP testing). J Otolaryngol 1996; 106:352–357. Weingarten C. Snare uvulopalatoplasty. Laryngoscope 1995; 105:1033–1036. Walker RP, Gatti WM, Poirier RN, et al. Objective assessment of snoring before and after laser-assisted uvulopalatoplasty. Laryngoscope 1994; 106(11): 1372–7. Erratum in: Laryngoscope 1997; 1:143. 1996; 106:1372–1377. Brietzke SE, Mair EA. Injection snoreplasty: how to treat snoring without all the pain and expense. Otolaryngol Head Neck Surg 2001; 124:503–510. 7.4.4 Additional Information SNAP Laboratories LLC Phone: 800 SNAP786/847 657–8100/847 657–8586 www.snaplab.com

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Figure 20 A picture of a typical tracing of the Watch-PAT100 study. (See color insert.) 7.5 Machine 5 Name: Watch-PAT100 Company: Itamar Medical Ltd. Size: 2.0cm by 6.5cm by 12.4cm

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Weight: 110g Channels: Three sensors, four derived signals Recording capacity: 10hr (16Mb memory)

Figure 21 A picture of the Remmers unit on a patient. Measurements: Peripheral arterial tone (PAT) signal Pulse rate (PAT derived) Pulse oximetry Actigraphy

7.5.1 Dispensing The unit is provided to the patient in the office. The usual instruction time is 5min. The patient uses the unit for a single night and returns the unit the next day. The overall automatic data process takes 2min: download, automatic scoring, and compiling of the findings to comprehensive report (numerical and graphical displays). The automatic scoring of the Watch-PAT100 device detects respiratory events and separates sleep periods from wakefulness (FDA approved). Therefore, the calculated respiratory disturbance index (RDI) is derived solely from sleep periods, rather than from

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the total recording time. Additionally, by detecting sleep arousal and REM sleep (submitted to the FDA), sleep architecture and fragmentation are assessed. 7.5.2 Diagnosis and Treatment Codes Description

Codes

Snoring

ICD.9

ENT examination

CPT

Fiberoptic laryngoscopy

780.5 99203/4 31575

Sleep diagnosis

None

Figure 22 A picture of a typical tracing of the Remmers study.

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7.5.3 Validation References Bar A, Pillar G, Dvir I, Sheffy K, Schnall RP, Lavie P. Evaluation of a portable device based on arterial peripheral tonometry (PAT) for unattended home sleep studies. Chest 2003; 123(3):695–703. Grote LB, Ding Z, Murphy P, Peker P, Lindblad U, Hedner J. Detection of sleep disordered breathing in a general population based on the peripheral arterial tone. Sleep 2002; 25(abstr suppl):352. Pittman SD, Pillar G, Ayas NT, Suraiya S, Maholtra A, White DP. Can obstructive sleep apnea be diagnosed in the home using a wrist-mounted device with automated analysis of peripheral arterial tonometry, pulse oximetry, and actigraphy? Sleep 2002; 25(abstr suppl):42. O’Donnell CP, Allan L, Atkinson P, Schwartz AR. The effect of upper airway obstruction and arousal on peripheral arterial tonometry in obstructive sleep apnea. Am J Respir Crit Care Med 2002; 166:965–971. Schnall RP, Shlitner A, Sheffy J, Kedar R, Lavie P. Periodic, profound peripheral vasoconstriction—a new marker of obstructive sleep apnea. Sleep 1999; 22(7):939–946. 7.5.4 Additional Information Itamar Medical Ltd Boston, MA 617–878–2161, www.itamar-medical.com 7.6 Machine 6 Name: Remmers Sleep Recorder (formerly SnoreSat) Company: SagaTech Electronics Inc. Size: 4.5cm by 19cm by 20cm Weight: 1000g Recording capacity: 8–45hr (dependent on configuration) Recorded signals: Blood oxygen saturation Heart rate Nasal airflow (nasal cannula pressure) Snoring Body position Respiratory movement Respiratory airflow during treatment study (pneumotachograph) CPAP pressure (compatible with any brand) EMGs

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7.6.1 Dispensing The Remmers is a seven-channel sleep recorder with automatic analysis of data. The calculated RDI has been validated in a large randomized clinical study. The computergenerated analysis eliminates the need for manual scoring because it provides an RDI that correlates closely with the polysomnographic AHI (R=0.97). The RDI calculated by the automated analysis algorithm has a sensitivity of 98% and a specificity of 88% in diagnosing sleep apnea, using an AHI threshold of 15 events per hour. The Remmers is designed for convenient unattended studies. The device is dispensed from the office, and instruction takes ≈15min. The probes are easily applied by the patient, and a visual analog scale on the front of the recorder provides feedback, validating adequate signal integrity before the study begins. This results in a technical success rate of 98%. The analysis and reporting software operates on any Windows-based computer, making it easy to configure and download studies. A one-page report summarizes a night’s study, and the raw data from all channels can be displayed and printed. 7.6.2 Case study A 50-year-old carpenter presents with a history of heavy snoring, and his wife has noted that he occasionally stops breathing during sleep. He reports that he is sleepy while driving but has not had an auto accident. He has medically controlled hypertension but no other significant illnesses. Physical exam reveals an obese male with a large neck (neck circumference 45cm). A 2mm overbite and a large tongue were noted. The adjusted neck circumference is 55cm (neck circumference plus 3cm for snoring plus 3cm for witnessed apnea plus 4cm for hypertension; N Engl J Med 2002; 347:498– 504). This indicates a high probability of sleep apnea. A Remmers Sleep Recorder test was performed, revealing heavy snoring (snoring index of 420 per hour), an RDI of 43 per hour, and severe hypoxemia (30% of the night with oxygen saturation <90%). In view of the patient’s symptoms and the severity of sleep apnea, the patient was given a therapeutic trial of CPAP using an automatically adjusting CPAP device. The patient reported dramatic improvement in daytime symptoms. A follow-up test with the Remmers Sleep Recorder test, while on CPAP, revealed an RDI of 3.2 and normal arterial oxygenation. 7.6.3 Diagnosis and Treatment Codes Description

Codes

Snoring

ICD.9

780.5

SDB without hypersomnolence

780.53

SDB with hypersomnolence

780.57

ENT examination Fiberoptic laryngoscopy

CPT

99203/4 31575

Home Sleep Testing

159

Sleep diagnosis unattended

95806

Oximetry

94762

7.6.4 Validation References Vazquez JC, Tsai WH, Flemons WW, Masuda A, Brant R, et al. Thorax 2000; 55:302– 307. 7.6.5 Additional Information SagaTech Electronics (403) 228–4214 www.sagatech.ca or remmers@ sagatech.ca 7.7 Machine 7 Name: Edentrace Company: Puritan Bennett Size: 3.5″ by 7.4″ by 11.2″ Weight: 3.3lb Channels: Six internal and two external Measurements: Nasal/oral airflow Breath sounds/snoring level SpO2 via pulse oximeter Transthoracic impedance Heart rate Body position

7.7.1 Dispensing The unit is provided to the patient from the physician’s office. The instruction time is under 30min. The patient uses the unit for a single night and returns it the following morning. The data are downloaded to a Pentium II 200 or higher computer and then automatically and/or manually scored. A report is generated. Auto analysis takes <5min. Manual analysis takes <45min. The unit allows simultaneous data display via printer or computer while continuously recording. For infant studies interface with a heart and respiration monitor is available.

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7.7.2 Diagnosis and Treatment Codes Description

Codes

Snoring

ICD.9

780.5

SDB without hypersomnolence

780.53

SDB with hypersomnolence

780.57

ENT examination

CPT

99203/4

Fiberoptic laryngoscopy

31575

Sleep diagnosis unattended

95806

Oximetry

94762

CPAP titration

94660

7.7.3 Validation References Emsellem HA, Corson WA, Rappaport BA, Hackett S, Smith LG, Hausfeld JN. Verification of sleep apnea using a portable sleep apnea screening device. South Med J 1990; 83(7):748–752. Redline S, Tosteson T, Boucher MA, Millman RP. Measurement of sleeprelated breathing disturbances in epidemiologic studies. Assessment of the validity and reproducibility of a portable monitoring device. Chest 1991; 100(5):1281–1286. 7.7.4 Additional Information Nellcor Puritan Bennett (Melville) Ltd., 141 Laurier Avenue West, Suite 700, Ottawa, ON K1P5J3, Canada 1–(800) 663–3336 www.sandmansleep.com

8. NIGHT-TO-NIGHT VARIABILITY Is there night-to-night variability and does it matter? There is a 10% night-to-night variability (34,35). In the ideal world without artificial AHI cutoffs, this would not make a difference. However, in today’s world with insurance company guidelines and authorizations it does make a difference. Remember, anyone with an AHI of 5 or more has SDB. The insurance companies generally use an AHI of 15 as the cutoff or 5 with two comorbidities. The issue is what is the difference between an AHI of 14 and 15? If a patient strongly suspect for SDB has an AHI between 10 and 14, do you argue with the insurance company or repeat the test, possibly with a glass of wine to insure a poorer result? There is a phenomenon called the first-night effect (36–38). This is a research issue for subjects undergoing in-house PSG. The first-night effect is normally not operant for multichannel home sleep testing.

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For research purposes night-to-night variability for multichannel home sleep testing is insignificant. When groups are studied as means, night-to-night variability is 1–2%. However, for individual tests there is 10% variability. This probably reflects the intrinsic variability of normal sleep, auto score machine variability, or for some a firstnight effect. The autoscoring of the sleep machines is most accurate for higher AHIs. There is as much as a 10% variability for manual vs. autoscoring. One can also change the scoring parameters, i.e., 10–8sec for an apnea or hypopnea. One can also define apnea or hypopnea with or without oxygen desaturation and if one employs oxygen desaturation can one use a 2% or a 4% desaturation? Can one include or exclude other parameters? For example, is a 4% O2 desaturation without a 50% decrease in respiration a respiratory event? The same question can be asked for sudden changes in respiration (gasping implies an apneic episode) or sudden change in heart rate. There are also differences in sleep machines. Table 5 shows comparisons for Embletta, Bedbug, and SNAP. Embletta and Bedbug with a 2% desaturation were similar. SNAP and Bedbug with a 4% desaturation reported lower AHIs. I have not done comparison and validation with the other machines. For those with moderate and severe SDB with AHIs of 30 or greater, these are academic issues of no clinical significance. However, for surgeons treating snoring in patients with AHIs of 5–20, night-to-night variability can be an issue. The general recommendation is that the diagnosis of SDB is based on the history, the examination, and the sleep test. If the insurance company requires an AHI >15, but the sleep test AHI is lower and the clinical impression is that the patient has the disease, you can repeat the sleep test. If you wish to insure a worse result, an alcoholic beverage prior to sleep will certainly help your patient relax. Alternatively, you can argue in favor of the diagnosis based on the clinical findings.

9. EVALUATION AND TREATMENT ALGORITHM Evaluation and treatment can be made simple or complex. I prefer to make it simple (Fig. 23). Snoring is the premier symptom of SDB. Hence, anyone with snoring loud or bad enough to bring them to medical attention warrants an upper respiratory tract examination, fiberoptic laryngoscopy included, and a sleep test. While treatment is discussed elsewhere by others in this book, it is to some degree part of the diagnostic paradigm and so is included here. Having been increasingly disappointed in surgery for SDB, I have come to the opinion that the treatment of choice for SDB is CPAP. This is based on several observations: First, surgeries like septoplasty, turbinate reduction, endoscopic sinus surgery (ESS), laser assested uvulo palatoplasty (LAUP), uvulo palatophay plasty (UP3), cautery assested palatal stiffening operation (CAPSO), tongue-base reductions and resections, suture and tongue advancements have not been uniformly successfully for OSA.

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Second, there is little scientific, evidence-based literature documenting the benefit of surgery.

Table 5 Comparisons for Embletta, Bedbug, and SNAP BedBugg vs. Embletta Background: The devices were worn by 14 patients. Results: Correlation coefficient between Embletta and BedBugg AHI scores was 0.823, which was significant at the p<0.0001 level. I did not calculate classification, but few would have been misclassified by the BedBugg (except for the individual who had an AHI of 28 on Embletta and almost 0 on the BedBugg). Figure: Scatterplot of the AHI derived from each device.

Snap vs. Embletta—different nights Background: The devices were worn on different nights by 16 patients (1 woman and 15 men) with a mean age of 39 (range: 15–60), mean BMI of 28.1 (range: 20.8–37.4), mean Epworth sleepiness score of 10.8 (range: 0–25). Note: Eleven of the 16 patients had AHI data on both the nights. Results: Correlation coefficient between Embletta and SNAP AHI scores was 0.60, which was significant at the p=0.05 level. Given an AHI classification of <5 being mild, 5–30 being moderate and >30 being severe, it appears that the SNAP would classify the apnea level quite consistently with the Embletta. (Note: There were two cases where SNAP had an AHI score of 6 while the Embletta had a score of <5.) It should be noted that this study is significantly limited by the low number of data points; however, it does offer preliminary evidence.

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Figure: Scatterplot of the AHI derived from each device.

Classification The contingency tables below classify AHI into two groups—(mild: 0–9.99, moderate: 10–19.99, and moderate to severe: ≥20) and (mild: 0–4.99, moderate: 5–19.99, and moderate to severe: ≥20). For this analysis, the Embletta is considered the gold standard test and the SNAP is being evaluated.

What the tables show is that in the diagonals, 5 and 6 of the total of 11 cases (45% and 54%), respectively, were classified correctly. There appears to be a clear trend for the SNAP to result in a higher AHI than the Embletta—see numbers. This could be due to one of several things: (1) natural night-to-night variability, (2) SNAP is indeed overestimating AHI, or (3) Embletta scoring results in under estimation of TST, which then artificially lowers AHI. I would recommend rescoring of the records to rule out possibilities

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(2) and (3), which would increase the confidence in other explanations.

Snap vs. Embletta-same night Background: The devices were worn on the same night by 8 patients (two women and six men) with a mean age of 43.6 (range: 27–66), mean BMI of 29.5 (range: 22.7–43.8), mean Epworth sleepiness score of 11.3 (range: 0–17). Results: Correlation coefficient between Embletta and SNAP AHI scores was 0.987, which was significant at the p <0.0001 level. Given an AHI classification of <5 being mild, 5–30 being moderate, and >30 being severe, it appears that the SNAP would classify the apnea level quite consistently with the Embletta. (Note: There were two cases where SNAP had an AHI score of 6 while the Embletta had a score of <5.) It should be noted that this study is significantly limited by the low number of data points; however, it does offer preliminary evidence. Figure: Scatterplot of the AHI derived from each device.

Third, there is concern that soft palate surgery may predispose to mouth leak (39). If the surgery fails and the patient is required to treat with CPAP, mouth leak is difficult to manage, often requiring a full-face mask, and so impairs future CPAP use. Fourth, SDB progresses with age, probably as a result of increasing BMI and as a function of increasing tissue laxity. Hence, I worry about surgery on a 30-year-old snorer, surgery that has no evidence-based validity, which may fail with time and may ultimately impair that individual’s ability to use CPAP.

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Snoring requires an upper respiratory tract sleep examination, laryngoscopy included, and then a sleep test. Now, one has to make a decision regarding medical vs. surgical therapy. I contend that a CPAP trial hurts no one and if the patient finds benefit, then the right treatment is CPAP.

Figure 23 Snoring examination and multichannel home sleep test algorithm. Algorithms for the evaluation and treatment of snoring can be simple or complex. The above is a simple algorithm to initiate one’s decision-making. The sleep test, and ultimately the AHI, is the primary objective measure of SDB. This unfortunately has potential errors. While it may be true that for the average adult male an AHI cutoff of 5, 10, 15, or 20 may reasonably reflect disease severity, it is increasingly clear that this is not true of other populations. Children, for example, can be significantly symptomatic with AHIs of 5–15. Women will also be symptomatic with AHIs <15, sometimes <5. In some individuals an AHI may not even be recorded and yet there is restriction of breathing and arousal. If the patient does poorly with CPAP, the surgeon must make one of several decisions: 1. Snoring without EDS with AHI <15

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• With examination suggesting snoring is palatal, the patient is treated with palatal resection or stiffening, whether by lasers, submucosal cautery, injection of sclerosing agent, or placement of an implant. • With examination suggesting snoring is caused by other correctable anatomic lesions such as nasal polyps or 3+ or 4+ tonsils, the patient is also treated with surgery directed at the site of obstruction. • With examination suggesting snoring is not easily surgically corrected and will progress with time, the patient is treated with CPAP. If CPAP is declined, repeat the sleep evaluation annually. Do not perform surgery as “Let’s try and see.” 2. Snoring with EDS with AHI <15, CPAP failure • Four-plus anatomic obstruction, i.e., polyps or tonsils: The patient is recommended for surgery. • No obvious 3+ or 4+ anatomic obstruction: Consider snoring surgery but repeat sleep test 3 months postoperative. 3. AHI 15–30: The treatment is CPAP. If it fails • Obvious 3+ or 4+ anatomic resection: Treat with surgery. • No obvious anatomic obstruction: Re-encourage the patient to use CPAP. If there is truly no benefit and the patient desires snoring therapy, you are removing the patient’s warning symptom of SDB, but with informed consent, it is probably acceptable. 4. AHI ≥30: the treatment is CPAP. If it fails • Obvious 3+ or 4+ anatomic obstruction, surgery may be considered: Do not resect soft palate. • CPAP failure secondary to nighttime nasal obstruction

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Figure 24 Alternate algorithm for evaluation and treatment of SDB. Hx and Px—suggesting SDB. Hx major— snoring, witnessed apneic episodes, EDS, falling asleep driving or at meetings plus hypertension, heart failure, and nocturnal arrhythmias. Hx minor—associated illnesses, nocturia, gastro esophageal reflux (GERD), asthma, diabetes, and arteria deficit

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and artertion deficit hyperactivity disorder (ADD&ADHD). Px— suggesting SDB. Px—BMI >30, neck circumference >40cm, Mallampatti III or IV, tonsils III or IV, nasal polyps, narrow pharynx, and edematous uvula. • Try autotitrating CPAP and add heated humidification • If this fails, consider nasal surgery. • CPAP failure without obvious 3+ or 4+ anatomic obstruction: This patient will require maxillomandibular advancement or tracheostomy. At this point I would like to suggest a different approach to the evaluation/ treatment algorithm. I am of the opinion that no one, in the absence of SDB, will benefit from CPAP. Therefore, the most effective and least expensive paradigm is to take all snorers and perform an examination to rule out neoplasm. Assuming no neoplasm, place the patient on autotitrating CPAP. Those that benefit, by definition, have the disease and have the proper treatment. Those who do not benefit will require a multichannel home sleep test and then consideration of CPAP, snoring therapy, or surgical therapy. This is depicted in Fig. 24.

10. CONCLUSION Sleep testing is a mandatory component of the evaluation of patients with snoring. Multichannel home sleep testing is accurate, i.e., highly specific and highly sensitive, when compared to PSG. The multichannel home sleep test is less expensive then PSG, is better tolerated by patients, can be administered by otolaryngologists and primary care physicians, and is easy to score. Based on accuracy, sensitivity, specificity, ease of application, physician acceptance, expense, and patient acceptance, multichannel home sleep testing is the preferred sleep test for patients with snoring and a presumptive diagnosis of SDB.

ADDITIONAL READING 1. Dement WC, Vaughan C. The Promise of Sleep: A Pioneer in Sleep Medicine Explores the Vital Connection between Health, Happiness, and a Good Night’s Sleep. A well-written book covering all of sleep medicine. Easy to read and an absolute must for all in sleep medicine. 2. Principles and Practice of Sleep Medicine. 3rd edition by Kryger, Roth, and Dement. A twovolume classic text on sleep medicine. This is the authoritive text on sleep. 3. Sleep Primer—Paige, Ancoli, and Davidson. www.surgery.ucsd.edu/ent/ DAVIDSON/SleepDisorders.pdf. A simple online resource on sleep. Excellent for medical students and primary care physicians. 4. Additional literature: The sleep literature is voluminous and difficult to interpret.

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The surgical literature reports studies demonstrating the benefits of a given procedure. Crossover studies are rarely conducted. Author bias confounds the conclusions. Shortterm follow-up is also a concern. Sleep physician (nonsurgical) literature is seriously compromised by two elements. First, whatever is written is invariably presented to insure that only a board certified sleep specialist can render the diagnosis and treatment, invariably using inhouse PSG. This is most evident in the multichannel home sleep testing literature. Second, the sleep physicians have become obsessed with evidence-based medicine and often spend more time identifying weaknesses in their studies than explaining the obvious, simple, clinically useful conclusions.

REFERENCES 1. Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleepdisordered breathing among middle-aged adults. N Engl J Med 1993; 328:1230–1235. 2. He J, Kryger MH, Zorick FJ, Conway W, Roth T. Mortality and apnea index in obstructive sleep apnea. Experience in 385 male patients. Chest 1988; 94:9–14. 3. Lacasse Y, Godbout C, Series F. Health-related quality of life in obstructive sleep apnoea. Eur Respir J 2002; 19:499–503. 4. Weinger MB, Ancoli-Israel S. Sleep deprivation and clinical performance. J Am Med Assoc 2002; 287:955–957. 5. Mitler MM, Carskadon MA, Czeisler CA, Dement WC, Dinges DF, Graeber RC. Catastrophes, Sleep, and Public Policy: Consensus Report. Sleep 1988; 11:100–109. 6. Lyznicki JM, Doege TC, Davis RM, Williams MA. Sleepiness, driving, and motor vehicle crashes. Council on Scientific Affairs, American Medical Association. J Am Med Assoc 1998; 279:1908–1913. 7. Driving with sleep apnea. N Engl J Med 1999; 340 (editorial). 8. Teran-Santos J, Jimenez-Gomes A, Cordero-Guevara J, the Cooperative Group BurgosSantander. The association between sleep apnea and the risks of traffic accidents. N Engl J Med 1999; 340:847–851. 9. Powell NB, Schechtman KB, Riley RW, Li K, Troell R, Guilleminault C. The road to danger: the comparative risks of driving while sleepy. Laryngoscope 2001; 111:887–893. 10. Young T, Peppard P, Palta M, Hla KM, Finn L, Morgan B, Skatrud J. Population-based study of sleep-disordered breathing as a risk factor for hypertension. Arch Intern Med 1997; 157:1746–1752. 11. Peppard PE, Young T, Palta M, Skatrud J. Prospective study of the association between sleepdisordered breathing and hypertension. N Engl J Med 2000; 342:1378–1384. 12. Nieto FJ, Young TB, Lind BK, Shahar E, Samet JM, Redline S, D’Agostino RB, Newman AB, Lebowitz MD, Pickering TG. Association of sleep-disordered breathing, sleep apnea, and hypertension in a large community-based study. Sleep Heart Health Study. J Am Med Assoc 2000; 283:1829–1836. 13. Bixler EO, Vgontzas AN, Lin HM, Ten Have T, Leiby BE, Vela-Bueno A, Kales A. Association of hypertension and sleep-disordered breathing. Arch Intern Med 2000; 160:2289– 2295. 14. Pepperell JC, Ramdassingh-Dow S, Crosthwaite N, Mullins R, Jenkinson C, Stradling JR, Davies RJ. Ambulatory blood pressure after therapeutic and subtherapeutic nasal continuous positive airway pressure for obstructive sleep apnoea: a randomized parallel trial. Lancet 2002; 359:204–210. 15. Malhotra A, White DP. Obstructive sleep apnoea. Lancet 2002; 360:237–245.

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16. Peker Y, Hedner J, Kraiczi H, Loth S. Respiratory disturbance index: an independent predictor of mortality in coronary artery disease. Am J Respir Crit Care Med 2000; 162:81–86. 17. Midelton GT, Frishman WH, Passo SS. Congestive heart failure and continuous positive airway pressure therapy: support of a new modality for improving the prognosis and survival of patients with advanced congestive heart failure. Heart Dis 2002; 4:102–109. 18. Wessendorf TE, Wang YM, Thilmann AF, Sorgenfrei U, Konietzko N, Teschler H. Treatment of obstructive sleep apnoea with nasal continuous positive airway pressure in stroke. Eur Respir J 2001; 18:619–622. 19. Wessendorf TE, Thilmann AF, Wang YM, Schreiber A, Konietzko N, Teschler H. Fibrinogen levels and obstructive sleep apnea in ischemic stroke. Am J Respir Crit Care Med 2000; 162:2018–2020. 20. Hajduk IA, Jasani RR, Strollo PJ, Atwood CW, Sanders MH. Nocturia in sleep disordered breathing. Sleep Med 2000; 1:263–271. 21. Chervin RD, Archbold KH, Dillon JE, Panahi P, Ptuch KJ, Dahl RE, Guilleminault C. Inattention, hyperactivity, and symptoms of sleep-disordered breathing. Pediatrics 2002; 109:449–456. 22. Nassem S, Chaudhary B, Collop N. Attention deficit hyperactivity disorder in adults and obstructive sleep apnea. Chest 2001; 119:294–296. 23. Bohadana AB, Hannhart B, Teculescu DB. Nocturnal worsening of asthma and sleepdisordered breathing. J Asthma 2002; 39:85–100. 24. Valipour A, Makker HK, Hardy R, Emegbo S, Toma T, Spiro SG. Symptomatic gastroesophageal reflux in subjects with a breathing sleep disorder. Chest 2002; 121:1748– 1753. 25. Ohayon MM, Li KK, Guilleminault C. Risk factors for sleep bruxism in the general population. Chest 2001; 119:53–61. 26. Lefcourt LA, Rodis JF. Obstructive sleep apnea in pregnancy. Obstet Gynecol Surv 1996; 51:503–506. 27. Halvorson DJ, Porubsky ES. Obstructive sleep apnea in women. Otolaryngol Head Neck Surg 1998; 119:497–501. 28. Friedman M, Tanyeri H, La Rosa M, Landsberg R, Vaidyanathan K, Pieri S, Caldarelli D. Clinical predictors of obstructive sleep apnea. Laryngoscope 1999; 109:1901–1907. 29. Somers VK, Dyken ME, Clary MP, Abbound FM. Sympathetic neural mechanism in obstructive sleep apnea. J Clin Invest 1995; 96:1897–1904. 30. El-Solh AA, Mador MJ, Sikka P, Dhillon RS, Amsterdam D, Grant BJB. Adhesion molecules in patients with coronary artery disease and moderate-to-severe obstructive sleep apnea. Chest 2002; 121:1541–1547. 31. Woodson TB, Hans J. Snoring: a cardinal symptom of sleep disordered breathing. Otolaryngol Head Neck Surg 2000; 123:P139. 32. Mallampati SR, Gatt SP, Gugino LD, Desai SP, Waraksa B, Freiberger D, Liu PL. A clinical sign to predict difficult tracheal intubation: a prospective study. Can Anaesth Soc J 1985; 32:429–434. 33. Condos R, Norman RG, Krishnasamy I, Peduzzi N, Goldring RM, Rapoport DM. Flow limitation as a noninvasive assessment of residual upper-airway resistance during continuous positive airway pressure therapy of obstructive sleep apnea. Am J Respir Crit Care Med 1994; 150:475–480. 34. Davidson TM, Gehrman P, Ferreyra H. Lack of night-to-night variability of sleep-disordered breathing during home monitoring. Ear Nose Throat J. In press. 35. Stepnowsky CJ, Orr WC, Davidson TM. Nightly variability of sleep-disordered breathing measured over 3 nights. Otolaryngol Head Neck Surg 2004; 131:837–843. 36. Agnew HW, Webb WB, Williams RL. The first night effect: an EEG study of sleep. Psychophysiology 1966; 2:263–266.

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37. Schmidt HS, Kaelbing R. The differential laboratory adaptation of sleep parameters. Biol Psychiatry 1971; 3:33–5. 38. Webb WB, Campbell SS. The first night effect revisited with age as a variable. Waking Sleeping 1979; 3:319–324. 39. Mortimore IL, Bradley PA, Murray JA, Douglas NJ. Uvulopalatopharyngoplasty may compromise nasal CPAP therapy in sleep apnea syndrome. Am J Respir Crit Care Med 1996; 154:1759–1762.

7 Video Sleep Nasendoscopy V.J.Abdullah and C.A.van Hasselt Division of Otolaryngology, Department of Surgery, Prince of Wales Hospital, Chinese University of Hong Kong, Shatin, Hong Kong 1. VIDEO SLEEP NASENDOSCOPY The study of upper airway dynamics in obstructive sleep apnea syndrome (OSAS) has always posed a challenge to the interested. Until the dynamics in OSA is well understood, treatment options cannot be comprehensive. To date, continuous positive airway pressure (CPAP) remains the most efficacious first-line treatment as it stents open the entire upper airway without the need for prior knowledge of the dynamics in OSA. Many patients are, nevertheless, not amenable to its lifelong use. Support is important for this group of patients, particularly if surgical or non-surgical options other than CPAP can alleviate, if not cure. The much disfavored tracheostomy with all its unpleasant problems is known to help in OSAS of an understanding of the dynamics of the upper airway above the glottis in OSAS, and has achieved the best long-term survival (1,2). This confirms the importance especially if effective surgery is to be designed. From the surgical viewpoint, the clear establishment of the obstructive sites is essential for the planning of effective treatment, if available. The Muller maneuver, once a popular technique for selecting patients for uvulopalatopharyngoplasty (UVPP) (3), is at best an easy to perform estimation of tissue collapse in the upper airway under inspiratory suction. The findings may differ quite significantly from the sleep breathing situation (4). Cine CT and Cine MRI are ideal but not practicable in terms of costs and the difficulties involved in the overnight study of an OSAS patient in a confined space. There is always the additional worry of irradiation in detailed cine CT. Inspection of the upper airway of the sleeping patient through the night with the fiberoptic nasopharyngeal endoscope is ideal but time and manpower consuming. It is seldom well tolerated and often results in significantly disturbing the patient and thus the normal/abnormal sleep pattern. The surgeon understandably prefers to see the actual events during sleep breathing difficulties to guide his plans for the appropriate surgical intervention. Video sleep nasendoscopy (VSE) (5) in the, albeit simulated, sleep breathing situation is our preferred technique for assessing the surgical candidates in our unit in Hong Kong. Its findings are probably the closest to the truth or, at most, closest to the worst situation that stands to be corrected.

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2. INDICATIONS VSE in our establishment is reserved for research protocols, selected snorers, and the OSAS surgical candidates as selected by our multidisciplinary team. Our multidisciplinary team consists of respiratory physicians, psychiatrists, neurologists, otolaryngologists, pediatricians for the pediatric cases, and physiotherapists for our weight control program for the obese. VSE is not used for the diagnosis of OSAS and is interpreted in the light of a full night’s polysomnographic sleep study (PSG). Our criteria for surgical intervention in adult patients are the PSG proven snorers, upper airway resistance syndrome, OSAS patients with a body mass index (BMI) of <30, and patients with correctable craniofacial deficits, e.g., “South China chin,” retrognathia, which is common in our locality in the Cantonese population. Surgical candidates in our institution should be under 60 years of age. All our surgical candidates are required to have tried CPAP with the present-day selection of masks for at least 6 months. The procedures performed at our institution for the different VSE established sites of obstruction in OSAS patients are summarized in Table 1. VSE is only useful if there is a surgical procedure to treat effectively the diagnosed sites of obstruction. We have adopted a reserved approach of no surgical intervention unless our repertoire of procedures is appropriate for the observed obstructive sites. The surgical patients are informed that they may experience an improvement but not necessarily a cure. Many medium and long-term failures of surgical treatment are related to the fundamental design of the surgical procedure. The stiffness or extra room achieved by scarring, tightening, or widening procedures is unable to counter the natural laxity of pharyngeal tissue, which yields to the upper airway negative pressure with time, resulting in re-obstruction. In obese patients with multiple medical problems and invariably multilevel obstruction, our experience with surgery has been disappointing. These patients are not subjected to VSE. They are patiently counseled and recommended for CPAP. Bilevel Positive Airway Pressure (BIPAP) ventilation is recommended for the obese hypoventilation patients under the supervision of our respiratory physicians, or a tracheostomy can be offered if they should select this option.

Table 1 Surgical Procedures Performed at the Prince of Wales Hospital, Chinese University of Hong Kong for Different Sites of Obstruction Nasal obstruction

Septoplasty; turbinoplasty; FESS for nasal polyposis

Velopharyngeal obstruction

Limited uvulopalatopharyngoplasty (tonsillectomy, uvulectomy, and tonsillar pillar suture)

Tonsillar obstruction

Tonsillectomy

Lateral pharyngeal Tonsillectomy and pillar suture wall Tongue-base obstruction

Hyoid hitch; phase I surgery for nonreceding chin; sliding genioplasty for receding chin; radiofrequency tongue-base reduction (under evaluation); distraction osteogenesis under evaluation in children; phase II surgery not

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performed to date Epiglottic flop

One-third to half laser epiglottic trim

VSE in our unit has also been assessed for the establishment of the CPAP level and has proven to be of great promise as an efficient and cost-effective means of CPAP titration.

3. THE PROCEDURE OF VSE Patients who are surgical candidates are admitted as a day case. An intravenous site is established for access during the procedure. The patient is monitored for transcutaneous oxygen saturation, ECG, and blood pressure. Simultaneous PSG with EEG monitoring is at present used in our unit for research purposes. The sleep endoscopy laboratory is equipped with oxygen, suction, a conveniently adjustable BIPAP/ CPAP machine, and the standard resuscitation equipment. The more patent nostril is selected and 10% Xylocaine spray is delivered to the nasal cavity as well as the nasopharynx using a long cannula. An awake flexible nasopharyngoscopy is performed to exclude static obstructive lesion. A Muller maneuver is performed for correlation. Four milligrams of Midazolam is given as an induction bolus with saline flush. The light is dimmed and the patient is encouraged to sleep. The dose is increased 1mg at a time with saline flush until the patient sleeps. A minimal 5min wait is recommended after the first bolus and between increments. Increments are only needed if the patient shows no sign of sleep onset. The ceiling dose in our unit is limited at 7.5mg i.v., after which the patient is deemed to have failed sedation. The average dose in our experience is 0.06mg/kg in OSAS cases. The dose for snorers is variable and we have applied the same ceiling dose of 7.5mg for this group of patients. Once the patient has slept, obstructive episodes are observed and the endoscopic examination is carried out after at least two episodes or cycles of obstruction and arousal. If the SaO2 should fall below 70%, the CPAP mask is applied and examination is resumed after 5min of unobstructed breathing. The endoscopic examination is performed using an Olympus P4 flexible nasopharyngoscope inserted via the anaesthetized nostril. In the location of obstructive sites, attention is paid to the following levels: Soft palate Lateral pharyngeal wall Tonsils Base of the tongue Epiglottis Hypopharynx (the pyriform fossae squashing in around the larynx)

Once the level/levels of obstruction are established, the patient is reversed with the slow injection of flumazenil (Anexate) IV (300–500mcg). It is important to be aware that the

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mean elimination half-life of flumazenil which is 35.5min is shorter than that of midazolam which is 107min. It, nevertheless, helps to shorten the duration of sedation. The patient is then turned on his side and airway monitored in our recovery area and then in the high dependency area of our ward. 3.1 Snorers Snorers are the most difficult group of patients to sedate optimally for viewing asleep, as they are usually not hypersomnolent. They are easy to oversedate. We performing VSE less frequently in this group of patients as most would benefit from any

Table 2 Summary of Snore Generation Sites in 30 Snorers by VSE Recordings Snore generation sites

No. of patients

Percentage of total

Soft palate

26

87

Tonsils

12

40

Base of the tongue

4

13

Posterior pharyngeal wall

2

6.5

12

40

Epiglottis

of the present range of soft palate and uvula procedures. When we do perform VSE in this group of patients to tailor make surgical procedures after their PSGs, they are sedated with a similar protocol as the one for OSAS patients with the ceiling dose of midazolam set at 7.5mg, and no obstructive or desaturation events should be seen throughout the procedure. Tables 2–4 summarize our study of video captured nasen-doscopic findings of snore generation sites in 30 successfully sedated snorers, 28 males and 2 females (mean age: 41.4 years). It was interesting that in this study, 75% (n=9) with single-site snoring had the snore generated by the soft palate and 54% (n=7) of the two-site snorers had soft palate plus epiglottic snores. Epiglottic and tonsillar vibrations seem to feature significantly in snore generation. In our experience of VSE in OSAS patients, epiglottic flutter is commonly seen as an important source of the loud wake-up snore after the obstructive cycle. The above findings also support the concept that the use of palatal stiffening procedures for snorers is likely to be effective in the majority of patients. 3.2 Obstructive Sleep Apnea Syndrome This group of patients is easy to sedate and most will sleep with the initial 4mg of midazolam with their hypersomnolence. Their respiratory events have to be watched carefully throughout the procedure and they should be administered CPAP or reversed with flumazenil if SaO2 should fall below 70% or if arrhythmic episodes should develop other than the usual mild cyclical slowing down and recovery of the heart rate with the

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obstructive episodes. We recommend waiting for two obstructive cycles prior to viewing the events. The viewing usually takes no longer then 15min in experienced hands. With the help of intermittent CPAP, sleep stage correlated events can be recorded when simultaneous PSG is used for study purposes. We are in the process of data collection for this group of patients. Between October 1992 and January 2002, we have performed 893 sleep nasendoscopy procedures

Table 3 Summary of Single/Multiple Snore Generation Sites in 30 Snorers by VSE Recordings Number of snoring sites

No. of patients

Percentage of total

Single site

12

40

2

13

44

3

3

10

4

1

3

5

1

3

Table 4 The Different Combinations of Snore Generation Sites in 30 Patients Studied by VSE Recordings Single site

Two sites

Three sites

Four sites

Five sites

SP—9

SP+T—3

SP+T+TB—1

SP+T+TB+E—1

SP+T+TB+PP+E—1

T—3

SP+E—7

SP+T+E—2

T+PP—1 SP+TB—1 SP+E—1 Note: SP, soft palate; T, tonsils; PP, posterior pharyngeal wall; TB, tongue base; E, epiglottis.

for different research and investigation protocols and have not experienced any untoward event. Our data on OSAS patients indicated that 87% of our patients have multilevel obstruction. In a recent study we conducted on 93 patients with a mean respiratory disturbance index (RDI) of 48.4 (RDI range: 15–89) selected for surgical assessment, the levels of obstruction and their different combinations were analyzed in detail. Of the 93 patients, 4 patients (4.3%) failed sedation. The 89 patients analyzed consisted of 11 females (mean age: 46.9 years) and 78 males (mean age: 39.7 years). The mean BMI of the 89 patients was 27.2, the mean BMI for the female patients was 26.7, and that for the males was 27.4. The number and percentages of single/multiple site obstruction as well as the mean BMI of each subgroup are given in Table 5.

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As can be seen from the findings, the percentage of patients with single-site obstruction is low at 14.61%. Despite the observable trend of a higher BMI being affiliated with four or more sites of obstruction as compared to single-site obstruction, no conclusion can be fairly drawn from this select group of patients. Many of these potential surgical candidates with lower BMI would have obvious or subtle facial skeletal deficits as the main contributor to their OSAS. Apart from one patient with an RDI of 15 with two-site obstruction adequately treated with phase I surgery, all patients were in the moderate to severe OSA range. Interestingly, the number of obstructive levels does not necessarily reflect the severity of OSAS and vice versa. In the selected few with singlelevel tonsillar obstruction, a simple tonsillectomy is curative for severe OSAS. In our institution, we do not see so many of the milder cases as they are referred for dental devices or CPAP at lower acceptable pressures, although they may be the best candidates for surgery. The different obstructive sites and their combinations are listed in Table 6. Figures 1– 4 illustrate the typical appearance on still pictures of different sites of

Table 5 Summary of VSE Findings in OSAS Patients Selected for Surgery with Regard to Single/Multiple Site Obstruction Number of obstructive sites

No. of patients

Percentage of total

Mean BMI

Single site

13

14.61

23.8

Two obstructive sites

16

17.98

25.5

Three obstructive sites

17

19.10

24.4

Four obstructive sites

20

22.47

28.3

Five obstructive sites

12

13.48

25.4

Six obstructive sites

11

12.36

27.2

Table 6 Obstructive Sites in 89 Patients for Surgical Assessment and Different Site Combinations as Seen in VSE Obstruction sites involved (total 302) I

Palate

69 22.8%

II

Lateral Pharynx

64 21.2%

III Tonsils

41 13.6%

IV Base of the tongue 62 20.5% V Epiglottis

37 12.3%

VI Hypopharynx

29 9.6%

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100% Site combinations number of patients and % I

Palate

4

4.49%

I+II

4

4.49% I+III

0

I+IV

5 5.62% I+V

1 1.12%

I+II+III

6

6.74% I+III+IV

0

I+IV+V

1 1.12% I+VI

0

I+II+IV

5

5.62% I+III+V

0

I+IV+VI

0

I+II+V

1

1.12% I+III+VI

0

I+IV+V+VI 0

I+II+VI

I+III+IV+V

I+V+VI 0

0

I+II+III+IV

7

7.87% I+III+IV+VI

1 1.12%

I+II+III+V

2

2.25% I+III+V+VI

0

I+II+III+VI

2

2.25% I+III+IV+V+VI 0

I+II+IV+V

4

4.49%

I+II+IV+VI

3

3.37%

I+II+V+VI

0

I+II+III+IV+V

3

3.37%

I+II+III+IV+VI

4

4.49%

5

5.62%

I+II+III+V+VI I+II+IV+V+VI

I+II+III+IV+V+VI 11 12.3% II

III

IV

Lateral pharynx

2

2.25%

II+III

1

1.12%

II+III+IV

II+IV

0

0

II+IV+V

1

II+III+V

0

II+IV+VI

2

II+III+VI

0

II+V+VI

0

II+III+IV+V

1

II+IV+V+VI

0

II+III+IV+VI

0

Tonsil

1

1.12%

III+IV

1

1.12%

III+V

1

III+IV+V

0

III+VI

0

III+IV+VI

0

III+V+VI

0

III+IV+V+VI

0

Tongue Base

4

1.12%

4.49%

II+V

0

1.12%

II+VI

0

2.25%

II+V+VI

0

1.12%

Video sleep nasendoscopy

V

VI

IV+V

3

3.37%

IV+V+VI

1

1.12%

Epiglottis

2

2.25%

V+VI

0

Hypopharynx

0

IV+VI

179

0

Figure 1 Velopharyngeal obstruction showing side-to-side as well as anteroposterior collapse. This situation is difficult to correct with mere anterior scarring procedure. obstruction. As is evident from these findings, the three obstructive sites which featured equally commonly are the soft palate, the lateral pharyngeal wall, and the base of the tongue. Within the present-day surgical spectrum, the lateral pharyngeal wall at the oropharyngeal level is the least attended to. The tonsils are usually not the culprit. This is the area which is most difficult to treat or to treat with any sustained effect. We have observed side-to-side, concentric, as well as oblique collapse of this region. In terms of single-site obstruction, the soft palate obstructed equally commonly as the base of the tongue. The hypopharynx, interpreted as the pyriform fossae squeezing concentrically around the larynx, interestingly, never featured as a single-site obstruction. This level of collapse is likely to be a secondary effect of higher-level obstruction. Our Muller maneuvers correlated poorly with our VSE findings. Figures 5(a) and (b) illustrate this point. The different combinations of obstructive sites are challenging to the interested surgeon. It is the humbling truth that the lasting cure for all these levels of obstruction

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Figure 2 Tonsillar obstruction at the oropharyngeal level.

Figure 3 Tongue-base obstruction with oblique pharyngeal wall collapse. is not in place at this point in time. The continued study of upper airway dynamics is an important adjunct to the fine-tuning of the present-day surgical procedures and the design of new procedures for OSAS.

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3.3 VSE and CPAP Titration VSE can be employed to establish the CPAP in an OSAS patient. This procedure can be conveniently performed at the end of the VSE examination by placing a CPAP mask over the nose of the patient gently with the flexible endoscope in situ. Despite the presence of the scope, a seal can easily be achieved (Fig. 6). We have a picture in picture oximetric tracing on the video monitor screen to facilitate pressure establishment while watching the changes in the upper airway. The aim is to achieve unobstructed breathing at the lowest level of CPAP with minimal snoring. It is interesting that a large airway lumen is not usually necessary to achieve this in the majority of our patients. In our study of 43 cases (40 males and 3 females), we had managed to achieve a 67% precise correlation of established CPAP values using

Figure 4 (a) Epiglottic obstruction, open position. (b) Epiglottis closing over laryngeal introitus obstructing airway.

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Figure 5 Muller maneuver and sleep breathing discrepancy. (a) Muller maneuver showing side-to-side collapse of the lateral pharyngeal wall over the base of the tongue. (b) VSE observation of oblique pharyngeal wall collapse against the base of the tongue. our technique when compared with those established manually overnight in the sleep laboratory. If ±1cm H2O is accepted as the error margin, a 77% correlation is achieved, and 90% correlation if ±2cm H2O is the accepted error margin. The technique is simple and quick. It is still our preference to titrate CPAP pressure manually overnight in the sleep laboratory. We have found this to be more reliable than the autotitrators. The VSE technique, nevertheless, can be a very cost-effective technique of CPAP titration when perfected, as it takes no longer than 10min to perform.

4. VSE: WHERE DOES IT STAND? Since Croft and Pringle (5) described their technique of sleep nasendoscopy (5), reception has been mixed. Criticism was generated by the disappointing results of

Figure 6 CPAP mask on nose and endoscope for VSE-guided CPAP titration.

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the once popular UVPP (6,7) for which this technique was employed to select the appropriate UVPP candidates. The second reason for skepticism is the use of sedation in VSE. This is unnatural sleep and may relax the tongue muscles, thus worsening the pharyngeal collapse. UVPP failed because of its design, as the created scar lies in a region which is constantly massaged by the act of swallowing. The stiffness could not possibly last for long. UVPP also fell into disrepute because only a limited number of OSAS patients have single-site obstruction at the soft palate and this operation was once performed for all. Different agents have been used for sleep endoscopic examination, halothane (8) in children, midazolam (5), diazepam (9), and propofol (10). The Osaka group evaluated diazepam-induced sleep nasendoscopy under PSG control in 50 patients. The non-rapid eye movement (REM) parameters were observed to be equal to those of their nocturnal PSG and the only difference was in the duration of REM sleep (9). Supporters of VSE for surgical evaluation are more than a few (11,12). In days to come, the optimal sedation for sleep endoscopy would require PSG-controlled evaluation. Surface electromyography would help clarify the suspected base of the tongue relaxation effect. We believe that the small controlled dose in our protocol would be hypnotic in the hypersomnolent OSAS patients rather than muscle relaxing. PSG data are being collected for midazolam. Our 10-year experience of its use in over 800 cases supports its safety if performed correctly. At present, however, sleep nasendoscopy should only be used for surgical evaluation, which should be interpreted in the light of a nocturnal PSG. Though a simulated sleep breathing situation, it undoubtedly provides quality information on upper airway dynamics closest to the truth in a cost-effective manner. This is invaluable information in surgical planning and procedure design.

REFERENCES 1. Partinen M, Jamieson A, Guilleminault C. Long term outcome for obstructive sleep apnea syndrome patients. Mortality Chest 1989; 96(3):703–704. 2. Guilleminault C, Simmons FB, Motta J, Cummiskey J, Rosekind M, Schroeder JS, Dement WC. Obstructive sleep apnea syndrome and tracheostomy. Long-term follow-up experience. Arch Intern Med 1981; 141(8):985–988. 3. Sher AE, Thorpy MJ, Spielman AJ, Burack B, Mcgregor PA. Predictive value of Muller manoeuvre in selection of patients for uvulopalatopharyngoplasty. Laryngoscope 1985; 95:1483–1487. 4. Pringle MB, Croft CB. A comparison of sleep nasendoscopy and the Muller manoeuvre. Clin Otolaryngol 1991; 16:559–562. 5. Croft CB, Pringle M. Sleep nasendoscopy: a technique of assessment in snoring and obstructive sleep apnoea. Clin Otolaryngol 1991; 16:504–509. 6. Fujita S, Conway W, Zorick F, Roth T. Surgical correction of anatomic abnormalities in obstructive sleep apnea syndrome: uvulopalatopharyngoplasty. Otolaryngol Head Neck Surg 1981; 89:923–934. 7. Fujita S. UPPP for sleep apnoea and snoring. Ear Nose Throat J 1984; 63:73–86. 8. Croft CB, Thomson HG, Samuels MP, Southall DP. Endoscopic evaluation and treatment of sleep-associated upper airway obstruction in infants and young children. Clin Otolaryngol 1990; 15:209–216.

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9. Sadaoka T, Kakitsuba N, Fujiwara Y, Kanai R, Takahashi H. The value of sleep nasendoscopy in the evaluation of patients with suspected sleep related breathing disorders. Clin Otolaryngol 1996; 21(6):485–489. 10. Roblin G, Williams AR, Whittet H. Target-controlled infusion in sleep endoscopy. Laryngoscope 2001; 111(1):175–176. 11. Camilleri AE, Ramamurthy L, Jones PH. Sleep nasendoscopy: what benefit to the management of snorers? J Laryngol Otol 1995; 109(12):163–1166. 12. Takeda K. Sleep nasendoscopy in the selection of surgical treatments for simple snoring and sleep apnea syndrome. J Med Soc Toho Univ 1998; 45(2):250–260.

8 Special Diagnostic Studies in Sleep Apnea Mike Yao Department of Otolaryngology/Head and Neck Surgery, University of Illinois at Chicago, Chicago, Illinois, U.S.A. Pamela H.Nguyen Department of Radiology, Mercy Hospital and Medical Center, Chicago, Illinois, U.S.A. 1. INTRODUCTION The diagnosis of obstructive sleep apnea (OSA) is currently based on apneic and hypopneic episodes recorded on polysomnography (PSG). These studies indicate those patients with OSA, but do not give further information on the cause of the obstruction, the best method of cure, nor the likelihood of cure. Many diagnostic studies, including lateral cephalometric x-rays, computed tomography (CT), magnetic resonance imaging (MRI), fluoroscopy, flexible pharyngoscopy, upper airway pressure measurements, and acoustic reflection techniques, have been used in an effort to make diagnoses, direct corrective intervention, and predict outcome for interventions. The perfect diagnostic study would distinguish normal nonsnoring patients from snoring patients from OSA patients, be inexpensive, widely available, and reproducible, indicate the cause of the obstructive episodes, and thus the best intervention, predict the level of success for each intervention, and allow for intraoperative monitoring to optimize results for each intervention. Based on these criteria, the perfect study could be done awake and upright in the examination chair using the tools present in all otolaryngology clinics. This would obviate the need for a sleep laboratory to do asleep studies and the need for special instrumentation. Currently, no single diagnostic study fulfills all of these criteria. Many studies have been performed in a quest for the best diagnostic modality, and the results are presented in the following sections.

2. LATERAL CEPHALOMETRIC X-RAYS Lateral cephalometric x-rays have been used for the study of OSA patients due to their wide availability and low cost. Lateral cephalometric x-rays can identify those patients with skeletal, as well as some soft tissue, defects which predispose them to OSA. Attempts have been made to use lateral cephalometric x-rays to distinguish snorers from OSA patients, choose more successful candidates for surgery, determine the appropriate type of surgery, and evaluate the outcome of surgery.

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2.1 Distinguishing Apnea from Control Patients In a study of OSA patients, 153 of 155 had significantly different cephalometric landmarks from the normative data in the literature (1). Common findings were retropositioning of the mandible [Fig. 1—decreased SNBa (sella, nasion, supramentale) angle], more acute cranial base flexure (Fig. 1—decreased NSBa (nasion, sella, basion) angle), and displacement of the hyoid bone to a lower position than expected [Fig. 1— longer mandibular plane (plane parallel to the inferior border of the body of the mandible) to hyoid distance (MP-H)]. Concomitant changes were seen in the soft tissues anchored to the skull and mandible shown by a significantly longer soft palate and a narrowed posterior airway space in OSA patients. The findings of narrowed retrolingual airspaces, longer soft palate, and inferiorly placed hyoid bones (longer MP-H) in OSA patients were first described in 1983 (2) and, subsequently, have been confirmed (3–10). In a more extensive analysis of lateral cephalometric x-rays, deBerry-Borowiecki et al. (6) found that OSA patients differed from controls by having larger tongues and soft palates, inferiorly displaced hyoid bones, elongated faces due to an inferior displacement of the mandibular body, retropositioned maxilla [Fig. 1—decreased SNA (sella, nasion, subspinale) angle] with elongation of the hard palate, and reduced oropharyngeal and hypopharyngeal airways. Statistical measures have been used to combine multiple parameters from physical examination, PSG, and lateral cephalometric x-rays to better differentiate between normal and OSA patients. Bacon et al. (11) described a discriminate function analysis which correctly classified 80% of patients into OSA vs. normal groups based on length of the maxilla, length of the cranial base, and lower facial height. They found that OSA patients had a shorter maxillary length, a shorter anterior

Figure 1 Lateral cephalometric analyses, normal subject (left) and subject with obstructive sleep apnea (right). S=sella; N=nasion;

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B=supramentale; ANS=anterior nasal spine; PNS=posterior nasal spine; Gn=gnathion; Go=gonion; MP=mandibular plane; H=hyoid; Ba=basion. (Reproduced from Ref. 1.)

Figure 2 Tracing of a cephalometric radiograph. PAS=posterior airway space; MPAS=minimal posterior airway space; PUS=posterior uvular space; TT-TB= distance from the central incisor to the tongue base; MPH=distance from the mandibular plane to the hyoid. (From Ref. 13.) cranial base, and an increased lower facial height (11). Since only 80% of patients were correctly categorized, they concluded that factors other than those seen on lateral cephalometric x-rays may determine OSA (11). Zucconi et al. (12) performed multiple regression correlation analysis, and found that the MP-H, SNB, SNA, posterior airway space (PAS) (Fig. 2)—measured as the distance between the base of the tongue and the posterior pharyngeal wall along the line from the supramentale to the gonion, tongue size, and body mass index (BMI) correlated significantly to the respiratory disturbance index (RDI). The combination of these variables only explained 33% of the variance of the RDI (12). In contrast to other studies, they did not find a significant difference in PAS, SNA, and SNB between the OSA patients and normal subjects (12).

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Tsuchiya et al. (14) classified OSA patients into two groups using cluster analysis based on apnea index (AI) and BMI, and then performed multiple regression analysis for each group. For the group with a high AI to BMI ratio, 65% of the AI variability could be explained by a combination of the factors measuring BMI, mandibular plane angle, anteroposterior discrepancy between the maxilla and mandible, and an inferior and anterior position of the hyoid bone. For the group with a low AI to BMI ratio, 68% of the AI variability could be explained by a combination of factors measuring BMI and upper airway volume (nasopharynx, oropharynx, and hypopharynx volume estimated using CT scan data). Lateral cephalometric x-rays provide important information about patients and their proclivity toward OSA, but as these regression analyses show, only a fraction of the variability in sleep indices can be explained based on the data from these x-rays. 2.2 Predicting Successful Uvulopalatopharyngoplasty Candidates Long-term follow-up has shown that uvulopalatopharyngoplasty (UPPP) alone cures fewer than 50% of patients with OSA (15–18). Simmons et al. (17) were not able to reliably predict success nor failure of UPPP based on the anatomic appearance of the palate and lateral pharyngeal walls. In a review of cephalometric data in patients who underwent unsuccessful UPPP, Riley et al. (5) reported significantly smaller PAS and more inferiorly placed hyoid bones (increased MP-H). Those patients with significant improvement following UPPP had PAS and MP-H measurements similar to those of the controls (5). Riley et al. (5) concluded that UPPP alone was not a successful treatment for OSA when hypopharyngeal obstruction exists as shown by abnormal PAS and MP-H measurements. Another retrospective study showed a significant difference in tongue size and mandibular-hyoid angle between responders and nonresponders to UPPP (19). In a large retrospective review of nine papers containing raw data on 168 patients, OSA patients with narrowing of only the retropalatal region had a 52.3% response rate to UPPP while those patients with some retrolingual narrowing had a 5.3% response rate (p <0.0001) (18), supporting the findings of Riley et al. (5). The three prospective studies in the literature do not support the findings of these retrospective studies. In the first study, 34 consecutive OSA patients were evaluated and no significant difference in the PAS and MP-H between the responder and nonresponder groups was found (20). In the second study, 60 consecutive OSA patients were evaluated and a significantly smaller PAS in responders vs. nonresponders was noted (21). A smaller PAS in responders to UPPP was completely in contrast to the findings of Riley et al. (5). In the third study, 30 consecutive OSA patients were evaluated and no significant difference in PAS between groups was noted (22). However, lowered hyoid position (longer MP-H), increased cranio-cervical angle, and shortening of the maxilla were significantly associated with poor UPPP outcome (22). A predictive model containing these three cephalometric measurements and hypersomnia correctly classified 83% of the patients in the study (22). Thus, the data about the predictive value of lateral cephalometric x-rays for the success of UPPP are contradictory. The bulk of the data predict that patients with narrowing of the retrolingual region will have a poor outcome following UPPP (5,18,19).

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However, the more statistically sound prospective studies all indicate that this has no effect on the success of UPPP (20–22). A number of different explanations for this discrepancy in the predictive value of the PAS exist. First, the retrospective studies may be skewed due to bias. The prospective studies are less likely to suffer from this error. Second, the parameters from the lateral cephalometric x-rays may not provide adequate information for predicting the outcome of UPPP, and only a portion of the variability in outcome is due to the change in cephalometric parameters. This last explanation is unlikely due to the strong statistical significance of the second prospective study by Ryan et al. (21) with p <0.0005. Third, each of the studies uses a different method of distinguishing responders from nonresponders. Fourth, differences in the extent of resection with UPPP would vary the results; however, the descriptions of surgical techniques are all very similar. 2.3 Predicting Successful Nasal Surgery Candidates Similar to the use of lateral cephalometric x-rays in OSA patients undergoing UPPP, these x-rays have been used to predict the efficacy of nasal surgery on OSA patients (23). In a study of 14 OSA patients treated with septoplasty, turbinectomy, and polypectomy, the patients with normal lateral cephalometric x-rays showed significant improvement of their RDI, while patients with abnormal x-rays (increased MP-H or decreased PAS) had an increase in RDI. As with the initial UPPP studies, this study provides evidence that hypopharyngeal obstruction seen on lateral cephalometric x-rays predicts a poor outcome for OSA patients undergoing nasal surgery. 2.4 Predicting Successful Multilevel Pharyngeal Surgery Other authors have used lateral cephalometric x-rays to evaluate OSA patients prior to multilevel pharyngeal surgery. Multilevel surgery addresses narrowing at the palate and the base of the tongue. In a review of 55 OSA patients treated with inferior sagittal mandibular osteotomy with hyoid myotomy and suspension, responders had a significantly different SNB angle from nonresponders (81.0±2.0° vs. 75.5±1.5°) (24). The decreased SNB angle represents a retruded mandible causing a narrowed hypopharyngeal airway. Riley et al. (24) concluded that OSA patients with these severe mandibular deficiencies (SNB <74°), and who do not benefit from this surgical procedure, need further surgical correction of their bony abnormalities to alleviate their OSA. 2.5 Assessing Outcome Three studies have used lateral cephalometric x-rays to assess outcome following multilevel sleep apnea surgery. All of the studies show changes in the PAS and MP-H following OSA surgery; however, none of the studies found a correlation between the change in cephalometric parameters and PSG data (13,25,26). The first study reviewed 40 OSA patients who had failed treatment with limited mandibular osteotomy with hyoid advancement, and were subsequently treated with advancement of the maxilla by Le Fort

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I osteotomy with rigid fixation and advancement of the mandible by bilateral sagittal ramus split (25). Significant changes were seen in the SNA, SNB, PAS, and MP-H measurements, but no direct relationship was found between the changes in the PAS and the changes in PSG data (25). The second study reviewed 12 OSA patients following inferior sagittal osteotomy with sliding mandibular osteotomy and hyoid bone suspension, and found a significant increase in the PAS and a decrease in MP-H which was not statistically significant (26). No pre- or postoperative cephalometric measurements or change in these measurements was correlated with the amount of reduction in the RDI or the change in the lowest nocturnal oxygen saturation (26). The third study reviewed 19 OSA patients following UPPP, mandibular osteotomy with genioglossus advancement, and hyoid myotomy with advancement (13). Changes in the PAS and MP-H approached statistical significance, and once again, these changes could not be correlated to changes in PSG data (13). Based on the results of these three studies, we conclude that changes are noted following multilevel pharyngeal surgery; however, the changes on lateral cephalometric x-ray do not accurately reflect the impact that surgery has on the severity of sleep apnea.

3. COMPUTED TOMOGRAPHY When evaluating the upper airway for obstruction, CT scans offer greater anatomic detail than lateral cephalometric x-rays. If anatomic abnormalities are the cause of OSA, CT scans should better delineate these abnormalities and should better direct surgical interventions toward the abnormal anatomic sites than plain x-rays. However, as the studies below will show, anatomy of the upper airway while awake only represents the static dimensions of the awake airway and has not shown a high predictive value for diagnosing OSA. Further efforts have been made to control variables during CT scanning. Respiratory efforts have been shown to change upper airway dimensions. Using fast-CT scans to evaluate changes in upper airway anatomy during different stages of the respiratory cycle has controlled variations due to the respiratory cycle. Asleep upper airway anatomy varies from awake anatomy. Efforts have been made to perform CT scans while asleep to assess the sleep anatomy, but little work has been done to evaluate the ability of asleep CT scans to direct surgical intervention. Despite the low sensitivity of CT scans for the diagnosis of OSA, CT scans are able to show correlation of anatomic changes to improvement of OSA parameters in contrast to lateral cephalometric x-rays. 3.1 Distinguishing Apnea from Control Patients Several awake CT studies have shown statistically significant narrowing of the oropharynx, especially in the retropalatal region, in OSA patients compared with controls (p<0.001 for all three studies) (27–29). Figure 3(a) and (b) shows the larger crosssectional area of the upper airway in a control patient as compared to the smaller airway of a patient with sleep apnea in Fig. 3(c) and (d) (29). These studies fsdiffered in their findings of nasopharyngeal and hypopharyngeal cross-sectional areas with two showing significant differences between OSA patients and controls (p<0.05) (27,28) and one

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showing no difference (29). A fourth study showed narrowing in the oropharynx in OSA patients compared with controls (p=0.052 in inspiration and no significant difference in expiration), but contradicted the previous studies by showing significant widening of the hypopharynx on expiration in OSA patients compared with controls (p=0.009) (30). Shepard et al. (31) reported that 70% of their patients were correctly classified as either normal subjects or OSA patients based on a minimal upper airway cross-sectional area (Amin) of 1cm2 or less for OSA patients. This 70% sensitivity for distinguishing OSA patients from normal controls is not high enough to make CT scanning a useful diagnostic test. Data from two of these studies showed that no normal controls were noted to have complete obstruction at the level of the oropharynx (28,29) and 6 of 20 (28) and 5 of 10 (29) OSA patients were noted to have complete obstruction at this level. Thus, complete obstruction at the level of the oropharynx on CT scan had 100% specificity for OSA, but poor sensitivity. These studies compared OSA to normal patients, but did not address the more clinically relevant question of distinguishing OSA from snoring patients. One study addressed the problem of distinguishing OSA from snoring patients. Significantly wider tongue widths and wider genioglossus muscles were found in OSA patients compared to snoring and normal patients (p<0.001) (Figs. 4 and 5), although considerable overlap was present between the three groups (32). Data showing narrowing of the oropharynx on CT scan in OSA patients support the data from lateral cephalometric x-rays (3–10). Furthermore, in a study of 16 men with OSA comparing lateral cephalometric x-rays to CT scans, a statistically significant correlation (r=0.92, p<0.005) was found between the PAS and the smallest volume measured behind the base of the tongue (33). With this high degree of correlation, the added anatomic accuracy of CT scans did not appear to significantly increase the sensitivity of the radiological diagnosis of OSA. CT scans and lateral cephalometric x-rays represent static soft tissue and bony dimensions, which are only indirectly related to the dynamic changes responsible for obstructions during sleep. In order to more accurately define the site of obstruction during sleep, one group performed CT scans in OSA patients both while awake and while asleep (34). Five of eight patients required Temazepam 10mg in order to aid the onset of sleep. Horner et al. (34) showed that the narrowest segment of the upper airway was the segment posterior to the soft palate in the majority of the patients and that the Amin was significantly narrowed in OSA patients as compared to control patients (p<0.05). While asleep, all patients showed obstruction of the segment of the airway posterior to the soft palate and approximately half had obstruction extend below the level of the soft palate. It was hypothesized that those patients with obstruction below the level of the soft palate would have a low likelihood of cure with UPPP, but this hypothesis remains untested (34).

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Figure 3 CT scan of control subject at a lower level. The upper arrow points to the oral airway, the lower arrow to the retropalatal airway, and the asterisk is on the soft palate. (A) CT scan of

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control subject at a higher level. The tongue rests against the soft palate obliterating the oral airway. The arrow points to the retropalatal airway. (B) CT scan of a patient with severe obstructive sleep apnea at a lower level. The vertical arrows point to the back of the tongue, the asterisk is on the soft palate, and the horizontal arrow points to the retropalatal airway. (C) CT scan of a patient with severe obstructive sleep apnea at a higher level. Complete occlusion of the airway posterior to the soft palate. A small oral airway is visible anterior to the soft palate. (From Ref. 29.)

Figure 4 Schematic illustration showing the points for measuring the tongue and indirect signs of macroglossia. The tongue width is measured between the outer convex borders of the hyoglossus muscles (1). The genioglossus width is measured at

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the intersection with the hyoglossus muscles (2). The thickness of the hyoglossus muscle is measured (3). Indirect signs of tongue enlargement are displacement of the submandibular salivary glands (4) and a visible midline cleft of the tongue surface (5). (From Ref. 32.)

Figure 5 (A) Normal tongue and oropharynx. Axial CT scan through the middle portion of the base of the tongue. The tongue surface is separated from the posterior pharyngeal wall by the oropharyngeal airway. (B) Patient with OSA. CT scan through the low base of the tongue. The genioglossus and hyoglossus muscles are wider than normal and the lateral margins of the tongue are resting against the posterior pharyngeal wall (crossed arrow). The submandibular salivary glands are displaced, causing a bulge in the overlying platysma (arrow). M=mandible; gg=genioglossus muscle; hg=hyoglossus muscle; mh=mylohyoid

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muscle; sm=submandibular gland. (From Ref. 32.) 3.2 Predicting Successful UPPP Candidates A few studies have used CT scan to predict surgical efficacy of UPPP. Two studies have found differences in surgical efficacy of UPPP between groups distinguished based on CT scan results. The first study showed significantly poorer success with patients with widened tongue and genioglossus muscles (p<0.05) (32). The second study showed greater surgical efficacy of UPPP patients with Amin less than 1cm2 and with obstruction at a level 20mm below the hard palate (35). Overall, these studies indicate that it might be possible for CT scans to distinguish responders from nonresponders to UPPP and allow for selection of more appropriate surgical interventions for those deemed as nonresponders. Further studies will need to be performed to evaluate the utility of CT scans in this setting. 3.3 Assessing Outcome Changes in airway dimensions on axial CT scans following UPPP correlate well with cure of sleep apnea. Two studies showed significant widening of Amin (minimal upper airway cross-sectional area) to >100mm2 in patients cured by UPPP and <100mm2 in patients not cured by UPPP (Fig. 6) (35,36). Similarly, a third study showed greater widening of the oropharynx following UPPP in good responders as compared to nonresponders (37). The ability of CT scans to correctly identify cured OSA patients following UPPP is in contrast to the lack of change seen on lateral cephalometric x-rays following multilevel pharyngeal surgery (13,25,26). The CT changes seen following UPPP may reveal either inadequately performed UPPP surgeries or other causes of retropalatal narrowing not addressed by UPPP. These issues will require further study. 3.4 Three-Dimensional CT Scans Three-dimensional reconstructed CT scans provide an easier way to assess the caliber of the upper airway than unreconstructed CT scans. An initial study using this modality showed significant correlation between AI and the ratio of tongue volume to airway volume in OSA patients (95% confidence level) (38). A larger follow-up study including the previous cohort of patients showed no correlation between polysomnographic data and upper airway volume measurements (39). A second prospective study evaluating three-dimensional airway CT supported the findings from the second study by showing no statistically significant differences in airway dimensions between OSA patients and control patients. Overall, the studies with three-dimensional CT show no statistical differences in airway dimensions between OSA patients and control patients. Three-dimensional reconstructed CT scans showed a difference in airway volumes for OSA patients who responded to UPPP compared with nonresponders.

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Figure 6 Forty-two-year-old man with severe OSA. (A) Axial CT at the level of the C2 vertebrae. The narrowest oropharyngeal cross-sectional area is less than 50mm2. (B) Sagittal CT reconstruction showing uvulopalatal narrowing (arrow). (C) Axial CT at the narrowest oropharyngeal level after uvulopalatopharyngoplasty with resolution of OSA. The oropharyngeal cross-sectional area is more than 100mm2. (D) Sagittal CT reconstruction after uvulopalatopharyngoplasty showing no narrowing of the pharynx. (From Ref. 36.) Smaller upper airway volumes (p<0.05), smaller upper airway to tongue volume ratios (p<0.01), and smaller oropharynx to soft palate volumes (p<0.05) were found in OSA patients who responded to UPPP than in nonresponders (39). These prospective results with three-dimensional reconstructed CT scans corroborate the previous findings, which showed that CT scans (35) and lateral cephalometric x-rays (21) are useful for choosing successful UPPP candidates.

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3.5 Dynamic CT Imaging Static imaging may show areas of narrowing that predispose individuals to obstruction, but dynamic imaging can actually show episodes of obstruction. Cine CT or ultrafast CT scans allow for acquisition of eight contiguous slices every 0.7sec. This rapid scan time allows for dynamic assessment of the upper airway, as with fluoroscopy, with the added superior anatomic localization of CT imaging. This technology allows for observation of dynamic obstructions of the upper airway (Fig. 7). Use of cine technology has shown that airway compliance can play a significant role in contributing to airway obstruction. Compliance is defined as a percentage change in the area of the airway. Using ultrafast CT, smaller oropharyngeal airways (p<0.001) and nasopharyngeal airways (p<0.001) were found in OSA patients than in normal controls (40). As previously mentioned, greater compliance of the oropharynx (p<0.001) and nasopharynx (p=0.001) was found in OSA patients than in normal controls (40). To precisely correlate cine CT slice acquisition with the respiratory cycle, cine CT scans were acquired during simultaneous monitoring of the respiratory cycle

Figure 7 Ultrafast axial CT sections at the level of the oropharynx posterior to

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the tongue in a patient with OSA. Large arrow demonstrates marked narrowing of the airway during awake tidal breathing. Small arrow points to the anterior portion of the mandible. (From Ref. 40.) using a pneumotachograph (41). Comparison of snorers to OSA patients was performed to find distinguishing characteristics between these clinically similar groups (41). The findings from this study agreed with the previous study showing smaller low retropalatal and retroglossal cross-sectional areas in awake OSA patients compared with snorers (p<0.05) and normal controls (p<0.001) (41). The greater compliance of the OSA airway was also confirmed with significantly greater changes in upper airway size in OSA patients compared with snorers (p=0.03) and with normal controls (p=0.007) (41). Significant correlations were found between the minimal airway caliber and the RDI (r=0.59, p<0.0001) and lowest O2 saturation (r=0.56, p<0.0001). This high degree of correlation suggests that the awake minimal airway caliber is related to the asleep obstructive episodes. With this ability to localize the likely anatomic obstruction, it should be possible to better direct surgical intervention and assess postoperative results in OSA patients. This last hypothesis remains to be proven by a study which uses cine CT to identify the site of the obstruction and properly direct intervention in a manner to maximize success. Overall, the CT modalities show that OSA patients possess smaller retropalatal and retroglossal cross-sectional areas and that OSA patients with smaller upper airway volumes have a greater response to UPPP. Unfortunately, CT scans provide a poor diagnostic test for distinguishing patients with OSA from those with simple snoring due to the significant overlap in the degree of narrowing of the upper airway. Cine CT findings suggest that greater compliance of the airways contributes to OSA, but further study of this technique will be needed to determine its value. In contrast to lateral cephalometric x-rays, the greater anatomic detail of CT scans allows responders to be distinguished from nonresponders to UPPP surgery.

4. MAGNETIC RESONANCE IMAGING MRI provides unparalleled anatomic definition of soft tissue structures, allows for direct multiplanar imaging, and does not expose patients to radiation. Unfortunately, MRI imaging is expensive and slow, making assessment of the dynamic changes occurring in the upper airway during normal tidal breathing difficult to interpret. Newer MRI technologies allow for faster scan times (up to five images per second), which allow for dynamic imaging (42). However, dynamic MRI while sleeping has been difficult due to the noise produced by the scanners. Some investigators have tried sleep depriving their patients prior to scanning, while others have resorted to the use of sedatives. Use of sedatives causes selective reduction of the upper airway muscles, altering the pattern of obstruction from those patients who are not sedated. Monitoring the level of sleep during

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the scan has been difficult in the MRI scanner due to the bulk of the machine and the limitation imposed by the magnetic field. Some studies have relied on verbal response to determine wakefulness, while others have instituted EEG monitoring during MRI scanning. A few studies have used MRI to try to distinguish between OSA, snoring, and normal patients. Three of these studies have shown no difference (43–45), while three have shown a difference (42,46,47). No significant difference in awake pharyngeal volumes was noted between seven snoring and seven nonsnoring patients (44), no significant difference in pharyngeal cross-sectional area was noted between nine snoring, six OSA, and eight normal patients (45), and no correlation was found between pharyngeal volumes and RDI in awake OSA patients (43). Conversely, a preliminary study of one OSA patient and two normal controls showed narrowing of the retropalatal region in the OSA patient (47), five OSA patients had smaller pharyngeal volumes than five normal control patients (46), and 16 OSA patients had significantly greater obstruction during Muller maneuver and simulated snoring than six healthy volunteers (Figs. 8 and 9) (42). In the last study, among the OSA patients the degree of obstruction as shown on MRI showed no correlation to the RDI (42). In aggregate, all these six studies are too small to determine the efficacy of MRI for distinguishing patients with OSA from normal patients. Furthermore, in eight patients evaluated prior to and 2–3 days after laser assisted uvulopalatopharyngoplasty (LAUP), cross-sectional area at the palate was not significantly changed (p>0.5), while RDI nearly doubled, although not statistically significantly (p>0.1), and AI was significantly increased (p<0.03) (48). This striking change in RDI and AI with lack of change in oropharyngeal cross-sectional area provides further evidence that MRI is not sensitive to changes which effect sleep parameters on PSG. MRI has been used to assess the effects of continuous positive airway pressure (CPAP) on the upper airway of OSA patients. The results are conflicting with one study of five patients, which showed an increase in oropharyngeal cross-sectional area (p<0.05) after 4–6 weeks of nightly CPAP use (21), and another study of 12 patients, which showed no change in pharyngeal volumes (49).

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Figure 8 Healthy volunteer. Spin density-weighted 2D-FLASH sequence, sagittal projection, during Muller maneuver, shows no narrowing of the pharynx (arrow). (From Ref. 42.) Initial studies utilizing dynamic MRI with a 1.1sec per slice acquisition time during druginduced sleep have shown qualitative correlation with fiberoptic examination in children with sleep disordered breathing (50). Ultrafast MRI (one image per 0.8sec) was used to compare the velopharyngeal airway in OSA patients with that in controls during different phases of the respiratory cycle. This study confirmed the findings of the previous CT studies by showing narrowing of the velopharynx in OSA patients and greater compliance of the velopharynx in OSA patients as compared to controls (Fig. 10) (51). For MRI studies performed during sleep, few investigators have monitored the level of sleep. Schoenberg et al. (52) performed concurrent EEG during MRI scanning without using sedatives to induce sleep. This monitoring verifies sleep at the initiation and during

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the entire, loud scanning process. The MRI scans showed complete obstruction of the pharynx during apneic episodes in patients with OSA (Fig. 11). Narrowing seen on MRI during awake Muller maneuvers in OSA patients did not correlate well with the extent of obstruction during sleep in the same patients. These findings may explain the inability of the Muller maneuver to select successful candidates for sleep apnea surgery. Quantitative MRI signals can show differences in the level of cellular activity. Schotland et al. (53) found a difference in T2 signal in the genioglossus and geniohyoid muscles between OSA and control patients. They hypothesized that this difference in T2 signal represents a difference in the activity level of these muscles between

Figure 9 Patient with OSA. Spin density-weighted 2D-FLASH sequence. (A) Transnasal shallow respiration at rest, sagittal projection, shows no narrowing of the pharynx (arrow). (B) Muller maneuver, sagittal

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projection, shows increased mobility of the posterior pharyngeal surface (arrows) and obstruction of the oropharynx (arrowhead). (C) Transnasal shallow respiration at rest, axial projection, shows no obstruction of the oropharynx (arrows). (D) Muller maneuver, axial projection, shows an obstruction of the oropharynx (arrow). (From Ref. 42.)

Figure 10 Comparison of an axial MRI in the velopharynx region of a normal subject showing (A) maximum and (B) minimum area, an awake apneic patient showing (C) maximum and (D) minimum area, and a sleeping apneic patient showing (E) maximum and (F) minimum area. (From Ref. 51.)

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Figure 11 Dynamic single-slice images in the medial sagittal plane of a 33-year-old man during sleep apnea. The first two images (from left) with a time interval of >5sec show a complete naso-, oro-, and hypopharyngeal obstruction. In the third image, the beginning of the arousal phase is seen, with widening of the previously collapsed pharynx. The last image shows complete pharyngeal widening at the end of the arousal period. (From Ref. 52.) the two groups (53). The relationship between genioglossus and geniohyoid activity and severity of sleep apnea is not clear and bears further study. In this quantitative MRI study, the level of the T2 signal did not correlate to the severity of sleep apnea (53). This type of quantitative evaluation may help us to better understand the mechanisms of OSA, but may not be useful for distinguishing OSA from control patients. Overall, the MRI characteristics studied do not appear to correlate well with the findings on PSG. The long scan times make precise measurement of the dynamic anatomy imprecise and are probably the cause of the poor correlation to PSG findings. MRI scans while sleeping offer a more accurate anatomic description of obstructive events, but the configuration of the MRI machines makes monitoring of the level of sleep difficult and the loudness of the MRI makes induction and maintenance of sleep difficult. Advances in MRI technology will be needed before this becomes a useful modality in assessing patients with OSA.

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5. FLUOROSCOPY Fluoroscopy provides a widely available modality for performing dynamic observations of the upper airway in OSA patients, and can be performed asleep in order to observe obstructive episodes in OSA patients. Drawbacks include a high radiation dose, and superimposition of structures, especially in patients with thick and short necks. One of the earlier studies from 1983 utilized fluoroscopy to study the site of collapse in OSA patients (29). They studied awake OSA patients lying with their head and trunk inclined at 30° above the horizontal. Thick barium was used to coat the pharyngeal mucosa to improve visibility of the pharyngeal structures. In all of the OSA patients, obstruction was initiated at the junction between the soft palate, base of tongue, and posterior pharyngeal wall (Fig. 12) (29).

Figure 12 Left panel shows position of tongue, soft palate, and posterior pharynx during unobstructed breathing in sleeping patients with obstructive sleep apnea. Right panel shows the position of these structures during obstruction when the same patient is attempting to inspire. (From Ref. 29.) Two subsequent studies utilizing digital fluoroscopy to examine awake supine OSA patients examined the collapsibility of the upper airway and the use of fluoroscopy to predict the outcome of OSA surgery. In the first, no difference in velopharyngeal area and velopharyngeal collapsibility was seen between controls and patients with complete obstruction (54). In the second study, no predictors for successful outcome of LAUP were found (55). However, after LAUP, a greater percentage of responders had a

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minimum anteroposterior dimension within the normal range (p=0.0086) and less collapsibility at the velopharyngeal level (p<0.03) as compared to nonresponders (55). Fluoroscopy did not select patients with a higher likelihood of successful LAUP, but did show changes in the upper airway dimensions which correlated with successful LAUP. Asleep fluoroscopy, or somnofluoroscopy, was used to make observations on 40 OSA patients, and showed that a great variability existed in the pattern of obstruction seen in this group of OSA patients (56). Somnofluoroscopic findings of hypopharyngeal collapse in OSA patients correlated well with MP-H measurements, but did not correlate well with CT measurements of the hypopharynx (57). Successful outcome for UPPP increased from 42% to 67% by selecting patients with the narrowest level of airway and initial level of obstruction in the oropharynx (58). In these studies utilizing fluoroscopy, asleep studies appear to have had better success in differentiating responders from nonresponders.

6. PHARYNGOSCOPY Fiberoptic pharyngoscopy has been used to evaluate patients both awake and asleep. Sleep studies are probably better for assessing the dynamics of upper airway obstruction but require a sleep laboratory and, thus, are not easily performed. The modified Muller maneuver (MMM) is easily performed in the clinic with a flexible laryngoscope, and has been hypothesized to show areas predisposed to anatomic obstruction in OSA patients. Four studies compared MMM with video sleep endoscopy and/or sleep manometry in the determination of the anatomic level of obstruction and found that MMM findings correlated poorly with obstructive episodes while sleeping (59–62). Five studies used the MMM to distinguish patients who respond to UPPP from those who do not respond. The results were conflicting with two studies showing greater success when MMM was used (63,64) and three studies showing no predictive value for MMM (22,65,66). Sher et al. (64) selected OSA patients with only palatal collapse using sitting and supine MMM, and found that after UPPP, 87% had >50% decrease in AI and 73% had >50% decrease in RDI. No control patients were studied, but these results compared favorably with those for historical controls (64). In a controlled retrospective study, Aboussouan et al. (63) performed supine MMM examinations and divided their patients into a group with velopharyngeal collapse only and a group with hypopharyngeal collapse. The velopharyngeal collapse group had a significantly greater percentage of patients with >50% reduction in RDI (p= 0.05) and a significantly greater percentage of patients with >90% decrease in RDI and postoperative RDI <15 (p=0.04) (63). Conversely, three prospective studies showed no predictive value for MMM (22,65,66). Overall, the retrospective studies show improved success of UPPP after selecting patients with MMM; however, the more statistically sound prospective studies do not verify this improved success. For now, MMM does not appear to improve the likelihood of success with UPPP. Asleep studies probably allow for more accurate assessment of obstructive episodes. Early studies with asleep videopharyngoscopy described the anatomic actions causing obstruction of the upper airway (67–69), but no studies correlated these findings to PSG sleep parameters. Launois et al. (70) found that OSA patients with exclusive nasopharyngeal collapse on asleep videopharyngoscopy had a significant improvement in

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RDI at 4 months (p<0.001) and at 14 months (p<0.05) following UPPP, while the patients with obstruction at other sites did not have significant changes in RDI. An asleep videopharyngoscopy study with midazolam-induced sleep, showed a 94% cure rate of snoring with UPPP in patients with simple palatal snoring or single palatal obstruction compared with 61% cure in an unselected population (p=0.017) (71). Sleep videopharyngoscopy shows promise for predicting efficacy of UPPP. Further study of sleep videopharyngoscopy will be needed to better define its role in the care of OSA patients.

7. MANOMETRY Manometry techniques use catheters in the upper airway to measure pressure at various sites in the airway. Both awake and asleep manometry measurements have been performed to identify areas of collapse. In awake patients, externally provided negative pressure or patient provided negative pressure have been used to collapse the airway artificially for study purposes. Asleep manometry has the advantage of localizing regions of obstruction without introducing externally induced pressures, and removes the confounding effects of upper airway muscular tone. Unfortunately, this technique requires a sleep laboratory for the sleep studies, is dependent on precise placement of pressure catheters to correlate findings to anatomic structures, and is not well tolerated by all individuals. The pressure catheters only measure pressure, not flow, and are therefore unable to identify areas of flow limitation, increased resistance, and increased collapsibility, which may be important in restricting air movement (72). Four studies show conflicting results with awake manometry. Two studies show that manometry can distinguish OSA patients from controls and two studies show no correlation of manometry findings to OSA parameters. Of the studies supporting the efficacy of manometry, one showed greater collapse in the upper airway of awake OSA patients in response to externally applied negative pressures. During application of negative pressure via a tightly fitting facemask, obstruction was noted on manometry in 10 of 12 OSA patients, while no obstruction was noted in any of the seven control patients (73). The second study supporting manometry showed a significant correlation between nasopharyngeal resistance and RDI (r=0.71, p<0.001) (74). Conversely, two studies showed that anatomic identification of obstructive areas on awake manometry studies have shown poor correlation to asleep manometry studies. Induced obstruction and snoring while awake in the sitting and supine positions showed different areas of obstruction from asleep manometry (75), and a study of nine OSA patients found awake measurement of the pressure gradient across the hypopharynx and palate to correlate poorly with the site of obstruction when asleep (76). Asleep manometry shows a high level of correlation to polysomnographic data. Reda et al. (77) showed 100%, 90%, 80%, and 100% sensitivity in identifying patients with severe, moderate, mild, and no OSA, respectively. Similarly, collapse of the upper airway from negative pressures generated by nasal obstruction showed that OSA patients have collapse at low levels of negative pressure (78), snorers at higher levels of negative pressure (79), and normal patients do not collapse despite high levels of negative pressure (80). Studies comparing asleep manometry to asleep endoscopy found that the extent of

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base of tongue collapse and collapsibility did not correlate well between the two different methods of examination (60), and that endoscopy identified caudal areas of narrowing in four of nine patients with palatal collapse which were not identified by manometry alone (81). These areas of narrowing may represent pathologic areas of increased resistance, which.are clinically significant and missed by manometry measurements. Studies using asleep manometry to predict response to UPPP have been largely unsuccessful. Shepard et al. (82) reported that only one of six patients responded to UPPP, and on asleep manometry, that patient was predicted to have a poor outcome due to obstruction in the oropharynx. Metes et al. (83) reported that three of nine patients with retropalatal and one of three patients with retrolingual obstruction had relief of obstruction based on postoperative pressure measurements. However, one of the responder patients with preoperative retropalatal obstruction had a postoperative RDI of 36. Examination of the PSG sleep indices showed that six of nine patients with retropalatal and one of three patients with retrolingual obstruction had a greater that 50% decrease in RDI (83). Hudgel et al. (84) found no difference in the change in RDI between patients with palatal and hypopharyngeal collapse preoperatively on asleep manometry. This poor predictive value for asleep manometry is probably a result of those clinically significant areas of narrowing, which are not identified by manometry alone. Upper airway resistance syndrome was described in 1993 based on a group of patients with the hallmark symptoms of OSA without evidence of hypopneas or apneas on PSG (85). These patients had excessive daytime somnolence, sleep fragmentation due to transient EEG arousals, and abnormal increases in upper airway resistance during sleep (85). Diagnosis of this syndrome requires identification of abnormally low peak inspiratory esophageal pressure. Since this diagnosis was introduced, a significant number of patients have been identified with this syndrome, making the use of esophageal pressure catheters an important addition to the armamentarium for diagnosis of sleep disordered breathing. Overall, asleep manometry is very sensitive for making the diagnosis of sleep apnea and may identify a group of patients with clinically significant sleep disordered breathing without evidence of frank apneas. Thus far, the role of awake manometry is not clear and manometry does not appear to select for successful surgical candidates.

8. ACOUSTIC REFLECTION Acoustic reflection measures the cross-sectional area of the upper airway as a function of distance using reflected sound waves. This technique’s advantages are that it is simple, fast, done while awake, and requires no exposure to radiation. Disadvantages of this technique include a need for special equipment, difficulty in performing the study asleep, and only measurement of the oropharyngeal and hypopharyngeal but not the nasopharyngeal airway. Correlation of pharyngeal cross-sectional areas between CT and acoustic reflection have shown statistically significant correlation between measurements (r=0.95, p<0.0001) (86). This technique has been used to study OSA, snoring, and normal control patients awake in supine and sitting positions. A study of 70 male and 84 female patients showed no difference in pharyngeal area between those who snored and normal nonsnoring patients (87). Multiple prospective studies have shown statistically

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significant differences in pharyngeal cross-sectional area between OSA patients and normal controls (88–90). Rivlin et al. (90) showed a significant correlation between AI and pharyngeal cross-sectional area in nine OSA patients (r=0.87, p<0.01). Different methods for evaluating pharyngeal compliance (change in pharyngeal cross-sectional area with change in pressure) have shown OSA patients to have greater pharyngeal compliance than normal controls (88,89,91,92). Some controversy exists about whether acoustic reflection reliably distinguishes snorers from OSA patients. Two studies comparing OSA and snoring patients have reported similarly small pharyngeal cross-sectional areas but greater pharyngeal compliance in OSA patients (88,91). Subsequently, an unpublished report on over 300 patients found that OSA and nonapneic snorers may be indistinguishable as far as measurements of awake pharyngeal mechanics are concerned (93). Further studies will be needed to better understand the ability of acoustic reflection to diagnose patients with OSA. Only one study has used acoustic reflection to evaluate postoperative results. Following UPPP, eight snoring patients had increased pharyngeal cross-sectional areas (p<0.01) and decreased pharyngeal compliance (p<0.05) (94). Thus far, acoustic reflection has not been used to choose, successful OSA surgical candidates or to assess the upper airways of OSA patients following surgery. If this technique accurately portrays the collapsibility of the upper airway, it holds great promise for possible intraoperative studies to direct intervention at the time of surgery.

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52. Schoenberg SO, Floemer F, Kroeger H, Hoffmann A, Bock M, Knopp MV. Combined assessment of obstructive sleep apnea syndrome with dynamic MRI and parallel EEG registration: initial results. Invest Radiol 2000; 35(4):267–276. 53. Schotland HM, Insko EK, Schwab RJ. Quantitative magnetic resonance imaging demonstrates alterations of the lingual musculature in obstructive sleep apnea. Sleep 1999; 22(5):605–613. 54. Tsushima Y, Antila J, Svedstrom E, Vetrio A, Laurikainen E, Polo O, Kormano M. Upper airway size and collapsibility in snorers: evaluation with digital fluoroscopy. Eur Respir J 1996; 9(8):1611–1618. 55. Tsushima Y, Antila J, Laurikainen E, Svedstrom E, Polo O, Kormano M. Digital fluoroscopy before and after laser uvulopalatopharyngoplasty in obstructive sleep apnea. Importance of pharyngeal collapsibility and hyoid bone position. Acta Radiol 1997; 38(2):214–221. 56. Walsh JK, Katsantonis GP, Schweitzer PK, Verde JN, Muehlbach M. Somnofluoroscopy: cineradiographic observation of obstructive sleep apnea. Sleep 1985; 8(3):294–297. 57. Pepin JL, Ferretti G, Veale D, Romand P, Coulomb M, Brambilla C, Levy PA. Somnofluoroscopy, computed tomography, and cephalometry in the assessment of the airway in obstructive sleep apnoea. Thorax 1992; 47(3):150–156. 58. Katsantonis GP, Walsh JK. Somnofluoroscopy: its role in the selection of candidates for uvulopalatopharyngoplasty. Otolaryngol Head Neck Surg 1986; 94(1):56–60. 59. Pringle MB, Croft CB. A comparison of sleep nasendoscopy and the Muller manoeuvre. Clin Otolaryngol 1991; 16(6):559–562. 60. Woodson B, Wooten M. Comparison of upper-airway evaluations during wakefulness and sleep. Laryngoscope 1994; 104:821–828. 61. Skatvedt O. Localization of site of obstruction in snorers and patients with obstructive sleep apnea syndrome: a comparison of fiberoptic nasopharyngoscopy and pressure measurements. Acta Otolaryngol (Stockh) 1993; 113(2):206–209. 62. Croft CB, Pringle M. Sleep nasendoscopy: a technique of assessment in snoring and obstructive sleep apnoea. Clin Otolaryngol 1991; 16(5):504–509. 63. Aboussouan LS, Golish JA, Wood BG, Mehta AC, Wood DE, Dinner DS. Dynamic pharyngoscopy in predicting outcome of uvulopalatopharyngoplasty for moderate and severe obstructive sleep apnea. Chest 1995; 107(4):946–951. 64. Sher AE, Thorpy MJ, Shprintzen RJ, Spielman AJ, Burack B, McGregor PA. Predictive value of Muller maneuver in selection of patients for uvulopalatopharyngoplasty. Laryngoscope 1985; 95(12):1483–1487. 65. Katsantonis GP, Maas CS, Walsh JK. The predictive efficacy of the Muller maneuver in uvulopalatopharyngoplasty. Laryngoscope 1989; 99(7 Pt 1):677–680. 66. Wittig R, Fujita S, Fortier J, Zorick F, Potts G, Roth T. Results of uvulopalatopharyngoplasty (UPPP) in patients with both oropharyngeal and hypopharyngeal collapse on Muller maneuver. Sleep Res 1988; 17:269. 67. Rojewski TE, Schuller DE, Clark RW, Schmidt HS, Potts RE. Synchronous video recording of the pharyngeal airway and polysomnograph in patients with obstructive sleep apnea. Laryngoscope 1982; 92(3):246–250. 68. Rojewski TE, Schuller DE, Clark RW, Schmidt HS, Potts RE. Videoendoscopic determination of the mechanism of obstruction in obstructive sleep apnea. Otolaryngol Head Neck Surg 1984; 92(2):127–131. 69. Borowiecki B, Pollak CP, Weitzman ED, Rakoff S, Imperato J. Fibro-optic study of pharyngeal airway during sleep in patients with hypersomnia obstructive sleep-apnea syndrome. Laryngoscope 1978; 88(8 Pt 1):1310–1313. 70. Launois SH, Feroah TR, Campbell WN, Issa FG, Morrison D, Whitelaw WA, Isono S, Remmers JE. Site of pharyngeal narrowing predicts outcome of surgery for obstructive sleep apnea. Am Rev Respir Dis 1993; 147(1):182–189. 71. Camilleri AE, Ramamurthy L, Jones PH. Sleep nasendoscopy: what benefit to the management of snorers? J Laryngol Otol 1995; 109(12):1163–1165.

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9 Clinical Staging for Sleep Disordered Breathing: A Guide to Diagnosis, Treatment, and Prognosis Michael Friedman and Hani Ibrahim Department of Otolaryngology and Bronchoesophagology, RushPresbyterian-St. Luke’s Medical Center, and Division of Otolaryngology, Advocate Illinois Masonic Medical Center, Chicago, Illinois, U.S.A. 1. INTRODUCTION Sleep disordered breathing (SDB) is a clinical syndrome resulting from obstruction of the upper airway during sleep. Clearly, the syndrome is not the result of any single site and cause of obstruction, as many potential sites and reasons for obstruction have been identified. In addition, since the primary treatment for SDB is continuous positive airway pressure (CPAP), the precise site and cause of obstruction is not always crucial. Historically, descriptions of upper airway abnormalities were qualitative in nature; quantitative standardized descriptions were not previously available. Surgical correction of SDB is site specific and unlike CPAP, any single surgical procedure would not be expected to correct all patients with SDB. Despite this obvious observation, uvulopalatopharyngoplasty (UPPP) became a standard treatment for SDB. However, UPPP only reduces soft palate and tonsil obstruction but does not always improve obstruction at the level of the hypopharynx. In fact, meta-analysis of reported data indicates that the procedure has only a 40% success rate (1). Of greater concern, however, are the findings by Senior et al. (2) that some patients showed both objective and subjective signs of worsening SDB following UPPP. The severity of the sleep disturbance as measured by polysomnography does not predict success with UPPP; the success rate for treatment of mild SDB was only 40%, not different from that of more severe SDB (2). Thus, the key to the appropriate use of this potentially curative procedure is identification of the right candidates. A simple, quantifiable, reproducible staging system could provide a basis to identify those patients likely to benefit from UPPP and those patients likely to fail (3). In addition to guiding surgical treatment, a clinical staging system would also be helpful as a diagnostic tool to predict the presence and severity of SDB based on physical examination (4). As with many diseases, the diagnosis of SDB is usually symptom driven. However, the patient may be unaware of some symptoms such as snoring and apnea, and in denial about others. This may account for the small percentage of patients with SDB that are actually referred for diagnosis and treatment. A simple, reproducible, quantitative staging system

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could facilitate SDB assessment as part of every routine physical examination. Clinical findings suggestive of SDB could alert the physician to search for additional history from a bed partner or others, and to refer the patient for definite diagnosis. This chapter reviews our experience with a proposed staging system and its value as a guide to predicting the presence and severity of SDB, as well as a guide to identifying those patients likely to benefit from UPPP. The staging system can direct appropriate surgical treatment when UPPP alone is not likely to succeed and thereby ultimately improve surgical success.

2. STAGING CRITERIA Palate position had been previously studied and found to be a clinical indicator of SDB (3). This palate classification is based on observations by Mallampati, who published a paper on palate position as an indicator of the ease or difficulty of endotracheal intubation by standard anesthesiologist techniques. There are two major modifications that we have incorporated into our staging criteria: (a) The anesthesiologist’s assessment is based on the patient sticking out their tongue and the observer then notes the relationship of soft palate to tongue. Our grading is based on the tongue in a neutral, natural position inside the mouth (Fig. 1). (b) The original grading system had only three grades; we believe that four grades are essential (Fig. 1). The reason for the first modification is that the tongue during sleep apnea is certainly not related to a protruded position. Therefore, we chose to assess the tongue inside the mouth. The reason for adding a fourth grade is that the majority of patients fall into the intermediate grades of 2 and 3, but patients with extreme positions (1 and 4) seem to have extreme behavior with respect to both the presence and the treatability of SDB. Since this is a modified palate position grading system, we are identifying it not as Mallampati but as Friedman palate position (FPP) grades 1–4. We do credit Mallampati for bringing this important physical finding to our attention. Palate grade was assessed as previously described (3,4). The procedure involves asking the patient to open their mouth wide without protruding their tongue. The procedure is repeated five times so that the observer can assign the most accurate level. At times there can be some variation with different examinations, but the most consistent position is assigned as the palate grade. Palate grade 1 allows the observer to visualize the entire uvula and tonsils or pillars (Fig. 1A). Palate grade 2 allows visualization of the uvula but not the tonsils (Fig. 1B). Palate grade 3 allows visualization of the soft palate but not the uvula (Fig. 1C). Palate grade 4 allows visualization of the hard palate only (Fig. 1D). Tonsil size was graded from 0 to 4. Tonsil size 1 implies tonsils hidden within the pillars (Fig. 2A). Tonsil size 2 implies the tonsil extending to the pillars (Fig. 2B). Size 3 tonsils are beyond the pillars but not to the midline (Fig. 2C). Tonsil size 4 implies tonsils that extend to the midline (Fig. 2D). Weight (kg) and height (m2) of the patients were recorded at the initial visit and the body mass index (BMI) (kg/m2) was calculated using the formula BMI=weight

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Figure 1 (A) FPP 1 allows visualization of the entire uvula and tonsils/pillars. (B) FPP 2 allows visualization of the uvula but not the tonsils. (C) FPP 3 allows visualization of the soft palate but not the uvula. (D) FPP 4 allows visualization of the hard palate only. (kg)/height2 (m2). The BMI was graded as grade 0 (<20kg/m2), grade I (20kg/m2), grade II (25–30kg/m2), grade III (30–40kg/m2>), and grade IV (>40kg/m2) according to previously published standards for obesity (5). A BMI >40 was selected as an automatic inclusion into clinical stage IV. Although somewhat controversial, most surgeons have

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found that patients with BMI >40 have a poor prognosis for corrective UPPP. Therefore, patients with BMI >40 were automatically assigned to stage IV. Neck circumference has been shown to correlate well as a clinical predictor, but BMI is an alternative measure that was used for creating the SDB score and staging. Stage I disease was arbitrarily defined as those patients with palate position 1 or 2, tonsil size 3 or 4, and BMI <40 (Table 1). Stage II disease is defined as palate position 1 or 2 and tonsil size 0, 1, or 2, or palate position 3 and 4 with tonsil size 3 or 4, and BMI <40. Stage III disease is defined as palate position 3 or 4 and tonsil size 0, 1, or 2. All patients with a BMI >40 were included in stage IV. In addition, all patients with skeletal deformities such as micrognathia or midface hypoplasia are considered stage IV.

Figure 2 (A) Tonsils, size 1, are hidden within the pillars. (B) Tonsils, size 2, extend to the pillars. (C) Tonsils, size 3, extend beyond the pillars but not to the midline. (D) Tonsils, size 4, extend to the midline. 3. PHYSICAL FINDINGS AS A CLINICAL PREDICTOR OF SDB Based on the three physical findings described (FPP, tonsil size, and BMI), an SDB score can be calculated to identify patients likely to have SDB. The score is calculated by adding the numerical values of each physical finding:

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SDB score=FPP(0–4)+tonsil size(0–4)+BMI value(0–IV) A positive SDB score is designated as the sum of FPP+tonsil size+BMI >8. A positive SDB score has a positive predictive value of moderate SDB [apnea-hypopnea index (AHI) >20] of 90%. A positive SDB score was 74% effective in predicting severe SDB (AHI ≥45) (see Table). A negative SDB score was designated as the sum of FPP+tonsil size+BMI <4. The value of a negative SDB score in predicting an AHI <20 was 67% (Table 1).

Table 1 Staging System Stage I

II

III

FPP

Tonsil size

BMI

1

3, 4

<40

2

3, 4

<40

1, 2

1, 2

<40

3, 4

3, 4

<40

3

0, 1, 2

Any

4

0, 1, 2

Any

Table 2 Success Rate of Uvulopalatopharyngoplasty in the Treatment of SDB Stage

Unsuccessful

Successful

Total

I

6 (19.4%)

25 (80.6%)*

31 (100%)

II

18 (62.1%)

11 (37.9%)*

29 (100%)

III

68 (91.9%)

6 (8.1%)*

74 (100%)

4. STAGES AS A PREDICTOR OF SUCCESSFUL UPPP Table 2 illustrates the success and failure rates of UPPP for the treatment of SDB according to stage. Chi-square analysis demonstrates a highly significant relationship between stage and success of surgery. The Pearson chi-square=54.2, with two degrees of freedom, and a two-sided p<0.0001. Successful treatment of SDB with UPPP was most likely achieved in stage I patients (80.6%) and least likely in stage III patients (8.1%). To further explore the relationship between the severity of SDB (stage) and the efficacy of surgical treatment with UPPP, a stepwise multivariate discriminant analysis can be performed. The preoperative criteria used to stratify patients into stages (BMI, tonsil size, and palate position score) were the only indices introduced into the stepwise analysis. The success or failure of surgical treatment with UPPP was used as the

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categorical end point. Using F values of 3.84 for entry and 2.71 for removal, the stepwise analysis eliminated BMI, keeping tonsil size and palate position score as the best combination of indices for differentiating between success and failure. The classification coefficients calculated for tonsil size and Mallampati score were used to construct Fisher’s linear classification functional equations. Fisher’s linear classification equation for each group takes the form: CF=tonsils(Coeftonsils)+MMP(CoefMMP)+constant where CF=group classification function tonsils=tonsil size Coeftonsils=group classification coefficient for tonsil size MMP=FPP score CoefMMP=group classification coefficient for Mallampati score constant=group classification constant A separate equation is constructed for each result, unsuccessful and successful. In the present case: Unsuccessful result=[(tonsils)0.870]+[(MMP) 5.319]+(−10.563) Successful result=[(tonsils)2.284]+[(MMP) 2.333]+(−6.001) To predict the success of UPPP surgery in patients with SDB, enter the patient’s tonsil size and palate position into each of the above formulas and calculate. The equation totaling the numerical highest value is the predicted result. In the validation study, the above formulas were applied casewise to the 134 patients and correctly predicted 95.0% of the cases by result.

5. DISCUSSION Classic medical diagnosis is based on symptoms and physical findings, which are then confirmed by laboratory tests. SDB is easily diagnosed when symptoms are presented. Many patients, however, do not provide accurate snoring or sleep histories for a variety of reasons. Patients who sleep alone are not aware or snoring or apneic events and are often unaware or in denial about daytime fatigue, somnolence, and many other SDBrelated symptoms. Even patients who are aware of snoring and apnea will usually not volunteer this information on routine physical examination. When patients present with a classical history, the diagnosis of SDB is relatively routine, but physicians have no clear criteria to identify SDB based on physical examination alone. Use of the clinical staging system based on palate position, tonsil size, and BMI will provide a simple, reliable, reproducible screening assessment tool to identify those patients likely to have SDB. UPPP is the most common and in many situations the only surgical procedure performed by most otolaryngologists for the treatment of SDB. Many studies have documented three important issues that must be considered in recommending the surgical procedure to a patient: (a) A meta-analysis of unselected patients treated with UPPP revealed that only 40.79% of patients had “successful” surgery defined by an AHI

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reduction of 50% and a postoperative AHI <20 or an apnea index (AI) reduced by 50% and a postoperative AI <10 (1). (b) Despite some data indicating that preoperative selection criteria may identify those patients likely to fail, prior to this staging system there have been no clear-cut, reproducible physical findings that have been shown to consistently help in the selection process. (c) A study published by Senior et al. (2) demonstrated that UPPP not only does not cure SDB in 60% of cases but also often makes it worse. It has been a common misconception to assume that although UPPP has only a 40% success rate, the responders would be those with mild disorders. Therefore, the procedure is often recommended for patients with mild and moderate SDB. Senior et al. have demonstrated that within this subgroup the risk of failure and the risk of aggravating the disease are extremely high. These findings are consistent with our own observations and data. They have also been shown to be true for patients treated with laser assisted UPPP. The procedure not only fails 60% of the time, but often makes the condition worse. Surgery with a 40% success rate is certainly less than ideal. Our ultimate goal is, of course, to develop a treatment with a high success rate. In the absence of that treatment, however, our goal should be to identify those patients who are likely to benefit from UPPP, which is a valuable procedure for those patients who can be cured with it. The ideal identification process would identify those patients with a high likelihood of success of UPPP vs. those with a high likelihood of failure and therefore a need to treat other areas of the upper airway. The ideal selection process would be noninvasive, costeffective, and reproducible. We propose that our staging system satisfies these criteria for an ideal prediction assessment for some patients (stage I and stage III), who can then be guided to appropriate treatment. Patients with stage I disease have better than an 80% chance of success with UPPP and should therefore undergo the procedure when nonsurgical treatment has failed. Even patients with severe SDB had an 80% success rate if they had stage I disease based on our staging system. Patients with stage III disease should never undergo UPPP alone as a surgical cure for SDB. With an 8.1% success rate, the surgery is destined to fail. They should be treated with a combination of procedures that address both the palate and the hypopharynx. In our study, 78.3% of patients can be stratified to stage I or III. Patients with stage II disease do not fall into either extreme but probably should be treated similar to stage III patients. The failure of UPPP to cure SDB has been clearly associated with sites of obstruction in the upper airway not corrected by the procedure, such as the hypopharynx (7). Fujita (7) originally described multiple levels of obstruction. Riley et al. (8) have demonstrated these abnormalities with cephalometric data. Routine use of preoperative cephalometric studies has not been shown to be worthwhile in the selection criteria. The complexity of the studies combined with conflicting reports on their value in treatment selection has relegated their use to research rather than as a clinical tool. Numerous other methods have been used to predict the location of the upper airway obstruction. These include physical examination, computed tomography, magnetic resonance imaging, and fluoroscopy. As with cephalometric studies, these studies are all valuable in research studies but have not been shown to be of clinical value. The most commonly used test is the Muller maneuver (MM). Borowiecki and Sassin (9) first described this maneuver for the preoperative assessment of SDB. The MM consists of having the patient perform a forced inspiratory effort against an obstructed airway with

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fiberoptic endoscopic visualization of the upper airway. The test is widely used and simple to perform. Despite this, its use is controversial and certainly no studies have been able to associate the maneuver as a tool to select patients who are likely to succeed with UPPP. Criticism of the test is based on three points. One criticism of the test is that it is subjective. Terris et al. (10) have clearly shown that in their institution the maneuver can easily be taught to residents at all levels of training and is clearly reproducible. Their institution, however, is highly focused on sleep disorders and treats a large number of patients on a regular basis. The level of reproducibility may be reduced by the general otolaryngologist and by residents seeing patients with SDB less frequently. Another criticism is that many patients are incapable of producing a full force inspiratory effort. Patient compliance can vary significantly from patient to patient and even from examination to examination with the same patient. Any test that relies on patient cooperation has some level of variability. The third point of criticism is whether the use of MM helps predict the success of UPPP. Terris et al. (10) and Sher et al. (11) were the first investigators who suggested that the use of MM for patient selection could increase the success of UPPP. Other researchers, however, have found that the MM is not helpful in predicting the success of UPPP. In addition, we have found that patients with minimal collapse of the hypopharynx as determined by MM before UPPP may have moderate or severe collapse in the base of the tongue (by MM) after UPPP. Katsantonis et al. (12) found that the prediction efficacy of the MM was only 33% in selected patients. Doghramjii et al. (13) similarly found no benefit of MM in the prediction value for success of UPPP. Other reports substantiate these negative findings questioning the reproducibility of MM as a predictive tool (14). Any staging system is not a substitute for detailed evaluation through clinical examination and radiological studies, but it provides stratification of patients, which helps in treatment selection and assessment of results. Similarly, this staging system for patients with SDB will help create reproducible physical data and help in treatment selection. The treating physician can continue to use vague and nonreproducible terms such as “low soft palate,” “thick soft palate,” “crowded oropharynx,” etc., but the staging system should be used in addition to these terms. Ideally, the goal of surgery for SDB would be procedures that result in ≥80% success. In the absence of that simple procedure, stratification of patients that allows for preoperative selection will in effect result in 80% success. Obviously, only 25% of patients suffering from SDB can achieve this result with UPPP as an isolated procedure. Seventy-five percent of patients should not be treated with UPPP as an isolated curative surgical procedure. Patients with stage II and stage III disease should have adjunctive procedures to address their hypopharynx if surgery is contemplated. Depending on surgeon bias and patient selection, some of them may require tongue-base advancement procedures or maxillary mandibular advancement procedures. If patients with stage III disease are treated with UPPP alone they should be forewarned that they likely will need secondary procedures since the likelihood of initial success is less than 10%. Further studies by Friedman et al. have used the staging system to direct surgical treatment. Patients are never considered for surgical therapy unless CPAP has failed. Patients with stage I disease are treated with UPPP as an isolated procedure. Patients with stage II and stage III disease are treated with UPPP and tongue-base reduction with

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radiofrequency technique. Using this staging-directed approach, the rate of successful treatment has been improved for stage II patients from 37.9% to 74%. Success rate for stage III patients improved from 8.1% to 43.8% (14).

6. CONCLUSIONS This study identifies three physical findings that can be quantified in a reproducible manner to predict the presence of SDB and to identify the location of the obstruction. Based on palate position (using the FPP score of 1–4), tonsil size (scored between 0 and 4), and BMI, the patient can be staged (stages I through III). Staging can be helpful in directing the patient toward surgical treatment with UPPP if nonsurgical treatment fails. Patients with an SDB score >8 are likely to have moderate SDB, whereas patients with an SDB score <4 are likely to have a normal polysomnogram. Patients with stage I disease have an 80% chance of successful cure with UPPP while those patients with stage III disease have only an 8.1% chance of cure. Staging-directed treatment has been shown to significantly improve success rates. Stage II and stage III patients should have treatment directed at the hypopharynx in addition to UPPP.

REFERENCES 1. Sher AE, Schectman KB, Piccirillo JF. The efficacy of surgical modifications of the upper airway in adults with obstructive sleep apnea syndrome. Sleep 1996; 19(2):156–177. 2. Senior BA, Rosenthal L, Lumley A, et al. Efficacy of uvulopalatoplasty in unselected patients with mild obstructive sleep apnea. Otolaryngol Head Neck Surg 2000; 123(3):179–182. 3. Friedman M, Tanyeri H, LaRosa M, et al. Clinical predictors of obstructive sleep apnea. Laryngoscope 1999; 109:1901–1907. 4. Friedman M, Ibrahim H, Bass L. Clinical staging for sleep-disordered breathing. Otolaryngol Head Neck Surg 2002; 127:13–21. 5. Andreoli TE, Cecil RL Cecil Essentials of Medicine. xiv. 2nd ed.. Philadelphia, PA: Saunders, 1990:830. 6. Simmons FB, Guilleminault C, Miles LE. The palatopharyngoplasty operation for snoring and sleep apnea: an interim report. Otolaryngol Head Neck Surg 1984; 92:375–380. 7. Fujita S. UPPP for sleep apnea and snoring. Ear Nose Throat J 1984; 63:227–235. 8. Riley R, Guillominault C, Powell N, et al. Palatopharyngoplasty failure, cephalometric roentgenograms, and obstructive sleep apnea. Otolaryngol Head Neck Surg 1985; 93:240–244. 9. Borowiecki BD, Sassin JF. Surgical treatment of sleep apnea. Arch Otolaryngol 1983; 109:506– 512. 10. Terris DJ, Hanasono MM, Liu YC. Reliability of the Muller maneuver and its association with sleep-disordered breathing. Laryngoscope 2000; 110:1819–1823. 11. Sher AE, Thorpy MJ, Shprintzen RJ, et al. Predictive value of Muller maneuver in selection of patients for uvulopalatopharyngoplasty. Laryngoscope 1985; 95:1483–1487. 12. Katsantonis GP, Maas CS, Walsh JK. The predictive efficacy of the Muller maneuver in uvulopalatopharyngoplasty. Laryngoscope 1989; 99:677–680. 13. Doghramji K, Jabourian ZH, Pilla M, et al. Predictors of outcome for uvulopalatopharyngoplasty. Laryngoscope 1995; 105:311–314.

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14. Petri N, Suadicani P, Wildschiodtz C, et al. Predictive value of Muller maneuver, cephalometry and clinical features for the outcome of uvulopalatopharyngoplasty. Acta Otolaryngol (Stockh) 1994; 114:565–571. 15. Friedman M, Ibrahim H, Joseph N. Staging of sleep disordered breathing: a guide to appropriate treatment. Presented at the Middle Section Meeting of the Triological Society, Indianapolis, IN, Jan 18, 2003.

10 Continuous Positive Airway Pressure in Obstructive Sleep Apnea Syndrome Susmita Chowdhuri Division of Pulmonary/Critical Care and Sleep Medicine, Department of Medicine, John D.Dingell Veterans Affairs Medical Center, Wayne State University School of Medicine, Detroit, Michigan, U.S.A. Jed Black Stanford Sleep Disorders Center, Stanford University, Palo Alto, California, U.S.A. 1. INTRODUCTION Sullivan et al. (1) first introduced continuous positive airway pressure (CPAP) as a mode of treatment for obstructive sleep apnea syndrome (OSAS) in 1981. A CPAP unit consists of a blower that generates positive pressure, which is then delivered via a hose through an appropriate interface to the patient. It acts as a pneumatic splint, and prevents the upper airway from collapsing cyclically during sleep in OSAS. It has become a standard of treatment for OSAS (2). In 1997, Wright et al. (3) concluded in a review article that the “relevance of sleep apnea to public health has been exaggerated” and that “the effectiveness of continuous positive airway pressure in improving healthcare has been poorly evaluated.” This was attributed to the lack of large randomized placebo controlled trials of CPAP vs. other modes of treatment. However, this review had methodological shortcomings (4). In addition, many randomized placebo controlled trials since then have strongly refuted the above claim. Results from a large multicenter longitudinal National Institutes of Health sponsored epidemiologic study, the Sleep Heart Health Study (SHHS) (5,6), have started yielding data that clearly associate OSAS with negative effects on the cardiovascular and neurocognitive systems. Whether the use of CPAP will prevent the development of these negative consequences is yet to be determined; however, recent large clinical outcomes trials support this view.

2. MECHANISM OF ACTION CPAP splints the upper airway open by raising the intraluminal upper airway pressure above the positive critical transmural pressure of the upper airway (7). In addition to acting as a splint (8) for the collapsible upper airway tube and hence improving nocturnal oxygenation and decreasing the respiratory disturbance index (RDI) in OSAS, CPAP

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possibly also works by increasing the awake ventilatory drive (9) and the airway tone (10). CPAP eliminates both obstructive and mixed apneas (11). Central apneas may also be eliminated.

3. INDICATIONS FOR CPAP CPAP is effective in the treatment of patients with clinically important OSAS (2). 3.1 Severe OSAS The general consensus is that patients with severe OSAS, defined as an RDI of ≥30/hr, should be treated with CPAP (12). This is based on the findings of increased risk of hypertension (HTN) in these subjects noted from the Wisconsin Sleep Cohort and the SHHS data (13,5). 3.2 Mild to Moderate OSAs The current consensus also is that when comorbid factors, e.g., symptoms of sleepiness, impaired cognition, mood disorders, or documented cardiovascular diseases, are present, then patients with mild (RDI of 5–15/hr) or moderate OSA (RDI 15–30/hr) may experience benefit from CPAP therapy (12). One may question whether CPAP is indicated in patients with mild OSA (RDI 5– 15/hr) who do not have associated symptoms of sleepiness, cognitive dysfunction, or underlying cardiovascular diseases. Many patients with a mild degree of abnormality will not have subjective symptoms of sleepiness. Instead, some may have symptoms of insomnia or may present with neuropsychological deficits that are evident only upon objective testing (14–16). Hence, one cannot rely solely on subjective symptoms to make a judgment regarding the need for CPAP. Indeed, motor vehicle accident risk correlates much more highly with RDI than measures of sleepiness, with evidence of a marked increased risk even in mild OSA (17). Additionally, many studies have shown that CPAP objectively improves neuropsychological functioning even in mild sleep-related breathing disorder (18,19). Moreover, we now know from the SHHS (4) that even an RDI as low as 5/hr in asymptomatic subjects poses a risk of HTN, ischemic heart disease, stroke, and other cardiovascular diseases. However, controlled outcome studies demonstrating reversal of cardiovascular morbidity and mortality are few in this group of individuals. Longitudinal studies are needed to evaluate these concerns. Such studies would help to elucidate the role of chronic CPAP use in mild asymptomatic OSA.

4. INITIATION OF CPAP TREATMENT Under the current guidelines, following a diagnostic nocturnal polysomnography or following the diagnostic portion of a “split-night” study, patients who meet OSAS diagnostic criteria undergo CPAP titration in the sleep laboratory (2,12). The minimum

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parameters for a monitored study include electroencephalography, electrooculography, oronasal airflow, chest wall effort, body position, snoring microphone, electrocardiogram, and oximetry. The patient is initially educated about the indications for CPAP. The patient is allowed to adapt to the equipment and different masks. An initial short period of desensitization prior to the study is recommended, which allows the patient to get accustomed to the idea of wearing it through the night. An attended study is most accurate and allows for technologist intervention for mask leaks, lost leads, as well as adjustment of CPAP according to body positions and rapid eye movement (REM) sleep. Due to OSAS variability across patients, no precise protocol for CPAP titration exists, but general recommendations have been established. Usually, one starts at a low pressure of 4–5cm, gradually increasing by 1–2cm every 15–20minutes until the apneas, hypopneas, respiratory effort-related arousals, and snoring are abolished. Patients who hypoventilate or who have other comorbidities [e.g., chronic obstructive pulmonary disease, congestive heart failure (CHF)] may require in-line oxygen to correct hypoxia, generally only after obstructive events are controlled. The determinants for optimal CPAP also lack precision. Prediction equations have been suggested for empiric CPAP pressures. Generally, such equations are based on neck circumference, body mass index (BMI), and apnea-hypopnea index (AHI) (20,21). The models perform better for men. They are not accurate enough to distinguish between patients with or without OSAS but may be useful in prioritizing patients for split-night polysomnography (22). Re-titration may be indicated for weight change (>15%), for persistent or recurrent symptoms, and for reassessment after upper airway surgery or oral appliances (OAs) (23). The positive airway pressure may need to be increased in the supine position or during REM sleep. One study noted that in most OSAS patients, the optimal CPAP level was significantly higher in the supine position than it is in the lateral position (24). This was true for REM and non-REM sleep, for obese and nonobese patients, for patients with different degrees of severity, and for young and old OSA patients. The authors concluded that no CPAP titration should be considered complete without the patient having slept in the supine posture during REM sleep. Unrelated to the above parameters, the differences in optimal CPAP between the supine and lateral postures were similar, ranging between 2.31 and 2.66cm H2O.

5. SPECIAL PAP DELIVERY SYSTEMS Occasionally, positive pressure therapy can be optimized through the application of variable or bilevel rather than continuous pressure. Bilevel pressure allows for independent adjustment of inspiratory and expiratory pressures and can provide partial spontaneous ventilatory assist in a variety of settings including obesity hypoventilation, neuromuscular disease, and conditions yielding central apneas and reduced ventilatory drive (25). Bilevel pressure may be indicated when patients cannot tolerate CPAP due to discomfort while exhaling against positive pressure or when aerophagia is problematic. A back-up rate is not required for bilevel pressure in OSAS. Bilevel pressure is not routinely indicated as an alternative to CPAP in OSAS because, although the mean

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pressure used may be lower, in most cases this does not affect compliance or increase the hours of usage (26). Traditionally, all-night CPAP titration is performed to optimize CPAP pressure. Frequently, diagnostic testing and CPAP titration can be accomplished in a split-night fashion for patients with moderate to severe OSA. A split-night protocol may be sufficient to determine the effective CPAP pressure (27), especially in patients with an RDI>20. But a split-night study may be too limited in some patients to determine a satisfactory prescription. Patients with milder OSAS are more likely to have unsuccessful split-night studies because more prolonged monitoring is needed to establish the diagnosis (28). However, a study using classical symptoms of OSAS as the indication for split-night studies found that there were no differences in long-term CPAP use compared to full-night studies and that it resulted in shorter time from referral to treatment (29). Advances in CPAP technology have yielded CPAP devices with sensors, which indirectly detect airflow and automatically adjust pressure according to built-in algorithms. In theory, such autotitrating CPAP (APAP) devices automatically adjust the pressure up or down to maintain upper airway patency at the lowest effective pressure. Berry et al. (30) have reviewed the efficacy of APAP for the treatment of OSA and the American Academy of Sleep Medicine has made recommendations (31) regarding the use of these devices. APAP may be used for treatment only after an attended titration with standard CPAP or APAP is completed. It is not currently recommended for patients with CHF, significant lung disease, obesity, hypoventilation, or respiratory failure. Patients who do not snore (due to surgery or naturally) should not be titrated with an APAP device that relies solely on vibration or sound to monitor compromised airflow. Mask leaks may prevent adequate titration with APAP. APAP is not recommended for use in split-night studies. Devices using differing technologies may yield dissimilar results in a given patient. There is conflicting evidence that compliance is increased with APAP compared to CPAP (30).

6. POTENTIAL CPAP-USE DIFFICULTIES Ultimately, the efficacy of CPAP as a treatment modality depends on long-term compliance, which in turn is related to the frequency of side effects among other factors. The common side effects of CPAP are related to nasal symptoms of dryness, congestion, sneezing, and rhinorrhea, which may affect 25–65% of the users (32). Patients may also complain of sinusitis and conjunctivitis. They may develop pressure sores on the face from the mask or complain of discomfort from the pressurized air and some may complain of difficulty tolerating noise from the equipment. In one study, 50% of the patients complained of at least one side effect related to the mask—allergic reaction, abrasion of the bridge of the nose, or mask air leaks; 65% complained of dryness of the nose or mouth; sneezing and nasal drip were noted in 35% and nasal congestion in 25% of the subjects, air swallowing in 16%, sinusitis in 8%, and nosebleed in 4% of the subjects (32). Higher levels of pressure and longer hours of use were not associated with higher prevalence of side effects. Although machine noise was noted by 34% of patients in this study, it is probably less of a problem today with newer, quieter machines.

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There have been reports of chest discomfort from the pressure, one case of pneumocephalus (33), a postcoronary artery bypass pneumopericardium (34), and one case report of meningitis related to recurrent sinusitis (35). There are no absolute contraindications for CPAP use but bouts of recurrent acute sinusitis following CPAP use may be a relative contraindication (35). There is a potential risk of rebreathing in the event of equipment or electric failure in the absence of an alarm system (36).

7. STRATEGIES FOR COMPLIANCE OPTIMIZATION Follow-up of patients should focus on efficacy, side effects, and compliance. The outcome measures of treatment efficacy include improved vigilance, daytime performance, quality of life measures, and effect on cardiovascular morbidity including HTN, as noted earlier (37). Kribbs et al. (38), found that only 46% of patients used at least 4hr of CPAP on 70% of the nights. Patients generally overestimate the hours of CPAP use. Most CPAP machines have built-in meters to record the duration of time that the machine has been running or has been in actual use and can be used to objectively measure compliance. Predictors of continued CPAP use include severity of sleepiness [Epworth Sleepiness Scale score (ESS>10)] as well as severity of AHI (AHI>15) and snoring. In one study, long-term use could be predicted most reliably by the average nightly use of CPAP during the first 3 months (39); patients using CPAP for less than 2hr/night at 3 months were unlikely to continue with long-term treatment. Overall CPAP use in those taking CPAP home was 68% at 5 years (39). Measures to counteract the side effects of CPAP have been found to improve compliance (40). Some of the measures include proper mask selection, humidification, nasal steroids and anticholinergic nasal sprays, use of chinstrap, pressure ramp, and, in certain instances, bilevel airway pressure. Available interfaces include nose mask, nasal pillows, full-face mask, and oral devices. The adequacy and comfort of mask fit and appropriate selection of pressure level greatly affect compliance. Compliance is greater with nose mask than with full-face mask due to greater comfort and fewer mask leaks with a nose mask despite more mouth-leak-related problems (41). Patients who complain of claustrophobia may be given oronasal mask, nasal pillows, or oral mask. When claustrophobia or other CPAP use related anxiety persists, desensitization protocols often become essential. The flow of cold air dries the nasal mucosa and may increase nasal airway resistance (although enhanced nasal flow is reported by some patients). Excessive drying of nasal mucosa has been shown to induce the release of vasoactive leukotrienes leading to increased resistance and mouth breathing which in turn leads to drying of mouth mucosa (42,43). Humidification can be in the form of cold passover humidity or heated humidity. The effect of cold or heated humidification with nasal CPAP on nasal symptoms and compliance has been studied (44,45). Compliance was improved with heated but not cold humidity. Although both types of humidity provided greater satisfaction compared to no humidity, patients were more refreshed and complained of fewer adverse effects, such as dry mouth or dry nose, with heated vs. cold humidification. There was no change in the ESS scores, however. In these studies, the predictors for the need for additional heated

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humidification with nasal CPAP include age >60 years, drying medication, symptoms of chronic mucosal disease, and previous uvulopalatopharyngoplasty. Fifty-six percent of the patients described development of disabling nasal discomfort with nasal CPAP. Heated humidification was necessary in 50% of the patients complaining of nasal discomfort after failure of cold humidification (45). Radiofrequency reduction of nasal turbinate hypertrophy may benefit nasal obstruction and hence compliance with CPAP use (46). Studies have also shown that consistent follow-up, trouble shooting, and regular feedback to patients and physicians can improve CPAP compliance rates to 85% over a period of 6 months (47). Cognitive-behavioral therapy with education regarding the consequences and efficacy of CPAP tends to improve compliance (48). Also, education with an additional phone call or printed literature about CPAP use can elicit greater compliance at 12 weeks from patients especially when applied at the start of CPAP therapy compared to no additional intervention (49).

8. TREATMENT OUTCOMES Several studies have documented that optimal CPAP implementation can normalize RDI and oxygenation. In addition, many studies have suggested that intervention with CPAP serves to ameliorate the (i) cardiovascular and (ii) neuropsychological consequences of OSAS. 8.1 Placebo Controls One of the strongest criticisms of CPAP efficacy studies has been the lack of an appropriate placebo control (2). In order to demonstrate a significant CPAP effect, one must compare with placebo. Placebo tablets and sham or placebo CPAP (at 1–3cm H2O) have been used as control. Placebo tablets are given to the subjects with the instruction that they will improve their sleep apnea syndrome (18). Sham CPAP has been described by Farre et al. (50) as a device that can be used as placebo when assessing the usefulness of CPAP in treating OSAS. To implement sham CPAP, airflow resistance of the exhalation port on the nasal mask is almost eliminated by drilling a hole, leading to decreased pressure (0.4–1cm H2O). When comparing sham CPAP with no treatment, no significant differences in sleep efficiency, arousals, and RDI were found. However, neither are perfect placebos. The compliance rates are lower with sham CPAP, whereas a placebo tablet does not produce the same absolute effect as CPAP. The subsequent paragraphs summarize the findings of placebo controlled studies. 8.2 Beneficial Effects of CPAP on the Cardiovascular System Studies have demonstrated that OSAS is associated with elevated blood pressure (BP) (4,13). A randomized double-blinded placebo controlled trial of CPAP vs. sham CPAP evaluated treatment impact on BP in 39 patients with sleep (51). Treatment was initiated following the discontinuation of antihypertensive medications and a 3-week washout

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period. Nighttime BP decreased to a greater extent in patients who received active CPAP vs. sham CPAP after 1 week of use. However, daytime mean BP also decreased significantly in both active CPAP and placebo CPAP groups, suggesting a possible placebo response or an inadequate antihypertensive washout period (51). Interestingly, Faccenda et al. (52) showed that CPAP causes normotensive patients with sleep apnea to experience small but significant decreases in 24-hour diastolic BP compared to a placebo tablet (52). Adequate therapy with nasal CPAP also may lower nocturnal systolic and diastolic BP in hypertensive patients with occult, unrecognized OSAS compared to nonapneic controls with HTN (53). In one study, 15/22 subjects who were “nondippers” (subjects failing to show the normally expected 10–20mm Hg drop in BP during the night) before treatment with CPAP became “dippers” (54). Moreover, a high heart rate and high pulse pressure at baseline may be the predictor of a beneficial effect of CPAP on BP (55). 8.3 Possible Mechanisms of BP Elevation in OSAS It has been shown that during each apnea or hypopnea, chemoreflex stimulation occurs as a result of acute hypoxia and hypercapnia, which in turn acutely increases peripheral vasoconstriction and raises BP (56). This repetitive phenomenon, occurring nightly, may lead to or contribute to HTN. Arousal from sleep may also play a role in BP elevation, but its effect may be less important in the presence of more severe levels of chemoreflex activation. Increased urine norepinephrine levels and decreased lymphocyte β2 adrenergic receptor sensitivity suggest that daytime sympathetic nervous activity is elevated in patients with RDI>15/hour (57). Other apnearelated acute cardiovascular effects have been reported which may play a role in the development of HTN. It is plausible that the elimination of sleep apnea and hypopnea with nasal CPAP and the resulting reduction in chemoreflex stimulation and arousals mediates, at least partially, the reduction of nocturnal BP with CPAP treatment. Four weeks of CPAP use also decreased sympathetic nerve activity when compared to noncompliant subjects (58). Approximately 20–40% of OSAS patients without other lung or heart disease evidence mild pulmonary hypertension (59). CPAP has been shown to improve pulmonary hemodynamics (without significant change in resting left ventricular function) at 4 months in subjects with OSAS (mean RDI 48±5/hr) (60). There was no control group in this study, however. In addition, in pharmacologically treated patients with CHF with OSAS, CPAP is a nonpharmacologic means of further reducing afterload and BP and improving left ventricular systolic function (61). One month of therapy with CPAP resulted in a 9% absolute increase and a 35% relative increase in left ventricular ejection fraction, with significant reductions in left ventricular end-systolic dimension, daytime systolic BP, and heart rate (61). CPAP therapy has also been shown to improve sleep-related respiratory stability and reduce mortality in CHF (62). There is evidence that OSA can contribute to myocardial ischemia in patients with coronary artery disease and that nasal CPAP therapy can successfully correct the sleep apnea with a resolution of the nocturnal angina and EKG ST-segment changes on the electrocardiogram (63,64). There is evidence that undertreated OSA can contribute to stroke (65,66). One of the mechanisms of increased cardiovascular events may be

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associated with in vivo platelet activation during sleep. After one night of CPAP therapy, a trend toward reduced levels of activated platelets has been reported (67). This needs to be studied further. 8.4 CPAP and Improved Neuropsychological Functioning 8.4.1 Acute Effects CPAP therapy prevents upper airway collapse, leading to improved oxygen delivery, reduced work of breathing, and fewer arousals resulting in a more restful night of sleep. Multiple case-series and prospective studies provide evidence of the benefits of CPAP therapy in restoring normal sleep architecture, cognition (68), and daytime functioning and in relieving daytime sleepiness (69). Neuropsychological test results improved in subjects receiving adequate treatment with CPAP compared to sham CPAP (70). CPAP use has been found to be correlated with improved psychosocial function as suggested by improved short form-36 (SF-36) and ESS scores as well as marital satisfaction, compared to conservative treatment at 3 months in a nonrandomized but controlled study (71). Determinants of usage were not identified, but benefits and usage were positively correlated. Similar findings of general improvement in health status have been noted with short-term (3 months) treatment and maintained with long-term (12 months) CPAP use (72). CPAP may also improve driving performance. Reduction in MVA with CPAP has been described following CPAP use (averaging 5.8 days/week for an average of 5.9hr/night) (73). CPAP treatment has also been found to improve subjective sleep quality not only of patients with OSAS but also of their bed partners (74). 8.4.2 Long-Term Effects As described earlier, long-term (12 months) treatment with CPAP has been associated with improved general health status and quality of life in OSAS (72,75). 8.4.3 Other Benefits of CPAP Treatment with CPAP has been reported to decrease frequency of nocturnal gastroesophageal reflux symptoms by 48% (76). CPAP may also decrease elevated BP in pre-eclamptic pregnant women (77).

9. CPAP VS. OTHER NONSURGICAL MODES OF THERAPY Since an average 10% of patients refuse to use CPAP altogether (78), and an estimated additional 15–30% may be partially to completely noncompliant, other nonsurgical modes of therapy may be offered to the patient.

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9.1 Positional Therapy A prospective randomized crossover study compared CPAP with positional therapy in a group of patients with positional OSA with mean AHI of 17 [±18 (SD)]. The improvement in sleep architecture, ESS scores, maintenance of wakefulness testing sleep latency, psychometric measures, mood, and quality of life measures was similar in both groups. The study did find that positional treatment was highly effective in reducing the time spent supine. However, CPAP had a greater effect on the respiratory indices with a significantly lower AHI (mean difference of 6.1/hour, 95% CI, 1–8%, p=0.007) and higher minimum oxygen saturation in the CPAP group in comparison to positional therapy (79). 9.2 Oral Appliances OAs can be useful alternatives to CPAP therapy. A randomized crossover study comparing an OA with CPAP therapy in 25 subjects revealed that both the OA and CPAP were effective in reducing symptoms of OSAS in subjects with mild to moderate disease (80). However, the OA was not as effective in reducing excessive daytime sleepiness as CPAP. Residual snoring was noted in 24% of subjects using OA vs. none in those on CPAP. Side effects were more common and subjects were less satisfied with CPAP vs. OA therapy (77). Only 55% of subjects using OA had successful treatment (AHI <10 and relief from symptoms) vs. 70% of CPAP subjects (81). Five percent of the subjects on OA failed to or were unwilling to use the appliance vs. 30% of subjects on CPAP. Although, no difference was noted in side effect, there was greater patient satisfaction with OA (81). A more recent randomized crossover study, involving 20 patients with mild to moderate OSA, showed that after 6 weeks of treatment, normalization of the respira-tory parameters was seen only with CPAP and not with the OA (82). However, patients considered the OA to be easier to use and demonstrated better compliance when compared to CPAP (82). In another study (n=48), AHI, effectiveness rating, symptoms, functional outcomes of sleepiness questionnaire, SF-36 health survey mental component, and health transition scores, all were better with CPAP vs. OA. Objective sleepiness, cognitive performance, and preference for treatments were not different (83). More research is needed to clarify the role of OA vs. CPAP in the treatment of OSA.

10. CONCLUSION In general, CPAP is considered to be the initial treatment of choice in OSAS. The current indications of CPAP may have to be revisited once the results from the longitudinal follow-up of the SHHS are made available. CPAP is safe and cost-effective (84); however, patient acceptance and compliance is less than optimal initially and compliance may decline over time. Continued improvement in technology with better mask-patient interface may help to improve compliance. Further research providing greater insights into the pathophysiology of OSAS will help in the development of more innovative modes of therapy.

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21. Hoffstein V, Mateika S. Predicting nasal continuous positive airway pressure. Am J Respir Crit Care Med 1994; 150:486. 22. Rowley JA, Aboussouan LS, Badr MS. The use of clinical prediction formulas in the evaluation of obstructive sleep apnea. Sleep 2000; 23:929–938. 23. Standards of Practice Committee of the ASDA. Practice parameters for the indication for polysomnography and related procedures. Sleep 1997; 20:402–422. 24. Oksenberg A, Silverberg DS, Arons E, Radwan H. The Sleep supine position has a major effect on optimal nasal continuous positive airway pressure: relationship with rapid eye movements and non-rapid eye movements sleep, body mass index, respiratory disturbance index, and age. Chest 1999; 116:1000–1006. 25. Criner GJ, Brennan K, Travaline JM, Kreimer D. Efficacy and Compliance with noninvasive positive pressure ventilation in patients with chronic respiratory failure. Chest 1994; 116(3):667–675. 26. Reeves-Hoche MK, Meck R, Zwillich CW. Nasal CPAP: an objective evaluation of patient compliance. Am J Respir Crit Care Med 1994; 149:149–154. 27. Sanders MH, Costantion JP, Strollo PJ Jr, Studnicki K, Atwood CW Jr. The impact of splitnight polysomnography for diagnosis and positive pressure therapy titration on treatment acceptance and adherence in sleep apnea/hypopnea. Sleep 2000; 23(1):17–24. 28. Yamashiro Y, Kryger MH. CPAP titration for sleep apnea using a split-night protocol. Chest 1995; 107:62–66. 29. McArdle N, Grove A, Devereux G, Mackay-Brown L, Mackay T, Douglas NJ. Splitnight versus full-night studies for sleep apnoea/hypopnoea syndrome. Eur Respir J 2000; 15(4):670– 675. 30. Berry RB, Parish JM, Hartse KM. The use of auto-titrating continuous positive airway pressure for treatment of adult obstructive sleep apnea. An American Academy of Sleep Medicine review. Sleep 2002; 25:148–173. 31. AASM Standards of Practice Committee. Practice parameters for the use of auto-titrating continuous positive airway pressure devices for titrating pressures and treating adult patients with obstructive sleep apnea syndrome. An American Academy of Sleep Medicine report. Sleep 2002; 25:143–147. 32. Pepin JL, Leger P, Veale D, Langevin B, Robert D, Levy P. Side effects of nasal continuous positive airway pressure in sleep apnea syndrome. Study of 193 patients in two French sleep centers. Chest 1995; 107:375–381. 33. Jarjour NN, Wilson P. Pneumocephalus associated with nasal continuous positive airway pressure in a patient with sleep apnea syndrome. Chest 1989; 96:1425–1426. 34. McEachern RC, Patel RG. Pneumopericardium associated with face-mask continuous positive airway pressure. Chest 1997; 112:1441–1443. 35. Bamford CR, Quan SF. Bacterial meningitis—a possible complication of nasal continuous positive airway pressure therapy in a patient with obstructive sleep apnea syndrome and a mucocele. Sleep 1993; 16:31–32. 36. Farre R, Montserrat JM, Ballester E, Navajas D. Potential rebreathing after continuous positive airway pressure failure during sleep. Chest 2002; 121(1):196–200. 37. McNicholas WT. Follow-up and outcomes of nasal CPAP therapy in patients with sleep apnea syndrome. Monaldi Arch Chest Dis 2001; 56(6):535–539. 38. Kribbs NB, Pack AI, Kline LR, Smith PL, Schwartz AR, Schubert NM, Redline S, Henry JN, Getsy JE, Dinges DF. Objective measurement of patterns of nasal CPAP use by patients with obstructive sleep apnea. Am Rev Respir Dis 1993; 147(4):887–895. 39. McArdle N, Devereux G, Heidarnejad H, Engleman HM, Mackay TW, Douglas NJ. Long-term use of CPAP therapy for sleep apnea/hypopnea syndrome. Am J Respir Crit Care Med 1999; 159:1108–1114. 40. Engleman HE, Martin SE, Douglas NJ. Compliance with CPAP therapy in patients with the sleep apnea/hypopnea syndrome. Thorax 1994; 49:263–266.

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41. Mortimore IL, Whittle AT, Douglas NJ. Comparison of nose and face mask CPAP therapy for sleep apnoea. Thorax 1998; 53(4):290–292. 42. Richards GN, Cistulli PA, Ungar RG, Berthon-Jones M, Sullivan CE. Mouth leaks and increased nasal resistance. Am J Respir Crit Care Med 1996; 154(1):182–186. 43. Togias AG, Naclerio RM, Peters SP, Nimmagadda I, Proud D, Kagey-Sobotka A, Adkinson NF Jr, Norman PS, Lichtenstein LM. Local generation of sulfidopeptide leukotrienes upon nasal provocation with cold, dry air. Am Rev Respir Dis 1986; 133(6):1133–1137. 44. Massie CA, Hart RW, Peralez K, Richards GN. Effects of humidification on nasal symptoms and compliance in sleep apnea patients using continuous positive airway pressure. Chest 1999; 116:403–408. 45. Rakotonanahary D, Pelletier-Fleury N, Gagnadoux F, Fleury B. Predictive factors for the need for additional humidification during nasal continuous positive airway pressure therapy. Chest 2001; 119:460–465. 46. Powell NB, Zonato AI, Weaver EM, Li K, Troell R, Riley RW, Guilleminault C. Radiofrequency treatment of turbinate hypertrophy in subjects using continuous positive airway pressure: a randomized, double-blind, placebo-controlled clinical pilot trial. Laryngoscope 2001; 111(10):1783–1790. 47. Sin DD, Mayers I, Man GC. Long-term compliance rates to continuous positive airway pressure in obstructive sleep apneas: a population based study. Chest 2002; 121(2):430–435. 48. Aloia MS, Di Dio L, Ilniczky N, Perlis ML, Greenblatt DW, Giles DE. Improving compliance with nasal CPAP and vigilance in older adults with OAHS. Sleep Breath 2001; 5(1):13–21. 49. Chervin RD, Theut S, Bassetti C, Aldrich MS. Compliance with nasal CPAP can be improved by simple interventions. Sleep 1997; 20(4):284–289. 50. Farre R, Hernandez L, Montserrat J, Rotger M, Ballester E, Navajas D. Sham continuous CPAP for placebo-controlled studies in sleep apnea. Lancet 1999; 353:1154. 51. Dimsdale JD, Loredo JS, Profant J. Hypertension 2000; 35:144–147. 52. Faccenda J, Mackay TM, Boon NA, Douglas NJ. Randomized placebo-controlled trial of continuous positive airway pressure on blood pressure in the sleep apnea-hypopnea syndrome. Am J Respir Crit Care Med 2001; 163:344–348. 53. Hla M, Skatrud JB, Finn L, Palta M, Young T. The effect of correction of sleep-disordered breathing on BP in untreated hypertension. Chest 2002; 122:1125–1132. 54. Akashiba T, Minemura H, Yamamoto H, Kosaka N, Saito O, Horie T. Nasal continuous positive airway pressure changes blood pressure ‘non-dippers’ to ‘dippers’ in patients with obstructive sleep apnea. Sleep 1999; 22:849–853. 55. Sanner BM, Tepel M, Markmann A, Zidek W. Effect of continuous positive airway pressure therapy on 24-hour blood pressure in patients with obstructive sleep apnea syndrome. Am J Hypertens 2002; 15(3):251–257. 56. Fletcher EC, Lesske J, Qian W, Miller CC III, Unger T. Repetitive episodic hypoxia causes diurnal elevation of BP in rats. Hypertension 1992; 19:555–561. 57. Ziegler MG, Mills PJ, Loredo JS, Ancoli-Israel S, Dimsdale JE. Effect of continuous positive airway pressure and placebo treatment on sympathetic nervous activity in patients with obstructive sleep apnea. Chest 2001; 120:887–893. 58. Waradekar NV, Sinoway LI, Zwillich CW, Leuenberger UA. Influence of treatment on muscle sympathetic nerve activity in sleep apnea. Am J Respir Crit Care Med 1996; 153:1333–1338. 59. Sajkov D, Cowie RJ, Thornton AT, Espinoza HA, McEvoy RD. Pulmonary hypertension and hypoxemia in obstructive sleep apnea syndrome. Am J Respir Crit Care Med 1994; 149:416– 422. 60. Sajkov D, Wang T, Saunders NA, Bune AJ, McEvoy RD. Daytime pulmonary hypertension in patients with obstructive sleep apnea: the effect of continuous positive airway pressure on pulmonary hemodynamics. Am J Respir Crit Care Med 2002; 165:152–158.

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61. Kaneko Y, Floras JS, Usui K, Plante J, Tkacova R, Kubo T, Ando S-I, Bradley TD. Cardiovascular effects of continuous positive airway pressure in patients with heart failure and obstructive sleep apnea. N Engl J Med 2002; 346:1074–1082. 62. Sin DD, Logan AG, Fitzgerald FS, Liu PP, Bradley TD. Effects of continuous positive airway pressure on cardiovascular outcomes in heart failure patients with and without Cheyne-Stokes respiration. Circulation 2000; 102(1):61–66. 63. Franklin K, Nilsson J, Sahlin C, Naslund U. Sleep apnoea and nocturnal angina. Lancet 1995; 345:1085–1087. 64. Philip P, Guilleminault C. ST segment abnormality, angina during sleep and obstructive sleep apnea. Sleep 1993; 16:558–559. 65. Partinen M, Guilleminault C. Long-term outcome for obstructive sleep apnea syndrome patients: mortality. Chest 1988; 94:1200–1204. 66. Partinen M, Guilleminault C. Daytime sleepiness and vascular morbidity at seven-year followup in obstructive sleep apnea patients. Chest 1990; 97:27–32. 67. Geiser T, Buck F, Meyer BJ, Bassetti C, Haeberli A, Gugger M. In vivo platelet activation is increased during sleep in patients with obstructive sleep apnea syndrome. Respiration 2002; 69(3):229–234. 68. Engleman HM, Martin SE, Deary IJ, Douglas NJ. Effect of continuous positive airway pressure treatment on daytime function in sleep apnea/hypopnea syndrome. Lancet 1994; 343:572–575. 69. Engleman HM, Martin SE, Deary IJ, Douglas NJ. Effect of CPAP therapy on daytime function in patients with mild sleep apnea/hypopnea syndrome. Thorax 1997; 52:114–119. 70. Jenkinson C, Davies RJ, Mullins R, Stradling JR. Comparison of therapeutic and subtherapeutic nasal continuous positive airway pressure for obstructive sleep apnea: a randomized prospective parallel trial. Lancet 1999; 353:2100–2105. 71. McFadyen TA, Espie CA, McArdle N, Douglas NJ, Engleman HM. Controlled, prospective trial of psychosocial function before and after continuous positive airway pressure therapy. Eur Respir J 2001; 18(6):996–1002. 72. Sin DD, Mayers I, Man GCW, Ghahary A, Pawluk L. Can continuous positive airway pressure therapy improve the general health status of patients with obstructive sleep apnea? A clinical effectiveness study. Chest 2002; 122:1679–1685. 73. George CF. Reduction in motor vehicle collisions following treatment of sleep apnea with nasal CPAP. Thorax 2001; 56(7):508–512. 74. McArdle N, Kingshott R, Engleman HM, Mackay TW, Douglas NJ. Partners of patients with sleep apnea/hypopnea syndrome: effect of CPAP treatment on sleep quality and quality of life. Thorax 2001; 56(7):513–518. 75. Sanner BM, Klewer J, Trumm A, Randerath W, Kreuzer I, Zidek W. Long-term treatment with continuous positive airway pressure improves quality of life in obstructive sleep apnea syndrome. Eur Respir J 2000; 16(1):118–122. 76. Kerr P, Shoenut JP, Steens RD, Millar T, Micflikier AB, Kryger MH. Nasal continuous positive airway pressure. A new treatment for nocturnal gastroesophageal reflux. Clin Gastroenterol 1993; 17(4):276–280. 77. Edwards N, Blyton DM, Kirjavainen T, Kesby GJ, Sullivan CE. Nasal continuous positive airway pressure reduces sleep-induced blood pressure increments in preeclampsia. Am J Respir Crit Care Med 2000; 162:252–257. 78. Westbrook PR. Treatment of sleep-disordered breathing: nasal CPAP. In: Issa FG, Suratt PM, Remmers JT, eds. Sleep and Respiration. New York: Wiley-Liss, 1990:387–394. 79. Jokic R, Klimaszewski A, Crossley M, Sridhar G, Fitzpatrick MF. Positional treatment versus continuous positive airway pressure in patients with positional obstructive sleep apnea syndrome. Chest 1999; 115(3):771–781. 80. Ferguson KA, Ono T, Lowe AA, Keenan SP, Fleetham JA. A randomized crossover study of an oral appliance versus nasal CPAP in the treatment of mild-moderate OSA. Chest 1996; 109:1269–1275.

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81. Ferguson KA, Ono T, Lowe AA, al-Majed S, Love LL, Fleetham JA. A short-term controlled trial of an adjustable oral appliance for the treatment of mild to moderate obstructive sleep apnoea. Thorax 1997; 52(4):362–368. 82. Randerath WJ, Heike M, Heinz R, Ruehle KH. An individually adjustable oral appliance versus continuous positive airway pressure in mild-to-moderate obstructive sleep apnea syndrome. Chest 2002; 122:569–575. 83. Engelman HM, McDonald JP, Graham D. Randomized crossover trial of two treatments for sleep apnea/hypopnea syndrome: continuous positive airway pressure and mandibular repositioning splint. Am J Respir Crit Care Med 2002; 166:855–859. 84. Douglas NJ, George CFP. Treating sleep apnea is cost effective. Thorax 2002; 57:93.

11 Nonsurgical Management: Oral Appliances James E.Eckhart Manhattan Beach, California, U.S.A. 1. SITES AND CAUSES OF SNORING AND OBSTRUCTIVE SLEEP APNEA Oral appliances are often effective in treating snoring and obstructive sleep apnea (OSA) because the sites of airway narrowing are in the pharynx immediately behind the mouth. The two most common sites of narrowing are behind the soft palate and lower, behind the tongue (Fig. 1). Major factors contributing to this narrowing include unfavorable anatomy such as a large soft palate, large tonsils, large tongue, large lingual tori (bony protuberances which crowd the tongue) (Fig. 2), or obesity. Additional physiological factors that lead to worsening include low pharyngeal muscle tone due to age, alcohol, and sleeping pills, and reduced airway patency due to sleeping on the back or sleeping with the head flexed by a large pillow. The pharyngeal airway patency can be assessed from a sagittal perspective by a lateral head film, but no radiographic method exists to quantify the coronal dimensions of the pharynx. Useful measurements from the lateral head film include the airway space behind the soft palate and behind the back edge of the tongue, the length and the thickness of the soft palate, the throat height from posterior nasal spine to the epiglottis, and the distance of the hyoid bone below the lower border of the mandible (Fig. 3) (1).

2. PATIENT EXAMINATION CRITERIA FAVORING ORAL APPLIANCES 2.1 History If patients have had a polysomnogram (PSG) and the apnea/hypopnea index (AHI) is mild (<20) to moderate (<40), they are potentially good candidates for an oral appliance, because these patients are less CPAP tolerant and more likely to be fully controlled with an oral appliance (2). If patients have refused or are intolerant of

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Figure 1 The two most common sites of airway narrowing. (From Eckhart, 2002.) CPAP, they may be candidates for an oral appliance. If patients have had an UPPP or other throat surgery and still have snoring/OSA, they may benefit from an oral appliance. If patients still snore while sleeping on their side they may improve with an oral appliance. Patients who are motivated by complaints or worries from their spouse seem to do well with oral appliances. Patients who do not do well with oral appliances include the morbidly obese and those individuals who assert they are unable to work for various reasons (3). 2.2 Questionnaire Before placing an oral appliance for snoring/OSA, a dentist/physician should question the patient sufficiently to evaluate how suspicious one should be of OSA. If a PSG has already been done, the questionnaire is less necessary, but if not, the answers to the questions might suggest a PSG be done. The standard of care suggests a PSG be done in most sleep disordered breathing, particularly if the patient answers yes to the following:

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Figure 2 Very large mandibular lingual tori. (Courtesy of John Coombs, Carson City, NV.)

Figure 3 Useful cephalometric measurements: (a) space behind soft palate; (b) space behind tongue; (c) length and thickness of soft palate; (d)

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throat height; (e) distance of hyoid from mandible. (From Eckhart, 2002.) 1. Does your bed partner say you stop breathing? 2. Do you often awake feeling un-refreshed? 3. Do you often wake with a headache? 4. Do you feel sleepy in the daytime? 5. Do you feel sleepy while driving? 6. Do you have memory loss or depression? 7. Has your job performance deteriorated? The absence of yes answers above does not rule out OSA, but somewhat reduces the likelihood. 2.3 Examination Before selecting an oral appliance for snoring/OSA, a dentist/physician should consider how heavy patients are, what neck sizes they have, whether their TMJs are free of clicking and pain and movement limitations, how complete the dentition is and what the bite is like (deep, shallow), and whether any tipped or extruded teeth would interfere with protruding the mandible. The health of the gums and cleanliness and stability of the teeth should be weighed before attaching any oral appliance. The tongue should be examined for size and ability to protrude (tongue tie). Indentations on the sides of the tongue from the teeth may mean a very large tongue (Fig. 4). The soft palate and uvula should be examined for size and battered or inflamed condition.

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Figure 4 Large tongue with indentations from teeth. (From Eckhart, 2002.) 3. TREATMENT OPTIONS OTHER THAN SURGERY OR CPAP 3.1. Position Aids Many people snore only on their back. There are cushions available with large foam cylinders worn on the back to assist people in sleeping on their sides (Fig. 5). Airway patency can be assisted by using a small pillow rather than a large one, so as not to flex the head/neck. Special pillows are available for this purpose as well.

3.2 Tongue Repositioners Tongue repositioners work by holding the jaws slightly apart and providing an opening for the tongue tip to protrude into. The soft chamber available for the tongue tip may be squeezed to form a light suction on the tongue tip, keeping the tongue forward and therefore away from the back wall of the pharynx. Furthermore, the muscle attachment of the palatoglossus muscle from the side of the tongue into the soft palate is also stretched when the tongue is protruded, and this tethering effect helps hold the soft palate away from the back wall of the pharynx too (Fig. 6). 3.2.1 Advantages Tongue repositioners are useful when there are no teeth or when the remaining teeth are too few or too weak to support mandibular advancers (MAs) [such as when there are

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severe periodontal (gum and bone) problems around the teeth]. Tongue advancers might also be used when the patient seems intolerant of stretching the TMJs due to pain or noise in the jaw joints. Tongue repositioners also are useful when a patient could not tolerate or wants to avoid the possible bite changes that can accompany MAs. Tongue repositioners are useful for people wearing orthodontic braces or dentures, where MAs could not fit or would cause sores. 3.2.2 Disadvantages Tongue repositioners have a bulb that protrudes beyond the lips, which is unsightly and the protrusion outside the lips takes getting used to. The tongue repositioners

Figure 5 Back cushions: (a) Original Silent Night Shirt™. (From Snoring and Apnea Solutions, Inc.); (b) Dr.

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Parker’s Snore Relief Cushion™. (From Innovative Sleep Products.)

Figure 6 Using the palatoglossus muscle as a tether to advance the soft palate. (From Eckhart, 2002.)

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Figure 7 Tongue stabilizing device. (From Great Lakes Orthodontics, Ltd.) are held in place by soft flanges, which fit between the lips and the alveolar process of the dental ridges, and the flanges impinge sometimes on the soft tissues, causing an arousal from sleep. They cause more drooling or pooling of saliva, which escapes the lips via the bulb and causes a feeling of wetness on the face. 3.2.3 Types of Tongue Repositioners Pre-Made. There are off-the-shelf tongue repositioners, premade and available in different sizes, which the clinician can purchase in advance or as needed. They are of fairly low cost. The tongue stabilizing device comes in four sizes. It is also available with its flanges intended to be intraoral or extraoral (Fig. 7). The Snor.X comes in two sizes (Fig. 8).

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Custom-Made. The tongue retaining device (Fig. 9) is one of the longest existing and well-documented oral appliances. Models of the teeth, along with the measurements of the tongue tip, are sent to a commercial lab for construction. It can also be made with breathing tubes if the patient cannot breathe nasally (Fig. 10). 3.3 Mandibular Advancers Mandibular advancers work by holding the lower jaw forward. Since the tongue is attached at the genial tubercles behind the chin, when the mandible moves forward

Figure 8 Snor.X. (From KD Knight.) so does the tongue. This moves the tongue away from the back wall of the throat, enlarging the lower pharyngeal airway. Also, the attachment of the palatoglossus muscle from the side of the tongue into the soft palate causes, via the tether effect, the soft palate to move forward away from the back wall of the throat, enlarging the upper pharyngeal airway too. 3.3.1 Design Variations There is an enormous diversity of designs and properties of MAs, and they are continuing to evolve. The sleep physician would be wise to work with an experienced dentist rather than attempt to manipulate oral appliances, because of the complexities and the value of dental experience.

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Methods of Retention. Mandibular advancers work best if they firmly attach to the teeth and reliably hold the lower jaw forward without allowing the muscles of the neck to pull the lower jaw down and back, out of the appliance. The methods of attaching to the teeth include clasps and firm-fitting plastic or elastomers.

Figure 9 Tongue retaining device. (From Space Maintainers Lab.)

Figure 10 Tongue retaining device with breathing tubes. (From Space Maintainers Lab.) Flexibility. The body material of the MAs may be hard plastic, soft elastomer, or thermal plastic, which slightly softens when warmed to body temperature, or a combination of a hard plastic casing with a softer thermal plastic surrounding the teeth.

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Adjustability. Some MAs are one-piece, which means that if the lower jaw advancement is to be increased, it is impossible, or it requires cutting the appliance in half and reassembling it, or it may require reheating and refitting in the mouth. For this reason, one-piece MAs are less popular. Two-piece appliances are more easily adjusted for jaw advancement. There are many mechanisms available for jaw advancement, including turnscrews, piston-and-rod assemblies, locking notches, straps, screw holes, and abutment surfaces. Vertical Opening. How much the lower jaw drops down somewhat effects the efficiency of MAs. If there is no vertical opening at all between the upper and lower incisors, the tongue is not encouraged as much to protrude way from the back wall of the throat. Even greater vertical opening also pulls the soft palate away from the back wall of the throat via the tether effect of the palatoglossus muscle. However, if there is extreme opening between the incisors, the lips cannot close and the mouth dries out and it is less comfortable to sleep. Freedom of Jaw Movement. One-piece MAs do not allow any side-to-side or forwardbackward movement of the lower jaw. For most people this is fine, but for tooth grinders it leads to appliance breakage. Tooth grinders will even break many of the two-piece MAs; the best MA for them is the elastic mandibular advancer (EMA) (Fig. 11) with its flexible elastic strips allowing generous side-to-side movement, or the Thornton adjustable positioner (TAP) (Fig. 12), with its wide range of lateral motion. Lab Construction vs. Office Construction. There are several versions of the officeconstructed MAs, some one-piece and some two-piece, which allow the dentist to take a premade appliance, heat it in water to soften an elastomeric material, and fit it directly onto the patient by inserting the warmed material and molding it to the mouth. The advantage is that there is no waiting for the lab to construct it, and the cost is less, but the disadvantage is that the retention of the elastomeric material to the teeth is not as good as with the harder plastic or with clasps, and the mandible often falls down away from the lower part of the appliance, with a return of snoring. These “boil and bite” MAs are not a reliable test of whether an MA will work for an individual. Lab-constructed MAs, although requiring models and bite registration and a longer waiting time and more cost, are superior in retention and adjustability and efficiency

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Figure 11 Elastic mandibular advancer (EMA). (From Space Maintainers Lab.) . Criteria for Selection of MAs. Experience has shown that the following are important criteria in choosing an MA, in decreasing order of importance: 1. reliably stops snoring, 2. adjustable, 3. simple delivery, 4. low bulk, 5. allows lip seal, 6. allows tongue to protrude, 7. does not disturb sleep by impinging on soft tissue, 8. does not bother the TMJ or encroach on tongue, 9. low cost, 10. allows lateral freedom.

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Figure 12 Thornton adjustable positioner (TAP). (From Space Maintainers Lab.)

Figure 13 Sleep apnea Goldilocks appliance (SAGA). (From Accutech Orthodontic Lab, Inc.) 3.3.2 Types of MAs There are dozens of MAs. In this section, only some of the reliable MAs that have achieved success in the market place are included. One-Piece MAs SAGA (Sleep Apnea Goldilocks Appliance) (Fig. 13). This is an upper and lower dualsplint, with each splint gaining retention to the teeth by the close fit of plastic, partly extending into the undercut area of the teeth. The two splints are fastened to each other

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with plastic. The relation of the splints together is determined by the wax bite made along with the impressions of the teeth. There is an anterior opening for the tongue to protrude into. Mandibular Advancer (Fig. 14). This is similar to the SAGA but is made all as one piece rather than assembled as two pieces. For retention it relies on clasps that engage the undercut areas of the back teeth. It also has a space for the tongue to protrude into. The advantages of the one-piece designs are their low bulk and lower cost. The disadvantages are their susceptibility to bite registration errors, their difficulty in changing the bite, and the absence of lateral freedom of movement for tooth grinders.

Figure 14 Mandibular advancer. (From Space Maintainers Lab.)

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Figure 15 Nocturnal oral airway dilator (NORAD). (From SullivanSchein Dental.) Two-Piece MAs The NORAD (Nocturnal Oral Airway Dilator) Appliance (Fig. 15). This is a two-piece premade appliance that consists of two splints each of which is a “boil and bite” type. A hard outer casing encloses the thermal plastic. The hard outer casings have step-like ramps and notches to position the two splints in variable degrees forward, and the twopiece assembly is held together with orthodontic elastics on the sides. The appliance comes in two different vertical openings. It is of very low cost and can be inventoried in the office. It does not provide an anterior space for the tongue to protrude into. The Silent Nite Appliance (Fig. 16). This is a two-piece lab-made appliance with each splint made of polyvinyl and held together with riveted nylon straps. The straps are replaceable with longer or shorter straps, as clinically desired. This appliance is very popular among dentists because of its low cost. It has a shorter lifetime due to its nonrobust construction. Since it has only one longer and one shorter pair of

Figure 16 Silent Nite appliance. (From Glidewell Labs.)

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Figure 17 Herbst sleep apnea appliance. (From Space Maintainers Lab.) straps, its adjustability is also limited. The nylon straps allow wide lateral movement of the jaws. This appliance does allow an anterior space for the tongue to protrude. The Herbst Sleep Apnea Appliance (Fig. 17). This consists of two lab-made splints relying on clasps for retention, positioned together with sleeve-rod assemblies that allow a wide range of adjustability. The assembly is held together with orthodontic elastics. Additional advancement is made by adding bushings onto the sleeve-rods. There is also a version of this appliance with an adjustable turn screw on the sleeve-rod instead of bushings. The Herbst is very reliable and useful in most nonedentulous cases except tooth grinders, which manage to break the attachments of the sleeve-rods due to the excessive lateral movements. The Herbst does allow an anterior space for the tongue to protrude into. The Elastic Mandibular Advancer (EMA) (Fig. 11). This is a two-piece lab-made appliance with the splints positioned with replaceable rubber straps that button onto the sides. The rubber straps come in three different lengths and three different strengths of stretchiness. Additional straps are purchasable as the straps eventually wear out. This appliance is a very good choice for tooth grinders, as the straps allow maximum lateral freedom of movement. The EMA provides an anterior space for the tongue to protrude. The company also makes a titration kit that allows variable forward movements of the lower jaw during a PSG, to reach the minimal level of snoring/OSA (Fig. 18). The Silencer (Fig. 19). This is a two-piece MA with the splints positioned via a plate in one splint with sagittally oriented screw holes, and a screw in the opposite splint which screws into one of those screw holes. The screw is mounted inside a plate that has a slot allowing the screw to slide right and left several millimeters, allowing some lateral

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freedom for tooth grinders. This appliance is a bit more expensive and requires more knowledge of jaw movements. It does not allow an anterior space for the tongue to protrude.

Figure 18 EMA titration kit. (From Space Maintainers Lab.) The Thornton Adjustable Positioner (Fig. 12). This is a two-piece lab-made appliance. Each splint can be either thermal plastic encased in a hard plastic shell or all of hard plastic. The jaw-positioning mechanism consists of a transverse bar in the lower splint behind the incisors, onto which a hook hanging vertically from the upper splint engages. The hook on the upper splint is adjustable in its anteriorposterior position by turning a knob. This allows a sleep technician to advance the lower jaw during a PSG until apneas disappear. The hook can slide right and left on the transverse bar, so there is ample lateral freedom of movement for tooth grinders. The position of the bar-hook assembly near the tip of the tongue interferes with the tongue being able to protrude between the teeth. Studies have shown, however, that because of its ability to markedly advance the lower jaw, the TAP is often very effective even in severe apneas. The knob on the front can be removed once the adequate advancement is achieved, and replaced later if more advancement is desired (Fig. 20). The knob violates lip seal.

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Figure 19 Silencer. (From Johns Dental Laboratory.)

Figure 20 Removable knob on TAP. (Courtesy Keith Thornton, Dallas, TX.) The Klearway (Fig. 21). This is a two-piece lab-made appliance with each splint made of a slightly soft plastic, and with the positioning mechanism being a turn screw mounted high in the palate vault. The Klearway has good lateral freedom of movement but has a feeling of encroachment on the top of the tongue. It has been extensively studied and there is considerable published literature on it. It does not allow an anterior space for the tongue to protrude.

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The PM Positioner (Fig. 22). This is a two-piece lab-made MA with turn screws on each side to produce jaw advancement. It is the most rigid of the two-piece MAs and allows no lateral freedom of movement and very little room for error in registering the bite. It is therefore more like an adjustable one-piece MA. It is made of thermal plastic and needs to be heated in warm water before placement in the mouth or else it will feel too tight on the teeth. It allows an anterior space for the tongue to protrude. The advantages of two-piece MAs are that, with the exception of the PM positioner, accuracy with the bite registration is not critical for the appliance to fit, they allow lateral freedom of movement for tooth grinders, they are easier than one-piece MAs to adjust forward or backward, and they have short simple delivery appointments.

Figure 21 Klearway. (From Great Lakes Orthodontics, Lt.)

Figure 22 PM positioner. (From Dental Services Group.)

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The disadvantages of the two-piece MAs are that they are somewhat bulkier due to the positioning apparatus and they cost more. There are many other MAs, one-piece and two-piece, premade and lab-made, existing in the market place. The MAs mentioned here have excellent market penetration and reliability. Combining MAs with CPAP or Oral Positive Air Pressure Sometimes patients do not tolerate the high pressures necessary for CPAP to eliminate OSA, and therefore resort to MAs, but find the MAs insufficient. For these patients, combinations of MA with CPAP at lower pressure have often been effective. The TAP has been used in combination with CPAP by modifying the TAP to support nasal hoses for CPAP (Fig. 23). Another system, CPAP Pro, can be used in combination with a variety of MAs (Fig. 24). Some patients cannot tolerate any positive air pressure nasally, either because of claustrophobia or because of nasal blockages, but have been able to tolerate OPAP, which combines an oral orthotic with an oral passageway for air into the pharynx (Fig. 25).

4. TREATMENT PROTOCOL FOR ORAL APPLIANCES 4.1. Acceptable Cases Cases that the American Sleep Disorder Association acknowledges are acceptable to be treated with oral appliances include primary snoring, mild and moderate OSA, anyone who is intolerant of CPAP, anyone who still snores after surgery to reduce snoring/OSA, adjunctive treatment along with CPAP in order to reduce the pressure required by CPAP alone, and occasional short-term substitutive therapy such as when a back packer would be unable to use CPAP in the mountains (2). 4.2. Contraindications Oral appliances are not indicated where there is a major component of central sleep apnea (nonobstructive), or when the patient is unmotivated to wear an oral

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Figure 23 Modifying the TAP to combine with CPAP. (Courtesy Keith Thornton, Dallas, TX.)

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Figure 24 CPAP Pro, a method to combine CPAP with MAs. (From Space Maintainers Lab.)

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Figure 25 OPAP, applying continuous air pressure orally. (From OPAP.com) appliance. Consideration must also be given to TMJ disorders and weak periodontal or edentulous conditions, but tongue repositioners may still help in these conditions. 4.3. Goals of Oral Appliance Therapy The goals of oral appliance therapy are to eliminate snoring or to get it to an acceptable level for the bed partner, and to eliminate daytime sleepiness and to get the RDI to under 10 or, if severe, to reduce it to less than half what it was, and to improve the oxygen saturation low point to above 90% and to reduce the number of desaturations by 50% (2). 4.4. Steps in Oral Appliance Therapy A sleep physician should refer an oral appliance candidate to a dentist experienced in oral appliance therapy. An accompanying letter of referral will help the dentist obtain medical insurance reimbursement for the patient. The dentist should obtain a history, do an examination, review the PSG, and recommend an appropriate oral appliance. The dentist advises the patient of sleep hygiene options, obtains an informed consent, and proceeds to make an appliance. At appliance delivery, the dentist adjusts the appliance, advises the patient of problems likely to require adjusting, explains how to place and remove the appliance and how to care for it, explains that it may take getting used to, and warns of common problems along with their solutions. The dentist sees the patient for periodic follow-ups to verify the comfort and efficiency of the appliance, as well as to look for

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unwanted bite changes. The patient is referred back to the sleep physician for a follow-up PSG if warranted. 4.5. Choices of Appliances Depending on the weights the dentist applies to the various factors, different appliances have different strong points. For TMJ-challenged patients and peri-odontally-at-risk or edentulous patients, or those in whom orthodontic braces are present, tongue repositioners are favored. For tooth grinders, the Silent Nite and EMA oral appliances allow the most lateral freedom of movement, followed by the TAP and the Silencer. For maximum ability to advance the lower jaw, the Herbst, the TAP, and Klearway have great potential. For simple delivery with little complications the Herbst and EMA are great. For low bulk and least impingement on soft tissues, the Norad, the MA, and SAGA are favorable. 4.6. Sleep Hygiene Instructions Overweight patients would probably improve their airway if they lost weight. A 10% weight loss has produced a 50% reduction in symptoms (3). Twenty minutes of daily exercise helps lose weight and improves the pharyngeal muscle tone, reducing the collapsibility of the airway. Avoiding alcohol after 6:00p.m. and avoiding sleeping pills helps reduce the paralysis of the pharyngeal muscles during sleep. Sleeping on the side helps avoid the tongue falling against the back wall of the throat. 4.7. Informed Consent An informed consent form for oral appliance therapy should explain the connection between snoring and OSA, suggest they see a physician if they have not already, explain how the oral appliance works, state that there is no guarantee oral appliances will work, and warn of possible intolerance of the oral appliances and possible side effects even if tolerated. 4.8. Steps Involved in Making Oral Appliances The premade tongue repositioners involve assessing the tongue size and trying in different sizes. The lab-made tongue positioner involves impressions of both jaws and a bite registration and measuring the tongue tip size. The premade MAs involve heating and cooling the thermal plastic, trying in the splint and molding it in the mouth, trimming the excess with a dental grinder outside the mouth, and polishing it. The lab-made MAs require impressions of both jaws and a bite registration. The Silencer requires additional jaw movement recordings. After construction, the lab-made

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MAs require try-in, checking tightness, proper seating, midline alignment, protrusion, TMJ comfort, balance of the bite (equal pressure on right and left sides), and soft tissue impingements. 4.9. Common Problems with Oral Appliances Sore jaw joints may mean the lower splint has been advanced too far. Sore teeth may mean the oral appliance is too tight in one area and needs to be adjusted. Dry mouth may mean the lips are apart implying either the oral appliance vertical dimension is excessive or the nasal airway is blocked, needing decongestants or nasal surgery. Bad smell or taste means that bacteria or saliva have not been removed from the oral appliance when it is removed in the morning. It can be cleaned with rinsing and

Figure 26 The bite may undergo permanent change. (From Eckhart, 2002.) scrubbed with a toothbrush, and soaked in a mouthwash or disinfectant. The bite may change (Fig. 26) and with MAs the back teeth are likely not to fit together well in the morning for a few hours. This is common. Permanent bite changes may also happen but clenching on a wafer of rubber between the incisors in the morning helps prevent this (Fig. 27) (4). If the breathing is still noisy, the nasal airway may need treatment or the MA may need more advancement. Drooling is common but usually reduces, but may be more persistent with tongue repositioners. Claustrophobia usually goes away if the patient is persistent in wearing the oral appliance.

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4.10. Follow-Ups and Retesting In the early stages, the dentist should see the patient frequently enough to ascertain the appliance is comfortable and effective at eliminating snoring. Once the snoring is

Figure 27 Clenching on an elastic wafer to correct the teeth-apart feeling after wearing an MA. (From Eckhart, 2002.) gone, a retest can be done by PSG to verify the OSA improvement. An Epworth Sleepiness Scale can also be done to verify an improvement in daytime sleepiness. Periodically, the dentist should recall the patient to establish the continued efficiency of the oral appliance, since it will change as people gain weight and change life styles. Also the dentist should look for bite changes. 4.11. Efficiency and Expected Compliance Snoring can be expected to be eliminated in 90% of selected cases using an oral appliance. OSA will be reduced around 60% with oral appliances. The oral appliance’s efficiency for OSA worsens as the original AHI worsens (5). Compliance with wearing oral appliances is higher than with CPAP, averaging around 80–90% and attenuating with time (6,7).

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REFERENCES 1. Bonham E, Currier G, Orr W, Othman J, Nanda R. The effects of a modified functional appliance on OSA. Am J Orthod Dentofac Orthop 1988; 94:384–392. 2. An American Sleep Disorders Association Report. Practice parameters for the treatment of snoring and obstructive sleep apnea with oral appliances. Sleep 1995; 18(6):511–513. 3. Lowe A. Oral devices for snoring and OSA. California Dental Association Scientific Meeting, Anaheim, 2002. 4. Abrahamsen T. Factors influencing the effect of oral appliance therapy. Academy of Dental Sleep Medicine Annual Meeting, Seattle, 2002. 5. Eveloff S, Rosenberg C, Carlisle C. Efficacy of a Herbst mandibular advancement device in obstructive sleep apnea. Am J Respir Crit Care Med 1994; 149:905–909. 6. Ferguson K, Ono T, Lowe A. A randomized cross-over study of an oral appliance vs. nasal CPAP in the treatment of mild-moderate OSA. Chest 1996; 190:1269–1275. 7. Pancer J, Al-Faifi S, Al-Faifi M, Hoffstein V. Evaluation of variable mandibular advancement appliance for treatment of snoring and sleep apnea. Chest 1999; 116(6):1511–1518.

12 Patient Selection for Surgery Samuel A.Mickelson The Atlanta Snoring & Sleep Disorders Institute, Advanced Ear, Nose & Throat Associates, Atlanta, Georgia, U.S.A. 1. INTRODUCTION In a patient with sleep disordered breathing, one of the most difficult issues is deciding who needs to be treated, when they should be treated, and what treatments are most appropriate. My treatment strategy is to first determine the patient’s concerns and complaints, exclude underlying medical conditions that may be causing or contributing to the current symptoms, assess severity of the disorder and underlying comorbidities, perform a thorough physical examination to determine sites of airway narrowing and collapse, clarify treatment objectives, and finally, select an appropriate course of therapy.

2. PATIENT CONCERNS AND COMPLAINTS It is important to listen to the patient and bed-partner in order to understand what is really bothering them and motivating them to seek evaluation for the problem. The patient may be concerned about the loudness of snoring and its effect on the bedpartner, the potential consequences of observed apnea, or the variety of nocturnal and daytime symptoms of sleep disordered breathing (Table 1). Not infrequently, the concerns of the patient or bedpartner do not coincide with the physicians concerns. This is most apparent when the patient only cares about the snoring, yet has severe sleep apnea. The patient’s concerns need to be addressed in order to achieve a satisfactory outcome for the patient. The severity of the symptoms may also help direct the type or timing of treatment. 2.1 Exclude Underlying Medical Conditions There are a variety of medical conditions that may cause or worsen sleep disordered breathing. These disorders usually manifest themselves by an increase or change in upper airway soft tissues. Such disorders include acromegaly (1), hypothyroidism (2), and upper airway masses. A sleep disordered breathing questionnaire which

Table 1 Symptoms of Sleep Disordered Breathing

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Nocturnal symptoms

Non-restorative sleep

Snoring

Excessive daytime sleepiness

Choking, gasping, awakening with fright

Personality changes

Observed apnea

Memory problems

Frequent awakenings

Reduced sexual performance

Increased motor activity

Automatic behavior, lapses

Nocturnal dyspepsia

Morning headaches

Nocturia, nocturnal enuresis

Morning dry mouth or sore throat

Heavy sweating

screens for the symptoms of acromegaly and hypothyroidism helps determine which patients may require further testing. Serum testing for these disorders is not needed in every patient. Upper airway masses are evaluated by a complete upper airway examination, a necessity for all patients presenting with sleep disordered breathing. There are a variety of other sleep disorders which may present with many of the same daytime symptoms as sleep apnea. Sleep disorders causing excessive daytime somnolence include insomnia, narcolepsy, and periodic limb movement disorder. Symptoms of these sleep disorders should be assessed with a sleep questionnaire, since they could cause the daytime symptoms or could be present in addition to sleep disordered breathing. For instance, a patient with primary snoring (but no sleep apnea) may present with daytime somnolence caused by the sleep fragmentation associated with periodic limb movement disorder. Other sleep disorders should be evaluated and treated, if present. Evaluation may require consultation with a psychiatrist, neurologist, or additional testing with a multiple sleep latency test (MSLT).

3. ASSESS THE SEVERITY OF THE DISORDER AND EVALUATE UNDERLYING CO-MORBIDITIES The presence and severity of sleep disordered breathing is determined primarily by a polysomnogram which measures sleep parameters [electroencephalography, electrooculography, and chin electromyography (EMG)], respiratory parameters (nasal/ oral airflow, chest and abdominal effort belts, pulse oximetry, snoring), cardiac parameters (electrocardiography), sleep position, leg movements (anterior tibialis EMG), and visual monitoring with video. Polysomnography not only allows determination of the presence and severity of sleep disordered breathing and its effect on sleep quality, but can also verify the presence of other sleep disorders such as restless leg syndrome, periodic limb movement disorder, insomnia, narcolepsy, sleep seizures, and a variety of parasomnias. An MSLT can be performed to objectively determine the severity of daytime somnolence. An MSLT should be performed in patients presenting with excessive

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daytime somnolence that is not explained by the severity of sleep apnea and with symptoms suggestive of narcolepsy (hypnogogic or hypnopompic hallucinations, sleep paralysis, automatic behavior, or cataplexy), or if narcolepsy is suggested on the polysomnogram [short rapid eye movement (REM) latency, short sleep latency, increased number of REM periods, and sleep fragmentation]. The MSLT is generally not performed routinely when evaluating sleep apnea.

Table 2 CMS Criteria for Treatment AHI ≥15 AHI 5–14 with any of the following: Documented symptoms of excessive daytime somnolence Impaired cognition Mood disorders or insomnia Documented hypertension Ischemic heart disease History of stroke CMS requirements for calculation of AHI include a minimum of 120min of recorded sleep. The definition of a hypopnea is ≥30% reduction of air-flow for at least 10sec with a ≥4% oxygen desaturation. Note: CMS, Centers for Medicare and Medicaid Services.

The patient’s health is very important in determining the type and aggressiveness of treatment. For example, in a patient with mild sleep disordered breathing, treatment may not be necessary in a healthy individual, yet treatment would be needed if the patient had significant underlying coronary artery disease. Co-morbidities that should be considered include those currently recognized by the Centers for Medicare and Medicaid Services (Table 2), diseases that may be exacerbated by the presence of sleep apnea (fibromyalgia, diabetes, autoimmune disorders, depression, cancer survival), and other abnormalities directly caused by the sleep apnea such as cardiac arrhythmias (brady-tachy arrhythmias, asystole, frequent Premature Ventricular Contractions (PVCs) with couplets or bigeminy, runs of ventricular tachycardia, atrial fibrillation) or nocturnal chest pain. Patients with upper airway resistance syndrome (UARS) also require treatment due to the daytime somnolence caused by this variant of sleep apnea.

4. PHYSICAL EXAMINATION: ASSESS SITES OF AIRWAY NARROWING AND COLLAPSE A thorough physical examination of the upper airway along with a fiberoptic examination or radiographic studies is required before initiating treatment. The nasal exam is needed to assess the patency of the nasal airway, as nasal patency impacts the potential use, efficacy, and compliance with nasal continuous positive airway pressure (CPAP) or

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bilevel positive airway pressure (BiPAP). An examination of the pharyngeal airway is performed to identify any abnormal masses which may be causing apnea. In addition, the pharyngeal examination helps determine the sites of airway narrowing and collapse. It is important to give the patient a reasonable expectation of the likelihood of success with surgical therapy and to identify which regions of the airway would need to be treated surgically. A thorough physical examination is recommended prior to initiation of CPAP since a localized site of airway narrowing would be more appropriately treated surgically than with lifelong therapy with CPAP. 4.1 Clarify Treatment Objectives The patient, bed-partner, and physician must agree on the goals of therapy. Many times, the patient and bed-partner focus on the snoring or daytime sleepiness only.

Table 3 Known Long-Term Adverse Effects of Sleep Disordered Breathing Hypertension Myocardial infarction Stroke Sudden death Motor vehicle crashes Loss of employment Un-insurability Marital discord

It is important for the physician to educate the patient and family of the potential current and future implications of untreated sleep disordered breathing. Indications for treatment include the presence of significant disease (snoring or apnea), significant current symptoms (Table 1), significant current morbidity (Table 2, and the co-morbidities listed earlier), or a significant risk of future morbidity (Table 3). The overall objectives of therapy should include the resolution of the signs and symptoms of sleep disordered breathing, improving the patient’s quality of life, and normalization of sleep parameters (AHI, oxyhemoglobin desaturation, and sleep fragmentation) as these polysomnographic measures of sleep disordered breathing are most likely to be associated with future morbidity. While primary snoring is not known to cause significant future morbidity, it may bother the bed-partner and cause marital discord. Primary snoring may be treated when it bothers the bed-partner. Prior to treatment of snoring, it is important to verify that snoring is really present, as a bed-partner with insomnia may be bothered by breathing noises that are otherwise insignificant. While a 10-point visual analog scale is useful to determine the changes in snoring during a research study, the Mickelson Snoring Scale (Table 4) is

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clinically more useful to determine the severity of snoring before and after treatment. Using this scale, a score of 3 or higher would warrant treatment of snoring. 4.2 Select Appropriate Treatment Surgical therapy is currently not performed as an initial therapy for moderate or severe sleep apnea but should be considered as primary therapy for primary snoring

Table 4 Mickelson Snoring Scale 5—Snoring is continuous and so loud, it can be heard despite being in a different room and using earplugs: “heroic snoring” 4—Snoring is continuous and so loud, I must go to another room or use earplugs in order to sleep: “persistent terrible snoring” 3—Snoring is frequently loud enough so that I awaken and nudge him/her so he/she will turn over and stop snoring: “persistent loud snoring” 2—Snoring occurs daily, but is a soft snore 1—Snoring is present, but does not disturb me or bother my sleep: “occasional soft snore” 0—No snoring

Table 5 Conservative Therapies for Sleep Disordered Breathing Behavior modification

Device therapy

Medication

Weight loss

CPAP, BiPAP, AutoPAP

Nasal medication

Sleep position training

Mandibular advancement appliance

Respiratory stimulants

Avoid sedatives and alcohol Improve sleep hygiene

Nasal dilators

REM reduction agents

Note: CPAP, continuous positive airway pressure; BiPAP, bilevel positive airway pressure; AutoPAP, automatic titrating positive airway pressure; REM, rapid eye movement.

and mild sleep apnea. In patients with significant nasal obstruction, isolated sites of airway narrowing, a low expectation of success with conservative therapy, or failure with, refusal of, or poor compliance with conservative therapy (Table 5), upper airway surgery should be performed as primary therapy or as an adjunct to CPAP, BiPAP, or an oral appliance. Decisions for therapy may be influenced by patient preferences, access to health care services, and the likelihood of compliance. The single most important determinant of treatment choice is severity of the disease. Severity is the most reliable predictor of success or failure with any treatment for obstructive sleep apnea. As the AHI increases, the chance of success declines with an oral appliance or any surgical procedure (except tracheostomy) and the chance of success increases with CPAP or BiPAP. Body mass index (BMI) and neck circumference are the

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next best determinants of treatment choice, since as BMI and neck size increase, it becomes more likely that airway narrowing will extend to the retrolingual or nasopharyngeal areas, and multiple surgical therapies will be required. Upper airway abnormalities are important when there are obvious masses or hypertrophic lymphoid tissues that narrow the airway. These findings dictate surgical therapy decisions for children and young adults who snore, but in severe apneic adults, isolated anatomical abnormalities are uncommon (3). Instead, disproportionate anatomy is common (4). The airway evaluation to determine the site of obstruction is important for the selection of surgical procedures for these patients (5). Identification of the sites of airway collapse substantially improves predictability of success with uvulopalatopharyngoplasty (UPPP) in patients with mild to moderate sleep apnea, but in those with obesity and severe apnea, it is less reliable (3). Surgical procedures are generally selected based on the severity of the disease and the sites of airway narrowing and collapse. This approach attempts to offer patients the most minimally invasive procedures available that have been shown to be efficacious for their problem (site-directed therapy approach). A treatment algorithm (6) is offered in Table 6, with the understanding that individual exceptions are often appropriate. 4.2.1 Primary Snoring, UARS, Mild Obstructive Sleep Apnea Syndrome Mild obstructive sleep apnea is currently defined as an apneahypopnea index (AHI) of 5– 15/hr, lowest oxygen saturation of 86–92%, and mild or no daytime somnolence. Primary snoring is defined as the presence of vibratory upper airway sounds during sleep that bother a bed-partner, but without any other respiratory distur-

Table 6 Algorithm for Management of Patients with Sleep Disordered Breathing Primary snoring, mild OSAS,

Moderate OSAS

Severe OSAS

UARS Tonsillectomy

CPAP, BiPAP, AutoPAP

CPAP, BiPAP, AutoPAP

Adenoidectomy

Nasal surgery

Nasal surgery

UPPP, tonsillectomy

UPPP, tonsillectomy

UPPP, tonsillectomy

UPP by

Genioglossus advancement

Genioglossus advancement

Cold instruments

Hyoid advancement

Hyoid advancement

Electro-cautery

Tongue suspension

Tongue suspension

Laser (LAUP)

Tongue surgical reduction

Tongue surgical reduction

Radio-frequency

Tongue RF reduction

Tongue RF reduction

Injection sclerosis

Combined surgeries

Maxillo-mandibular advancement

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Palatal implant

Oral appliance

273

Combined surgeries

Nasal surgery/medications

Tracheostomy

Oral appliance

Possible bariatric surgery

Note: OSAS, obstructive sleep apnea syndrome; UARS, upper airway resistance syndrome; CPAP, continuous positive airway pressure; BiPAP, bi-level positive airway pressure; Auto-PAP, automatic titrating positive airway pressure; UPPP, uvulopalatopharyngoplasty; UPP, uvulopalatoplasty; LAUP, laser-assisted uvulopalatoplasty. Source: Modified from Ref. 6.

bances or symptoms. UARS is defined as the presence of frequent episodes of airflow limitation (insufficient to be scored as hypopneas), which lead to arousals, sleep fragmentation, and excessive daytime somnolence. In this group of patients, a variety of anatomical problems may be at fault, either alone or in combination. The presence of daytime somnolence, nonrestorative sleep, benefit of behavioral self-help therapy, and co-morbid conditions determine whether these patients require treatment or not. CPAP may be effective for primary snoring, UARS, or mild sleep apnea caused by any of the above abnormalities. How-ever, in the absence of substantial daytime sleepiness, CPAP compliance is low (7). Anatomical abnormalities generally determine the choice of treatment: Uvula and Soft Palate. If these structures are elongated, retropositioned, thin, or webbed (and tonsils are small or absent), a uvulectomy or uvulopalatoplasty (UPP) by any of the following techniques may be beneficial [there is currently no evidence that one method is more efficacious than another (8–10), though the choice of palate procedure may be made on the basis of availability, cost, patient preference, or the amount of expected posttreatment pain]: • Cold surgical instrument resection • Electro-cautery resection (cautery-assisted palatal stiffening operation) • Laser-assisted UPP (LAUP) • Radiofrequency UPP • Injection sclerosis (injection snoreplasty) • Palatal implant of stiffening material. Tonsils and Adenoids. If these structures are significantly enlarged, their removal is recommended and is often curative, in both children and adults (11). Tonsils, Uvula, and Soft Palate. If all these compromise the airway, UPPP with tonsillectomy is recommended. Nose. If nasal obstruction or mouth breathing occurs during the day or night, and medical therapy does not improve the symptoms, nasal surgery should be considered. Surgical options include septoplasty, turbinate reduction, repair of the nasal valve, or polypectomy. Retrognathia, Micrognathia, Relative Macroglossia. If disproportionate anatomy exists in the retrolingual airway, an adjustable oral appliance (mandibular repositioning device) should be considered.

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4.2.2 Moderate Obstructive Sleep Apnea Syndrome Moderate obstructive sleep apnea is currently defined as an AHI between 15 and 30/ hr, lowest oxygen saturation of 70–85%, with moderate daytime somnolence. CPAP is generally recommended as the preferred treatment, unless surgically correctable isolated airway abnormalities are identified. Surgical procedures may be used to improve CPAP compliance or in those patients who fail or are noncompliant with CPAP therapy. Surgical procedures may be performed alone, in combination with others, or sequentially if there is concern about the length of the surgery or edema at multiple surgical sites. Nose. Nasal surgery as described above may be required to improve CPAP compliance or along with palatal or tongue base surgery as primary surgical therapy. Tonsils, Uvula, and Soft Palate. Surgical therapy for an elongated soft palate and uvula and retropalatal airway collapse usually requires UPPP with or without a tonsillectomy. UPPP may need to be combined with treatment of the retrolingual airway to achieve a successful outcome. Factors that increase the probability of a successful outcome include the presence of isolated palatal and pharyngeal abnormalities, enlarged tonsils, site of obstruction at the retropalatal and/or oropharyngeal level with absence of significant retrolingual airway collapse (3,5), no significant obesity, younger age, and lower degrees of apnea severity. LAUP has also been used for patients with mild to moderate degrees of obstructive sleep apnea. Success appears to vary with apnea severity: the higher the AHI, the lower the success of therapy (12). The efficacy of LAUP also tends to deteriorate over time. Several investigators have recommended against the use of LAUP for obstructive sleep apnea (13–16). There are currently no available outcome data on the efficacy of other minimally invasive palatal procedures in the treatment of moderate or severe sleep apnea. Retrognathia, Micrognathia, Relative Macroglossia. Retrolingual airway narrowing may be treated with a genioglossus advancement, a hyoid advancement, or a repose tongue suspension, alone or in combination with UPPP (17–19). These procedures may also be utilized for patients with isolated retrolingual narrowing or in those who have failed prior UPPP surgery. Tongue reduction procedures such as midline glossectomy or radiofrequency tongue reduction (20,21) may also be used alone or in combination with UPPP. Oral appliances may also be recommended as a nonsurgical option for these patients. An oral appliance is generally better tolerated than CPAP, but treatment success is lower than with CPAP in moderate or severe apnea patients (22). 4.2.3 Severe Obstructive Sleep Apnea Syndrome Severe obstructive sleep apnea is defined as an AHI>30, lowest oxygen saturation <70%, and severe excessive daytime somnolence. In this group of patients, CPAP is the preferred treatment. CPAP generally brings about a dramatic relief of daytime sleepiness and most of these patients use it regularly for the rest of their lives. Compliance with therapy tends to be very good in the majority of these patients. Surgical therapy is similar to that for patients with moderate obstructive sleep apnea syndrome (OSAS). However, most patients with severe sleep apnea are obese and UPPP with tonsillectomy often fails to correct the diffuse airway narrowing caused by fat

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deposition in and around the airway musculature. UPPP (with tonsillectomy) might be offered to those CPAP-intolerant patients who are not obese and have relatively isolated airway narrowing in the retropalatal and oropharyngeal region. UPPP (with tonsillectomy) in combination with nasal surgery and a combination of retro-lingual airway enlarging procedures may also be considered for patients who cannot tolerate CPAP or BiPAP in a manner similar to that described for moderate OSAS patients. In addition to the retro-lingual airway soft tissue procedures listed, mandibular and maxillary advancement is a reasonable treatment option for these patients, either alone if there are demonstrable abnormalities of the facial skeleton or following failure of the various soft tissue procedures. In patients with moderate or severe sleep apnea, studies have demonstrated efficacy that is equivalent to that of CPAP (23). Tongue reduction procedures (20,21) may also be considered in selected patients. Surgical reduction of the tongue, however, generally requires a temporary tracheostomy in the perioperative period, a possible deterrent for some patients. Morbidly obese patients may be candidates for bariatric surgery (24). Bariatric surgery has also been shown to be beneficial for sleep apnea; however, due to the long time required for weight loss, these patients should continue on their CPAP machine until a follow-up sleep study demonstrates resolution of sleep apnea. If these patients are not compliant with CPAP, then other airway enlarging procedures may be contemplated in addition to the bariatric surgery. Tracheostomy is the historical gold standard treatment with an ≈100% success rate and should be considered for patients intolerant to, noncompliant with, or unsuccessful with CPAP (25,26).

REFERENCES 1. Mickelson SA, Rosenthal LD, Rock JP, Senior BA, Friduss ME. Obstructive sleep apnea syndrome and acromegaly. Otolaryngol Head Neck Surg 1994; 111(1):25–30. 2. Mickelson SA, Lian T, Rosenthal L. Thyroid testing and thyroid hormone replacement in patients with sleep disordered breathing. Ear Nose Throat J 1999; 78(10):768–775. 3. Woodson BT. Predicting which patients will benefit from surgery for obstructive sleep apnea: the ENT exam. Ear Nose Throat J 1999; 78(10):792–800. 4. Rivlin J, Hoffstein V, Kalbfleisch J, et al. Upper airway morphology in patients with idiopathic obstructive sleep apnea. Am Rev Respir Dis 1984; 129:355–360. 5. Sher AE, Schechtman KB, Piccirillo JF. The efficacy of surgical modifications of the upper airway in adults with obstructive sleep apnea syndrome. Sleep 1996; 19:156–177. 6. Piccirillo JF, Duntley S, Schotland H. Obstructive sleep apnea. J Am Med Assoc 2000; 284:1492–1494. 7. Guilleminault C, Kim Y, Palombini L, et al. Upper airway resistance syndrome and its treatment. Sleep 2000; 23(suppl 4):5197–5200. 8. Gnuechtel MM, Keyser JS, Greinwald JH, Postma GN. Electrocautery versus carbon dioxide laser for uvulopalatoplasty in the treatment of snoring. Laryngoscope 1997; 107:848–854. 9. Blumen MB, Dahan S, Wagner I, et al. Radiofrequency versus LAUP for the treatment of snoring. Otolaryngol Head Neck Surg 2002; 126:67–73. 10. Brietzke SE, Mair EA. Injection snoreplasty: how to treat snoring without all the pain and expense. Otolaryngol Head Neck Surg 2001; 124:503–510.

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11. Verse T, Kroker BA, Pirsig W, Brosch S. Tonsillectomy as a treatment of obstructive sleep apnea in adults with tonsillar hypertrophy. Laryngoscope 2000; 110:1556–1559. 12. Mickelson SA, Ahuja A. Short-term objective and long-term subjective results of laserassisted uvulopalatoplasty for obstructive sleep apnea. Laryngoscope 1999; 109:362–367. 13. Ryan CF, Love LL. Unpredictable results of laser-assisted uvulopalatoplasty in the treatment of obstructive sleep apnea. Thorax 2000; 55:399–404. 14. Finkelstein Y, Stein G, Ophir D, et al. Laser-assisted uvulopalatoplasty for the management of obstructive sleep apnea, myths and facts. Arch Otolaryngol Head Neck Surg 2002; 128:429– 434. 15. Verse T, Pirsig W. Meta-analysis of laser-assisted uvulopalatopharyngoplasty: what is clinically relevant up to now. Laryngorhinootologie 2000; 79:273–284. 16. Littner M, Kushida CA, Hartse K, et al. Practice parameters for the use of laser-assisted uvulopalatoplasty: an update for 2000. Sleep 2001; 24:603–609. 17. Vilaseca I, Morello A, Montserrat JM, et al. Usefulness of uvulopalatopharyngoplasty with genioglossus and hyoid advancement in the treatment of obstructive sleep apnea. Arch Otolaryngol Head Neck Surg 2002; 128:435–440. 18. Riley RW, Powell NB, Li KK, Guilleminault C. Surgical therapy for obstructive sleep apneahypopnea syndrome. In: In: Kryger MH, Roth T, Dement WC, eds. Principles and Practice of Sleep Medicine. Philadelphia, PA: WB Saunders Co., 2000:913–928. 19. Woodson BT, DeRowe A, Hawke M, Wenig B, Ross EB, Katsantonis GP, Mickelson SA, Bonham RE, Bembidis S. Pharyngeal suspension suture with repose bone screw for obstructive sleep apnea. Otolaryngol Head Neck Surg 2000; 122(3):395–401. 20. Mickelson SA, Rosenthal L. Midline glossectomy and epiglottidectomy for obstructive sleep apnea syndrome. Laryngoscope 1997; 107:614–619. 21. Woodson BT, Nelson L, Mickelson SA, Huntley T, Sher A. A multi-institutional study of radiofrequency volumetric tissue reduction for OSAS. Otolaryngol Head Neck Surg 2001; 125(4):303–311. 22. Ferguson KA, Ono T, Lowe M, et al. A randomized crossover study of an oral appliance vs nasal continuous positive airway pressure in the treatment of mild-moderate obstructive sleep apnea. Chest 1996; 109:1269–1275. 23. Li K, Powell NB, Riley RW, et al. Morbidly obese patients with severe obstructive sleep apnea: is airway reconstructive surgery a viable treatment option? Laryngoscope 2000; 110:982–987. 24. Brolin RE. Gastric bypass. Surg Clin North Am 2001; 81(5):1077–1095. 25. Simmons FB. Tracheotomy in obstructive sleep apnea patients. Laryngoscope 1979; 89:1701– 1703. 26. Mickelson SA. Upper airway bypass surgery for obstructive sleep apnea syndrome. Otol Clin North Am 1998; 31(6):1013–1023.

13 Anesthesia Management for Sleep Apnea Surgery Terry Stephen Vitez San Jose, California, U.S.A. 1. INTRODUCTION Anesthetic management can be divided into two areas—patient-related problems and procedure-related problems. Patient-related problems are medical conditions that afflict the patient. These are problems that the anesthesiologist has to manage, regardless of the surgery. Procedure-related problems are problems related to the conditions required by the surgeon, and the effects that the surgery will have on the patient. An anesthetic for a procedure is divided into six phases: preinduction, induction, intubation, maintenance, emergence, and immediate recovery. In developing an anesthetic plan, the anesthesiologist must think through each of these phases, deciding what procedurerelated problems will occur, and what patient-related problems would be affected.

2. PREANESTHETIC EVALUATION 2.1 Associated Medical Problems Patients who come for sleep apnea surgeries often have medical problems related to obesity: hypertension, diabetes, gastroesophageal reflux, difficult airway, and restrictive pattern of pulmonary function. Terris et al. reported a 25% incidence of preoperative hypertension (27 of 109 patients) (1). Rarely, sleep apnea may be associated with severe hypoxemia, carbon dioxide retention, pulmonary hypertension, and cor pulmonale (2). Sleep apnea may occur in children as a result of tonsil and adenoid hypertrophy. 2.1.1 Morbid Obesity Morbidly obese patients present significant challenges to ventilation and oxygenation. Pulmonary function tests reveal significant restrictive pattern. The lower functional residual capacity (FRC) results in early airway closure and a tendency for desaturation. Spontaneous ventilation may be mostly diaphragmatic. The recumbent position exacerbates problems in ventilation by pushing the diaphragm further into the chest and impeding diaphragmatic excursion. Ventilation-perfusion mismatching can be severe. Significant desaturation can occur in the recumbent posture, even when the patient is

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awake. Ordinary anesthesia machine ventilators may not be able to deliver high enough pressures or inhalational profiles to avoid hypoxia and hypercarbia. In these instances, special ventilators (e.g., Siemens ventilator) may be required. Cardiac output, blood volume, and left ventricular work are elevated in obesity. Elevated systemic blood pressures are common. As left ventricular work increases, left ventricular hypertrophy develops. Hyperglycemia and hyperlipidemia are frequent. These metabolic and hemodynamic changes can lead to accelerated coronary artery disease and left ventricular dysfunction. In severe cases, where hypoxemia occurs, pulmonary hypertension develops. Cor pulmonale and biventricular failure can follow (3). Patients with significant cardiac sequelae may require inotropic support (e.g., dobutamine) and protection against myocardial ischemia (e.g., nitroglycerin). Beta blockade may be contraindicated in patients with severe ventricular failure. 2.1.2 Medications The history of current and past medical therapy is important to the anesthetic evaluation. Many patients with sleep apnea are treated with drugs that have implications for anesthetic management: antidepressants, drugs for weight reduction, and antihypertensives. A history of therapy with drugs for weight reduction has special implications. For example, fenfluramine, desfenfluramine, and phentermine were popular weight-reduction drugs in the early 1990s. However, they caused dysrhythmias, pulmonary hypertension, and valvular lesions, some of which were irreversible (4,5). More recently, concern has focused on herbal medications (6). St. John’s wort and ephedrine are common herbal medications that have caused concern about cardiovascular effects during anesthesia. Currently, there is little information upon which to construct rules regarding herbals. Some anesthesiologists believe that the best solution is to discontinue all herbal medications 2 weeks prior to elective surgery (7). Usually, antihypertensives are continued up to the day of surgery. However, angiotensin converting enzyme (ACE) inhibitors can cause severe hypotension following induction of anesthesia (8). The same problem may occur with angiotensin receptor blockers (9). Therefore, it might be prudent to discontinue ACE inhibitors and angiotensin receptor blockers the day prior to surgery. 2.1.3 Airway When anesthetizing patients for sleep apnea surgery, the primary question for the anesthesiologist is “Can I ventilate and oxygenate this patient?” The evaluation of the airway is designed to answer these two questions. An apnea-hypopnea index of >70 and a SPO2 <80% during sleep have been suggested as useful indicators for inability to ventilate and intubate (10). The best predictor of the ability to intubate the patient is a combination of the mouth opening, Mallampati score, assessment of neck length/mobility, neck circumference, jaw length, jaw protrusion, and protruding maxillary incisors (11– 13). If the anesthesiologist feels that the patient can be intubated, a usual induction-intubation sequence can be used. If the preoperative evaluation indicates a difficult intubation, a fiberoptic, light wand, Bullard scope, or other device must be used.

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Ventilating the sleep apnea patient is complicated by soft tissue obstruction. Adenoidal and tonsillar tissue may fill the airway. Excess adipose tissue in the airway may completely obstruct the airway when the patient is anesthetized. Thus, inspection of the oropharynx and the ENT surgeon’s physical findings will strongly influence the anesthetic management.

3. PREMEDICATION Sleep apnea patients are reported to be very sensitive to sedatives and opioids (14). Intravenous and inhalational anesthetics decrease motor tone in the muscles of the upper airway, leading to airway obstruction (15–17). Patients with sleep apnea appear to be unusually susceptible to these effects. The susceptibility to sedation leads to the practice of limiting preoperative sedation. Glycopyrrolate (0.2mg IV up to 0.8mg) is often administered as an antisialogogue, prior to induction. This helps prevent the secretions that accompany instrumentation of the airway. Some physicians administer decadron (10–12mg) in an attempt to decrease airway swelling.

4. INTRAOPERATIVE MANAGEMENT 4.1 Induction Most sleep apnea patients can be anesthetized without much deviation from normal induction techniques. The patient breathes 100% oxygen for several minutes prior to induction. During this period, the anesthesiologist instructs the patients to “Take as deep a breath as you can and blow it all out.” These vital capacity maneuvers denitrogenate the lung. The FRC is filled with oxygen, increasing the amount of time from apnea to desaturation. A rapid acting intravenous anesthetic (e.g., thiopental 3–5mg/kg, or propofol 2.5mg/kg) is administered; an attempt is made to ventilate the patient. If the patient is at risk for aspiration, cricoid pressure may be applied at the time the patient loses consciousness. Extrathoracic variable obstruction from soft tissue is common. This type of obstruction is usually managed easily by positive airway pressure. An oral airway may be needed to maintain patency. Nasal airways are more prone to cause bleeding, complicating attempts to intubate. 4.2 Intubation Succinylcholine is the agent of choice for neuromuscular blockade to facilitate intubation. The rapid onset (30–60sec) makes the airway accessible quickly. The short duration of action (3–8min) allows a quick recovery, in case intubation is impossible and fiberoptic techniques are required. A nerve stimulator is recommended to indicate the optimum time to attempt intubation (0 twitches on a train-of-four).

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Another effective method of securing the airway is to use a larygneal mask airway (LMA). An LMA can overcome the soft tissue obstruction, provide a portal for intubation, and allow suction of stomach contents. A specialized “intubating LMA” is recommended for blind intubation. Extra long, flexible endotracheal tubes are required for intubation via LMAs. If the preoperative evaluation predicts difficulty in both ventilating (with a bag and mask) and intubating the patient, then airway is secured with the patient awake. Fiberoptic intubation with the patient in the sitting position is the usual approach. The patients are pretreated with glycopyrrolate 0.4–0.8mg. The airway is anesthetized with aerosolized 4% lidocaine, cetacaine spray, or viscous lidocaine. Small amounts of sedation may be used (1mg increments of midazolam), but should not be substituted for good topical anesthesia. Opioids are avoided. Low flow (2–4L/ min) oxygen can be administered through the suction port of the fiberoptic scope. This helps oxygenate the patient, and propels secretions away from the lens. However, care must be taken that the flow rates are not high enough to force gas into the stomach or to dissect the pharyngeal mucosa. In the absence of tumor or other lesions distorting the anatomy, fiberoptic intubation is usually rapidly accomplished. It is best if the anesthesiologist and surgeon discuss and agree on the airway approach, especially the alternatives to the original plan. 4.3 Special Monitors The usual monitors used are automatic noninvasive blood pressure, oximetry, end-tidal CO2, and EKG. When mandibular osteotomy and tongue advancement is included in the operation, an arterial line is used. The arterial line allows the anesthesiologists to control the blood pressure more precisely. Arterial lines are also indicated in morbidly obese patients, even when mandibular osteotomy is not part of the procedure. In these patients, blood pressure cuffs may not read correctly, or may not even fit an extremity. In addition, the arterial line allows the anesthesiologist to monitor blood gases intra- and postoperatively. 4.4 Field Avoidance A small diameter oral endotracheal tube allows the surgeons to work around the tube. Usually, a 6mm tube suffices. Below 6mm, the resistance to airflow rises, and may restrict the ability to ventilate adequately. A reinforced (anode tube) is used to prevent kinking. The tube is secured to one side of the mouth. A plastic flex connector is attached to the endotracheal tube, and then to a rigid straight connector. This straight connector replaces the usual right angle connector in the standard circle system. In some anesthesia circuits, the port for gas analysis is incorporated into this connector. When this connector is used, the spot where the gas-analyzer tubing connects to the rigid connector is rotated toward the patient. This prevents the surgeons from leaning on and kinking the gas analyzer tubing. All connections are checked and pushed together as tightly as possible. The patient is turned 180° from the anesthesiologist. This requires extension tubes for the breathing circle, IV, and arterial lines.

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For maxillomandibular procedures, nasal intubation is required. The nares are prepared by spraying with oxymetazoline. A 6.5mm nasal RAE tube is soaked in hot water to soften the tube and well-lubricated to minimize trauma to the nasal mucosa. 4.5 Maintenance The brevity of the procedure and the need for rapid recovery of the airway dictates the use of agents with short half-lives. The usual technique is to use a volatile inhalational agent with varying concentrations of nitrous oxide. The low solubility and lack of airway irritation make sevoflurane the best alternative for mask induction. After securing the airway, desflurane’s low solubility may afford the most rapid change in anesthetic levels and most rapid emergence. The use of nitrous oxide may be limited by the necessity to use high concentrations of oxygen. Since nitrous oxide increases pulmonary vascular resistance, it is avoided in the presence of pulmonary hypertension and cor pulmonale. An alternative to an inhalational technique is total intravenous anesthesia. The short halflives of propofol and remifentanil make that combination an attractive strategy. Often, local anesthetic infiltration obviates the need for analgesics. If opioids are used, small amounts of short-acting opioids are administered. Fentanyl is the current favorite. Remifentanil is a new opioid of the fentanyl family. Remifentanil contains an ester group that allows it to be metabolized by serum cholinesterases. This metabolic degradation results in an extremely short half-life of 2min. When opioids are used, they should be given after intubation because they can cause severe rigidity. Also, if an awake intubation is required, the respiratory depression will complicate that technique. Doses of opioids and sedatives are limited, because sleep apnea patients are unusually susceptible to these drugs. Alternatives for opioids are partial agonist/antagonists (e.g., butorphanol) and nonsteroidal analgesics (e.g., ketorolac). When the surgeon infiltrates with local anesthetic, epinephrine is usually added to provide local vasoconstriction. The epinephrine can be absorbed rapidly causing tachycardia, hypertension, and dysrhythmias (PVCs, PACs). These manifestations usually disappear quickly, but may need to be treated with esmolol (10mg increments) or labetolol (5–10mg). Muscle relaxants may be required to provide adequate access to the pharynx. Intermediate acting agents are chosen. With a 35–45min duration of action, vecuronium may easily suffice for the duration of the procedure. The relaxant effect should be monitored with a nerve stimulator. The ideal level of relaxation is one to two twitches remaining on the train-of-four. Volatile inhalational agents augment the neuromuscular block and decrease the dose of the neuromuscular blocking agents. While hypertension is avoided, induced hypotension is usually not required. The exception is for mandibular osteotomy and tongue advancement. In this procedure, decreased bleeding markedly enhances surgical exposure. Nitroprusside is frequently combined with beta blockade (propanolol, esmolol, metoprolol) to control the blood pressure. Beta-blockers prevent the reflex tachycardia and increased cardiac output that complicates nitroprusside infusions. Another approach is to use labetolol, a combined alpha- and beta-blocker. Drug infusions used to control blood pressure are administered through a dedicated IV. This IV is often located in a vein in the foot or leg, so it is immediately available to the anesthesiologist.

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A mean arterial pressure of 60mmHg appears to provide good surgical conditions for mandibular osteotomy. When the patient is hypertensive, the need for lowered blood pressure must be factored against the potential damage of decreased perfusion to the brain, kidneys, and heart. The EKG can show evidence of inadequate regional myocardial perfusion. However, there are no reliable monitors to reflect the instantaneous adequacy of regional perfusion to the brain or kidneys. Some patients with hypertension have altered levels of cerebral autoregulation. In these patients, the lower limit of autoregulation may be raised from 50–60 to 80–100mm Hg mean arterial pressure. Therefore, the lower limit for blood pressure is often set between 80 and 100 MAP. When there are contraindications to the usual levels of induced hypotension, the anesthesiologists and surgeons discuss the problem and agree on limitations for induced hypotension.

Emergence The objective for emergence is to have the patient awake with adequate spontaneous ventilations as soon as possible. Many of the same concerns for induction are repeated in emergence. In addition, any continuing bleeding into the pharynx can precipitate laryngospasm. The usual technique is to insure adequate reversal of all muscle relaxants. If nitrous oxide was used, that agent is discontinued 5–10min prior to estimated end of surgery. The anesthetic is continued with volatile agent or propofol and 100% oxygen. As the volatile agent is discontinued, the patient is allowed to resume spontaneous ventilation. The bed is rotated back to its original position, with the patient’s head by the anesthesiologist. The stomach and pharynx are suctioned. Extubation is delayed until the patient opens his/her eyes to command, or spontaneously opens their eyes. At this point, the patients should be able to maintain and protect their airway. A reliable measure of adequate ventilation is the ratio of ventilatory rate to minute ventilation (in liters). If the ratio is <100, the patient should be able to maintain an adequate minute ventilation. After extubation, the adequacy of ventilation is assessed. If the airway is clear and the ventilation is adequate, the patient is transported to the PACU with supplemental oxygen. If laryngospasm occurs, positive pressure with oxygen and intravenous lidocaine (50– 100mg) will often resolve the problem. If the problem does not resolve and the intubation was easy, the patient can be reanesthetized briefly with 10–50mg of propofol. If airway obstruction continues, emergency strategies (retrograde wire, tracheostomy, Combitube, LMA) should be employed early, before desaturation occurs.

5. PACU/ICU The anesthesiologist’s primary concerns for the postoperative period center on the patency of the airway and the adequacy of ventilation/oxygenation. Potential edema, bleeding, or opioid induced airway obstruction/hypoventilation are the factors that have led to a tendency to monitor these patients in the ICU. However, newer information indicates that even “high-risk” patients need not be admitted to the ICU. In one report,

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the presence of preoperative hypertension was found to be the only correlate to the need for postoperative monitoring (1). In this series, Terris found that all complications requiring ICU care occurred within 2hr of the operation. Other more recent studies confirmed Terris’s findings (18,19). Patients without comorbidity factors, body mass index >35, and multiple surgical components were successfully managed outside the ICU. Therefore, it appears possible to eliminate ICU admissions by careful patient selection, and observing the patients in the PACU during the critical 2–3hr immediate postoperative period. Specific post-operative management is described elsewhere in this book.

6. KEY POINTS 1. The surgeon’s preoperative and the anesthesiologist’s preanesthetic evaluation identify the minority of patients who require fiberoptic or specialized intubation techniques. 2. Management can be complicated by obesity and its sequelae. 3. Pulmonary hypertension is a problem in only a very few patients. 4. Sleep apnea patients are often very susceptible to opioids and sedatives. 5. Field avoidance involves: head 180° away from the anesthesiologist, 6.0mm anode tube, rigorously secured endotracheal tube (sutured to skin) and anesthesia breathing system, extensions for IVs and breathing circuit. 6. Neuromuscular blockade is required for intraoral surgery. 7. Use induced hypotension for procedures involving mandibular osteotomy. 8. Use rapidly eliminated drugs to have patients maintaining own airway, at end case. 9. ICU admissions may be avoided by using nasal CPAP and observing the patient in the PACU for 2 hours.

REFERENCES 1. Terris DJ, Fincher EF, Hanasono M, Fee WE, Adachi K. Conservation of resources: indications for intensive care monitoring after upper airway surgery on patients with sleep apnea. Laryngoscope 1997; 107:1–6. 2. Boushra NN. Anaesthetic management of patients with sleep apnoea syndrome. Can J Anaesth 1996; 43:992–996. 3. Hamm CW, Koehler LS. The implications of morbid obesity for anesthesia. Anesthesiol Rev 1979; 6:29–35. 4. Connolly HM, Crary JL, McGoon MD, Hensrud DD, Edwards BS, Edwards WD, Schaff HV. Valvular heart disease associated with fenfluramine-phentermine. New Engl J Med 1997; 337:581–588. 5. Mark EJ, Patalas ED, Chang HT, Evans RJ, Kessler SC. Fatal pulmonary hypertension associated with short-term use of fenfluramine and phentermine. New Engl J Med 1997; 337:602–606. 6. Tsen LC, Segal S, Pothier M, Bader, A. Alternative medicine use in presurgical patients. Anesthesiology 2000; 93:148–151. 7. American Society of Anesthesiologists. What You Should Know About Your Patients’ Use of Herbal Medicines. Park Ridge, IL: American Society of Anesthesiology, www.ASAhq.org.

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8. Colson P, Ryckwaert F, Coriat P. Renin angiotensin system antagonists and anesthesia. Anesth Analg 1999; 89:1143–1155. 9. Brabant S, Eyraud D, Bertrand M, Coriat P. Refractory hypotension after induction of anesthesia in a patient chronically treated with angiotensin receptor antagonists. Anesth Analg 1999; 89:887–888. 10. Esclamado RM, Glenn MG, McCulloch TM, Cummings CW. Perioperative complications and risk factors in the surgical treatment of obstructive sleep apnea syndrome. Laryngoscope 1989; 99:1125–1129. 11. Rocke DA, Murray WB, Rout CC, Gouws E. Relative risk of factors associated with difficult intubation in obstetrical anesthesia. Anesthesiology 1993; 77:67–73. 12. Brodsky JB, Lemmens HJM, Brock-Utne JM, Vierra M, Saidman LJ. Morbid obesity and tracheal intubation. Anesth Analg 2002; 94:732–736. 13. Crosby ET, Cooper RM, Douglas MJ, Doyle, DJ, Hung OR, Labrecque P, Muir H, Murphy MF, Preston RP, Rose DK, Roy L. The unanticipated difficult airway with recommendations for management. Can J Anaesth 1996; 45:757–776. 14. Rafferty TD, Ruskis A, Saski C, Gee JB. Perioperative considerations in the management of tracheotomy for the obstructive sleep apnoea patient. Br J Anaesth 1980; 52:619–621. 15. Nanadi PR, Charlesworth CH, Taylor SJ, Nunn JF, Dove CJ. Effect of general anaesthesia on the pharynx. Br J Anaesth 1991; 66:157–162. 16. Beydon L, Lofaso F, Heyer L, Delaunay L, Goldenberg F. Nitrous oxide induces central and obstructive apneas in normal subjects. Br J Anaesth 1994; 72(suppl 1):A113. 17. Montravers P, Dureuil B, Desmonts JM. Effects of midazolam on upper airway resistance. Br J Anaesth 1992; 68:27–31. 18. Mickelson SA, Hakim I. Is postoperative intensive care monitoring necessary after uvulopalatopharyngoplasty? Otolaryngol Head Neck Surg 1998; 119:352–356. 19. Ulnick KM, Debo RF. Postoperative treatment of the patient with obstructive sleep apnea. Otolaryngol Head Neck Surg 2000; 122:233–236.

14 Nasal Surgery for Sleep Apnea Patients Richard L.Goode Department of Otolaryngology—Head and Neck Surgery, Stanford University Medical Center, Stanford, California, U.S.A. 1. INTRODUCTION Surgery to correct nasal obstruction has an important role in the treatment of sleep disordered breathing (SDB), particularly snoring and obstructive sleep apnea (OSA). Rarely will opening an obstructed nasal airway cure snoring and/or obstructive sleep apnea; however, it usually has a very positive effect on improving the quality of life in these patients and may substantially improve OSA in some (1). First and foremost, chronic nasal obstruction is an unpleasant symptom, independent of the presence of a sleep disorder. Indications for the surgical treatment of nasal obstruction are similar in patients with and without sleep disordered breathing: the presence of nasal obstruction secondary to septal deviation, chronically enlarged turbinates, or incompetent nasal valves plus failure or unacceptance of medical management, if indicated. A combination of these disorders may exist and other less common causes of obstruction may be present such as nasal polyps or other nasal and nasopharyngeal tumors. Nasal obstruction during sleep is particularly a problem in the patient with sleep disordered breathing since it leads to mouth breathing. These patients may breathe well during the day when upright, but have varying degrees of nasal obstruction when they are horizontal. Most have some complaints of daytime obstruction but are aware that it is worse at night. Confirmation of a nocturnal nasal obstruction may be difficult in cases when the daytime nasal examination is normal, but usually can be verified by the sleep partner observing an open mouth during sleep as well as symptoms of a dry mouth in the morning. A patent nasal airway must be present in order to successfully use nasal continuous positive airway pressure (CPAP) at the lowest possible pressure. This may be another reason for surgery in certain cases.

2. EVALUATION The evaluation of nasal obstruction in the sleep disordered breathing patient is the same as in any patient with this symptom. History is, of course, very important including whether the obstruction is unilateral, bilateral, or varying, seasonal or perennial, constant or intermittent, and whether it is worse at night when lying down. The effect of medications, symptoms of sinusitis and previous nasal surgery, including rhinoplasty,

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should be noted. The physical evaluation includes inspection of the turbinates and septum before and after use of a topical decongestant to perform a better examination, plus evaluate the effect of the decongestant on the turbinates and nasal breathing. Endoscopic evaluation may be necessary to make sure a nasopharyngeal tumor or other disease in the posterior nose or high in the nasal vault is not present. Examination of the internal and external nasal valves is part of the nasal evaluation. Nasal valve obstruction is invariably due to collapse of the internal valve at the junction of the upper and lower lateral cartilages (Fig. 1A). This is usually associated with aging or previous rhinoplastic surgery (Fig. 1B). Occasionally, when unilateral, it is secondary to a high deviation of the septum; rarely this can be bilateral. Inspection may reveal a pinched tip following rhinoplastic surgery producing an obvious obstruction on one or both sides due to valve collapse secondary to lower lateral cartilage removal. The diagnosis of a valve collapse is easy when the internal valve is collapsed onto the septum. More difficult is the diagnosis of weak cartilages that collapse inward at lower than normal inspiratory air pressures producing obstructive symptoms. In these cases, the Cottle test can be useful. The skin just

Figure 1 (A) The internal nasal valve. The medial boundary is the septum, the inferior boundary is the nasal floor, and the lateral boundary (arrow) is the

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caudal edge of the upper lateral cartilage. (B) Aging and rhinoplasty both can produce a separation at the junction of the upper and lower lateral cartilages leading to internal valve insufficiency. lateral to the ala is pushed upward and outward with a finger widening the nares and the effect of this maneuver on breathing is noted. Improvement or elimination of the obstruction suggests a valvular disorder. Use of a small cotton applicator placed on the upper aspect of the internal valve and pushing outward may be more specific. If this maneuver improves nasal breathing, it also supports an internal valve disorder. Short nasal bones may contribute to the collapse of the internal valve, particularly if a rhinoplasty has been previously performed. Sheen (2) found that most nasal bones extend half the distance between the radix and the angle of the septum. Those that extend 25% of that distance are considered short and predispose to valvular collapse. Drooping of the nasal tip due to age or trauma with an acute nasolabial angle can lead to valve collapse. The effect on nasal breathing of elevation of the tip with the finger can determine if this is a contributing factor.

3. THERAPEUTIC TRIALS Therapeutic trials are of two types: (a) to determine if nonsurgical treatment provides a long-term solution and (b) to help diagnose the site(s) of obstruction. Prior to surgery, an adequate trial of medical management should be performed if indicated. Usually, a topical corticosteroid, an oral sympathomimetic, and a nonsedating long acting antihistamine are prescribed. Allergic desensitization may be needed if allergies are a cause of nasal obstruction. Some patients have an excellent response to medical management, but desire surgery because of side effects from the medications, cost issues, a desire not to indefinitely use nasal medications, or some combination of these. A short therapeutic trial with a long-acting topical decongestant such as oxymetazoline (Afrin®) at night may provide important information as to the effect of turbinate shrinkage on snoring, daytime sleepiness, and the use of nasal CPAP. The sleep partner is an important part of this evaluation in order to determine if snoring is less during the Afrin® trial. Usually, a two- or three-night trial is adequate to determine the role of the turbinates in producing the nasal obstruction and snoring. The use of Breathe Right® nasal strips to open the valves as a trial may also be helpful in the diagnosis of nasal obstruction due to valvular collapse. They can have a beneficial effect in reducing snoring (3); if successful, they may be used for long-term treatment in appropriate patients. Trials with both modalities may be necessary in cases where obstruction is suspected due to both enlarged turbinates and weak valves. As part of the snoring evaluation, the sleep partner must note not only the effect of shrinkage of the turbinates on the loudness and duration of any snoring but whether the mouth is open or closed during the test period. Despite the presence of a temporarily open

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nose during sleep produced by either Afrin® or nasal valve support, the habit pattern of sleeping with an open mouth often continues. This is particularly true with loud snoring. It is difficult, though not impossible, to snore loudly with the mouth closed. Obviously, it is impossible to sleep with the mouth closed unless the nose is adequately open. In addition, an open mouth tends to cause the tongue to fall backward increasing obstruction, particularly when the patient is supine. In these patients, lying on the side usually decreases snoring and obstructive sleep apnea. Unfortunately, it is difficult to retrain individuals to sleep only in certain positions that minimize snoring. If the patient can be retrained to sleep with the mouth closed after an adequate nasal airway is obtained, this should provide improvement in snoring intensity. The use of an elastic chin support to close the mouth may aid in this regard. A careful evaluation of the oral cavity and hypopharynx is necessary as part of the physical examination, as is a careful history of the symptoms of sleep disordered breathing, particularly daytime sleepiness, hypertension, morning headaches, etc. Preoperative laboratory testing may require a coronal computed tomography (CT) of the sinuses to assess the presence of sinus disease. An overnight sleep study may already have been done in the majority of individuals with suspected sleep disordered breathing. If it has not been done, it should be carefully considered prior to surgery designed to correct the nasal obstruction. Nasal surgery is in a unique position since chronic nasal obstruction nonresponsive to medical management should be treated with surgery whether the patient has sleep apnea or not. This raises the question of whether every snorer with nasal obstruction should be evaluated with an overnight sleep test. Each case should be judged on its own merit and whether to routinely test or not will not be discussed further here; it has been discussed in a previous paper (4). An important point regarding nasal surgery in sleep apnea patients is that obstructing the nasal airway with packing may temporarily worsen the sleep apnea as well as make it difficult, if not impossible, to use nasal CPAP postoperatively (5,6). In patients with mild sleep apnea [respiratory disturbance index (RDI) 6–15 with a lowest oxygen saturation above 90%], this is usually not a major issue. However, in patients with moderate or severe sleep apnea and/or coexisting heart disease, a nasal airway placed within the packing and/or nonoccluding splints or no packing should be considered. In appropriate cases, nocturnal oxygen can be given until any packing is removed and nasal CPAP can be used again (7). Fortunately, the effects of nasal obstruction on sleep disordered breathing are usually mild; however, when surgery for nasal obstruction is combined with palatopharyngoplasty and/or tongue base surgery, the effects may be additive. This should be carefully considered in planning the postoperative care. Because of this concern, some physicians routinely recommend doing the nasal surgery first, assessing its effect, and following later with palate and/or tongue surgery so that nasal CPAP can be used in the postoperative period. Most patients, however, prefer only one surgery, if possible. While oronasal CPAP is available, it may not be as well tolerated as nasal CPAP.

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4. SITES OF OBSTRUCTION 4.1 Nasal Septum Deviations of the nasal septum, particularly in the area of the internal valve, produce nasal obstruction in many patients. The standard techniques of septoplasty have been well described and will not be repeated here. The role of septal deviations as a cause of nasal obstruction in patients who also have hypertrophic inferior turbinates may be difficult to assess. Since Afrin® affects only the turbinates, particularly the inferior turbinates, complete relief of nasal obstruction with an Afrin® trial suggests that the septum is not a major component in the obstruction, and surgery should be directed to reduction of the inferior turbinates and not the septum. Partial relief may imply a combination of factors producing the obstruction. We routinely combine conservative reduction of the anterior half of the inferior turbinates

Figure 2 High septal deflection in the valve area (a) may mimic a weak or collapsed valve on inspiration (b). with septoplasty in cases where this distinction is not clear. Furthermore, Afrin® can reduce the size of the entire inferior turbinate whereas the usual turbinate surgery is designed to decrease only the anterior one-third to one-half. In these cases when symptoms remain after turbinate reduction surgery, the septum may be suspected as the cause; however, if a postoperative Afrin® trial provides normal nasal breathing, reduction of the posterior half of the inferior turbinates should correct the nasal obstruction. In cases of minor septal deviations, particularly posterior, the role of the septum may be difficult to determine. We feel the septum should be straightened if there is any doubt as to its role in the nasal obstruction. High nasal deflections in the valve area are important to diagnose since these may present as a nasal valve problem when they are really a septal problem (Fig. 2). Postoperative packing or splinting should be minimally

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obstructive and removed as soon as possible in order to avoid aggravating SDB; we prefer magnetic splints (Fig. 3) (8).

Figure 3 Magnetic nasal splints are designed to hold the septal mucoperichondrial flaps in place after septoplasty and produce minimal nasal obstruction (8). A suture placed through the splints and septum helps prevent displacement. 4.2 Turbinates A variety of surgical techniques are available to reduce the turbinates (9). We divide turbinate reduction procedures into those that can be performed routinely in an office procedure room and those better performed in the operating room usually with septoplasty, septorhinoplasty, rhinoplasty, or endoscopic sinus surgery. Turbinate reduction surgery is regularly combined with palate and/or tongue surgery in the treatment of obstructive sleep apnea. In the clinic, we prefer the use of submucosal radiofrequency (RF) reduction of the anterior one-third to one-half of the inferior turbinate. This procedure, shown in Fig. 4, uses a needle electrode and temperature and power controlled RF energy (10–12). It can also be used in the operating room with palate and tongue surgery since it does not produce significant swelling and nasal packing is not required. This allows the use of nasal CPAP in the postoperative period, if indicated. After infiltrative anesthesia with lidocaine, the insulated monopolar needle electrode is inserted in one site in the anterior aspect of the inferior turbinate (Fig. 4). The energy setting is 500J with a desired peak temperature of 75°C. Two thermocouples in the needle

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control the tissue temperature and a grounding pad is required. If necessary, a second insertion is made, 1.5cm posterior to the first. The turbinate needle and RF generator are available from Gyrus Corporation. The technique produces minimal crusting and requires 8 weeks to produce maximum shrinkage. Treatments can be repeated if obstruction persists. The needle is short and difficult to use in the posterior half of the nose; fortunately, this is rarely required. Postoperative bleeding is extremely rare, no packing is required and any postoperative pain is usually controlled with acetaminophen. Nontemperature controlled submucosal electrocautery to the turbinates, both monopolar and bipolar, has been used for years and appears to be equally effective (13). The surgeon must be aware that the time and energy requirements are only approximate with these units. CO2 or YAG/KTP laser partial turbinate excision can also be performed in the office under local anesthesia. This technique also has the advantage of no postoperative packing and minimal postoperative bleeding. Again, the anterior one-third to

Figure 4 RF technique using a 10mm insulated needle electrode in one site in the inferior turbinate.

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Figure 5 Outfracture of the inferior turbinate. First the turbinate is infractured (a) and then outfractured (b) to open the nasal airway. one-half of the inferior turbinate is addressed at the initial treatment. This technique has a disadvantage in that it destroys the ciliated surface of the turbinate, producing crusting and slower healing. Outfracture of the inferior turbinate (Fig. 5) is regularly suggested but rarely has any long-term effect. The reason for conservatism in the initial treatment of enlarged turbinates is because of the complication of excessive dryness (rhinitis sicca) that can lead to thick mucous production, easy bleeding, and crusting. These symptoms may be quite distressing and can be difficult to treat. Atrophic rhinitis after inferior turbinate removal is rare; rhinitis sicca is more common and may exist prior to turbinate reduction. In these cases, opening the nose increases the dryness, which may be as aggravating as the obstruction. Turbinate reduction procedures performed in the operating room are of three types: (a) RF and laser turbinate reduction procedures, the same as performed in the office; (b) partial or total inferior turbinate removal (Fig. 6); and (c) submucosal tur- binoplasty (Fig. 7). We prefer (c) since the goal in inferior turbinate surgery is to remove as much of the submucosal erectile tissue as needed, yet maintain the surface mucosa intact to minimize crusting and dysfunction of the cilia. Submucosal turbinoplasty as commonly performed removes the anterior one-third to one-half of the inferior turbinate bone, although more can be removed if desired.

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Figure 6 Scissor excision of the free edge of the inferior turbinate. Initially, we use the more conservative excision as shown by the angled dotted line.

Figure 7 Submucosal turbinoplasty. Using an anterior-inferior incision, the anterior half of the inferior turbinate bone is removed with bone biting forceps.

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A modification described by Mabry (14) and shown in Fig. 8 is our preferred technique. The mucosa remains intact on the medial surface and nasal packing is required only for a few days. Tubing may be used within the packing for breathing but has the problem of frequently becoming occluded with mucous. Inferior turbinate reduction with a specialized submucosal microdebrider appears promising (15). While a submucosal turbinoplasty can be performed in a well-equipped office procedure room, we prefer to combine it with septoplasty in the operating room under general anesthesia, usually when both septum and turbinate surgery are indi-

Figure 8 Modification of the submucosal turbinoplasty where the lateral turbinate tissue is resected with the turbinate bone (a). The medial flap is then rotated laterally to meet the resected lateral flap of tissue (b). cated. These procedures allow removal of a known amount of turbinate tissue, an advantage over RF reduction. 4.3. Nasal Valve Many procedures have been described for the treatment of nasal valve insufficiency (16,17). Any time a large number of surgical procedures are described to correct a problem, the implication is that no one procedure has been found ideal. While this may be true, it is our feeling that the best single procedure to correct the problem is a cartilage batten graft placed in the area of the internal valve (Fig. 9).

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The batten lies parallel to the valve extending from the nasofacial groove laterally to the septum medially. The batten is placed internally via a cartilage-splitting incision (Fig. 10). Septal cartilage is an excellent implant, if available, while conchal cartilage is also good (18). We prefer irradiated costal cartilage since it is stiffer than conchal cartilage and does not require an ear dissection. Perforated polyethylene (Medpore)® alloplastic valve implants are available for this purpose (19), however, experience over the years with alloplastic implants in the nose has demonstrated that long-term results are often poor due to extrusion of the implant. Irradiated cartilage is an exception. It does not require donor site surgery but must be carved into the proper shape. The function is similar to placing a batten in a sail; it stiffens the valve area and prevents collapse. A potential disadvantage is that the implants can widen the nose in the valve area. Excessive widening will not be well tolerated despite a beneficial effect on nasal breathing. Valve implants may be combined with septal and turbinate surgery to decrease nasal resistance and, therefore, decrease the negative pressure required to produce adequate nasal airflow. Spreader grafts were described initially by Sheen (2) to treat nasal valve collapse (Fig. 11). The grafts were placed using an endonasal approach, whereas, now they are more commonly placed via an external rhinoplasty approach. They also widen the

Figure 9 Batten graft, placed at the junction of the upper and lower lateral nasal cartilages to stiffen the valve and prevent collapse. The graft is ideally placed parallel and medial to the valve cartilages, but it is usually easier to place it laterally. If the nose appears too wide after placement of the grafts,

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the remnant cartilage at the site of the grafts should be removed. The dotted line shows the incision.

Figure 10 Cartilage splitting approach to batten placement. The incision site is shown by the dotted line (a). A pocket is made in the valve area with fine blunt scissors. The pocket extends from the dorsum of the septum to the nasofacial groove. The carved graft is inserted (b and c) and the incision closed with 46 chromic sutures. Packing is placed in each nostril for 5

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days to support the grafts during healing.

Figure 11 Spreader grafts of septal or irradiated cartilage are inserted high in the nasal vault under the upper lateral cartilages beneath the septal mucoperichondrium (2). The grafts are usually 2mm thick, 2mm wide, and 15mm long. When in place they move the upper lateral cartilages outward, opening the valves.

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Figure 12 (a and b) Placement of cartilage grafts just inside the alar rim rather than in the internal valve area as described by Troell et al. (20). mid-nose pushing the upper lateral cartilages outward. Care must be taken that the implants do not slip anteriorly or inferiorly or they may be ineffective or contribute to nasal obstruction, similar to a deviated dorsal septum. The procedure can be combined with batten grafts in the valve. Troell et al. (20) described placement of irradiated cartilage grafts at the external valves (Fig. 12) and compared this with placement at the internal valves. They found the former procedure easier to perform and the results better (94.8% improved or free of obstruction vs. 85% with internal valve placement). Whether the widening is greater or less is not defined; both procedures do widen the nose. Battens in other positions in the lower nose have been described which

Figure 13 (a and b) Conchal cartilage placed over the dorsum of the septum in the area of the internal valves can widen the valve area and the nose. It can be placed by either an open or endonasal approach. The septum must be lowered below the graft site in order to avoid a post-operative “polly-beak” deformity.

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may have a lesser effect on widening but their mechanism of support is not clear. Sutures have been described to pull the upper lateral cartilages outward (21) or bow them in order to increase the airway (22). We have no experience with these techniques. M-plasty to widen the nasal valve area is recommended by some surgeons (23). A conchal cartilage graft placed over the septum in the area of the valve can provide valve support, correcting valve collapse (Fig. 13) (9,18). The dorsal septum must be lowered in the area of the graft to avoid a “polly-beak” deformity. The subjective benefits reported by patients after nasal surgery on the quality of sleep may be greater than the improvement seen on polysomnogram testing and occasionally vice versa. The reasons for this are not clear but subjective improvement should not be discounted. Surgery for nasal obstruction should be considered a regular part of surgery to improve the symptoms of sleep disordered breathing.

REFERENCES 1. Hoiuer V, Ejnell H, Hedner J, et al. The effects of nasal dilation on snoring and obstructive sleep apnea. Arch Otolaryngol Head Neck Surg 1992; 118:281–284. 2. Sheen JH. Spreader graft: a method of reconstructing the roof of the middle nasal vault following rhinoplasty. Plast Reconstr Surg 1984; 73:230–239. 3. Ulfberg J, Fenton G. Effect of Breathe Right® nasal strip on snoring. Rhinology 1997; 35:50–52. 4. Goode RL. Who needs a sleep test? The value of the history in the diagnosis of obstructive sleep apnea. Ear Nose Throat J 1999; 78:710–715. 5. Suratt PN, Turner BL, Wilhoit SC. Effect of intranasal obstruction on breathing during sleep. Chest 1986; 90:324–329. 6. Olsen KD, Kern EB, Westbrook PR. Sleep and breathing disturbance secondary to nasal obstruction. Otolaryngol Head Neck Surg 1981; 2:183–188. 7. Fletcher EC, Munafo DA. Role of nocturnal oxygen therapy in obstructive sleep apnea. When should it be used? Chest 1990; 98:1497–1504. 8. Goode RL. Magnetic internasal splints. Arch Otolaryngol 1982; 108:319. 9. Goode RL, Pribitkin E. Diagnosis and Treatment of Turbinate Dysfunction. Alexandria, VA: American Academy of Otolaryngology—Head and Neck Surgery Foundation, 1995. 10. Smith TL, Smith JM. Radiofrequency electrosurgery. Oper Tech Otolaryngol Head Neck Surg 2000; 11:66–70. 11. Li KK, Powell NB, Riley RW, et al: Radiofrequency volumetric reduction for hypertrophic turbinates. Oper Tech Otolaryngol Head Neck Surg 2000; 11:24–25. 12. Utley DS, Goode RL, Hakim I. Radiofrequency energy tissue ablation for the treatment of nasal obstruction secondary to turbinate hypertrophy. Laryngoscope 1999; 109: 683–686. 13. Shahinian L. Chronic vasomotor rhinitis. Arch Otolaryngol 1953; 57:475–489. 14. Mabry RL. Inferior turbinoplasty. Oper Tech Otolaryngol Head Neck Surg 1981; 2: 183–188. 15. Friedman M, Tanperi H, Lim J, et al. A safe, alternative technique for inferior turbinate reduction. Laryngoscope 1999; 109:1834–1837. 16. Goode RL. Surgery of the incompetent nasal valve. Laryngoscope 1985; 95:38–41. 17. Kern EB, Wang TD. Nasal valve surgery. In: Daniel EK, ed. Rhinoplasty. Boston, MA: Little, Brown and Company, 1993:613–630. 18. Stucker FJ, Hoasjoe DK. Nasal reconstruction with conchal cartilage: correcting valve and lateral nasal collapse. Arch Otolaryngol Head Neck Surg 1994; 120:653–658. 19. Romo T, Sclafani AP, Sabini P. Use of porous high-density polyethylene in revision rhinoplasty and in the platyrhine nose. Aesthetic Plast Surg 1998; 22:211–221.

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20. Troell RJ, Powell NB, Riley RW, et al. Evaluation of a new procedure for nasal alar rim and valve collapse: nasal alar rim reconstruction. Otolaryngol Head Neck Surg 2000; 122:204–211. 21. Paniello RC. Nasal valve suspension. Arch Otolaryngol Head Neck Surg 1996; 122: 1342– 1346. 22. Park SS. The flaring suture to augment the repair of the dysfunctional nasal valve. Plast Reconstr Surg 1998; 101:1120–1122. 23. Schulte DL, Sherris DA, Kern EB. M-plasty correction of nasal valve obstruction. Facial Plast Surg Clin North Am 1999; 7:405–09.

15 Uvulopalatopharyngoplasty Richard L.Goode Department of Otolaryngology—Head and Neck Surgery, Stanford University Medical Center, Stanford, California, U.S.A. 1. BACKGROUND Uvulopalatopharyngoplasty (UPPP) has been the most commonly used surgical procedure for the treatment of obstructive sleep apnea (OSA) and related snoring since its introduction by Fujita et al. (1) in 1981. It also has the distinction of being one of the longest names for a surgical procedure. Unfortunately, because of limitations in our ability to clinically diagnose the site(s) of obstruction in a given case of OSA, its success has been sub-optimal with regard to significant improvement in the apnea index (AI) or respiratory distress index (RDI). This is because this procedure was designed to open the airway at the level of the soft palate and retropalatal oropharynx; we now know that in the majority of cases the obstruction is also at the level of the base of the tongue and retrolingual hypopharynx. Fujita (2) later introduced a staging system to clarify the role of UPPP: type I—collapse during sleep occurs at the retropalatal level; type II—collapse at both the retropalatal and retrolingual areas; and type III—collapse at only the retrolingual area. The UPPP would be expected to be successful in most type I cases and in a certain percentage of type II cases and unsuccessful in type III cases. Since the majority of OSA cases are thought to be type II (60%) with about 20% each in types I and III, a success rate of around 50% would be expected, assuming that half of the type II cases have obstruction predominantly at the retropalatal level. Using Fujita’s original liberal criteria for surgical success of a 50% reduction in RDI, Sher et al. (3) found in a meta-analysis that the response rate was 53%. Using the stricter criteria of a 50% decrease in AI or RDI, plus a reduction of AI to <10 or the RDI to <20, the overall response rate for UPPP was 41%. If the cases were broken down by type, type I had a 52% response rate while types II and III had only a 5% response rate. This decreased over time following the procedure, thought primarily due to weight gain. Correction of snoring, felt to be usually due to vibration of the soft palate, would be expected to have a higher success rate. This has turned out to be the case; the UPPP appears to be a good procedure to decrease or eliminate loud snoring with success in ≈84% or greater of cases (4). Obviously, the stricter the criteria, the lower the successful result percentage will be. Furthermore, the subjective effect following surgery is very important. The operation should not be considered a success based on a significant drop in the RDI if the patient has no change in daytime sleepiness. The lowest O2 saturation must also be considered; a reasonable goal would be >85%. Ideally, the operation should provide results similar to

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nasal continuous positive airway pressure (CPAP) and should be maintained over time. As previously mentioned, a major problem in evaluating the effectiveness of the UPPP operation is our inability to accurately define the site(s) of obstruction in many OSA cases. An examination while awake in the office is no substitute for an assessment of the possible obstructive site(s) when the patient is asleep. The UPPP is not a perfect operation even in those type I candidates where the obstruction is thought to be solely at the soft palate level. Studies using multilevel pressure transducer measurements in patients following UPPP have demonstrated persistent obstruction at the retropalatal level, despite what was thought to be an adequate soft palate resection and oropharynx tightening (5,6). Surgeons vary in the amount of palate they resect based, in part, on concerns over creating long-term post-operative velopharyngeal insufficiency (VPI) with speech and swallowing problems. Variations in UPPP technique have been described by several authors and some appear to produce better results than others. It is difficult to compare different techniques because of differences in patient mix; prospective, randomized trials comparing techniques are needed, such as those performed by Thomas et al. (7) for tongue-base surgery. The role of the tonsils in retropalatal obstruction appears important and this is particularly true in cases of OSA in children with large tonsils and obstructing adenoids. A UPPP should not be performed as the initial procedure in children since a tonsillectomy and adenoidectomy is commonly successful. In adults with OSA, if large tonsils are present, their removal in combination with a UPPP provides better results than if the tonsils are absent or small (8). Large tonsils are thought to contribute to the obstruction and their removal further opens the airway at the retropalatel level. The role of each part of the UPPP is not understood, particularly the pharyngoplasty component. Does it add much in a given case? Other surgical procedures that shorten and/or tighten only the soft palate appear to produce similar results for OSA and loud snoring, implying that there is little or no value in tightening the oropharyngeal folds. The pharynx may look smoother but does the tightening have any value? We do not know at this time, but I suspect not.

2. PRE-OPERATIVE EVALUATION Using the methods described in Chapter 8, an effort is made to define the site(s) of obstruction. If the palate is thought to be a major contributor, then UPPP, with or without tonsillectomy, should be considered. It must be remembered that the results achieved with a UPPP are not dependent on the pre-operative RDI value; mild to moderate cases have the same likelihood of success as severe cases. Unfortunately, in the milder cases it is more likely that the OSA may become worse (8); understanding why some patients get worse after UPPP would be helpful in improving our surgical technique. Friedman et al. (9) have recently reported on a new simple clinical staging system based on body mass index, tonsil size, and soft palate position that provides additional help in patient selection for a UPPP. Their OSA patients were divided into three stages. Those falling in stage I had an 80% success rate with UPPP, much better than the 41% rate reported by Sher et al. (3); stage II achieved 38% success while stage III dropped to 8%.

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The pre-operative velopharyngeal distance is a factor in deciding how much soft palate to remove. The soft palate “dimple,” located just behind the levator palati muscle and seen when the palate elevates, is a useful landmark in this decision. It is identified preoperatively, because soft palate excision usually begins just posterior to this point, unless the velopharynx distance is longer than usual. In that case, less soft palate should be removed. Assessment of soft palate movement during speech (saying the letter “k”) is also necessary before surgery; occasionally there is bilateral or unilateral limitation of palatal movement secondary to neurologic disease, submucus cleft, or previous tonsillectomy or palate surgery. This may be a contraindication to a UPPP or limit the amount of palate resection. The combination of UPPP with procedures to open the nasal airway is regularly performed in an effort to correct nasal and retropalatal obstruction in one session. In many instances, UPPP is combined with procedures to open the retrolingual airway as well. The goal is to address all likely sites of obstruction with a minimal number of visits to the operating room. This makes good sense but should be tempered by the expected increase in postoperative complications as well as concern about temporarily making the airway worse during sleep in the postoperative period (10). In addition, nasal surgery to correct nasal obstruction may prevent the use of nasal CPAP in the postoperative period. In cases of moderate to severe OSA, particularly with significantly depressed O2 saturation levels, this may be an important safety consideration. This assumes, of course, that the patient can use CPAP. In such cases, performing the nasal surgery as a separate first procedure may be the best course, followed by procedures to correct any retrolingual or retropalatal obstruction. Each case must be evaluated on its own merit; this is discussed further in Chapters 34 and 35. Risks of the operation are discussed with the patient in detail. Ideally, this should be in writing and a copy given to the patient. Post-operative bleeding is uncommon, similar to tonsillectomy. Infection may occur but is also uncommon except for the expected lowgrade cellulitis in the tonsillar fossae produced by the mouth anaerobic bacteria. The risk of long term VPI needs to be mentioned as does the possible inability to produce a palatal “trill” during speech. This is not a problem in English but may be for some foreign languages, particularly French. Management of the postoperative airway during sleep is discussed as well as the potential risks of narcotic medications in the treatment of post-operative pain. If the patient can use CPAP in the post-operative period, this is strongly encouraged, particularly in the more severe cases. Otherwise, home O2 may be prescribed. Aspirin products, NSAIDs, and vitamin E are stopped 2 weeks prior to surgery; hypertension and any other existing comorbidity (heart disease, diabetes, etc.) must be under good medical control by the patient’s family physician prior to surgery.

3. METHOD The procedure is usually performed in the operating room under general anesthesia with an oral endotracheal tube. Tonsillectomy is considered part of the UPPP if it has not been previously performed. As previously mentioned, removal of large tonsils, defined as kissing or near kissing, improves the final postsurgical result. Removal of small tonsils

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appears to make no difference and only adds to the postoperative pain. The goal of the UPPP is to open the retropalatal area and the oropharynx the greatest amount possible without producing post-operative VPI, resulting in nasal reflux and/or hypernasal speech. Stiffening of the remaining soft palate may be an additional benefit, particularly in decreasing snoring. The UPPP consists of two separate procedures: (a) shortening the free edge of the soft palate (uvulopalatoplasty) and (b) tightening the oropharynx by pulling the posterior tonsillar pillars forward and sewing them to the anterior tonsillar pillars (pharyngoplasty). A balance between the two procedures is necessary since the pull of the former procedure is at right angles to that of the latter. This can result in a postoperative omega-shaped velopharyngeal opening which, in my experience, is often associated with a poor result. A complete tonsillectomy is recommended as part of the UPPP if tonsils are present; this improves the final result when the tonsils are large, but as previously stated, there is essentially no evidence to advocate performing a complete tonsillectomy if the tonsils are small. In our technique, large tonsils are completely removed using needle point electrocautery; small tonsils only need the upper one-third or less removed in order to perform an adequate upper pharyngoplasty and, more important, to produce a rectangular opening after uvulopalatoplasty. Partial tonsillectomy should produce less postoperative pain and a shorter healing time. If a previous tonsillectomy has been performed, the mucosa in only the upper one-third of the tonsillar fossa is removed between the anterior and posterior pillars prior to suturing them together. The tonsillectomy, if indicated, is performed first (Figs. 1 and 2). The UPPP is then performed. Our technique is similar to that described by Friedman et al. (11). A flap of palate mucosa on the nasal side of the soft palate is first elevated (Figs. 3 and 4). The incisions are made with needle point electrocautery. Back cuts are then performed through the superior aspect of the posterior and anterior tonsillar pillars where they reach the free edge of the soft palate. The back cuts are around 1.0cm in depth, occasionally deeper. This allows the anterior advancement of the soft palate flap to be separated from the lateral pull produced by sewing the upper aspect of the posterior pillar to the anterior pillar. An appropriate amount of soft palate is then resected using an incision that extends to the back cuts on each side (Figs. 5 and 6A). The mucosal flap is advanced over the resected border of the palate so that the suture line is not at the free edge but 5–10mm anteriorly (Fig. 6B).

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Figure 1 View of the oropharynx showing mildly enlarged tonsils and mucosal folds in the posterior pharyngeal wall. (From Ref. 11.)

Figure 2 The upper aspect of the tonsil is pulled medially with a clamp or

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forceps and excised using needle point coagulation. If the tonsils are small, only the upper one-third or less is removed, otherwise all of the tonsil is removed. (From Ref. 11.)

Figure 3 The uvula is grasped and pulled anteriorly so that the curved incision is made on the posterior undersurface of the uvula, developing a mucosal flap. (From Ref. 11.)

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Figure 4 The dissection of the mucosal flap on the posterior aspect of the uvula is shown from the side. (From Ref. 11.)

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Figure 5 Back cuts are made with the needlepoint cautery to separate the horizontal free edge of the soft palate from the vertically directed anterior and posterior pillars. The uvula and free edge of the soft palate are resected using a curved incision, shown by the dotted line, that extends just to the end of the back cuts.

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Figure 6 (A) Soft palate and uvula resection seen from the side. (B) Closure of the mucosal flap over the free edge of the resected palate using interrupted polyglactin 910 sutures. (From Ref. 11.) The key to producing a wide, rectangular velopharyngeal opening is to advance the superior edge of the posterior pillar, just below the back cut, forward and upward to meet the anterior pillar at its cut superior aspect (Fig. 7). The medial edge of the anterior pillars may need to be trimmed a small amount, depending on the width of the upper tonsillar fossa, so that the closure is snug but not under excessive tension. Interrupted 3–0 polyglactin 910 (Vicryl®) sutures on an atraumatic needle are used for the closure of the soft palate and fixing the posterior pillar to the anterior pillar (Fig. 8). Care must be taken to eliminate any dead space under this latter closure by including the middle constrictor muscle in the closure or using a two-layer closure.

Figure 7 The posterior pillar is pulled slightly upward and laterally and sewn to the anterior pillar using a twolayered closure of muscle and mucosa, or a single-layer closure incorporating both muscle and mucosa. This is to eliminate any dead space plus decrease tension on the mucosal suture line.

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Arrows show the direction of the soft palate and tonsillar pillar closure(s).

Figure 8 After the posterior pillar is sutured to the anterior pillar, the soft palate mucosal flap is pulled forward and sewn to the anterior cut edge, as shown by the arrow. The back cut must be deep enough so that the pillar closure is vertical. The left side shows the usual closure of only the upper one-third of the tonsillar fossa. The presence of a dead space will invariably lead to dehiscence as does too tight a closure. An advantage of the cautery technique is the absence of bleeding; however, with this technique there is an increased incidence of post-operative dehiscence compared with a cold knife technique. The final result should appear as in Fig. 9, producing a wide rectangular opening. The operation is regularly combined with nasal and/or tongue advancement surgery. An effort is made to minimize the total time the mouth gag is in place during

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Figure 9 At completion of surgery, the velo-pharyngeal opening should appear rectangular and not excessively oval, with the pillar closure vertical and the soft palate closure horizontal. Any dead space in the upper tonsillar fossa must be eliminated. The lower tonsillar fossa may be left open if a total tonsillectomy is performed. The arrows show the sites of the back cuts. the procedure since it may produce tongue edema, an undesirable condition. The palate and pharyngeal incisions are injected with 0.5% Marcaine® at the termination of the procedure to diminish post-operative pain. Usually, an antibiotic and corticosteroid are prescribed to decrease pain and swelling, similar to what is used for routine tonsillectomy. In children, only a tonsillectomy and adenoidectomy are performed in suspected sleep apnea cases. A UPPP is not performed until the effects of those procedures have been evaluated.

4. POST-OPERATIVE CARE Patients with milder OSA (RDI <40, lowest O2 saturation greater than 85%) are usually taken care of after surgery on the ward; a pulse oximeter is required. Patients with more severe sleep apnea or cardiac disease may be placed in an intensive care unit in order to

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provide better monitoring in the immediate post-operative period. Each case is evaluated on its own merits but routine placement of all patients in the ICU is not done (12). Our patients are nearly always kept in the hospital at least one night to assess pain, ability to eat, and ability to take oral medications as well as to monitor them overnight with a pulse oximeter. For more severe cases we recommend the use of nasal CPAP following surgery and advise that they bring their machine in with them. If they do not have a machine, a loaner can be provided. If they cannot or will not use CPAP, we evaluate them on room air during sleep using the pulse oximeter the night after surgery to ascertain whether they need supplemental oxygen to maintain O2 saturation above 85%. Pain is controlled with a patient controlled analgesia pump using morphine; sleeping medication is not prescribed. Pain medication is started at a low dose and gradually increased as needed to provide a compromise between adequate pain control and a reasonable lowest O2 saturation (>85%) during sleep. Usually, patients are discharged on the first or second postoperative day if only a UPPP was performed. If other procedures were performed, particularly tongue procedures, the patient may stay for a longer duration, usually because of difficulty in eating or for adequate pain control. Patients are advised to use their CPAP at home in the post-operative period; however, many of these patients do not have CPAP machines or cannot use them. Patients that drop their lowest oxygen saturation to below 85% on room air in the hospital are given supplemental oxygen to use during sleep at home, unless there are contraindications such as lung disease with a chronically elevated pCO2.(13) The effect of supplemental oxygen is evaluated during sleep in the hospital prior to discharge. The first postoperative evaluation is usually done at 1 week with a second evaluation 2–3 weeks later. Weight is measured and compared with the pre-operative weight. A loss of 5–10lb is common. A post-operative polysomnogram is usually performed 3 months after the surgery. This may vary depending on the symptoms of the patient and any delays in healing which may occur. In summary, the UPPP with a conservative pharyngoplasty provides good relief of OSA due to obstruction predominantly at the retropalate area. Removal of large tonsils increases the success rate. Snoring is regularly improved and postoperative complications are low.

ACKNOWLEDGMENTS The author wishes to thank Elsevier Publishing and Dr. Michael Friedman for permission to use figures from Ref. (11).

REFERENCES 1. Fujita S, Conway W, Zorick, et al. Surgical correction of anatomical abnormalities in obstructive sleep apnea syndrome: uvulopalatopharyngoplasty. Otolaryngol Head Neck Surg 1981; 89:923– 934.

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2. Fujita S. Midline laser glossectomy with lingualplasty: a treatment of sleep apnea syndrome. Oper Tech Otolaryngol Head Neck Surg 1991; 2:127–131. 3. Sher AE, Schechtman KB, Piccirillo JF. The efficacy of surgical modifications of the upper airway in adults with obstructive sleep apnea syndrome. Sleep 1996; 19(2):156–177. 4. Friberg D, Carlsson-Nordlander B, Larsson H, et al. UPPP for habitual snoring: a 5-year follow up with respiratory sleep readings. Laryngoscope 1995; 105:519–522. 5. Woodson BT, Wooten MR. Manometric and endoscopic localization of airway obstruction after uvulopalato-pharyngoplasty. Otolaryngol Head Neck Surg 1994; 111:38–43. 6. Metes A, Hoffstein V, Mateika S, et al. Site of airway obstruction in patients with obstructive sleep apnea before and after uvulopalatopharyngoplasty. Laryngoscope 1991; 101:1102–1108. 7. Thomas AJ, Chavoya M, Terris DJ. Preliminary findings from a prospective, randomized trial of two tongue-base surgeries for sleep-disordered breathing. Otolaryngol Head Neck Surg 2003; 129:539–546. 8. Senior BA, Rosenthal L, Lumley A, et al. Efficacy of uvulopalatoplasty in unselected patients with mild obstructive sleep apnea. Otolaryngol Head Neck Surg 2000; 123:179–182. 9. Friedman M, Ibrahim H, Lee G. Clinical staging for sleep-disordered breathing: a guide to surgical treatment. Oper Tech Otolaryngol-Head Neck Surg 2002; 13:191–195. 10. Burgess LPA, Derderian SS, Morin GV, et al. Postoperative risk following uvulopalatopharyngoplasty for obstructive sleep apnea. Otolaryngol Head Neck Surg 1992; 106:81–86. 11. Friedman M, Landsberg R, Tanyeri H. Submucosal uvuloplatopharyngoplasty. Oper Tech Otolaryngol Head Neck Surg 2000; 11:26–29. 12. Mickelson SA, Hakim I. Is postoperative intensive care monitoring necessary after uvulopalatopharyngoplasty? Otolaryngol Head Neck Surg 1998; 119:352–356. 13. Gold AR, Schwartz AR, Bleecker ER, et al. The effect of chronic nocturnal oxygen administration upon sleep apnea. Am Rev Respir Dis 1986; 134:925–929.

16 Surgery of the Palate and Oropharynx: Laser-Assisted Techniques Regina Paloyan Walker Loyola University Medical Center, Maywood, Illinois, and Hinsdale Hospital, Hinsdale, Illinois, U.S.A. 1. LASER-ASSISTED UVULOPALATOPLASTY Laser technology, with its application in the oropharynx, revolutionized surgical management of sleep-disordered breathing. Prior to the introduction of laser-assisted uvulopalatoplasty (LAUP) in 1990, the most common palatal procedure was uvulopalatopharyngoplasty (UPPP). The UPPP requires a general anesthetic in most cases and often requires hospitalization. The UPPP was a very expensive and invasive option for the treatment of snoring. The laser allowed physicians to perform palatal procedures in the office, making snoring treatment more accessible to the general public. The first series of patients treated with LAUP was published in 1990 by Dr Yves Victor Kamami of Paris, France (1). In this publication, he reported that 85% of snoring patients had complete or near complete elimination of their snoring. These promising results combined with media attention and consumer interest stimulated tremendous enthusiasm among patients. Snorers now had an accessible, reasonably priced procedure to explore as an option. By 1995, LAUP was the most common snoring procedure performed. As with any procedure, the indications for LAUP broadened over time to include patients with upper airway resistance syndrome (UARS) and obstructive sleep apnea syndrome (OSAS). After 10 years, this procedure was first performed in the United States, both otolaryngologists and sleep medicine physicians agree that LAUP is a viable and safe option for patients who snore (2). The controversy continues as to whether this procedure should be offered to patients suffering from OSAS of any severity. Over this same time period, the definition of OSAS and its severity levels has changed. Recently in the sleep literature, it is more common to see the expression "nonpathologic" apnea. This category of patients has not been shown to have the same symptoms or medical consequences commonly seen in a patient with more significant OSAS. Yet, the Sleep Heart Health Study, an ongoing study looking at the cardiac consequences of sleep disordered breathing (SDB), has shown a correlation between hypertension and all levels of sleep apnea (3). Thus, the degree of snoring and SDB clinically significant remains unclear (4). With this degree of uncertainty, choosing the correct snoring procedure for a patient is cloudy at best. Until more data are published, good clinical judgment combined with experience is the best method for determining which procedure is best for an individual patient.

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1.1 Pre-operative Evaluation An initial evaluation includes a sleep and medical history, a directed physical examination, and patient education. Input from the bed partner, a body mass index (BMI), and neck circumference should be obtained on all patients. All patients require objective testing prior to LAUP. A polysomnogram, overnight cardiorespiratory testing, or overnight oximetry is performed (5,6). If the lowest oxygen saturation is less than 85% on any of these studies, LAUP is not performed except when the patient is a regular user of nasal CPAP (nCPAP). LAUP is not recommended in patients with a hyperactive gag reflex, significant retrognathia, or a bleeding disorder. Patients are told to stop anticoagulant medications as well as herbal remedies for 10 days preoperatively. Preoperative antibiotics are used in patients who require antimicrobial prophylaxis for medical and dental procedures.

2. SURGICAL TECHNIQUES 2.1 Anesthesia LAUP is performed using local anesthesia. Vital signs and weight are recorded on all patients prior to beginning the procedure. An informed consent is obtained at this time. Due to the nature of this procedure, working with the gag reflex is often the most challenging part of the procedure. Most patients who snore have an elongated soft palate and/or uvula. Thus, more tongue blade pressure is needed to visualize the inferior aspect of the uvula. This pressure of the tongue blade on the tongue base often stimulates the gag reflex. Hence, a well-anesthetized patient is a necessity. First,

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Figure 1 Topical anesthesia being applied to the soft palate. Two or three metered doses are applied.

Figure 2 The location of the injection points (X) for the local anesthesia. Only the midline site is injected prior to the first procedure in the modified LAUP procedure with all three sites being injected for subsequent procedures. a topical spray anesthetic is applied to the soft palate concentrating on the area to be injected (Fig. 1). The nasopharynx can also be anesthetized with a topical anesthetic spray applied nasally; however, this is usually not necessary. Two or three applications of the topical anesthetic should be used, with a minute or two between each application. The topical anesthetic gives the patient the sensation of anesthesia as well as the feeling of dysphagia. Due to the uncomfortable sensation of dysphagia, only a minimal amount of local anesthetic spray is currently used prior to the injection. The patient often needs reassurance that this feeling of dysphagia will typically pass in 2–5min. Next, one to three injections of 2% lidocaine with epinephrine (1:100,000) mixed with Kenalog (Allscrips, Vernon Hills, IL) are injected into the soft palate (Fig. 2). A 2-cc syringe contains 1.8mL of lidocaine with epinephrine and 0.2mL of Kenalog 40mg/mL. A total of 1–2mL is used depending on the area to be treated. Allowing 10min to pass before beginning the procedure is best so that the epinephrine has taken effect. There should be minimal to no bleeding if this technique is used. However, the anesthetic spray usually wears off before the 10min has passed. Applying topical spray anesthetic to the palate

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just before beginning the procedure is reassuring to the patient and helpful in dulling the gag reflex. After the procedure is completed, an anesthetic lozenge can be given to the patient to prolong the pain-free period. 2.2 Surgical Techniques The original technique described by Dr Kamami included the creation of bilateral vertical transpalatal trenches followed by partial uvular ablation (Figs. 3 and 4). The patient is seated in an examination chair in an upright position. All personnel and the patient wear carbon dioxide (CO2) laser safety glasses. A CO2 laser with a special hand piece, known as the backstop hand piece, is utilized. This hand piece was specifically designed for this procedure; it protects the posterior pharyngeal wall while working on the soft palate. The hand piece also allows forward retraction of the soft palate, which helps keep the tissue under tension while using the laser to

Figure 3 The transpalatal trench formation with a hand piece designed specifically for the LAUP procedure (backstop hand piece). This is a 1cm vertical incision made with the CO2 laser in the continuous mode. cut or ablate tissue. Most patients require two to four procedures spaced a month or more apart to complete their treatment. In general, patients with OSAS require a greater number of procedures than patients with a diagnosis of snoring. Ladies and elderly patients have less soft tissue as compared with middle-aged men and often only require one procedure to obtain satisfactory results when snoring is the indication for treatment.

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Dr Kamami described the technique in the following sequence. First he created bilateral vertical trenches in the soft palate on either side of the uvula using a CO2 laser in the continuous mode. Next he ablated a portion of the uvula with a Swiftlase attachment (Sharplan Laser Inc, Israel). This instrument rotates the laser beam creating a 3mm spot size, thus producing less char while ablating the tissue more

Figure 4 The CO2 laser ablation of the free hanging uvula during the first session. Approximately two-thirds of the free hanging uvula is ablated. The power setting is 20–25W with the Swiftlase attachment.

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Figure 5 The vertical trenches are widened by ablating the medial (uvular) side of the trench. The trench is widened on the lateral side if the UPPP technique is used. rapidly. He then widened the trenches by ablating the medial (uvular) side of the trench (Fig. 5). At the completion of the first procedure the uvula is smaller and narrower, and there are wide trenches made in the soft palate. As with any procedure, most surgeons modify a procedure over time. With Dr Kamami’s technique, many patients did not note an improvement in their snoring until after the second or third procedure. LAUP is a painful procedure to recover from. Many patients underwent their first procedure, did not note any improvement, and thus they did not return for further treatment. The author modified the original procedure by eliminating the trench formation and only the uvula was partially ablated during the first session (7). Subsequent procedures are performed as first described by Dr Kamami. The end result of the modified standard technique is the same as the standard technique. However, a higher percentage of patients returned for a second procedure because their snoring volume was reduced. It is important to understand that the reduction in snoring is related to multiple factors. The length of the free hanging uvula is related to the snoring volume. If vertical trenches are created, as is done in the standard technique, even if the original uvula is reduced in size, the “neo” uvula may still be elongated because of the creation of the trenches. In the modified standard technique, during the first treatment session, no vertical trenches are made and the uvula is partially ablated. This difference in technique may enhance an initial snoring reduction seen in the modified technique. An increase in the snoring volume is occasionally seen on subsequent procedures if the vertical trenches are created and the “neo” uvula is not reduced to the same degree as was done on previous procedures. The original and modified techniques result in a smaller uvula as well as a shortening of the soft palate (Figs. 6 and 7). A uvula is left to help avoid creating a continuous scar, which increases the incidence of a postoperative foreign body sensation. The uvula also helps clear secretions form the nasopharynx. Another technique, known as the UPPP technique, was developed in the mid-1990s. The uvula is essentially completely ablated in this procedure. In addition, the vertical trenches are angled out laterally and the ablation of the inferior edge of the soft palate is carried out to the tonsillar fossa (Figs. 8 and 9). The final appearance of

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Figure 6 The preoperative soft palate and uvula. the soft palate resembles a post-UPPP palate. In addition, tonsil ablation can be performed with either the standard technique or the UPPP technique (Fig. 10). Tonsil ablation adds to the width of the pharyngeal airway and theoretically should enhance the clinical response to LAUP. Tonsil ablation can be a useful procedure even when LAUP is not needed. The CO2 laser can be used in the office to perform partial tonsil ablation for tonsil hypertrophy, tonsil liths, and cysts. Topical spray anesthesia can be used alone or in conjunction with infiltration of the tonsil fossa to anesthetize a patient for this procedure. Care must be taken when injecting the tonsil fossa due to its rich blood supply. Drawing back prior to injecting and using plain lidocaine is important in this situation. The straight hand piece is used with the Swiftlase attachment or a defocused beam can be used as well. There are also special curved noncontact tonsil hand pieces available. The tonsil is ablated from the superior pole to the inferior pole. A right angle ear instrument is useful in retracting the overhanging anterior tonsil pillar so that the superior portion of the tonsil can be reached. If the tonsil pillars are not traumatized during the tonsil ablation, patients rarely complain of more than a mild sore throat for a few days. This is in contrast to the severe sore throat experienced by patients undergoing LAUP. The ablation is done in stages. Two to five millimeters of lymphoid tissue is removed in each session. This procedure is best suited for patients with moderate tonsil hypertrophy. Patients with massive hypertrophy should be taken to the operating room for either a reduction tonsillectomy or standard tonsillectomy.

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Figure 7 The soft palate and uvula once the standard or modified LAUP procedure(s) is completed.

Figure 8 The preoperative soft palate and uvula. 2.3 Post-operative Care Patients are observed for 20–30min following the procedure. They are then discharged to home or work. Medications include an antibiotic for 7 days, pain medication, and steroids in select patients. Anesthetic lozenges are very helpful in reducing the postoperative pain. Narcotics are usually necessary and all patients need to be educated on how to titrate these medications to avoid the common side-effects of these agents. Patients are

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counseled to sleep upright for at least 3–5 days following the procedure. Patients are reminded to use their nCPAP beginning the night of the

Figure 9 The soft palate and uvula once the UPPP technique is completed.

Figure 10 Tonsil ablation with a CO2 laser with Swiftlase and a straight hand piece. procedure. Other comforting strategies such as keeping hydrated and using a vaporizer at the bedside are reviewed as well.

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2.4 Complications The complications associated with LAUP are typically minor and transient. The most commonly reported side-effects are bleeding, local infection, globus sensation, temporary velopharyngeal insufficiency, and taste alterations (8,9). Postoperative bleeding that requires medical attention occurs less than 2% of the time. Cauterization with silver nitrate in the office or emergency room is usually sufficient to control the bleeding. Local infection is usually limited to oral candidiasis and resolves with standard treatment. Globus sensation or a foreign body sensation is noted in as many as 25% of patients undergoing this procedure (9). This sensation dissipates over time in the majority of patients. In selective patients who continue to be symptomatic after 6 months, the author has successfully used the laser to break up the palatal scar band and alleviate the symptoms in multiple cases. Identifying which patients will benefit from a scar release is not obvious in most cases. The patient must be informed prior to attempting to release the scar that this may not improve the symptoms and could actually intensify the sensation. Velopharyngeal insufficiency should be avoidable in a staged procedure such as LAUP. Four to six weeks after each procedure, patients’ postoperative courses are reviewed prior to proceeding to the next treatment session. If a patient notes even a temporary sensation of nasal regurgitation that completely resolves before their postoperative visit, performing further procedures should be avoided in most cases. The patient may still note snoring in such a situation, but further palatal reduction procedures could create permanent insufficiency.

3. RESULTS Dr Kamami’s initial data on his LAUP snoring results were published in 1990 (1). The first group of snorers experienced a 77% complete or near complete elimination

Table 1 Efficacy of LAUP for Snoring (Subjective Results) Source

Year

Number of patients

Success rates (%)

Kamami

1990

31

77

Kamami

1994

741

70

Walker

1995

105

60

Mickelson

1996

34

92

Ikeda

1997

30

93

Osman

2000

29

83

of snoring and another 23% had persistent nondisturbing snoring. Following this first publication, many series were published reporting response rates ranging from 60% to 93% (Table 1) (1,10–14). These data are based on short-term subjective patient or bed

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partner observations. Self-reported data on snoring are limited by many factors. Hoffstein et al. compared the perception of the patient and on duty sleep technician to objective measurements of snoring obtained during polysomnography (15). The perception of the patient was poorly correlated with the objective findings; the sleep technologist’s perception was qualitative at best. Yet, it is the subjective complaints of the bed partner that drive patients to the doctors’ offices for treatment. Thus, subjective results are all that really matter to the bed partner and most patients. However, to objectively determine if a new procedure such as LAUP actually alters the snoring noise, objective testing was essential. LAUP has been studied to objectively evaluate the frequency, pattern, and volume of snoring prior to and following treatment (16). Oronasal respiration was recorded and a digital analysis was performed. Subjective results were reported by the patient and bed partners as well. The findings shown in Table 2 demonstrate that the LAUP procedure alters the snoring sound. The fundamental frequency and the respiratory noise loudness showed statistically significant changes following the completion of LAUP treatment. These objective results correlated well to the patient and bed partner subjective responses. LAUP has recently been compared to radiofrequency tissue ablation (RFTA) of the soft palate in two studies (Table 3) (17,18). Terris et al. (17) and Blumen et al. (18) reported on their results with these two procedures. Terris et al. conducted a prospective, randomized, crossover surgical trial at a university hospital. The preliminary findings in 17 patients demonstrated a 60% satisfactory resolution of snoring in the RFTA group versus 86% satisfactory resolution in the LAUP-treated patients.

Table 2 Objective LAUP Snoring Results (Sonographic Data)

Snoring index (snores/hr)

Pre-operative

Post-operative

353.6±36.3

245.5±35.9

13.9±1.5

4.5±1.4

106.4±10.0

178±17.1

87.2±1.9

59.6±6.8

Relative loudness (dB) Av. fundamental frequency (Hz) Palate-like snoring (%)

Note: Values are mean standard error of the mean. Post-operative values are recorded after all the procedures have been completed.

Table 3 LAUP vs. RFTA of the Palate (Subjective Snoring Results) Terris et al. (17) LAUP Number of patients Age (yr)

Blumen et al. (18)

RFTA

LAUP

RFTA

7

10

15

15

46.7

52.8

46.0

48.5

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28.6

26.7

25.2

25.7

Epworth (pre-operative)

6.0

7.8

6.2

8.9

Epworth (post-operative)

6.0

6.4

VAS snoring (pre-operative)

8.6

7.5

8.0

8.3

VAS snoring (post-operative)

2.9

3.1

2.7

1.7

15.1

7.0

Duration of pain (days)

Not reported

Not reported

Note: Data are expressed as the mean. BMI, body mass index; Epworth, Epworth sleepiness scale; VAS, visual analog scale.

The RFTA failures were salvaged with LAUP. Blumen et al. conducted a prospective nonrandomized study on 30 patients who were seeking treatment for habitual snoring. They concluded that both treatments were effective. The authors also noted that radiofrequency treatment was tolerated better than LAUP. Finally, LAUP for the treatment of OSAS remains controversial. In the 2000 Update of the practice parameters for the use of LAUP, the Standards of Practice Committee did not recommend LAUP for the treatment of sleep-related breathing disorders. This recommendation is based on the opinion that “adequate controlled studies on the LAUP procedure for sleep-related breathing disorders were not found in peer-reviewed journals” (2). A total of six controlled studies and six case series or historical cohort studies were reviewed for this updated practice parameters. Four of these series, reporting the efficacy of LAUP in patients with OSAS, are shown in Table 4 (10,12,19,20). As can be seen in these series, the results are favorable and no serious complications were reported. Yet these series are not classified as Level I data as defined by the American Academy of Sleep Medicine (AASM) (2). Although the AASM requires Level I data to classify a procedure as a standard of practice, current data do suggest that LAUP is a reasonable procedure based on a moderate degree of clinical certainty.

Table 4 Efficacy of LAUP for OSAS Source (Ref.)

N

BMI

Pre-op

Post-op

Pre-op

Post-op

RDI

RDI

LSAT

LSAT

Kamami (10)

63

29.4

41.3

20.3

NA

NA

Mickelson (12)

36

31.0

28.1

7.9

80.6

84.0

Walker (19)

40

30.5

25.0

15.3

83.5

85.3

Utley (20)

12

NA

8.9

10.3

86.0

88.6

Note: Values are expressed as the mean. OSAS, obstructive sleep apnea syndrome; RDI, respiratory disturbance index (events/hr); BMI, body mass index (kg/m2); LSAT, lowest oxygen saturation (%).

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REFERENCES 1. Kamami YV. Laser CO2 for snoring—preliminary results. Acta Otorhinolaryngol Belg 1990; 44:451–456. 2. Littner M, Kushida CA, Hartse K, Anderson WM, Davila D, Johnson SF, Wise MS, Hirshkowitz M, Woodson BT. Practice parameters for the use of laser-assisted uvulopalatoplasty: an update for 2000. Sleep 2001; 24:603–619. 3. Nieto FJ, Young TB, Lind BK, Shahar E, Samet JM, Radline S, D’Agostino RB, Newman AB, Lebowitz MD, Pickering TG. Association of sleep-disordered breathing, sleep apnea and hypertension in a large community-based study. The Sleep Heart Health Study. J Am Med Assoc 2000; 283:1829–1835. 4. Walker RP. Long-term health consequences of mild to moderate obstructive sleep apnea. Arch Otolaryngol Head Neck Surg 2001; 127:1397–1400. 5. An American Sleep Disorders Association Report. Practice parameters for the indications for polysomnography and related procedures. Sleep 1997; 20:406–422. 6. Levy P, Pepin JL, Deschaux-Blanc C, Paramelle B, Brambrilla C. Accuracy for oximetry for detection of respiratory disturbances in sleep apnea syndrome. Chest 1966; 109: 395–399. 7. Walker RP. Method of Walker: laser-assisted uvulopalatoplasty. In: Fairbanks D, ed. Snoring and Obstructive Sleep Apnea. Baltimore: Lippincott, Williams and Wilkins, 2003; 144–150. 8. Walker RP, Gopalsami C. Laser-assisted uvulopalatoplasty: postoperative complications. Laryngoscope 1996; 106:834–838. 9. Pinczower EF. Globus sensation after laser-assisted uvulopalatoplasty. Am J Otolaryngol 1998; 19:107–108. 10. Kamami YV. Outpatient treatment of snoring with CO2 laser: laser-assisted UPPP. J Otolaryngol 1994; 23:391–394. 11. Walker RP, Grigg-Damberger MM, Gopalsami C, Totten MC. Laser-assisted uvulopalatoplasty for snoring and obstructive sleep apnea: results in 170 patients. Laryngoscope 1995; 105:938– 943. 12. Mickelson SA, Ahuja A. Short-term objective and long-term subjective results of laserassisted uvulopalatoplasty for obstructive sleep apnea. Laryngoscope 1999; 109:362–367. 13. Ikeda K, Oshima T, Tanno N, Ogura M, Shimomura A, Suzuki H, Takasaka T. Laserassisted uvulopalatoplasty for habitual snoring without sleep apnea: outcome and complications. ORL. J Otorhinolaryngol Relat Spec 1997; 59:45–49. 14. Osman EZ, Osborne JE, Hill PD, Lee BWV, Hammad Z. Uvulopalatopharyngoplasty versus laser-assisted uvulopalatoplasty for the treatment of snoring: an objective randomised clinical trial. Clin Otolaryngol 2000; 25:305–310. 15. Hoffstein V, Mateika S, Anderson D. Snoring: is it in the ear of the beholder? Sleep 1994; 17:522–526. 16. Walker RP, Gatti WM, Poirier N, Davis JS. Objective assessment of snoring before and after laser-assisted uvulopalatoplasty. Laryngoscope 1996; 106:1372–1377. 17. Terris DJ, Coker JF, Thomas AJ, Chavoya M. Preliminary findings from a prospective, randomized trial of two palatal operations for sleep-disordered breathing. Otolaryngol Head Neck Surg 2002; 127:315–323. 18. Blumen MB, Dahan S, Wagner I, De Dieuleveult T, Chabolle F. Radiofrequency versus LAUP for the treatment of snoring. Otolaryngol Head Neck Surg 2002; 126:67–73. 19. Walker RP, Garrity T, Gopalsami C. Early polysomnographic findings and long-term subjective results in sleep apnea patients treated with laser-assisted uvulopalatoplasty. Laryngoscope 1999; 109:1438–1441. 20. Utley DS, Shin EJ, Clerk AA, Terris DJ. A cost-effective and rational surgical approach to patients with snoring, upper airway resistance syndrome, or obstructive sleep apnea syndrome. Laryngoscope 1997; 107:726–734.

17 Temperature-Controlled Radiofrequency Palatoplasty Lionel M.Nelson Department of Surgery, Stanford University School of Medicine, Stanford, California, U.S.A. 1. INTRODUCTION Sleep-disordered breathing (SDB) associated with upper airway obstructive events can range from primary snoring through upper airway resistance syndrome (UARS) to varying severity levels of obstructive sleep apnea syndrome (OSAS). When the soft palate is the site of the obstruction, particularly in the less severe forms of SDB, such as snoring, UARS, and mild OSAS, practitioners and patients presently have the option of replacing excisional surgical treatments with less invasive safe and effective alternatives. Temperature-controlled radiofrequency (TCRF) palatoplasty (palate Somnoplasty®) is one of these alternatives.

2. TEMPERATURE-CONTROLLED RADIOFREQUENCY BASICS The process of TCRF palatoplasty begins when radiofrequency spectrum (465 kHz) electromagnetic energy is delivered submucosally into palatal muscle tissue via an electrode. This energy forms a low-temperature (47–85°C) tissue coagulum which the body gradually resorbs (typically over 6–8 weeks), shrinking and stiffening the palate. The coagulum is the end state result of active frictional heat generated by ionic agitation in cells surrounding the electrode, isothermal passive conduction to adjacent cooler tissue, and dissipating heat convection to more peripheral tissue. This process occurs subsurface, hidden from the visual cues one usually depends on to control electrosurgical procedures. Therefore, to assure safety and predictability in this process, an alternate control mechanism to the surgeon’s direct visual assessment of tissue changes is needed. That alternate is temperature information fed back real-time from the tissue as the coagulum is being formed via thermocouples in the electrode. That information is then used by a computer-driven control unit that modulates energy output from a radiofrequency generator, thus enabling more precision in lesion formation based on predesignated energy and temperature parameters. Therefore, TCRF, unlike other radiofrequency instrumentation used in

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Figure 1 TCRF energy delivered via a straight electrode will produce a predictable prolate sphere lesion with a larger footprint than the dimensions of the electrode. In palate muscle, a 1-cm electrode programmed to deliver 600J of energy to a maximum tissue temperature of 85°C produces a threedimensional lesion submucosally that is approximately 15mm (major axis) by 8mm (minor axis). otolaryngology, allows a rapid and dynamic response and control to changing conditions in the treated tissue. TCRF technology is available for use in the upper airway as Somnoplasty® (Gyrus ENT, Bartlett, TN), giving the practitioner the capability to form sharply defined and accurate submucosal lesions. Using the 1cm straight electrode designed for palate Somnoplasty®, and preset maximum temperature and energy settings of 85°C and 600J, respectively, a predictable prolate sphere (“football” shape) submucosal tissue lesion will be formed in muscle measuring approximately 15mm in length by 8mm in width, with some minor variability due to existing tissue conditions (Fig. 1). Powell and Riley, who pioneered the first applications of TCRF in the upper airway, found that when applied to soft palate muscle, the target tissue would become stiffer and reduced in volume, but without overt changes in overall palate appearance other than a slight shortening effect of 5.5mm, as measured from the nasal spine to the tip of the uvula (1). TCRF palate lesions are designed to be placed in muscle, sparing surrounding mucosa. Intact mucosa avoids the open tissue wounds associated with more invasive palatal procedures. For the patient this means less discomfort, minimal changes in tissue

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physiology and anatomy when compared to excisional surgical techniques, and quicker return to normal activity. Minimal permanent change in palate anatomy also maintains the option for retreatment as needed, an attribute that often becomes an important consideration.

3. PATIENT SELECTION TCRF palatoplasty is primarily indicated for the treatment of palatal flutter snoring. Sleep studies in nonapneic to mildly apneic populations demonstrate no ultimate changes in respiratory disturbance indices (RDI) or oxygen saturation nadirs with treatment. They do, however, reveal statistically significant improvements in sleep efficiency (SE) and esophageal pressure (Pes) nadirs (1). This, along with observed improvements in Epworth Sleepiness Scale scores and snore indices (SI) (1), appears to indicate that the procedure may also be appropriate for the control of some of the more bothersome symptoms associated with UARS and mild OSAS. Since RDI and oxygen levels to not change, the procedure does not appear to be indicated for the treatment of more significant OSAS. Appropriate patient selection for TCRF palatoplasty, therefore, becomes important. Since Tami et al. (2) found that 72% of individuals seeking snoring treatment actually had unrecognized OSAS (42% of them severe), before embarking on treatment for the snoring patient, an apnea work-up, including sleep study, should be undertaken. Anatomy plays an important role in predicting outcomes in the snoring patient. In general, the best candidates for TCRF palatoplasty (as is true for most other surgical treatments for snoring) are those with normal appearing soft palates and upper airways. The ideal candidate for treatment, therefore, would be a nonapneic (apnea/hypopnea index, AHI, ≤5), nonoverweight (body mass index, BMI, ≤25) individual with a hypervibratory but anatomically normal appearing soft palate, and no significant facial skeletal or airway soft tissue abnormalities, or confounding lifestyle factors (such as cigarette smoking). However, individuals with mild OSAS (AHI ≤15 and oxygen saturations no lower than 85%), who are overweight but not obese (BMI ≤30), have mild degress of palate variation (such as increased tissue bulk, uvula size, velum webbing), and treatable lifestyle (smoking, sedative medications) and soft tissue airway factors are also acceptable candidates. For this second group, which is usually more typical of those who seek treatment, successful outcomes in snoring control can be attained in approximately 84% of patients with TCRF palatoplasty (3). Successful snoring control diminishes as the above parameters worsen. Contributory upper airway soft tissue factors (enlarged nasal turbinates, tonsils, or tongue) can be treated by other in-office Somnoplasty® procedures, as described elsewhere in this book. For those individuals with very large, pendular uvulas, adjunctive in-office surgical partial uvulectomy may be needed. The goal of TCRF palatoplasty treatment is adequate control of the offensive nature of the snoring. Rarely does complete snoring irradication result. This, along with snoring relapse rates over time, should be discussed with the patient and his/her bed partner as realistic expectations before treating. Since what will constitute objectionable snoring to a bed partner is subjective, a subjective 0–10 visual analog scale (the snore index or SI)

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seems appropriate to assess outcomes. Defining an SI scale where 0 is the absence of snoring, 1–3 is soft snoring not bothersome to the bed partner, 4–6 is snoring bothersome to the bed partner, 7–9 is snoring heard outside the room, and 10 is snoring bothersome enough that bed partner leaves the room, a successful treatment outcome is attained when the SI is reduced to ≤3 (3).

4. PROCEDURE TCRF palatoplasty is designed to be done as an in-office procedure under local anesthesia. Generally, no premedication or preprocedure restrictions are needed. Standard dosages of salicylates and anti-inflammatory medications need not be curtailed. Anticoagulants, such as coumadin, should be temporarily stopped in consultation with the patient’s other physicians. Although rarely needed, a mild oral sedative can be useful for those with extreme gag reflex control problems. Antibiotic coverage (unless needed as prophylaxis for other medical conditions) and steroids are not routinely given. A Somnoplasty® generator/control unit (Gyrus ENT, Bartlett, TN) with palate handpiece and groundplate is needed for the procedure. With the patient seated in an examination chair, and using headlight illumination and a tongue depressor, the palate is exposed and topically anesthetized (lidocaine or benzocaine spray). After evaluating the palate and oral cavity, the handpiece’s bendable electrode delivery tube is angled to the palate’s curvature. Local anesthetic (such as 1% lidocaine with 1:200,000 epinephrine and bicarbonate, or equivalent) is then infiltrated submucosally into the proposed palate treatment site. The pattern of injection and volume of anesthetic used is important. The risk of producing mucosal ulcerations can be minimized by “ballooning” the target tissue with local solution (usually 7–9cc is needed). Fluid injected into the tissue surrounding the thicker muscular palate will dissipate fairly rapidly, while that placed into the thinner distal uvular and velum tissue will not. Therefore, avoiding local anesthetic migration into these latter areas (areas which are not usually in the treatment target zone anyway) will minimize the discomfort of prolonged postoperative uvular swelling (Fig. 2). Proposed lesion placement sites should then be determined. With the electrode fully deployed in its operational position, it is placed over the surface of the palate, using the 1cm active electrode portion over the proposed site of the intramuscular lesion. Keeping in mind that the final lesion is larger (approximately 15×8mm) than the electrode, the mucosal entrance site to attain this lesion should be noted (it can be marked with a marking pen). All lesions planned for that treatment session should be outlined in a similar manner before producing any actual lesions. This will assist in tailoring the placements to the individual palate, and minimize lesion overlap, which could potentially increase complications. With the patient incorporated into the electrosurgical circuit via the dispersive (grounding) pad, the electrode is now placed into the palate. As a final placement check for proper positioning, the outline of the electrode can be seen under the mucosa by gently pulling forward on the handpiece. The soft palate, now tethered by the electrode, should move freely with handpiece movement. Once satisfied with placement, all tension on the handpiece should be released, allowing the electrode to

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Figure 2 Pattern of injected local anesthesia. Using enough solution (usually 7–9cc) to “balloon” the treatment site will minimize mucosal ulcerations.

Figure 3 Lateral cut-away view of electrode deployed in the soft palate.

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The electrode housing tube has been bent to conform to the palate’s curvature prior to placement. “float” in the tissue (the electrode’s outline under the mucosa should disappear). Energy flow is then activated and delivered to a maximum temperature setting of 85°C. Centering the electrode in the anteroposterior palate dimension, avoiding undue tension in gripping the handpiece, and observing for mucosal blanching will help attain a strictly submucosal lesion with intact mucosal surfaces (Fig. 3). Several different electrode placement patterns and energy settings have been utilized. Each has its advantages and shortcomings. The soft palate is thickest high in the midline. Limiting lesion placement to the midline or paramedian positions in the upper threequarters of the palate diminishes the risk of mucosal ulcerations and full thickness tissue necrosis that can be associated with treating the thinner more lateral

Figure 4 The single-midline lesion technique. The black line represents the electrode placement in muscle and the dotted line the resultant submucosal lesion.

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Figure 5 The two-midline lesion technique. or peripheral tissue. Proponents of this approach recommend sequential treatment sessions, treating either one site in the midline (Fig. 4), two midline sites with one superior and one inferior (Fig. 5), or two paramedian sites (Fig. 6) at each session (4). Although the amount of energy used is adjusted for palate thickness, in general, no more than 750J is given to any one lesion site. If the lower midline lesion treads into the uvula base where the muscle is thin, a lower level (350–500J) is recommended. Another approach is the placement of three lesions per treatment session, one midline and two angled laterally (Fig. 7), delivering 650–750J in the midline and 300–350J to each lateral site. A comparative multicenter study of 105 patients, demonstrated a higher rate of successful outcomes in snoring control with fewer treatment sessions using this triple lesion technique. Defining a successful outcome as a 2month posttreatment snore index of no more than 3, this approach produced a successful outcome in approximately 84% of treated patients, within a mean number of treatment sessions of 1.6 per patient. In this study, 56% attained this outcome with one treatment session. Complications rates were minimal, with 2.9% mucosal ulcerations, 1.9% small fistulas (all closing spontaneously), and 1.9% tissue slough (3).

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Figure 6 The two-paramedian lesion technique. Electrodes are placed on either side of the uvula muscle, leaving enough space so that the lesions formed do not overlap.

Figure 7 The three-lesion technique. In an effort to minimize the number of patients needing more than one treatment session, a more aggressive four-lesion approach has been introduced. Here, lesions are placed high midline at 700J, low midline at 350–500J (depending on tissue thickness) into the uvula base, and laterally at 500J each (Fig. 8). Total energy delivered is 2050–2200J. The rationale for using this amount of energy is based on study findings that, on average, a minimum total of 2000J, regardless of the number of treatment sessions, is needed to

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produce a substantial improvement in snoring (3). The potential importance of placing a lower midline lesion into the uvula base is supported by stroboscopic data showing the significant contribution of the distal midline palate and uvula in palatal flutter snoring (5). The four-lesion approach will attain a successful outcome with a single treatment in, on average, 80% of properly selected patients, thus decreasing the number of patients needing a second treatment. This more aggressive approach, however, does have a greater potential for temporary mucosal ulcerations and, on rare occasions, tissue slough. Technique becomes critical if risk of these complications is to be minimized. Since proper technique

Figure 8 The four-lesion technique. comes with experience, for those just starting to do TCRF palatoplasties, one of the less aggressive approaches is recommended initially. For those four-lesion patients needing a second treatment, placement of two paramedian lesions of 500J each on the lateral aspects of the uvula muscle is recommended (Fig. 6). Since lesion maturation is slow, results of a treatment may not be apparent for 6–8 weeks. Therefore, regardless of the lesion pattern used, repeated treatment if needed is not recommended before maturation time has elapsed.

5. COMPARATIVE OUTCOMES The initial success rates of TCRF palatoplasty appear to be comparable to other surgical treatment methods for snoring control. Kamani reported an initial success of 85% using laser-assisted uvulopalatoplasty (LAUP) (6). Coleman and Rathfoot noted an 85% initial success at snoring control with uvulopalatopharyngoplasty (UPPP) (7). However, unlike these other procedures, TCRF palatoplasty appears to be better tolerated with more rapid return to normal activity and significantly less postoperative pain. Troell et al. (8) found in their comparative study that only 9% of the TCRF patients

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needed narcotics for pain control as opposed to 100% of their LAUP and UPPP patients. Narcotics were needed, on average, for 0.2 days in the TCRF group and 11.8 and 12.4 days, respectively, in the LAUP and UPPP groups. The total number of days of pain was, on average, 2.6 for TCRF, 13.8 for LAUP, and 12.4 for UPPP. Typically, TCRF palatoplasty patients find that over-the-counter anesthetic lozenges and ibuprophen are adequate for discomfort control. Although small superficial mucosal ulcerations causing minor discomfort are not uncommon (particularly with more aggressive treatment patterns), deeper ulcerations, which can be quite painful, are rare. Patients reporting more significant pain following treatment should be evaluated for this contingency and consideration for prescription analgesic and possibly oral antibiotic therapy. Although relatively low in temperature, radiofrequency lesions still represent a thermal injury. Therefore, early palatal edema, often with concomitant temporary worsening of SDB symptoms, can be expected. Powell et al. (1) found that there was an initial posttreatment change for his study group in mean RDI from a baseline of 3.9 to 10.5 episodes per hour, and an oxygen saturation nadir drop from 91.2 to 86.5%. Both parameters returned to baseline levels as the edema resolved. Symptomatic treatment for this with head elevation on pillows at night is usually adequate posttreatment, but on rare occasions, short-term steroid use may be indicated. Long-term outcomes of surgical procedures for snoring control appear to be similar, regardless of the degree of invasiveness. Evident snoring recurs in 45% of patients at 18 months following LAUP (9), and in 41% of patients 13 months following UPPP (10). TCRF palatoplasty has a similar relapse rate. Li et al. (11) found that at 12–18 months 41% of their study patients had a recurrence of snoring. Although the snoring level did not return to pretreatment intensities (mean snore indices were initially 8.3 for their study group, diminishing to 1.9 with treatment, and recurring to 5.7 on extended follow-up), nonetheless it was loud enough to again be bothersome to the bed partner (SI>3). They also found that a single in-office TCRF palate retreatment in this relapse group could restore the result to an acceptable level (mean SI 3.3). Patient satisfaction with snoring procedures, and their willingness to undergo retreatment if needed, appears to be proportional to the level of discomfort associated with the technique used. Of the patients that had prior treatment, willingness to consider retreatment with the same modality was 70% for UPPP (12), 75% for LAUP (9), and 95% for TCRF (11). In addition, since the ability to retreat often hinges on the remaining anatomic integrity of the palate, excisional approaches that change basic palatal anatomy may exclude this option. Having the capability to easily retreat in a patient population that is receptive to this possibility is a great advantage, given the apparent high recurrence rates following all of the present surgical treatments for snoring.

6. CONCLUSIONS TCRF palatoplasty appears to give comparable results in snoring control to the more invasive surgical options presently available. Whether by decreasing the frequency of snore-related arousals during sleep, and/or by improving overall airway resistance, the procedure also produces a salutary effect on daytime sleepiness and sleep efficiency. For

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the patient, TCRF palatoplasty offers a well-tolerated, safe, and effective in-office procedure, with minimal posttreatment discomfort, complications, or disruption of normal activities. For the practitioner, the procedure is easy to perform with few postoperative problems. The absence of significant changes in palatal anatomy and function with TCRF not only allows retreatment, but also will not complicate future more invasive surgical approaches, or the use of oral appliances and positive airway pressure devices (cpap) should they be needed. Minimal invasiveness with comparable clinical effectiveness makes TCRF palatoplasty well suited as a first-line approach when a surgical option is sought for the control of symptoms associated with bothersome snoring, UARS, and mild OSAS.

ACKNOWLEDGMENT The author thanks Theodore R.Kucklick, BFA, for his invaluable assistance in rendering the illustrations for this chapter.

REFERENCES 1. Powell NB, Riley RW, Troell RJ, Li K, Blumen MB, Guilleminault C. Radiofrequency volumetric tissue reduction of the palate in subjects with sleep-disordered breathing. Chest 1998; 113:1163–1174. 2. Tami TA, Duncan HJ, Pfleger M. Identification of obstructive sleep apnea in patients who snore. Laryngoscope 1998; 108:508–513. 3. Sher AE, Flexon PB, Hillman D, Emery B, Swieca J, Smith TL, Cartwright R, Dierks E, Nelson L. Temperature-controlled radiofrequency tissue volume reduction in the human soft palate. Otolaryngol Head Neck Surg 2001; 125:312–318. 4. Troell RJ, Li KK, Powell NB, Riley RW. Radiofrequency of the soft palate in snoring and sleepdisordered breathing. Operative Techniques in Otolarygol-Head and Neck Surg 2000; 11(1):21– 23. 5. Brietzke SE, Mair EA. Injection snoreplasty: how to treat snoring without all the pain and expense. Otolaryngol Head Neck Surg 2001; 124:503–510. 6. Kamami Y. Laser CO2 for snoring—preliminary results. Acta Otorhinolaryngol Belg 1990; 44:451–456. 7. Coleman J, Rathfoot C. Oropharyngeal surgery in the management of upper airway obstruction during sleep. Otolaryngol Clin North Am 1999; 32(2):263–276. 8. Troell RJ, Powell NB, Riley RW, Li KK. Comparison of postoperative pain between laserassisted uvulopalatoplasty, uvulopalatopharyngoplasty, and radiofrequency volumetric tissue reduction of the palate. Otolaryngol Head Neck Surg 2000; 122:402–409. 9. Wareing MJ, Callanan VP, Mitchell DB. Laser assisted uvulopalatoplasty: six and eighteen month results. J Laryngol Otol 1998; 112:639–641. 10. Levin BC, Becker GD. Uvulopalatopharyngoplasty for snoring: long-term results. Laryngoscope 1994; 104:1150–1152. 11. Li KK, Powell NB, Riley RW, Troell RJ, Guilleminault C. Radiofrequency volumetric reduction of the palate: an extended follow-up study. Otoalryngol Head Neck Surg 2000; 122:410–414. 12. Macnab T, Blokmanis A, Dickson RI. Long-term results of uvulopalatopharyngoplasty for snoring. J Otolaryngol 1992; 21:350–354.

18 Coblation Techniques for Sleep Disordered Breathing Luc G.Morris and Kelvin C.Lee Department of Otolaryngology, New York University School of Medicine, New York, New York, U.S.A. 1. INTRODUCTION Because of the significant morbidity associated with traditional surgical interventions for snoring and sleep disordered breathing, minimally invasive methods of tissue reduction have received a great deal of attention. Many of these tissue reduction techniques utilize radiofrequency (RF) energy for ablation, relying upon heat to destroy tissue. Coblation is short for “cold ablation,” and uses an ionized plasma field as a surgical tool with unique characteristics. In otolaryngology, coblation has been primarily used for subtotal tonsillar reduction and total tonsillectomy. Coblation is unique in that it utilizes RF energy to create a plasma field of ionized particles, which ablates tissue without generating significant heat. The plasma field allows for precise molecular disintegration, while minimizing unintended peripheral damage. The base unit is a RF generator capable of performing coblation—bipolar radiofrequency volumetric tissue reduction (RFVR). The RF energy can also be used for bipolar coagulation, thus achieving hemostasis. One of the unique aspects of this modality is that coblation’s surgical characteristics can be dramatically altered based on wand design. Different coblation wands generate varying amounts of heat, and either ablate or volumetrically reduce tissue. This gives the coblation unit great versatility in almost any surgical situation, offering the surgeon a wide range of aggressivity in tissue removal, as well as heat generation to assist with hemostasis. Using a combination of tissue removal and volumetric tissue reduction, the coblation device is commonly used in the surgical management of snoring and sleep apnea, focusing on the turbinates, soft palate, base of tongue, and tonsils. This chapter will review the process of coblation and its utilization in the management of patients with sleep disordered breathing.

2. TECHNICAL ASPECTS OF COBLATION 2.1 Conventional Electrosurgery The technical basis for coblation is best understood in comparison to other forms of electrosurgery. Cushing and Bovie, in 1928, first described the use of conventional

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electrosurgery. Modern electrosurgical devices are essentially unchanged, and can be used for either cutting or hemostasis. A voltage difference between the electrode and the tissue eventuates in an electrical current arc across the intervening space. This locally heats and damages tissue, with the manner of tissue damage dependent on the character of the waveform used. If dessication or coagulation of tissue is desired, the device will generate a sinusoidal pulse with a frequency of 250–2000kHz, voltage of 300–2000V, and power of 80–200W. This pulsed energy generates extremely high temperatures, slowly drying tissue and arresting bleeding, with only limited destruction of cells. In order to cut tissue, a continuous waveform, of higher frequency, voltage, and power, must be used, vaporizing tissue by pyrolysis. Frequencies of 500kHz to 2.5Mhz, voltages of up to 9000V, and power of 100–750W are utilized. These devices may also cut and coagulate simultaneously by generating a blended waveform. In the higherpower cut mode, current penetrates between 0.3 and 3.5mm into tissue (1). 2.2 RF Ablation RF devices are also technically electrosurgical devices, but produce energy with a lower frequency, thus destroying tissue in a different manner. With RF ablation, the electrode is inserted into tissue, so that current does not arc, and the electrode has a larger surface area, so that current is distributed over a larger area. This causes regional necrosis with minimal cutting. RF devices produce less heat, which can be more specifically controlled. This modality can be used to create a predictable lesion in tissue, which can be precisely placed. In otolaryngology, monopolar coagulation necrosis is used for volumetric tissue reduction of the soft palate, base of tongue, and turbinates, and has been popularized using the Somnus device (Somnus Corporation, Mountain View, CA). The Somnus device operates at lower energy (2–10W and 80V) and lower temperatures (<100°C) than conventional electrosurgery, but still destroys tissue via a pyrolytic mechanism. Somnus electrodes are insulated to reduce thermal injury to the overlying mucosa and receive constant feedback though thermistors built into the tissue-treating electrodes, allowing the surgeon to control the maximal temperature reached in the target tissues. Somnoplasty volumetrically reduces tissue through coagulation, which progresses to necrosis over the first 72hr, and then to fibrosis over the next 10–12 days. Fibrotic tissue occupies a smaller area than normal tissue and retracts the surrounding tissue. This technique is also known as RFVR. 2.3 Coblation 2.3.1 Plasma-Mediated Ablation Coblation is a method of RF ablation which primarily shrinks tissue by molecular disintegration, rather than heat-induced necrosis and scarring. Technically, coblation is a form of electrosurgery, in that the mechanism is a voltage differential between the active and return electrodes. However, coblation operates at a lower frequency (100kHz) and

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lower voltage (100–300V), and also employs a conductive fluid, usually isotonic saline, between the electrodes. The device operates in two modes, depending on the voltage. At lower voltages, the device produces tissue damage in a manner similar to traditional RF ablation, generating some heat. However, when a sufficient voltage is applied, the saline fluid is converted into an ionized plasma field between the electrodes (2). Partial plasma generation begins at approximately 150V, and a luminous plasma discharge can be observed at approximately 200V (3). With higher coblation device settings (higher voltage), the generated power increases and the wand is more consistently maintained in plasma generation mode. In normal saline, the plasma discharge emanating from the coblation electrode will glow with an orange color, reflecting a narrow spectroscopic emission peak at 589nm; this is the sodium ionization wavelength, corresponding to Na+ cations in plasma phase. Smaller peaks also exist at 656nm (H+) and 306nm (OH−), representing dissociated water. Standard electrosurgical and other RF techniques in saline will instead emit a broad, continuous spectrum from 490 to 900nm, with no evidence of any ionized particles (2,3). Energized ions in the plasma field accelerate down the electrical gradient toward tissue cells with enough energy to dissociate individual molecular bonds. The carboncarbon bonds and carbon-nitrogen bonds in tissue molecules require 3–4eV to break; coblation generates a plasma field with energy of ≈8eV (2). As the molecules are broken apart, coblation removes tissue volumetrically, and releases gaseous biproducts, including oxygen, nitrogen, carbon dioxide, and methane. Under laboratory conditions, a stream of bubbles from these gases is observed at 200V (3). This is not steam as is seen with the use of CO2 lasers or electrocautery. This non-heat driven process of cellular destruction has also been termed ablative sublimation. In principle, this method of cold ablation is similar to excimer lasers, which dissociate molecular bonds using energized photons (4). Charged particles in the plasma do not travel far; as a result, molecular dissociation tends to occur only at the tissue adjacent to the coblation wand, penetrating to an estimated depth of 50–100µm (2). The bulk of tissue destruction is the result of this plasma-mediated process, although some RF heat energy will induce an additional degree of collateral tissue damage surrounding the small ablation zone. However, the heating of peripheral tissue is minimal in coblation when compared to other electrosurgical devices. Wand design can produce higher tissue temperatures during the process of coblation if these temperatures are desired. For example, the Coblator Reflex wands (ENTec, Sunnyvale, CA) utilize three electrodes to create a long, thin, submucosal thermal lesion surrounding the zone of coblation at the tip of the probe. Coblation in soft tissue produces immediate results, as tissue has been ablated and there is no need for resorption of necrotic tissue. Additionally, with time, any collateral necrosis from the thermal lesion will result in tissue volume reduction and tissue stiffening, similar to the coagulation necrosis described for RF ablation. 2.3.2 Histologic Evaluation Woloszko and Gilbride (2) in 2000 first described the heating aspects of coblation in the optical engineering literature. This study investigated the TurboVac coblation wand, used in arthroscopic surgery, in a saline bath. Counterintuitively, coblation maximally heats tissue at low voltages. Below 150V, the coblation system operates in a conventional RF

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resistive heating mode, simply coagulating tissue. The surface temperature will rise as high as 60–65°C after 20sec, and 45–50°C at a tissue depth of 1mm. This tissue heating is relatively minor, even when operating at lower voltages, when compared to other modalities. Conventional electrosurgical devices such as bovies and CO2 lasers operate in the 400–600°C range. Excimer lasers for photodissociation have been reported to operate at low temperatures, similar to coblation, although recent studies now suggest that their temperatures may transiently become >100°C (5). As voltage becomes >150V, the device enters the plasma coblation mode, so that maximum tissue temperature falls to <55°C, and <45°C at a depth of 1mm. Other investigators have confirmed 1mm as the maximum depth of significant heat penetration into tissue (6). These temperatures remain constant, even up to 300V. As long as the device is used in high-voltage coblation mode, tissue temperature will remain <60°C, the point at which most irreversible tissue damage is believed to occur (2,7). Identical results have been noted in otolaryngologic coblation wands (8). Chinpairoj et al. in 2001 (9) compared the degree of tissue damage in coblation to the degree of tissue damage in standard monopolar electrosurgery, using a rat tongue model for histologic evaluation. When incisions of equivalent size (approximately 1mm2) were produced using the two methods, significantly smaller surrounding areas of epithelial destruction and collagen denaturation were noted with coblation. Complete reepithelialization occurred by day 7 in coblation and day 14 in standard electrosurgery, with significantly less inflammation and granulation tissue in the coblation specimens (Fig. 1). This study verified that coblation causes less collateral damage in tissue, and permits faster wound healing, than conventional electrosurgery. Early studies of articular chondrocytes following coblation demonstrated that viable cells are found at a depth of <50µm from the surface, and that these cells remain viable for 180 days (10). One of the clear unique characteristics of coblation is that, beyond the zone of plasma-mediated ablation, there is minimal collateral heat damage to tissue. With reduced collateral heat injury to tissue and essentially no charring of surface tissue, postoperative pain and edema should be substantially lower. Rice et al. in 1999 (8) have additionally suggested that myelin sheath molecular bonding energy is twice that of connective tissue, thus providing a protective covering of nerves against plasma ablation. The clinical benefits of this differential ablation have not been investigated, but may make the use of coblation as a dissection tool more attractive. In cases when a larger lesion is desired, the coblation device can produce a tissue lesion of predictable size. Woloszko and Gilbride (2) have compared the thermal effects of coblation against somnoplasty in an animal model (chicken tissue). This study employed the Coblator device with the Reflex 55 wand at settings for soft palate ablation, in comparison to a Somnus Model 1000 device at 200, 300, and 600J settings and a temperature limit of 80°C. The Reflex wand is designed to ablate tissue, but also uses heat to generate a thermal lesion surrounding the ablation zone. Results of this study demonstrated that standard coblation created lesions intermediate in size between 300 and 600J somnoplasty: 285mm3 vs. 255 and 392mm3, respectively. Average temperatures were 59.3°C for coblation and 84.2°C for somnoplasty, with maximum temperatures of 76.2°C and 89.0°C, respectively. This limited study suggests that coblation using the Reflex style wands, with 10sec of dwell time, creates lesions roughly equivalent in size to 300J somnoplasty, but at substantially lower temperatures.

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Figure 1 This histologic comparison of coblation and monopolar electrocautery on the rat tongue reveals less tissue injury after creating equivalent incisions. At 7 days (b) there is a visible difference in the stage of healing and the inflammatory

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response seen in the wound. (From Ref. 9.) The coblation device, when operated at <150V, can also be used strictly for coagulation of tissue. At these low voltages, no plasma layer is generated, and the conductive saline liquid retains its normally low impedance. This permits some dissemination of heat energy into tissue, achieving hemostasis with some necrosis of tissue. The controller unit has a specific mode for hemostasis, with voltage limited to 65V. The newer controller units allow further increase of voltage and thus more effective cautery of tissue, but without the generation of a plasma field. The operator of the device may thereby achieve either hemostasis or ablation, or both, by selecting the appropriate power setting.

3. CLINICAL APPLICATIONS OF COBLATION 3.1 Overview Coblation was originally developed for use in arthroscopic surgery in 1995, since which time more than 400,000 cases have been reported. Since coblation is performed in a saline environment, this modality has been easy to integrate into arthroscopic surgery approaches. Orthopedists have also used coblation for a wide range of procedures, including chondroplasty, meniscectomy, meniscal tears, lateral release, synovectomy, and ligament reconstruction (11). Coblation has more recently found use by dermatologists for skin resurfacing, as coblation offers excellent precision for ablation of thin layers of epidermis (12,13). In otolaryngology, the Food and Drug Administration has approved coblation for “ablation and coagulation of soft tissue including head, neck, oral and sinus surgery” (14). Surgeons have used this surgical modality for a wide variety of procedures including head and neck surgery, turbinate surgery, and surgery of the oropharynx. For the surgical management of the sleep disordered breathing patient, coblation offers techniques for reduction of anatomical obstruction at the level of the nasal passages, oropharynx, and base of tongue.

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3.2 Tissue Ablation Techniques or Coblation Channeling Coblation has been useful for techniques that remove and stiffen tissue while leaving the mucosa largely undamaged, which has been called submucosal channeling. For these procedures, a thin coblation wand (ENTec Reflex wand) is employed, with three electrodes: a proximal and distal active electrode and a centrally located return electrode as seen in Fig. 2. The electrode need only be dipped in saline gel prior to insertion into tissue, after which the tissue’s sodium content is sufficient to allow the coblation process to occur. A channel is created by inserting a thin wand into tissue and ablating: this removes the volume of tissue displaced by the wand. Though the coblation process takes

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place with tissue ablation, the resultant lesion is also a product of heat generated inherent to the wand design, and can be thought of as bipolar RFVR technique. The commonly used wands will leave a lesion 4mm in diameter and 12mm in length after 10sec of activation. The coblation channeling method is useful for submucosal reduction of the inferior turbinate, soft palate, and base of tongue. 3.2.1 Turbinate Reduction Coblation turbinoplasty is used in patients when nasal obstruction is believed to be exacerbating snoring or sleep apnea. The ablated volume of tissue is believed to be removed immediately, and the thermal effect along the passage results in further reduction of tissue volume. Turbinate fibrosis will also promote adherence of the

Figure 2 The Reflex wand design utilizes three electrodes to produce a long slender thermal lesion in addition to tissue removal at the tip. Coblation occurs between the active tip electrode and the central return electrode that will remove tissue when activated. At the same time the distal active electrode and return electrode generate a heat-based lesion between them. The end result is a core of tissue removed

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and a surrounding thermal lesion of about 4mm×12mm.

Figure 3 This artist’s drawing simulates the lesion created with the placement and activation of the Reflex 45 wand into the inferior turbinate. The wand creates a submucosal lesion while preserving the overlying mucosa., which minimizes the crusting after surgery. Typically, one to three lesions are placed in various positions within the inferior turbinate when using this wand. mucosa to the periosteum and reduce regional blood flow, limiting edema. In addition to decreased pain and the minimal invasiveness of coblation turbinoplasty, an advantage over traditional turbinectomy is that submucosal ablation spares the nasal epithelium, allowing preservation of mucociliary clearance. Numerous techniques have been described, and the number and placement of lesions can depend on the surgeon’s perception of the patient’s degree and level of obstruction. The wand most commonly used is the Reflex 45 wand. The threeelectrode design of the Reflex wand has been described previously and is expected to create a 4mm×12mm lesion with 10sec of activation at a single submucosal location of the wand as seen in Fig. 3. The wand is first inserted into the midanterior portion of the inferior turbinate, and two additional entries are performed medially. A Coblator setting of 4, corresponding to 168–

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182V, is used, and the wand is activated in place for 10sec. As the wand is removed, it is activated in coagulation mode to ensure hemostasis of the highly vascular turbinates. An alternative type of wand is the hummingbird wand, which has only two electrodes, and is designed to primarily perform coblation at the tip. This wand is inserted submucosally into the turbinate and slowly advanced while activated. The surgeon has the flexibility to create as long a submucosal lesion as is desired. The technique described by Lee et al. (15) then utilizes the coagulation mode while slowly removing the wand, thereby creating an area of further tissue destruction and hemostasis along the channel. This author uses endoscopic guidance and places six lesions over the entire turbinate. In a study of coblation turbinate reduction using the Reflex 45 wand with three lesions per turbinate, the most common complaints were pain and nasal discharge, both of which diminished by postoperative day 2 (16). Mucosal erosion, bleeding, adherent crust, and prolonged rhinorrhea, all of which result with laser or electrocautery procedures, did not develop in any of the patients. By postoperative day 1, patients reported subjectively decreased nasal obstruction, and no trend toward relapse was found over 12 months. Acoustic rhinometry confirmed a significant

Figure 4 The use of the Reflex 55 wand for palatoplasty requires a twostep procedure for each lesion. Initial insertion is done with activation of the wand into the tissue as shown in (a). The wand is then bluntly advanced into position within the palate and then activated to create a lesion as shown in (b). The wand can be used to bluntly dissect in several directions through a single puncture site to create several lesions in a local area. increase in nasal cavity volume, and rhinomanometry confirmed significant improvements in nasal airflow: improvement in these parameters did not diminish over

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12 months of follow-up. Measurement of saccharine transit time and olfactory thresholds verified no adverse effects on epithelial clearance time and olfactory function. Other investigators (17) have found similarly successful outcomes at 12 months. 3.2.2 Soft Palate Reduction In the soft palate, the goals of treatment for snoring are reduction, stiffening, and stabilization of the soft tissue. RFVR of the palate has advantages over traditional uvulopalatopharyngoplasty (UPPP), offering less postoperative pain and avoidance of the long-term side disability of swallowing, regurgitation, taste, smell, and voice found in 40–60% of UPPP recipients (18). However, as described by others, multiple

Figure 5 The insertion sites of a typical palatoplasty is illustrated by the gray circles. The wand is then advanced along the direction of the arrows to create the submucosal lesions. Traditionally, three lesions are used for each treatment.

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Figure 6 A more aggressive approach to palatoplasty is illustrated with three insertion sites and seven lesions placed. The two lesions placed laterally through the midline insertion just above the uvula, represented by the gray arrows, are reserved for patients with long extended palates with heavy tonsillar pillars. RF procedures are usually required before the goal of reduction in snoring is achieved. The Reflex 55 wand can be used to produce palatal lesions with a similar end result for the palate. Coblation treatment of the soft palate utilizes central and lateral channels. The Coblator device is set to 6, corresponding to 235V. The wand is inserted 1cm distal to the midline soft/hard palate junction while activating the wand, then advanced along the soft palate with blunt dissection only as in Fig. 4. The wand is then held in place while activating the coblation mode for 10sec. An additional, more distal, central channel is sometimes introduced just above the uvula. Two paramedian channels are also created with the same insertion site, but angled 45° to each side of the central channel in a similar fashion (Fig. 5). The ablated channels close over the next 24–48hr, and some scarring and stiffening develops in the following weeks. The total dwell time of the wand for this procedure may be as short as 45sec, markedly shorter than that required by other monopolar RFVR techniques. Given the short time needed to create each palatal submucosal lesion using coblation, the main limitation of this approach is the patient’s ability to tolerate pain, and the avoidance of palatal perforation with each treatment. At present our approach includes a series of seven lesions as outlined in Fig. 6. This has been well tolerated by patients and

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often requires retreatment. The overall efficacy and relapse rate using this more aggressive approach have not been determined. To compare coblation’s effectiveness and morbidity with those of other traditional snoring procedures, Back and associates conducted a study of habitual snorers without sleep apnea, who received two coblation palatoplasty procedures, a week apart. At 9.5 months’ follow-up, subjective snoring significantly improved in up to 63% of patients, and was successfully eliminated in 37%. These numbers compare favorably to somnoplasty: 58% and 22%, respectively (19). Coblation also produced significant improvement in daytime sleepiness at 9.5 months. Comparison of precoblation and postcoblation MR cephalometric imaging has demonstrated significant retraction of the uvula but no significant changes in other palatal or pharyngeal distances. T1-weighted signal intensity changes reflected fibroid scar formation in most cases, although these findings did not correlate with snoring improvement (20). In terms of the morbidity of coblation palatoplasty, Back et al. (20) in 2002 identified peak pain on the day of surgery, which disappeared within 3 days. Patients required a median of two doses of pain medication. Swelling sensation, speaking, and eating all returned to normal within 3–4 days. These data are similar to reports from somnoplasty. Complications of coblation palatoplasty include mucosal blanching and abscess formation at the insertion point of the wand, and palatal swelling. Back et al. reported minor superficial blanching in 20% of patients and small abscesses requiring antibiotics in 10% of patients. Palatal edema can usually be managed by sleeping with the head elevated, but significant edema requiring corticosteroids occurs in 2.5% of patients. Abscesses and edema are reported to occur at similar frequencies in somnoplasty (21, 22). In this same study, relapse occurred in 6% of patients in the 9-month follow-up period. Most scar tissue matures and softens after 12–18 months, making some relapses unavoidable with this technique. However, because of the high acceptance of retreatment in coblation, additional treatments may improve outcomes and keep patients happy with the technique overall. This has been noted in somnoplasty of the palate, where 80% of patients would agree to retreatment, with good outcomes resulting after retreatment (19). Follow-up of coblation treated patients for more than 9 months or the success of retreatment of relapsed patients has not yet been reported. 3.2.3 Tongue-Base Reduction In patients with obstructive sleep apnea, the use of coblation channeling using the Reflex 55 wand for RFVR of the base of tongue has been described (23). As in other coblation channeling procedures, the wand is inserted while ablating, held in place for 10–15sec, and removed while coagulating. No clinical studies of coblation for tongue-base reduction exist yet in the literature, although results are likely similar to somnoplasty. The Reflex wand creates a single lesion with each activation, but given the 10sec treatment time, multiple lesions can be quickly created. Kao et al. (24) have described the placement of up to eight lesions per treatment with the Somnus device, and a similar number of lesions are likely needed with the coblation wand. Because of the location of the base of the tongue, there is increased potential for abscess formation and airway

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narrowing from postoperative edema. All patients should therefore receive a 10-day course of antibiotics and a 5-day course of corticosteroids. 3.2.4 Tonsillar Reduction Using Coblation Channeling The use of coblation channeling for tonsillar hypertrophy has been described as an office procedure that may allow the reduction of tonsillar size with minimal morbidity in adult patients. The concept is similar to the somnoplasty tonsillar reduction, and utilizes coblation for submucosal destruction of tonsillar stroma, achieving size reduction of the tonsil through ablation and thermal tissue destruction. The preservation of the mucosal surface and the avoidance of injury beyond the tonsillar capsule limit the morbidity of the procedure. In a retrospective study, Friedman et al. compared this procedure to other tonsillar techniques and found that though the morbidity of the procedure was limited, the total reduction of tonsillar tissue was on average limited to 53.6% (25). It is unclear whether this level of tonsillar reduction has a clear indication for use, except for the limited number of patients with obstructive disease who cannot tolerate general anesthesia. Further study of these types of limited tonsillar reduction is needed before they can be recommended. 3.3 Coblation-Assisted Tissue Excision As previously described, the coblation process can aggressively remove tissue with minimal heat production. This surgical modality has been used to remove tissue layer by layer, or as a surgical dissection tool for precise excision of structures. In either case the wand removes tissue 2–3mm in advance of the tip, and even after 20sec of activation, tissue temperature remains below 60°C (2) (Fig. 7). Hemostasis of vessels less than 1mm in diameter is easily achieved using the coblation device at voltages of 125–175V. In practice, this facilitates the smooth separation of tissue with little thermal damage. The wands used for this type of surgery can provide electrocautery coagulation by activating the unit’s coagulation mode. 3.3.1 Tonsillectomy Tonsillectomy is the most common procedure performed for sleep disordered breathing, particularly in the pediatric patient. The use of coblation in otolaryngology has been most closely associated with tonsil surgery. However, a review of the literature can be confusing because coblation wands have been used to perform tonsillar surgery using three very different approaches. Tonsillar reduction using coblation channeling has been described in the previous section. The E-vac 70 wand has been used to perform a traditional total tonsillectomy using a subcapsular complete excision of the tonsils. A tonsillar capsule-sparing subtotal tonsillectomy technique has been described removing 90–95% of the tonsil using the same wand design.

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Figure 7 The E-vac 70 wand has the components of the new wand design. The electrodes are immersed in the saline media from the self-irrigation system and immediately suctioned away by the central suction port. The gas and tissue particles produced by the coblation process are evacuated by the suction port as well, maximizing visualization of the electrodes. Hemostasis with cautery also occurs between the active and passive electrodes and thus requires positioning of the wand edge over the bleeding site to be effective. Total Coblation-Assisted Tonsillectomy. Traditional total tonsillectomy procedures result in significant morbidity, including 7–10 days of postoperative pain (26), and possible infection, airway compromise from edema, and dehydration secondary to odynophagia. The severe pain is believed to result from damage to the sensory nerves and pharyngeal muscle spasm. In addition, there is a 1–3.5% incidence of late postoperative bleeding, which may require rehospitalization and return to the operating room to control. Patients lose an average of 7 days from work or school, and sometimes require hospitalization for dehydration or respiratory problems, in addition to bleeding (27). Given the morbidity of these procedures, investigators have searched for a less morbid approach to tonsillar disease. Tonsillectomy has traditionally been performed either with “hot” electrodissection or CO2 laser, or with “cold” instruments (knife, scissors,

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dissectors, or snare). Proponents of electrosurgery cite its faster excision time and minimal blood loss, while proponents of instrument dissection claim a less painful recovery due to lack of thermal injury to tissue. Coblation, a cold excision technique with hemostatic properties, may be an effective compromise. While in coblation mode, small vessels are sealed as the dissection takes place, and more aggressive hemostasis can be achieved with the same wand operating in cautery mode (Fig. 8). Despite this, coblation subcapsular tonsillectomy may occasionally require the use of suction electrocautery to achieve complete hemostasis, as larger-caliber blood vessels are exposed. The use of monopolar cautery is associated with more wound tissue injury, which likely translates into more pain and a longer recovery time. In using coblation for subcapsular total tonsillectomy, the initial dissection is similar to that in traditional approaches. An incision is made and blunt dissection is initiated to identify the tonsillar capsule. Identification of the capsule is critical, and with retraction of the tonsil medially, wide exposure expedites the procedure. The coblation wand is then used to dissect the capsule from the muscles in the tonsillar fossa. With moderate power setting and the ablative flat surface of the wand tip directed toward the tonsil capsule, dissection is continued toward the inferior pole.

Figure 8 Dissection using the coblation wand for total tonsillectomy. The wand active surface should be directed toward the tonsil during the dissection and applied with minimal pressure. The wand should be in constant steady motion, similar to the use of a contact laser. The lower the coblation and the slower the movement the more effective the hemostasis achieved by the plasma field.

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(Illustration courtesy of Arthrocare— ENT.) At the middle power settings the wand will preferentially excise the fibrous tissue under the capsule, relative to the tonsillar tissue. Thus, the speed of excision in the subcapsular plane will be rapid, but slows down if the excision is extended into the tonsillar tissue. The heat generated is minimal, but sufficient to fuse small blood vessels. The wand’s coagulation mode can be used if more significant bleeding is encountered. Occasionally, additional hemostatic measures may be needed to achieve definitive control of hemorrhage. Shah et al. (28) in 2002 conducted a controlled, prospective study comparing coblation to electrosurgery for total tonsillectomy in pediatric patients. Electrocautery for hemostasis was employed after excision in all patients. Coblation was associated with a significantly longer surgical time than electrosurgery: 23.8min for coblation as against 16.2min for monopolar electrosurgery. This has also been reported in adult studies (29,30). This increased time is attributed to the fact that coblation includes extra irrigation and tubing, and requires greater care during tonsillectomy to avoid lateral injury from the 2–3mm zone of ablation preceding the wand tip. Also of note is the fact that in infrequent cases of brisk bleeding, coblation is slower to achieve hemostasis. Nevertheless, estimated blood loss is equivalent in the two procedures. Coblation was noted to leave less gross eschar. Histopathologic evaluation of surgical specimens in this pediatric study demonstrated that coblation caused significantly less thermal injury to tissue: a depth of 0.13mm with coblation vs. 0.63mm with electrosurgery. Despite this histologic difference, no statistically significant improvement was noted in subjective pain, morphine consumption, recovery of diet, activity, or parental return to work. A similar controlled study in adults by Back et al. (30) in 2001 compared coblation to traditional cold dissection, and used monopolar electrocautery liberally for hemostasis in all patients. This study also failed to identify significant differences in subjective pain or swelling, analgesic use, or recovery of eating, drinking, or speaking. This lack of improvement in postoperative measures may be due to the fact that during and following coblation excision, conventional electrocautery was invariably used to achieve complete hemostasis. This may undo the benefits of cold ablation. In contrast, a prospective, controlled study of total tonsillectomy in a pediatric population conducted by Temple and Timms (31) in 2001 also compared coblation to electrosurgery. This study utilized minimal adjunctive electrocautery for hemostasis. In this case, the investigators did find improved outcome with coblation. The day of peak pain was postoperative day 1 in the coblation group and postoperative day 4 in the electrosurgery group. Coblation patients returned to normal diet after a mean 2.4 days, while electrosurgery patients required a mean 7.6 days. Timms and Temple (32) in 2002 performed a similar study with adults using each modality on one tonsil in each patient. Pain persisted for a mean 5 days with coblation and >9 days with conventional electrosurgery. Most coblation tonsils had healed within 9 days, whereas no tonsillar fossa healed completely after electrosurgery in the follow-up period. Other investigators have reported consistent results (29). In the Temple studies and the Back study, no differences in perioperative complications were found.

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These studies suggest that coblation is as safe and effective for tonsillectomy as traditional techniques. The postoperative morbidity seems to be significantly decreased unless conventional electrocautery is used extensively for hemostasis during the procedure. Further study using larger groups of patients is needed to better define the advantages of coblation for subcapsular, total tonsillectomy. Capsule-Sparing Subtotal Coblation-Assisted Tonsillectomy. In the setting of sleep disordered breathing, when the tonsils are obstructive due to marked lymphoid hypertrophy, subtotal tonsillectomy (sometimes called tonsillotomy) is believed to be a suitable alternative to complete tonsillectomy. The goal of subtotal tonsillectomy is to remove as much of the tonsillar tissue as possible without damaging the tonsillar capsule. By preserving the tonsillar capsule, the surgeon avoids the larger blood vessels and dissection into the pharyngeal muscles. This facilitates faster healing, with reduced constriction and scarring (33), and may decrease the incidence of post-operative bleeding. In subtotal tonsillectomy, using the highest power settings, the wand (E-vac 70) is brushed over the tonsillar surface, removing tissue layer by layer, as seen in Fig. 9. This motion is continued systematically until approximately 90% of the tonsil has been removed. Most bleeding points in the body of the tonsil can be ignored, and further coblation controls most small-caliber vessels. For the final 5%, the power setting is reduced and the residual tonsil is carefully palpated. Any significant segment of palpable tonsil is then treated further. Special care is required to minimize any contact with the tonsillar pillars or penetration through the capsule. This action results in more bleeding immediately, and may translate to increased morbidity after surgery. The coagulation mode can be used when bleeding is encountered, resulting in an operative field that is typically bloodless (Fig. 10). Electrocautery diathermy is rarely needed with this technique. Coblation for subtotal tonsillectomy should not be employed if there is a suspicion of a neoplasm in the tonsil, because tissue will not be available for pathology. Lee and McLaughlin (34) in 2001 presented an initial report comparing coblation subtotal tonsillectomy to electrosurgical total tonsillectomy, in cases of obstructive tonsillar hypertrophy. This study identified dramatic differences between the two procedures. Mean visual-analog scale pain scores were 2.2 and 4.7 in the two groups, respectively. Duration of postoperative analgesic use was 2.6 and 6.0 days. Mean time for return to normal activity was 1.4 and 10.8 days. Mean time to resumption of normal diet was 2.4 and 11.6 days, respectively. There were no complications such as postoperative bleeding, substantial intraoperative blood loss, or respiratory compromise in patients of either group.

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Figure 9 Capsule-sparing subtotal tonsillectomy requires brushing the tonsil surface with the wand active surface under the highest settings. Wand positioning should insure coverage of the electrode with the conductive media, saline, at all times to maximize efficiency of the coblation process. (Illustration courtesy of Arthrocare—ENT.)

Figure 10 The final appearance of the tonsillar fossa after capsule-sparing

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subtotal tonsillectomy. Some visible tonsillar remnants sit in each fossa with elimination of all crypts and pockets but preservation of the tonsillar pillars. (Illustration courtesy of Arthrocare—ENT.) Subsequently, Chan et al. (35) presented a prospective, double-blinded randomized study comparing coblation-assisted subtotal tonsillectomy and total tonsillectomy using electrocautery in 50 pediatric patients with obstructive tonsillar hypertrophy. In this study, the patients who received subtotal tonsillectomy with coblation reported statistically significant reduction in time to resolution of pain, the first day without pain medications, and days to normal diet. In the 90-day and 1-year follow-up data, no differences in presenting symptoms could be found. A large retrospective review of 528 patients who underwent coblation-assisted subtotal tonsillectomy revealed a low incidence of complication (36). There were three cases (0.6%) of intraoperative complications: two wand malfunctions and one incidental tongue burn, which required no further treatment. There were five cases (0.95%) of postoperative bleeding from the tonsillar bed, only one of which required hospitalization, and a 0.6% incidence of dehydration necessitating hospitalization. Coblation for subtotal tonsillectomy therefore appears to offer a lower incidence of complications than traditional tonsillectomy. The study data at this time suggest that capsule-sparing subtotal tonsillectomy using coblation may be an approach that markedly reduces the morbidity of tonsillar surgery by both reducing pain after surgery and expediting recovery, while also reducing the incidence of posttonsillectomy hemorrhage. For tonsillar hypertrophy, no significant difference has been found with respect to control of obstructive symptoms up to 1 year later. Further long-term differences when compared to subcapsular total tonsillectomy need to reviewed over a longer time frame. The potential role for a capsule-sparing subtotal tonsillectomy in patients with recurrent tonsillar infections also needs to be formally studied. 3.3.2 Uvulopalatopharyngoplasty The most well known procedure for surgical management of sleep disordered breathing in the adult continues to be UPPP. However, with the limited success rate reported in the otolaryngologic literature, and the known postoperative morbidity, surgeons have become more critical in patient selection. Given the availability of techniques to reduce the morbidity of surgery for obstructive tonsillar hypertrophy, individuals with very large tonsils and more normally sized palate and uvula may benefit from tonsillectomy alone (37). Alternatively, these same coblation techniques can be applied to UPPP in addition to tonsillectomy, with a similar expectation of reduced postoperative morbidity. Coblation for total tonsillectomy, followed by the use of the same wand for excision of the palatal edge and uvula, can be easily performed. The resultant wound has minimal eschar and blanching of the mucosal edges. Closure of the coblation UPPP should be

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achieved in the same manner as UPPP using conventional electrocautery. Coblation offers rapid tissue excision with some hemostasis and minimal tissue damage in the resultant wound. There are no published reports in the literature concerning the use of coblation for UPPP.

4. CONCLUSION Coblation employs a cold plasma field to dissociate molecular bonds, thus ablating soft tissue without significant thermal injury. Coblation wand design determines the surgical characteristics of the process and thus gives the surgeon a flexible surgical modality that can be adapted to many situations. The wands may be used for submucosal channeling, which volumetrically reduces tissue, or for outright excision of tissue structures. Coblation has been studied in reduction of the turbinates, soft palate, and base of tongue, in UPPP, and in total or subtotal tonsillectomy. In these procedures, coblation appears to be safe and effective, and achieves outcomes comparable with traditional techniques, while in many cases causing less pain, and permitting faster return to normal activity. Further study is needed to fully understand the impact of this unique modality on the efficacy and safety of these procedures as well as to appreciate the other potential uses of this technology.

REFERENCES 1. Tucker RD, Platz CE, Landas SK. Histologic characteristics of electrosurgical injuries. J Am Assoc Gynecol Laparosc 1997; 4(2):201–206. 2. Woloszko J, Gilbride C. Coblation technology: plasma mediated ablation for otolaryngology applications. In: Anderson R, Bartels KE, Bass LS, eds. Proceedings of the SPIE. Lasers in Surgery: Advanced Characterization, Therapeutics and Systems X. 3097. Bellingham, WA: SPIE The International Society for Optical Engineering, 2000; 306–316. 3. Stalder KR, Woloszko J, Brown IG, Smith CD. Repetitive Plasma Discharges in Saline Solutions. Sunnyvale, CA: Arthrocare Corp, 1997. 4. Lubatschowski H, Kermani O, Otten C, Haller A, Schmiedt KC, Ertmer W. Ar-F excimer laser induced secondary radiation in photoablation of biological tissue. Lasers Surg Med 1994; 14(2):168–177. 5. Ishihara M. Measurement of the surface temperature of the cornea during ArF excimer laser ablation by thermal radiometry with a 15-nanosecond time response. Lasers Surg Med 2002; 30(1):54–59. 6. Hecht P, Hayashi K, Cooley AJ. The thermal effect of monopolar radiofrequency energy on the properties of joint capsule: an in vivo histologic study using a sheep model. Am J Sports Med 1998; 26:808–814. 7. Chen SS, Wright NT, Humphrey JD. Heat-induced changes in the mechanics of a collagenous tissue: isothermal, isotonic shrinkage. J Biomech Eng 1998; 120:382–388. 8. Rice D, Eggers P, Thapliyal H. Coblation: a novel method for head and neck soft tissue management. Res Outcomes Otorhinolaryngol 1999; 1(2):1–5. 9. Chinpairoj S, Feldman MD, Saunders JC, Thaler ER. A comparison of monopolar electrosurgery to a new multipolar electrosurgical system in a rat model. Laryngoscope 2001; 111(2):213–217.

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10. Kaplan L, Uribe JW, Saskin H, Markarian G. The viability of articular cartilage following radiofrequency generated energy treatment. J Arthros Relat Surg 1999; 15(5):569–570. 11. Eggers PE, Thapliyal HV, Matthews LS. Coblation: a newly described method for soft tissue surgery. Res Outcome Arth Surg 1997; 2:1–4. 12. Bortnick DP. Coblation: an emerging technology and new technique for soft-tissue surgery. Plast Reconstructr Surg 2000; 107(2):614–615. 13. Mancini PF. Coblation: a new technology and technique for skin resurfacing and other aesthetic surgical procedures. Aesthetic Plast Surg 2001; 25:372–377. 14. Arthrocare Corp. AccENT Head and Neck Electrosurgery System Indications Statement. Sunnyvale, CA: Arthrocare Corp, 1997. 15. Lee KC, Hwang PH, Kingdom TT. Surgical management of the inferior turbinate hypertrophy in the office: three mucosal sparing techniques. Oper Tech Otolaryngol Head Neck Surg 2001; 12(2):107–111. 16. Back LJJ, Hytonen ML, Malmberg HO, Ylikoski JS. Submucosal bipolar radiofrequency thermal ablation of inferior turbinates: a long-term followup with subjective and objective assessment. Laryngoscope 2002; 112(10):1806–1812. 17. Elwany S, Gaimaee R, Fattah HA. Radiofrequency bipolar submucosal diathermy of the inferior turbinates. Am J Rhinol 1999; 13(2):145–149. 18. Hagert B, Wikblad K, Odkvist L, Wahren LK. Side effects after surgical treatment of snoring. ORL J Otorhinolaryngol Relat Spec 2000; 62:76–80. 19. Trotter MI, D’Souza AR, Morgan DW. Medium term outcome of palatal surgery for snoring using the Somnus unit. J Laryngol Otol 2002; 116:116–118. 20. Back LJJ, Tervahartiala PO, Piilonen AK, Partinen MM, Ylikoski JS. Bipolar radiofrequency thermal ablation of the soft palate in habitual snorers without significant desaturations assessed by magnetic resonance imaging. Am J Respir Crit Care Med 2002; 166:865–871. 21. Powell NB, Riley RW, Troell RJ, Li K, Blumen MB, Guilleminault C. Radiofrequency volumetric tissue reduction of the palate in subjects with sleep-disordered breathing. Chest 1998; 113(5):1163–1171. 22. Sher AE, Flexon PB, Hillman D, Emery B, Swieca J, Smith TL, Cartwright R, Dierks E, Nelson L. Temperature-controlled radiofrequency tissue volume reduction in the human soft palate. Otolaryngol Head Neck Surg 2001; 125(4):312–318. 23. Senders C. The Macroscopic and Microscopic Effects of Radiofrequency Injury in the Porcine Tongue Treated with Radiofrequency Ablation. Nashville, TN: Triologic Society Presentation, 2003. 24. Kao YH, Shnayder Y, Lee KC. The efficacy of anatomically based multiple-level surgery for obstructive sleep apnea. Otolaryngol Head Neck Surg. In press. 25. Friedman M, LoSavio P, Ibrahim H, Ramakrishnam V. Radiofrequency tonsil reduction: safety, morbidity, and efficacy. Laryngoscope 2003; 113:882–887. 26. Blomgren K, Qvamberg YH, Valtonen HJ. A prospective study on the pros and cons of electrodissection tonsillectomy. Laryngoscope 2001; 111:478–482. 27. Nelson LM. Radiofrequency treatment for obstructive tonsillar hypertrophy. Arch Otolaryngol Head Neck Surg 2000; 126(6):736–740. 28. Shah UK, Galinkin J, Chiavacci R, Briggs M. Tonsillectomy by means of plasmamediated ablation. Arch Otolaryngol Head Neck Surg 2002; 128:672–676. 29. Hall DJ, Littlefield PD, Birkmirc-Peters DP, Holtel MR. Radiofrequency ablation versus electrocautery in tonsillectomy. Presented at Pacific Coast Otolaryngology and Ophthalmology Society Meeting, 2001. 30. Back L, Paloheimo M, Ylikoski J. Traditional tonsillectomy compared with bipolar radiofrequency thermal ablation tonsillectomy in adults: a pilot study. Arch Otolaryngol Head Neck Surg 2001; 127(9): 1106–1112. 31. Temple RH, Timms MS. Paediatric coblation tonsillectomy. Int J Ped Otorhinolaryngol 2001; 61:195–198.

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32. Timms MS, Temple RH. Coblation tonsillectomy: a double blind randomized controlled study. J Laryngol Otol 2002; 116:450–452. 33. Roure RM, Lee KC, Bernstein JM. Complete excision versus tonsil ablation for surgical management of tonsillar disease. Curr Opin Otolaryngol Head Neck Surg 2002; 10: 185–187. 34. Lee KC, McLaughlin LAH. Subtotal tonsillar ablation using coblation for tonsillar hypertrophy. Presented at the Eastern Section Meeting of the American Triological Society, 2001. 35. Chan KH, Friedman NR, Allen GC, Yarenchuck K, Wirtschaffer A, Bikazi N, Bernstein JM, Lee KC. Treatment of tonsillar hypertrophy by subtotal tonsillectomy using ionized field ablation: a randomized multi-center trial. Presented at ASPO, Nashville, TN, 2003. 36. Lee KC, Altenau MM, Barnes DR, Bernstein JM, Bikhazi NB, Brettscheider FA, Caplan CH, Ditkowsky WA, Ingber CF, McLaughlin LAH, Moghaddassi MH. Incidence of complications for subtotal ionized field ablation of the tonsils. Otolaryngol Head Neck Surg 2002; 127(6):531– 538. 37. Verse T, Kroker BA, Pirsig W, Brosch S. Tonsillectomy as a treatment of obstructive sleep apnea in adults with tonsillar hypertrophy. Laryngoscope 2000; 110(9):1556–1559.

19 Cautery-Assisted Palatal Stiffening Operation Eric A.Mair Department of Otolaryngology, Wilford Hall USAF Medical Center, San Antonio, Texas, U.S.A.

Cautery-assisted palatal stiffening operation (CAPSO) is a single office-based surgical procedure that treats both snoring and obstructive sleep apnea syndrome (OSAS) at the level of the soft palate. CAPSO uses standard electrocautery to remove an oral mucosal strip from the midline soft palate. The wound heals by secondary intention inducing a scar that stiffens the floppy palate. It is a safe, simple, and cost-effective procedure with comparable success rates to other palatal surgeries that treat primary palatal snoring or OSAS (1–3).

1. PATIENT SELECTION Those who suffer from snoring at the level of the soft palate after nonsurgical methods have failed will benefit most from CAPSO. The patient is encouraged to bring their sleeping partner to the initial evaluation where a thorough interview and examination is performed. The nasal cavity, nasopharynx, oropharynx, hypopharynx, and larynx are viewed with fiberoptic nasopharyngolaryngoscopy (NPL) while the patients approximate the snoring sound in the presence of their sleeping partner, or an audio tape of their snoring if no sleeping partner is available. Only patients with significant awake voluntary palatal flutter at the level of the soft palate as evidenced by NPL or acoustic polysomnography (e.g., SNAP test) are considered for CAPSO. Exclusion criteria include uncontrolled hypothyroidism or considerable obstruction at other sites on NPL, 3–4+ tonsillar hypertrophy, notable nasal polyposis or septal deviation, or significant hypopharyngeal collapse without palatal flutter. Patients with documented OSAS are asked to quantify subjective symptoms of sleepiness via the Epworth Sleepiness Scale (ESS) before the procedure (3). This is in addition to objective measures of OSAS via polysomnography.

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Figure 1 (a) Pre-operative view. There is an elongated soft palate without evidence of tonsillar hypertrophy or a submucous cleft palate. Voluntary palatal flutter is seen on office nasopharyngolaryngoscopy. (b) Topical anesthesia. The 14% benzocaine “gargle and spit” is sprayed on the palate. It provides excellent topical anesthesia along with a benzocaine gel “lollipop.” (c) Local anesthesia. About 5mL of lidocaine with epinephrine is injected submucosally into the central soft palate. (d) Dissection outline. An inverted “U” is mapped with cautery over the midline soft palate after injection with local anesthesia. Electrocautery is set on a blend of cut and coagulate to outline the mucosal dissection. Instrumentation is simple: cautery, tongue blade, suction, and forceps. (e) Mucosal elevation. A 2-cm central soft palatal mucosal flap is developed. Flap elevation begins on the soft palate 1cm from the junction of the hard and soft palate and is easily dissected down to the uvula. The midline soft palatal mucosa is easily peeled down after identifying the mucosa-muscle plane. (f) Identify uvular ridge. The mucosal uvula is gently elevated, and the muscular uvular ridge is identified on the nasal surface of the uvula. (g) Uvular dissection. A smaller inverted “U” incision is made to dissect the mucosa off the muscular uvular ridge. A significant portion of the uvula may

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consist of mucosa. The muscle remains intact. Cauterization of the midline mucosa on the nasal surface of the uvula will enhance the stiffening effect. (h) Completion. The mucosal specimen is dissected free, and the central palatal muscle (palatopharyngeus and muscularis uvulae) remain intact. (i) Palatal stiffening. By 1 month after surgery, the soft palate is stiffened with a midline palatal scar. Snoring is either eliminated or greatly reduced. Voluntary palatal flutter is no longer seen on examination. 2. PROCEDURAL TECHNIQUE CAPSO is a 10-min surgical procedure performed in the otolaryngology clinic with the patient sitting in the examination chair. The soft palate is examined with the mouth comfortably open (Fig. 1a). Topical anesthesia is first administered with 14% benzocaine (Cetylite Inc., Pennsauken, NJ) oral spray (Fig. 1b) followed by a benzocaine gel “lollipop” (200mg/g gel; Henry Schein, Port Washington, NY) applied on the end of a tongue depressor. The “lollipop” is held against the soft palate for 5 minutes. Next, a 27gauge needle is used to inject 5mL of 2% lidocaine with 1:100,000 units of epinephrine submucosally in the midline soft palate extending 1cm laterally on each side (Fig. 1c). The cautery is set to a blend of cut and coagulate (“Blend 3” on Valleylab electrosurgical generator, Boulder, CO). This mode provides optimal hemostasis while minimizing excessive postoperative pain and thermal injury. A tonsil suction evacuates cautery smoke. A sheathed needle-tip cautery outlines an inverted “U” on the soft palate. The outlined points are then connected with the cautery (Fig. 1d). A 2-cm strip of midline soft palate mucosa is developed staying 1cm distal to the hard/soft palate junction (Fig. 1e). The mucosal strip is peeled off the palatopharyngeal muscle toward the uvula. The uvula is lifted (Fig. 1f) and the mucosal uvulae are dissected off the muscular uvulae (Fig. 1g). The wound is left to heal by secondary intention (Fig. 1h). The patient is observed after the procedure for 10min and then sent home. Resected palatal mucosa may be examined by means of routine histology. One month after the procedure, a midline palpable scar is noted and the palatal snoring is successfully treated (Fig. 1i).

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3. SUBSEQUENT MANAGEMENT The patient leaves the office with a 2cm midline soft palate mucosal defect and exposed palatopharyngeus muscle (Fig. 2a). After 2 days, a white fibrinous exudate

Figure 2 (a) CAPSO post-operative follow-up: immediately after removal of the soft palate mucosa. Exposed

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palatal muscle is present. Hemostasis is assured with cautery. (b) CAPSO post-operative follow-up: after 2 days, a white fibrinous debris forms over the muscle resembling the posttonsillectomy fossae. The patient usually experiences discomfort as long as the white debris is in place. (c) CAPSO post-operative follow-up: after 3–5 days, peripheral granulation is prominent and the wound actually widens. (d) CAPSO post-operative follow-up: by 7–9days postoperatively, the white fibrinous debris is totally replaced by red granulation tissue. The wound now starts contracting. (e) CAPSO post-operative follow-up: the palate has remucosalized by 11–13 days after surgery. By this time, the patient is in no discomfort; however, snoring may still persist. (f) CAPSO post-operative follow-up: by 4 weeks after surgery, the palate appears healed, contracted, and stiffened. Palatal snoring is no longer a problem. (g) CAPSO postoperative follow-up: over 2 years after surgery, the soft palate remains stiffened with prominent muscularis uvulae. (See color insert.) forms over the exposed muscle (Fig. 2b) resembling the tonsillar fossae 2 days after tonsillectomy. By post-operative days 3–5, red granulation tissue begins to replace the white fibrinous debris (Fig. 2c). By post-operative days 7–9, the fibrinous debris is totally replaced by granulation tissue, and the wound begins to contract (Fig. 2d). By 11–13 days after surgery, the palate is remucosalized and any patient discomfort is gone (Fig. 2e). By 1 month after surgery, the palate is notably stiffened and the snoring and voluntary awake palatal flutter are greatly diminished (Fig. 2f). The palate remains stiffened with a palpable midline scar and a prominent muscularis uvulae (Fig. 2g).

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Pain is notable on post-operative days 3–10, peaking on days 5–7 after the surgery. Topical aspirin oral rinses (325mg, 80–100 tablets dissolved in 1 L of water, 5–10mL swish and spit every 30min as necessary) provide significant relief without appreciable systemic absorption or bleeding. Additional pain management includes cool mist vaporizers to moisten the palate during nighttime, anesthetic lozenges, and acetaminophen with or without codeine. Prophylactic acyclovir (Zovirax 400mg by mouth twice daily) is prescribed in patients with a history of oral aphthous ulcers. No steroids or antibiotics are given because these medications may diminish the desired palatal scarring. The patient follows up at 4–6 weeks post-surgery, allowing sufficient time for palatal stiffening to take place. In addition, the OSAS patient is given a postsurgical ESS and polysomnogram to quantify the improvement of their OSAS.

4. POSSIBLE COMPLICATIONS The great majority of the patients that we have treated at our institution have had no major complications. Most describe thickened mucus and a “scratchy” palate during the first 3 weeks after the procedure. In our initial study of 206 people undergoing CAPSO for the treatment of primary palatal snoring, 10% of patients experienced asymptomatic tiny vesicles at the surgical site for up to 2 months after the surgery. The vesicles were most likely minor salivary gland pseudocysts and resolved as the palatal scar matured. Four percent of patients had prolonged throat pain that resolved beyond 10 days. A total of 1.5% of patients reported temporary xerostomia and taste changes. Less than 1% had temporary velopharyngeal incompetence or bleeding. There were no reported cases of voice change, wound infection, or nasopharyngeal stenosis (2).

5. DISCUSSION Stiffening the soft palate to diminish extensive snoring is not a new idea. As early as 1852, surgeons from the UK performed midline intrapalatine resection of the soft palate mucosa and muscle with primary closure to achieve tightening of the soft palate (Fig. 3). In 1943, Strauss described a palatal “flutter ratio” and proposed placing a scar along the soft palate to stiffen the floppy palate (4). More recently, Ellis et al. (5) demonstrated successful early results in treating snoring by stripping off the midline soft palate with a laser on patients under general anesthesia. We modified these concepts by devising an office procedure requiring routine electrocautery instead of a laser. The laser is a precision instrument used to minimize scar; electrocautery promotes scarring to stiffen the floppy palate. CAPSO is a simple, econom- ical, and safe palatal stiffening procedure performed as a single outpatient clinic visit while under local anesthesia. The electrocautery procedure does not require expensive, cumbersome, and potentially hazardous laser equipment with multiple staging procedures.

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Figure 3 Palatal stiffening for snoring is not a new idea. This 1852 London surgical print depicts central intrapalatine excision of muscle and mucosa to tighten the soft palate and prevent snoring. Costs vary between institutions, but our experience shows CAPSO to cost about $150 (1,2). This makes CAPSO about 10 times less expensive than complete treatment of snoring with laser-assisted uvulopalatoplasty (LAUP) or radiofrequency ablation (RFA), and 70 times less expensive than uvulopalatopharyngoplasty (UPPP) with an overnight monitored hospital stay (1). CAPSO is as effective as UPPP or LAUP in the short- and long-term treatment of palatal snoring and as effective as UPPP or LAUP in the management of OSAS (1–3). CAPSO has a 48% success rate of decreasing apnea-hypopnea index (AHI) by >50% which correlates to an overall 52.8% success rate of UPPP found on metaanalysis. CAPSO has a 48% success rate of decreasing AHI by >50% with a final AHI <20, which corresponds favorably with the 40.7% success rate of UPPP (6). Similarly, in early

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studies, LAUP decreased the AHI by 50% in about 50% of patients (7–9). However, more recent studies tend to show treatment response to LAUP to be variable and unpredictable with up to 30% of patients having a worse AHI after LAUP (10). The American Sleep Disorders Association subsequently has not recommended LAUP for the treatment of OSA (11). Unfortunately, long-term data for the treatment of OSA by palatal surgery (UPPP, LAUP, RFA, injection snoreplasty, and CAPSO) is unflattering in many studies (1,12). CPAP is the treatment of choice for OSA, yet poor patient acceptance and compliance remain problematic. Palatal surgical options are warranted in carefully chosen patients. CAPSO is a single office procedure that does not rely upon expensive laser systems or generators and handpieces. Revisions are rare. In 4 years, less than 1% of over 500 patients that we have treated with CAPSO required repeat surgery (2). LAUP commonly requires multiple painful staged procedures. In our practice, many patients refuse more than one LAUP secondary to pain. RFA, although less painful than CAPSO, requires multiple procedures and is notably more expensive than CAPSO. CAPSO success rates are comparable to other palatal surgeries.

REFERENCES 1. Littlefield PD, Mair EA. Snoring surgery: which one is best for you? Ear Nose Throat J 1999; 78:861–868. 2. Mair EA, Day RH. Cautery-assisted palatal stiffening operation. Otolaryngol Head Neck Surg 2000; 122:547–556. 3. Wassmuth Z, Mair EA, Loube D, Leonard D. Cautery-assisted palatal stiffening operation for the treatment of obstructive sleep apnea syndrome. Otolaryngol Head Neck Surg 2000; 123:55–60. 4. Strauss JF. A new approach to the treatment of snoring. Arch Otolaryngol 1943; 38:225–229. 5. Ellis PD, Willians JE, Shneerson JM. Surgical relief of snoring due to palatal flutter: a preliminary report. Ann R Coll Surg Engl 1993; 75:286–290. 6. Sher A, Schechtman K, Piccirillo J. The efficacy of surgical modifications of the upper airway in adults with obstructive sleep apnea sundrome. Sleep 1996; 19:156–177. 7. Maisel R, Antonelli P, Iber C, et al. Uvulopalatopharyngoplasty for obstructive sleep apnea: a community’s experience. Laryngoscope 1992; 102:604–607. 8. Walker R, Grigg-Damberger M, Gopalsami C, Totten M. Laser-assisted uvulopalatoplasty for snoring and obstructive sleep apnea: results in 170 patients. Laryngoscope 1995; 105:938–943. 9. Mickelson S. Laser-assisted uvulopalatoplasty for obstructive sleep apnea. Laryngoscope 1996; 106:10–13. 10. Ryan CF, Love LL. Unpredictable results of laser assisted uvulopalatoplasty in the treatment of obstructive sleep apnoea. Thorax 2000; 55:399–404. 11. Verse T, Pirsig W. Meta-analysis of laser-assisted uvulopalatopharyngoplasty. Laryngorhinootologie 2000; 79:272–284. 12. Brietzke SE, Mair EA. Injection snoreplasty: extended follow-up and new objective data. Otolaryngol Head Neck Surg 2003; 128:605–615.

20 Transpalatal Advancement Pharyngoplasty B.Tucker Woodson Department of Otolaryngology and Communication Sciences, Medical College of Wisconsin, Milwaukee, Wisconsin, U.S.A.

Successful outcomes for pharyngeal surgeries to treat obstructive sleep apnea continue to be inadequate. Surgical procedures have the goal of enlarging the upper pharyngeal airway, removing redundant and obstructive tissues, and decreasing collapsibility. It is the goal of this chapter to describe a technique of pharyngoplasty using transpalatal advancement and the rationale for a modified approach. The pharynx and palate have historically been the major focus for the surgical treatment of obstructive sleep apnea (OSA) and snoring. Uvulopalatopharyngoplasty (UPPP), described by Fujita et al. (1), was the first specific procedure to reconstruct the upper airway for surgical treatment of OSA. The UPPP was based on Ikematsu’s pharyngoplasty developed to treat snoring and which predated the description of OSA. This procedure separately modified the uvula, palate, and pharynx (2). Initial case series review of UPPP suggested a high success rate of these procedures, yet subsequent series have demonstrated decreased success rates using more stringent criteria in non-selected patients. A meta-analysis by Sher et al. (3), demonstrated UPPP had a 40% overall success rate. Although both Ikematsu and Fujita identified and tried to correct structural changes associated with sleep apnea and snoring, the UPPP has not predictably corrected the problems. Attempts to improve palatopharyngoplasty success rates have included modifications in both technique and patient selection. Technical modifications have included aggressive palatal excision, techniques of pillar advancement, modification of lateral wall, and application of new technologies such as laser and radiofrequency (4–6). Unfortunately, none have been accepted as demonstrating substantially higher success rates than the original UPPP. An alternative to improve UPPP success has also included combining UPPP with other surgical procedures. Multilevel surgeries likely improve UPPP success rates where more than one level is obstructive, however, multilevel upper airway surgeries have been slow to be applied to a wide population with only a small subgroup willing to accept the perceived morbidity with these surgeries (7). Identifying favorable candidates and eliminating potential failures are attractive alternatives, which could theoretically increase success. Assumptions that failure occurs due to obstructions at non-palatal sites has focused this strategy on identifying patients with lower pharyngeal obstruction. Methods have included using endoscopy, manometry, and physical exam (8–10). No widely available method has yet prospectively demonstrated any significant benefit. Most UPPP predictors have identified failures without markedly improving success rates (11). Studies suggest that certain subgroups do

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poorly with UPPP. Subjects who demonstrate endoscopic obstruction at the tongue base with Mueller’s maneuver or who have on physical exam small tonsils and an unfavorable Mallampati score may demonstrate a UPPP success rate of 10% or less (10,11). Inconsistent outcomes of all types of palatopharyngoplasty for OSA continue to frustrate and hamper attempts to surgically treat the disease. Much attention has been directed at the proximate outcome of clinical failure such as the polysomnogram. This is despite the dilemma that the ultimate causes of how the procedure alters the upper airway to explain failure and success have yet to be adequately explained. Inadequate objective data exist on structural effects of UPPP to guide treatment. Without this knowledge, attempts to improve the procedure are rudderless. Historically, surgical snoring procedures have subsequently been extended and applied to treat OSA. Although physiologically related, snoring and apnea differ potentially explaining why snoring procedures fail to adequately treat OSA. Snoring is noise, turbulence, oscillation, and flutter. These result from partial airway obstruction and from exposure to alternating collapsing and dilating forces. Changing airway compliance and stiffness may improve the noise characteristics, flutter, and oscillation characteristics of the upper airway; however, these may not fundamentally alter the abnormalities of OSA, which are predominantly airflow limitation and airway obstruction. What can be done to address OSA? It is known that the sites and levels of obstruction in sleep apnea vary but occur in the soft tissue pharynx. The site of obstruction varies depending on sleep state and body position. However, endoscopy, manometry, and other methods of airway imaging all consistently identify the retropalatal airway segment as a primary location of obstruction during sleep (12,13). Data studying UPPP failures have consistently identified that abnormal narrowing often persists at this site following conventional palatopharyngoplasty (Fig. 1). Using manometry, the primary site of initial obstruction in UPPP failures continues to be localized in 80% of subjects to the upper pharynx (14,15). Computerized tomography before and after UPPP identified that patients with successful UPPP differed from non-successful UPPP only the difference in enlargement in the retropalatal airway in the former but not the latter (Fig. 2) (16). These data suggest that part of the explanation of UPPP failure is technical failure of the procedure at the retropalatal level of the airway. To address this failure, a different approach is required. Transpalatal advancement pharyngoplasty was developed to increase the size of the upper oropharynx by advancing the soft palate anteriorly (17). Transpalatal advancement pharyngoplasty removes the posterior portion of the maxilla to advance the soft palate (Fig. 3). This pulls the soft palate forward. Conceptually, similarities exist to maxillary advancement where the entire maxilla including dentition is moved anteriorly. Potential advantages of this are that palatal advancement does not require either more aggressive surgical excision of the velopharyngeal port or movement of dentition. During the procedure, palatine bone is removed, the soft palate is mobilized, and soft tissues are advanced into the defect. Compared to UPPP, significant increases in cross sectional area and decreases in pharyngeal collapsibility have been observed (18,19).

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Figure 1 A midsagittal magnetic resonance image of the pharyngeal airway before and after uvulopalatopharyngoplasty. Although the palate is clearly shortened following the procedure, anterior posterior airway size is not significantly changed. (Adapted from Schwab R.J., Goldberg A.N,: Upper airway assessment: radiography and other imaging techniques. Octalatyngol Clin North Am 1998; 31(6):931–968). 1. PATIENT SELECTION Patient selection for transpalatal advancement pharyngoplasty continues to evolve as more is learned about OSA and the airway. Multiple elements of clinical exam, anatomy, disease severity, and patient preferences must be factored into the decision of which palatal procedure to utilize for a given patient. Clinical factors that need to be considered include causes of treatment failure, swallowing function, and severity of disease. Most patients who undergo surgery for OSA are medical treatment failures. Defining ineffective medical treatment is beyond the scope of this chapter but occurs when treatment fails to achieve adequate adherence or symptomatic benefit despite

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Figure 2 Cross-sectional area following uvulopalatopharyngoplasty is shown before and after treatment in successful responders (red) and failures (blue). Cross sectional area (cm2) is shown as it relates to distance from the hard palate. Patients with successful uvulopalatopharyngoplasty significantly increased cross-sectional area in the region adjacent to the hard palate. Velopharyngeal airway size was different in the successful versus failure groups not tongue base size. (Adapted from Ref. 16.)

Figure 3 The concept of palatal advancement pharyngoplasty is

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depicted. Traditional UPPP would resect palatal length (spickled left). With palatal advancement, the posterior hard palate is removed (hatched left). The palate is then pulled forward enlarging the airway (right). appropriate intervention. Given that even limited pharyngeal surgeries pose a risk to patients, efforts at medical therapy are appropriate. Identifying and correcting nasal continuous positive airway pressure (CPAP) failure as well as attempts at controlling known risk factors such as weight loss may be needed. Swallowing is potentially at risk with all pharyngeal surgeries. Since patients who have abnormalities postoperatively may have some evidence of abnormalities preoperatively, preexisting swallowing dysfunction should be identified. Endoscopy should demonstrate adequate lateral pharyngeal wall movement with swallow. Despite concerns about creating swallowing dysfunction, dysphagia or velopharyngeal incompetence is rarely associated with surgeries that advance the palate. Maxillomandibular advancement (MMA) surgery, which creates significant advancement, has been demonstrated to have a small risk of causing swallowing abnormalities even following UPPP (20). Severity of sleep apnea may impact the clinical selection of patients. Patients treated with maxillofacial surgery may rarely have disruption of the greater palatine vessels during maxillary surgery, which may result in poor healing or even theoretically necrosis of the maxilla. If collateral blood supply from the attached soft tissues is disrupted such as with palatal advancement pharyngoplasty, chances of this complication are potentially increased. For this reason if maxillofacial surgery is a likely option, this potential risk should be discussed with the patient. It should be noted that the risk of palatal necrosis or dysfunction is theoretical only. In a small number of patients where palatal advancement has been performed in combination with maxillofacial surgery (and even UPPP), no major complications have occurred. Since scar tissue formation on the distal palate is minimal with palatal advancement, snoring may not be affected to the same degree as following UPPP or laser-assisted palataopharyngoplasty. Ancillary snoring procedures such as radio-frequency may be required post-operatively. The procedure should not be advocated for primary snoring. Contraindications for palatal advancement continue to evolve, but may include a cleft palate, known swallowing dysfunction, or impaired healing of the soft or hard palate such as following radiation therapy. Anatomical or structural findings of patients who may be considered for the procedure may include prior uvulopalatopharyngoplasty/laser-assisted uvulopalatoplasty (UPPP/LAUP) failure with persistent retropalatal airway obstruction, a narrow nasopharyngeal airway superior to the proposed line of resection with traditional UPPP, or retropalatal/nasopharyngeal obstruction (such as superiorly located adenoid in a patient with obstructive lateral wall hypertrophy) that cannot be approached or visualized transorally or endoscopically.

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Poor candidates for palatal advancement may include those with severe OSA having a high likelihood of MMA as a second stage procedure, significant retropalatal airway lateral wall bulge, poor pharyngeal lateral wall movement, other pharyngeal swallowing problems, and cleft or submucosal cleft palate. Since the palatal flap is dependent on random blood supply, prior tissue ablation of the base of the flap using sclerotherapy or radiofrequency may increase risk of flap necrosis.

2. SURGICAL TECHNIQUE Palatal advancement pharyngoplasty is an evolving technique and has been modified since initially described with changes in methods of flap mobilization and suture placement (Fig. 4). Ongoing refinements will continue. The procedure is performed under general anesthesia delivered oroendotracheally. Patients are placed supine in the Rose position, and operative exposure is obtained with a Dingman mouth gag (Pilling Instrument Co., Philadelphia, PA). The Dingman mouth gag facilitates handling of multiple sutures during closure. All patients are administered perioperative antibiotics (Ancef 1–2g and Flagyl 500mg) and dexamethasone 10mg. For hemostasis, 1% lidocaine with 1:100,000 epinephrine is infiltrated into the greater palatine foramen and the incision sites prior to the procedure. This includes the junction of the hard and soft palate, the tissues over the hamulus and lateral soft palate,

Figure 4 Diagrammatic procedure of transpalatal advancement pharyngoplasty. (A) The gothic arch incision is outlined medial to the greater palatine foramen and flared

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laterally over the hamulus. (B) Flap elevated. Dotted line depicts the osteotomy to separate the hard and soft palate. (C) The soft and hard palates are separated exposing nasopharynx. The osteotomy is separated from the posterior nasal septum (not shown). (D) The posterior hard palate is removed, and palatal drill holes are placed. The tensor tendon is incised laterally. (E) The soft palate is advanced with permanent anterior and lateral sutures. (F) The flap is advanced into the “T” and closed with multiple interrupted sutures. and the line of incision of the mucosal flap over the hard palate. Oxymetazolinesoaked pledgets are placed along the floor of the nose to reduce nasal bleeding from the nasal mucosa when placing drill holes and sutures. For description, the procedure is divided into several steps: (a) palatopharyngoplasty of the distal palate, (b) soft palate mobilization, (c) soft palate advancement, and (d) wound closure. 2.1 Distal Palatopharyngoplasty In patients with an anatomically normal palate and uvula, no surgery of the uvula and distal palate is required. In patients with redundant palate, pillar mucosa, uvula, or tonsils, conservative UPPP (such as uvulopalatal flap) or tonsillectomy may be performed. In other patients, UPPP may have been performed as a previous procedure. 2.2 Incision and Mobilization A palatal incision is outlined beginning at the central hard palate posterior to the alveolus immediately medial to the greater palatine foramen in a curvilinear “gothic arch” fashion. Anteriorly, a midline “T” incision is made on the hard palate to create a defect into which the soft tissue flap may be advanced. The incision is then flared laterally over the palpable process of the hamulus after passing posterior to the greater palatine foramen (Fig. 4A). The length of the flap varies, but should extend proximal to the planned bone removal and drill holes. The mucosa lateral to the “T” incision is elevated. Extra mucosa is not trimmed and should be preserved for closure. Bleeding is usually minor and may be controlled with additional infiltration of anesthetic into the mucosal margins and judicious electrocautery. A mucoperiosteal flap is elevated, thereby exposing the hard palate and the proximal soft palate (Fig. 4B). Centrally, the mucosa is usually thin, and

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care must be taken to avoid tearing it. Laterally, the flap is thicker. The fibro-adipose tissue is bluntly dissected. A mastoid curette is useful in flap elevation. Both flap elevation and subsequent closure are more difficult to perform in patients with high arched palates. Flap elevation is done superficial to the tensor aponeurosis and exposes 5–7mm of tensor tendon. Elevation is not performed too far posteriorly to preserve blood supply to the flap from the muscular palate. The soft palate has been advanced and mobilized using several techniques. The first method was using electrocautery to separate the soft from the hard palate at the insertion of the tensor aponeurosis. This exposed the nasopharynx (Fig. 4C). Mobilization of the central soft palate was achieved by fracturing the hamulus and therefore releasing stress on the tensor tendon. Since otitis media with effusion was observed postoperatively in some individuals, this was abandoned. Without mobilization, midline palate advancement was then achieved by vigorous traction on the soft palate using a retractor to pull the palate forward while closing the wound. Lateral palatal advancement was achieved with mucosal incisions along the lateral margin of the soft palate carried inferiorly to the superior border of the palatoglossal folds. A limited undermining of the flaps was then performed and the medial soft palate mucosa and muscle were pulled forward. A “corner” suture (using 3–0 vicryl) firmly secured this to the posterior alveolar periosteum. Multiple absorbable sutures were placed to distribute tension. Incisions were mucosal and superficial to the muscular soft palate. Advancement and mobilization has now been significantly altered. Mobilization of the soft palate aggressively incises the tensor aponuerosis medial to the hamulus with the tendon incised posteriorly to approximately the level of the levator muscle. Repositioning the palate is significantly improved with this maneuver. Advancement is at the discretion of the surgeon. Due to the major forces applied to the palate with speech and swallowing, simple soft tissue sutures (even into the tensor aponuerosis) are inadequate. Instead, a posterior osteotomy is performed leaving the tensor tendon attached to bone. Bone and tendon are then advanced. A posterior 0.5–1.0cm margin of the hard palate (palatine bone) is removed to provide space to move the soft palate anteriorly. Bone removal is performed with a small angled sagittal saw to make initial cuts and then residual bone removed with a rotatory drill. The central palate overlying the posterior nasal septum is also removed (Fig. 4D). A significant problem occurred initially with release of the tensor tendon. Although incising the tensor tendon markedly improves mobilization, it exposes the closure to the forces and posterior pull of the levator muscle with swallowing and movement. This has resulted in a 10–20% oronasal fistula rate. Although none has required intraoperative closure, the use of a short-term palatal splint has been required. To minimize this wound dehiscence, the “osteotomy” method of mobilization has been developed leaving a 2– 3mm margin of bone attached to the soft palate (Fig. 5). By leaving the soft palate insertion intact, advancement appears augmented and wound strength improved. 2.3 Advancement Palatal drill holes are placed at a 45° angle to the palate, extending from the oral surface of the palate into the nasal cavity (Fig. 5). A strong solid segment of bone must be left between these drill holes and the excised bony margin. A free needle is then

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Figure 5 Initial soft tissue technique, palatal advancement pharyngoplasty as well as the modified osteotomy method are shown. In the soft tissue technique (upper left), the hard and soft palate are separated at the junction of the hard and soft palate. Bone is removed. Drill holes are placed and the suture is placed into the tensor aponeurosis. The swallowing forces and speech place the soft tissue closure (lower left) at risk of dehiscence. In contrast, the osteotomy technique preserves the bony attachments of the soft palate (upper right). Bone is removed (arrow). The suture is placed around the bony butrus (middle right). Preserving the normal anatomic attachments decreases the likelihood of dehiscence (lower right). used to pass suture through the drill holes into the nasopharynx. After the suture is grasped in the nasopharynx, it is withdrawn into the mouth. If space allows, sutures may be placed in a simple fashion from the nasopharyngeal side around the osteotomy into the tensor tendon and out the oral cavity. If space is insufficient, the suture may be place from the oral cavity around the osteotomy and the suture drawn out the nasopharynx.

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This then requires passing the suture through the palatal drill holes from the nasopharynx. This may be achieved by passing separate loops of suture through the drill holes. The primary suture may then be placed through these loops and the loops with engaged primary suture pulled through the drill holes. Primary sutures are 2–0 Tevdek or other braided non-absorbable suture that are placed medially and laterally in the tensor tendon. Care must be taken in passing the sutures so they do not cut or tear the tensor tendon. Additional absorbable sutures are placed in the lateral tendon to reapproximate the tensor tendon and the tissues around the hamulus. Sutures are tied while an assistant pulls the palate forward with a curved retractor or blunt-tipped Yankauer suction. 2.4 Closure Excess or redundant tissue of the palatal is present after advancement. All mucosa is usually preserved. Since the posterior flap is thicker than the original hard palate mucosa, extra mucosa broaches this difference. Only fatty and fibroadipose tissue is trimmed as required. The anterior flap is closed with interrupted long-lasting absorbable sutures. Closure is difficult due to the angle of the hard palate. Closure is easier when midline sutures are initially placed only in the lateral (hard palate) mucosa. After all other sutures are placed, the midline sutures are completed and placed into the flap. Sutures are tied without tension. No bolster dressing is required. A soft diet is begun on the first day. The use of an upper denture is avoided for at least 4 weeks, or until healing is completed. If wound breakdown is noted, an upper palatal splint may be easily fashioned by most dentists and worn until healing has been achieved. Initial experience with transpalatal advancement pharyngoplasty noted significant reductions in respiratory disturbance index (RDI) and apnea index (AI). A 67% successful response rate with an RDI of less than 20 events/hr was observed in patients who only underwent transpalatal advancement. Respiratory disturbance index in the responder group decreased from 52.8 to 12.3 events/hr. Seven of 11 patients (64%) had RDI reduced to less than 20 events/hr. This group was skewed by several individuals with massive redundant nasopharyngeal lymphoid tissue that when removed contributed to such marked improvement. Subsequent evaluation has demonstrated significant postoperative acute and long-term enlargement in the retropalatal space. The velopharynx is increased in both anterior posterior dimension, but more significantly, recent data also suggests enlargement of the lateral pharyngeal ports (Fig. 6).

3. COMPLICATIONS Postoperatively, all patients have had complete velopharyngeal closure. No cases of velopharyngeal insufficiency (VPI) have been observed. This is similar to maxillofacial surgery where VPI is rare even following UPPP (20). As with UPPP, transient symptoms of mild nasopharyngeal reflux may occur immediately postoperatively.

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Figure 6 Preoperative (left) and 6 months post operative (right). The photographs of the retropalatal airway are shown. Preoperative airway is compromised from both anterior posterior as well as lateral wall collapse. Palatal advancement has significantly enlarged the velopharyngeal lateral airway ports (right). (See color insert.) Dysphagia may occur for several weeks postoperatively. The reason for this is uncertain, but increased pharyngeal volume or effects of UPPP may decrease bolus pressures and contribute to delayed pharyngeal clearance. Palatal flap necrosis and a subsequent oronasal fistula may occur. All have closed with conservative treatment including the creation and wearing of an upper palatal prosthesis for 1–3 weeks. No fistula has required an operative procedure to close secondarily. Gentle tissue technique, careful hemostasis, perioperative antibiotics, and placement of the site of incision to minimally overlap the bone removal are recommended to lessen this complication. Smokers may be particularly prone to poor healing and fistula. Transpalatal advancement pharyngoplasty offers a potential alternative to aggressive UPPP in an attempt to enlarge the upper oropharyngeal airway and improve respiratory function. With this procedure the soft palate, although mobilized, is not excised at the velopharynx. The enlargement of the airway occurs with advancement of the tensor tendon. The tendon advancement affects the central palate; however, lateral pharyngeal wall appear to be altered as well. It is speculated that advancing the palate and associated structures may tense the pharyngobasilar fascia, which in turn opens the lateral pharynx is some patients. The bony hard palate and alveolar periosteum provide a strong structural framework to suspend tissues anteriorly. This is in contrast to the thin mucosa and musculature of the palatoglossal fold, which in some techniques is the primary anterior support in UPPP. Transpalatal advancement is only a part of the surgical procedure for the treatment of OSA. Multiple areas of obstruction contribute to OSA (8). All segments of the airway—

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nasal, palatal, tongue base, and hypopharyngeal—need to be treated appropriately. Although the respiratory effects of this procedure demonstrate dramatic postoperative improvements in some patients with severe OSA, experience is limited. Nonetheless, and despite the potential for fistula using earlier techniques, this procedure markedly alters the airway similar to that of bimaxillary advancement. Given the known limitations of traditional UPPP, palatal advancement offers significant advantages.

REFERENCES 1. Fujita S, Conway W, Zorick F, et al. Surgical correction of anatomic abnormalities of obstructive sleep apnea syndrome: uvulopalatopharyngoplasty. Otolaryngol Head Neck Surg 1981; 89:923– 934. 2. Ikematsu T. Palatopharyngoplasty and partial uvulectomy method of Ikematsu: a 30 year clinical study of snoring. In: Fairbanks DNL, Fujita S, Ikematsu T, Simmons FB, eds. Snoring and Sleep Apnea. 1st ed. New York: Rivlin Press, 1987; 130–134. 3. Sher AE, Schechtman KB, Piccirillo JF. The efficacy of surgical modifications for the upper airway in adults with obstructive sleep apnea syndrome. Sleep 1996; 19:156–177. 4. Zohar Y, Finkelstein Y, Strauss M, et al. Surgical treatment of obstructive sleep apnea: comparison of techniques. Arch Otolaryngol Head Neck Surg 1993; 119:1023–1029. 5. Ryan CF, Love LL. Unpredictable results of laser assisted uvulopalatoplasty in the treatment of obstructive sleep apnoea. Thorax 2000; 55:399–404. 6. Blumen MB, Dahan S, Wagner I, et al. Radiofrequency versus LAUP for the treatment of snoring. Otolaryngol Head Neck Surg 2002; 126:67–73. 7. Riley RW, Powell NB, Guilleminault C. Obstructive sleep apnea syndrome: a review of 306 consecutively treated surgical patients. Otolaryngol Head Neck Surg 1993; 108: 117–125. 8. Morrison DL, Launois SH, Isono S, et.al. Pharyngeal narrowing and closing pressures in patients with obstructive sleep apnea. Am Rev Respir Dis 1993; 148:606–611. 9. Skatvedt O, Akre H, Godtlibsen OB. Continuous pressure measurements in the evaluation of patients for laser assisted uvulopalatoplasty. Eur Arch Otorhinolaryngol 1996; 253:390–394. 10. Aboussouan LS, Golish JA, Wood BG, et al. Dynamic pharyngoscopy inpredicting outcome of uvulopalatopharyngoplasty for moderate and severe obstructive sleep apnea. Chest 1995; 107:946–941. 11. Skatvedt O. Continuous pressure measurements in the pharynx and esophagus during sleep in patients with obstructive sleep apnea syndrome. Laryngoscope 1992; 102:1275–1280. 12. Katsantonis GP, Moss K, Miyazaki S, et al. Determining the site of airway collapse in obstructive sleep apnea with airway pressure monitoring. Laryngoscope 1993; 103:1126–1131. 13. Friedman M, Ibrahim H, Bass L. Clinical staging for sleep-disordered breathing. Otolaryngol Head Neck Surg 2002; 127:13–21. 14. Shepard JW, Thawley SE. Localization of upper airway collapse during sleep in patients with obstructive sleep apnea. Am Rev Respir Dis 1990; 141:1350–1355. 15. Woodson BT, Wooten MR. Manometric and endoscopic localization of airway obstruction after uvulopalatopharyngoplasty. Otolaryngol Head Neck Surg 1994; 111:38–43. 16. Caballero P, Alvarez-Sala R, Garcia-Rio F. CT in the evaluation of the upper airway in healthy subjects and in patients with obstructive sleep apnea syndrome. Chest 1998; 113:111–116. 17. Woodson BT, Toohill RJ. Transpalatal advancement pharyngoplasty for obstructive sleep apnea. Laryngoscope 1993; 103:269–276. 18. Woodson BT. Retropalatal airway characteristics in UPPP compared to transpalatal advancement pharyngoplasty. Laryngoscope 1997; 107:735–740.

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19. Woodson BT. Acute effects of palatopharyngoplasty on airway collapsibility. Otolaryngol Head Neck Surg 1999; 121:82–86. 20. Li KK, Troell RJ, Riley RW, Powell NB, Koester U, Guilleminault C. Uvulopalatopharyngoplasty, maxillomandibular advancement, and the velopharynx. Laryngoscope 2001; 111:1075–1078. 21. Schwab RJ, Goldberg AN. Upper airway assessment: radiographic and other imaging techniques. Otoloryngol Clin North Am 1998; 31(6):931–968.

21 Injection Snoreplasty Scott E.Brietzke Department of Otolaryngology, Walter Reed Army Medical Center, Washington, D.C., U.S.A. Eric A.Mair Department of Otolaryngology, Wilford Hall USAF Medical Center, San Antonio, Texas, U.S.A.

Injection snoreplasty is a recently described office procedure that treats palatal flutter snoring. A sclerotherapy agent is injected into the midline soft palate submucosa in order to reduce or eliminate primary palatal snoring by inducing scarring or controlled fibrosis. There are several office procedures available for the treatment of palatal flutter snoring but injection snoreplasty has the relative advantages of being simple to perform, producing minimal comparative discomfort, and being very inexpensive. The technique described in this chapter was first introduced through a prospective, nonrandomized human-use pilot study at Walter Reed Army Medical Center (1). Intermediate-term data as well as objective data confirming palatal stiffening efficacy were also recently published (2).

1. PATIENT SELECTION The patient who will benefit the most from injection snoreplasty is the one with primary palatal snoring who has failed standard nonsurgical therapy. The patient is interviewed and examined. The sleeping partner is also encouraged to attend the initial visit. The nasal cavity, nasopharynx, oropharynx, and hypopharynx are examined by fiberoptic nasopharyngolaryngoscopy. During the evaluation, the patient attempts to recreate the snoring sound with the assistance of the sleeping partner. The soft palate is observed for flutter. Various objective tools are available which help qualify primary snoring, which include home polysomnography with acoustical analysis (i.e., SNAP testing) and standard polysomnography. The acoustical analysis of the snoring flutter frequency can assist in establishing the primary anatomic location of the snoring noise (3). A lower snoring frequency (≈60Hz) corresponds to soft palate flutter and the higher frequency sounds may correspond to other anatomic sites of tissue vibration, e.g., the tongue or epiglottis. Absolute exclusion criteria include significant tonsillar hypertrophy, uncontrolled hypothyroidism, or any comorbid disease that might interfere with normal healing (uncontrolled diabetes, vascular disease, or significant periodontal disease). Relative exclusion criteria include a history of prior surgical snoring operations and

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significant obstructive sleep apnea syndrome (OSAS). A limited study investigating the efficacy of injection snoreplasty with OSAS demonstrating limited benefit has been completed by the authors and is pending publication.

2. PROCEDURAL TECHNIQUE Injection snoreplasty is a short procedure performed in the office with the patient seated in the examination chair. The supplies required are simple and inexpensive. Topical anesthesia is first administered with Benzocaine oral spray (14%, Betylite Inc, Pennsauken, NJ) followed by a mint flavored benzocaine gel “lollipop” (200mg/gm gel; Henry Schein, Port Washington, NY) applied on the end of a tongue depressor. The gel is held against the soft palate for approximately 5min. Injected local anesthetic is not used since it would likely decrease the effect of the sclerosing agent by dilution and cause it to leak from the soft palate. The physician then injects up to 2.0mL of the selected sclerotherapy agent with a single-needle penetration into the midline soft palate within the submucosal plane, just above the uvula (Fig. 1). This is done with a 0.75 in., 27-gauge needle bent to a 30–45° angle. Two sclerotherapy agents have been used safely and effectively in the injection snoreplasty procedure by the authors. Sodium tetradecyl sulfate (STS) (10mg/mL sotradecol, Elkins-Sinn, Cherry Hill, NJ, or multiple sources worldwide) was the first agent described for use with injection snoreplasty (1). STS was chosen due to its longstanding excellent safety record as a sclerosing agent as well as its low cost. A translucent bubble of fluid is seen as the STS is injected into the submucosal plane (Fig. 2). This bubble turns a hemorrhagic color within 2–3min after injection, as the sclerosing agent takes effect (Fig. 3). Fifty percent ethanol (99% dehydrated alcohol diluted with 2% lidocaine without epinephrine) has also been used as a palatal sclerotherapy agent by the authors and has been found to be comparable to 3% STS in effectiveness and safety in both animal and human studies that are awaiting publication. The injection procedure with 50% ethanol is identical to that with 3% STS although the visual appearance of the palate is

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Figure 1 Midline soft palate injection after topical anesthesia is a simple, well-tolerated clinic procedure. Supplies for performing injection snoreplasty include cetacaine oral spray, benzocaine gel, tongue blades, STS, and a 3cc syringe with bent 0.75 in., 27-gauge needle. (See color insert.)

Figure 2 Soft palate immediately after injection demonstrates the clear bulla of submucosally injected sclerosing agent. (See color insert.) distinctly different (Fig. 4). As with 3% STS, the patient is then observed for ≈10min before being sent home.

3. SUBSEQUENT MANAGEMENT Pain control is usually adequate with acetaminophen. No antibiotics or steroids are given. Snoring symptoms generally worsen for 2–3 days, then gradually improve over 2–3 weeks. The patient is followed up at a minimum of 6 weeks postinjection, allowing for the greatest sclerosing-effect possible. The scar should be inspected and palpated for stiffness and the patient reassessed for the ability to reproduce the snoring sound (Fig. 5). Postprocedural palatal stroboscopy or acoustic analysis can provide optional objective confirmation of palatal stiffening. Most important in the decision to reinject the soft

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palate is the patient or sleeping partner’s satisfaction with the response to the procedure. The response is deemed inadequate if the snoring is not gone or subjectively is still a problem. The average number of injections needed to

Figure 3 Soft palate several minutes after injection is purplish in color demonstrating the sclerosing agent taking effect. (See color insert.)

Figure 4 Soft palate immediately after injection with 50% ethanol diluted with 2% lidocaine without epinephrine. (See color insert.)

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achieve treatment success at our institution with 3% STS or 50% ethanol is approximately 1.2 injections per patient. For the patient undergoing a repeat injection, the injection sites differ. Reinjection into the midline is usually difficult due to the already stiffened soft palate scar. As a result, the soft palate is reinjected laterally to the initial site, with 1cc of agent on each side (Fig. 6). If the prior injected site in the midline is inadequately stiffened, it can also be reinjected. The overall trend with palatal stiffening operations (uvulopalatopharyngoplasty, laser assisted uvulopalatopharyngoplasty, radiofrequency ablation (RFA), and cautery-assisted palatal stiffening operation (CAPSO) is that their effect lessens with time (4–8). Recently published intermediate-term results demonstrate that injection snoreplasty will also likely follow this trend (2). Unlike other palatal snoring surgeries, however, repeat application of the injection snoreplasty is simple, well tolerated, and inexpensive.

Figure 5 Soft palate several weeks after injection demonstrates a midline scar that is easily palpated. The stiffened palate prevents palatal snoring. (See color insert.)

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Figure 6 If a second injection is needed, the site of injection is usually modified. Typically, the midline palatal scar after the first injection makes reinjection in this area difficult. Two injections of 1mL 3% STS on either side of the midline soft palate further stiffen the floppy palate. (See color insert.) 4. POSSIBLE COMPLICATIONS In well over 200 patients treated to date at our institution, the great majority have had no complications (no VPI, infection, or symptomatic airway edema). Most describe a nonobstructing “lump” in their throat (injected site), which resolves in 2–5days. There is relatively painless mucosal breakdown in the majority of patients within 5 days postprocedure, which has resolved in every case without sequelae. The injection should be placed slightly above the uvula to avoid uvular swelling. Four cases of soft palate fistula have occurred, all of which resolved quickly without intervention within 1 week of identification. There have been no postinjection difficulties with speech production, swallowing, excessive scarring, or anaphylaxis to the sclerosing agents.

5. DISCUSSION The concept of palatal sclerotherapy as a method of treating excessive snoring is not a new one. In 1943, Strauss (9) proposed lateral soft palate injections to dampen the “flutter ratio” of the soft palate with “controlled fibrosis.” Our animal model revealed optimal

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palatal dampening and scarring from midline submucosal injection of the sclerotherapy agent (10). A central scar stiffens the soft palate much like a central mast on a ship stiffens the sail. The sclerotherapy agents that we presently prefer are STS and ethanol, although there are likely many other effective agents. Injection snoreplasty enjoys distinct advantages over other palatal procedures. It is easily accomplished in a routine 15min visit to the clinic and is very inexpensive with little pain or disruption to the patient’s daily lifestyle. Extended follow-up success and snoring relapse rates of injection snoreplasty are similar to those of other palatal treatments (2). However, unlike other palatal procedures, retreatment with injection snoreplasty, if necessary, is simple, effective, well tolerated, and inexpensive. Relapse after all forms of palatal snoring procedures is common, and maintenance therapy may be required. Complications from injection snoreplasty are uncommon and self-limiting, typically requiring no treatment (2).

REFERENCES 1. Brietzke SE, Mair EA. Injection snoreplasty: how to treat snoring without all the pain and expense. Otolaryngol Head Neck Surg 2001; 124:503–510. 2. Brietzke SB, Mair EA. Injection snoreplasty: extended follow-up and new objective data. Otolaryngol Head Neck Surg. 2003; 128(5):605–615. 3. Miyazaki S, Itasaka Y, Ishikawa K, Togawa K. Acoustic analysis of snoring and the site of airway obstruction in sleep related respiratory disorders. Acta Otolaryngol (Stockh) 1998; 537(suppl):47–51. 4. Macnab T, Blokmanis A, Dickson RI. Long-term results of uvulopalatopharyngoplasty for snoring. J Otolaryngol 1992; 21:350–354. 5. Levin BC, Becker GD. Uvulopalatopharyngoplasty for snoring: long term results. Laryngoscope 1994; 104:1150–1152. 6. Wareing MJ, Callanan VP, Mitchell DB. Laser assisted uvuloplasty: six and eighteen month results. J Laryngol Otol 1998; 112:639–641. 7. Li KK, Powell NB, Riley RW, Guilleminault C. Radiofrequency volumetric reduction of the palate: an extended follow-up study. Otolaryngol Head Neck Surg 2000; 122: 410–414. 8. Mair EA, Day RH. Cautery-assisted palatal stiffening operation. Otolaryngol Head Neck Surg 2000; 122:547–555. 9. Strauss JF. A new approach to the treatment of snoring. Arch Otolaryngol 1943; 38: 225–229. 10. LaFrentz JR, Brietzke SE, Mair EA. Evaluation of palatal snoring surgery in an animal model. Otolaryngol Head Neck Surg 2003; 129:343–352.

22 Skeletal Techniques: Mandible Robert J.Troell Beauty By Design, Las Vegas, Nevada, U.S.A. KEY POINTS • A preoperative analysis for hypopharyngeal collapse, usually with the fiberoptic nasopharyngoscopy with the Müller maneuver and a lateral cephalometric radiograph, is essential to determine if base of tongue obstruction exists and if mandibular skeletal surgery is warranted. • Hypopharyngeal obstruction may include base of tongue and/or lateral pharyngeal wall collapse. • Mandibular skeletal surgery to improve the patency of the upper airway has been established to be an effective alternative treatment for hypopharyngeal obstruction. • A preoperative mandibular panoramic radiograph should be acquired to determine the presence of periapical dental disease, the length of the incisor tooth roots, and aid in identifying the precise location of the genioglossus muscle insertion. • The mandibular osteotomy with genioglossus advancement (GA) is the optimal surgical technique for base of tongue obstruction, while the hyoid myotomy and suspension is the preferred technique when lateral pharyngeal wall collapse exists. • Multilevel pharyngeal surgery is both safe and effective in selected patients with obstructive sleep apnea syndrome (OSAS). • Patients with more severe sleep-disordered breathing (SDB) are more likely to have multilevel obstruction. • Combining mandibular skeletal surgery with other hyopharyngeal procedures, such as tongue base radiofrequency or the hyoid myotomy and suspension, can produce significant tongue swelling. This swelling may require a more vigilant postoperative monitored setting, such as the intensive care unit, or additional treatment modalities, such as parenteral antihypertensive medications, steroids, and/or nasal positive airway pressure. • The modified mortise genioglosssus advancement technique is preferred in patients with mandibular deficiency for efficacy and esthetic advantages.

1. INTRODUCTION Upper airway resistance syndrome (UARS) and OSAS encompass a spectrum of sleeprelated upper airway obstruction collectively referred to as SDB. If medical therapy has been unsuccessful, surgical therapy is a therapeutic option. A preoperative assessment

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estimates the areas of the upper airway that may be causing obstruction. Base of tongue collapse may be a component of this obstruction. The surgical armamentarium of procedures to improve the posterior airway space (PAS) includes the mandibular osteotomy with GA. The practice parameters for the surgical treatment of obstructive sleep apnea published by the American Academy of Sleep Medicine states that “of the procedures directed at enlarging the retrolingual region, inferior sagittal mandibular osteotomy and genioglossus advancment with or without hyoid mytomy and suspension appears to be the most promising” (1).

2. BACKGROUND The limited initial surgical results in the surgical treatment of OSAS using the uvulopalatopharyngoplasty (UPPP) by Fujita et al. (2,3) and Simmons et al. (4) led to an evaluation of the mechanisms and sites of obstruction. A study evaluating the upper airway with fiberoptic nasopharyngoscopy concluded that OSAS patients present with “disproportionate anatomy,” consisting of a large base of the tongue, narrow mandibular arch, and mandibular deficiency (5). Cephalometric analysis of UPPP patients with incomplete surgical success, by Riley et al. (6), concluded that radiographically the base of the tongue was a cause of the persistent obstruction. Magnetic resonance imaging of the upper airway determined that collapse of the lateral pharyngeal wall was a significant component to the etiology of sleep-related airway obstruction (7). When surgical therapy is contemplated, a comprehensive preoperative assessment to identify the sites of airway obstruction should improve surgical success rates. When the base of the tongue is suspected as a component in the upper airway collapse, surgical management directed at this site of obstruction is indicated.

3. MANDIBULAR ANATOMY The genioglossus muscle (GGM) is an extrinsic muscle of the tongue that extends upward into the intrinsic tongue musculature. The origin of this muscle is from the mental spine or genial tubercle (geniotubercle), which are on each side of the midline or often fused together in the midline. The GGM also originates from the internal surface of the mandible adjacent to the geniotubercle (Fig. 1) (8). The muscle radiates into a broad sheet in the sagittal plane and inserts into the anterior portion of the intrinsic tongue musculature, posterior portion of the intrinsic tongue musculature, or the most inferior fibers insert into the superior-midline aspect of the hyoid bone. The GGM arises from the mandible above the geniohyoid muscle. Understanding the anatomical relationships and size of the GGM insertion can aid the surgeon in performing the specific technique of GA for the individual patient’s anatomy, precise mandibular osteotomies for optimal geniotubercle advancement, and optimal cosmetic concerns.

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Figure 1 Cadaveric surgical anatomy of the rectangular geniotubercle modification of the genioglossus advancement. (See color insert.) The sclerotic area of the mandible noted on panoramic radiographs in the midline corresponds to the bone of the geniotubercle as noted by previous anatomical studies (8). Two modifications of the GA technique are currently being used to produce adequate advancement and successful clinical outcomes with the least morbidity and complications (Fig. 2) (9). The rectangular geniotubercle osteotomy modification of the GA procedure advances only the geniotubercle. This technique augments the anterior chin the least degree and has the lowest risk of mandibular fracture, while including all of the GGM fibers in the advanced bony fragment. The modified mortise technique provides an improved success rate by advancing additional musculature and significantly augments the anterior mandible. Thus, this modification of the procedure improves the cosmetic appearance in patients displaying retrognathia.

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Figure 2 Genioglossus advancement surgical modifications: (A) horizontal inferior sagittal osteotomy; (B) mortise osteotomy; (C) modified mortise osteotomy; (D) rectangular geniotubercle osteotomy. (From Powell NB, Riley RW, Guilleminault C. The hypopharynx: upper airway reconstruction in obstructive sleep apnea syndrome. In: Fairbanks DNF, Fujita S., eds. Snoring and Obstructive Sleep Apnea. 2nd ed. New York: Raven Press, Ltd., 1994.) Understanding the anatomical relationships and size of the GGM insertion enables the surgeon in performing the modification of GA for the individual patients anatomy, precise mandibular osteotomies for optimal geniotubercle advancement, and optimal cosmetic concerns. In summary, the inferior sagittal mandibular osteotomy and GA is performed through an intraoral approach designed to enlarge the retrolingual area. The genial tubercle, which is the anterior attachment of the GGM, is mobilized by osteotomies. A comprehensive understanding of this technique, the caveats, and pitfalls will offer the surgeon another surgical procedure to address hypopharyngeal obstruction and increase the overall surgical success rate in treating patients with SDB.

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4. PRESURGICAL EVALUATION Nearly all patients with documented SDB are candidates for surgical intervention. The decision to perform base of tongue reconstructive surgery is based on the preoperative evaluation that this site is at least partially involved in the upper airway collapse. The typical preoperative assessment includes a head and neck comprehensive physical examination, fiberoptic nasopharyngoscopy, and a lateral cephalometric analysis. Physical examination findings of a small soft palate, a postoperative palatal surgical result, a narrowed mandibular skeletal arch, and a large tongue suggest that the base of tongue is involved in upper airway collapse. Fiberoptic nasopharyngoscopy confirms the existence and degree of tongue base obstruction (Fig. 3A). The Müller maneuver aids in identifying the sites of obstruction by creating negative intraluminal pressure, accentuating obstructive forces (Fig. 3B). A lateral cephalometric radiograph may suggest base of tongue obstruction by noting a narrowed PAS of less than 11mm (Figs. 4 and 5). The degree of mandibular development is important, because if skeletal deficiency exists, there is a higher incidence of

Figure 3 Fiberoptic nasopharyngoscopy: (A) view of hypopharynx; (B) view of hypopharynx during the Müller maneuver.

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Figure 6.12 A summary graph.

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Figure 6.14 A picture of a typical tracing of the Stardust study.

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Figure 6.14 A summary graph.

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Figure 6.16 A picture of a typical tracing of the NovaSom on (a) study night 1, (b) study night 2 (see insert p. 5), and (c) study night 3 (see insert p. 6).

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Figure 6.20 A picture of a typical tracing of the Watch-PAT100 study.

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Figure 19.2 CAPSO post-operative follow-up: (a) immediately after removal of the soft palate mucosa; (b) at day 2; (c) after 3–5 days; (d) days 7– 9; (e) days 11–13; (f) 4 weeks after surgery; (g) more than 2 years after surgery. (See p. 310 for full caption.)

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Figure 20.6 Preoperative (left) and 6 months post operative (right). The photographs of the retropalatal airway are shown. Preoperative airway is compromised from both anterior posterior as well as lateral wall collapse. Palatal advancement has significantly enlarged the velopharyngeal lateral airway ports (right).

Figure 21.1 Midline soft palate injection after topical anesthesia is a

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simple, well-tolerated clinic procedure. Supplies for performing injection snoreplasty include cetacaine oral spray, benzocaine gel, tongue blades, STS, and a 3cc syringe with bent 0.75in., 27-gauge needle.

Figure 21.2 Soft palate immediately after injection demonstrates the clear bulla of submucosally injected sclerosing agent.

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Figure 21.3 Soft palate several minutes after injection is purplish in color demonstrating the sclerosing agent taking effect.

Figure 21.4 Soft palate immediately after injection with 50% ethanol

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diluted with 2% lidocaine without epinephrine.

Figure 21.5 Soft palate several weeks after injection demonstrates a midline scar that is easily palpated. The stiffened palate prevents palatal snoring.

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Figure 21.6 If a second injection is needed, the site of injection is usually modified. Typically, the midline palatal scar after the first injection makes reinjection in this area difficult. Two injections of 1mL 3% STS on either side of the midline soft palate further stiffen the floppy palate.

Figure 22.1 Cadaveric surgical anatomy of the rectangular geniotubercle modification of the genioglossus advancement.

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Figure 22.5 Cephalometric preoperative radiograph—base of tongue obstruction and a narrowed posterior airway space evident.

Figure 22.6 Panoramic radiograph: (A) pre-operative; (B) post-operative. Note increased sclerotic area at the

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symphyseal mandibular area, correlating to the location of the geniotubercle. The estimate of the geniotubercle fragment to incorporate all of the genioglossal muscle fibers was drawn from the pre-operative radiograph.

Figure 22.12 Genioglossus advancement: modified mortise osteotomy modification. Cadaver dissection revealing the attached musculature.

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Figure 22.14 Cephalometric radiograph: (A) preoperative view; (B) postoperative view after rectangular osteotomy modification of genioglossus advancement.

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Figure 23.1 Hypopharyngeal view: (A) pre-Müller maneuver; (B) during Müller maneuver.

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Figure 30.8 Appearance of an adult patient pretreatment (A) and at 3 months post-TCRF tonsil reduction (B).

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Figure 4 Standard cephalometric tracing. S, sella; N, nasion; A, subnasale; B, supramentale; SNA, maxilla to cranial base; SNB, mandible to cranial base; ANS, anterior nasal spine; PNS, posterior nasal spine; P, tip of uvula; PNS-P, length of soft palate; PAS, posterior airway space; MP, mandibular plane; H, hyoid; Go, gonion; Gn, gnathion. obstruction at the level of the base of the tongue. But, if the PAS radiographically is normal, it does not rule out tongue base obstruction. All of these presurgical evaluations are important in determining the presence of base of tongue obstruction (Table 1). A preoperative panographic radiograph of the mandible is required to provide vital information for surgery: identify the presence of periodontal disease, aid in

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Figure 5 Cephalometric preoperative radiograph—base of tongue obstruction and a narrowed posterior airway space evident. (See color insert.) Table 1 Factors Suggesting Base of Tongue Obstruction Obesity (body mass index >31) Severe sleep apnea (apnea-hypopnea index >40) Small soft palate anatomy PAS <11mm noted on lateral cephalometric radiograph Base of tongue obstruction noted on fiberoptic examination

estimating the location of the GGM insertion by noting the increased sclerotic area of the symphyseal mandibular area, determining the height of the mandible, and noting the incisor root lengths (Fig. 6A). All of these measurements are involved in determining the surgical position and size of the surgically created geniotubercle bony fragment (Fig. 6B).

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5. TREATMENT PHILOSOPHY There are potentially different phases of upper airway reconstruction. The initial phase of surgery directs treatment to the specific areas of obstruction. Persons with isolated obstruction at the level of the soft palate receive a palatal surgical procedure and patients with obstruction at the level of the base of tongue undergo a procedure designed to improve this region. If the patient has both palatal and base of tongue obstruction, they receive procedures directed at both sites, either simultaneously or staged. The determination of the timing of surgery is dictated by the following: the patient’s ability to use nasal CPAP to protect the upper airway from collapse postoperatively, the severity of SDB, the safety and stability of the upper airway, and the number and sites of upper airway reconstructive procedures. When nasal obstruction is identified, it is usually addressed with a staged nasal procedure before or after the palate and/or hypopharyngeal areas are treated. If the patient does not have severe SDB, nasal surgery may be elected to proceed along with other upper airway reconstructive procedures. Presently, the best surgical procedures addressing the soft palate in SDB are the UPPP and the uvulopalatal flap (UPF) (10). Sher et al. (11) have statistically evaluated the results with upper airway reconstruction using only the UPPP in SDB and revealed a 39– 40% surgical success rate. The mandibular osteotomy and GA is the author’s preferred first-line procedure to address the hypopharyngeal

Figure 6 Panoramic radiograph: (A) pre-operative; (B) post-operative. Note increased sclerotic area at the symphyseal mandibular area, correlating to the location of the geniotubercle. The estimate of the geniotubercle fragment to incorporate all of the genioglossal muscle fibers was drawn from the pre-operative radiograph. (See color insert.) obstruction caused by the base of tongue. This can be combined with radiofrequency (RF) volumetric tissue reduction. RF uses an insulated probe at 465kHz to reduce the

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tongue volume by producing coagulation necrosis, and subsequent scarring with muscle and soft tissue contraction (12).

6. SURGICAL TECHNIQUE 6.1 Genioglossus Advancement: The Rectangular Geniotubercle Osteotomy Technique If simultaneously performing other upper airway reconstructive procedures, the GA is performed last to avoid blood altering visualization during these procedures. An injection of a local anesthetic solution containing 1:100,000 epinephrine is placed along the planned labiogingival sulcus and floor of mouth for hemostasis. The labiogingival sulcus is incised with a knife blade to avoid postoperative dehiscence by thermal injury to the mucosa from electrocautery (Fig. 7). A periosteal elevator raises the periosteum and mentalis muscle from the mandibular cortex. Assessment of the depth of the GGM insertion to the geniotubercle is determined by digital palpation of the floor of mouth by the surgeon and by evaluating the panorex radiograph. The rectangular osteotomy is completed using an oscillating saw with the parallel vertical cuts medial to the canine dentition (Fig. 8). The inferior horizontal osteotomy is placed at least 6–8mm from the inferior mandibular border and the superior osteotomy is placed 8–12mm above the inferior osteotomy. This osteotomy is an estimated distance of at least 5mm below the incisor root apices, parallel to the inferior osteotomy. The horizontal osteotomies are cut upward at approximately a 15° angle to ensure that all of the GGM fibers are incorporated in the geniotubercle fragment, especially with long dental roots. A 1.5mm hole is drilled into the center of the geniotubercle fragment and a 2mm width and 10mm length titanium mini-screw (Stryker-Leibinger, Portage, MI) placed.

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Figure 7 Labiogingival sulcus incision. A knife blade produces an incision and periosteum is raised using a Molt elevator. (From Ref. 22.).

Figure 8 The rectangular mandibular osteotomy modification. The horizontal osteotomies are parallel and the vertical osteotomies, medial to the canine dentition, are performed parallel. (From Ref. 22.) The geniotubercle fragment is inspected to ensure acquisition of the GGM fibers. A modified straight Kocher clamp grasps the screw and advances the fragment anteriorly. The geniotubercle fragment is rotated with a straight Kocher clamp only to allow bony overlap over the adjacent anterior mandibular symphyseal bone (Fig. 9). Immobilization of the fragment to the inferior border of the mandible is performed by a “lag screw” technique. An approximately 2.0mm hole is drilled into the geniotubercle fragment, then a 1.5mm hole drilled into the underlying inferior mandibular cortex. A 2mm width and 10mm length titanium mini-screw immobilizes the fragment (Fig. 10). Occasionally, a 1.2mm titanium micro-screw is needed at the superior border of the fragment to completely immobilize the fragment. The mentalis muscle is closed with a horizontal mattress and the mucosa is reapproximated with simple interrupted sutures. The rectangular geniotubercle fragment is advanced to the width of the mandible containing all of the GGM fibers.

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Figure 9 The rectangular mandibular osteotomy modification. The surgically created genitoubercle fragment is advanced and rotated to allow bony overlap. (From Ref. 22.)

Figure 10 The rectangular mandibular osteotomy modification. The outer cortex of the surgically created genitoubercle fragment is removed and the fragment is immobilized using a “lag” screw technique. (From Ref. 22.)

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6.2 Genioglossus Advancement: Modified Mortise Osteotomy Technique This modification of the original GA differs in that the initial osteotomy is an inferior horizontal osteotomy approximately 8–10mm from the inferior border of the mandible (Fig. 11A). This fragment is down-fractured with a periosteal elevator and the exact location of the GGM insertion can be observed after this segment is down-fractured. A superior horizontal osteotomy is performed to the width of the central incisor dentition. A beveled osteotomy connecting the superior osteotomy to the inferior osteotomy creates a trapezoid shaped fragment, where the lingual cortex containing the GGM insertion is wider than the outer or buccal cortex (Fig. 11B). This outer cortex of the geniotubercle fragment is removed and contoured for cosmetic concerns (Fig. 11C). The lower border fragment containing the geniohyoid, mylohyoid, and digastric muscles is advanced and immobilized (Fig. 12). There is an increased risk of mandible fracture with this technique, but also a greater success rate and reduced relapse rate.

7. SURGICAL ANATOMY CONCERNS There are concerns regarding the position of each specific osteotomy. The most important issue regarding the position of the superior osteotomy is to avoid the incisor root apices. Mintz et al. (13) evaluated 41 adult human skulls by linear cross-sectional tomography to determine the geniotubercle bony anatomical relationship to the dentition. The mean distance from the incisor root apices to the superior aspect of the geniotubercle after dividing by a magnification factor of 1.10 was 6.5±3.3mm with a range of 1–14mm and 35% less than 5mm. In contrast, Silverstein et al. (14) split the mandible in the midline with a handsaw and evaluated the relationships of the GGM anatomy itself without radiographs. The distance from the incisor apices to the GGM insertion was a mean of 11.8mm and a range of 9–15mm. This distance is almost twice that of the results of Mintz et al. (13). This difference may be due to the variation in the position where the distances were

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Figure 11 Genioglossus advancement: modified mortise osteotomy

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modification. (A) Inferior horizontal osteotomy. (B) Trapezoid osteotomy encompassing the genioglossus muscle. (C) Removal of the outer mandibular cortex followed by immobilization of the inner cortex and inferior border segments with titanium screws. measured. Bell et al. (15) recommended at least a 5mm distance below the incisor dentition to an osteotomy to prevent devitalization of the dentition. Troell (16) revealed the postoperative radiographic distance from the incisor root apices to the superior osteotomy of the geniotubercle fragment was 8.4±3.8mm with a range of 3–16mm. This investigation noted the actual GGM

Figure 12 Genioglossus advancement: modified mortise osteotomy modification. Cadaver dissection revealing the attached musculature. (See color insert.) insertion would be located more inferiorly than those of Mintz et al., correlating to those findings by Silverstein et al. (14). Another concern is to encompass all the GGM fibers in the advanced fragment. Mintz et al. (13) noted the mean height and width of the tubercle from the bony protuberance of the skulls were 4.8 and 6.0mm, respectively. The problem with the bony skull study is

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that it evaluated only the bony relationships of the geniotubercle. The GGM originates not only from the mental spine or genial tubercle (geniotubercle), but also from the adjacent internal (lingual) surface of the mandible (8). Evaluation of the soft tissue relationships is essential to accurately depict the muscular anatomy. Silverstein et al. (14) measured the width of the GGM 2mm from the mandibular insertion with a mean of 13.8mm and a range of 13–15mm. Another investigation (16) revealed the muscle insertion at the lingual surface of the mandible to be larger, between one and two times the size of the geniotubercle bony protuberance. The mean GGM width immediately at the insertion to the mandible was 8.3±1.6mm with a range of 4–10mm and the mean height was 7.7±2.8mm with a range of 4–12mm (Fig. 13). Some of the discrepancies of the width of these two studies may be the location of the measurement of the GGM width, ethnic variations of the specimens, and damage to the anatomy from the surgical genioglossus procedure or cadaver dissection. If one assumes that future patients have similar anatomy to the cadaver specimens, to be certain of capturing the entire width of the GGM insertion, the minimum osteotomy needs to be at least 14mm. A width of 12.4mm would capture 95% of the patients’ entire GGM insertion. Troell’s data noted that the GGM insertion maybe asymmetric between 2 and 7mm from the midline (16). Mintz’s (13) results revealed that the geniotubercle is medial to the canine tooth roots in all specimens. Thus, to completely acquire the GGM insertion and avoid the long root apices of the canine dentition the vertical osteotomies need to be placed medial to the canine roots. The concern regarding the location of the inferior osteotomy is to maintain the postoperative strength of the anterior mandible, while ensuring adequate GGM fiber acquisition. In Silversteins’ (14) cadaver dissection, the mean distance from the

Figure 13 Relationship of geniotubercle fragment (GF): the genioglossus advancement— rectangular geniotubercle osteotomy modification. (A) Anterior view; (B) lateral view: A—superior aspect of GF

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to the incisor crown; B—superior aspect of GF to superior border of mandible; C—inferior aspect of GT to inferior border of mandible; D— mandibular height; E—distance from dental root apices to superior aspect GF; W—width of GF; H—height of GF. inferior border of the mandible was 14.2mm. The cadaver results and surgical findings in the study by Troell (16) revealed the mean distance of the GGM insertion to the inferior border of the mandible to be 11.3mm and the distance of the geniotubercle fragment to the inferior border of the mandible to be 6.9mm. The surgical results reveal the inferior osteotomy closer to the inferior mandibular border than the anatomical insertion, because the surgeon wanted to ensure that none of the GGM fibers were missed in the geniotubercle fragment advancement. The amount of GA is directly related to the thickness of the symphyseal area of the mandible at the location of the geniotubercle. Silverstein et al. (14) revealed a mean geniotubercle bony thickness of 12.6mm with a range of 9–15mm, while the surgical results of the study by Troell (16) revealed similar findings with a mean thickness of the geniotubercle fragment of 11.4mm and a range of 8–15mm. Another variable in the efficacy of the advancement is the tension noted in the geniotubercle fragment after the complete osteotomy is created. Some patients are difficult to advance, which suggests the final result will create more tension in the muscle. This tension will decrease the risk of base of tongue displacement during the pathophysiologic hypotonia noted in SDB patients.

8. RESULTS The success of surgical treatment of SDB with UPPP alone is only about 39–40% (11). The results using the GA have been in protocols using other upper airway reconstructive procedures including the palatoplasty. The GA improves the tension on the GGM and may improve the PAS on lateral cephalometric radiographic analysis (Fig. 14A, B). Riley et al. (17) revealed an overall success rate of 61% in a review of 239 patients undergoing a GA, hyoid suspension, and UPPP. There was approximately 75% success rate in patients with mild to moderately severe sleep apnea [apnea-hypopnea index (AHI) <60], which declined to 42% when patients demonstrated severe disease (AHI >60). Success was defined as an AHI <20 with at least a 50% reduction.

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Figure 14 Cephalometric radiograph: (A) preoperative view; (B) postoperative view after rectangular osteotomy modification of genioglossus advancement. (See color insert.) Johnson and Chinn (18) revealed a mean reduction in the AHI by 44.1 from a preoperative value of 58.7 to a postoperative value of 10.5 in patients undergoing a UPPP and GA. Using a success rate of an AHI <10, (7/9) 78% were successfully treated. Ramirez and Loube (19) revealed in morbidly obese patients a 42% success rate. Utley et al. (20) revealed a (8/14) 57% success rate defined as an AHI <20 in patients undergoing a GA, hyoid suspension, and UPPP. Troell (21) revealed a 64% (7/11) success rate as defined as an AHI <10 with resolution of excessive daytime sleepiness by the same protocol. These studies support the improved outcomes of multi-level pharyngeal surgery addressing both retropalatal and retrolingual areas of collapse.

9. COMPLICATIONS AND AVOIDANCE STRATEGIES The most immediate and significant postoperative complication is upper airway obstruction. Patients with SDB often have underlying hypertension or hypertension when surgically stressed. Bleeding from the mandibular diploe can result in a floor of mouth hematoma, which can result in airway obstruction or increase the risk of postoperative infection. Control of postoperative hypertension to maintain the mean blood pressure

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below 100mm Hg with intravenous antihypertensive medications is essential. Ice to the anterior chin may also aid in decreasing edema to the tongue postoperatively. If multiple upper airway reconstructive procedures are performed, or if observed upper airway swelling is discovered postoperatively, intensive care unit monitoring should be carefully considered. The use of nasal CPAP in the postoperative period stabilizes blood pressure, reduces edema, and protects the airway from sleep-related obstruction. Many of the potential complications (Table 2) can be avoided by proper surgical technique. A panorex radiograph rules out any significant anterior mandibular

Table 2 Complications Labiogingival incision dehisence Wound infection Dental root injury Dental paresthesia Lower lip paresthesia Mandible fracture Floor of mouth hematoma Postoperative upper airway obstruction

bone or dental disease. The location of the geniotubercle on panoramic x-ray and digital palpation of the floor of mouth aid in estimating the height of the GGM insertion. This method of determining the location of the osteotomies reduces the risk of amputating dental roots, reduces the risk of mandible fracture from weakening the mandible by an excessively large genioglossus fragment, or unsuccessfully advancing all of the GGM fibers by an inadequate fragment.

10. DISCUSSION Knowledge of the anatomical relationships and size of the geniotubercle and GGM fiber insertion can aid the surgeon in performing the specific technique of the GA procedure for the individual patient’s anatomy and precise mandibular osteotomies for optimal geniotubercle advancement. The main concerns regarding the GA surgical procedure is to construct the osteotomy to the largest extent possible to increase the chance of acquiring all of the GGM fibers. Also, optimal surgical technique limits the size of the fragment to decrease the risk of dental injury or weakening the bony mandibular integrity without limiting acquisition of the muscle fibers. Thus, these two concerns limit the size and position of the surgically created geniotubercle fragment in each individual patient. When a comprehensive presurgical evaluation identifies the site of airway obstruction to be the base of the tongue, surgical therapy using the GA provides a surgical technique to advance the tongue base effectively with a low morbidity.

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REFERENCES 1. Practice parameters for the treatment of obstructive sleep apnea in adults: the efficacy of surgical modifications of the upper airway. Sleep 1996; 19(2):156–177. 2. Fujita S, Conway W, Zorick F, et al. Surgical correction of anatomic abnormalities in obstructive sleep apnea syndrome: uvulopalatopharyngoplasty. Otolaryngol Head Neck Surg 1981; 89:923. 3. Fujita S, Conway WA, Zorck F, et al. Evaluation of the effectiveness of uvulopalatopharyngoplasty. Laryngoscope 1985; 95:70. 4. Simmons FB, Guilleminault C, Miles L. The palatopharyngoplasty operation for snoring and sleep apnea: an interim report. Otolaryngol Head Neck Surg 1984; 4:375. 5. Rojewski TE, Schuller DE, Clark RW. Video endoscopic determinations of the mechanisms of obstructive sleep apnea. Otolaryngol Head Neck Surg 1984; 92:127. 6. Riley R, Guilleminault C, Powell N, et al. Palatopharyngoplasty failure, cephalometric roentgenograms, and obstructive sleep apnea. Otolaryngol Head Neck Surg 1985; 93:240. 7. Schwab RJ, Gefter WB, Hoffman EA. Dynamic upper airway imaging during awake respiration in normal subjects and patients with sleep disordered breathing. Am Rev Respir Dis 1993; 148:1385. 8. Hollinshead WH. The jaws, palate, and tongue. In: Anatomy for Surgeons: The Head and Neck. Vol. 1. 3rd ed. Hagerstown: Harper & Row Publishers, 1982:346–348, 367–370. 9. Powell NB, Riley RW, Guilleminault C. The hypopharynx: upper airway reconstruction in obstructive sleep apnea syndrome In: Fairbanks DNF, Fujita S, eds. Snoring and Obstructive Sleep Apnea. 2nd ed. New York: Raven Press, Ltd., 1994. 10. Powell N, Riley R, Guilleminault C, et al. A reversible uvulopalatal flap for snoring and obstructive sleep. Sleep 1996; 19:593. 11. Sher A, Schechtman K, Piccirillo J. The efficacy of surgical modifications of the upper airway in adults with obstructive sleep apnea syndrome. Sleep 1996; 19(2): 156. 12. Troell RJ, Li KK, Powell NB, Riley RW. Radiofrequency tongue base reduction in sleepdisordered breathing. In: Woodson T, ed. Otolaryngologic Operative Techniques in Otolaryngology-Head and Neck Surgery Vol. 11(1). Philadelphia, PA: WB Saunders, Inc. 2000:47–49. 13. Mintz SM, Ettinger AC, Geist JR, Geist RY. Anatomic relationship of the genial tubercles to the dentition as determined by cross-sectional tomography. J Oral Maxillofac Surg 1995; 53:1324–1326. 14. Silverstein K, Costello BJ, Giannakpoulos H, Hendler B. Genioglossus muscle attachments: an anatomic analysis and the implications for genioglossus advancement. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000; 90:686–688. 15. Bell WH, Proffit WR, White RP. Surgical Correction of Dentofacial Deformities. 1st ed. Philadelphia, PA: WB Saunders, Inc., 1980:1218–1226. 16. Troell RJ. Genioglossus advancement in sleep-disordered breathing: anatomical relationships. Laryngoscope. Submitted. 17. Riley R, Powell N, Guilleminault C. Obstructive sleep apnea syndrome: a review of 306 consecutively treated surgical patients. Otolaryngol Head Neck Surg 1993; 108:117. 18. Johnson NT, Chinn J. Uvulopalatopharyngoplasty and inferior sagittal mandibular osteotomy with genioglossus advancement for treatment of obstructive sleep apnea. Chest 1994; 105:278. 19. Ramirez SG, Loube DI. Inferior sagittal osteotomy with hyoid bone suspension for obese patients with sleep apnea. Arch Otolaryngol Head Neck Surg 1996; 122:953. 20. Utley DS, Shin EJ, Terris DJ. A cost-effective and rational surgical approach to patients with snoring, upper airway resistance syndrome or obstructive sleep apnea syndrome. Laryngoscope 1997; 107:726. 21. Troell R. Contemporary surgical approaches to upper airway reconstruction in sleep disordered breathing. Otorhinolaryngol Nova 2000; 10:138–148.

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22. Terris DJ. Multilevel pharyngeal surgery for obstructive sleep apnea: indications and techniques. Oper Techn Otolaryngol Head Neck Surg 2000; 11:12–20.

23 Skeletal Techniques: Hypopharynx Robert J.Troell Beauty By Design, Las Vegas, Nevada, U.S.A. KEY POINTS • A preoperative analysis for hypopharyngeal collapse, usually with fiberoptic nasopharyngoscopy with the Müller maneuver and a lateral cephalometric radiograph, is essential to determine if lateral pharyngeal collapse exists and if hyoid myotomy and suspension is warranted. • Hypopharyngeal obstruction may include base of tongue and/or lateral pharyngeal wall collapse. • Hyoid suspension surgery improves the patency of the upper airway and has been established to be an effective alternative treatment for hypopharyngeal obstruction, improving both lateral pharyngeal wall collapse and base of tongue obstruction. • The hyoid myotomy and suspension is the preferred technique when lateral pharyngeal wall collapse exists. The mandibular-maxillary advancement is the only other surgical procedure that directly affects the collapse of the lateral pharyngeal wall. • Multi-level pharyngeal surgery is both safe and effective in selected patients with obstructive sleep apnea syndrome (OSAS). • Patients with more severe sleep-disordered breathing (SDB) are more likely to have multi-level obstruction. • Combining hyoid myotomy and suspension surgery with other hyopharyngeal procedures, such as tongue base radiofrequency or the genioglossus advancement (GA), can produce significant tongue swelling. This swelling may require a more vigilant postoperative monitored setting, such as the intensive care unit, or additional treatment modalities, such as parenteral antihypertensive medications, steroids, and/or nasal positive airway pressure. • Placement of a drain and a pressure dressing reduces the risk of seroma and hematoma formation postoperatively.

1. INTRODUCTION Due to the limited surgical success rates using the uvulpalatopharyngoplasty (UPPP) alone in patients with SDB, an investigation for other sites of obstruction and surgical alternatives was undertaken. Diagnostic testing revealed that the hypopharynx may be a potential component of upper airway collapse in SDB. The hypopharyngeal sites of obstruction included the base of tongue and the lateral pharyngeal walls. Surgical

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procedures designed to treat this hypopharyngeal obstruction or collapse were subsequently implemented. The hyoid myotomy and suspension was designed to prevent both base of tongue collapse and, more significantly, lateral pharyngeal wall collapse. Modifications to the initial description have been attempted to improve the surgical success rate, while minimizing complications.

2. BACKGROUND Patton et al. (1) described an “expansion hyoidplasty” in the canine model to enlarge the hypopharyngeal airway. This technique was attempted by Fujita as well as Riley and Powell in human subjects, but was abandoned because of disappointing results. These investigators found an inferior quality to the hyoid bone for placement of metallic screws and plating systems. Kaya presented a case report of two patients with sleep apnea treated by sectioning the hyoid bone in acromegalics. Only one had postoperative improvement, but no further studies were continued using this approach (2). Van de Graf et al. (3) confirmed an improvement of airway patency and decreased airway resistance from anterior hyoid advancement using a canine model. Modifications of the original hyoid expansion procedure to advance the hyoid bone superiorly and anteriorly was examined. Riley et al. (4) described a case report in 1984 of a patient with obstructive sleep apnea undergoing a mandibular osteotomy and hyoid bone advancement.

3. HYOID ANATOMY The hyoid bone is the only bony structure supporting the upper airway in the cervical area. The middle constrictor muscle inserts on the greater cornu of the hyoid bone. This muscle is the key to lateral pharyngeal wall collapse. The anterior body of the hyoid bone reveals the insertion of the geniohyoid and genioglossus muscles. Understanding the anatomical relationships of the hyoid bone and supporting musculature can aid the surgeon in performing the procedure for the optimal advancement, while minimizing complications.

4. PRESURGICAL EVALUATION Hypopharyngeal obstruction has been documented by a variety of diagnostic modalities, including the initial studies using electromyography, then endoscopy with the Müller maneuver, and finally radiographic analysis using cephalometric radiography, computerized tomography, and magnetic resonance imaging. Presently, most surgeons use preoperative lateral cephalometric radiography and/or fiberoptic

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Figure 1 Hypopharyngeal view: (A) pre-Müeller maneuver; (B) during Müeller maneuver. (See color insert.) nasopharyngoscopy with the Müeller maneuver as a cost-effective technique to estimate the existence of hypopharyngeal collapse. The addition of the Müller maneuver with or without pharyngeal pressure monitoring may assist in determining areas of collapse during the upper airway endoscopy exam (Fig. 1A, B). The Müeller maneuver is performed with the patient inhaling against a closed glottis with the nose and mouth closed to generate negative pressure in the pharynx. Numerous studies have described the benefits and limitations of this examination for preoperative prediction of effectiveness of the uvulopalatopharyngoplasty. There are a number of findings that suggest the existence of hypopharyngeal obstruction preoperatively (Table 1). Physical examination alone cannot confirm hypopharyngeal obstruction.

5. TREATMENT PHILOSOPHY There are potentially different phases of upper airway reconstruction. The initial phase of surgery directs treatment to the specific areas of obstruction. Persons with isolated obstruction at the level of the soft palate receive a palatal surgical procedure and patients with obstruction at the level of the hypopharyngx undergo a procedure designed to improve this region. If the patient has both palatal and hypopharyngeal obstruction, they receive procedures directed at both sites, either simultaneously or staged. The determination of the timing of surgery is dictated by the following: the patient’s ability to use nasal CPAP to protect the upper airway from collapse post-operatively, the severity of SDB, the safety and stability of the upper airway, and the

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Table 1 Factors Suggesting Hypopharyngeal Obstruction Obesity (body mass index >31) Severe sleep apnea (apnea-hypopnea index >40) Small soft palate anatomy PAS <11mm noted on lateral cephalometric radiograph Lateral pharyngeal wall narrowing noted on fiberoptic examination Lateral pharyngeal wall collapse noted during the Müller maneuver

number and sites of upper airway reconstructive procedures. The hyoid myotomy and suspension is designed to improve both lateral pharyngeal wall and base of tongue obstruction. The goal is to successfully treat or significantly improve the underlying SDB.

6. SURGICAL MODIFICATIONS After the limitations of the initial hyoid expansion described by Patton et al. in human subjects, Riley et al. described a hyoid advancement and suspension procedure (4). The hyoid bone is mobilized and suspended to the anterior mandible (Fig. 2). A variety of techniques and substances were attempted. The final material selected to suspend the hyoid bone reliably to the anterior aspect of the mandible was fascia lata. This procedure was effective in treating SDB patients. The technique was abandoned because of the increased risk of anterior mandibular fracture when performed with a mandibular osteotomy, extensive dissection in the submental region, and the need to harvest fascia lata from the lateral thigh. A modification was designed to suspend and advance the intact hyoid bone anteriorly and inferiorly to the superior aspect of the thyroid cartilage (Fig. 3) (5). A recent modification of the hyoid suspension procedure divided the hyoid bone in the midline and suspended the hyoid bone to the anterior body of the mandible using Repose tongue suspension equipment.

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Figure 2 Original hyoid myotomy and suspension procedure.

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Figure 3 Modified hyoid myotomy and suspension procedure. The modified hyoid myotomy and suspension technique currently in use suspends the hyoid bone and supporting musculature to the superior thyroid cartilage. The operation is similar to the thyroglossal duct cyst excision approach (Sistrunk procedure). A cervical horizontal incision is made over or immediately inferior to the location of the hyoid bone (Fig. 4). The platysma and soft tissues are divided to expose the anterior cervical strap muscles (Fig. 5). Once the hyoid bone is exposed, the inferior hyoid musculature attachments are released (Fig. 6). Occasionally, the stylohyoid ligament needs to be excised from the superior extent of the lesser cornu to allow adequate mobilization. The hyoid bone is secured to the superior aspect of the thyroid cartilage with four permanent sutures of 1–0 Ticron (Fig. 7). All sutures are tied while the hyoid bone is pulled anteriorly over the thyroid cartilage to allow maximum advancement (Fig. 8).

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Figure 4 Horizontal anterior cervical incision. (From Ref. 10.)

Figure 5 Division of the platysmal muscle and soft tissues. (From Ref. 10.) The incision is closed in layers after hemostasis is attained. A Penrose drain and pressure dressing is placed for 24hr to decrease the risk of hematoma and seroma formation.

7. SURGICAL RESULTS In a review of 239 patients treated between 1989 and 1992, with most requiring phase I surgery, which entails a GA, hyoid suspension, and UPPP (6), the overall results revealed a successful treatment in 61% of the patients. When evaluating those with mild to moderately severe OSAS (i.e., RDI <60), there was an approximately 75% success rate.

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The surgical success declined to 42% when patients had severe OSAS (RDI >60). Ramirez and Loube in 1996, using the same protocol, revealed in morbidly obese patients a 42% success rate, which was identical to the success rate in the study by Riley et al. in those with severe OSAS (7). Utley et al. noted the results of phase I surgery in 14 patients, revealing a 57.1% (8/14) success rate, defined as a reduction in the RDI by 50% and a postoperative RDI of <20 (8). Troell revealed 7 of 11 patients (63.6%) were successfully treated as defined by an RDI<10 with resolution of EDS by a combination of UPPP, GA, and HM (9). The treatment outcomes of multiple-level pharyngeal surgery addressing both the retropalatal and retrolingual areas of collapse using the hyoid suspension in the surgical protocol yielded promising surgical results.

Figure 6 Infrahyoid musculature release. (From Ref. 10.)

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Figure 7 Hyoid bone advancement and placement of permanent sutures. (From Ref. 10.) A study reviewed the results with an isolated modified hyoid suspension to suspend the intact hyoid bone to the superior aspect of the thyroid cartilage (5). Postoperative sleep studies and subjective symptomatology revealed that 75% of subjects had correction of their excessive daytime sleepiness and marked improvement in their sleep disorders. The mean preoperative and postoperative RDI were 44.7 (SD 22.6) and 12.8 (SD 6.9), respectively, while the mean preoperative and postoperative LSAT were 82% (SD 6%) and 86% (SD 5%), respectively. The conclusions were that in selected patients, the modified HM procedure appears to offer significant adjunctive treatment to hypopharyngeal obstruction.

8. SURGICAL COMPLICATIONS This procedure is technically a simple procedure with minimal risks of complications (Table 2). Dissection should be limited to the midline of the anterior neck and to the tissue immediately adjacent to the hyoid bone. Dissection medially to the lesser

Figure 8 Immobilization of the hyoid bone to the superior thyroid cartilage. (From Ref. 10.) Table 2 Complications Hematoma formation Seroma formation Wound infection

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Hyoid bone fracture Cervical scar formation Dysphagia Hypoglossal nerve injury Superior laryngeal nerve injury Postoperative upper airway obstruction

cornu limits the risk of superior laryngeal nerve injury and dissection with limited exposure superior to the hyoid bone limits the risk of hyoglossal nerve injury. Advancement of the hyoid bone should be performed cautiously to prevent hyoid bone fracture. Occasionally, the thyroid cartilage is ossified and a drill to create an avenue for passing the suture is required.

9. CONCLUSIONS The hyoid myotomy and suspension is a technically simple procedure with good surgical results and minimal risks that can improve both lateral pharyngeal wall collapse and base of tongue obstruction in SDB.

REFERENCES 1. Patton TJ, Ogura JH, Thawley S. Expansion hyoidplasty. Laryngoscope 1983; 93:1387–1396. 2. Kaya N. Sectioning the hyoid bone as a therapeutic approach for obstructive sleep apnea. Sleep 1984; 7(1):77–78. 3. Van de Graaf WB, Gottfried SB, Mitra J, et al. Respratory function of hyoid muscles and hyoid arch. J Appl Physiol 1984; 57:197–204. 4. Riley R, Guilleminault C, Powell N, et al. Mandibular osteotomy and hyoid bone advancement for obstructive sleep apnea: a case report. Sleep 7(1):79–82. 5. Riley R, Powell N, Guilleminault C. Obstructive sleep apnea and the hyoid: a revised surgical procedure. Otolaryngol Head Neck Surg 1994; 111:717. 6. Riley R, Powell N, Guilleminault C. Obstructive sleep apnea syndrome: a review of 306 consecutively treated surgical patients. Otolaryngol Head Neck Surg 1993; 108:117. 7. Ramirez SG, Loube DI. Inferior sagittal osteotomy with hyoid bone suspension for obese patients with sleep apnea. Arch Otolaryngol Head Neck Surg 1996; 122:953. 8. Utley DS, Shin EJ, Terris DJ. A cost-effective and rational surgical approach to patients with snoring, upper airway resistance syndrome or obstructive sleep apnea syndrome. Laryngoscope 1997; 107:726. 9. Troell R. Contemporary surgical approaches to upper airway reconstruction in sleep disordered breathing. Otorhinolaryngol Nova 2000; 10:138–148. 10. Terris DJ. Multilevel pharyngeal surgery for obstructive sleep apnea: indications and techniques. Oper Techn Otolaryngol Hrod Neck Surg 2000; 11:12–20.

24 Skeletal Techniques: Mandible and Maxilla Kasey K.Li Sleep Disorders Clinic and Research Center, Stanford University Medical Center, Stanford, California, U.S.A.

Obstructive sleep apnea syndrome (OSAS) has been shown to increase cardiovascular morbidity and mortality (1,2). The psychomotor sequelae of OSAS including excessive daytime sleepiness, fatigue, and poor quality of sleep resulting from sleep fragmentation are also well recognized (3,4). Therefore, treatment of OSAS is clearly indicated. Tracheotomy was the first treatment of OSAS. It bypasses all forms of obstruction in the upper airway. However, the associated morbidity of tracheotomy prevents its use in a majority of the patients. Sullivan et al. (5) first reported the application of nasal continuous positive airway pressure (CPAP) to maintain upper airway patency for OSAS. Because of its effectiveness, nasal CPAP is currently the first-line treatment of OSAS. However, patient compliance remains a major problem, and the long-term use of CPAP is an unrealistic expectation for many patients (6–8). Since the first tracheotomy performed by Kuhlo et al. (9), several major surgical advances have significantly improved the understanding and treatment of patients with OSAS. Uvulopalatopharyngoplasty (UPPP) was initially described by Ikematsu (10) and later popularized by Fujita et al. (11). UPPP improves oropharyngeal obstruction and is the most commonly performed procedure for the treatment of OSAS. With the increased recognition that hypopharyngeal airway obstruction is a major contributing factor of OSAS, genioglossus and hyoid advancement were later developed to improve treatment outcomes (12,13). In the early 1980s, numerous investigators found that mandibular advancement surgery can improve OSAS (14–16). To maximize the extent of mandibular advancement, concurrent maxillary advancement was subsequently advocated (17). Presently, UPPP, genioglossus and hyoid advancement, as well as maxillomandibular advancement (MMA) are widely used to improve upper airway obstruction in OSAS. Of the available surgical interventions, MMA is clearly the procedure with the highest success rate (17–20).

1. RATIONALE FOR MAXILLOMANDIBULAR ADVANCEMENT The contributing causes that lead to OSAS are multifactorial. They may have negative influence on the delicate balance necessary for airway patency during sleep. In addition to obesity, male gender, age, and ethnicity (21–23), craniomaxillofacial abnormality is a

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well-recognized predictor of OSAS (24–26). MMA was initially advocated based on the finding that maxillofacial skeletal abnormality, that is, maxillary and/or mandibular deficiency are frequently found in patients with OSAS, and that maxillomandibular deficiency results in diminished airway dimension, which leads to nocturnal obstruction. MMA achieves enlargement of the pharyngeal and hypopharyngeal airway by physically expanding the skeletal framework. In addition, the forward movement of the maxillomandibular complex improves the tension and collapsibility of the suprahyoid and velopharyngeal musculature. Recent evidence further suggests that MMA improves lateral pharyngeal wall collapse (27), which has been shown to be a major contributor in OSAS (28–30).

2. PATIENT SELECTION MMA can be performed as the initial surgical treatment, or reserved as the “last resort” when other procedures have insufficiently improved the patient (31). The debate continues on whether patients should undergo less invasive procedures such as UPPP with genioglossus/hyoid advancement first, or a single-stage reconstruction consisting of MMA alone or in conjunction with other “adjunctive” procedures (19,32). In the author’s experience, although the less invasive procedures are often attempted first, some patients have elected to proceed directly to MMA. These patients usually have either severe sleep apnea or significant maxillomandibular deformity. Although patients with maxillomandibular deficiency are considered “good” candidates for MMA, it should also be considered in patients without “disproportionate” maxillofacial features (33). This is because recent evidence suggests that previous concerns of MMA resulting in a compromised facial esthetics have been insignificant in most patients (33,34). It may be that most of the patients with OSAS are middle-age adults, and most of them are showing signs of facial aging due to soft tissue sagging. MMA achieves facial skeletal expansion, and thus enhances the facial esthetics by improving soft tissue support (33,34). Surgical decision is usually based on the surgeon’s preference, experience, the patient’s body habitus, airway/skeletal anatomy, the severity of OSAS, the patient’s desire, and other comorbid factors (35).

3. MAXILLOMANDIBULAR ADVANCEMENT PROCEDURE Although MMA for the treatment of OSAS is similar to the procedure performed to correct skeletal facial deformities for malocclusion, it must be emphasized that there are a few major differences. Since the occlusion must be preserved while the maxilla and the mandible are advanced the same distance, either arch bars or orthodontic bands are required prior to the osteotomies. A Le Fort I maxillary osteotomy (Fig. 1) is performed above the apices of teeth. The maxilla is down fractured after pterygomaxillary separation. The descending palatine arteries are identified and are preserved if possible. The mobilized maxilla is manipulated and advanced approximately 10–12mm. During the mobilization, the

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integrity of the descending palatine artery must be observed. If excessive tension is noted, the artery should be clipped and divided to prevent

Figure 1 Le Fort ostetomy. (From Operative Techniques of Otolaryngology.) excessive bleeding due to tearing of the vessels. The maxilla is stabilized with rigid fixation using four plates and the bone grafts are placed in the osteotomy sites. The alignment of the maxilla in relation to the mandible, dentition and the face is crucial to ensure acceptable occlusion and aesthetics. Mandibular osteootomy is performed via the sagittal split technique (Fig. 2). The medial and lateral cortex of the mandible is separated at the ramus region while preserving the inferior alveolar nerve. The dentated mandibular segment is advanced the same distance as the maxilla thus occlusion is restored. Rigid fixation is achieved with three positional screws on each side (plates are often also used to bridge the osteotomy sites to ensure rigidity) after the mandible is stabilized via intermaxillary fixation. Following the completion of the procedure (Fig. 3), intermaxillary fixation can be maintained for 7–10 days, or the occlusion can be supported by guiding elastics, depending on the rigidity of the fixation.

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Figure 2 Sagittal split osteotomy. (From Operative Techniques of Otolaryngology.)

Figure 3 Completed maxillomandibular advancement. (From Operative Techniques of Otolaryngology.)

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4. PERIOPERATIVE MANAGEMENT As always, anesthesia induction and intubation is especially critical for OSAS patients, and the surgeons should be present at all times. An awake fiberoptic intubation or tracheotomy should be considered in difficult airway situations, especially in obese patients with an increased neck circumference and associated skeletal deformities (mandibular deficiency and low hyoid bone) (36). Although blood transfusion is often unnecessary, we prefer to have two units of autologous blood available. All patients are awakened and extubated following surgery in the operating room. All patients are monitored in the intensive care unit (ICU) for the first postoperative day and arterial line is used for blood pressure monitoring. The use of narcotics should be closely monitored due to the increased potential of airway compromise. Either humidified oxygen (35%) via face tent or nasal CPAP is used throughout the hospitalization. Nasal trumpets are necessary if nasal CPAP is used to prevent subcutaneous emphysema from the intraoral incisions. The patients are transferred to the ward the following day, and discharge criteria include a stable airway, adequate oral intake of fluids and satisfactory pain control.

5. SURGICAL OUTCOMES Approximately 400 MMA procedures have been performed for the treatment of OSAS at Stanford. An analysis of 175 patients between 1988 and 1995 demonstrated 166 patients have had a successful outcome, with a cure rate of 95% [if using the criteria of achieving the respiratory disturbance index (RDI) less than 20 events per hour and greater than 50% reduction]. The mean preoperative RDI was 72.3 events per hour. The mean postoperative RDI was 7.2 events per hour. The mean lowest oxygen saturation (LSAT) improved from 64.0% to 86.7%. Eighty-six patients who failed UPPP/genioglossus/hyoid advancement underwent MMA. The cure rate in this group was 97% (83/86 patients). To date, 59 patients (49 men) have had long-term follow-up results (37). The mean age was 47.1 years. The mean body mass index (BMI) was 31.1kg/m2. Nineteen patients had only subjective (quality of life) results. These patients refused long-term polysomnography due to various reasons including inconvenience, being time consuming, and cost. Sixteen of the 19 patients continued to report subjective success with minimal to no snoring, no observed apnea, and no recurrence of excessive daytime sleepiness (EDS). All patients reported stable (unchanged) weight to mild weight gain (<5kg). Three patients reported recurrence of snoring and EDS. Long-term polysomnographic data were available in 40 patients (33 men). The mean age was 45.6 years. The mean BMI was 31.4kg/m2. The preoperative RDI and LSAT were 71.2 events per hour and 67.5%, respectively. The 6-month postoperative RDI was 9.3 events per hour and the LSAT was 85.6%. The mean follow-up period was 50.7 months, and longterm RDI and LSAT were 7.6 events per hour and 86.3%, respectively. Due to different factors such as the individual patient’s lifestyle and treatment expectations, the subjective outcomes can be highly variable, and may not correlate with the objective outcomes. To evaluate the patient’s perspective on the outcomes after MMA, a study using a questionnaire was conducted. Six months after MMA,

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questionnaires were sent to 56 patients who have undergone MMA for persistent OSA after UPPP/genioglossus/hyoid advancement (38). Forty-two (75%) patients (36 men) completed and returned the questionnaires. The mean age was 46.3 years and the mean BMI was 32.1kg/m2. The mean RDI improved from 58.7 to 10.0 events per hour. The mean LSAT improved from 76.3% to 87.3%. Thirty-seven patients (88%) were cured and all 42 patients reported improved sleep quality with a mean visual analog scale (VAS) of 8.7 (VAS 0–10). Temporary postoperative paresthesia of the inferior alveolar nerve distribution occurred in all of these patients, however, only four patients (10%) did not report either total or near total recovery within 6 months. No major infection was encountered. Minor infection involving the mandibular osteotomy sites occurred in three patients (7%) that completely resolved with local care and oral antibiotics. Although the questionnaires identified 10 patients with changes in speech, the changes were extremely subtle and insignificant with nine of the patients marked 0 on the VAS (mean VAS 0.08). Five patients reported changes in swallowing, the VAS scores were 0.5, 0.9, 1.0, 2.7, and 6.9 (mean VAS 2.4). The perceived pain and suffering following UPPP/genioglossus/hyoid advancement (mean VAS 5.9) was found to be similar to MMA surgery (mean VAS 5.1). Eighteen patients felt that the pain and suffering following phase I surgery was worse. However, 16 patients felt that the pain and suffering was worse following MMA. The remaining eight patients felt that the postoperative recovery was not significantly different between the two phases. Forty patients (95%) were satisfied with their results and would go through the reconstruction all over again. Two patients (5%) responded that they would not go though the reconstruction again in retrospect. The first patient was a 54-year-old man with the complaint of severe daytime fatigue and sleepiness. Polysomnographic findings were consistent with severe OSA (RDI 56, LSAT 86%). Despite total upper airway reconstruction, he continued to have significant symptoms of daytime sleepiness and the postoperative polysomnography demonstrated persistent OSAS (RDI 35.7, LSAT 91%). The second patient was a 43year-old man with severe OSAS (RDI 76.2, LSAT 82%). Although an improvement was achieved following the completion of airway reconstruction (RDI 20, LSAT 77.5%), he continued to have complaints of daytime sleepiness that affected his daily activity. This patient also reported significant changes in his swallowing (VAS 6.9), which contributed to the dissatisfaction. Fourteen (25%) patients (all men) did not respond to the questionnaire. They were younger (mean age 41.4 years) and less obese (mean BMI 28.4kg/m2). The severity of OSA was similar, however, the cure rate was higher in this group with 13 patients (93%) achieving a RDI≤20. The mean RDI improved from 57.1 to 9.3 events per hour. The mean LSAT improved from 79.9% to 87.9%.

6. COMPLICATIONS OF MMA 6.1 Maxillary Vascularity Aseptic necrosis of the maxilla is a feared, but fortunately, unusual consequence following maxillary osteotomies (39). Aseptic necrosis of the maxilla is a potential

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concern in performing MMA for OSAS due to the amount of advancement required. In large advancements, the soft tissue envelope of the maxilla will be “stretched” to its maximum physiological limit. In order to maintain optimal blood supply to the maxilla, we routinely try to preserve the descending palatine arteries. However, during the advancement process, the arteries can be torn since the arteries may not always accommodate the extent of the advancement. Therefore, the surgeon must be cognizant of this issue and be prepared to control the torn arteries during the advancement. The surgeon must also carefully monitor the viability of the maxilla throughout the procedure. If the viability of the maxilla is significantly compromised, the surgeon should consider placing the maxilla in its preoperative position and discontinuing the procedure. In over 400 MMAs performed at our center, two cases of MMA were discontinued due to this issue. No cases of aseptic necrosis have occurred. 6.2 Skeletal Fixation The majority of OSAS patients are men and most are obese. In a review of 21 morbidly obese patients undergoing OSAS surgery, four of the five complications were related to the stability of the fixation or suspension (40). These events could be related to the patients’ obesity in that the conventional fixation methods may be inadequate in this patient population due to the increased tissue mass, and consequent forces exerted on the plates and screws. Therefore, improved rigidity and fixation may be necessary in this patient population. 6.3 Occlusion Because the majority of OSAS patients require expedited treatment, arch bars are routinely used instead of orthodontics to establish the occlusion. Although this method is usually adequate, significant malocclusion can occur due to skeletal relapse from large advancement, early functioning by uncooperative patients, or increased forces exerted on the fixation device(s) by obese patients. Despite diligent efforts, postoperative malocclusion may be unavoidable in this patient population and postoperative orthodontic therapy may be necessary. Occasionally, revision surgery may be necessary due to significant malocclusion. In over 400MMAs performed, six cases have required revision surgery. 6.4 Velopharyngeal Insufficiency It is well known that velopharyngeal insufficiency (VPI) is a potential risk following UPPP. The risk of VPI may be even greater in patients who undergo MMA after UPPP since the forward movement of the maxilla increases the anterior-posterior dimension of the velopharynx, and thus further compromises the velopharyngeal closure. Interestingly, we have found that despite the combined effect of UPPP and maxillary advancement on the velopharynx, the risk of VPI is low, in that less than 10% of the patients had very mild symptoms of VPI (41). The low incidence of VPI could also be due to the inherently narrowed pharyngeal airway, and the increased collapsibility of the pharyngeal tissues

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and soft palate that are usually found in OSA patients. The anatomic and physiologic characteristics that predispose these patients to the development of OSAS might have provided some “protective effect” on the development of VPI after MMA. However, it must be emphasized that the risk of VPI is a potential complication in these patients. Therefore, preoperative consultation regarding the possibility of VPI should be considered, especially in patients with excessively foreshortened soft palates due to aggressive UPPP, when there are preexisting VPI symptoms.

7. CONCLUSION MMA is an extremely effective therapy for the treatment of OSAS. When properly executed, it is associated with minimal morbidity and is well accepted by the patients.

REFERENCES 1. Shahar E, Whitney CW, Redline S, et al. Sleep-disordered breathing and cardiovascular disease: cross-sectional results of the Sleep Heart Health Study. Am J Respir Crit Care Med 2001; 163:19–25. 2. Partinen M, Jamieson A, Guilleminault C. Long-term outcome for obstructive sleep apnea: experience in 385 male patients. Chest 1988; 94:9–14. 3. Gottlieb DJ, Whitney CW, Bonekat WH, et al. Relation of sleepiness to respiratory disturbance index: the Sleep Hearth Health Study. Am J Respir Crit Care Med 1999; 159:502–507. 4. Bonnet MH. The effect of sleep disruption on performance, sleep, and mood. Sleep 1985; 8:11– 19. 5. Sullivan CE, Berthon-Jones M, Issa FC, et al. Reversal of obstructive sleep apnea by continuous positive airway pressure applied through the nares. Lancet 1981; 1:862–865. 6. Kribbs NB, Redline S, Smith PL, et al. Objective monitoring of nasal CPAP usage in OSAS patients. Sleep Res 1991; 20:270–271. 7. Reeves-Hoche MK, Meck R, Zwillich CW. Nasal CPAP: an objective evaluation of patient compliance. Am J Respir Crit Care Med 1994; 149:149–154. 8. Waldhorn RE, Herrick TW, Nguyen MC, et al. Long-term compliance with nasal continuous positive airway pressure therapy of obstructive sleep apnea. Chest 1991; 99:855–860. 9. Kuhlo W, Doll E, Frank MD. Erfolgreiche Behandlung eines Pickwick-syndroms durch eine Dauertrachealkanule. Dtsch Med Wochenschr 1969; 94:1286–1290. 10. Ikematsu T. Study of snoring. 4th report. Therapy. J Jpn Otol Rhinol Laryngol Soc 1964:434– 435 (in Japanese). 11. Fujita S, Conway W, Zorick F, Roth T. Surgical correction of anatomic abnormalities of obstructive sleep apnea syndrome: uvulopalatopharyngoplasty. Otolaryngol Head Neck Surg 1981; 89:923–934. 12. Riley RW, Guilleminault C, Powell NB, Derman S. Mandibular osteotomy and hyoid bone advancement for obstructive sleep apnea: a case report. Sleep 1984; 13. Li KK. Lower pharyngeal airway surgery: hyoid suspension/advancement. In: Fairbanks DNF, Mickelson SA, Woodson BT, eds. Snoring and Obstructive Sleep Apnea. 3rd ed.. Philadelphia, PA: Lippincott Williams & Wilkins, 2003. 14. Powell NB, Guilleminault C, Riley RW. Mandibular advancement and obstructive sleep apnea syndrome. Bull Eur Physiopathol Respir 1983; 19:607–610.

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15. Bear SE, Priest JH. Sleep apnea syndrome: correction with surgical advancement of the mandible. J Oral Surg 1980; 38:543–549. 16. Kuo, PC, West RA, Bloomquist DS, et al. The effect of mandibular osteotomy in three patients with hypersomnia and sleep apnea. Oral Surg Oral Med Oral Pathol 1979; 48:385–392. 17. Riley RW, Powell NB, Guilleminault C. Obstructive sleep apnea syndrome: a review of 306 consecutively treated surgical patients. Otolaryngol Head Neck Surg 1993; 108:117–125. 18. Li KK, Riley RW, Powell NB, Gervacio L, Troell RJ, Guilleminault C. Obstructive sleep apnea surgery: patients’ perspective and polysomnographic results. Otolaryngol Head Neck Surg 2000; 123:572–575. 19. Prinsell JR. Maxillomandibular advancement surgery in a site-specific treatment approach for obstructive sleep apnea in 50 consecutive patients. Chest 1999; 116: 1519–1529. 20. Hochban W, Conradt R, Brandenburg U, et al. Surgical maxillofacial treatment of obstructive sleep apnea. Plast Reconstr Surg 1997; 99:619–626. 21. Young T, Palta M, Dempsey J, et al. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med 1993; 328:1230–1235. 22. Kripke DF, Ancoli-Israel S, Klauber MR, et al. Prevalence of sleep-disordered breathing in ages 40–64 years: a population-based survey. Sleep 1997; 20:65–76. 23. Ancoli-Israel S, Klauber MR, Stepnowsky C, et al. Sleep-disordered breathing in AfricanAmerican elderly. Am J Respir Crit Care Med 1995; 152:1946–1949. 24. Riley R, Guilleminault C, Powell N, et al. Palatopharyngoplasty failure, cephalometric roentgenograms, and obstructive sleep apnea. Otolaryngol Head Neck Surg 1985; 93:240–243. 25. Jamieson A, Guilleminault C, Partinen M, Quera-Salva MA. Obstructive sleep apneic patients have craniomandibular abnormalities. Sleep 1986; 9:469–477. 26. DeBerry-Borowiecki B, Kukwa A, Blanks R. Cephalometric analysis for diagnosis and treatment of obstructive sleep apnea. Laryngoscope 1988; 98:226–234. 27. Li KK, Riley RW, Powell NB, Guilleminault C. Obstructive sleep apnea and maxillomandibular advancement: an assessment of airway changes using radiographic and nasopharyngoscopic examinationa. J Oral Maxillofac Surg 2002; 60:526–530. 28. Schwab RJ, Gefter WB, Hoffman EA, Gupta KB, Pack AI. Dynamic upper airway imaging during respiration in normal subjects and patients with sleep disordered breathing. Am Rev Respir Dis 1993; 148:1385–1400. 29. Suratt PM, Dee P, Atkinson RL, Armstrong P, Wilhoit SC. Fluoroscopic and computer tomographic features of the pharyngeal airway in obstructive sleep apnea. Am Rev Respir Dis 1993; 127:487–492. 30. Schwab RJ, Gupta KB, Gefter WB, Metzger LJ, Hoffman EA, Pack AI. Upper airway and soft tissue anatomy in normal subjects and patients with sleep-disordered breathing. Significance of lateral pharyngeal walls. Am J Respir Crit Care Med 1995; 152: 1673–1689. 31. Li KK, Powell N. Lower pharyngeal airway surgery: maxillomandibular advancement. In: Fairbanks DNF, Mickelson SA, Woodson BT, eds., eds. Snoring and Obstructive Sleep Apnea. 3rd ed. Philadelphia, Pensylvania, Lippincott: Williams & Wilkins, 2003:182–189. 32. Hendler BH, Costello BJ, Silverstein K, Yen D, Goldberg A. A protocol for uvulopalatopharyngoplasty, mortised genioplasty, and maxillomandibular advancement in patients with obstructive sleep apnea: an analysis of 40 cases. J Oral Maxillofac Surg 2001; 59:892–897. 33. Li KK, Riley RW, Powell NB, Guilleminault C. Maxillomandibular advancement for persistent OSA after phase I surgery in patients without maxillomandibular deficiency. Laryngoscope 2000; 110:1684–1688. 34. Li KK, Riley RW, Powell NB, Guilleminault C. Patient’s perception of the facial appearance after maxillomandibular advancement for obstructive sleep apnea syndrome. J Oral Maxillofac Surg 2001; 59:377–380.

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35. Li KK. Discussion on “A protocol for uvulopalatopharyngoplasty, mortised genioplasty, and maxillomandibular advancement in patients with obstructive sleep apnea: an analysis of 40 cases.” J Oral Maxillofac Surg 2001; 59:898–899. 36. Riley RW, Powell NB, Guilleminault C, Pelayo R, Treoll RJ, Li KK. Obstructive sleep apnea surgery: risk management and complications. Otolaryngol Head Neck Surg 1997; 117:648–652. 37. Li KK, Powell NB, Riley RW, Troell RJ, Guilleminault C. Long-term results of maxillomandibular advancement surgery. Sleep Breath 2000; 4:137–139. 38. Li KK, Riley RW, Powell NB, Gervacio L, Troell RJ, Guilleminault C. Obstructive sleep apnea surgery: patients’ perspective and polysomnographic results. Otolaryngol Head Neck Surg 2000; 123:572–575. 39. Lanigan DT, Hey JH, West RA. Aseptic necrosis following maxillary osteotomies: report of 36 cases. J Oral Maxillofac Surg 1990; 48:142–156. 40. Li KK, Powell NB, Riley RW, Zonato, A, Gervacio L, Guilleminault C. Morbidly obese patients with severe obstructive sleep apnea syndrome: is airway reconstructive surgery a viable option? Laryngoscope 2000; 110:982–987. 41. Li KK, Troell RJ, Powell NB, Riley RW, Guilleminault C. Uvulopalatopharyngoplasty, maxillomandibular advancement and the velopharynx. Laryngoscope 2001; 111: 1075–1078.

25 Radiofrequency Tissue Volume Reduction of the Tongue Samuel A.Mickelson The Atlanta Snoring & Sleep Disorders Institute, Advanced Ear, Nose & Throat Associates, Atlanta, Georgia, U.S.A. 1. INTRODUCTION Macroglossia causing retrolingual airway collapse is a known cause of sleep disordered breathing (1). Several methods have been developed to reduce the tongue in size including cryotherapy (S.Fujita, unpublished data), CO2 laser excision via a transoral route (2–4), and transcervical excision (5). The potential use of submucosal radiofrequency (RF) energy to reduce the tongue in size was introduced as a less invasive technique by Powell et al. (6) in 1997.

2. BASIC SCIENCE OF RF TISSUE VOLUME REDUCTION RF energy has been used for many applications including tissue cutting, vessel coagulation, and tissue volume reduction. RF energy is applied to tissue by creating a circuit through the body with a large surface grounding pad and a very small treatment site electrode or by way of a bipolar treatment electrode with both electrodes in close approximation to one another. In this manner, the energy is focused in the region of the treatment electrode. In order to cause tissue volume reduction, RF energy is applied at low energy levels with the needle electrode in full contact with the tissues. The RF energy causes the surrounding tissues to heat up, creating a lesion of nonviable tissue around the electrode. By keeping the temperature below the boiling point, the continued application of energy allows heat to spread, leading to larger lesions with increasing energy delivery. Tissue volume reduction has been applied to many bodily sites including liver, prostate, and cardiac tissue. Powell and Riley introduced RF energy to reduce tongue volume in 1997. The prototype electrode was a 1.6cm needle (distal electrode exposed and proximal electrode insulated) intended to heat deeper tissues while protecting mucosa. Two temperature sensors were attached: one at the distal electrode in order to monitor tissue temperature and one on the insulation to monitor temperature near the mucosa. A computer was programmed to control RF energy delivery (Somnus Medical Technologies, now Gyrus ENT, Sunnyvale, CA) in order to maintain the target tissue temperature at a preprogrammed setting (6).

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When RF energy is applied to the tongue in this way, there is necrosis of the muscle with preservation of mucosa. Powell et al. (6) showed that as energy was increased from 500 to 2400J, the size of the treated lesion increased from 1.4cm×0.5cm to 1.5cm×1.7cm and the cross-sectional area of the lesion increased from 0.7cm2 to 1.4cm2 (6). After lesion creation, the initial 2.5cm2 lesion increased to 7cm2 after 2 days but then shrank to 1cm2 over the next 21 days. Application of 2400J to the tongue was estimated to cause an overall tissue volume reduction of 0.84g of muscle tissue (6). RF energy delivery requires the presence of water and electrolytes in the treatment tissue. The heating effect, tissue volume reduction, and clinical outcome with RF energy application are improved by administration of electrolytes to the tissue treatment area (7,8). Injection of 1–2cc of saline into the tissue, prior to application of RF energy, causes a more rapid delivery of energy and possibly a larger lesion.

3. PATIENT SELECTION RF tissue volume reduction may be performed in any patient with mild to severe obstructive sleep apnea syndrome (OSAS) with macroglossia, or relative macroglossia due to retrognathia or micrognathia. If performed under local anesthesia, a patient should be cooperative, have no significant gag reflex, and not have trismus. Tongue RF may be combined with other upper airway procedures. Patients should be willing to use continuous positive airway pressure (CPAP) for at least a few days after treatment. In patients with severe OSAS who cannot tolerate CPAP, a tracheostomy may be required.

4. TECHNIQUE There are currently three basic techniques that have been described: transoral through the tongue dorsum, transoral through the ventral aspect of the tongue, and transcervical above the hyoid bone. The transmucosal approach on the tongue dorsum is the most common method and is described here. Prior to the procedure, in order to reduce the risk of posttreatment infection, the patient is given a broad-spectrum antibiotic to cover oral anaerobic bacteria (amoxicillin, cephalexin, clindamycin, or metronidazole) and a topical antibacterial agent to rinse the mouth (Chlorhexidine). Steroids are administered prior to the procedure in order to reduce edema. When performed under local anesthesia, the patient should be NPO for a few hours. The planned treatment sites are marked with a skin marker. Local anesthesia is achieved with a topical anesthetic (xylocaine or benzocaine) to the planned mucosal treatment site and each lesion site is injected with 1–2cc of a local anesthetic with epinephrine. Injection of 1cc of sterile normal saline can also be used. The local anesthetic is usually injected into the same place as the planned lesion. The electrode is then inserted in order to treat the submucosal region, remembering that the area to be treated is generally 1–2cm from the needle insertion site. Care must be taken to avoid treatment of the lingual tonsils and mucosa and to stay near the midline so as to avoid the neurovascular bundle. The electrode insertion sites are

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Figure 1 Electrode insertion sites on the base of the tongue: 1—treatment session 1, 2—treatment session 2, 3— treatment session 3, 4—treatment session 4, 5—treatment session 5, 6— treatment session 6. placed just at or anterior to the circumvallate papilla. Lesions should not be too close together in order to avoid a large region of nonviable tissue. Treatment is limited to the central 2–3cm of the tongue and may be from 5 to 7cm in length (Fig. 1). Most of the research studies published to date have been performed with the same technology used by Dr.Riley and Dr.Powell. Using this generator and hand piece (Somnus Medical Technologies, now Gyrus ENT, Sunnyvale, CA), the impedance will usually range from 100 to 200Ω, the treatment temperature is 85°C, and a total of 750J of energy is applied to each lesion site. At each treatment session, three to four lesions are applied for a total of 2000–3000J. Immediately following treatment, the patient is given ice or a popsicle in order to reduce tongue edema. The patient is asked to sleep with the head elevated, continue intermittent ice application to the tongue for several days, and to use CPAP when sleeping. If sleep apnea is severe or there is significant edema, steroids may also be

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continued. For pain, the patient is usually given ibuprofen, acetominophen or a mild narcotic agent. Most patients are able to go home following treatment. Treatment sessions are repeated every 4–6 weeks until snoring and other OSA symptoms resolve. A follow-up sleep study is performed on completion of the treatments or between treatments to check for improvement.

5. TREATMENT RESULTS Powell et al. (9) performed the first human study of RF of the base of the tongue, with administration of a mean 8490J of energy over 5.5 treatment sessions. They

Table 1 Treatment Results of RF on the Base of the Tongue Author (Ref.)

No. of patients Mean no. of treatments

Pre-AHI Post-AHI

Powell et al. (9)

18

5.5

39.6

17.8

Woodson et al. (7)

56

5.4

40.5

32.8

38.8

17.2

Saline injection Stuck et al. (12)

20

3.4

32.1

24.9

Riley et al. (13)

20

4.6

35.1

15.1

Hohenhorst et al. (14)

10

2.5

47

24

demonstrated a radiographic reduction of tongue volume by a mean of 17% and >50% reduction in apnea-hypopnea index (AHI) from baseline (Table 1). The lowest oxygen saturation improved from 81.9% to 88.3%. Similar results were obtained by Stuck et al. (10–12) after only two treatment sessions with treatment of four lesions with 700J of energy (total 2800J per treatment session) and by Woodson et al. (7) with 5.4 treatment sessions (Table 1). Alternative approaches to the base of the tongue have also been studied. Instead of only treatment of the dorsum of the tongue, Riley et al. (13) applied the RF electrode to both the dorsum and the ventral aspect of the tongue with similar results (Table 1), though with lower energy and fewer treatment sessions compared to his earlier studies. Robinson et al. applied treatment of the base of the tongue through a transcervical approach under general anesthesia. In order to apply a larger amount of energy at one treatment session, they identified the neurovascular bundle with ultrasound. When combined with uvulopalatopharyngoplasty (UPPP), they were able to achieve a response rate of 80%. Similarly, Hohenhorst et al. (14) treated only the ventral aspect of the tongue with three lesions at each of two to three treatment sessions. They felt there was less pain and gagging with the ventral application and had similar treatment results (Table 1). Long-term results with 16 patients undergoing tongue-base RF have been reported by Li et al. (15) with a mean follow-up of 28 months. The initial AHI of the group was 39.6/hr, dropping to 17.8/hr soon after treatment and increasing to 24.9/hr at 28 months.

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The oxygen saturation at baseline was 81.9%, rising to 88.3% and then dropping to 85.8% at long-term follow-up. These results indicate that while there is still improvement long-term, there is some deterioration that occurs over time. Tongue-base RF has been shown to improve quality of life measures including the Epworth Sleepiness Score (ESS), Functional Outcome of Sleep Questionnaire (FOSQ), Snore 25, and SF-36 questionnaires (7,9,13,15). Woodson et al. (7) also showed that the improvement in quality of life measures was comparable to the use of CPAP. Tongue-base RF can be performed along with other upper airway procedures. Tonguebase RF has been shown to be safe and effective when combined with UPPP. Nelson (16) compared seven patients with only retropalatal collapse treated with only UPPP, with 10 patients with retropalatal and retrolingual collapse treated with tongue-base RF and UPPP. The success rates were similar in both groups (57% vs. 50%). Stuck et al. (17) performed RF to the base of tongue and palate in 18 patients. In addition to improvement in the ESS and snoring visual analog scales, the respiratory disturbance index fell from a mean of 25.3–16.7/hr. The injection of saline into the base of the tongue just prior to RF delivery may improve treatment results. As suggested by basic science studies, the addition of saline not only increases the speed of energy delivery, but it may also increase the size of the treatment area (7,8). The effects of prednisone and ibuprofen on RF tissue reduction were studied by Han and Woodson (18). While both reduced the acute edema, there was no significant long-term effect on tissue reduction by either medication. Tongue-base RF treatment is generally well tolerated. Posttreatment pain is usually mild to moderate on day 1 [4.5 on a 10-point Visual Analogue Scale (VAS)] and virtually gone by day 5 (7). There has not been any reported persistent dysphagia or voice change.

6. COMPLICATIONS AND AVOIDANCE STRATEGIES 6.1 Mucosal Ulceration and Infection Mucosal ulceration will occur if the electrode is too superficial. When present, the patient will experience severe throat pain and otalgia. Treatment should entail oral and topical antibiotics until all pain subsides and the ulcer is gone. If a tongue abscess develops, there will be severe pain, tongue swelling, dysphagia, and fever. Definitive diagnosis is made with MRI or CT. Treatment must be aggressive in order to prevent airway obstruction. While outpatient treatment with broad-spectrum antibiotics may be effective early on, some patients may require hospitalization, intravenous antibiotics, and transoral surgical drainage or debridement. Tracheostomy should be considered if the airway is compromised. Tongue abscess or infection occurs in approximately 3.1% of patients (7). The risk of infection should be reduced with pretreatment oral antibiotics and a topical antibacterial mouth rinse. Placement of the electrode should be deep into the tongue, in order to avoid affecting the mucosa. Lesions should not be placed too close together in order to avoid creating a single large nonviable region of tongue base.

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6.2 Tongue Paralysis, Bleeding Tongue paralysis is possible if the treatment sites are too close to the major branches of the hypoglossal nerves. In order to avoid these nerves, the treatment electrode should be kept in the middle third of the tongue. The midline of the tongue should be marked with a skin marker to maintain orientation. If extensive treatment of the tongue is planned in one treatment session, consideration should be given to ultrasound localization of the neurovascular bundle (19). While temporary weakness can rarely occur, permanent tongue paralysis has not been reported (7,9). While bleeding is a potential complication with any procedure, it has not been reported after tongue-base RF (7,9–12,16,20). Similar to avoiding neural injury, in order to prevent significant bleeding, treatment should be kept in the middle one-third of the tongue in order to avoid the neurovascular bundle. 6.3 Taste Sensation Loss or altered taste sensation may occur if the mucosa is injured, or due to submucosal RF energy effect on the lingual or glossopharyngeal nerves. Despite this risk, altered taste sensation has not been reported after RF of the tongue (7,9–12,16,20). 6.4 Dysphagia Dysphagia and aspiration may occur due to limitation of tongue motion, scar formation within or on the surface of the tongue, or paralysis of branches of the hypoglossal nerves. Despite this potential, persistent dysphagia has not been reported (7) (9–12,16,20). 6.5 Airway Obstruction Airway obstruction is a risk of any procedure for sleep apnea due to the combination of tissue edema, effect of narcotic analgesics, and effects of anesthetic agents. Powell et al. (6) showed that tongue edema peaks 2 days following RF treatment. Tissue edema may be reduced by administration of steroids, cooling of the treatment area, and head elevation. CPAP or bilevel positive airway pressure (BiPAP) use should be considered for patients with moderate or severe sleep apnea, in order to reduce edema and maintain airway patency. The risk of airway obstruction is low but tracheostomy has been reported to be needed in up to 3.9% (2 of 51) of patients (20). In patients with severe sleep apnea who are unable to use CPAP or BiPAP, more aggressive monitoring with continuous pulse oximetry in the hospital or extended recovery unit, or a planned tracheostomy should be considered.

REFERENCES 1. Fujita S, Conway WA, Zorick F, et al. Surgical correction of anatomic abnormalities in obstructive sleep apnea syndrome: uvulopalatopharyngoplasty. Otol Head Neck Surg 1981; 89:923–934.

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2. Fujita W, Woodson BT, Clark JL, Wittig RL. Laser midline glossectomy as a treatment for obstructive sleep apnea. Laryngoscope 1991; 101 (8):805–809. 3. Woodson BT, Fujita S. Clinical experience with lingualplasty as part of the treatment of severe obstructive sleep apnea. Otol Head Neck Surg 1992; 107(1):40–48. 4. Mickelson SA, Rosenthal L. Midline glossectomy and epiglottidectomy for obstructive sleep apnea syndrome. Laryngoscope 1997; 107:614–619. 5. Chabolle F, Wagner I, Blumen MB, Sequert C, Fleury B, De Dieuleveult T. Tongue base reduction with hyoepiglottoplasty: a treatment for severe obstructive sleep apnea. Laryngoscope 1999; 109(8):1273–1280. 6. Powell NB, Riley RW, Troell RJ, Blumen MB, Guillemenault C. Radiofrequency volumetric reduction of the tongue. A porcine pilot study for the treatment of obstructive sleep apnea syndrome. Chest 1997; 111:1348–1355. 7. Woodson BT, Nelson L, Mickelson SA, Huntley T, Sher A. A multi-institutional study of radiofrequency volumetric tissue reduction for OSAS. Otol Head Neck Surg 2001; 125(4):303– 311. 8. Livraghi T, Goldberg SN, Monti F, et al. Saline-enhanced radio-frequency tissue ablation in the treatment of liver metastases. Radiology 1997; 202(1):205–210. 9. Powell NB, Riley RW, Guillemenoult C. Radiofrequency tongue base reduction in sleepdisordered breathing: a pilot study. Otol Head Neck Surg 1999; 120(5):656–664. 10. Stuck BA, Maurer JT, Hormann K. Tongue base reduction with radiofrequency tissue ablation: preliminary results after two treatment sessions. Sleep Breath 2000; 4(4): 155–162. 11. Stuck BA, Maurer JT, Hormann K. Tongue base reduction with radiofrequency energy in sleep apnea. HNO 2001; 49(7):530–537. 12. Stuck BA, Maurer JT, Verse T, Hormann K. Tongue base reduction with temperaturecontrolled radiofrequency volumetric tissue reduction for treatment of obstructive sleep apnea syndrome. Acta Otolaryngol 2002; 122(5):531–536. 13. Riley RW, Powell NB, Li KK, Weaver EM, Guilleminault C. An adjunctive method of radiofrequency volumetric tissue reduction of the tongue for OSAS. Otol Head Neck Surg 2003; 129(1):37–42. 14. Hohenhorst W, Stoohs R, Knaack L, Gruenwald S, Koester U, Lamprecht J. Radiofrequency of the tongue by ventral approach. Otol Head Neck Surg 2003; 129(2): 180 (abstract). 15. Li KK, Powell NB, Riley RW, Guilleminault C. Temperature-controlled radiofrequency tongue base reduction for sleep-disordered breathing: long-term outcomes. Otol Head Neck Surg 2002; 127(3):230–234. 16. Nelson LM. Combined temperature-controlled radiofrequency tongue reduction and UPPP in apnea surgery. Ear Nose Throat J 2001; 80(9):640–644. 17. Stuck BA, Starzak K, Hein G, Verse T, Hoermann K, Maurer JT. Combined radiofrequency surgery on tongue base and soft palate in obstructive sleep apnea. Otol Head Neck Surg 2003; 129(2):200–201 (abstract). 18. Han JK, Woodson BT. Effects of prednisone and ibuprophen on radiofrequency volume tissue reduction in a rabbit model. Ann Otol Rhinol Laryngol 2002; 111:968–971. 19. Robinson S, Lewis R, Norton A, McPeake S. Ultrasound-guided radiofrequency submucosal tongue-base excision for sleep apnoea: a preliminary report. Clin Otolaryngol 2003; 28(4):341– 345. 20. Pazos G, Mair EA. Complications of radiofrequency ablation in the treatment of sleepdisordered breathing. Otol Head Neck Surg 2001; 125(5):462–426.

26 Tracheotomy Vincent D.Eusterman and Wayne J.Harsha Department of Otolaryngology—Head and Neck Surgery, Madigan Army Medical Center, Fort Lewis, Washington, U.S.A. 1. INTRODUCTION Tracheotomy is the ultimate surgical treatment for obstructive sleep apnea (OSA). It has the highest success rate for all therapies for OSA and is considered an important adjunct in treating severe life-threatening disease. Tracheotomy was once the only treatment for OSA and has been replaced by more conservative site-specific surgical stiffening and dilation of the upper airway. In addition, nasal continuous positive airway pressure (CPAP) and other nonsurgical therapies have proven highly effective in treating mild, moderate, and some severe forms of OSA. Tracheotomy is generally reserved for temporary airways, severe OSA failing CPAP, and life-threatening cardiac disease resulting from OSA. Tracheotomy and tracheostomy are used synonymously in the medical literature. Trache(o)—referring to the trachea, from Greek tracheia arteria [Gr. meaning rough artery] and tomy [Gr. tome a cutting] to cut the trachea, or stomy [Gr. stomoun to furnish with an opening] referring to the opening in the trachea. The procedure is probably the oldest surgical procedure in recorded history dating back 5600 years. Egyptian tablets circa 3600 BC depict images of what appears to be a knifewielder surgeon performing a throat incision. Tracheotomy was first described in the sacred book of Hindu medicine, the Rig Veda and later in Western medical text in the eight century BC when Homer described the opening of the trachea for the relief of a choking patient. In the first century BC, Asclepiades first described it in an elective setting. The Dark Ages saw little use for the tracheotomy, which at the time was considered both dangerous and useless. Robert Hook (1667) described the ability to sustain a dog’s life by ventilating the dog with a bellows placed in the severed trachea. Heister (1739) was the first to use the term “tracheotomy” to describe placement of a straight tube into the trachea using a straight trocar. Following several reports of the use of the tracheotomy as a means to alleviate acute airway obstruction in croup, the procedure saw a surge in its use with many physicians performing tracheotomies for airway obstruction secondary to diphtheria, croup, trauma, and airway foreign bodies. There were controversies as to the best technique and proper indication for tracheotomy. In 1909, Chevalier Jackson advocated a large incision and the division of the thyroid isthmus to clarify some of these issues. Jackson’s advances were profound and may have led to the overuse of the tracheotomy. Many advocated its use for dozens of medical ailments, including its use in all major surgery. The indications for tracheotomy became streamlined with three advances. The first was when Carte and

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Giuseppe proved that tracheotomy decreased the ventilatory dead space, aiding those suffering from chronic pulmonary conditions like chronic bronchitis and emphysema. The second was the invention of intermittent positive pressure ventilation led to the modern indication for use of tracheotomy. And finally, in 1965, oral and nasal intubations became popularized as a safe and effective way to secure an airway and reduced the operative indication for tracheotomy (1). In 1969, Kuhlo first described the use of tracheotomy to treat sleep apnea in a morbidly obese patient suffering from “Pickwickian syndrome” (2). Although the first descriptions of the use of a “permanent tracheotomy” for respiratory disorders were by Penta (1960) and by Mayer (1961), it was Fee and Ward (1977) who first described the technique of the permanent tracheotomy for the treatment of OSA (3). At that time, the tracheotomy was the only surgical procedure and cure for OSA. Since then, newer surgical and nonsurgical procedures discussed elsewhere in this book have been shown to be effective in treating less severe forms of OSA. Despite these new advancements in the treatment of OSA, tracheotomy remains an important option for patients with severe lifethreatening disease.

2. INDICATIONS Indications for tracheotomy in OSA vary between authors (3–6). These indications are listed in Table 1. Most agree that the patient must have oxygen desaturation below 70%, life-threatening arrhythmias during sleep, morbid obesity (body mass index, BMI ≥35kg/m2), severe daytime hypersomnolence, failed attempts at weight loss, and failed an adequate trial of CPAP. Additional indications include cor pulmonale, chronic alveolar hypoventilation, and the exacerbation of other comorbid conditions associated with obstructive nocturnal hypoxemia. Mickelson (4) designated “severe OSA” as a respiratory disturbance index (RDI) >50 and significant nocturnal hypoventilation as an SaO2 <60%. Riley et al. (5) describe severe OSA as RDI >60 and severe desaturation as an SaO2 <60%. Fairbanks (6) recommends tracheotomy in patients with SaO2 <50%.

Table 1 Indications for Tracheotomy in OSA Hypoventilation/hypoxemia/desaturation (SaO2 <50–70%) Life-threatening arrhythmias/bradycardia (HR ≤40–45bpm) Morbid obesity (BMI >40 or >35 with significant comorbidity) Failure/intolerance of CPAP Severe OSA (RDI >50–60) Disabling daytime hypersomnolence Exacerbation of comorbidities (seizures, CAD, and COPD) Retrognathia or skeletal deformities Cor pulmonale, CO2 retention, chronic alveolar hypoventilation Source: From Refs. 3–6.

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In addition to the permanent tracheotomy, temporary tracheotomy may be indicated in patients who may not meet the above criteria. Piccirillo and Thawley (7) recommend the use of temporary tracheotomy followed in 6 weeks by uvulopharyngopalatoplasty (UPPP) or tracheotomy at the same time as UPPP. When the patient recovers from UPPP, a polysomnogram (PSG) is performed with the tracheotomy capped and uncapped. If successful, the tracheotomy is decannulated and the wound is allowed to heal by secondary intention (7). Mickelson (4) also advocates tracheotomy for patients scheduled for other operative procedures that cannot tolerate perioperative CPAP. Thatcher and Maisel’s (8) recent retrospective study of 79 patients with severe OSA (mean BMI=41, RDI=81) showed that tracheotomy is 100% successful in treating the disease, but that decannulation occurred in only 16 patients (20%). Of the 16, five patients were decannulated after switching to CPAP, three were cured after UPPP, two lost weight and were successfully decannulated, and the remaining requested tracheotomy removal (8). To augment successful decannulation the surgeon should consider UPPP at the time of tracheotomy and include diet and weight loss counseling following surgery. Patients failing weight loss therapy may be candidates for bariatric surgery. Candidates for gastric bypass should have a BMI ≥40kg/m2 or be at least 200% of their IBW. Exceptions to this rule include patients with a BMI ≥35kg/m2 who suffer from obesity-related comorbidity. These comorbidities include cardiopulmonary disease, sleep apnea, diabetes, and physical conditions like severe osteoarthritis or chronic back pain that interferes with lifestyle (9,10). Long-term development of “vascular comorbidity” from OSA remains the ultimate concern physiologic concern to sleep specialists. Vascular comorbidity is the result of intermittent obstructive breathing, which produces intermittent cellular hypoxia with the release of reactive oxygen species. The result is an ischemia-reperfusion insult which upregulates sympathetic tone, releases catecholamine and elevates systemic and pulmonary blood pressure. The American Academy of Sleep Medicine Task Force (1999) recommends grading sleep apnea as mild (RDI 5–15), moderate (RDI 15–30), and severe (RDI >30) (11). This metric statistically correlates the presence of sleepiness, neurocognitive impairment, and vascular risk (12–14). Strollo (15) considers the asymptomatic, CPAP noncompliant OSA patient to be at the greatest risk for vascular comorbidity. He states, “other than CPAP, tracheotomy is the only surgical procedure, supported by data that can effectively treat the intermittent obstruction producing the vascular comorbidity related to OSA” (15).

3. SURGICAL TECHNIQUE 3.1 Preoperative Considerations Vascular and systemic comorbidity are common in the OSA patient. Coronary artery disease, hypertension, cerebrovascular disease, hypertriglyceridemia, cardiomyopathy, diabetes mellitus, gastroesophageal reflux, back pain, endocrine abnormalities, hepatobiliary disease, malignancies, degenerative joint disease, respiratory abnormalities, coagulopathy, and sudden death are considerations that should be taken into account in the perioperative work-up. When history and physical examination suggests concomitant

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disease further evaluation is appropriate. Preoperative laboratory studies include EKG, hematocrit, coagulation factors, and bleeding time. Chest radiographs, and possibly lateral neck and spine or computed tomography to access spine and anatomic concerns in the obese neck. Pulmonary concerns of postoperative aspiration can be addressed with simple exercise testing or by formal spirometry to assess the forced vital capacity (FVC) and forced expiratory volume (FEV1). Preoperative examination of the pharynx and larynx by flexible nasal—pharyngeal endoscopy gives helpful airway information to the surgeon and anesthesiologist. General anesthesia is recommended over local anesthesia due to discomfort associated with neck extension when positioning the patient for surgery. A variety of tubes should be available for establishing a stable airway. These include standard tracheotomy tubes, adjustable length tubes, and armored endotracheal tubes. Levine et al. (16) described custom fabrication a long tracheotomy tube using an endotracheal tube as an alternative method to bypass tracheal strictures when standard tubes are not available. Bronchoscope and emergent airway sets should be readily available in anticipation of a difficult airway during intubation. Perioperative sedation can precipitate an acute airway emergency and should be avoided in the OSA patient unless required. The tracheotomy patient may have significant psychosocial problems, including depression, spousal rejection, and problems in the workplace. The family, support personnel and surgery staff should be aware of these needs. Preoperative education not only includes the patient’s physical needs of wound care, tracheotomy tube cleaning, and airway suctioning but the care of the patients psychological needs as well. 3.2 Relevant Anatomy The larynx is comprised of the epiglottis, thyroid, arytenoids, and cricoid cartilages. The reversed signet ring cricoid is attached anteriorly to the thyroid cartilage by the cricothyroid membrane and cricothyroid muscle. This muscle arises from the anterior cricoid and travels superiorly and posterolaterally to attach to the lateral surface of the thyroid cartilage and rotates the thyroid anteriorly lengthening the vocal cords. Injury to the cricoid or thyroid cartilage during cricothyrotomy or tracheotomy could affect voice and airway patency. The innominate artery or brachiocephalic trunk crosses the anterior trachea at the thoracic inlet and is vulnerable to injury during and after tracheotomy. The trachea has cartilaginous rings anterolaterally and is membranous posteriorly and between these rings. The thyroid gland isthmus crosses the trachea anteriorly in the area of the second and third tracheal ring. Paratracheal structures of concern include the carotid arteries, jugular veins, thyroid gland, and recurrent laryngeal nerves. Surgical access to the brachymorphic neck is limited and difficult; a thorough knowledge of these structures is essential to avoid damaging them during tracheotomy. 3.3 Open Tracheotomy Variations exist in performing an open (temporary) tracheotomy in the OSA patient. General anesthesia is recommended, induction is undertaken with the anesthesiologist at the head of the bed to control the endotracheal tube and assist the surgeon. The neck is extended with a shoulder roll or by lowering the head of the table. Exceptionally large individuals with “no neck” require taping the shoulder girdle and pectoral fat inferiorly

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and taping the chin and submental fat superiorly (Fig. 1). Reverse Trendelenburg position recruits gravity to assist in this process. The thyroid notch, cricoid cartilage, and sternal notch landmarks are identified and marked. The skin incision for the correct curvature of the tube should be placed above the tracheal entrance

Figure 1 Large individuals with difficult cervical anatomy require special positioning for tracheotomy. Here surgical tape is used to position the shoulder girdle and pectoral fat inferiorly and extend chin and submental tissue superiorly. site. This is above the third tracheal ring level just below the cricoid cartilage depending on neck thickness. In the same regard, the skin incision would be placed lower in a defatted neck because the curve of the tube would start closer to the tracheal opening. As discussed earlier, a variety of tracheotomy tubes, including an adjustable tracheotomy tube (Fig. 2) should be on hand and tested before the procedure. The skin and subcutaneous tissue is infiltrated with 1% lidocaine with 1:100,000 epinephrine. A 3cm horizontal (cosmetic) or vertical (hygienic) incision is made inferior to the cricoid cartilage. Skin and subcutaneous tissue flaps are elevated and the median raphe of the strap muscles is identified. Midline dissection is important for hemostasis and avoiding paratracheal structures. Strap muscles are separated away from the thyroid gland using electrocautery and retracted laterally.

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Figure 2 Temporary adjustable tracheotomy tube (Bivona). The thyroid gland isthmus is carefully undermined and elevated off the trachea. The isthmus is isolated, cross-clamped, divided using electrocautery and suture ligated with 2–0 silk. An intact thyroid isthmus could be irritated by the tracheostomy tube and cause postoperative bleeding. The remaining gland and soft tissue is cleaned off the pretracheal fascia from the level of the cricoid to the level of the fourth tracheal ring. Following meticulous hemostasis, the inferior aspect of the incision is palpated for the location of the innominate artery. The anesthesiologist is asked to deflate the endotracheal balloon and advance the endotracheal tube toward the right main stem bronchus before reinflating it. This technique avoids cuff injury from injection and incision and allows the airway to be sealed should bleeding occur. The trachea is anesthetized by transtracheal injection of lidocaine to reduce postoperative coughing. The cricoid is elevated superiorly with a hook to help control the tracheal incisions. The incision is centered over the third tracheal ring and can be an inverted U flap or H- or T-shaped depending on surgeon preference. The FiO2 should be <20% to reduce the risk of airway fire when entering the airway with electrocautery. Tracheal cartilage flaps are sutured to the skin or subcutaneous tissue with resorbable suture to facilitate emergent tube replacement if dislodged. Tracheal cartilage resection is generally reserved for permanent tracheotomy and contraindicated in temporary tracheotomy because cartilage loss may result in tracheal stenosis. Tracheal cartilages are separated with a tracheal spreader to facilitate tube placement. The anesthesiologist retracts the endotracheal tube to a level above the proximal opening. The tracheotomy tube with obturator is inserted. The obturator is removed, inner cannula inserted and balloon cuff inflated to the proper pressure. Wetting or lubricating the balloon cuff before insertion can help avoid puncture by calcified tracheal cartilage. Respiration is tested, and confirmed by carbon dioxide monitors. The tracheotomy tube is secured to the skin in the four quadrants using 2–0 silk sutures. Umbilical tape

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tracheotomy ties are then placed to prevent dislodgement of the tube by ventilator tubing. Skin may be left open to prevent subcutaneous emphysema and or pneumomediastinum. Post-operative chest x-ray is ordered to show the relationship of the tracheotomy tube to the carina, the status of the lung and mediastinum and tissue spaces in the neck. Percutaneous dilatational tracheotomy (PDT) has become safer when using bronchoscope guidance (17), however, it is not considered safe in the obese neck. Cialgia and Graniero (18) do not recommend the PDT for those with morbid obesity or those whose cricoid cartilage cannot be palpated. 3.4 Permanent Tracheotomy Like open tracheotomy, there are a number of accepted techniques for performing the permanent tracheotomy for OSA, with a few governing principles that remain the same. Foremost is the need to create a continuous epithelial lined stoma with direct anastomosis between the tracheal epithelium and the skin. The second is debulking peristomal fat to create a shallow stoma to comfortably accept a tracheotomy tube. Finally, the obese neck has redundant submental fat and skin, which can be a surgical challenge when it occludes the permanent tracheotomy at night despite an adequate stoma size. The first of three methods of permanent tracheotomy is the technique described by Fee and Ward (3) in their 1977 article. The skin incision is marked with the patient’s head preferably in the neutral position. The incision is in the shape of a “horizontal H” with the inferior most incision line placed low in the neck for easier

Figure 3 Permanent tracheotomy skin incisions. (A) Fee and Ward (3) “horizontal H” incision. (B) Sahni et al. (19) describe a “horizontal H” with 135° angled extensions. (C) Eliachar et al. (20) and Gross et al. (21) make a superiorly based U-shaped flap. manual occlusion during phonation. Each horizontal incision measures about 2–3cm in length, the vertical connecting incision is 1.5cm in height (Fig. 3A).

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Horizontal skin flaps are raised with an adequate amount of vascular subcutaneous tissue and retracted laterally in one of several atraumatic methods. Skin is undermined laterally and superiorly to release adequate tissue to prevent tension at the stoma anastomosis. A large amount of subcutaneous fat is then debulked laterally to the sternocleidomastoid muscles, inferiorly to the sternal notch, and superiorly to the hyoid bone or thyroid notch. Meticulous attention is paid to hemostasis (3). The strap muscles are identified, separated in the midline, and retracted laterally. The thyroid isthmus is elevated from the trachea, clamped and divided using electrocautery. The free margins of the thyroid are then oversewn and trachea injected and approached in the same fashion as the open tracheotomy technique discussed earlier. Following cricoid elevation, a scalpel is used to make a “vertical H” shaped incision in the trachea. The horizontal incision is placed between the second and third or third and fourth tracheal rings and should measure 1.5cm in width. The vertical incisions are made at the lateral aspect of the trachea and should extend superiorly 1cm and inferiorly 1.5cm (Fig. 4A) (3). The length of the vertical incisions may vary with each patient, as the ultimate goal is to have tracheal flaps that are long enough to reach the skin flaps without tension on the suture lines. The tracheal flaps are sewn to the horizontal skin edges. The lateral skin flaps are reflected into the wound and sewn to the vertical portions of the tracheal incision to complete the stoma opening (Fig. 4B). A standard cuffed nonfenestrated

Figure 4 Permanent tracheotomy. (A) Lateral skin flaps after “horizontal H” incisions and tracheal flaps after “vertical H” incision. (B) Tracheal flaps are sewn to the horizontal skin edges, lateral skin flaps are sewn into the vertical tracheal margins completing the stoma. tracheotomy tube or a reinforced endotracheal tube is then placed into the trachea for deep tracheal suctioning in the postoperative period.

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Sahni et al. (19) described a very similar procedure with some modifications of the skin incision (Fig. 3B). They shorten the horizontal portions of the H-shaped skin incisions to approximately 1.5cm and then extend these incisions at a 135° angle for another 1.5cm on each side of both the inferior and superior incisions (19). The tracheal incisions are carried out in the same manner as mentioned earlier. The results are a slightly larger final stoma with four diagonally oriented skin incisions closed with nonabsorbable sutures, which are later removed. Eliachar et al. (20) and Gross et al. (21) advocate skin incisions that resemble a thyroidectomy incision made low in the neck proceeding to an omega-shaped superior extension in the midline (Fig. 3C). Eliachar et al. create a superiorly based U-shaped flap incision in the trachea. They suture the tracheal flap superiorly to the skin and the skin flap inward toward the trachea (20). Gross et al. use an additional submental lipectomy incision and removes a small square portion of the tracheal ring (21). 3.5 Lipectomy A common problem that plagues tracheotomies in OSA patients is the occlusion of the tracheotomy by submental fat and soft tissue at night. Gross et al. describe a large open technique of cervical lipectomy through the incision they make for the tracheotomy. The lipectomy extends laterally to the sternocleidomastoid muscles, superiorly to the level of the hyoid, and inferiorly to the sternal notch. They also remove potentially obstructive redundant submental skin and fat through an elliptical excision, which extends deep to the mylohyoid muscle. The incisions are closed over bilateral Penrose drains (21). Clayman and Adams in 1990 (22) described a method of cervical lipectomy through an elliptical tracheotomy incision. They raised superior and inferior horizontal subplatysmal flaps. Enough skin and soft tissue is removed to prevent occlusion of the tracheostoma yet closed without placing tension on the wound (22). Fedok et al. (23) mentioned the use of suction-assisted lipectomy during tracheotomy, which allows for soft tissue repositioning and prevention of stoma occlusion at night.

4. POST-OPERATIVE CARE The immediate post-operative care is directed at teaching the patient and family about tracheotomy care. Again, psychosocial issues, depression, spousal rejection, and workplace problems must be addressed. The tracheotomy appliance can be changed on the first or second postoperative day to an uncuffed fenestrated inner and outer cannula. Some wait until the fifth postoperative day to allow additional healing and reduce the risk of subcutaneous emphysema or false passage on tube reinsertion. The skin-lined stoma of the permanent tracheotomy is far less likely to create false passages on reinsertion than the standard temporary tracheotomy. The patient and family are educated on the proper cleaning and care of the inner cannula as well as changing the entire inner and outer cannula system. They are trained in deep tracheal suctioning, and are advised to purchase a home suctioning device prior to discharge from the hospital. In addition, humidified tracheotomy-mask oxygen is advised for the first 3–4 weeks to help prevent crusting and aid in the healing of the stoma site. The patient is typically discharge on about the fourth

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to fifth postoperative day once the patient and family have demonstrated competence in dressing changes, suctioning, changing, and cleaning both the inner and outer cannula. Longer-term tracheotomy care issues over the next 3–4 months are concerned with granulation tissue formation, tube fit, and stenosis. Approximately 50% of patients will have granulation tissue formation primarily at the superior margin of their stoma (6). This presents about 4 weeks after surgery and often is heralded by small venous bleeds. It may be due to pressure and irritation from the tracheotomy tube possibly from the superior pull of the tracheotomy ties and the low lying trachea short obese neck (4). Other sites include the fenestration and distal cannula opening, again causing chronic irritation of the respiratory epithelium. Granulation tissue can be managed in one of several ways. After applying a topical or local anesthetic, silver nitrate applications directly on small amounts of the granulation tissue are often sufficient in the outpatient setting. More extensive granuloma formation often requires sharp debridement and/or electrocautery in a similar setting or in the operating room. A water-based topical antimicrobial ointment several times a day can help prevent further tissue growth. Caution! Some petrolatum-based ointments can weaken some silicone and plastic tubes. A second issue is the fit and comfort of the tracheotomy appliance. Despite an extensive removal of subcutaneous adipose tissue, standard tracheotomy tubes are often not long enough for an accurate fit. Coughing and pain can be produced with head movement. Obstruction of the fenestration in the standard tube in a nonstandard neck with large skin to trachea distances can result in difficult speech. Most often these issues can be resolved with the accurate measurement and fitting of a custom tracheotomy tube, detailed in the following text. Long-term issues include stoma stenosis and hygiene. Stenosis of the “permanent” tracheotomy can occur much like that of the total laryngectomy patient if improperly cared for. Permanent tracheotomy for OSA is a side tracheostome unlike the end tracheostome in the laryngectomy patient and may close more rapidly. Stoma hygiene is improved when patients have two or more appliances so that a clean cannula can be replaced daily while the other(s) are cleaned. Some patients report stoma closure when leaving the tube out for more than a few hours. Stoma cleaning and tracheotomy tube exchange should happen expeditiously. Patients must understand that good stoma care is important to avoid stoma stricture and operative stoma revision. Cleaning solutions should be limited to disinfectants based on active oxygen and exposure times. Concentrations and exposure times should be according to the manufactures recommendations. Usually half strength 3% hydrogen peroxide (equal amounts of hydrogen peroxide and distilled water) is recommended. Patients should practice good hand washing before and after tube exchange. After soaking for 2min, the obturator and inner and outer cannula are scrubbed with a brush or cotton pipe cleaners. The tube is rinsed in distilled or sterile water then dried and placed in a zip-lock bag for storage. Organic solvents must be avoided as they harden the tube. Exceeding disinfectant concentrations and soak times may penetrate the tube and cause mucosal irritation when reused. If necessary, rinse water may be sterilized by boiling tap water for 5–10min. It can be poured into jars or plastic containers previously cleaned with soapy water and stored 3 days at room temperature.

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5. CUSTOM TRACHEOTOMY Custom tracheotomy may be required for OSA patients who have abnormal skin to trachea dimension or who have a complication from a standard tracheotomy tube. Custom tubes are often required for the patient with unsuccessful lipectomy or when other surgical treatment to alteration of the neck anatomy is ineffective or not indicated. The tube is custom ordered by taking two measurements of a stable tracheotomy tract. The first measurement is the skin to trachea distance; the second is the overall length of tracheotomy tube. Ill-fitting standard tracheotomy tubes can injure the tracheal wall and produce granulation tissue at the distal opening. This condition is the result of the rigid nature of the tube and chronic irritation of the distal end against the tracheal mucosa. Treatment requires tube removal and bypassing the injured site with a flexible or custom tracheotomy tube. Granulation tissue can also form at the fenestration site when the hole is not centered in the trachea lumen. This can lead to obstruction of the fenestration and the loss of phonation. An accurate measurement of these distances is important for proper fit. We have found the flexible nasal endoscope to be a valuable tool in taking curvilinear measurements and for follow-up evaluation of proper fit. The first measurement is the skin to trachea distance that represents the “proximal fenestration margin”. The flexible endoscope is inserted into the tracheotomy tract. As the tip of the scope reaches the trachea this distance is marked by finger position on the scope at the stoma-skin junction as shown in Fig. 5. The proximal fenestration distance is this measurement and an additional 3–4mm, which is added for tracheotomy flange displacement out of the stoma. If the tracheotomy tube flange holds the tube out farther, this distance should be measured and added to the fenestration measurement and shaft measurement. Once the custom tube has been inserted the scope is used within the tube to verify that the fenestration and shaft length are accurate. Most OSA patients usually maintain the same measurements over time, but should be rechecked with the flexible scope before ordering additional tubes. The second measurement or “shaft length” uses the same technique in measuring the site for the distal opening. When replacing an ill-fitting tube producing a tracheal injury, the scope is extended through the open tracheotomy to the defect and 10mm is added to the shaft length. The new tube will extend 10mm beyond the defect allowing the tracheal injury to heal and improve ventilation when bypassing obstructing granulation tissue. If no tracheal defect is present the shaft length should be about 70– 80mm in length and extend at least 20mm beyond the fenestration and no less than 20mm above the carina.

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Figure 5 Flexible endoscope technique for accurate measurement of tracheotomy tube fenestration and overall tube length.

Figure 6 Differences between standard tracheotomy tube (A) and an actual custom tracheotomy tube (B) designed for a patient with severe OSA. Note that the custom tube’s fenestration is more distal and the tube is longer than the standard tube. Considerable differences exist between a standard and custom tracheotomy tube. The standard tracheotomy (Fig. 6, upper) tube length is 67–79mm and a fenestration at 30mm. The second tube (Fig. 6, lower) is a custom tracheotomy tube for a 75-year-old patient with severe OSA and CHF caused by a compressive inoperable thyroid goiter. The tube length is 92mm and the fenestration distance is 61mm. This patient recovered, became ambulatory and continues wearing the same size custom tracheotomy for the past 4 years.

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OSA patients with tracheal compression, tracheal stenosis, or large necks who cannot be treated successfully with surgical methods are ideal candidates for a custom tracheotomy. Custom tubes are available from a number of companies, two of which are Mallinckrodt (Shiley, 800–635–5267), and SIMS Portex Inc. (Portex & Bivona, 800– 258–5361). Custom tracheotomy forms (Fig. 7) help the surgeon relay accurate information about the patient’s anatomy for the best tube fit. Special needs including abnormal angles formed at the stoma can be measured using a protractor or with custom measurements and drawings. Dental impression compounds have been used to fabricate accurate stoma buttons for speech prosthesis and could one day be adapted to build and even more accurate custom tracheotomy tube. Newer silicone custom tubes are flexible and rarely require special measurements. The initial custom tube is ordered and evaluated for fit and function; subsequent tubes are modified based on this evaluation. Patients are encouraged to change the tube daily to improve hygiene and prevent granulation tissue formation. Correct cleaning methods and replacement techniques are discussed with the patient and care givers. Care kits, speaking valves, and other accessories are available from the manufacture, on the Internet (www.mallinckrodt.com and www.portex.com/airway/home.asp), and from excellent patient information sites (www.tracheostomy.com). Apnea patients are generally not tracheotomy dependent but should be counseled to the risks of tube occlusion and given instructions in emergency care.

6. COMPLICATIONS In a recent comprehensive article on the postoperative complications of tracheotomy, Goldenberg et al. (24) report 1130 consecutive tracheotomies done at their institution. Although none were performed for the treatment of OSA, this review provides a good look at the complications of the surgical airway. A total of 49 patients (4.3%) had major complications. Subglottic or tracheal stenosis occurred in 21 patients, significant postoperative bleeding occurred in nine patients including two patients who developed tracheoinnominate artery fistulas. Less common complications occurred in 14 patients (1.2%) that included infection, decannulation, obstruction, subcutaneous emphysema, pneumomediastinum, pneumothorax, and tracheoesophageal fistula (24).

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Figure 7 Custom tracheotomy tube order form. Postobstructive pulmonary edema (POPE) has been recently described as a complication relatively isolated to tracheotomies performed for OSA. In a retrospective study of 45 OSA patients, Burke et al. (25) report 30 patients (67%) treated by tracheotomy had evidence of POPE, whereas only five (20%) of 25 in the control group had evidence of pulmonary edema. The remaining patients in both groups had no change or had improved pulmonary status. Of the 30 who developed pulmonary edema, 22 (73%) were mild, 6 (20%) moderate, and 2 (7%) were severe. The two severe cases died of complications related to cor pulmonale in the postoperative period. The pathophysiology of POPE may be related to chronic respiratory obstruction producing vasoconstriction and pulmonary hypertension. The result is increased intrathoracic hydrostatic pressure favoring transudate into the pulmonary parenchyma. The auto PEEP mechanism counterbalances transudate formation. Once auto PEEP is removed with tracheotomy the imbalance in the transudative forces produces pulmonary edema. Surgeons should be aware of the development of POPE in the OSA patient who undergoes tracheotomy. Treatment includes diuretics and positive pressure ventilation, which often resolves the condition within days (25). Longer-term complications with tracheotomy include poor fit, granulation formation, and stoma stricture as discussed previously in the postoperative care section. Most of these complications can be treated by proper hygiene, revision surgery, or placement of custom tracheotomy tube described in earlier sections.

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7. RESULTS Tracheotomy remains the standard for the treatment of severe OSA, having been studied extensively in both medical and surgical literature. Guilleminault et al. (26) and Guilleminault and Cummiskey (27) at Stanford University produced one of two comprehensive articles from a medical and surgical experience (26,27). In the first of his two articles, Guilleminault reported a retrospective review of 50 patients that underwent tracheotomy for OSA evaluated by preoperative and postoperative polysomnography. The average preoperative apnea index was 81 (range 65–120). All patients had significant sinus arrhythmias during sleep, and all had nighttime oxygen saturations <70% with 49/50 dropping at least once below 30%. Postoperative PSG performed between 6 weeks and 3 months postoperatively showed dramatic improvement. Apnea indices for all patients were under 5. Twenty-four hr Holter monitoring demonstrated resolution of all cardiac arrhythmias, including sinus arrhythmia, severe bradycardia, A-V block and ventricular tachycardia. Central apneas gradually decreased over time and normalized within 6–12 months after surgery. Subjective morning headache, confusion, nocturnal enuresis, sleepwalking, abnormal movements during sleep and heavy snoring were eliminated. Erratic behavior, personality changes, and sexual dysfunctions disappeared. Revision surgery was required for chin fat obstructing the tracheotomy tube. Thirty-eight patients were monitored by PSG in an attempt to decannulate. These patients had return of the sleep apnea when the tracheotomy was occluded and were “unable to close any of the tracheotomies permanently” (26). In his second study published the following year, Guilleminault documented the progressive improvement after tracheotomy using the patient’s ventilatory response (VE) to CO2 and the apnea index (AI). In this prospective study, he followed five patients by PSG at 5–7 weeks preoperatively and then again at 2–3 days, 4–5 weeks, and >3 months postoperatively. His results are summarized in Table 2. He found a dramatic decrease in the apnea index immediately after surgery and a slower recovery of central AI over time. Four of the five patients actually doubled their ventilatory response to CO2 after surgery which he feels provides evidence of a “resetting” of a receptor threshold that can be measured following tracheotomy (27). In 1998, Kim et al. (28) retrospectively reviewed PSG and hemoglobin desaturation data on three groups of OSA patients at the Johns Hopkins Sleep Disorders Center who received a tracheotomy. Patients in Group 1 had preoperative PSG and failed conservative management from CPAP and upper airway surgery (UPPP). Group 1

Table 2 Results of Tracheotomy on Apnea Index and Oxygen Saturation

Apnea index Lowest O2 sat.

Before

2–3 days after

4–5 weeks after

>3 months after

65±14

13±3

7±1

2±2

39±16%

87±3%

88±3%

90±3%

Source: From Ref. 27.

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Table 3 Results of Tracheotomy on AHI and SaO2 Pre-operative

Tracheotomy closed

Tracheotomy open

NREM

REM

NREM

REM

NREM

REM

AHI

79.7±19.7

59.3±29.5

50.9±23.0

26.2±19.63

5.7±5.3

8.9±14.3

Low SaO2

83.8±6.9

72.3±14.9

91.6±2.4

88.1±5.3

89.1±3.9

88.9±5.3

AHI

102.3±47.6

57.8±38.4

63.9±47.7

45.7±28.5

30.6±30.9

39.2±34.7

Low SaO2

69.2±17.8

56.5±18.3

80.3±7.7

77.6±10.2

83.3±9.6

80.2±11.0

AHI

N/A

N/A

57.1±39.2

80.2±21.4

5.3±5.1

1.7±3.5

Low SaO2

N/A

N/A

90.1±3.0

83.0±9.5

90.6±2.5

91.7±3.2

Group 1a

Group 1b

Group 2

Source: From Ref. 28.

was broken down into Group 1a (10 patients with severe OSA with no cardiopulmonary decompensation) and Group 1b (13 patients with severe OSA with cardiopulmonary decompensation, morbid obesity, hypoventilation and hypoxia, and right-sided heart failure). Group 2 consisted of 5 patients receiving tracheotomy to avoid airway compromise while undergoing other airway surgery. These patients received a PSG when attempts at decannulation failed prompting concern for the presence of OSA. In Group 1a, the mean rapid eye movement (REM) and non-REM (NREM) apnea-hypopnea indices (AHI) dropped from 79.7 and 59.3 to 5.7 and 8.9, respectively, with the tracheotomy open postoperatively. In Group 1b, (cardiopulmonary decompensation and morbid obesity) tracheotomy showed dramatic improvement but the AHI remained in the 30–40 range. The mean REM and NREM AHI fell from 102.3 and 57.8 to 30.6 and 39.2, respectively. Group 2 patients showed posttracheotomy PSG differences between the capped and uncapped AHI. The REM and NREM AHI drop was similar to Group 1a, from 57.1 and 80.2 to 5.3 and 1.7, respectively. These results are summarized in Table 3. Group 1b (with cardiopulmonary decompensation and morbid obesity) improved less in this study compared to the other groups (28). This difference could be due to fat and skin obstruction, poor tracheotomy fit, central apnea that corrected beyond the length of the study, or other physiologic factors associated to cardiopulmonary health. Thatcher’s long-term longitudinal cohort study of 79 patients suggests tracheotomy for severe OSA is very effective and well tolerated in the long term. Significant morbidity and mortality are low and complications of tracheotomy are well tolerated and easily treated. Decannulation in Thatcher and Maisel’s (8) and Guilleminault et al.’s (26) studies is unlikely even in cases with resolution of OSA. Severe OSA patients who undergo tracheotomy should have concurrent UPPP and weight counseling if decannulation is anticipated. Tracheotomy patients who meet criteria for gastric bypass

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surgery should be considered for this type of treatment to enhance the probability of decannulation.

REFERENCES 1. Frost EAM. Tracing the tracheotomy. Ann Otol 1976; 85:618–624. 2. Kuhlo W, Doll E, Franck MC. Erfolgreiche Behandlung eines Pickwick Syndroms durch eine Dauertrachekanuele [Successful management of Pickwickian syndrome using longterm tracheostomy]. Dtsch Med Wochenschr 1969; 94(24):1286–1290. 3. Fee WE, Ward PH. Permanent tracheostomy. Ann Otolaryngol 1977; 86:635–637. 4. Mickelson SA. Upper airway bypass surgery for obstructive sleep apnea syndrome. Otolaryngol Clin North Am 1998; 31(6):1013–1023. 5. Riley RW, Powell NE, Li KK, Guilleminault C. Surgical therapy for obstructive sleep apneahypopnea syndrome. In: In: Kryger M, Roth T, Dement W, eds., eds. Principles and Practice of Sleep Medicine. 3rd ed.. Philadelphia, PA: WB Saunders, 2000:913–928. 6. Fairbanks DN. Tracheotomy for obstructive sleep apnea: indications and techniques. In: In: Fairbanks DNF, Fujita S, eds., eds. Snoring and Obstructive Sleep Apnea. 2nd ed. New York: Raven Press, 1994:169–177. 7. Piccirillo JF, Thawley SE. Sleep-disordered breathing. In: In: Cummings CW, ed. Otolaryngology Head & Neck Surgery. 3rd ed.. St. Louis, MO: Mosby, 1998:1546–1571. 8. Thatcher GW, Maisel RH. The long-term evaluation of tracheostomy in the management of severe obstructive sleep apnea. Laryngoscope 2003; 113(2):201–204. 9. Albert M, Spanos C, Shikora S. Morbid obesity: the value of surgical intervention [Review article]. Clin Fam Pract [serial online]. 2002; 4(2):447. Available at http://home.mdconsult.com. Accessed February 24, 2003. 10. National Institutes of Health. Gastrointestinal surgery for severe obesity: National Institutes of Health Consensus Development Conference Statement. Am J Clin Nutr 1992; 55:615–619. 11. Sleep-related breathing disorders in adults: recommendations for syndrome definition and measurement techniques in clinical research. The report of an American Academy of Sleep Medicine Task Force. Sleep 1999; 22(5):667–689. 12. Gottlieb DJ, Whitney CW, Bonekat WH, Iber C, James GD, Lebowitz M, Nieto FJ, Rosenberg CE. Relation of sleepiness to respiratory disturbance index: the Sleep Heart Health Study. Am J Respir Crit Care Med 1999; 159(2):502–507. 13. Peppard PE, Young T, Palta M, Skatrud J. Prospective study of the association between sleepdisordered breathing and hypertension. N Engl J Med 2000; 342(19):1378–1384. 14. Shahar E, Whitney CW, Redline S, Lee ET, Newman AB, Javier-Nieto F, O’Connor GT, Boland LL, Schwartz JE, Samet JM. Sleep-disordered breathing and cardiovascular disease: cross-sectional results of the Sleep Heart Health Study. Am J Respir Crit Care Med. 2001; 163(1):19–25. 15. Strollo PJ. Indications for treatment of obstructive sleep apnea in adults. Clin Chest Med 2003; 24(2):307–313 (Review). 16. Levine PA, Sasaki CT, Kirchner JA. The long tracheostomy tube: alternative management of distal tracheal stenosis. Arch Otolaryngol 1978; 104:108–110. 17. Polderman KH, Spijkstra JJ, de Bree R, Christiaans HM, Gelissen HP, Wester JP, Girbes AR. Percutaneous dilational tracheostomy in the ICU: optimal organization, low complication rates, and description of a new complication. Chest 2003; 123(5):1595–1602. 18. Ciaglia P, Graniero KD. Percutaneous dilatational tracheostomy: results and long-term followup. Chest 1992; 101:464–467. 19. Sahni R, Blakley B, Maisel RH. Flap tracheostomy in sleep apnea patients. Laryngoscope 1985; 95:221–223.

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20. Eliachar I, Zohar S, Golz A, Joachims HZ, Goldsher M. Permanent tracheostomy. Head Neck 1984; 7:99–103. 21. Gross ND, Cohen JI, Andersen PE, Wax MK. ‘Defatting’ tracheotomy in morbidly obese patients. Laryngoscope 2002; 112:1940–1944. 22. Clayman GL, Adams GL. Permanent tracheostomy with cervical lipectomy. Laryngoscope 1990; 100:422–424. 23. Fedok FG, Houck JR, Manders EK. Suction-assisted lipectomy in the management of obstructive sleep apnea. Arch Otolaryngol Head Neck Surg 1990; 116(8):968–970. 24. Goldenberg D, Ari EG, Golz A, Danino J, Netzer A, Joachims HZ. Tracheotomy complications: a retrospective study of 1130 cases. Otolaryngol Head Neck Surg. 2000; 123(4):495–500. 25. Burke AJ, Duke SG, Clyne S, Houry SA, Chiles C, Matthews BL. Incidence of pulmonary edema after tracheotomy for obstructive sleep apnea. Otolaryngol Head Neck Surg 2001; 125(4):319–323. 26. Guilleminault C, Simmons FB, Motta J, Cummiskey J, Rosekind M, Schroeder JS, Dement WC. Obstructive sleep apnea syndrome and tracheostomy: long-term followup experience. Arch Intern Med 1981; 141:985–988. 27. Guilleminault C, Cummiskey J. Progressive improvement of apnea index and ventilatory response to CO2 after tracheostomy in obstructive sleep apnea syndrome. Am Rev Respir Dis 1982; 126:14–21. 28. Kim SH, Eisele DW, Smith PL, Schneider H, Schwartz AR. Evaluation of patients with sleep apnea after tracheotomy. Arch Otolaryngol Head Neck Surg 1998; 124:996–1000.

27 Surgery for Pediatric Sleep Apnea David H.Darrow Departments of Otolaryngology and Pediatrics, Eastern Virginia Medical School, Children’s Hospital of The King’s Daughters, Norfolk, Virginia, U.S.A. 1. INTRODUCTION As in adults, sleep-related breathing disorders (SRBD) in children are characterized by episodic obstruction of airflow through the upper airway during sleep. Children with SRBD often demonstrate decreased caliber of the airway due to skeletal anatomy, compliant or excessive pharyngeal soft tissues, or neuromuscular compromise, complicated by the diminished muscle tone and neurophysiologic changes that typically accompany sleep. Attempts to overcome the obstruction by increasing respiratory effort often exaggerate collapse of the airway, resulting in a paradoxical increase in resistance to airflow. The physiologic sequelae may include hypoxemia, hypercapnia, and acidosis, which in turn signal central and peripheral chemoreceptors and baroreceptors to initiate the arousals and sudden pharyngeal dilation that characterize SRBD. Management of sleep apnea in children depends on accurate identification of the site of obstruction and the severity of obstruction. Although hyperplasia of the tonsils and adenoid account for the vast majority of cases, the potential offending pathologies causing SRBD in children are more diverse than those in adults and can affect any site in the upper respiratory tract. In small children, the distance between these sites may be quite small, resulting in stertor or stridor whose source is difficult to localize. In such cases, careful assessment using flexible and rigid endoscopic examination of the airway and videofluoroscopy may be necessary to determine appropriate intervention.

2. CAUSES OF SRBD IN CHILDREN Causes of SRBD in children may be grouped on the basis of age, simplifying the differential diagnosis for a given patient (Table 1). Neonates and infants rarely have significant lymphoid hyperplasia, and SRBD in these children are usually related to their immature respiratory physiology or to congenital obstructing lesions. In premature babies, neural pathways that control ventilation, coordination of the larynx and diaphragm, and chemoreceptor responses are not yet fully developed. In such

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Table 1 Causes of Sleep-Related Breathing Disorders in Children Neonates and infants Nasal aplasia, stenosis, or atresia Nasal or nasopharyngeal masses Craniofacial anomalies Hypoplastic mandible (Pierre Robin, Nager’s, Treacher Collins) Hypoplastic maxilla (Apert’s, Crouzon’s) Macroglossia (Beckwith-Wiedemann) Vascular malformations of tongue and pharynx Neuromuscular disorders Toddlers and older children Rhinitis, nasal polyposis, septal deviation Syndromic narrowing of nasopharynx (Hunter’s, Hurler’s, Down’s, achondroplasia) Adenotonsillar hyperplasia Obesity Macroglossia (Down’s) Vascular malformations of tongue and pharynx Neuromuscular disorders Iatrogenic Nasopharyngeal stenosis

children, hypoventilation, central apnea, and periodic breathing are common, resulting in reflex bradycardia. Hypoxemia and hypercapnia, which are less common due to the short duration of the apneic events, do not reliably evoke compensatory mechanisms. Apnea in infants may also be associated with gastroesophageal reflux, either as a direct result of soiling of the upper airway or due to vagally mediated reflexes that inhibit inspiration. In such cases, management by medical therapy or Nissen fundoplication may be warranted. Since babies depend primarily on nasal breathing, obstruction of the nose or nasopharynx is more significant than in older children. Common causes include neonatal rhinitis, pyriform aperture stenosis, choanal atresia, dacryocystoceles, and nasal/choanal stenosis related to craniofacial syndromes such as Apert’s or Crouzon’s. Dermoids, teratomas, gliomas, and encephaloceles of the nose and nasopharynx are also seen. Oropharyngeal obstruction in this age group is usually related to micrognathia or macroglossia. Micrognathia may be syndromic, as in children with Treacher Collins or Nager’s syndromes, or developmental, as in Pierre Robin sequence. Macroglossia is common in Down and Beckwith-Wiedemann syndromes. Vascular malformations of the

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pharynx and tongue may also cause obstruction in this age group. Laryngeal abnormalities more often result in severe stridor while awake than in collapse of soft tissues during sleep. Neuromuscular disorders, which may be complicated by impaired pharyngeal tone, impaired excursion of the diaphragm, or effects of medical therapy, begin to cause obstruction in this age group and often progress as the child ages due to adenotonsillar enlargement. Toddlers and older children are more affected during sleep by disorders that have had an opportunity to-progress. Hyperplasia of the tonsils and adenoid is unquestionably the most common cause of upper airway obstruction in children resulting in sleep disordered breathing. Severe allergic rhinitis may also develop in children, causing or complicating airway obstruction due to other causes. Similarly, weight gain also begins to become an issue in older children, and the accumulation of fat in the fascial planes surrounding the pharynx of obese individuals may be a cause of surgical failure following adenotonsillectomy. Some children are affected by syndromes involving progressive reduction of the pharyngeal airway such as Down’s syndrome, achondroplasia, and the mucopolysaccharidoses (Hunter’s and Hurler’s syndromes). In the latter group, surgical intervention may actually precipitate deposition of mucopolysaccharide. In adolescence, lymphoid hyperplasia becomes a less important cause of SRBD as the pharynx increases in size and the tonsils and adenoid recede. As in adults, sleep disordered breathing is more commonly associated with redundant pharyngeal tissues, obesity, macroglossia, and septal deviation. Progression of neuromuscular disorders may also necessitate surgical intervention in this age group. Iatrogenic stenosis of the nasopharynx following adenotonsillectomy, uvulopalatopharyngoplasty, or surgery for cleft palate or velopharyngeal insufficiency may result in significant sleep apnea. Corrective surgical intervention for this disorder is often complicated by recurrence.

3. DIAGNOSIS OF SRBD IN CHILDREN In most studies, snoring occurs during sleep in 3–12% of children (1), although a recent study suggests a prevalence as high as 27% (2). However, only those with hypoventilation, apnea, hypoxemia, or repeated arousals are considered to have SRBD. In its mildest form, SRBD is recognized as upper airway resistance syndrome (UARS). Affected children demonstrate episodic arousals resulting from partial obstruction of the upper airway, associated with symptoms of heroic snoring, mouth breathing, sleep pauses or breathholding, gasping, perspiration, and enuresis. Daytime manifestations of sleep disturbance include behavioral and neurocognitive disorders, morning headache, dry mouth, and halitosis. Hypersomnolence may occur in older children and adolescents. Other signs and symptoms include audible breathing with open mouth posture, hyponasal speech, and chronic nasal obstruction with or without rhinorrhea. Approximately 40% of children who snore demonstrate more significant degrees of obstruction characteristic of obstructive hypopnea syndrome (OHS) or obstructive sleep apnea syndrome (OSAS) as defined below (1). The most severely affected patients may develop cor pulmonale, right ventricular hypertrophy, congestive heart failure, alveolar hypoventilation, pulmonary

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hypertension, pulmonary edema, or failure to thrive, and are at risk for permanent neurological damage and even death. Physical examination of children with SRBD should include assessment of the patient’s weight and body habitus, a complete examination of the head and neck with attention to potential sites of obstruction, and auscultation of the patient’s heart and lungs. Findings of mouth-breathing, hyponasal speech, mandibular hypoplasia, drooling, neuromuscular deficit, and tonsillar hyperplasia all suggest some degree of upper airway obstruction. Fiberoptic assessment of the nasal vault, the adenoid pad, and the distal pharynx and larynx may be useful in selected cases. Ancillary studies including chest radiography and electrocardiography should be performed in severely obstructed children. In many cases of nasal obstruction in infants and young children, computed tomography (CT) scanning is desirable in order to define the bony anatomy and to assess the relationship of nasal masses to the sinonasal tract and the central nervous system. In most cases, candidacy for surgical intervention cannot be established solely on the basis of a history and physical examination (3–10). SRBD occurs primarily during rapid eye movement (REM) sleep when children are less likely to be observed by their parents (11), and in many cases of UARS and OHS parents may misinterpret the symptoms only as snoring in the absence of obstruction. In addition, while hyperplasia of the tonsils and adenoid likely predispose to airway obstruction, airway dynamics during sleep cannot be determined by static examination in the office setting. Furthermore, fiberoptic assessment of the airway is useful in determining anatomic obstruction but offers a distorted wideangle view of obstructing tissues and will not demonstrate the dynamics of the nasopharynx during sleep. Similarly, radiographic assessment of the adenoid tissue and tongue base may be difficult to interpret (12–15). Polysomnography (PSG) remains the gold standard for objective correlation of ventilatory abnormalities with sleep disordered breathing (4). In most laboratories, such testing includes objective assessment of chest wall excursion (respiratory effort), airflow at the nose or mouth, arterial oxygen saturation, electrocardiography, electromyography to determine episodes of arousal, and occasionally electroencephalography to monitor stages of sleep. However, although the definition of hypopnea (paradoxical respiratory effort with reduction of airflow to <50% of baseline with oxygen desaturation of ≥4%) is the same in children as that in adults, experts differ on the definition of obstructive apnea (paradoxical respiratory effort with cessation of airflow for 6–15sec) (16). Furthermore, there is no consensus on the level at which the apnea-hypopnea index (AHI) (average apneas plus hypopneas per hour) becomes clinically significant (4). Children with an AHI >5 may be considered “at risk”; however, polysomnographic data must be interpreted within the context of symptoms of airway obstruction or sleep disturbance. In addition, there are no data that demonstrate a correlation between polysomnographic abnormalities and adverse outcomes in SRBD (2). In contrast to their adult counterparts, disturbance of sleep architecture and sleep efficiency are unusual in children with SRBD. The expense and scheduling difficulties associated with PSG make this a cumbersome method of assessment in many otolaryngology practices. Other techniques of assessment including audiotaping (5,7), videotaping (17), and home PSG (18) have demonstrated favorable results, but require further study. Abbreviated PSG (i.e., overnight oximetry or nap PSG) has demonstrated a high positive predictive value and a low negative predictive

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value, suggesting that patients with negative results may still require additional studies (19–21).

4. MANAGEMENT OF SRBD IN CHILDREN Treatment of SRBD in children is tailored to the etiology of the airway obstruction. Medical management, such as thioxanthines and methylphenidate, may be useful in cases of central apnea. Pharmacotherapy may also be considered in less severe cases of obstructive apnea, or when surgical intervention does not address the pathology. Examples of such disorders include obesity, allergic rhinitis, and acute tonsillitis. In cases of chronic upper airway obstruction, mechanical correction by prostheses, positive airway pressure, or surgery is usually necessary. In most cases, including those such as obesity and neuromuscular disorders in which airway dynamics are affected, surgical management is generally considered prior to use of positive airway pressure or oral prostheses, since these interventions are rarely tolerated in children and often ineffective. However, such modalities should be entertained should obstruction persist following surgery. Rarely, in the most severe or refractory cases, tracheotomy must be considered. Postoperative respiratory distress is common after surgery for SRBD due to effects of anesthesia, bleeding, edema, and residual airway compromise. Patients at greatest risk include those with severe OSAS, diminished neuromuscular tone (i.e., cerebral palsy), morbid obesity, skeletal and craniofacial abnormalities such as hypoplasia of the midface and/or mandible or nasopharyngeal vault, and very young children (under the age of 2–3 years) (21–25). Preoperative planning for such individuals who are undergoing even routine procedures such as adenotonsillectomy should include hospital admission to a high visibility bed with continuous cardiac and oxygen saturation monitoring. Intraoperative use of steroids and postoperative placement of nasopharyngeal airways may reduce the risk of airway compromise after surgery. Narcotics and sedatives should be used sparingly in severely obstructed children. Patients with reduced neuromuscular tone may benefit from airway support with positive airway pressure. In the most extreme cases, overnight endotracheal intubation may be desirable. 4.1 Adenotonsillar Hyperplasia and Oropharyngeal Obstruction Adenotonsillectomy is generally considered first line therapy in most patients with SRBD, provided they have at least mild adenotonsillar hyperplasia. Improvements in snoring and polysomnography may be anticipated postoperatively in such patients (8,9,26,27). Even obese children seem to have reduced obstruction after surgery (28,29); however, available studies lack long-term follow-up and symptoms may return in those who do not additionally pursue weight loss. Children with SRBD who exhibit abnormalities in body growth preoperatively often demonstrate increased body mass after surgery (30–32). Improvement following adenotonsillar surgery has also been demonstrated in children with preoperative enuresis (33) and in those with orthodontic abnormalities prior to surgery (34). Validated surveys suggest an overall improvement in quality of life after adenotonsillectomy (35,36).

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Several new techniques of tonsillectomy and adenoidectomy have been proposed in recent years as technology has evolved. For decades, guillotine and cold steel removal of the tonsils were fraught with complications of bleeding and postoperative pain. The use of electrocautery in these procedures reduced the problem of surgical blood loss considerably and decreased operating time, but postoperative pain remained a significant morbidity (37,38). Over the last 20 years, instrument makers have competed for supremacy in adenotonsillectomy by introducing devices with the promises of decreased pain, decreased bleeding, and decreased operative time. Although no device seems to have definitively accomplished these goals, changes in surgical technique may be getting closer. Initial reports of tonsillectomy using lasers yielded variable and occasionally disappointing results (39–42). However, with the report by Krespi and Ling (43) of serial tonsillectomy with CO2 laser in the outpatient setting came the notion that partial tonsillectomy was safe and less painful than traditional tonsillectomy for patients with tonsil hyperplasia. It is theorized that the exposure of muscle resulting from removal of the tonsil capsule is the cause of pain associated with tonsillectomy, and that leaving some small portion of the tonsil behind may vastly diminish this sequela (44). Proposed many years ago, the technique had been abandoned due to the risk of tonsil regrowth at a time when most such procedures were performed for recurring infection. Recent literature suggests that single stage intracapsular tonsillectomy, or “tonsillotomy” using the CO2 laser is safe, rapid, and effective with little loss of blood (45,46). Similar results have been achieved using microdebrider instrumentation, which reduces the cost of the procedure but may be associated with somewhat more bleeding (44). The Harmonic scalpel (Ethicon Endo-Surgery; Cincinnati, OH) is a devices that uses ultrasonic technology to cut and coagulate with minimal tissue damage. Early reports of tonsillectomy using this device suggest that pain may be modestly decreased compared to standard techniques (47–49). Hemorrhage rates are equivalent, but surgical time may be somewhat longer and the cost of the disposable blade is high. Radiofrequency devices, such as the Somnoplasty system (Somnus Medical Technologies, Sunnyvale, CA) and the ArthroCare Coblation system (ArthroCare Corp., Sunnyvale, CA) have not been studied extensively, but seem to yield similar results, with further decrease in postoperative pain when the tonsil is reduced rather than excised (50–53). Techniques of adenoidectomy include curettage, suction electrocautery ablation, and removal by power-assisted devices. Traditional curettage is inexpensive but is the least precise of these techniques and is associated with hemorrhage that must be controlled before leaving the operating room. Electrocautery dissection, by definition, is associated with less bleeding and is also a precise and inexpensive device (54–56). However, high settings are required on the cautery device with the potential for thermal injury to deep structures. Surgical times have been variable. Studies of power-assisted (microdebrider) techniques (Figs. 1A and B) have demonstrated excellent precision with rapid removal of tissue; however, additional time for cautery is still necessary and the disposable blades add significant expense (57,58). Uvulopalatopharyngoplasty is not commonly performed in children, perhaps since most children with sleep apnea do not demonstrate the redundant tissue found in adults with similar symptoms. Several studies have demonstrated that the procedure is efficacious in the most difficult-to-treat patients with SRBD, particularly

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Figure 1 Power-assisted adenoidectomy using the Straight Shot® microdebrider (Medtronic/Xomed; Jacksonville, FL) outfitted with the RADenoid® blade. The microdebrider is used at 2500rpm. (From Darrow DH, Weiss DD. Management of sleep-related breathing disorders in children. Oper Tech Otolaryngol Head Neck Surg 2002; 13:111–116.) those with obesity (59), neurological impairment (60–62), or Down syndrome (63– 65). However, these reports are retrospective, and it remains unclear whether resection of the palate and uvula add significantly to tonsillectomy with plication of the tonsil pillars, which is usually performed simultaneously. In addition, nasopharyngeal stenosis remains a significant risk when the procedure is performed at the same time as adenoidectomy (66,67). 4.2 Nasal and Nasopharyngeal Obstruction SRBD due to nasal and nasopharyngeal masses is best addressed by removal of the mass. Depending on the pathology, the procedure may be as simple as a transoral, retropalatal approach for adenoidectomy or marsupialization of nasolacrimal duct cysts, or as complex as an anterior craniofacial approach for encephalocele. Nasal and nasopharyngeal neoplasms may require aggressive resection, as well as preoperative embolization (juvenile nasopharyngeal angiofibroma) or postoperative radiation therapy or chemotherapy (malignancies).

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Bilateral choanal atresia causes obstructive apnea in neonates and requires early intervention. Such infants can be temporized with oropharyngeal airways, but should not leave an intensive care setting until a secure airway is established by tracheotomy is performed or repair of the atresia. Timing of the repair is controversial; early repair with avoidance of tracheotomy is always desirable, however children several weeks to months old will better tolerate bleeding from transpalatal repair and better accommodate instruments for transnasal repair. While the transpalatal and transnasal approaches each have their proponents, improvements in endoscopic and powered instrumentation have made the transnasal approach the first choice for most otolaryngologists (68,69) In small children, the procedure is best performed using a small rigid rod-lens telescope and a protected microdebrider such as the Straight Shot® instrument by Medtronic/Xomed (Jacksonville, FL) (Fig. 2). After creation of mucosal flaps with a sickle knife, the microdebrider can be fitted

Figure 2 Endoscopic transnasal repair of choanal atresia using Straight Shot® microdebrider. (From Darrow DH, Weiss DD. Management of sleeprelated breathing disorders in children. Oper Tech Otolaryngol Head Neck Surg 2002; 13:111–116.)

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Figure 3 After mucoal flaps are created, bone removal is accomplished without soft tissue injury using the

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microdebrider with a pediatric round bur (A) and Silver Bullet® blade (B). (From Darrow DH, Weiss DD. Management of sleep-related breathing disorders in children. Oper Tech Otolaryngol Head Neck Surg 2002; 13:111–116.) with a small round bur (Fig. 3A) or a conical cutting bur (Silver Bullet®) (Fig. 3B) for removal of bone with protection of the mucosa from the turning shaft (Fig. 3C). Use of a 120° telescope in the mouth affords a view of the nasopharynx to determine the extent of the drilling. Back-biting forceps are used to remove the posterior portion of the vomer. The opened choanae may be treated with mitomycin C to reduce the risk of restenosis (70), followed by stenting for several weeks using endotracheal tubes or Albouker-type stents. In cases of pyriform aperture stenosis, the offending bone may be approached through a sublabial approach and reduced using similar instrumentation (71). Nasopharyngeal stenosis, once a common complication of syphilis, may result as a complication of adenotonsillectomy, uvulopalatopharyngoplasty, or surgery for cleft palate or velopharyngeal insufficiency. This disorder often causes obstruction of the upper airway that is even more significant than the disorder the original surgery was intended to correct. Typically, cicatrix forms circumferentially in the nasopharynx as a result of removal of excessive mucosa from opposing surfaces. Simple release of the scarred area results in recurrence, and treatment must therefore include the movement of fresh, well-vascularized tissue to cover the denuded bed. A variety of techniques has been recommended, including Z-plasty (72), laterally based pharyngeal flaps (Fig. 4) (73), other advancement and rotation flaps (74–76), radial forearm, and jejunal free flaps (76,77). Many authors advocate the use of intralesional steroids and topical application of mitomycin C to the surgical site to reduce the risk of recurrence. Postoperative stenting with nasopharyngeal airways or oropharyngeal prostheses (78) is mandatory, although the necessary duration of such stenting is controversial.

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Figure 4 Laterally based pharyngeal flap for correction of nasopharyngeal stenosis. (A) A lateral incision is made from velopharyngeal opening into lateral scar on one side (top) and deepened (bottom). (B) Mucosal flaps are elevated from the scar inferolaterally and the scar is excised. (C) (Top) A laterally based posterior pharyngeal flap is incised incorporating a back cut, then elevated with the underlying muscle (center). (Bottom) Points A1 and B1 are closed to points A and B, respectively, covering the denuded area. (From Ref. 73.)

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4.3 Hypoplasia of the Midface and Mandible Upper airway obstruction due to hypoplasia of the midface and mandible is usually associated with craniofacial syndromes. Micrognathia due to Pierre Robin sequence

Figure 5 Glossoptosis in a child with micrognathia due to Pierre Robin sequence. (From Darrow DH, Weiss DD. Management of sleep-related breathing disorders in children. Oper Tech Otolaryngol Head Neck Surg 2002; 13:111–116.) often improves within the first 2 years of life without surgical intervention for the mandible. In cases of mild airway obstruction, children with competent caretakers may be managed by prone positioning and nasopharyngeal stenting via nasal trumpet or similar device (79). When symptoms are more severe, temporary repositioning of the ptotic tongue by labioglossopexy (Figs. 5 and 6) has been advocated (80). However, results from this procedure are variable and the procedure carries the risks of dehiscence, tongue lacerations, and deformation of the lip and speech impairment due to scar formation (81).

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Figure 6 Labioglossopexy for glossoptosis. After denuding mucosa from the anterior ventral tongue, floor of mouth, and oral vestibule (A), the tongue is fixed to the lip with sutures. The base of the tongue is supported using a translingual fixation suture brought over the anterior mandible and fixed externally under the chin (B). (From Darrow DH, Weiss DD. Management of sleep-related breathing disorders in children. Oper Tech Otolaryngol Head Neck Surg 2002; 13:111–116.) Subperiosteal release of the floor of the mouth has also been reported but has not been used widely. Temporary tracheotomy seems to be the most reliable and least morbid means of airway management providing the patient shows signs of mandibular “catchup” growth within the first few months. When this is not the case, distraction osteogenesis should be considered. First described in 1969 by Ilizarov and Ledyaev (82) in the treatment of limb length discrepancies, osteotomy with distraction of bone is now widely accepted as the procedure of choice in the early management of airway obstruction due to craniofacial disproportion (83–85). The procedure takes advantage of the rapid healing and capacity for growth in the pediatric skeleton. Distraction osteogenesis has been used for over a decade to advance the mandible in cases of retrognathia and micrognathia, but indications have expanded to include neuromuscular disorders. With modifications to the expansion

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devices, distraction of the midface is also beginning to replace Leforte osteotomies with bone grafting. Prior to surgery, all candidates for mandibular distraction undergo airway endoscopy and craniofacial assessment by three-dimensional CT scanning. Airway patency is estimated in relaxed and jaw-thrust positions, and precise bony measurements are taken from the scan. Distraction osteogenesis is divided into four phases: surgery, distraction, consolidation, and removal. The surgical approach we recommend is an initial internal incision along the oblique line of the mandible (Fig. 7). The incision tracks along the angle of the mandible and is taken down to the periosteum. The angle of the mandible is exposed both medially and laterally. The lateral surface of the mandible is marked for a standard bilateral sagittal split osteotomy. The lingula is identified and the future medial cortex osteotomy is marked above this. Four 2–4mm incisions are made externally for pin placement using a #11 blade. The incisions on the body of the mandible are made with the skin pinched in order to decrease the amount of linear scarring once distraction is started. The distraction pin is placed through the incision and passed to the level of the bone. Once in contact with the bone, the drill is attached and the pin is advanced bicortically. Two pins are set above the future osteotomy site and two below (Fig. 7). In neonates, one of the pins on either side

Figure 7 Planned bone cuts and pin placement for mandibular distraction. Bone cuts are designed as in a bilateral sagittal split osteotomy. Two pins are placed on either side of the osteotomy. In neonates, one pin is passed straight through from one side of the mandible to the other. (From Darrow DH, Weiss DD. Management of sleep-related breathing disorders in children. Oper

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Tech Otolaryngol Head Neck Surg 2002; 13:111–116.)

Figure 8 The medial osteotomy is prepared by scoring the bone. The bone is released with a gentle twist of the osteotome. (From Darrow DH, Weiss DD. Management of sleeprelated breathing disorders in children. Oper Tech Otolaryngol Head Neck Surg 2002; 13:111–116.) of the osteotomy is passed transorally all the way through the opposite side of the mandible. This prevents the pins from loosening or cheese-cutting through the soft bone. The osteotomies are made in a stair step fashion using a #15 blade in neonates or a sagittal saw in older children. An osteotomy is performed on the lateral cortex, followed by a superior cortex cut made in an angled fashion. A subperiosteal tunnel is made vertically along the medial cortex. The bone is scored and then freed using an osteotome (Fig. 8). The distraction device is placed over the pins and tightened incompletely. Finally, the medullary connection is separated with gentle rotation of the osteotome. With the bone completely mobile the distraction device is fully tightened. The distractor is then turned 2−3mm to assure surgical release has been completed (Fig. 9). After a lag phase of 24–72hr, distraction is started. We generally distract at a rate of 2mm/day, with adjustments of 1mm every 12hr. Once the desired length of the mandible has been achieved, adequacy of the airway is verified by flexible or rigid laryngoscopy prior to consolidation. In children who already have a tracheostomy, downsizing and bedside occlusion can be performed. The consolidation phase is usually about 8 weeks, but should last at least two times as long as the distraction period. The hardware may be left in place during this time. The final stage is removal of the hardware and minor scar revision. Avoidance of or decannulation from tracheotomy in appropriately selected patients undergoing distraction of the mandible is >90% (84,85).

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Figure 9 The multivector distractor applied to the inserted pins. Distraction may proceed at a rate of 2–3mm/day. (From Darrow DH, Weiss DD. Management of sleep-related breathing disorders in children. Oper Tech Otolaryngol Head Neck Surg 2002; 13:111–116.)

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Figure 10 Approaches to surgical reduction of the tongue. None of these methods reliably treats obstruction at the tongue base. (From Darrow DH, Weiss DD. Management of sleeprelated breathing disorders in children. Oper Tech Otolaryngol Head Neck Surg 2002; 13:111–116.) 4.4 Macroglossia and the Ptotic Tongue Children with macroglossia generally have Beckwith-Wiedemann syndrome (macroglossia, omphalocele, visceromegaly, cytomegaly of the adrenal cortex), Down syndrome, or a vascular malformation of the tongue. Complications of macroglossia include aberrant dental eruption and malocclusion, maldevelopment of the maxilla and mandible, excessive drying of the tongue with ulceration, and airway obstruction.

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Unfortunately, surgical reduction of the tongue is generally effective only for the first three indications, and less so for airway obstruction. The procedure usually consists of a resection of the lingual margin or a wedge resection with or without aggressive resection at the foramen cecum (86), and therefore fails to address obstruction at the distal oropharynx and tongue base (Fig. 10). As a result, airway obstruction persists in many children undergoing tongue reduction for macroglossia (87). Regrowth of tongue tissue following the procedure has also been reported (88). Other methods of managing macroglossia include suture suspension of the tongue, radiofrequency ablation, and intralesional laser therapy for vascular malformations. The tongue suspension suture technique has not been reported in children. To date, only case reports document the success of radiofrequency ablation for pediatric macroglossia due to lymphatic malformation of the tongue (89), and Down syndrome (EA Mair, personal communication). Venous malformations of the tongue have demonstrated a variable response to superficial and intralesional Nd:YAG laser therapy (90,91), but may also be treated by alcohol sclerosis and/ or excision.

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81. Leblanc SM, Golding-Kushner KJ. Effect of glossopexy on speech sound production in Robin sequence. Cleft Palate Craniofac J 1992; 29:239–245. 82. Ilizarov G, Ledyaev V. The replacement of long tubular bone defects by lengthening distraction osteotomy of one of the fragments. Vestnik Khururgii 1969; 6:78–84. 83. McCarthy JG, Schreiber J, Karp N, Thorne CH, Grayson BH. Lengthening the human mandible by gradual distraction. Plast Reconstr Surg 1992; 89:1–8. 84. Sidman JD, Sampson D, Templeton B. Distraction osteogenesis of the mandible for airway obstruction in children. Laryngoscope 2001; 111:1137–1146. 85. Imola MJ, Hamlar DD, Thatcher G, Chowdury K. The versatility of distraction osteogenesis in craniofacial surgery. Arch Facial Plast Surg 2002; 4:8–19. 86. Morgan WE, Friedman EM, Duncan NO, Sulek M. Surgical management of macroglossia in children. Arch Otolaryngol Head Neck Surg 1996; 122:326–329. 87. Kacker A, Honrado C, Martin D, Ward R. Tongue reduction in Beckwith-Wiedemann syndrome. Int J Pediatr Otorhinolaryngol 2000; 53:1–7. 88. Kopriva D, Classen DA. Regrowth of tongue following reduction glossoplasty in the neonatal period for Beckwith-Wiedemann macroglossia. J Otolaryngol 1998; 27:232–235. 89. Cable BB, Mair EA. Radiofrequency ablation of lymphangiomatous macroglossia. Laryngoscope 2001; 111:1859–1861. 90. EA Mair. Personal communication. 91. Clymer MA, Fortune DS, Reinisch L, Toriumi DM, Werkhaven JA, Ries WR. Interstitial Nd:YAG photocoagulation for vascular malformations and hemangiomas in childhood. Arch Otolaryngol Head Neck Surg 1998; 124:431–436. 92. Chang CJ, Fisher DM, Chen YR. Intralesional photocoagulation of vascular anomalies of the tongue. Br J Plast Surg 1999; 52:178–181.

28 Surgery for the Upper Airway Resistance Syndrome James Newman Division of Otolaryngology—Head and Neck Surgery, Stanford University Medical Center, Stanford, California, U.S.A.

The upper airway resistance syndrome (UARS) defines a group of patients with clinical signs and symptoms of excessive daytime somnolence in the absence of obstructive sleep apnea. Snoring is oftentimes present in these patients but is not a necessary symptom of UARS. Patients have increased upper airway resistance, which is characterized by partial collapse of the airway resulting in the increased resistance to airflow. The resistance to airflow is typically subtle and does not result in apneic or hypopneic events; therefore, a normal respiratory disturbance index is recorded. Physical findings include excessive palatal tissue and narrowing of the oropharynx and hypopharynx. An increased respiratory effort is required to maintain airflow to the lungs and may result in multiple sleep fragmentations as measured by very short alpha electroencephalogram (EEG) arousals (1). Repetitive alpha arousals during sleep are thought to be responsible for symptoms of excessive daytime somnolence, which is the principal symptom of UARS. The sites of airway obstruction and increased airway resistance are similar to those in frank obstructive sleep apnea syndrome but the degree of collapse or relaxation of muscle tone in the palate or tongue is less. Narrowing or partial collapse occurs both at the retropalatal and hypopharyngeal airway. The factors to be considered in each patient include the individual anatomic variation in depth of the nasopharynx and posterior airway space, the presence of redundant palate tissue, hypertrophy, or persistence of lymphoid tissue in Waldeyer’s ring, and the inhibition of the baseline tone of the skeletal muscles of the chest and upper airway during sleep. Several studies have confirmed that closure of the palate against the posterior pharyngeal wall producing increased resistance to airflow in the nasopharynx was found to correlate with loss of tonic activity of the tensor veli palatini muscles (2,3). Further evidence of narrowing of the hypopharynx has been documented as a result of decreased genioglossus muscle tone (4). Continued narrowing of the airway is promoted by compliance of the upper airway from the loss of muscle tone. Partial collapse occurs when subatmospheric pressures are generated within the pharyngeal lumen by inspiration against proximal resistance (Fig. 1). This narrowing leads to a vicious cycle, manifesting the Bernoulli principle. As increasing airflow

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Figure 1 Schematic drawings depicting (A) normal upper airway in the presence of normal thoracic pressure and (B) partial collapse of the upper airway, producing increased upper airway resistance, which results in increasingly negative intrathoracic pressure. velocity is required to maintain minute ventilation, a decrease in the transluminal pressure within the upper airway promotes further airway collapse (5). If the transluminal pressure is overcome and closure of the airway occurs, an apnea may result. In order to understand the physiology, researchers have been measuring the transluminal pressure, which gives a direct value of airway collapse known as the closing pressure for the system. The normal closing pressure of the upper airway in normal individuals is 13.3cm H2O, diminishes to 5.8cm H2O in nonapneic snorers, and decreases

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to 3.1cm H2O in patients with obstructive sleep apnea (6). Airway resistance increases in patients who snore and in those with sleep apnea, with quite significant changes compared to their baseline states. One report shows that individuals’ upper airway resistance increased 230% during non-rapid-eye-movement sleep when compared to their wakeful states (7). To overcome the rises in airway resistance, a person has to achieve increasingly negative intrathoracic pressures to drive air into the lungs. The rise in negative intrathoracic pressure during inspiration is measured using an esophageal manometer as an adjunct to a polysomnogram. When the esophageal pressure readings exceed −10cm H2O, the work of breathing is increased. Catheters or balloons with pressure transducers can be placed in the esophagus as an indirect measurement of intrathoracic pleural pressure and values more negative than –10cm H2O are considered abnormal (7). The occurrence of

Figure 2 Polysomnogram tracing of UARS demonstrating an alpha EEG arousal (small arrow) with quantitative evaluation of esophageal pressure (Pes). Pes is at its nadir in the two breaths just prior to the arousal (large arrows). There is no desaturation on pulse oximetry and no significant change in airflow consistent with an apnea or a hypopnea. these elevated intrathoracic pressures are correlated with sleep arousals seen as spikes in alpha brain wave activity (Fig. 2). In patients with UARS, a polysomnogram with EEG

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monitoring will pick up these alpha arousals. As seen in Fig. 2, when the intrathoracic pressure increases to −30 to −50cm H2O, an alpha arousal is seen in the EEG tracing. The frequency of these alpha arousals during sleep is thought to be the major contributing factor to daytime somnolence. Because there are no registered apneas with these events, a patient will have a normal respiratory disturbance index. The administration of continuous positive airway pressure (CPAP) during these episodes corrects the pressure changes and the frequency of alpha spike arousal diminishes and correlates with fewer symptoms of excessive daytime somnolence. Making a diagnosis of UARS rests on symptoms of excessive daytime somnolence coupled with polysomnographic documentation of more than 10 EEG arousals per hour of sleep. The surgical treatment of UARS is primarily aimed at preventing retropalatal tissue collapse and removal of excess tissues crowding the oropharyngeal inlet. Some cases will also require tightening of the genioglossus muscle to prevent hypoharyngeal narrowing (5). Treatment for UARS includes CPAP, somnoplasty of palate and base of tongue, tonsillectomy and adenoidectomy, uvulopalatophayrngoplasty, laser-assisted uvulopalatoplasty, snare uvulectomy, and genial tubercle advancement. As all of the procedures have been discussed in detail in other chapters, the process of snare uvulectomy will be discussed in detail as it represents a minimally invasive outpatient clinic procedure. Equipment needed includes a headlight, tongue depressor, bayonet forceps with Brown-Adson tissue grasping tips, and a standard cautery source for attachment to a standard hand-controlled snare. Several manufacturers supply cautery snares for otolaryngology, including Karl Strorz Instruments (Culver City, CA) and Ellman International Inc. (Hewlett, NY). The anesthetic technique is similar to that of preparation for laser uvulopalatoplasty. The oropharynx is sprayed with 20% benzocaine (Hurricaine Spray, Beutlich, Waukegan, IL) followed by injection with 1.5cc of an equal mixture of 1% Lidocaine with 1:100,000 epinephrine (Abbott, North Chicago, IL) and 0.25% bupivicaine through a 1.25 in., 27guage needle attached to a 3cc syringe. In performing injections and instrumentation in the oropharynx, the patients are instructed to open their mouth and to breathe in and out through their mouth only. This action relaxes the genioglossus muscle and allows an unimpeded view of the uvula and palate. In some cases with larger tongues, an assistant may need to hold the tongue depressed with a standard sweetheart tongue depressor. During the preoperative examination, the patient is asked to elevate the palate for general muscle tone and the palate is palpated to assess for any submucous cleft of the hard palate. The thickness of the palate and uvula base is also assessed to help determine the duration of cauterization and speed of snare tightening. The snare is always tested prior to introduction and then relaxed so that the initial diameter of the loop opening is the size of a quarter. A “dry run” placement of the snare is performed so that the operator can anticipate movements of the palate and to determine the position of the uvula amputation. Sometimes a cautery mark is scored with the tip of the snare to mark the level of amputation and to confirm adequate anesthesia. After pretreatment preparations are checked and proper grounding is ensured an assistant stands to the right of the patient with a hand-held suction and tongue depressor. The patient is given a 500cc emesis basin to hold. The physician with a headlight,

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Brown-Adson bayonet forceps in the left hand and the control snare in the right hand, is ready to begin the procedure. With the mouth open, the procedure is initiated by engaging the uvula and snugging the snare at the indicated level for amputation (Figs. 3 and 4). The cautery settings depend on the source to be used. In the author’s, three different cautery sources have been utilized with equally satisfactory results in hemostasis. The Cameron Miller radiofrequency source is typically

Figure 3 Depressing the tongue and securing the snare around the uvula.

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Figure 4 Snare is tightened around the base of the uvula and heat cauterization is initiated. set between 3 and 4. The Ellman radiotron box is set on 4–5 with a partially rectified current. The Valley Lab Force 2 electrosurgical generator is set in the cut mode with a blend of 2 and a power setting of 3–6. Regardless of the generator used, one should be familiar with the current device and practice the procedure on a template from an uncooked piece of chicken breast. The procedure is then begun with depression of the footswitch and closing of the snare loop. During the procedure, there is an absence of smoke plume because no tissue is being vaporized as in laser or free-hand cautery techniques. This is an important fact, which is why there is no visual obstruction by an assistant’s hand or suction tip device trying to evacuate a plume. The procedure culminates in the forceful closure of the snare, resulting in amputation of the uvula, which is then removed from the mouth with the bayonet forceps (Fig. 5). After the specimen is removed, the stump is observed for any potential sites of bleeding (Fig. 6). If any red spots are seen, they can be point cauterized with the partially drawn closed free snare, which makes the end into a narrow wire cautery tip. The patients are usually impressed by the brief nature of the procedure and the lack of discomfort. Patients are observed for 15min and then allowed to go home with a prescription for 3 days of penicillin and 1 week’s supply of liquid codeine with acetaminophen or liquid hydrocodone with acetaminophen. Patients are instructed to return to the office in 3 weeks. If there is bleeding or increased pain after the first 3 days, they are encouraged to come in for an office visit prior to their routine 3-week visit. Their return visit at 3 weeks usually shows a well-healed mucosa and normal palate contraction.

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This particular procedure seems to offer several advantages when compared to similar treatments for UARS or even snoring. It is a single procedure with minimal risks and does not require the expense of a unique piece of equipment for the sole purpose of snare uvulectomy. The anatomic configuration of the uvula makes it an ideal candidate for amputation with a snare. The ability to produce circumferential cauterization and cutting makes for excellent hemostasis and also limits the lateral collateral thermal damage. Loop tip cauteries have limited collateral damage when used in pure cutting modes. Performance of the procedure requires

Figure 5 Grasping of the uvula from the oral cavity after its transection by closing the snare across the base of the uvula. an appreciation of the anatomy and a feel for the amount of manual squeeze over the course of the procedure. The main risks of other uvulectomy procedures include bleeding and excessive scarring, resulting in stenosis of the oropharynx inlet. Compared to the laser, there is less chance of pass pointing or posterior wall injury. Compared to free-hand bovie tip cautery amputation, there is less chance of collateral heat damage and less smoke. A more stable target is present as the single instrument both grasps and cuts. The lack of smoke plume makes for better visualization when compared to other techniques and the limited lateral thermal damage to the palate makes for quick recovery and diminished discomfort when compared to laser uvulectomy or laser palatoplasty.

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Figure 6 Open wound at the base of the uvula upon completion of the procedure. Choosing the location of amputation is the most variable part of the procedure as a low, mid, or high amputation can be performed. A low amputation is defined as a site of tissue cut inferior to the midway length of the uvula, the mid amputation is defined as the site of tissue cut exactly at the midline length of the uvula. A high amputation is defined as a site of tissue cut above the midway length of the uvula. The length of the uvula is observed beginning at the muscular base and extending to the free tip of the uvula. Treatments for simple snoring can also be performed at similar locations. More risk of bleeding has been reported when high amputations are performed, possibly due to the larger-diameter vessels, which includes arterioles in this location. Possible complications include vasovagal responses from patients during local anesthetic administration, bleeding, and excessive scarring (8). Patients have reported pain lasting from 3 to 20 days. No cases of stenosis, voice disturbance, infection, or excessive scarring have been noted in the author’s experience. The author is not aware of any other complications associated with this procedure and continues to offer it for cases of UARS and simple snoring. Most patients report that their symptoms of excessive daytime somnolence and snoring, when present, have been eliminated or significantly reduced at 6-month and 1year visits posttreatment. We have been unsuccessful in our attempts to universally obtain posttreatment polysomnograms with esophageal monitoring to confirm the abatement of signs associated with UARS. In practice, successful treatment of UARS is often correlated with an improvement or elimination of excessive daytime somnolence as reported by the patient. Monitoring of the condition and symptom scores as measured on the Epworth sleepiness scale should be carried out annually and should involve repeat

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polysomnography if there is a worsening of the symptoms. In cases where the symptoms of excessive daytime somnolence have not improved, CPAP, radiofrequency treatments, or surgery to address tongue-base collapse should be considered.

REFERENCES 1. Guilleminault C, Stoohs R. The upper airway resistance syndrome. Sleep Res 1991; 20:250. 2. Guilleminault C, Stoohs R, Clerk A, Cetel A, Maistros P. A cause of excessive daytime sleepiness: the upper airway resistance syndrome. Chest 1993; 104:781–787. 3. Gleadhill IC, Schwartz AR, Shubert N. Upper airway collapsibility in snorers and in patients with obstructive hypopnea and apnea. Am Rev Respir Dis 1991; 143:1300–1303. 4. Remmers JE, DeGroot WJ, Sauerland EK, Anch AM. Pathogenesis of upper airway occlusion during sleep. J Appl Physiol 1978; 44:931–938. 5. Newman JP, Moore M, Utley D, Terris DJ, Clerk A. Recognition and surgical management of the upper airway resistance syndrome. Laryngoscope 1996; 106:1089–1093. 6. Lopes JM, Tabachnik E, Muller NL, Levison H, Bryan AC. Total airway resistance and respiratory muscle activity during sleep. J Appl Physiol 1983; 54:773–777. 7. Hudgel DW, Martin RJ, Johnson B, Hill P. Mechanics of the respiratory system and breathing pattern during sleep in normal humans. J Appl Physiol 1984; 56:133–137. 8. Coleman J, Rathfoot C. Oropharyngeal surgery in the management of upper airway obstruction during sleep. Otolaryngol Clin North Am 1999; 32:263–276.

29 Electrical Stimulation for Sleep Disordered Breathing David W.Eisele Department of Otolaryngology—Head and Neck Surgery, University of California, San Francisco, California, U.S.A. Alan R.Schwartz and Philip L.Smith Division of Pulmonary and Critical Care Medicine, Johns Hopkins Sleep Disorders Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, U.S.A. 1. INTRODUCTION Obstructive sleep apnea (OSA), caused by recurrent episodes of upper airway obstruction during sleep, is associated with periodic arousals from sleep and oxyhemoglobin desaturations. Sleep disturbance and abnormal oxygenation are thought to be the primary cause of the clinical sequelae of OSA. These sequelae include daytime hypersomnolence, arterial and pulmonary hypertension, and cardiopulmonary failure. Treatment of OSA is directed toward the relief of upper airway obstruction so that the clinical manifestations of the disorder are resolved or are avoided. Numerous methods have been utilized to restore upper airway patency during sleep for patients with OSA. No single treatment modality, however, has been shown to provide complete reversal of upper airway obstruction during sleep in all patients with this disorder. Furthermore, the cause of OSA, which is considered to be related to diminished genioglossus muscle activity during sleep, is not addressed by current treatments (1). In order to address this problem, we conducted investigations into the effect of neuromuscular stimulation of the tongue muscles and direct hypoglossal nerve stimulation on upper airway patency in patients with OSA during sleep. In this chapter we will discuss our investigations of the effects of selective neuromuscular tongue and direct hypoglossal nerve stimulation on upper airway airflow mechanics in patients with OSA during sleep and the feasibility of this intervention for the treatment of OSA.

2. NEUROMUSCULAR STIMULATION OF THE TONGUE Multiple prior investigations have addressed the concept of electrical stimulation of the tongue in OSA. Approaches have included attempts to stimulate the tongue with surface electrodes placed in the skin of the upper neck (2,3), sublingual mucosa (4,5), base of tongue mucosa (6), and soft palate (7). Percutaneous wire electrodes, directed near the

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hypoglossal nerve, have also been utilized (8,9). The methodology utilized in these studies, however, lacked selectivity in stimulating the genioglossus muscle or hypoglossal nerve and induced recurrent arousals from sleep. Therefore, a generalized arousal from sleep resulting in pharyngeal muscle activation could have caused the improvements in pharyngeal airway patency reported in these earlier investigations. In light of the limitations of the these studies, we began to investigate electrical stimulation of the tongue muscles with three primary objectives: first, to develop methods to selectively stimulate the genioglossus muscle in volunteers and OSA patients; second, to determine the effect of the selective stimulation of the genioglossus muscle on upper airway airflow dynamics during sleep in OSA patients; and third, to treat patients for OSA with an implantable electrical stimulation system. Initially, methods for selective neuromuscular stimulation of the tongue muscles with transorally directed hook-wire electrodes were developed. Tongue motor responses with these methods were correlated with those resulting from selective hypoglossal nerve stimulation performed during open neck surgeries. This correlation provided confirmation of proper transoral electrode placement into the genioglossus muscle based on the motor response observed with stimulation. The observed response to neuromuscular and selective hypoglossal nerve stimulation of the genioglossus muscle was tongue protrusion and deviation to the contralateral side. Neuromuscular stimulation of the genioglossus muscle was then examined during sleep in OSA patients (10). The level of maximal airflow before, during, and after stimulation was measured with standard polysomnographic recording techniques. Arousal from sleep during or after stimulation was excluded by monitoring electroencephalography (EEG), electromyography (EMG), the pattern of respiration, and the heart rate. All OSA patients studied were morbidly obese with significant apneahypopnea indices. Neuromuscular stimulation of the genioglossus muscle resulted in an improvement in inspiratory airflow of ≈200–250mL/sec (Fig. 1). Improvement in airway patency was observed to be limited to the duration of stimulation of the genioglossus muscle. An important result of this study was the confirmation that electrical stimulation of the upper airway could be achieved during sleep in OSA patients without arousal from sleep. The airway opening effect produced by stimulation was noted to be directly related to genioglossus neuromuscular activation rather than a global arousal from sleep.

3. DIRECT SELECTIVE HYPOGLOSSAL NERVE STIMULATION Another study was undertaken to determine the effect of direct hypoglossal nerve stimulation on upper airway patency in OSA patients during sleep (11). A tripolar halfcuff electrode (Medtronic 3990, Medtronic, Inc., Minneapolis, MN) was used for nerve stimulation. This electrode was designed to limit the electrical current to the nerve and to prevent nerve entrapment. The hypoglossal nerve was exposed through an upper neck incision in patients with OSA. Two sites of hypoglossal nerve stimulation, the distal branch to the genioglossus muscle and the main nerve trunk, were examined. The level of maximal inspiratory airflow before, during, and after stimulation was measured during

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sleep with standard polysomnography. Lack of arousal from sleep was confirmed by monitoring EEG, EMG, the respiratory

Figure 1 Mean maximal inspiratory airflow (VImax) levels for eight OSA patients before, during, and after neuromuscular stimulation of the genioglossus muscle during sleep. (From Ref. 10.) pattern, and the heart rate. Electrical stimulation of the hypoglossal nerve at both stimulation sites resulted in a marked improvement in inspiratory airflow during stimulation, compared to unstimulated breaths, without patient arousal from sleep (Fig. 2). It was concluded from this study that airway obstruction in OSA patients was alleviated by hypoglossal nerve stimulation, not only when the genioglossus muscle was stimulated, but also when the tongue retrusor muscles were coactivated with the genioglossus muscle.

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4. IMPLANTABLE HYPOGLOSSAL NERVE STIMULATION SYSTEM Following the studies mentioned previously, which confirmed the success of electrical stimulation methods for opening the airway in OSA patients without arousal from sleep, as well as additional animal studies (12), an FDA-approved feasibility study was undertaken to investigate the treatment of OSA patients with a fully implantable hypoglossal nerve stimulation system. This system, the Inspire I (Medtronic, Inc., Minneapolis, MN), consists of components that were designed to reliably predict the onset of the inspiratory phase of respiration and to stimulate the hypoglossal nerve during inspiration. The system components include an implantable pulse generator (IPG), a respiratory pressure sensor, and a tripolar, half-cuff peripheral nerve stimulation electrode. The IPG contains a programmable microprocessor that allows stimulus frequency, duration, and amplitude to be adjusted

Figure 2 Mean maximal inspiratory airflow (VImax) in five OSA patients before, during, and after hypoglossal nerve stimulation during sleep. Closed

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circle indicates stimulation of the hypoglossal nerve branch to the genioglossus muscle. Open circle indicates main trunk hypoglossal nerve stimulation. (From Ref. 11.) transcutaneously by a physician programmer. The peripheral nerve lead and the respiratory pressure sensor interface with the IPG (Fig. 3). Surgical implantation of the hypoglossal nerve stimulation system is described in detail elsewhere (13,14). Briefly, the system is surgically implanted under general anesthesia with the use of three surgical incisions: an upper lateral neck incision, a

Figure 3 Schematic diagram of Inspire I hypoglossal nerve stimulation system. (From Medtronic Inc, Minneapolis, MN.)

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Figure 4 Half-cuff stimulation electrode placement around the distal branch of the hypoglossal nerve to the genioglossus muscle. (From Ref. 13.) lower midline neck incision, and an infraclavicular incision. The hypoglossal nerve is exposed by dissection via the upper neck incision. The stimulation electrode is placed on the peripheral hypoglossal nerve branch to the genioglossus muscle (Fig. 4). Proper placement on the desired nerve is confirmed by stimulation of the nerve with a hand-held pulse generator and observation of tongue protrusion and deviation to the contralateral side (Fig. 5).

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Figure 5 Tongue at rest (A). Tongue protrusion and deviation to the right with selective left hypoglossal nerve stimulation (B).

Figure 6 Pressure transducer placement through a drill hole in the manubrium. (From Ref. 13.)

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Through the midline lower neck incision, the pressure transducer is placed flush with the posterior aspect of the manubrium via a drill hole and the transducer housing is secured to the manubrium with a miniscrew (Fig. 6). An infraclavicular pocket, superficial to the pectoralis major muscle fascia, is created via the infraclavicular incision (Fig. 7). A tunneling device is then utilized to tunnel the nerve electrode lead and the pressure transducer lead to the IPG pocket. The leads are then

Figure 7 IPG placement in an infraclavicular pocket superficial to the pectorialis major muscle fascia. The nerve electrode lead and pressure transducer lead are tunneled to the IPG pocket and connected to the IPG. (From Ref. 13.) connected to the IPG and the wounds closed. The system is then checked for functional integrity prior to awakening the patient from anesthesia. Further testing of the system is deferred for about 1 month to allow for adequate healing and stabilization of the implanted system.

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5. THERAPEUTIC HYPOGLOSSAL NERVE STIMULATION IN OBSTRUCTIVE SLEEP APNEA Recently, the results of a multi-institutional, prospective trial to investigate the therapeutic efficacy of the Medtronic Inspire I hypoglossal nerve stimulation system for OSA were reported (14). The system was implanted in eight middle-aged, moderately overweight men with moderate to severe OSA during rapid eye movement (REM) and non-REM (NREM) sleep. Nightly unilateral hypoglossal nerve stimulation was initiated at 4 weeks after system implantation. These patients initiated nightly electrical stimulation with a self-controlled programming unit. A preset delay in system activation allowed the patients to fall asleep before the start of electrical stimulation. Sleep and breathing patterns were examined at baseline and at 1, 3, and 6 months postoperatively. The results of this clinical trial indicated that unilateral hypoglossal nerve stimulation decreased the severity of the OSA throughout the entire study period. Specifically, stimulation reduced the mean apnea-hypopnea indices in non-REM and REM sleep compared to baseline values (Fig. 8). In addition, the severity of oxyhemoglobin desaturations was significantly reduced. All patients were able to tolerate long-term stimulation at night and there were no

Figure 8 NREM apnea-hypopnea indices for a night without stimulation (baseline) and for entire-night and continuous periods with hypoglossal nerve stimulation. Patients’ values for

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the entire night are the mean of values at 1, 3, and 6 months and the last follow-up. (From Ref. 14.) adverse effects related to system implantation or to nerve stimulation. Small, consistent increases in stimulus parameters were required early in the protocol to maintain therapeutic responses to stimulation. After 3 months, however, little further increase in stimulus intensity was required, suggesting that the nerve-electrode interface had stabilized during this early postoperative period. The results of this prospective study demonstrate the feasibility and therapeutic benefit of unilateral hypoglossal stimulation in OSA. Prior to wider application of an electrical stimulation system for the treatment of OSA, some system technical issues require resolution. Electrode breakage or respiratory sensor malfunction occurred in some patients, resulting in compromise of long-term stimulation. Patients who remained free from stimulator malfunction, however, were able to continue to use the device as primary therapy for OSA. In addition, further studies are necessary to optimize patient selection criteria for therapeutic hypoglossal nerve stimulation. Patient selection may be based on baseline differences in upper airway collapsibility or the site of pharyngeal obstruction. In addition, therapeutic responses may be augmented by the use of multiple-site stimulation such as bilateral hypoglossal nerve stimulation or stimulation of other combinations of upper airway and cervical muscles. Most importantly, the impact of electrical stimulation of the upper airway on measures of daytime sleepiness, performance, and cardiopulmonary function must be assessed before this treatment modality can be established as an effective therapeutic option for OSA.

6. CONCLUSION Recent studies have shown that neuromuscular stimulation of the genioglossus muscle and direct stimulation of the hypoglossal nerve can be performed selectively and safely. Such stimulation, delivered below the arousal threshold, can modulate airflow during sleep in patients with OSA. Furthermore, the feasibility and potential of upper airway stimulation for the treatment of sleep disordered breathing has been demonstrated. Further studies and stimulation system refinements are presently under way with the goal of establishing electrical stimulation of the upper airway as a therapeutic option for this challenging disorder.

REFERENCES 1. Remmers JE, de Groot WJ, Sauerland EK, Anch AM. Pathogenesis of upper airway occlusion during sleep. J Appl Physiol 1978; 44:931–938.

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2. Miki H, Hida W, Chonan T, Kikuchi Y, Takishima T. Effects of submental electrical stimulation during sleep on upper airway patency in patients with obstructive sleep apnea. Am Rev Respir Dis 1989; 140:1285–1289. 3. Edmonds LC, Daniels BK, Stanson AW, Sheedy PF, Shepard JW. The effects of transcutaneous electrical stimulation during wakefulness and sleep in patients with obstructive sleep apnea. Am Rev Respir Dis 1992; 146:1030–1036. 4. Guilleminault C, Powell N, Bowman B, Stoohs R. The effects of electrical stimulation on obstructive sleep apnea syndrome. Chest 1995; 107:67–73. 5. Oliven A, Schnall RP, Pillar G, Oliven A, Schnall RP, Pillar G, Gavriely N, Odeh M. Sublingual electrical stimulation of the tongue during wakefulness and sleep. Respir Physiol 2001; 127:217–226. 6. Schnall RP, Pillar G, Kelsen, Oliven A. Dilatory effects of upper airway muscle contraction induced by electrical stimulation in awake humans. J Appl Physiol 1995; 78: 1950–1956. 7. Schwartz RS, Salome NN, Ingmundon PT, Rugh JD. Effects of electrical stimulation to the soft palate on snoring and obstructive sleep apnea. J Prosthet Dent 1996; 76:273–281. 8. Decker MJ, Haaga J, Arnold JL, Atzberger D, Strohl KP. Functional electrical stimulation and respiration during sleep. J Appl Physiol 1993; 75:1053–1061. 9. Fairbanks DW, Fairbanks DNF. Neurostimulation for obstructive sleep apnea: investigations. Ear Nose Throat J 1993; 72:52–57. 10. Schwartz AR, Eisele DW, Hari A, Testerman R, Erickson D, Smith P. Electrical stimulation of the lingual musculature in obstructive sleep apnea. J Appl Physiol 1996; 81: 643–652. 11. Eisele DW, Smith PL, Alam DS, Schwartz AR. Direct hypoglossal nerve stimulation in obstructive sleep apnea. Arch Otolarygol Head Neck Surg 1997; 123:57–61. 12. Goding GS, Eisele DW, Testerman R, Smith, PL, Roertgen K, Schwartz AR. Relief of upper airway obstruction with hypoglossal nerve stimulation in the canine. Laryngoscope 1998; 108:162–169. 13. Eisele DW, Schwartz AR, Smith PL. Electrical stimulation of the upper airway for obstructive sleep apnea. Oper Tech Otolaryngol Head Neck Surg 2000; 11:59–65. 14. Schwartz, AR, Bennet, ML, Smith PL, Backer, WD, Hedner J, Boudewyns A, Van de Heyning P, Ejnell H, Hochban W, Knaack L, Podszus T, Penzel T, Peter JH, Goding GS, Erickson DJ, Testerman R, Ottenhoff F, Eisele DW. Therapeutic electrical stimulation of the hypoglossal nerve in obstructive sleep apnea. Arch Otolaryngol Head Neck Surg 2001; 127:1216–1223.

30 Temperature-Controlled Radiofrequency Tonsil Reduction Lionel M.Nelson Department of Surgery, Stanford University School of Medicine, Stanford, California, U.S.A. 1. INTRODUCTION It hurts to have one’s tonsils taken out. Whether excised by traditional snare resection, dissection, electrocautery, or laser, the significant postoperative pain is fairly similar (1). The pain, resulting from transected sensory fibers, disruption of overlying mucosa, and spasm of exposed tonsil fossa pharyngeal musculature, typically persists for 7–10 days as exposed tissue heals slowly by secondary intention (2). Resultant problems of poor oral intake with weight loss and dehydration, side effects of frequent and prolonged narcotic analgesic use, and loss of work or school time are well recognized (1,3). In an effort to reduce the discomfort of tonsillectomy when treating obstructive disorders caused by enlarged tonsils, various methods of subtotal reduction (tonsillotomy), such as laser, electrodessication, plasma-mediated ablation technologies, and microdebriders have been introduced. These reduce discomfort by sparing capsule and adjacent tonsil lymphoid tissue, thus avoiding underlying muscle exposure. However, they all ablate overlying mucosa in the process, still leaving a relatively large open wound in the oral cavity with its associated discomfort and other comorbidities. Temperature-controlled radiofrequency (TCRF) soft tissue reduction in the upper airway, a procedure known as Somnoplasty® (Gyrus ENT, Bartlett, TN), takes a different approach. For tonsil reduction, it is designed to ablate targeted subsurface lymphoid tissue, effectively shrinking tissue bulk while essentially sparing overlying mucosa and underlying capsule. This accounts for the diminished pain and rapid return to normal activity for both the adult (4) and pediatric (5) patients who have undergone this procedure. It makes tonsil Somnoplasty® the least invasive approach to the treatment of tonsil-related obstructive disorders in the upper airway presently available to the practitioner.

2. BASIC TECHNOLOGY TCRF technology works by forming a low-temperature (47–85°C) thermal lesion via an electrode placed submucosally within the target tissue. The body then gradually (usually over a 6–8 week period) heals this area, resorbing the damaged submucosal tissue, which results in overall tissue volume reduction while leaving overlying mucosa intact. This

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entire process is designed to take place subsurface, and is therefore hidden from the visual cues we usually rely on to assure accuracy and safety when utilizing electrosurgery. An alternative control mechanism is therefore needed. That mechanism is temperature information fed back real-time from the lesion as it is being formed through thermocouples within the electrode. This information is then utilized by a computerized control unit/radiofrequency generator, which in turn modulates the flow of energy needed to produce a precise, predesignated lesion. Unlike other radiofrequency instrumentation presently in use in otolaryngology, this technology allows a rapid and dynamic response to changing conditions in the treated tissue. It therefore gives the surgeon a predictable and safe method to form submucosal lesions. For TCRF tonsil reduction (tonsil Somnoplasty®), two parallel blunt tipped electrodes are deployed into tonsil lymphoid tissue through a handpiece that incorporates a sharp nonconducting penetrator template to breach the tonsil mucosa. The handpiece is designed to minimize the risk to underlying subcapsular tissue and overlying mucosa while concentrating the lesion in the target tonsil tissue (Fig. 1). An in vivo study involving tonsil removal after TCRF lesion placement demonstrated rare puncture penetration (1 of 11 tonsils) of the underlying fibrous tonsil capsule, and no thermal or mechanical damage to tonsil fossa musculature or vascular structured in any of the study patients (4). The lesions that are formed by one placement of this device have the configuration of two parallel “football” shapes (prolate spheres). When formed by 500J of energy, controlled by temperature feedback information to a maximum temperature of 85°C, the three-dimensional lesion generated in tonsil lymphoid tissue by each of the 8mm active electrodes is approximately 16mm in length along its major axis, and 10mm in width along its minor axis, with some minimal variability due to tissue conditions (Fig. 2).

Figure 1 Close-up of tonsil Somnoplasty® handpiece tip. The

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sharp-tipped insulated penetrator template punctures through the tonsil mucosa. By sliding a switch on the hand-piece, the blunt-tipped active electrodes are then deployed into underlying tonsil tissue.

Figure 2 Electrode dimensions and approximate lesion size in tonsil. Prior to activating energy flow for lesion formation, lateral pressure on the handpiece should be released and the electrodes allowed to “drift” back medially about 5mm. Since the lesion produced will be larger than the electrode, this will further reduce the chance of potential capsular and subcapsular thermal injury. 3. PATIENT SELECTION The procedure is indicated for the reduction of chronically enlarged tonsils, particularly when associated with obstructive sleep-disordered breathing (SDB) conditions, such as habitual snoring, upper airway resistance syndrome, and sleep apnea, or when associated with related dysphonia, dysphagia, or malocclusion. It has also proved useful in the treatment of recalcitrant cryptic tonsil disease (chronic inflammatory cryptitis and tonsillith formation). As is the case with other methods of subtotal reduction, since tonsil tissue remains, it is probably not indicated for control of recurrent infectious tonsillitis.

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4. PROCEDURE TCRF tonsil reduction is well tolerated as an in-office or outpatient procedure under local anesthesia for adult and older teenage patients. Systemic sedation is usually not needed. Therefore, no specific restrictions need be placed on activity or diet for the day of treatment. For adults and older teenagers, the ability to undergo a tonsil procedure with minimal disruption to work or school schedules is a considerable advantage. Since there is no significant bleeding either with or after the procedure, non-excessive use of anti-inflammatory or salicylate medications is permissible. As with other procedures, patients on anticoagulant therapy (such as coumadin) should stop their medication temporarily with an appropriate timetable as designated in consultation with the patient’s other physicians. For pediatric patients, the procedure is performed in an operating room under general anesthesia. Since significant bleeding is not an issue, it has been demonstrated that a laryngeal mask airway (LMA) can be used as a safe alternative to endotracheal intubation (5). Concurrent curette adenoidectomy, which is usually indicated in this age group, is carried out at the same time. Other than the mode of anesthesia and the patient’s position (upright in an examination chair for adults and teenagers in-office or in the standard “T&A” Rose position in the operating room for children), the procedure as described below is the same. A commercially available Somnoplasty® control unit/generator (Gryus ENT, Bartlett, TN) with two-channel capability and tonsil handpiece (model 2420) will be needed for the procedure. Perioperative antibiotics and steroids are recommended. Ampicillin/clavulanate or cephalexin is started on the day of treatment, and continued for 7 days. For adults, prednisone is given for 2 days, starting with 30mg twice daily on the day of treatment (initial dose, preferably 4hr prior to treatment and second dose about 6hr postprocedure), and 20mg twice daily on the day after treatment. For children, appropriate antibiotic and steroid doses by weight are used, with the initial doses of both administered intravenously at the time of general anesthesia. For local procedures, a topical anesthetic level is first established (20% benzocaine or 4% lidocaine sprays or equivalent). Treating one tonsil at a time, the tissue is then injected with 1% lidocaine (or equivalent) with 1:200,000 epinephrine and sodium bicarbonate (optional to minimize injection discomfort when done under local anesthesia). Under general anesthesia, anesthetic injection is still recommended as it diminishes any mucosal bleeding from the sharp penetrating tips and “hydroplanes” the tonsil medially away from the underlying fossa. Injections are first placed into the pillar mucosa, then into the subcapsular plane to mediallize the tonsil, and, finally, into the tonsil mucosa and tissue (Fig. 3). Just prior to placing the electrode into the tonsil, 5–6cc of normal saline (0.9%) is injected into the tonsil tissue submucosally. Although not needed to form a TCRF lesion, saline in the target tissue appears to increase lesion size and subsequent volume of tissue reduced (6). The electrodes are placed by approaching the tonsil in a medial to lateral direction (Fig. 4), rather than anteroposteriorly. To breach the mucosa, the handpiece’s penetrator template is firmly pressed into the tonsil so that the full length of its insulated sharp tips is buried submucosally (Fig. 5). With the penetrator tips in place, and without applying

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any additional lateral pressure, the active electrodes are then deployed by using a sliding switch in the handpiece, advancing them into the tonsil.

Figure 3 Pattern of local anesthesia placement, injecting first into the pillar mucosa (1), then into subcapsular plane (2), and finally into tonsil mucosa and tissue (3).

Figure 4 Electrode placement. The tonsil is approached in a medial to lateral direction.

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This maneuver should be done gently. Forceful deployment with too much additional lateral pressure could potentially cause the blunt electrode tips to puncture through the underlying tonsil capsule (Fig. 6). Since the radiofrequency ablation pattern may typically extend approximately 3–4mm beyond the active electrode tips, all lateral compression force should be released and the handpiece allowed to “drift” back medially toward the oral cavity about 5mm prior to switching on energy flow to establish the lesion. This last maneuver moves the electrode tips away from the tonsil capsule. Despite the fact that the capsule is fibrous and has a more limited response to low-temperature thermal input, this should further diminish the chance of extending the ablation outside of the target tonsil tissue (Fig. 2). The recommended parameters for lesion formation are 500J of energy per lesion delivered to a maximum temperature of 85°C (4). Formation of the TCRF lesion should be painless. For the patient undergoing the procedure under local anesthesia, if pain is experienced, it could indicate deep ablation beyond the capsule into muscle. Under this circumstance, handpiece position should be evaluated to be sure that lateral pressure is not being applied. The

Figure 5 Electrode placement. The penetrator template is pressed firmly through the tonsil mucosa so that the full lengths of its insulated sharp tips are submucosal.

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Figure 6 Electrode placement. Once the template tips are in position, and without exerting additional lateral pressure on the handpiece, the active electrodes are gently deployed, advancing them into the tonsil tissue. handpiece can be allowed to drift more medially, as long as the penetrator template tips remain submucosal. If pain persists, energy flow should be paused (the system’s control unit has that capability), the electrodes disengaged from the tonsil, so that more local anesthetic can be placed and the device repositioned. When performed under general anesthesia, in the absence of patient feedback, strict adherence to avoiding lateral pressure is important. Depending on the size of the tonsil, this dual electrode device is usually placed four to six times in each tonsil, forming 8–12 TCRF lesions (4000–6000J total energy) per tonsil. Device placements should be spaced about 1cm apart, covering the tonsil’s medial surface (Fig. 7). Each ablation (formation of two lesions) takes about 1.5–2min to complete. After treatment of the first tonsil is completed, the above procedure is repeated on the contralateral tonsil.

5. POSTTREATMENT CARE TCRF tonsil reduction is significantly less painful than tonsillectomy or tissue resecting tonsil reduction, but it is not painless. Most adult patients describe a sore throat

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Figure 7 Various patterns of device placement, spacing each set of lesions approximately 1cm apart over the medial tonsil surface. similar in intensity to that experienced with a typical viral upper respiratory tract infection that abates over 3–5days. Few need prescription analgesics, and most find overthe-counter analgesics or anesthetic lozenges/sprays adequate. Patients will experience early tonsil and peritonsil tissue edema. This starts within 2–4hr of the procedure, peaks at 12–18hr, and abates rapidly over the ensuing 24hr. Edema is limited to directly contiguous mucosa, submucosa, and tonsil tissue. It is not accompanied by trismus or muscle spasm, and therefore does not appear to limit oral intake. However, changes in voice quality and more fitful sleep patterns with increased snoring may occur over this period. Sleeping with head elevated is recommended. When treating patients with very large tonsils (3+ or greater) or an airway of concern for any reason, this acute edematous phase could temporarily add to airway compromise. For those individuals, an overnight hospital stay for airway observation should be considered. An alternative approach to the adult or older teenage patient with very large tonsils who is undergoing the procedure under local anesthesia in-office is to treat one tonsil at a time, with the second side treated about 5–7days later, thus avoiding hospitalization. Since the degree of edema is energy dependent, incremental, repetitive treatments using less energy to both tonsils per session is another alternative. For children undergoing TCRF tonsil reduction under general anesthesia, an overnight in-hospital observation usually follows. Since children with SDB usually start with large tonsils, and since the need for a general anesthetic dictates that enough energy be used bilaterally to attain the expected result with one treatment session, close airway observation appears warranted for the initial 18hr postprocedure (5). Following TCRF tonsil reduction, diet and activity are as tolerated without any specific restrictions. For most adults and teenagers, a soft diet can be tolerated as soon as the local anesthetic resolves, and normal activity is resumed within 1–2 days (4). For children operated under a general anesthetic, all have been able to take liquids fairly well in recovery room, and have been able to achieve sustainable oral hydration within the first 24hr. Most eat soft solids within 6hr of the procedure. In the pediatric case series study group, 80% of the children resumed their regular diet by day 5 and all were back to normal activity by 3.9±2.1days (5).

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Despite the fact that the penetrator template is insulated, as a result of tissue thermal conductance, areas of localized mucosal slough often develop at the electrode placement sites. These rarely need treatment or cause pain and heal within 1–2 weeks. To date, no significant bleeding, airway obstruction, or infections requiring intervention have been noted in either the adult (4) or pediatric (5) study groups, or in my practice.

6. DISCUSSION TCRF tonsil reduction is a safe, minimally invasive treatment for symptomatic chronic tonsil enlargement. It has also proved useful in some recalcitrant cases of cryptic tonsil disease. For most adults and older teenagers, its ease of toleration as an in-office procedure under local anesthesia has clear advantages. The minimal pain with rapid return to normal diet and activity, and associated low morbidity (bleeding, infection, dehydration, and weight loss), makes TCRF an appealing alternative to tonsillectomy or more invasive tonsil reductive techniques in both adult and pediatric patients. For the practitioner, the procedure is easy to learn, with high patient acceptance and low risk of complications. Since the procedure spares the subcapsular plane, it will not compromise a future tonsillectomy if this becomes necessary. Although tonsil reduction always occurs following treatment, the specific amount of tissue volume reduced using identical treatment parameters may vary between patients. Despite the fact that outcomes, therefore, are not completely predictable, a single treatment appears sufficient to control tonsillar obstructive symptoms in most patients (4,5). A single treatment in an adult case series study showed, on average, a 70.8% reduction in tonsil size. Using 0–10 visual analog scales (VAS), at 3 months following treatment, this group demonstrated a reduction in snoring from 7.7 to 4.4, dysphonias from 1.7 to 0.3, dysphagias from 2.3 to 0.3, and chronic throat discomfort (often described as “throat fullness” or “irritation”) from 3.5 to 1.0. On average, Epworth Sleepiness Scale scores changed from 7.7 to 4.4 (4). A pediatric case series study (ages 4–13) showed similar improvements. Tonsil size, on a clinical 0 to 4+ scale (where “0” is no discernable tonsil tissue, a “1+” tonsil is well within the fossa, a “2+” extends to the posterior pillar, a “3+” is well beyond the posterior pillar but not to midline, and a “4+” is to midline), decreased from a baseline of 3.2+ to 0.8+ (a reduction of about 75%). For these pediatric patients, who also underwent a concurrent curette adenoidectomy if adenoids were present, by VAS (0–10 scale), there were statistically significant reductions in snoring from 7.0 to 0.9, OSA-18, a validated apnea quality of life survey (7), scores from 44.2 to 26.3, and improvements in daytime sleepiness, and speech and swallowing problems. Sleep studies at 3 months showed improving trends, with a mean Apnea/ Hypopnea Index change from 8.8 to 4.2 episodes per hour (5). Retreatment as an in-office procedure under local anesthesia is feasible for the adult patient with inadequate symptom control after one treatment. For example, one patient with minimal improvement following his first treatment underwent a second treatment 6 months later resulting in reductions in VAS scores for snoring from 7.5 to 0, throat discomfort from 7.5 to 0, and Epworth Sleepiness Scale score from 19 to 9 (8). For

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children, where retreatment is less practical, given the need for a general anesthetic, total energy (number of lesions placed) at the initial procedure should be maximized to improve the probability of a one-stage optimal outcome. Although the amount of initial edema is energy dependent, no significant airway problems have been noted to date in the pediatric population (5) on short-stay hospital observation. Improvement in initial obstructive symptoms is usually first noted by the patient about 2 weeks following treatment. Since lesion absorption with consequent submucosal tissue volume reduction continues over a 6–8week period, further improvement occurs gradually, and eventually stabilizes by 3 months (Fig. 8). Adult

Figure 8 Appearance of an adult patient pretreatment (A) and at 3 months post-TCRF tonsil reduction (B). (See color insert.) (8) and pediatric (5) studies show no clinical evidence of tonsil tissue regrowth or relapse of symptoms over 1 year follow-up.

7. CONCLUSIONS TCRF tonsil reduction is another treatment approach for symptomatic obstructive tonsils and recalcitrant cases of cryptic tonsil disease. As the least invasive surgical approach, its greatest advantage to the patient resides in its ease of tolerance, minimal posttreatment discomfort, and rapid return to productive activity. For the adult and older teenager, the capability to accomplish this in-office under a local anesthetic is also appealing. These factors often lower the bar of acceptance in patients (and pediatric patients’ parents) that were previously reluctant to accept surgical treatment. TCRF tonsil reduction is not designed to supplant traditional tonsillectomy in all cases, but for the properly selected patient, it has become a welcome addition to the surgeon’s armamentarium.

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ACKNOWLEDGMENT The author thanks Theodore R.Kucklick, BFA, for his invaluable assistance in rendering the illustrations for this chapter.

REFERENCES 1. Randall DA, Hoffer ME. Complications of tonsillectomy and adenoidectomy. Otolaryngol Head Neck Surg 1998; 118:61–68. 2. Murthy P, Laing MR. Dissection tonsillectomy: pattern of post-operative pain, medication and resumption of normal activity. J Laryngol Otol 1998; 112:41–44. 3. Colclasure JB, Graham SS. Complications of outpatient tonsillectomy and adenoidectomy: a review of 3,340 cases. Ear Nose Throat J 1990; 69:155–160. 4. Nelson LM. Radiofrequency treatment for obstructive tonsillar hypertrophy. Arch Otolaryngol Head Neck Surg 2000; 126:736–740. 5. Nelson LM. Temperature-controlled radiofrequency tonsil reduction in children. Arch Otolaryngol Head Neck Surg. 2003; 129;533–537. 6. Woodson TB, Nelson LM, Mickelson S, Huntley T, Sher A. A multi-institutional study of radiofrequency volumetric tissue reduction in OSAS. Otolaryngol Head Neck Surg 2001; 125:303–311. 7. Franco RA Jr, Rosenfeld RM, Rao M. Quality of life for children with obstructive sleep apnea. Otolaryngol Head Neck Surg 2000; 123:9–16. 8. Nelson LM. Temperature-controlled radiofrequency tonsil reduction: extended follow-up. Otolaryngol Head Neck Surg 2001; 125:456–461.

31 Harmonic Scalpel in Tonsillectomy Ashkan Monfared Department of Otolaryngology—Head and Neck Surgery, Stanford University Medical Center, Stanford, California, U.S.A. David J.Terris Department of Otolaryngology-Head and Neck Surgery, Medical College of Georgia, Augusta, Georgia, U.S.A. 1. INTRODUCTION Presently an indispensable part of many surgical disciplines, ultrasonically activated instruments such as the harmonic scalpel (HS) (Ethicon Endosurgery, Cincinnati, OH) are becoming progressively applied to the field of head and neck surgery. Harmonic shears have already become the instrument of choice for thyroidectomy and similar operations at many institutions (1–3). The most widespread use of HS in the field of otolaryngology is in tonsillectomy. The preliminary reports suggest that the HS might be the much sought after compromise between the precision and fast healing of the cold scalpel and the lower postoperative bleeding risk of the electrocautery (4). In this chapter, we will first delineate the technical aspects of this new technology, then expound upon the surgical technique and practical recommendations regarding usage of HS in tonsillectomy, and last, discuss the advantages as well as the limitations of HS compared to the more conventional methods of tonsillectomy.

2. TECHNOLOGICAL CONSIDERATIONS The HS technology is based on rapid longitudinal vibrations of the blade at 55,000Hz over a distance of 50–100µm. The vibrations are produced by the expansion and contraction of piezoelectric crystals in the hand piece of the scalpel, which are transferred to the tip via the blade extenders. The mechanical vibration is transferred to the tissue and the “frictional” energy denatures the proteins by breaking the hydrogen bonds at temperatures between 50° C and 100°C (4). Unlike with the electrocautery instruments, there is no electrical current involved and the patient does not have to be grounded. The harmonic system consists of a generator, a hand piece, blades, and a foot pedal (Fig. 1). The harmonic generator has power settings of 1 through 5, which

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Figure 1 Harmonic shears power generator with the foot pedal set on top. dictate the distance that the blade will vibrate across at the same frequency; hence, the lower settings (shorter excursion of the blade) are optimal for operations demanding maximum coagulation and the higher ones (longer excursion of the blade) for cutting through avascular tissue. At all settings the foot pedal or hand control switch offers two blade speeds of “Full” and “Variable,” which are used for cutting and coagulation, respectively. Ethicon has recently mounted “Variable” and “Full” control buttons on the hand piece, thus eliminating the less desired foot pedal. The HS offers a variety of blades with different handle lengths. The two most popular blades are the “dissecting hook” and the “curved” blade (Fig. 2a and b). The former has an inner sharp concave edge, suitable for sharp dissection, and a dull flat side surface optimal for coagulation of vascular beds. The two cutting edges of the curved blade allow easier and more precise tissue separation at the cost of lower coagulation surface-area. Both blades are offered with 10 and 14cm blade extenders.

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Figure 2 Harmonic scalpels: (A) curve blade and (B) hook blade. (From Ethicon, Johnson & Johnson.)

Figure 3 The patient is positioned as for a traditional tonsillectomy, with a

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mouth gag of choice positioned to obtain exposure of the oropharynx. (From Operative Techniques in Otolaryngology—Head and Neck Surgery, Vol. 13, No. 2 (Jun), 2002.) 3. SURGICAL TECHNIQUE Patient positioning, anesthesia method, and placement of the mouth retractors are identical to the more conventional methods of tonsillectomy (Fig. 3). In our experience, a hook blade on a 10cm handle on power setting of 3 has proven optimal for tonsillectomy operations. The HS is held like a cold knife and the blunt edge of the hook blade is used for the entire procedure (Fig. 4). The tonsil is retracted medially using an Allis clamp (Fig. 5). Starting from the superior portion of the anterior tonsillar pillar (mucosal covering of the palatoglossus muscle), the plane of dissection is defined between the tonsillar capsule and the tonsillar bed. As in conventional tonsillectomy, the goal is to minimize the amount of mucosa resected. Due to its minimal lateral thermal dissipation, larger vessels are not as easily coagulated with the HS as with the monopolar electrocautery. For this reason it is imperative to gently move the blade medially and laterally while advancing parallel to the tonsillar capsule to avoid any bleeding. In the highly vascular areas, such as the inferiormost

Figure 4 Harmonic scalpel, here shown with hand-controlled buttons, is held like a pen and the dull part of the hook blade used for the dissection. (From Ethicon, Johnson & Johnson.)

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Figure 5 The tonsil is retracted medially, placing the tissue on tension. The harmonic scalpel is then turned to a setting of 3, on the “Full” mode, and the anterior pillar mucosa is divided, exposing the tonsillar capsule. Dissection continues in this plane, as for a traditional tonsillectomy. (From Operative Techniques in Otolaryngology—Head and Neck Surgery, Vol. 13, No. 2 (Jun), 2002.) part of the anterior and posterior tonsillar pillars, the blade should be advanced very slowly on the “Variable” setting in order to achieve better hemostasis. Should bleeding ensue, gently apply the flat part of the blade for a few seconds using the “Variable” mode (Fig. 6). A white coagulum coats the dissected area after the tonsils are removed, but char is conspicuously absent from the tonsillar fossae (Fig. 7).

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Figure 6 Modest bleeding may be controlled by holding the flat surface of the hook blade against the tissues while activating the “Variable” foot pedal. Hemostasis may require several seconds of energy delivery. (From Operative Techniques in Otolaryngology—Head and Neck Surgery, Vol. 13, No. 2 (Jun), 2002.)

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Figure 7 The appearance of the tonsillar fossae after harmonic scalpel tonsillectomy; char is conspicuously absent, while the bed is typically coated with a white coagulum. (From Operative Techniques in Otolaryngology—Head and Neck Surgery, Vol. 13, No. 2 (Jun), 2002.) Due to the steep learning curve of HS tonsillectomy, it is advisable to have suction electrocautery at the surgeon’s disposal during the first few operations, especially in pediatric cases in which the tonsillar bed is highly vascular. Surgeons should be cognizant of the fact that unlike the electrocautery, which is only effective on grounded tissue, the harmonic blade will cut any object that it comes in contact with. In a case reported by Hayakawa et al. (5), the thin tube connected to the cuff of the endotracheal tube was inadvertently severed by the blade, which resulted in a potentially hazardous leak around the tube. Additionally, all parts of the blade are ultrasonically active, so care must be taken to avoid any unintentional tissue contact.

4. ADVANTAGES A few groups have recently compared the HS to the more conventional techniques in tonsillectomy. Despite such studies, a clear advantage of the HS over the electrocautery remains controversial at this time. In a prospective study comparing patients who have

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undergone tonsillectomy by the HS vs. by the electrocautery, Walker et al. demonstrated that a higher percentage of the former group were able to ingest food 24 and 72hr postoperatively. The same study demonstrated that the postoperative use of analgesics was similar in both groups. Also, there was no statistical significance in post- and perioperative bleeding between the two groups (4). Contrary to these results, Morgenstein et al. (6) demonstrated no immediate or short-term difference in postoperative analgesia requirement and days to regular diet between the two groups. Compared to the blunt dissection method, the HS was shown to cause significantly less intraoperative and immediate postoperative pain. However, when compared over a 2week period, otalgia and pharyngeal pain were significantly higher in the HS group (7). Arguably the major advantage of the ultrasonically activated instrument is the smaller lateral thermal injury compared to the electrocautery. It has been demonstrated that the lateral thermal injury caused by the HS is 0–1000µm compared to 240µm to 15mm by the electrocautery (8). However, since no significant neurovascular bundle is present in the immediate vicinity of the dissection area, this advantage of the HS is not of great significance in tonsillectomy.

5. LIMITATIONS In terms of the speed of the operation, the electrocautery is generally the fastest instrument. However, it should be noted that there is a significantly steep learning curve for the HS (4,9). In one study comparing the HS and the electrocautery, the surgeons initially used the electrocautery to control bleeding in the HS group (4). Once surgeons become familiar with the technique and the capabilities of the HS, the operation time is comparable to that of the monopolar electrocautery. The set-up time of the two instruments is nearly identical as well. As to the precision of the instruments, it has been our experience that the finer tip of the electrocautery provides a finer incision. Unlike with the harmonic scalpel, the electrical current easily divides the tissue under tension without applying extra pressure from the blade. Also, the white coagulum produced by the HS distorts the plane of dissection. Hence, using the cutting and coagulating modes of the monopolar electrocautery allows for a much easier definition of the dissection plane. Although HS does not produce any char or smoke, this advantage is similarly not of great significance when the “coagulation” mode of the electrocautery is used judiciously. Although harmonic shears have been proven to be able to ligate vessels up to 2mm such as the thyroid arteries (1), HS is not suitable for control of brisk bleeding. In one study the surgeons used the electrocautery as a backup when hemostasis was not achieved by HS (4). As mentioned before, at least during the initial cases and cases when excessive bleeding is anticipated, such as in older children and in chronic tonsillitis, having an electrocautery system already set up is highly advised. As for the cost of this new technology, considering the advantages of the HS, as mentioned in the previous section, especially in the field of laparoscopic surgery, many General Surgery and Obstetrics/Gynecology departments have already purchased the power supply unit. For this reason, only the cost of the reusable blade is incurred by the hospital when using HS for tonsillectomy. In a study performed at a community hospital

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it was shown that HS tonsillectomy on average costs an additional $300–400 when compared to the traditional electrocautery. The cost was attributed to the cost of HS hand piece and blades since the operation time was virtually identical between the two groups.

6. CONCLUSION Preliminary data suggest that the HS provides slight, yet not negligible, benefits over the electrocautery in tonsillectomy. Although the two major advantages of the HS, namely, smaller lateral thermal injury and absence of char and smoke, are not directly beneficial in tonsillectomy, one study has shown that patients return to regular diet and activity earlier when the HS is used to perform the tonsillectomy. On the other hand, HS requires additional training and extra cost to the institution. Whether such advantages are significant enough to warrant adoption of the new technology for tonsillectomy needs to be further investigated.

REFERENCES 1. Sheman L. Thyroidectomy using the harmonic scalpel: analysis of 105 consecutive cases. Otolaryngol Head Neck Surg 2002; 127:284–288. 2. Miccoli P, Berti P, Raffaelli M, Materazzi G, Conte M, Galleri D. Impact of harmonic scalpel on operative time during video-assisted thyroidectomy. Surg Endosc 2002; 16(4): 663–666. 3. Siperstein AE, Berber E, Morkoyun E. The use of the harmonic scalpel vs. conventional knot tying for vessel ligation in thyroid surgery. Arch Surg 2002; 137(2):137–142. 4. Walker RA, Syed ZA. Harmonic scalpel tonsillectomy versus electrocautery tonsillectomy: a comparative pilot study. Otolaryngol Head Neck Surg 2001; 125(5):449–455. 5. Hayakawa M, Morimoto Y, Kemmotsu O. Tracheal tube damage by harmonic scalpel during tonsillectomy. Masui 2000; 49(11):1261–1262 (in Japanese). 6. Morgenstein SA, Jacobs HK, Brusca PA, Consiglio AR, Donzelli J, Jakubiec JA, Donat TL. A comparison of tonsillectomy with the harmonic scalpel versus electrocautery. Otolaryngol Head Neck Surg 2002; 127:333–338. 7. Akural EI, Koivunen PT, Teppo H, Alahuhta SM, Lopponen HJ. Post-tonsillectomy pain: a prospective, randomized and double-blinded study to compare an ultrasonically activated scalpel technique with the blunt dissection technique. Anaesthesia 2001; 56(11):1045–1050. 8. McCarus SD. Physiologic mechanism of the ultrasonically activated scalpel. J Am Assoc Gynecol Laparosc 1996; 3:601–608. 9. Sood S, Corbridge R, Powles J, Bates G, Newbegin CJ. Effectiveness of the ultrasonic harmonic scalpel for tonsillectomy. Ear Nose Throat J 2001; 80(8):514–516.

32 Post-operative Management of Obstructive Sleep Apnea Patients Edgar F.Fincher and David J.Terris Department of Otolaryngology-Head and Neck Surgery, Medical College of Georgia, Augusta, Georgia, U.S.A. KEY POINTS • The identification of risk factors for most post-operative complications remains elusive. • The majority of patients do not require intensive care unit monitoring following surgery. • Patients with pre-existing hypertension are at the greatest risk for needing intensive post-operative care, primarily to manage labile blood pressure. • Decisions regarding the need for intensive care unit monitoring can usually be made during the immediate post-operative period. • The use of continuous positive airway pressure (CPAP), or the performance of a tracheotomy in severely affected patients should be considered to prevent airway complications. • Judicious use of narcotics may obviate many post-operative airway complications. • The use of steroids may be beneficial in avoiding post-operative airway edema and the subsequent consequences of airway compromise. • There is insufficient evidence to condemn a surgical approach that combines nasal and oropharyngeal procedures in a single stage. • Outpatient management of patients with mild obstructive sleep apnea (OSA) (or combined with CPAP use in patients with moderate or severe OSA) has been proven safe and reliable. • Posttreatment polysomnography should be obtained between 3 and 6 months after surgery. • Tonsillectomy and adenoidectomy are effective means of treating children with OSA and avoiding the severe sequelae associated with upper airway obstruction. • Complications in the pediatric population appear to occur at a higher rate than in adults. • Studies on the use of post-operative CPAP in the pediatric population are warranted.

1. INTRODUCTION The post-operative management of patients with obstructive sleep apnea (OSA) has attracted a great deal of attention and comment over past years. Much of this discussion and debate has to do with what the appropriate treatment guidelines should be for these

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patients in the immediate post-operative period. Several authors have argued that these patients are extremely susceptible to severe post-operative morbidity and mortality and therefore should be monitored routinely in an intensive care unit (ICU) setting during the initial post-operative period. Much of the support for this philosophy stems from published experiences documenting major catastrophic complications, including deaths, in these patients following surgery. Additionally, OSA patients have a high incidence of comorbid conditions (hypertension, arrhythmias, pulmonary disease) that must be addressed in the post-operative setting, and considered in the planning for post-operative care. The objectives of this chapter are to review the published series that describe the postoperative courses of OSA patients, to analyze the types of complications that are likely to occur in OSA surgical patients, to briefly discuss the underlying physiological mechanisms that might contribute to these complications, and to attempt to identify warning signs or predictors of such events. Additionally, a set of patient-care guidelines will be offered that will help direct physicians in both their pre-operative preparation of these patients for surgery, as well as the post-operative decisions as to the appropriate level of monitoring of OSA surgical patients.

2. IDENTIFICATION OF RISK FACTORS A review of the past literature is important for understanding the current dilemma that exists in preparing for and anticipating the post-operative outcomes of the OSA patient. Multiple accounts of significant post-operative morbidity and mortality in OSA patients have been described. These findings have led some to believe that OSA patients are inherently predisposed to develop severe life-threatening complications and therefore should be monitored routinely in an ICU environment during the immediate postoperative period. Efforts have been made to identify predictors of post-operative morbidities in these patients, however no clear consensus has been reached. The inability to predict which patients will have poor outcomes has caused many caregivers to adopt more conservative approaches to their post-operative patients. Fairbanks published a list of complications experienced at 72 different centers in patients who underwent uvulopalatopharyngoplasty (UPPP) (1). In this series, 16 fatalities and eight near fatalities were reported; the majority were the result of airway compromise, one due to exsanguination, and three others of unknown causes that were attributed to myocardial infarction, arrhythmias, and pulmonary embolism. The major factor thought to contribute to the airway complications was difficult intubation, which resulted in upper airway edema. In a separate series reported by Esclamado et al. (2), 135 patients who underwent multiple types of surgery for their OSA were found to experience complications in 13% of cases, including one death from airway compromise. Again, the number one cause of post-operative complications was airway difficulty, with hemorrhage and arrhythmias being responsible for other significant complications. In that study, the airway complications were further analyzed after distinguishing them as either difficult intubations, or extubation problems. The authors concluded that patient obesity was a factor in the cases of difficult intubation that eventually led to airway compromise, although this factor was not statistically significant. In the instances where difficulty was

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encountered with extubation, oversedation with narcotics was found to be a contributing factor. Additionally, these authors reported a statistically significant relationship between the patient’s preoperative respiratory disturbance index (RDI) and the lowest oxygen desaturation (LSAT), as well as the amount of narcotics used intraoperatively and the frequency of post-operative complications. A past medical history of heart disease or pulmonary disease was not found to be a significant contributing risk factor. Haavisto and Suonpää (3) reported on yet another series of patients undergoing UPPP. They reported a 25% incidence of post-operative complications in their series of 101 OSA patients, including one death as a result of airway compromise. Their conclusions were that the patient’s weight, past history of heart disease, and the preoperative RDI and LSAT were statistically correlated to the occurrence of post-operative complications. Analysis of these findings reveals, as previously stated, that there are differing results with regard to both the incidence of complications as well as the identified risk factors. We recently reported on a series of 125 surgical encounters of patients undergoing various surgeries for the treatment of their OSA (4). In our group there were no deaths and only one respiratory event, which occurred immediately after surgery and was reversed with naloxone. The major complication in our group was hypertension during the post-operative period, with several patients requiring ICU admission to receive potent antihypertensive medications that are only given under monitored conditions. A separate study, by Riley et al. (5), also reported hypertension as the most common post-operative complication in their series. We were unable to discern any statistical correlation between the occurrence of complications and the patient’s RDI, LSAT, amount of narcotic medication, or body mass index. Two major factors that we believe contributed to our low rate of post-operative airway compromise were the practice of using a short course of perioperative steroids to reduce postoperative airway edema, and the policy of continuing patients on their CPAP during the perioperative period when appropriate. We also found that the majority of complications could be identified during the immediate postoperative period, in the recovery room. The data from our series argue against the need for routine admission to the ICU and in favor of a delayed and more appropriate decision based upon the individual patient’s early surgical outcome. The study by Riley et al. (5) resulted in similar conclusions. They reviewed 182 cases of upper airway surgery performed on patients with documented OSA. These authors routinely placed patients with severe OSA on perioperative CPAP. In this study, there were no reports of airway complications, and as previously stated, the most common complication reported was hypertension (70.5%). ICU monitoring was recommended only for patients undergoing multiple procedures or in patients undergoing single procedures who had coexistent comorbid medical conditions (hypertension, coronary artery disease). Empiric knowledge supports the use of perioperative corticosteroids in OSA surgery to reduce the amount of upper airway edema, despite the lack of solid evidence to support its usefulness. Several studies have been published on the effectiveness of corticosteroids in reducing airway and oral edema following oral surgery and intubation, however, the results have been inconsistent (6–9). We recommend a short course of corticosteroids (24mg of dexamethasone in three divided doses) for OSA patients. A randomized controlled study on the use of corticosteroids in OSA surgery patients, however, will still be necessary to confirm their effectiveness in this population.

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While the guidelines for monitoring OSA patients post-operatively remain controversial, the use of tracheotomy or nasal CPAP for patients with severe sleep apnea has become a widely accepted practice. The preoperative polysomnogram (PSG) is most useful in determining the indications for the use of these two techniques. Tracheotomy, the first therapeutic procedure described for OSA, was previously the gold standard for treatment of patients with OSA (discussed in detail in another chapter). With the advent of CPAP, however, tracheotomy is usually reserved for definitive treatment only in patients with severe sleep apnea, and is rarely used for perioperative airway protection. Several authors have demonstrated the usefulness of perioperative nasal CPAP in avoiding post-operative oxygen desaturation and complications in patients with OSA who undergo upper airway surgery (5,10,11). These authors demonstrated a significant decrease in the number of post-operative airway complications in patients who were prescribed CPAP during the early post-operative period. They concluded that CPAP is beneficial even in the most severely affected patients. In their prospective 1988 study, Powell et al. (10) demonstrated that CPAP had a protective effect in post-operative OSA patients. Although their study included a small sample size (n=10), they convincingly suggested that severely affected OSA patients could avoid the previously mandatory placement of a protective tracheotomy if they utilized CPAP in the perioperative period. Their patients all had LSATs >90% post-operatively and none suffered any severe airway compromise. Rennotte et al. (11) further demonstrated that OSA patients who were treated with perioperative CPAP could be given usual doses of sedatives, narcotics, and anesthetics without risk of post-operative airway compromise. These studies provide compelling evidence for the utilization of perioperative CPAP in preventing post-operative airway complications in patients with severe OSA. In order to be maximally effective, these patients should be maintained on their CPAP for at least 2 weeks prior to surgery, and should be continued on their preoperative level of CPAP until a follow-up PSG is performed at 3–6 months post-operatively.

3. CONSIDERATION OF COMORBID RISK FACTORS OSA has been linked to many comorbid physiologic conditions that may increase the risk of post-operative complications. Although most studies failed to show a strong correlation between preoperative medical conditions and post-operative complications in OSA patients, there are certain illnesses that should be considered in the decision regarding the level and acuity of post-operative monitoring. Patients with sleep-related breathing disorders (SRBD) have a high prevalence of hypertension, arrhythmias, and pulmonary disease. Many of these comorbid conditions are the result of the hypoxic periods that occur with SRBD and the resultant physiologic responses (sympathetic and otherwise) that subsequently occur. Hypertension is common among OSA patients, typically approaching 30% (12) [24.7% in our series (4)] and also is a frequent perioperative phenomenon in non-sleep apnea surgery. In fact, in two separate studies (4,5) hypertension was the most common complication identified. The potential need for additional pharmacologic management of hypertension during the post-operative period, including the infrequent need for potent antihypertensive medications that are only given

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under monitored conditions (nitroprusside, labetalol), should therefore be a consideration in all surgical OSA patients. The majority of the arrhythmias consist of bradycardic episodes associated with apneic/hypopneic periods and the subsequent tachycardia that follows during the recovery phase. These arrhythmias, as well as other more severe underlying arrhythmias, may be detected during the preoperative PSG, thereby affecting the decision of the level of post-operative monitoring required. Careful assessment of a patient’s comorbid conditions, either by identification during the preoperative PSG or by close monitoring in the recovery room, may provide the surgeon with indications that the patient may require prolonged cardiac monitoring or continuous infusion medications for refractory hypertension, therapies that often can only be provided in an ICU environment.

4. POST-OPERATIVE MANAGEMENT IN THE PEDIATRIC POPULATION OSA in the pediatric population represents a potentially serious affliction that has been, until recent years, poorly understood. The clinical presentation, evaluation, and management of this disorder in children differ from that of adults in many important respects. This realization has led to several studies which attempt to define a set of guidelines for the appropriate diagnosis, evaluation, management, and post-operative care of these patients. OSA syndrome in the pediatric population often presents with symptoms of daytime sleepiness, poor school performance, developmental delay, failure to thrive, cor pulmonale and occasionally sudden infant death (13,14) and as such represents a major cause of morbidity in this age group. A study published by Brouillette et al. (15) identified common adverse sequelae in children suffering from OSA in whom a delay in diagnosis had occurred. In their population of 22 patients, they found that 73% had developed symptoms commonly attributable to patients with OSA. Cor pulmonale was identified in 55%, failure to thrive in 27%, developmental delay in 23%, and permanent neurological sequelae in 9%. Other symptoms identified were hypersomnolence and behavioral disturbances. Twenty-one of these 22 patients had radiographic studies performed, all of which demonstrated evidence of upper airway narrowing (defined as tonsillar and/or adenoidal hyperplasia, micrognathia, or facial abnormalities). Furthermore, all children who were followed after tonsillectomy and/or adenoidectomy (T&A) demonstrated reversibility of their cor pulmonale, hypersomnolence, and failure to thrive. This study is significant in that it demonstrates the severe sequelae of OSA in children as well as the effectiveness of surgery for treating OSA and preventing the associated comorbidities. A 1992 retrospective study performed by McColley et al. (16) examined the complications experienced following surgical correction for OSA in a pediatric population. The purpose of this study was to identify preoperative risk factors for the development of post-operative respiratory compromise. Sixty-nine patients under 18 years of age with OSA documented by preoperative PSG were monitored in a pediatric ICU setting for 24hr after undergoing T&A for their OSA. The prevalence of respiratory

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compromise (defined as a drop in the oxygen saturation to <70% or evidence of hypercapnia, PaCO2 >45mm Hg) was found to be 23%. Preoperative parameters that were found to be predictive of post-operative respiratory compromise were age <3 years, weight <5th percentile for age, an abnormal EKG or echocardiogram, craniofacial anomalies, and the severity of the preoperative PSG findings. The prevalence of respiratory compromise in these patients (23%) was significantly higher than a quoted 0– 1.3% prevalence seen with children undergoing T&A for indications other than OSA. Based upon these data, the authors recommended that all children undergoing T&A for OSA be monitored in the hospital during the initial 24-hr post-operative period. In a separate study, Rosen et al. (17) retrospectively examined the outcomes from a population of 37 children age <16 years with documented OSA who underwent T&A for surgical correction of their upper airway obstruction. These authors also attempted to define a set of preoperative criteria that could help predict the occurrence of postoperative upper airway obstruction in this population. Ten of 37 (27%) patients experienced post-operative airway compromise, defined as oxygen desaturations <80% or causing significant respiratory compromise. The patients who experienced airway compromise were found to be younger (mean age of 1.8 vs. 5.2 years), had higher preoperative RDIs and lower LSATs, and were also found to have a higher prevalence of comorbidities: craniofacial anomalies, hypotonia, failure to thrive, morbid obesity, prior upper airway trauma, or cor pulmonale. Additionally, post-operative CPAP/BiPAP appeared to be an effective means of managing the post-operative airway compromise of many of these patients. Four patients in this population were placed on CPAP or BiPAP during the post-operative period following respiratory compromise, and subsequently demonstrated improvement in their respiratory parameters. Rosen et al. (17) proposed a list of criteria for predicting post-operative airway compromise in the pediatric population consisting of the following: (1) age <2 years; (2) midface and pharyngeal craniofacial anomalies; (3) failure to thrive; (4) hypotonia; (5) cor pulmonale; (6) upper airway trauma; (7) morbid obesity; and (8) high-risk PSG criteria (RDI >40 and LSAT<70). These authors recommended that high-risk patients be monitored with a pulse oximeter and apnea monitor in a closely observed environment during the initial post-operative period. Additionally, they suggested that CPAP/BiPAP could be an effective tool in preventing or managing post-operative respiratory compromise in the pediatric population. CPAP is an accepted means of treating adult patients with OSA. Despite its proven utility in adults, the use of CPAP in the pediatric population is a relatively new treatment modality. Several studies have addressed the use of CPAP as a potential method for the management of upper airway obstruction in the pediatric population (14,18,19). These studies examined the use of CPAP with specific emphasis on the effectiveness of therapy, patient compliance and the need for monitoring CPAP therapy in the maturing child. Marcus et al. (14) examined the use of CPAP on 94 patients aged 19 years and younger and reported an 86% success rate and 87% compliance. Success, in these cases, was judged by both a decrease in the patient’s RDI as well as an improvement in other clinical measures such as a decrease in the clinical signs of OSA and an improvement in intellectual functioning. Waters et al. (18) reviewed 175 children aged 15 years and younger who were treated with T&A for their OSA. In their population, 80 patients failed to demonstrate clear improvement in their OSA symptoms following T&A, but

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subsequently showed improvement in their sleep and clinical parameters after treatment with CPAP. Although the purpose of these studies was not to examine the effectiveness of post-operative CPAP in preventing post-operative airway compromise, they do provide solid evidence that CPAP is an effective, and well-tolerated means of treating OSA in children and adolescents. One may conclude that routine post-operative CPAP in children with severe OSA may be a useful therapy for avoiding unwanted airway complications. There remain no studies which specifically look at the routine use of CPAP/ BiPAP in the post-operative period for preventing respiratory compromise in children. The closest to this was the study by Rosen et al. (17) which reported on the use of CPAP in five of their patients during the post-operative period. These authors observed that the postoperative course in these five patients was without incident, and they subsequently proposed that CPAP may have a role in preventing post-operative airway complications in the pediatric population. A randomized trial of CPAP following surgery for OSA, vs. surgery alone would better address the indications and utility of CPAP in the postoperative pediatric patient.

5. CONCLUSIONS There continues to be an absence of any definite clinical indicators that allow surgeons to predict adverse events during the post-operative period. The decision of whether to monitor the patient in an ICU setting should be based upon the individual patient, the severity of his or her disease, the presence of any underlying cardiac or respiratory disease that would mandate closer monitoring, as well as treatment directed at minimizing symptoms of these diseases (e.g., monitoring and control of arrhythmias or labile hypertension). Additionally, the occurrence of complicating preoperative events such as traumatic intubation or the excessive use of narcotics and sedatives should alert the surgeon to have a heightened suspicion for post-operative respiratory compromise, lowering the threshold for placing the patient in a more closely monitored environment. Furthermore, the vast majority of significant adverse events are manifested during the immediate post-operative period (during the time the patient is in the recovery room) allowing for a delayed decision regarding admission to the ICU. There are several factors that should be routinely considered in the preoperative evaluation and the post-operative management of patients with OSA who undergo major upper airway surgery: (1) preoperative PSG; (2) the presence of comorbid conditions (arrhythmias and hypertension); (3) protective tracheotomy or nasal CPAP in severe sleep apneics; and (4) the use of perioperative steroids.

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REFERENCES 1. Fairbanks DNF. Uvulopalatopharyngoplasty complications and avoidance strategies. Otolaryngol Head Neck Surg 1990; 102:239–245. 2. Esclamado RM, Glenn MG, McCulloch, et al. Perioperative complications and risk factors in the surgical treatment of obstructive sleep apnea syndrome. Laryngoscope 1989; 99:1125–1129. 3. Haavisto L, Suonpää J. Complications of uvulopalatopharyngoplasty. Clin Otolaryngol 1994; 19:234–247. 4. Terris DJ, Fincher EF, Hanasono MM, et al. Conservation of resources: indications for intensive care monitoring following upper airway surgery on patient with obstructive sleep apnea. Laryngoscope 1998; 108:784–788. 5. Riley RW, Powell NB, Guilleminault C, et al. Obstructive sleep apnea surgery: risk management and complications. Otolaryngol Head Neck Surg 1997; 117:648–652. 6. Gersema L, Baker K. Use of corticosteroids in oral surgery. J Oral Maxillofac Surg 1992; 50:270–277. 7. Tellez DW, Galvis AG, Storgion SA, et al. Dexamethasone in the prevention of postextubation stridor in children. J Pediatr 1991; 118:289–294. 8. April MM, Callan ND, Nowak DM, et al. The effects of intravenous dexamethasone in pediatric adenotonsillectomy. Arch Otolaryngol Head Neck Surg 1996; 122:117–120. 9. Darmon J, Rauss A, Dreyfuss D, et al. Evaluation of risk factors for laryngeal edema after tracheal extubation in adults and its prevention by dexamethasone. Anesthesiology 1992; 77:245–251. 10. Powell NB, Riley RW, Guilleminault C, et al. Obstructive sleep apnea, continuous positive airway pressure, and surgery. Otolaryngol Head Neck Surg 1988; 99:362–369. 11. Rennotte M, Baele P, Aubert G, et al. Nasal continuous positive airway pressure in the perioperative management of patients with obstructive sleep apnea submitted to surgery. Chest 1995; 107:367–374. 12. Fletcher EC. The relationship between systemic hypertension and obstructive sleep apnea: Facts and theory. Am J Med 98. 1995; 118–128. 13. Guilleminault C, Korobkin R, Winkle R. A review of 50 children with obstructive sleep apnea syndrome. Lung 1981; 159:275–287. 14. Marcus CL, Davidson Ward SL, Mallory GB, et al. Use of nasal continuous positive airway pressure as treatment of childhood obstructive sleep apnea. J Pediatr 1995; 127: 88–94. 15. Brouillette RT, Fernbach SK, Hunt CE. Obstructive sleep apnea in infants and children. J Pediatr 1982; 100(1):31–40. 16. McColley SA, April MM, Carroll JL, et al. Respiratory compromise after adenotonsillectomy in children with obstructive sleep apnea. Arch Otolaryngol Head Neck Surg 1992; 118:940–943. 17. Rosen GM, Muckle RP, Mahowald MW, et al. Postoperative respiratory compromise in children with obstructive sleep apnea syndrome: can it be anticipated? Pediatrics 1994; 93:784– 788. 18. Waters K, Everett FM, Bruderer JW, et al. Obstructive sleep apnea: the use of nasal CPAP in 80 children. Am J Respir Crit Care Med 1995; 152:780–785. 19. Guilleminault C, Nino-Murcia G, Heldt G, et al. Alternative treatment to tracheostomy in obstructive sleep apnea syndrome: nasal continuous positive airway pressure in young children. Pediatrics 1986; 78:797–802.

33 Avoidance of Complications in Sleep Apnea Patients Samuel A.Mickelson The Atlanta Snoring & Sleep Disorders Institute, Advanced Ear, Nose & Throat Associates, Atlanta, Georgia, U.S.A. 1. INTRODUCTION Obstructive sleep apnea syndrome (OSAS) is a prevalent condition resulting from a decrease in upper airway size and patency during sleep. Safe perioperative management of patients with obstructive sleep apnea requires special attention to preoperative, intraoperative, and postoperative care. These patients are more likely to be obese, and are at greater risk of hypertension (1), cardiac arrhythmias (2), myocardial infarction (3), and stroke (4). Anatomical features in these patients may lead to potential difficulty with ventilation and intubation. Airway narrowing may also predispose to increased risk of complications related to anesthetic agents and postoperative analgesics including aspiration with intubation, intraoperative airway obstruction, postoperative airway obstruction, myocardial infarction, stroke, cardiac arrhythmia, sudden death, deep vein thrombosis (DVT), pulmonary emboli, and dehydration. There is growing evidence that sleep apnea is a risk factor for anesthetic morbidity and mortality (5–9). These risks are present when undergoing upper airway surgery as well as a general surgical procedure. The care of these patients requires vigilance before, during, and after surgery in order to minimize the risks associated with their underlying diseases. This chapter discusses these potential complications along with avoidance strategies.

2. PRE-OPERATIVE CONCERNS 2.1 Use of Continuous Positive Airway Pressure While the impact of general anesthesia on sleep is poorly understood, there is significant alteration of sleep prior to and after surgery (10,11). Many patients are sleep deprived prior to surgery due to untreated sleep apnea, as well as anxiety about the upcoming surgery. Sleep deprivation is also common postoperatively due to the pain of surgery and ongoing nursing care. Once these factors are gone, patients likely are able to enter deeper levels of sleep and are likely predisposed to more severe sleep apnea (7). It would seem beneficial therefore to have a patient use continuous positive airway pressure (CPAP)

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preoperatively for several weeks in order to prevent some of the sleep deprivation following surgery. Using CPAP prior to surgery may also reduce the risk of postobstructive pulmonary edema (12,13). CPAP is considered the gold standard in the treatment of sleep apnea because it controls the apnea immediately when used at predetermined pressures. Unfortunately, CPAP cannot be used in many patients prior to surgery because of their unwillingness or inability to use it. 2.2 Use of Narcotics and Sedative Agents Unsupervised use of narcotics or sedative agents should be avoided or minimized prior to surgery. There have been reports of deaths due to sedatives administered to sleep apnea patients in the preoperative holding area (9). While it is common practice to give an antianxiety agent or sedative hypnotic in the preoperative area to a patient undergoing surgery, this approach should be avoided in patients with sleep apnea. These agents may decrease respiratory effort and blunt the arousal response to hypoxia, hypercapnia, and airway obstruction. Benzodiazapine receptor agonists have a direct effect on upper airway muscle tone and may lead to a worsening of sleep apnea (14). Flurazepam and ethyl alcohol have been shown to result in a worsening of the apnea index in elderly patients (15) and triazolam increases the arousal threshold to airway occlusion, the duration of apnea/hypopnea events, and oxygen desaturation (16). If a sleep apnea patient has to be sedated prior to surgery, these patients should be given supplemental oxygen, or monitored with continuous pulse oximetry or cardiac monitoring. 2.3 Reflux/Aspiration Precautions Many patients with sleep disordered breathing are overweight and therefore at increased risk of gastroesophageal reflux (17,18). Morbidly obese patients have a larger volume of intra-abdominal fat, which leads to a higher intra-abdominal pressure and an increased incidence of hiatal hernia. Ninety percent of these patients will have a gastric fluid volume greater than 25cc and a gastric fluid pH under 2.5, and will be at greater risk of aspiration during induction of anesthesia (19). In order to reduce the risk of aspiration of the acidic stomach contents, obese patients undergoing surgery should receive an antacid, a proton pump inhibitor, an H2 blocker, and/or an esophageal motility stimulant prior to surgery (20). 2.4 Medical/Anesthesia/Cardiology Clearance In patients with complex comorbid conditions such as hypertension, coronary artery disease, or diabetes, a medical, cardiac, or anesthesia clearance should be considered. The selection of consultation with an internist, cardiologist, or anesthesiologist is at the discretion of the surgeon, and is typically based on the availability and expertise of the consulting physicians. The purpose of this preoperative consultation is to make the anesthesiologist and surgeon aware of the severity of the comorbid conditions, as well as optimize control of these conditions prior to surgery.

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2.5 Selection of Operating Suite The surgeon must select an operating room with personnel and equipment adequate for an elective and controlled management of the patient’s airway. It is the responsibility of the surgeon to advise the anesthesia team on the anticipated difficulty in airway control and assist the anesthesiologist when necessary since most OSAS patients will be more difficult to ventilate or intubate than a patient without sleep apnea. It is often hard to predict which OSAS patients will have serious airway problems. Patients with a large tongue, retrognathia, or micrognathia are the most challenging to ventilate and intubate. If the larynx is not visible with indirect laryngosopy with a mirror, intubation will usually be more difficult. In these patients, the anesthesiologist is notified of the potential for a difficult airway in order to have appropriate equipment and personnel available. To maintain optimal safety, the surgeon and anesthesiologist should be in the operating room at the time of induction, intubation, and extubation for all sleep apnea patients.

3. INTRA-OPERATIVE CONCERNS 3.1 Preparation for Intubation (Airway Ventilation) It is important to maintain continuous control of the airway by the patient or anesthesiologist. Prior to surgery, an antireflux agent and antisialogogue should be used to reduce the risk of reflux and excess saliva production (20). Anesthetic agents cause relaxation of the dilator airway muscles including the genioglossus and hyoglossus muscles leading to airway collapse and potential obstruction. In order to ventilate the upper airway, the anesthetized patient is typically treated with positive pressure breathing by mask, extension of the head and neck, jaw extension, and insertion of an oral airway of proper size to hold the base of the tongue out of the airway. A two-person ventilation approach may be needed, one for jaw positioning and mask seal and the other for ventilation, in the obese patient (21). A 3–5min period of ventilation is used to increase oxyhemoglobin saturation and reduce the rate of desaturation as much as possible in case of a difficult intubation. In the sleep apnea patient, however, these measures alone may not be sufficient and additional measures may be needed to ventilate the patient (22). A variety of methods are available to maintain ventilation (Table 1). The simplest approach is to insert a long nasopharyngeal airway that extends inferior to the soft palate and base of tongue. Regular nasopharyngeal tubes are often too short to extend beyond the level of airway obstruction. A laryngeal mask airway (LMA) (22,23) is also an excellent way to stabilize the airway and allow ventilation. The LMA is inserted blindly to sit just above the larynx. Due to its shear bulk and design, the LMA keeps the base of tongue and epiglottis from collapsing posteriorly. Other options include the use of an esophageal-tracheal combitube, a rigid ventilating bronchoscope, or the placement of a 14-gauge angiocath into the cricothyroid membrane along with transtracheal jet ventilation.

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Table 1 Available Methods for Difficult Ventilation Oral and nasopharyngeal airways Laryngeal mask airway Esophageal-tracheal combitube Rigid ventilating bronchoscope Intratracheal jet stylet Transtracheal jet ventilation

Table 2 Available Methods for Difficult Intubation Light wand Fiberoptic Intubation through LMA Retrograde intubation Blind nasal intubation

3.2 Intubation The sleep apnea patient can be a challenge to intubate due to the large amount of oropharyngeal and hypopharyngeal soft tissue, skeletal deficiency, and a relatively anterior larynx. If the patient can be easily ventilated after initial induction, then paralyzing agents may be used, though preferably with a short-acting agent such as succinylcholine. While muscle paralysis may facilitate intubation, there can be severe oxygen desaturation if the patient cannot be adequately ventilated. A standard oral intubation may not be feasible if the larynx cannot be visualized. Alternative methods are available for a difficult intubation (Table 2). Despite the patient discomfort, some anesthesiologists prefer an awake oral or nasal intubation since the patient continues breathing. Another simple option is the use of a light wand in a darkened room. The light wand places a light at the end of an endotracheal tube stilet. The tube is guided into the trachea with the room lights turned off. The safest intubation is likely with a planned awake transnasal fiberoptic intubation performed after adequate topical anesthesia with the patient in a sitting or semisitting position. On rare occasions, a patient requires a planned temporary or skinned lined tracheostomy. Planned tracheostomy should be considered in patients who have failed intubation at a prior surgery, severe sleep apnea with failure of nasal CPAP, or lifethreatening cardiac arrhythmias or severe oxygen desaturation (24). Tracheostomy should also be performed when significant edema is expected postop (e.g., tongue resection procedures), or with isolated upper pharyngeal surgery in a patient with persistent lower pharyngeal airway collapse. Finally, an emergency tracheostomy or cricothyrotomy may be needed when a patient cannot be adequately ventilated or intubated.

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3.3 Type of Anesthesia There are no data and no consensus as to whether it is safer to perform surgery with local anesthesia with or without sedation, regional anesthesia with or without sedation, or general anesthesia. Theoretically, surgery may be safest when performed under local anesthesia without sedation; however, when performing upper airway surgery, there may be increased risk due to bleeding into the upper airway, aspiration, or reduced control of secretions due to local anesthetic agents. General anesthesia may pose more risk with intubation and extubation but allows more control of the airway from blood and secretion. Anesthetic agents, muscle relaxants, narcotic analgesics, sedative hypnotics, sedating antihistamines, and sedating antidepressants may all reduce upper airway muscle tone and worsen obstructive sleep apnea. These agents are best administered in a titrated fashion or used on an “as-needed” basis. 3.4 Extubation Extubation is another critical time during the management of the sleep apnea patient due to airway obstruction and inability to ventilate. Most anesthesiologists prefer not to extubate while “deep” due to the risk space of loss of airway. There may also be an increased risk of postobstructive pulmonary edema with deep extubation due to negative pressure breathing against a closed glottis or collapsed airway. On the other hand, if the patient was easy to ventilate prior to intubation, there is no reason to believe that there should be any difficulty ventilating after extubation. The benefits of a deep extubation are less coughing, breath holding, and straining and therefore less bleeding into the airway following surgery. When extubating the patient “light,” the patient should have purposeful movement, recovery of neuromuscular activity, sustainable head lift for at least 5sec, and an adequate voluntary tidal volume. The endotracheal tube should be removed in the operating room, recovery room, or intensive care unit (ICU) with appropriate personnel present so as to be able to replace the tube if necessary. Airway control is performed with an oropharyngeal or nasopharyngeal airway as is done prior to intubation. There is no consensus as to the safest use of adjunctive agents at the end of the operation. Use of local anesthetic blocks at the end of surgery may be helpful to minimize the need for systemic analgesics but may also worsen apnea due to blocking of the airway mechanoreceptors that contribute to the arousal stimulus and lead to apnea termination (25). Narcotic reversal agents are helpful in reversing the sedating effects of narcotics, but should be used with caution since their effectiveness may be shorter than that of the narcotic agent. This may lead to a recurrence of sedation after the reversal agent has worn off. Short-acting anesthetic agents are preferred to those with a longer half-life. Muscle relaxants should be short acting or reversed at the end of the procedure.

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4. POST-OPERATIVE CONCERNS Several studies have shown that sleep apnea is generally unchanged one to two nights after uvulopalatopharyngoplasty (UPPP) and in some cases is worse (26,27). Following surgery, vigilance is required to reduce factors that may exacerbate the sleep apnea or cause complete airway obstruction and to monitor patients in a manner that can alert the nursing personnel or give early warning of serious airway complications. The first 24hr after surgery is probably the most critical time. However, deaths from complications have also occurred later than 24hr, potentially from the accumulated effects of sleep deprivation, analgesic agents, and rapid eye movement rebound (28,29). 4.1. Reducing Airway Edema The OSAS patient already has a small airway. Despite excision of tissues and enlargement of the airway, the edema from surgical trauma or a difficult intubation may cause airway compromise. Reducing airway edema is important for all patients undergoing sleep apnea surgery, especially those with severe apnea, multiple sites of airway compromise, and multiple airway surgeries. Tissue edema occurs after all upper airway surgeries including laser and radiofrequency procedures performed under local anesthesia (30,31). Use of systemic steroids can reduce edema in the upper airway (32). Dexamethasone (10–15mg/dose in adults) is generally the preferred corticosteroid agent due to the limited effect on sodium retention. Steroids are best administered just prior to surgery and in several doses following surgery. Elevation of the head of the bed after surgery helps reduce soft tissue edema in the airway, reduces turbinate engorgement, and improves the nasal airway. Since there are no valves in the veins of the head and neck, lying flat increases venous pressure and increases tissue edema. Soft tissue edema may also be reduced by tissue cooling either before or following surgery. Tissue precooling reduces edema in thermal wounds from lasers (32) or cautery units. Application of ice packs to the neck and sucking on ice chips are soothing to the patient and may also reduce swelling. Gentle handling of soft tissues and judicious use of lasers and electosurgery units are important aspects of proper surgical technique that can reduce tissue edema. Use of topical or systemic antibiotic prophylaxis may also reduce edema by reducing subclinical contamination or infection at the surgical site. Perioperative use of a broadspectrum systemic agent with anaerobic coverage is generally recommended with oral or nasal surgery. In addition, use of topical Chlorhexidine oral rinses reduces bacterial counts in the oral cavity. 4.2 Use of Narcotic and Sedative Agents Upper airway reconstructive surgeries are often painful and require narcotic agents for adequate pain control (33). All opiate agents including morphine, meperedine, hydromorphone, and fentanyl cause depression of respiratory drive, a decreased respiratory rate, decreased tidal volume, and CO2 retention (34). These agents cause

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respiratory suppression that increases with their dosage (35). The combination of tissue edema, lingering effects of anesthetic agents, and use of narcotics may worsen sleep apnea, oxygen desaturation, CO2 retention, serious cardiac arrhythmia, and lead to cardiac or respiratory arrest. Narcotic agents should be titrated and used on an as-needed basis. Strong narcotic agents should only be used when weaker analgesic agents are not adequate, and only with proper monitoring to allow early detection of pending airway complications. Other options includeuse of an agonist/antagonist agent such as Nalbuphine hydrochloride (10–15mg/dose IM). While respiratory depression may occur with the usual doses of Nalbuphine, the depression does not increase with larger doses. Mild to moderate pain may be relieved by oral opioid agents including codeine, hydrocodone, oxycodone, and propoxyphene. Most physicians prefer these agents since in the usual doses, there are only mild respiratory suppressing effects. Centrally acting nonopioid agents such as Tramadol hydrochloride also have less respiratory suppression than morphine. Acetominophen is adequate for mild pain and may be used in combination with opioid agents. Nonsteroidal anti-inflammatory agents (ibuprophen, naproxen, ketolorac tromethamine) may also be helpful and may reduce the need for a narcotic agent but must be used with caution due to antiplatelet actions and the potential for increased bleeding. Newer COX-2 nonsteroidal anti-inflammatory agents (Rofecoxib, Celocoxib, and Valdecoxib) have minimal or no risk of increased bleeding and when administered prior to surgery, may reduce postoperative analgesic requirements. Topical anesthetics (Benzocaine) are also helpful in controlling postoperative pain. Sedatives hypnotics are frequently administered after surgery to help insomnia. As discussed in the preoperative section, long-acting agents should be avoided due to adverse effects on apnea duration and severity. Short-acting non-benzodiazapine hypnotic agents may be safer in sleep apnea patients. Zalaplon (half-life 1hr) and Zolpidem Tartrate (half-life 2.5hr) have no significant effect on the apnea-hypopnea index compared to placebo in mild to moderate sleep apnea patients (36). While Zaloplon had no effect on the oxygen saturation, Zolpidem reduced the lowest oxygen saturation compared to placebo. 4.3 DVT Prophylaxis Many patients with sleep apnea are obese. Obesity predisposes to DVT and pulmonary emboli, especially with long surgical procedures. Methods to reduce the risk of DVT include application of sequential compression stockings, elastic stockings, and subcutaneous heparin. DVT prophylaxis is indicated for the majority of patients undergoing surgery for sleep apnea. 4.4 Blood Pressure Control Patients with OSAS are at increased risk of hypertension due to an increased sympathetic drive (37,38). To maintain blood pressure under 160/90, over half of the patients undergoing upper airway surgery will require an antihypertensive agent (S.Mickelson, unpublished observations) following surgery. Adequate blood pressure control during and following surgery is important since elevated blood pressure will increase the risk of bleeding and lead to increased tissue swelling. Blood pressure control is most important

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after osteotomies, since bleeding from bone will continue when blood pressure is elevated. 4.5 Use of CPAP Post-operatively CPAP can be safely used after most upper airway surgeries to control the sleep apnea and prevent desaturation (39). Following surgery, use of CPAP may also reduce the risk of gastroesophageal reflux (40). Patients can bring their own CPAP or bilevel positive airway pressure machine to the hospital and use it whenever asleep at the pre-established pressure. However, CPAP pressure requirements may change after surgery: they may become either higher due to edema and muscle relaxation from narcotics or lower due to enlargement of the upper airway. Therefore, even with use of CPAP, the patient’s breathing and oximetry should be monitored following surgery. CPAP is generally avoided when undergoing maxillary advancement due to the potential for subcutaneous emphysema. CPAP is also not easily used following nasal surgery until nasal swelling has subsided. A CPAP full-face mask can be used in some patients even after nasal surgery though this type of mask is usually poorly tolerated and air leaks are common. Supplemental oxygen may be considered if the patient has desaturation and CPAP cannot be used. 4.6 Maintaining a Patent Nasal Airway After Surgery Nasal obstruction may cause or worsen sleep apnea (41), while improving the nasal airway can improve sleep apnea (42). Nasal packing should be avoided in patients undergoing nasal surgery. Alternatives to nasal packing include use of quilting septal sutures, or septal splints. Nasal tubes may also maintain patency such as Doyle septal splints or nasopharyngeal airways sewn into place. Use of a decongestant nasal spray (oxymetazoline) or a systemic decongestant for several days postop is helpful in reducing turbinate swelling following nasal surgery or a nasal intubation. 4.7 Site, Type, and Length of Post-operative Monitoring Upper airway surgery in sleep apnea patients can temporarily worsen the sleep apnea and lead to serious and potentially fatal complications including acute upper airway obstruction, hypoxemia, myocardial infarction, cardiac arrhythmias, stroke, and death. Prevention of these complications requires early detection of pending airway problems. Postoperative monitoring is performed in order to detect and prevent potential complications. The decision to do outpatient surgery or to admit to a 23hr unit (extended recovery room), regular hospital room, or an ICU is made with consideration of associated medical problems, severity of apnea, sites of airway narrowing, and types of surgery being performed. Care should be taken in selecting patients for outpatient procedures. Patients with mild sleep apnea or those only undergoing nasal surgery may safely be treated as outpatients, depending on the procedure performed and associated comorbid conditions. The quality of the hospital nursing care and the skill of the anesthesiologist also have an

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impact on the level and type of postoperative monitoring. For example, some hospitals can perform continuous pulse oximetry in the extended recovery unit or regular nursing unit while others require an ICU to administer this same level of care. Continuous pulse oximetry affords the easiest and most reliable method for early detection of postoperative hypoxemia and can alert the nursing staff and physician of a potential airway or cardiovascular complication. In most cases, continuous pulse oximetry alone is adequate after sleep apnea surgery. Most patients with moderate or severe sleep apnea and those undergoing surgery at multiple sites will require continuous pulse oximetry. There is no consensus on whether cardiac monitoring affords any protection to the patient after sleep apnea surgery. Certainly, if there is a history of significant cardiac or pulmonary disease or cardiac arrhythmias, cardiac monitoring may be warranted. Monitoring in an intensive care setting has been recommended as a measure to decrease the potential risk of airway complications after sleep apnea surgeries (43,44). Following UPPP, sleep apnea may be better, the same, or even worse during the first 24– 48hr following surgery (26,27,43,45). Some physicians have recommended ICU monitoring since low oxygen saturation could lead to cardiac arrhythmias (26,27). Other authors have advocated ICU monitoring due to the high incidence of serious airway complications ranging from 13% to 25% of patients undergoing surgery (44,46). Several authors have found an association between an elevated apnea index, respiratory disturbance index, and low oxygen saturation and the rate of airway complications (44,46). Postobstructive pulmonary edema may also occur following sleep apnea surgery, requiring treatment with diuretics, intubation, and positive end expiratory pressure ventilation. It is possible that the high complication rates noted above were due to less aggressive peri-operative precautions to reduce edema and sedation. Mickelson and Hakim (47) used the precautions noted in this chapter and evaluated 347 consecutive patients undergoing surgery for OSAS. The overall complication rate was 4%: 1.4% due to airway problems and 1.4% due to bleeding. Complications did not correlate with apnea severity or type of monitoring but rather with the number of simultaneous surgeries being performed. It is important to be cautious with sleep apnea patients undergoing surgery as serious complications can occur. Complications may be reduced by avoiding potent narcotic agents and other sedatives, and taking special precautions to reduce airway edema and nasal obstruction. Those at greatest risk of perioperative complications are patients who are morbidly obese, have severe sleep apnea, or are undergoing multiple surgeries.

Table 3 Standard Pre-operative Orders for Sleep Apnea Surgery Vioxx 50mg PO 30−60min prior to surgery Pepcid 20mg PO 30−60min prior to surgery Reglan 10mg PO 30−60min prior to surgery Robinul 0.2mg IM 308722−60min prior to surgery Ancef 1g IVPB 30−60min prior to surgery

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Dexamethasone 10mg IV 30−60min prior to surgery Oxymetazoline nasal spray, three sprays for each nostril, to be given on call if patient is to undergo nasal surgery or nasal intubation No narcotic or sedative agents to be given prior to surgery

4.8 Generic Patient Care Protocols Patient care protocols for preoperative and postoperative sedation and analgesia are often utilized in operating room settings. Individual institution protocols should be examined to be sure the routine orders are appropriate for the sleep apnea patient (see Tables 3 and 4). If the generic protocol is not appropriate or does not provide

Table 4 Standard Post-operative Orders After Sleep Apnea Surgery 1.

Recovery room orders: no IV or IM narcotics 30min prior to transfer to room.

2.

Wean oxygen to room air (maintain O2 saturation above 90%).

3.

Vitals: per recovery room, then routine.

4.

Check patient breathing effort every 2 hours.

5.

Continuous pulse oximetry.

6.

Elevate head of bed 30−45°.

7.

Ice collar to neck prn.

8.

Sequential compression stockings to be on while in bed.

9.

Clear liquid diet; advance as tolerated; encourage PO intake; monitor oral intake.

10. IV D5 LR at—cc/hr. 11. Cefazolin sodium 1g IVPB q 8 hours. 12. Patient is to wear his/her own CPAP machine whenever sleeping (exception: nasal surgery) 13. For pain: 14. Chloroseptic spray to oral cavity prn, keep at bedside. 15. Mild: codeine and acetaminophen elixir 12/120mg/tsp:—tsp PO q 3–4hr prn or 16. Mild: hydrocodone and acetaminophen elixir 2.5/166mg/tsp:—tsp PO q 6hr prn 17. Moderate: oxycodone and acetaminophen tabs 5/325mg: one PO q 6hr prn 18. Severe: Nalbuphine hydrochloride 10–15mg IM or slow IV q 3–6hr prn. 19. Dexamethasone sodium phosphate 10mg IVPB at—p.m. today and—a.m. tomorrow. 20. Oxymetazoline nasal spray: three sprays to each nostril q 8hr 21. For blood pressure elevation: systolic >160 or diastolic >90, give:

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22. Apresoline 5−10mg IV, may be repeated q 15min up to four doses total or 23. Labatolol 5−10mg IV, may be repeated q 15min up to four doses total 24. Call physician for 25. Active bleeding from nose or mouth. 26. Any evidence of respiratory distress. 27. Oxygen saturation below 90% or inability to wean off supplemental oxygen. 28. Temperature above 101° (oral) 29. Systolic BP >160, diastolic BP >90, not controlled with prescribed medication

adequate levels of postoperative monitoring, individual alterations in the care should be made. 4.9 Discharge Requirements Dysphagia and odynophagia following surgery can result from the changes in anatomy, soft tissue edema, and pain from surgery and may lead to dehydration. Intravenous fluids should be administered during and following surgery in order to maintain hydration. The patient should not be discharged until swallowing is adequate and there is adequate pain control with oral analgesics.

5. CONCLUSIONS Obstructive sleep apnea increases the risk of anesthetic and perioperative complications, including life-threatening cardiorespiratory and neurologic complications. The sleep apnea patient poses a significant challenge for safe perioperative care. To reduce this risk, precautions are required before, during, and after surgery. These precautions are taken due to anticipated difficulty in airway management, presence of obesity, postoperative airway edema, and airway muscle atonia. The important concepts in perioperative care are constant control of the airway during surgery, judicious use of medications, and proper monitoring following surgery. The recommendations presented here are based on a culmination of experience supported by the peer-reviewed medical literature available.

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30. Terris DJ, Clerk AA, Norbash AM, Troell RJ. Characterization of postoperative edema following laser-assisted uvulopalatoplasty using MRI and polysomnography: implications for the outpatient treatment of obstructive sleep apnea syndrome. Laryngoscope 1996; 106:124– 128. 31. Powell NB, Riley RW, Troell RJ, Blumen MB, Guillemenault C. Radiofrequency volumetric reduction of the tongue. A porcine pilot study for the treatment of obstructive sleep apnea syndrome. Chest 1997; 111:1348–1355. 32. Sheppard LM, Werkhaven JA, Mickelson SA. The effect of steroids or tissue pre-cooling on edema and tissue thermal coagulation after CO2 laser impact. Lasers Surg Med 1992; 12:137– 146. 33. Troell RJ, Powell NB, Riley TW, et al. Comparison of postoperative pain between laser assisted uvulopalatoplasty, uvulopalatopharyngoplasty, and radiofrequency volumetric tissue reduction of the palate. Otol Head Neck Surg 2000; 122:402–409. 34. Bailey PL, Egan TD, Stanley TH. Intravenous opioid anesthetics. In: In: Miller RD, ed., ed. Anesthesia. 5th ed.. Philadelphia, PA: Churchill Livingstone, 2000:273–376. 35. American Medical Association. General Analgesics. In: AMA Drug Evaluations. 4th ed. Chicago, IL: American Medical Association, 1980:chap 6, 55–88. 36. George CFP. Perspectives on the management of insomnia in patients with chronic respiratory disorders. Sleep 2000; 23(suppl 1):S31–S35. 37. Worsnop CJ, Pierce RJ, Naughton M. Systemic hypertension and obstructive sleep apnea. Sleep 1993; 16:S148–S149. 38. Bonsignore MR, Marrone O, Insalaco G, Bonsignore G. The cardiovascular effects of obstructive sleep apnoeas: analysis of pathogenic mechanisms. Eur Respir J 1994; 7:786–805. 39. Powell NB, Riley RW, Guilleminault C, Murcia GN. Obstructive sleep apnea, continuous positive airway pressure, and surgery. Otol Head Neck Surg 1988; 99(4):362–369. 40. Kerr P, Shoenut JP, Millar J, Buckle P, Kryger MH. Nasal CPAP reduces gastroesophageal reflux in obstructive sleep apnea syndrome. Chest 1992; 101(6):1539–1544. 41. Olsen KD. The nose and its impact on snoring and obstructive sleep apnea. In: Fairbanks DNF, ed. Snoring and Obstructive Sleep Apnea. New York: Raven Press, 1987:199–226. 42. Dayall VS, Phillipson EA. Nasal surgery in the management of sleep apnea. Ann Otol Rhinol Laryngol 1985; 94:550–554. 43. Macaluso RA, Reams C, Vrabec DP, Gibson WS, Matragrano A. Uvulopalatopharyngoplasty: post-operative management and evaluation of results. Ann Otol Rhinol Laryngol 1989; 98:502– 507. 44. Esclamado RM, Gleen MG, McCulloch TM, Cummings CW. Perioperative complications and risk factors in the surgical treatment of obstructive sleep apnea syndrome. Laryngoscope 1989; 99:1125–1129. 45. Burgess LP, Derderian SS, Morin GV, Gonzolez C, Zajtchuk JT. Postoperative risk following uvulopalatopharyngoplasty for obstructive sleep apnea. Otolaryngol Head Neck Surg 1993; 106(1):81–86. 46. Haavisto L, Suonpaa J. Complications of uvulopalatopharyngoplasty. Clin Otolaryngol 1994; 9:243–247. 47. Mickelson SA, Hakim I. Is post operative intensive care monitoring necessary after uvulopalatopharyngoplasty? Otolaryngol Head Neck Surg 1998; 119(4):352–356.

34 Failure Analysis in Sleep Apnea Surgery K.Christopher McMains and David J.Terris Department of Otolaryngology—Head and Neck Surgery, Medical College of Georgia, Augusta, Georgia, U.S.A. 1. BACKGROUND Guilleminault et al. (1) coined the term “obstructive sleep apnea” (OSA) to describe patients with disrupted nocturnal breathing. In 1969, Kuhlo et al. (2) performed the first tracheotomy to bypass upper airway obstruction, which represented the first definitive surgical intervention in OSA. In 1979, Fujita et al. (3) introduced uvulopalatopharyngoplasty (UPPP) for treatment of OSA. In 1981, Sullivan et al. (4) published the first study of continuous positive airway pressure (CPAP) for nonsurgical treatment of OSA. As with tracheotomy, CPAP eliminates excessive daytime sleepiness (EDS) and cardiopulmonary sequelae of OSA (5) including normalization of blood pressure (6). Only complete compliance with CPAP was shown to be sufficient to derive treatment benefits from this therapy (7). Problematically, incomplete compliance with CPAP was prevalent (8–10). Despite increased compliance with auto-titrating CPAP, a substantial proportion of patients remained ineffectively treated (11). This led to a shift in attention toward surgical treatment for OSA. In a meta-analysis, Sher et al. (12) noted success of UPPP in 41% of all patients; however, in patients with tongue-base obstruction UPPP was successful in only 6% of the cases. This finding is further supported by Isono et al. (13) who demonstrated that collapsibility at the level of the retroglossal airway is the most significant determinant of UPPP outcome. Failure of UPPP in many patients made it clear that multiple anatomic sites contribute to obstruction (14–16). Methods for evaluating levels of obstruction were sought to improve preoperative assessment and surgical outcomes. Studies used included the Muller maneuver, cephalometric analysis, CT, and volumetric MRI. The Muller maneuver can demonstrate the level of obstruction and dimensions of obstruction, though it does not accurately predict surgical success (17). Cephalometric analysis correlates with 3-D CT analysis (18). CT provides good airway and bony resolution, though it does not delineate the upper airway soft tissue as well as MRI (19). Sagittal MRI evaluates distances from the palate and the base of the tongue to the posterior pharyngeal wall (20). MRI provides good soft tissue resolution and supine evaluation in multiple dimensions; however, patient weight, claustrophobia, pacemaker placement, and high cost limit its application. Responding to the limitations of UPPP, Riley et al. (21) introduced the Stanford Protocol, which involved inferior sagittal osteotomy of the mandible, and hyoid myotomy or suspension. Later, Riley et al. published a two-phase protocol. Phase I involved UPPP

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for palatal obstruction, and genioglossus advancement with hyoid myotomy or suspension for tongue-base obstruction. This was successful in 70–80% of patients with mild to moderate OSA as measured by polysomnogram (PSG). For patients with severe OSA, success was achieved in only 42% of the cases. Additionally, surgical treatment improved sleep architecture and increased lowest oxygen saturation levels to those achieved by CPAP. For patients who suffered from residual OSA by postoperative sleep study and who desired further treatment, phase II involved maxillary-mandibular advancement and achieved 97% success (22). Updates on clinical outcomes from the Stanford group continue to report similar outcomes for phase I (23) and phase II (24). In recent years, a growing number of procedures aimed at surgical cure for OSA have been described in the literature. Laser-assisted uvuloplasty (LAUP) was investigated and proved to be an effective treatment for snoring (25), but there are conflicting data on its efficacy in the treatment of OSA (26). Preliminary studies on tonguebase suspension sutures demonstrate a modest effect on PSG results (27) and a small improvement in functional outcomes, sleepiness, and snoring (28). Radiofrequency energy has been employed to decrease the volume of palatal tissue (29), turbinate tissue (30,31) and base of tongue (32–34), with mixed results. Bariatric surgery has also been employed to reduce the severity of OSA by decreasing the degree of obesity. This assortment of treatment modalities and methods of reporting outcomes raises two fundamental questions: What constitutes success or failure, and why do specific interventions succeed or fail by these measures?

2. MEASURING SUCCESS AND FAILURE A thorough understanding of the pathologic features of OSA is necessary to fully understand the approaches to intervention in OSA. Several tools have been used for diagnosing OSA, assessing its severity, and assessing the response to treatment. These include purely subjective patient-reported measures, subjective physician-graded measures, and physiologic monitoring. A brief review of the major modalities follows. 2.1 Epworth Sleepiness Scale Principal among the symptoms resulting from OSA is EDS. Using EDS in assessing disordered sleep incorporates subjectivity in reporting. Additionally, EDS is not limited to patients with OSA. EDS was found in 21% of patients with respiratory disturbance index (RDI) <5 vs. 35% of patients with RDI >30 (35). First described by Johns (36), the Epworth (EPW) Sleepiness Scale (EPW), is an instrument used to evaluate severity of symptoms from OSA in a semiquantitative way. The EPW is a self-administered survey of a patient’s likelihood of dozing during eight activities. For each activity, the patient rates his or her chances of falling asleep while engaged in the activity. Scores range from 0 (never dozing in a situation) to 3 (always dozing).

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2.2 Quality of Life Scales (General and Disease Specific) Early work in the field used global measures of health to assess the impact of OSA. These were originally designed to measure aggregate health characteristics and provide synoptic information regarding a patient’s own perception of health. The Medical Outcome Survey Short Form 36 (SF-36) includes eight domains to measure health and well-being (37). Briones et al. (38) showed the correlation between the EPW score and vitality, emotional health, and general health domains, while the multiple sleep latency test (MSLT) correlated with only the vitality domain. Another study using the SF-36 showed improvement in energy/vitality, mental functioning, and physical functioning domains, though another measure used in the study failed to identify these effects (39). Oxygen desaturation also negatively affects quality of life (QOL) measured by SF-36 (40). Mild to moderate sleep disordered breathing (SDB) was associated with a decreased vitality measure on the SF-36, while severe SDB was associated with a global decrease in QOL (41). All dimensions of QOL were significantly diminished on the SF-36 in OSA patients as compared to controls. Improvement in QOL was related more to the degree of perceived disability than to the RDI or arousal index (42). The Nottingham Health Survey compared OSA patients to controls and found significant differences in energy, pain, sleep, social isolation, and physical mobility. However, no difference was noted in EDS between these groups. No difference in QOL was identified among patients with different levels of severity of OSA (43). Concern about the sensitivity of nonspecific measures in capturing subtle QOL changes specific to OSA led to the development of disease-specific measures of QOL. The Calgary Sleep Apnea Quality of Life Index (SAQLI) demonstrated validity in assessment of OSA. SAQLI also demonstrated a higher magnitude of effect and responsiveness index than did the SF-36 (44). The Functional Outcomes Sleep Questionnaire (FOSQ) was designed to assess the impact of sleep-related symptoms on five daily activities. It demonstrated validity in evaluating functional disability related to sleep disturbance and response to treatment (45). The obstructive sleep apnea patient oriented severity index was designed for use in the OSA Treatment Outcome Pilot Study (OSATOPS). It separates questions into five subscales to which both importance and magnitude of effect are assigned. A symptom impact score of the importance and the magnitude is generated from the product. The OSATOPS study demonstrated lower QOL in all domains except body pain for OSA patients compared to controls (46). A revised version, the SNORE-25, excluded seven items from the index used in OSATOPS and dispensed with symptom-impact scoring, instead reporting the average-magnitude score. This instrument correlated well with the patient’s subjective response to treatment (47). 2.3 Multiple Sleep Latency Test The MSLT evaluates the degree of impairment of daytime alertness experienced by a patient with sleep disturbance (48). This test involves recording the sleep initiation time for multiple naps separated by at least 2hr during a patient’s normal waking period. This instrument can be used either to diagnose upper airway resistance syndrome (UARS) (49)

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or as an assessment of treatment effect. In the absence of UARS, the MSLT can be used to diagnose narcolepsy. Many consider it the “gold standard” for evaluating daytime somnolence and sleep latency. A moderate correlation exists between the sensation of being overcome by sleep, or “irresistible sleepiness,” and MSLT. However, patients with SDB and irresistible sleepiness were not identified as having a pathologic MSLT (50). 2.4 Muller Maneuver The Muller maneuver (MM) arose from attempts to evaluate various levels of upper airway obstruction. The examiner views the upper airway through the nasopharyngocope first at rest, then with maximal inspiratory effort against closed nose and mouth. The base of tongue, lateral pharyngeal walls, and palate are examined for collapse. The examiner rates collapsibility of each structure from 0 (minimal collapse) to 4+ (complete collapse). MM score was shown to be moderately correlated with preoperative SDB severity, and its reproducibility has been verified between examiners (51). In another study, collapse of the palate on MM was highly correlated with RDI, while lateral wall collapse was moderately correlated, and base of tongue collapse was not correlated (52). 2.5 Pclose Pclose (closing pressure) is the pressure at which the upper airway collapses. This value is a significant discriminator between normal subjects and OSA patients who have abnormal collapsibility (53). In apneics, Pclose tends toward higher values than in controls, with airway collapse occurring at the level of the palate or tongue base. Positive Pclose predicted treatment effect in OSA patients. For patients with positive Pclose, nocturnal oxygenation was normalized following UPPP in 27%, whereas oxygenation was corrected in 73% of patients with negative Pclose (13). Palatal advancement, UPPP, and tracheal traction each results in a decrease in Pclose (54,55). 2.6 Cephalometrics Cephalometric radiographs are obtained and evaluated in a standardized fashion (56). Relationships among landmarks have been assessed for predictive value in diagnosing OSA and evaluating surgical outcome. Changes in ANB and SNB angles were correlated with postoperative changes in apnea-hypopnea index (AHI) (57). Other studies correlated increased posterior airway length, increased hyoid-mandibular length, and increased posterior airway space with postoperative outcomes (58,59). Li et al. (60) report a high success rate following maxillomandibular advancement with an increase in pharyngeal length and depth of 48% and 53%, respectively. However, a study by Yao et al. (52) found that postoperative cephalometric radiographs reflect anatomic changes, but these changes did not correlate with efficacy as measured by improvements in the AHI.

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2.7 Polysomnogram The PSG was first described in 1974 by Holland et al. (61) Since that time, PSG has become the “gold standard” in diagnosis and follow-up of sleep apnea because it provides physiologic data on sleep and respiratory status. Originally, only apneas were evaluated; however, analysis has expanded to include hypopneas and respiratory effort-related arousals described previously. Diagnosis is typically made on the basis of the sum of these events per hour, or RDI. In the level I study, pulse oximetry, ECG, nasal and/or oral airflow, respiratory effort, extremity EMG, submental EMG, electro-oculogram, positionally dependent sleep changes, and EEG evidence of arousal data are recorded and interpreted (62). Responding to the pressures of medical economics, other less expensive studies have been explored that attempt to adequately diagnose OSA without incurring the costs of a level I study. Other evaluations range from fully monitored home studies to overnight oximetry, though each has limitations in the data collected. The AHI and oxygen desaturation index (ODI) detected in a nap study correlate with the severity of OSA as determined by PSG (63). Data reported from portable PSG correlated with those obtained with a laboratory-based control for AHI and diagnosis, although there was reduced confidence in respiratory scoring secondary to signal quality (64). Parra et al. (65) showed 89% concordance between AHI measured by a home device, the portable monitor of respiratory parameters, and traditional PSG. Kapur et al. (66) reported that unattended home sleep studies were acceptable for the evaluation and diagnosis of OSA in 90.6% of cases.

3. WHY SURGICAL PROCEDURES FAIL The complex interactions causing dysfunction in OSA make guaranteeing effective treatment in an individual patient difficult. The perfect treatment for OSA would eliminate sleep disturbance, reverse dangerous physiologic changes, restore restful sleep, eliminate symptoms, and be well-tolerated by patients. The principal failure of CPAP is an individual patient’s inability to tolerate this treatment. Tracheotomy bypasses airway obstruction at all levels and yields objective results comparable to CPAP, but is poorly tolerated by many patients due to inconvenience and social stigma. Paradoxically, in some cases, UPPP may decrease the maximal pressure tolerated on CPAP by creating oral air escape, thus decreasing CPAP effectiveness (67). Patient selection based on careful examination affects the likelihood of success. In early work, Sher et al. (17) showed that selecting patients with pharyngeal collapse isolated to the region of the tonsillar fossae and soft palate increased the success rate of UPPP. For patients completing phase II surgical treatment, over 90% have a successful surgical result as measured by RDI. However, after phase I surgery, many patients who do not have a successful surgical outcome as defined by PSG parameters do not elect to complete phase II surgery. This limits the generalizability of the results reported in the literature for OSA surgery (68). Answers to the questions “What prevents success in earlier stages of surgical treatment?” and “How does one maximize the likelihood of a given patient achieving cure from their disease?” may lie in the variability of OSA.

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The association of OSA and obesity cannot be disputed. Significant weight gain is associated with surgical failures, although there is no negative effect from minor weight gain and aging (69). Failure following UPPP is related to preoperative BMI and postoperative weight gain (70). Bariatric surgery has been explored in the treatment of OSA with variable results. Several authors report that bariatric surgery provides significant long-term reduction in weight and OSA severity (70–73), while other data suggest a considerable relapse rate among treated patients (74). Aggressive weight reduction programs represent an important component of comprehensive OSA treatment. Significant differences in disease presentation and characteristics of OSA are seen between male and female patients. Presenting symptoms for males included snoring and stoppage of breathing, while females reported headache on awakening (75). In another study of SDB, both genders presented with similar symptoms of snoring and EDS. This same study showed that women suffered from much milder disease than men despite having significantly smaller oropharyngeal airways. Additionally, upper airway size correlated with severity of disease for men only (76). Among women with AHI >5, a higher death rate is noted than in similarly affected men (77). The association between BMI and RDI is weaker in women than in men. In a study of obese patients, Vgontzas (78) reported OSA in 40% of men and only 3% of women. Another study of morbidly obese patients showed that 77% of these men and only 7% of these women had OSA (79). Taken together, these observations suggest important gender differences in sleep disorders. Further exploration of the nature of these differences may result in a higher percentage of surgical success. Collapse of the lateral pharyngeal wall contributes significantly to obstruction. Bettega et al. (80) wrote, “No data are available on the effects of phase I surgical techniques on dilator muscle activity, contraction efficiency, and upper airway collapsibility.” This view is disputed by Schwab et al. (56), who reported that skeletal advancement surgery increased tension on constrictors, and thereby decreased lateral wall collapse. Li et al. (24) found that maxillomandibular osteotomy (MMO) improves the tension and collapsibility of the velopharyngeal and suprahyoid musculature. In a later study, Li et al. (81) reported that MMO decreases retrodisplacement of the tongue, and more dramatically improves lateral wall stability. Thut et al. (82) showed that elongation of the airway had the greatest effect on collapsibility (82). When changing from the upright to supine position, pharyngeal length increases significantly in OSA patients as compared to controls (47). A distance of less than 21mm from the mandibular plane to the hyoid was significantly associated with UPPP failure (83). Exploration of airway lengthening procedures may exploit the insight gained through Thut’s research to the benefit of OSA patients. Other comorbidities may contribute to the challenge of effective OSA treatment. “Disproportionate anatomy” of the base of tongue, and narrow or hypoplastic mandible affect upper airway dynamics (16). This disproportion can be seen in syndromic patients and in isolation from other abnormalities. Allergy may also play a role in the pathogenesis of OSA. Allergic response not only increases airway resistance intranasally, but also results in edema of pharyngeal segments and predisposes to collapse (84). Hypoventilation syndrome can occur concomitantly with OSA and can cause continued sleep disturbance despite treatment of obstruction. Recognizing and addressing these and other comorbidities may positively affect surgical outcomes.

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4. BEST CURRENT METHODS OF EVALUATION Despite using RDI as a standard for diagnosis and treatment effectiveness, there is some suggestion that RDI may not completely describe all aspects of the disease and responses to treatment. Piccirillo (85) described the principal limitations in the use of PSG for diagnosis and evaluation of treatment response in OSA: 1. Assignment of severity based on RDI, rather than including ODI, sleep fragmentation, or patient symptoms. This criticism is supported by Kingshott et al. (86), who demonstrated that neither apneas nor hypopneas account for more than a small percentage of the variation in objective or subjective sleepiness. RDI showed poor correlation with EDS (87), neuropsychological functioning (88), or rates of MVA (77). Oxygen desaturations negatively affect QOL measured by SF-36 (40). This suggests an influence from desaturation independent of RDI. While ODI has been shown to be specific for OSA diagnosed by PSG (89), ODI coupled with CT90 (percentage of time saturation levels remain below 90%) and oximetry is both sensitive and specific for OSA (90). Sleep fragmentation results from short alpha EEG arousals during sleep, which correlate with the increased work of breathing (91). Though RDI and minimum SaO2 were improved on therapeutic CPAP, no significant difference in sleep architecture was seen between therapeutic CPAP and placebo CPAP (92). Therefore, patients “effectively” treated as assessed by RDI alone may not receive the physical benefits of restored sleep architecture. Patient perception of treatment effect may differ dramatically from the objective data provided by PSG. The distinction between PSG data and patient perception is highlighted by the fact that tracheotomy and CPAP can decrease QOL secondary to inconvenience, discomfort, and social stigma despite effective bypass or splinting of obstruction (93). This disparity has also been demonstrated for LAUP (26), UPPP (94), and dental appliances (95). EPW correlates with patient-identified sleepiness but does not correlate with MSLT (96), AHI, or minimum SaO2 (97). In contrast, another study found an association between RDI and QOL measures (98). Li et al. (93) showed correlation among RDI, minimum SaO2, and visual analog scale reporting of symptoms. The majority of patients report subjective improvement in symptoms after UPPP, although this subjective improvement does not correlate with the sleep architecture or apnea index for many patients. Resistance to postoperative sleep studies is often encountered since symptomatic improvement decreases a patient’s desire to undergo additional testing (94). In a study of mild OSA patients, no benefit was seen over placebo with CPAP treatment on SF-36 or FOSQ, suggesting that the placebo effect may obscure subjective reporting of the findings (99). Additionally, snorers without OSA suffer decrements in QOL comparable to patients with OSA as measured on the Nottingham Health Profile (100). Response bias has been shown to affect data collected through medical outcomes surveys (101). PSG data and subjective data are competing and cloud conclusions about the relationship between these measures. 2. There is a lack of correlation between AHI and the overall health status (43) or QOL (102). The conflicting data about the relationship to OSA diagnosed by PSG and various measures of health have been presented previously (pathophysiology of OSA). Data addressing the relationship between PSG results and QOL have been presented

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previously in this section. Questions about the strength of each of these relationships persist. 3. Apneas/hypopneas are not reported in a uniform way. Although efforts to standardize definitions of these occurrences have been made (48), considerable variability in definition, evaluation, and reporting continues to cloud comparisons (103). Various cutoffs are used in different studies for diagnosis, benefit, and cure. This situation further complicates interpretation of PSG data. Different methods of recording AHI yield dramatically different diagnoses and severity assignments (104). For example, thermistors have the potential to be less sensitive to hypopneas than other methods of recording (80). Sher (105) states that intraesophageal manometry is the most effective method of distinguishing apnea from hypopnea. In contrast, Skatvedt et al. (106) showed no statistical difference in any sleep quality parameter except duration of non-REM sleep with oxygen saturation below 90% between patients undergoing PSG with and without pressure monitoring. Use of different criteria for diagnosis, definitions for respiratory disturbance, and measures of success is perhaps the most significant limitation in evaluating and comparing outcomes from various interventions. 4. Frequency of apneas and hypopneas may vary from night to night. Because sleep quality may vary from night to night due to myriad physical and psychosocial influences, a one-night study may be inaccurate (107). A corollary to this observation is that monitoring may cause arousal artifact secondary to mask placement or perception of other monitoring devices. This criticism has been refuted by data that show no significant difference between first- and second-night sleep studies (108). Another study saw reclassification of disease or severity in only a few patients based on subsequent night sleep studies (109). Though data conflict on this point as well, attention to the possibility of nightly variation may guide decisions regarding repeating sleep studies or proceeding with surgical treatment in cases that fall close to diagnostic cutoffs. Steps have been taken already to incorporate some of these principles in the diagnosis and treatment of OSA. The composite clinical-severity index, described by Piccirillo et al. (46), includes EPW, BMI, presence of redundant pharyngeal tissue, RDI, and minimum O2 saturation in assignment of disease severity. A second iteration of this instrument, the SNORE-25, has been developed and the initial study reported (47). Friedman et al. (110) proposed a staging system for SDB based on palate position, tonsil size, and BMI that describes the likelihood of surgical success with a UPPP alone. Although exploration of this type of multidimensional analysis is in its infancy, this approach represents a significant step toward thorough diagnosis and assessment by considering both objective and subjective measures.

5. FUTURE STRATEGIES Future strategies for OSA treatment will incorporate studies exploring new methods of assessment and intervention. Though related, assessment and intervention are distinct fields of investigation. Much progress has been made already in the field of assessment. Clear definition and uniform reporting of respiratory disturbances will help establish more reliable, valid comparisons among different studies. To date, the relative contributions of apneas, hypopneas, and RERAs to symptomatology and downstream

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health effects have not been well defined. Research into the relative contributions by each type of respiratory disturbance may provide insight into the true impact of treatment. Despite its utility as a quantitative measure, traditional PSG reported in terms of RDI alone has limitations. Recognition of these limitations has already motivated the development of instruments that include multiple pertinent variables. Additionally, continued exploration of the neural interface between sleep and awake states may provide new frontiers in OSA treatment. Future advances in treatment will likely parallel those made in assessment. On the nonsurgical front, vigorous educational efforts on the part of the medical community aimed at raising public awareness of OSA can affect health behaviors and the social stigmata assigned to various treatment modalities. Such educational efforts have been reported to increase compliance with CPAP treatment (111). Finding new and unique approaches to preventing collapse while decreasing morbidity will likely drive additional advances in treatment. Continued work on lateral wall collapse offers one area of potential improvement. Early success has been reported in electrical stimulation of the genioglossus resulting in decreased pharyngeal critical pressure (112). Procedures designed to lengthen the airway may prove to be important components of future treatment. Work will likely continue on applications of radiofrequency energy in OSA. Other devices may also demonstrate utility in the treatment of OSA. Jokic et al. (113) reported decreasing surface tension and decreased AHI by applying a topical lubricant to upper airway tissues. Further work in these areas will likely add to the armamentarium in OSA treatment. The complexity of OSA and its variability of expression among individual patients make identification of one “best method” of assessment and intervention difficult. As new techniques for treatment continue to evolve, methods of reporting will continue to evolve to more thoroughly illuminate the complex relationships at work in OSA.

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35 The Ideal Procedure for Snoring and Obstructive Sleep Apnea Richard L.Goode Department of Otolaryngology—Head and Neck Surgery, Stanford University Medical Center, Stanford, California, U.S.A.

Currently (2005), there is no ideal surgical procedure for obstructive sleep apnea (OSA), including the upper airway resistance syndrome (UARS). Surgical treatment of snoring without evidence of obstruction is a different matter; several reasonably successful procedures are available for office treatment of snoring, providing improvement or cure for the majority of patients treated. While these procedures are not yet ideal, they are closer to that goal than the procedures available for OSA.

1. SNORING WITHOUT OSA For snoring, the ideal operation should be one-stage, performed in the office under local anesthesia without sedation, and should eliminate snoring in ≥90% of cases. Furthermore, complications should be few and minor in nature. Postoperative pain should also be minimal and well controlled with the usual oral pain medications. Pain medication should be required only for a few days. Since the procedure is not reimbursed by the usual health insurance policies, the costs should be reasonable. With an ideal operation the results should be long lasting, and any failures could be re-treated with the expectation of a similar high incidence of success. This would bring the overall success rate to ≈100%, a laudable goal. Currently, procedures that come closest to achieving this goal are (1) soft palate tightening procedures using radiofrequency (RF) energy delivered submucosally into several sites by a needle electrode (1,2) and (2) injection of a sclerosing solution into the palate to produce scarring and soft palate stiffening called injection snoreplasty (3). The resultant stiffening or shortening of the palate prevents excessive vibration of the posterior edge of the soft palate, thought to produce the snoring noise in the majority of cases. Both these procedures can be performed in the office under local anesthesia without the need for sedation. Postoperative pain is usually mild and the complications minor. The cost of palate injection is extremely low; the cost of RF treatment is higher and may require purchase of a disposable RF needle electrode, an additional expense. In addition, an RF generator is needed and this cost must be amortized, adding to the expense. Over time, the effectiveness of the RF treatment decreases and may need to be repeated (4); the same will probably be true for injection snoreplasty.

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Uvulectomy in the office using scissors, snare (5), cautery, or laser appears to be similarly effective, but results in greater pain during the postoperative period, lasting a week or more in most patients. The same is true for extended uvulectomy procedures that remove more of the free edge of the soft palate, termed uvulopalatoplasty (UPP). The uvulopalatal flap (5) is a variation that has the potential to be reversed if needed; this is rarely indicated. These procedures may have the long-term complaint of a feeling of “mucus” or dryness on the nasopharynx side of the palate border; if the free edge of the palate could be spared, it would eliminate this symptom. Laser-assisted uvulopalatoplasty (LAUP) is a multistage office procedure that requires a CO2 or equivalent laser but does not need a new hand piece for each treatment (6). Since the cost of the laser must be amortized, the expense of the procedure is necessarily higher than that of nonlaser procedures. The associated pain is greater than with RF submucosal tightening and the need for multiple procedures is a drawback. Some surgeons perform LAUP as a onestage procedure, which produces greater pain but eliminates the need for multiple office visits. Other surgical procedures designed to shorten and tighten the palate, such as the cautery-assisted palatal stiffening operation, appear to be equally effective (7). All of these procedures appear to have some effectiveness in the treatment of OSA and UARS due to obstruction at the palate level. It is unfortunate that opening an obstructed nose with standard nasal procedures is not regularly effective in improving snoring, although it will improve nasal breathing, including nocturnal breathing. There are several studies that found subjective improvement; one describes a 69% success rate (8). In patients who have nasal obstruction, whether just at night or both in the day and at night, opening the nose would be appropriate independent of any effect on snoring. Assuming a straight nasal septum, a short trial of a long-acting, topical, alpha adrenergic spray, such as oxymetolazine, at bedtime to shrink the turbinates overnight will provide information to the surgeon and the patient regarding the role of nasal obstruction in producing snoring. If there is adequate snoring improvement, an office procedure to decrease the size of the inferior turbinates can be performed. Procedures to decrease the size of the turbinates can be performed at the same time as procedures that tighten or shorten the soft palate. Submucosal RF cautery to the turbinates to open the nose can be performed at the same time that the soft palate is treated in the office. Correction of symptomatic nasal septal deflections is usually performed in an operating room, commonly in combination with turbinate reduction. No information exists on the effectiveness of this combination of nasal and palate surgery on snoring or sleep apnea vs. a soft palate procedure alone; however, it makes sense that opening an obstructed nose should make the patient feel better. This is discussed in more detail in another chapter. Unfortunately, the nature of snoring is such that it is almost impossible for us to have hopes for an ideal snoring operation. There are three reasons for this, two which we can address and attempt to solve; the third is more difficult. The first is a diagnostic issue as to the exact site of the sound produced by the snorer. It is generally assumed that the majority of snoring comes from vibration of the soft palate free edge. The data for this are not as clear as we would like. Certainly, if the loud snoring which regularly accompanies OSA and UARS is due to the palate, then it would appear logical that nocturnal airway obstruction is due to the same cause. This is usually not the case, with the base of the tongue and/or hypopharynx being a major component with or without

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palate level obstruction. The nose can produce noise at night due to narrowing and possibly the presence of thick mucus. This nasal snoring group are the patients whose snoring improves with nasal surgery. In addition, nasal obstruction leads to mouth breathing and the presence of an open mouth during sleep increases the sound intensity of the snoring. While it is possible to snore with the mouth shut, the sound levels achieved are not as great. Some snorers snore during the exhalation stage rather than while inhaling, and some snore on both inhalation and exhalation; the significance of this in regard to treatment is unclear. There appear to be snorers in whom the tongue is a component of the snoring noise and this may be the sole component after the palate has been shortened and/or tightened. Basically, our inability to identify the site or sites of the snoring noise hampers our ability to provide an appropriate operation. To operate on the palate of a snorer whose tongue is the major reason for the snoring makes no sense but is probably performed all the time. The second problem is that even if we are sure the snoring noise is coming from soft palate vibration, we do not know how much palate removal or tightening is required in a given case to totally eliminate the snoring. Since we do not want to produce velopharyngeal insufficiency, there is a limit to what can be done to surgically correct snoring from this site. This is common as evidenced by the fact that snoring is rarely completely eliminated after UPP. We need better tests to determine the site of the snoring, so that the effect of palatal stiffening or shortening can be evaluated prior to any surgery. This is similar to what we do in the nose by evaluating the effect on snoring of a topical long-acting alpha adrenergic spray to decrease the size of the inferior turbinates. If it is helpful, we consider medical or surgical treatment to correct turbinate hypertrophy. Acoustic analysis of the snoring sound has been performed by several investigators but is not used routinely in the pretreatment evaluation of snoring. Many home- and hospital-based polysomnography systems include a measurement of the intensity and duration of snoring, which is helpful but not enough. One method of home analysis (SNAP) claims to analyze the snoring sound to determine the site(s) of the snoring; however, no convincing data are provided to support this claim. It does provide objective information on snoring duration, loudness, and frequency (9). Another approach would be the temporary immobilization of the free edge of the palate and uvula, to validate the potential effectiveness of a palate procedure in eliminating snoring. The simplest test would be to temporarily attach the uvula forward onto the soft palate, using a suture, in order to evaluate the effect on snoring for one or two nights, releasing the temporary attachment after the evaluation. This technique could also be used in predicting the effect of soft palatal tightening/resection on the respiratory disturbance index in cases of OSA. In this case, the temporary attachment would be performed just before a nocturnal home polysomnogram (PSG). The third problem in achieving an ideal snoring operation is that the evaluation of the snoring result is done by the bed partner, so that no matter what the objective data are, if the sleep partner says that snoring is still objectionable, the operation is considered a failure. It is difficult to objectively evaluate “improvement” in snoring since anyone who has slept with a snorer knows it only takes two or three episodes to wake one up in the middle of the night, become angry, and move out of the bed (or make the snorer move

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out). There are few areas in surgery where the evaluation of success or failure of a procedure is done not by the patient but by an individual that the surgeon may not even know. What is the relationship between the snorer and the sleep partner? Is it hostile? Is the sleep partner an insomniac who wakes up at the slightest noise and then cannot go back to sleep? The lack of acceptance of earplugs at night by the sleep partner, which in theory should help, has been a disappointment. The same is true for other devices worn by the snorer and designed to reduce snoring. They either do not work or are too uncomfortable for the majority of patients.

2. OBSTRUCTIVE SLEEP APNEA The problem of determining site is also a major issue in the treatment of OSA and UARS. Preoperative assessment of the site(s) of obstruction is simply not good enough at this time. Physical examination, Mallampati evaluation, lateral cephalometric x-rays, and fiberoptic endoscopy with Mueller maneuver all have severe limitations as to determining the site or sites of obstruction in a given patient. The OSA patient needs to be evaluated during sleep. The best objective test, in my opinion, to determine the site of obstruction is a multilevel pressure measurement during sleep (10). This is not routinely performed for a number of reasons. Sleep laboratories have no incentive to do such testing since nasal continuous positive airway pressure corrects obstruction at all levels; site(s) determination is of interest primarily to the surgeon. Current reimbursement schemes would need to be modified to pay for such additional testing; sleep laboratories would need to receive incentive from surgeons to perform such tests or the surgeons would need to support specialized testing systems that provide such data. Esophageal pressure measurements during sleep have allowed us to diagnose UARS; a single pressure measurement in the upper esophagus reflects the negative intrathoracic pressure needed for inspiration during sleep. A similar test using multilevel pressure sensors would provide us with a measurement of obstruction at the palate and base of the tongue. Induction of artificial sleep using intravenous medications while the surgeon looks at the potential areas of obstruction with a fiberoptic endoscope has promise but is expensive and time-consuming, unless performed at the time of surgery for OSA. This is not routinely done and there are questions as to whether sleep produced by intravenous drugs is the same as normal sleep. Volume CT and MRI during artificial sleep have the same limitations, cost, and risks as fiberoptic endoscopy. The end result of eliminating excessive daytime sleepiness, etc., is determined by the patient for the most part. This may not always correlate with the results of the PSG. How do we score a case where the PSG shows marked improvement of the sleep apnea while the patient reports no improvement or may even claim he/ she is worse? What about the reverse when the patient is delighted at how they feel but the PSG shows no or minimal change? Certainly, in explaining why some patients do not feel much better despite improvement in the PSG, the answer is that we have probably simply moved the patient from OSA to UARS or there is another cause for the excessive sleepiness. The uvulopalatopharyngoplasty (UPPP) appears to be an “adequate” operation for the 25% or so of OSA cases where the obstruction is limited to the soft palate level, assuming we know who these patients are, a debatable point. I believe the major

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limitation today in surgery in the treatment of OSA is the lack of a suitable operation for tongue-base obstruction that has acceptable morbidity and cost. While maxillomandibular advancement is an excellent operation as far as success is concerned (11), it is a technically difficult operation with substantial morbidity and expense. Tracheotomy is much easier to perform, invariably successful, and of relatively low cost, but the presence of an opening in the neck is unacceptable to most OSA patients. We need a better tonguebase procedure. RF tongue reduction has promise (12) but the need for five or more procedures to achieve moderate success is unacceptable. Protocols are needed to safely allow the creation of a larger number of RF lesions at one time so that adequate tongue-base tightening and shrinkage occur. Tongue-base resection has been tried and continues to be explored; however, morbidity is high and the results, unfortunately, remain unpredictable. Distraction osteogenesis is not the answer at this time—it is too morbid and takes too much time to achieve a result (13). A combination of treatment modalities may provide an answer, for example combining RF to the tongue and genioglossus muscle advancement or Repose suture suspension (14) may provide a solution that one modality cannot. The addition of a dental device to further advance the lower jaw during sleep may improve the final result (15). We have evaluated hyoid suspension combined with UPPP in 29 patients and found it added little over UPPP alone (16). In summary, the ideal operation is not yet here for either snoring or OSA and unless we address the diagnostic issues we will find it difficult to develop an ideal operation for these conditions.

REFERENCES 1. Powell NB, Riley RW, Troell RJ, et al. Radiofrequency volumetric tissue reduction of the palate in subjects with sleep disordered breathing. Chest 1998; 113:1163–1174. 2. Coleman SC, Smith TL. Midline radiofrequency tissue reduction of the palate for bothersome snoring and sleep-disordered breathing: a clinical trial. Otolaryngol Head Neck Surg 2000; 122(3):387–394. 3. Brietzke SE, Mair EA. Injection snoreplasty: how to treat snoring without all the pain and expense. Otolaryngol Head Neck Surg 2001; 124:503–510. 4. Li KK, Nelson BP, Riley RW, et al. Radiofrequency volumetric reduction of the palate: an extended follow-up study. Otolaryngol Head Neck Surg 2001; 122(3):410−411. 5. Huntley T. The uvulopalatal flap. Oper Tech Otolaryngol Head Neck Surg 2000; 11: 30–35. 6. Walker RP, Grigg-Damberger MM, Gopalsami C, et al. Laser-assisted uvulo-palatoplasty for snoring and obstructive sleep apnea: results in 170 patients. Laryngoscope 1995; 105:938–943. 7. Mair EA, Day RH. Cautery-assisted palatal stiffening operation. Otolaryngol Head Neck Surg 2000; 122:547–556. 8. Woodhead CJ, Allen MB. Nasal surgery for snoring. Clin Otolaryngol 1994; 19:41–44. 9. Walker RP, Gatti WM, Poirer N, et al. Objective assessment of snoring before and after laserassisted uvulopalatoplasty. Laryngoscope 1996; 106:1372–1377. 10. Skatvedt, O. Localization of the site of obstruction in snorers and patients with obstructive sleep-apnea: a comparison of fiber optic nasopharyngoscopy and pressure measurements. Acta Otolaryngol 1993; 113:206–209. 11. Li KK, Powell NB, Riley RW, et al. Long-term results of maxillomandibular advancement surgery. Sleep Breath 2000; 4:137–139.

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12. Woodson BT, Riley L, Mickelson SA, et al. A multi-institutional study of radiofrequency volumetric tisse reduction for OSAS. Otolaryngol Head Neck Surg 2001; 125(4):303–311. 13. Wang X, Wang X-X, Liang C, Yi B, Lin Y, Li Z-L. Distraction osteogenesis in correction of micrognathia accompanying obstructive sleep apnea syndrome. Plast Reconstr Surg 2003; 112:1549–1557. 14. Thomas AJ, Chavoya M, Terris DJ. Preliminary findings from a prospective, randomized trial of two tongue-base surgeries for sleep-disordered breathing. Otolaryngol Head Neck Surg 2003; 129:539–546. 15. Millman RP, Rosenberg CL, Carlisle CC. The efficacy of oral appliances in the treatment of persistent sleep apnea after uvulopalatopharyngeoplasty. Chest 1998; 113:992–996. 16. Bowden MT, Kezirian EJ, Utley D, et al. Outcomes of hyoid suspension for the treatment of obstructive sleep apnea. Arch Otolaryngol Head Neck Surg 2005; 131:440–445.

Index

Acoustic reflection, 155 Actigraphy, 129 Adenotonsillectomy, 393 postoperative pain, 393 Adenoidectomy, curette, 429 Airway, 234 from anterior hyoid advancement, 348 compliance, 316 compromise, 433, 446 edema, 457 patency and decreased airway resistance, 348 upper, 389 Airway narrowing, 203 large lingual tori, 203 large soft palate, 203 large tongue, 203 large tonsils, 203 obesity, 203 sites of, 203 Alpha arousal, 409 American Academy of Sleep Medicine (AASM), 84 American Sleep Disorder Association, 217 Anesthesia, 266, 429 general, 266 local, 266 management, 233 patient-related problems, 233 procedure-related problems, 233 topical spray, 267 Angiotensin converting enzyme (ACE) inhibitors, 234 Anterior mandibular fracture, 350 Apnea, nonpathologic, 265 Apnea index (AI), 184, 255, 322 Apnea-hypopnea index (AHI), 9, 31, 54, 81, 95, 182, 191, 227, 234, 279, 342, 368, 392, 418, 434, 458, 468 moderate obstructive sleep apnea syndrome, 229 severe obstructive sleep apnea syndrome, 229 success and failure rates, 183 Arousal responses, 71 hypercapnia, 72

Index

591

increased airway resistance, 72 isocapnic hypoxia, 72 respiratory effort-related arousal (RERA), 73 Autotitrating CPAP (APAP), 192 Balance of forces in sleep apnea, 59 Bernoulli principle, 409 Bilateral vertical transpalatal trenches, 267 Bilevel positive airway pressure (BiPAP), 225, 370, 459 Bipolar coagulation, 287 Body mass index (BMI), 9, 144, 157, 191, 227, 266, 279 Buccal speech, 35 Calgary Sleep Apnea Quality of Life Index (SAQLI), 467 Candidiasis, oral, 272 Cauterization, 272 with silver nitrate, 272 Cautery-assisted palatal stiffening operation (CAPSO), 307, 480 complications, 311 cost, 312 management, 309 procedural technique, 307, 309 success rate, 312 Centers for Medicare and Medicaid Services, 225 Central sleep apnea, 217 Cephalometric analysis, 332 Cephalometric radiograph, 347 Circadian Pacemaker, 68 Closing pressure, 410 Coblation channeling, 293 soft palate reduction, 295 tongue-base reduction, 297 tonsillar reduction, 297 turbinate reduction, 293 Coblation turbinoplasty, 293 clinical applications, 292 technical aspects, 287, 288 Comorbidity, 375 incidence of, 446 obesity-related, 375 vascular, 375 Computed tomography (CT), 155, 348 Constrictor muscles, 18 inferior, 19 middle, 19 Continuous positive airway pressure (CPAP), 51, 82, 95, 143, 166, 179, 189, 225, 256, 355, 366, 373, 411, 454, 465, 482 compliance optimization, 193 delivery systems, 191

Index

592

indications, 190 initiation, 190 mechanism of action, 189 potential, 192 treatment outcomes, 194 use difficulties, 192 Contralateral tonsil, 432 Cottle test, 242 CPAP. See Continuous positive airway pressure (CPAP) Craniobase angulation, 36 Cryptic tonsil disease, 433 Curette adenoidectomy, 429 Custom tracheotomy, 382 Daytime sleepiness, 285 Decongestants, 220 Deep vein thrombosis (DVT), 453 preoperative concerns, 453 Dingman mouth gag, 319 Displacement of the soft palate, dorsal, 35 Distal palatopharyngoplasty, 320 Distraction osteogenesis, 400 Dorsal displacement of the soft palate, 35 Dysphagia, 267, 429 Dysphonia, 429 Edema, 433 contiguous mucosa, 433 submucosa, 433 tonsil tissue, 433 Elastic mandibular advancer, 214 Electro-oculography (EOG), 83 Electrocautery, 337, 378, 437 Electroencephalography (EEG), 82, 190 Electromyography (EMG), 83, 348 Electrosurgery, 428 Electrosurgical procedures, 277 Endotracheal intubation, 429 Epworth Sleepiness Scale (ESS), 69, 70, 193, 222, 278, 307, 415, 466 subjective symptoms, 307 Esophageal pressure nadir, 278 Esophageal pressure, 81 Esthetics, facial, 356 Excessive daytime sleepiness (EDS), 95, 359, 465 Expansion hyoidplasty, 348 Extubation, 455 intraoperative concerns, 455 postoperative concerns, 457

Index

593

Facial esthetics, 356 Factors contributing to this narrowing, 203 large lingual tori, 203 large soft palate, 203 large tongue, 203 large tonsils, 203 obesity, 203 Fiberoptic nasopharyngolaryngoscopy, 325 Fiberoptic nasopharyngoscopy, 331, 347 Fisher’s linear classification, 183 Floor of mouth hematoma, 343 due to bleeding from the mandibular diploe, 343 Fluoroscopy, 155 Foramen magnum, 32, 33 Fossil records, 37 Functional Outcomes Sleep Questionnaire (FOSQ), 467 Gag reflex, 266 Gag reflex control, 279 Gastroesophageal reflux, 454 Genial tubercle, 332 Genioglossus advancement, 347 EMG activity, 51 muscle, 331, 417 Harmonic scalpel (HS), 394, 437 advantages, 441 limitations, 442 surgical technique, 439 technological considerations, 437 tonsillectomy for, 394 Hematoma, floor of mouth, 343 Hemostasis, 287, 337, 351, 352, 378, 440 Herbst Sleep Apnea Appliance, 214 Home sleep test, Multichannel, 96 Hyoglossal, 354 Hyoid bone, 348 Hyoid myotomy, 331, 347 with suspension, 331 Hyoid suspension surgery, 347 Hypercapnia, 50 Hypoglossal nerve stimulation system, 419 patient selection, 424 surgical implantation, 420 therapeutic efficacy, 423 Hypoglossal nerve, 9 Hypopharyngeal airway, 348 Hypopharyngeal collapse, 331, 347

Index

594

preoperative analysis, 347 Hypopharyngeal obstruction, 331, 347 base of tongue obstruction, 347 lateral pharyngeal wall collapse, 347 Hypopharynx, 348 Hhypotonia, pathophysiologic, 342 Hypoventilation, 71 Hypoxemia, 47, 72 Hypoxia, 48 Hyoidplasty, expansion, 348 ICU care, 238 Impaired wakefulness, 70 Inferior mucosa layer (IML), 2 Injection snoreplasty, 325, 479 patient selection, 325 possible complications, 329 procedural technique, 326 subsequent management, 327 Intraoperative management, 235 field avoidance, 236 induction, 235 intubation, 235 special monitors, 236 Intrathoracic pressure, 410 Intubation, 453 endotracheal, 429 Invasive palatal procedures, 278 Klearway, 216 Klinorynchy, 31 Labiogingival sulcus, 337 Laryngeal descent, 32, 33 Larygneal mask airway (LMA), 235, 429 Laryngoscopy grade, 100, 101, 102 Laser-assisted uvulopalatoplasty (LAUP), 166, 284, 312, 466, 480 Lateral cephalometric radiograph, 331 Lateral cephalometric x-ray, 155 Lateral mucosa layer (LML), 2 Lateral pharyngeal collapse, 331, 347 Lateral thermal injury, 442 Lesion maturation, 284 Lipectomy, 380 Lowest oxygen desaturation (LSAT), 108, 447 Lowest oxygen saturation, 256, 466 Macroglossia, 402 children with, 402

Index

595

complications of, 402 Magnetic resonance imaging (MRI), 40, 155, 332, 348 of the upper airway, 332 Mallampati, 102 evaluation, 482 score, 183 Malocclusion, 429 Mandibular advancers, 206 adjustability of, 210 criteria for selection of MAs, 211 flexibility, 210 freedom of jaw movement of, 210 lab vs. office construction, 210 retention, methods of, 209 vertical opening of, 210 Mandibular osteotomy, 331 with genioglossus advancement, 331 Mandibular skeletal surgery, 331 Maxilla, 360 Maxillary-mandibular advancement, 466 Maxillomandibular advancement (MMA), 318, 355 complications of, 360 patient’s perspective, 359 procedure, 356 rationale For, 355 surgery, 318 Maxillomandibular osteotomy (MMO), 470 Mechanoreceptors, 48 Medial mucosal layer (MML), 2 Mentalis muscle, 338 Mickelson Snoring Scale, 226 Midface and Mandible, hypoplasia of, 398 Modified mortise osteotomy technique, 338, 339 Monitoring OSA patients, 448 guidelines for, 448 Morbid obesity, 233 ventilation, 233 Motor innervation, 9 Mouth gag, Dingman, 319 Mucosal ulcerations, 281 temporary, 283 Müller maneuver, 143, 166, 185, 331, 347, 468, 482 modified, 170 Multichannel home sleep test, 96 night-to-night variability, 133 sleep diagnostic machines, 112 Multiple sleep latency test (MSLT), 69, 224, 467

Index

596

Nasal airway, 1 Nasal CPAP, 448 Nasal obstruction, 241 common causes, 241 during sleep, 241 surgical treatment, 241 Nasal obstruction, evaluation of, 241 effect of medications, 241, 242 history, 241 valve collapse, 242 Nasal positive airway pressure, 347 Nasal septum, 244 deviations of, 244 Nasal surgery, 220 Nasendoscopy, video sleep (VSE), 143 Nasopharyngolaryngoscopy (NPL), 307 Nerve injury, 353, 354 Neuromuscular stimulation, 417 Neuromuscular tone, 47 Nocturnal oral airway dilator, 213 Non-rapid eye movement (NREM), 46 Nonpathologic apnea, 265 Obstructive hypopnea syndrome (OHS), 391 Obstructive sleep apnea (OSA), 6, 39, 45, 70, 95, 155, 241, 255, 315, 373, 417, 446, 465, 479 post-operative management of, 446 Obstructive sleep apnea patient oriented severity index, 467 Obstructive sleep apnea syndrome (OSAS), 81, 143, 189, 230, 307, 347, 355, 366, 391, 453 contributing causes, 355 psychomotor sequelae of, 355 Obstructive sleep disordered breathing (OSDB), 1, 429 habitual snoring, 429 sleep apnea, 429 upper airway resistance syndrome, 429 Occlusion, 360 One-piece MAs, 212 sleep apnea Goldilocks appliance, 212 Ontogenetic development, 37 Open Tracheotomy, 376 variations, 376 Oral airway, 5 tongue, 5 Oral appliance therapy, 220 informed consent for, 220 Oral appliances (OAs), 191, 203 patient examination criteria favoring oral appliances, 203 treatment protocol for, 217 Oral candidiasis, 272

Index

Oronasal respiration, 273 Oropharyngeal tongue, 36 Oropharynx, 25, 265 Osteotomy, 331, 356 mandibular o, 331 Otolaryngology, 277, 278, 428 Oxygen desaturation index (ODI), 469 Oxygen saturation nadirs, 278 Pclose (closing pressure), 468 Pain management, 311 topical aspirin oral rinses, 311 Palatal advancement, 318 contraindications for, 318 Palatal edema, 284 Palatal flutter ratio, 311 Palatal flutter snoring, 278, 325 Palatal procedures, invasive, 278 Palatal stroboscopy, 327 Palatoglossus muscle, 209 tether effect, 209 Palatopharyngoplasty, distal, 320 Partial uvular ablation, 267 Pathophysiologic hypotonia, 342 Patient-care guidelines, 446 Pearson chi-square, 183 Penetrator template, 433 Percutaneous dilatational tracheotomy (PDT), 378 Periapical dental disease, 331 Periodic limb movement disorder (PLMD), 91 Peri-operative management, 358 anesthesia induction and intubation, 358 surgical outcomes, 358 Peri-operative work-up, 375 aseptic necrosis of, 360 nasal-pharyngeal endoscopy, 376 Permanent Tracheotomy, 378 governing principles, 378 Pharyngeal airway, 11, 12 laryngopharynx, 12 nasopharynx, 12 oropharynx, 12 patency, assessment of, 203 Pharyngeal plexus, 17 Pharyngeal soft tissue, 55 Pharyngeus muscles, 21 palatopharyngeus, 21 salpingo, 21 stylo, 21

597

Index

598

Pharyngobasilar fascia, 20 Pharyngoplasty, 315 success rate, 315 technical modifications, 315 Pharyngoscopy, 155 Pharynx coronal dimensions of, 203 Phasic upper airway muscle, 48 Physical examination, 225, 391 body habitus, 391 head and neck, 391 Pickwickian syndrome, 374 PM positioner, 216 Pneumotachometer, 84 Polysomnogram (PSG), 203, 266, 375, 448, 466 Polysomnographic sleep study (PSG), 144 Polysomnography (PSG), 81, 96, 155, 392 Positional therapy, 196 Posterior airway space (PAS), 6, 157, 332 Post-operative care, 380 long-term issues, 381 in the pediatric population, 449 psychosocial issues, 380 Post-operative complications, 384 airway difficulty, 446 postobstructive pulmonary edema (POPE), 384 predictors of, 446 Post-operative dehiscense, 337 Post-operative outcomes, 446 Post-operative pain, 427 disruption of overlying mucosa, 427 spasm of exposed tonsil fossa pharyngeal musculature, 427 transected sensory fibers, 427 Post-operative respiratory distress, 393 Preanesthetic evaluation, 233 Preoperative radiograph, 335 Proximal fenestration margin, 382 Pulse oximetry, 83, 454 Quality of life (QOL), 467 Radiofrequency (RF) energy, 287, 365 Temperature-controlled, 427 Radiofrequency lesions, 284 Radiofrequency palatoplasty, 277 in-office procedure, 279 temperature controlled, 277 Radiofrequency tissue ablation, 273 Radiofrequency volumetric tissue reduction (RFVR), 287, 336, 337 Rapid eye movement (REM), 71, 83, 104, 191, 224, 423

Index

599

Recalcitrant cryptic tonsil disease, 429 in-office, 429 outpatient procedure, 429 Reconstructive surgery, 334 Rectangular geniotubercle osteotomy technique, 337 Relevant Anatomy, 376 larynx, 376 Repose tongue suspension, 350 Respiration, oronasal, 273 Respiratory distress index (RDI), 255 Respiratory disturbance index (RDI), 81, 129, 147, 157, 190, 278, 322, 358, 368, 411, 447, 460, 466, 481 patient care protocols, 460, 461 perioperative complications, 460 Respiratory effort-related arousal (RERA), 81, 191 Respiratory inductance plethysmography (RIP), 84 Respiratory physiology, 71 normal sleep, 71 Respiratory tract, upper, 25 Retrognathia, 334 Retrolingual, collapse, 352 Retropalatal, collapse, 352 RF Ablation, 288 Sagittal split technique, 357 intermaxillary fixation, 357 Sclerotherapy agent, 325 Sedatives and opioids, 235 Sensory innervation, 4 Septum, nasal, 244 Severe OSA, 374 Silencer, 214 Silent Nite appliance, 213 Sites of airway narrowing, 203 Skeletal fixation, 360 Skeletal surgery, Mandibular, 331 Sleep apnea, 233, 287, 316, 389 in children, 389 management of, 389, 392 sites and levels of obstruction in, 316 Sleep architecture, 71 Sleep disordered breathing (SDB), 25, 45, 81, 95, 167, 179, 204, 205, 223, 241, 265, 277, 287, 331, 347, 365, 424, 454, 467 abnormal respiratory patterns, 89 anatomic correlations, 37 upper airway obstructive events, 277 Sleep efficiency nadir, 278, 285 Sleep examination, 99 Sleep fragmentation, 49, 71, 409, 470, 471

Index

Sleep Heart Health Study (SHHS), 189 Sleep history, 99 Sleep hygiene instructions, 220 Sleep stages, 81 NREM Sleep, 87 REM Sleep, 88 Sleep testing, 95 rationale, 95 Sleep-related airway obstruction, 332 Sleep-related breathing disorders (SRBD), 389, 448 Sleepiness, 68 daytime, 285 objective, 69 subjective, 69 Slow-wave sleep (SWS), 72 SNA (sella, nasion, subspinale), 11 Snare uvulectomy, 411 anesthetic technique, 412 complications, 415 equipment needed, 411 preoperative examination, 412 procedure, 413 SNB (sella, nasion, supramentale) angle, 11 Snore index, 279 Snoreplasty, injection, 325, 479 Snoring, 241, 265, 307, 315 elongated soft palate, 266 obstructive sleep apnea, 203 soft palate, 307 sites and causes of, 203 uvula, 266 Snoring evaluation, 243 Snoring Scale, Mickelson, 226 Sodium tetradecyl sulfate (STS), 326 Soft palate advancement, 320 drill holes, 321 suture, 321, 322 Soft palate mobilization, 320 flap elevation, 320 hamulus, 320 tensor aponeurosis, 320 Somnofluoroscopy, 170 Somnoplasty®, 277, 427 South China chin, 144 SRBD in Children, 389 causes of, 389 diagnosis of, 391 Staging criteria, 180 body mass index (BMI), 180

600

Index

Friedman palate position (FPP), 180 SDB score, 182 tonsil size, 180 Stanford Sleepiness Scale (SSS), 69 Starling resistor, 59 Submucosal turbinoplasty, 247, 248 septoplasty, 248 Suprachiasmatic nucleus (SCN), 68 Supralaryngeal vocal cord tract (SVT), 25 anatomy, 26 changes, 30 Surgery, nasal, 220 Surgery, reconstructive, 334 Surgical intervention, 392 Swallowing dysfunction, 318 Swiftlase attachment, 268 Symphyseal mandibular area, 336 Temperature-controlled radiofrequency, 427 Temporary tracheotomy, 400 Tensor veli palatini, 17 Therapeutic trials, 243 types, 243 Therapy, positional, 196 Thermal injury, lateral, 442 Thornton adjustable positioner, 215 Thrombosis, deep vein, 453 Thyroglossal duct cyst excision, 351 Thyroid cartilage, 350 Tissue necrosis, 281 Tissue slough, 283 Tissue volume reduction, 365 basic science, 365 complications and avoidance strategies, 369 patient selection, 366 technique, 366 treatment results, 367 Tomography, 339 cross-sectional tomography, 339 Tongue, oropharyngeal, 36 Tongue base obstruction, degree of, 334 Tongue base radiofrequency, 331, 347 Tongue collapse, base of, 332 Tongue repositioners, 206 custom-made, 208 premade, 208 Tongue stabilizing device, 208 Tongue-base resection, 483 Tonsil, contralateral, 432

601

Index

Tonsil disease, cryptic, 433 Tonsil and peritonsil tissue edema, 433 Tonsil hypertrophy, 271 massive, 271 moderate, 271 Tonsil lymphoid tissue, 428 Tonsil mucosa, 428 Tonsil-related obstructive disorders, 427 in the upper airway, 427 Tonsillar fossa, 269 cysts, 270 tonsil hypertrophy, 270 tonsil liths, 270 Tonsillectomy and/or adenoidectomy (T&A), 449 Tonsillectomy, 298, 427 subtotal coblation-assisted tonsillectomy, 300 total coblation-assisted tonsillectomy, 298 Tonsils, 390, 427 by traditional snare resection, 427 dissection, 427 electrocautery, 427 hyperplasia of the, 390 laser, 427 Total sleep time (TST), 103 Tracheal cartilage, 378 Tracheal tug, 56 Tracheotomy, 355, 373, custom, 382 in recorded history, 373 indications for, 374 open, 376 permanent, 378 temporary, 400 Tracheotomy appliance, 381 fit and comfort of, 381 Transcutaneous carbon dioxide (TcCO2), 81 Transluminal pressure, 410 Transpalatal advancement, 315 Treatment, 226 guidelines, 446 objectives, 225 Treatment Outcome Pilot Study (OSATOPS), 467 Turbinates, 246 reduction procedures, 246 Underlying co-morbidities, 224 Underlying medical conditions, 223 Upper airway, 389 dynamics, 143

602

Index

603

muscle, Phasic, 48 obstruction, 72, 81 patency, 355, 417 reconstruction, 336, 349 resistance syndrome (UARS), 74, 89, 95, 144, 172, 225, 265, 277, 332, 391, 409, 467, 479 Upper airway collapse, 45 active, 46 dynamic forces, 47 passive, 46 static, 47 structural abnormalities, 51 Upper respiratory tract, 25 Uvular ablation, partial, 267 Uvular swelling, 280 postoperative, 280 Uvulectomy, 480 Uvulopalatal flap, 336 Uvulopalatopharyngoplasty (UPPP), 157, 179, 227, 255, 295, 315, 355, 368, 446, 457, 465, 482 laser-assisted, 166, 284, 312, 466, 480 method, 257 oropharyngeal obstruction, 355 postoperative care, 263 preoperative evaluation, 256 primary snoring, 227 Uvulopalatoplasty (UPP), 265, 480 laser-assisted, 265 Valve implants, 249 Velopharyngeal insufficiency (VPI), 256, 272, 322, 361, 481 Video sleep nasendoscopy (VSE), 143 indications, 144 procedure, 145 Visual analog scale (VAS), 279, 359, 434 Wakefulness, 67 impaired, 70 Waldeyer’s ring, 17, 18 superior, 18 Wound closure, 320