Laryngology [First edition.] 9789351524571, 9351524574

Table of contents :
Cover
Contributors
Foreword
Preface
Acknowledgments
Contents
SECTION 1 : Anatomy And Physiology
1 - The Evolution Of The Human Voice And Speech: Key Components In The Story Of Our Uniqueness
2 - History Of Laryngology
3 - Gross Anatomy Of The Larynx
4 - Microanatomy Of The Vocal Folds
5 - Biomechanics, Fundamentals Of Vibration, And Flow
6 - Basics Of Voice Acoustics–a Tutorial
7 - Whisper
8 - Nervous System, Proprioception, And Reflexes
9 - Genetics And Voice
SECTION 2 : Evaluation Of The Voice And Larynx
10 - Multidisciplinary Evaluation And Voice Lab
11 - The Voice History
12 - Wellness, Health And Voice
13 - The Head And Neck Evaluation Of A Vocalist
14 - Voice Sound Perception
15 - Objective Voice Assessment
16 - Measuring Voice-related Quality Of Life
17 - Visualizing The Larynx
18 - Stroboscopy And High-speed Video Examination Of The Larynx
19 - Ct Scan For Voice Disorders: Virtual Endoscopy—virtual Dissection
20 - Laryngeal Electromyography
21 - Image Storage And Retrieval: The Present And The Future
SECTION 3 : General Principles of Treatment
22- Principles Of Voice Therapy
23 - Treating The Singing Voice
24 - Medical Therapy, Medication And The Voice
25 - Complementary And Alternative Medicines And Voice
26 - Assessing Outcomes Of Voice Treatment
27 - Perioperative Management For Phonomicrosurgery
28 - Anesthesiology And Clinical Airway Management: A Brief Introduction For Laryngologists
29 - Phonomicrosurgery Setup And Instrumentation
30 - Principles Of Phonomicrosurgery
31 - Laser Physics And Principles
32 - Voice Rest
33 - Care Of The Professional Voice
SECTION 4 : Voice Disorders
34 - Etiology, Incidence, And Prevalence Of Laryngeal Disorders
35 - Dynamical Disorders Of Voice
36 - Functional Dysphonia
37 - Posture And Muscle Tension
38 - Neurologic Disorders Of The Voice
39 - Spasmodic Dysphonia
40 - Surgical Management Of Spasmodic Dysphonia
41 - Environment And Allergies
42 - Acute Laryngitis
43 - Chronic Laryngitis
43A - Autoimmune Disorders Of The Larynx: Common Conditions, Symptoms, And Treatments
44 - Laryngopharyngeal Reflux
45 - Dysphagia In Esophageal Disorders
46 - Cough
47 - Pulmonary Disorders And Voice
48 - Diagnosis And Treatment Of Pediatric Voice Disorders
49 - The Aging Voice
50 - Hormones And The Female Voice
51 - Laryngeal Trauma
SECTION 5 : Benign Lesions And Masses Of The Larynx
52 - Nomenclature Of Laryngeal Lesions
53 - Nodules And Polyps: Assessment And Treatment
54 - Laryngeal Cysts
55 - Laryngeal Granulomas
56 - Vocal Fold Scar
57 - Reinke’s Edema/polypoid Corditis
58 - Laryngoceles And Saccular Cysts
59 - Laryngeal Papilloma
60 - Benign Tumors Of The Larynx
SECTION 6 : Vocal Fold Paralysis/Paresis
61 - Principles And Timing Of Treatment—unilateral
62 - Classification Of Laryngoplasty
63 - Vocal Fold Injection
64 - Medialization Laryngoplasty (thyroplasty) And Arytenoid Rotation/adduction
65 - Reinnervation
66 - Surgery For Bilateral Vocal Fold Immobility
67 - Reinnervation For Bilateral Vocal Fold Paralysis
SECTION 7 : Airway Obstruction and Stenosis
68 - Laryngotracheal Stenosis— Definitions And Pathogenesis
60 - Tracheostomy
70 - Managing Glottic Stenosis
71 - Subglottic Stenosis
72 - Tracheal Stenosis
SECTION 8 : Premalignant and Early Laryngeal Cancers
73 - Leukoplakia
74 - Premalignant And Early Malignant Lesions Of The Larynx
75 - Classification Of Transoral Laser Microsurgery
SECTION 9 : Office Laryngeal Surgery
76 - Setup And Safety In Office Procedures
77 - Anesthesia For Office-based Laryngology
78 - Excisions Of Laryngeal Masses
79 - Office-based Laryngeal Laser Surgery
80 - Office-based Esophagology
SECTION 10 : Voice Practice and New Innovations
81 - New And Emerging Technology
82 - Developing A Voice Practice
83 - Laryngeal Transplantation
Index
A
B
C
D
E
F
G
H
I
J
K
L
M
N
O
P
Q
R
S
T
U
V
W
X
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Z

Citation preview

Series Editor: Robert T Sataloff

 

SATALOFF'S COMPREHENSIVE TEXTBOOK OF OTOLARYNGOLOGY HEAD AND NECK SURGERY MD DMA FACS

LARYNGOLOGY

Series Editor: Robert T Sataloff

 

SATALOFF'S COMPREHENSIVE TEXTBOOK OF OTOLARYNGOLOGY HEAD AND NECK SURGERY MD DMA FACS

LARYNGOLOGY Vol. 4

Volume Editor

Michael S Benninger MD Chairman, Head and Neck Institute The Cleveland Clinic Professor of Surgery Lerner College of Medicine of Case Western Reserve University Cleveland, Ohio, USA

The Health Sciences Publisher New Delhi | London | Philadelphia | Panama

 

Jaypee Brothers Medical Publishers (P) Ltd

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The views and opinions expressed in this book are solely those of the original contributor(s)/author(s) and do not necessarily represent those of editor(s) of the book. All rights reserved. No part of this publication may be reproduced, stored or transmitted in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without the prior permission in writing of the publishers. All brand names and product names used in this book are trade names, service marks, trademarks or registered trademarks of their respective owners. The publisher is not associated with any product or vendor mentioned in this book. Medical knowledge and practice change constantly. This book is designed to provide accurate, authoritative information about the subject matter in question. However, readers are advised to check the most current information available on procedures included and check information from the manufacturer of each product to be administered, to verify the recommended dose, formula, method and duration of administration, adverse effects and contraindications. It is the responsibility of the practitioner to take all appropriate safety precautions. Neither the publisher nor the author(s)/editor(s) assume any liability for any injury and/or damage to persons or property arising from or related to use of material in this book. This book is sold on the understanding that the publisher is not engaged in providing professional medical services. If such advice or services are required, the services of a competent medical professional should be sought. Every effort has been made where necessary to contact holders of copyright to obtain permission to reproduce copyright material. If any have been inadvertently overlooked, the publisher will be pleased to make the necessary arrangements at the first opportunity. Inquiries for bulk sales may be solicited at: [email protected] Sataloff’s Comprehensive Textbook of Otolaryngology: Head and Neck Surgery: Laryngology (Vol. 4) First Edition: 2016 ISBN: 978-93-5152-457-1 Printed at

Contributors Mona Abaza MD Associate Professor Department of Otolaryngology University of Colorado Aurora, Colorado, USA Katherine Verdolini Abbott PhD CCC-SLP Professor Department of Communication Science and Disorders University of Pittsburgh Pittsburgh, Pennsylvania, USA Jean Abitbol MD Ear, Nose, Throat University of Paris 7 Paris, France Patrick Abitbol MD Ear, Nose, Throat University of Paris 7 Paris, France Lee M Akst MD Assistant Professor Director, Laryngology Department of Otolaryngology— Head and Neck Surgery Johns Hopkins University Baltimore, Maryland, USA Kenneth W Altman MD PhD Professor and Vice Chair for Clinical Affairs Bobby R. Alford Department of Otolaryngology—Head and Neck Surgery Baylor College of Medicine Houston, Texas, USA Milan R Amin MD Associate Professor Department of Otolaryngology New York University School of Medicine New York, New York, USA Ronald J Baken PhD Vocal Tract Physiologist New York Eye and Ear Infirmary of Mount Sinai New York, New York, USA

Peter C Belafsky MD PhD Professor Director of Voice and Swallowing University of California Davis Health System Department of Otolaryngology Sacramento, California, USA Michael S Benninger MD Chairman, Head and Neck Institute The Cleveland Clinic Professor of Surgery Lerner College of Medicine of Case Western Reserve University Cleveland, Ohio, USA Jennifer L Bergeron MD Ear Institute of Texas San Antonio, Texas, USA Gerald S Berke MD Professor and Chair Department of Head and Neck Surgery David Geffen School of Medicine at University of California Los Angeles Los Angeles, California, USA Craig Berzofsky MD New York Eye and Ear Infirmary New York, New York, USA Simon RA Best MD Assistant Professor Department of Otolaryngology— Head and Neck Surgery Johns Hopkins School of Medicine Baltimore, Maryland, USA Steven A Bielamowicz MD Professor and Chief Department of Otolaryngology— Head and Neck Surgery The George Washington University Washington DC, USA Christopher M Bingcang MD Assistant Professor Otolaryngology—Head and Neck Surgery University of Nebraska Medical Center Omaha, Nebraska, USA

Edward Blake Physiotherapist, Physio Ed Medical London, United Kingdom Diane M Bless PhD Professor Emerita Department of Surgery Division of Otolaryngology Department of Communicative Disorders University of Wisconsin—Madison Madison, Wisconsin, USA Joel H Blumin MD FACS Professor, Otolaryngology Medical College of Wisconsin Milwaukee, Wisconsin, USA Joseph P Bradley MD Assistant Professor Department of Otolaryngology— Head and Neck Surgery Washington University in St. Louis School of Medicine St. Louis, Missouri, USA Ryan C Branski PhD Assistant Professor Department of Otolaryngology— Head and Neck Surgery New York University School of Medicine New York, New York, USA Paul C Bryson MD Assistant Professor of Surgery Head, Section of Laryngology Director, Cleveland Clinic Voice Center Head and Neck Institute The Cleveland Clinic Cleveland, Ohio, USA Brian B Burkey MD Med Professor and Vice-Chairman Head and Neck Institute The Cleveland Clinic Foundation Cleveland, Ohio, USA James A Burns MD Associate Professor Division of Laryngeal Surgery Massachusetts General Hospital Harvard Medical School Boston, Massachusetts, USA

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Linda M Carroll PhD Senior Voice Scientist Children’s Hospital of Philadelphia Philadelphia, Pennsylvania, USA Private Practice New York, New York, USA Research Scientist Montefiore Medical Center Bronx, New York, USA Albert Castro MD University of Paris Paris, France R Eugenia Chavez MD Professor Director Centro de Foniatria y Audiologia Mexico DF, Mexico Jason Chesney DO Chief Resident Department of Otolaryngology McLaren Oakland Regional Medical Center Pontiac, Michigan, USA Aliza P Cohen MA Division of Pediatric Otolaryngology— Head and Neck Surgery Cincinnati Children’s Hospital Medical Center Cincinnati, Ohio, USA Mark S Courey MD Professor University of California San Francisco Department of Otolaryngology, Head and Neck Surgery Director, Division of Laryngology University of California San Francisco San Francisco, California, USA Lise Crevier-Buchman MD PhD Professor Voice and Speech Lab Otolaryngology— Head and Neck Surgery European Georges Pompidou Hospital HEGP Phonetics and Phonology Lab University Paris 5 Descartes University Paris 3, Sorbonne-Nouvelle Paris, France

Roger L Crumley MD Professor Emeritus, Otolaryngology Senior Associate Dean for Clinical Affairs Department of Otolaryngology— Head and Neck Surgery University of California, Irvine School of Medicine— Otolaryngology Irvine, California, USA Seth H Dailey MD Associate Professor Department of Surgery University of Wisconsin School of Medicine and Public Health Madison, Wisconsin, USA Alessandro de AlarcÓn MD MPH Associate Professor Department of Otolaryngology— Head and Neck Surgery Cincinnati Children’s Hospital Medical Center Cincinnati, Ohio, USA Craig S Derkay MD Professor Department of Otolaryngology and Pediatrics Eastern Virginia Medical School Norfolk, Virginia, USA Conor Devine MD Resident Head and Neck Institute The Cleveland Clinic Cleveland, Ohio, USA

Robert L Eller MD Lt Col USAF Chief Department of Otolaryngology RAF Lakenheath Suffolk, United Kingdom Elizabeth Erickson-DiRenzo PhD CCC-SLP Assistant Professor Division of Laryngology Department of Otolaryngology— Head and Neck Surgery Stanford University School of Medicine Stanford, California, USA Daniel S Fink MD Assistant Professor Department of Otolaryngology— Head and Neck Surgery Louisiana State University Health Sciences Center New Orleans, Louisiana, USA Susanne Fleischer MD Department of Voice, Speech and Hearing Disorders University Medical Center Hamburg Hamburg, Germany Charles N Ford MD FACS Emeritus Professor Department of Surgery, Division Otolaryngology University of Wisconsin Madison, Wisconsin, USA

Gregory R Dion MD MS CPT MC USA San Antonio Military Medical Center Department of Otolaryngology— Head and Neck Surgery San Antonio, Texas, USA

Marvin P Fried MD Professor and University Chairman Department of Otorhinolaryngology— Head and Neck Surgery Albert Einstein College of Medicine Montefiore Medical Center Bronx, New York, USA

D John Doyle MD PhD Professor of Anesthesiology Department of General Anesthesiology The Cleveland Clinic Cleveland, Ohio, USA

Gerhard Friedrich MD Professor of Otolaryngology Hals-Nasen-Ohren-Universitätsklinik Phoniatrics and Speech Pathology ENT-University Hospital Graz Graz, Austria

Natalie Edmondson MD Senior Physician Department of Head and Neck Surgery University of California Los Angeles Los Angeles, California, USA

Michael P Gailey DO Pathologist Department of Pathology University of Iowa Hospitals and Clinics Iowa City, Iowa, USA

Contributors Danielle L Gainor MD Surgical Resident Department of Otolaryngology The Cleveland Clinic Foundation Cleveland, Ohio, USA

Jeanne L Hatcher MD Assistant Professor Emory Voice Center Department of Otolaryngology Emory University School of Medicine Atlanta, Georgia, USA

Harry T Hoffman MD Professor Department of Otolaryngology— Head and Neck Surgery University of Iowa Iowa City, Iowa, USA

Glendon M Gardner MD Otolaryngology— Ear, Nose and Throat Henry Ford Hospital Detroit, Michigan, USA

Thomas E Havas MD FRACS FRCSE FACS Associate Professor Otolaryngology—Head and Neck Surgery University of New South Wales Sydney, Australia

C Gaelyn Garrett MD Professor Department of Otolaryngology Vanderbilt University Nashville, Tennessee, USA

Mary J Hawkshaw BSN RN CORLN Philadelphia Ear, Nose and Throat Associates American Institute for Voice and Ear Research Philadelphia, Pennsylvania, USA

Matthew R Hoffman PhD Research Specialist Department of Surgery— Division of Otolaryngology Head and Neck Surgery University of Wisconsin School of Medicine and Public Health Madison, Wisconsin, USA

Thomas R Gildea MD MS FCCP Head, Section of Bronchology Transplant Center Pulmonary Disease The Cleveland Clinic Cleveland, Ohio, USA Amanda I Gillespie PhD Assistant Professor Department of Otolaryngology University of Pittsburgh Pittsburgh, Pennsylvania, USA Philip Goetz Resident D-Scope Systems Brooklyn, New York, USA Stacey L Halum MD FACS Otolaryngology— Head and Neck Surgery The Voice Clinic of Indiana Carmel, Indiana, USA Georg P Hammer MD General Hospital Vienna— Medical University Campus Vienna, Austria Gady Har-El MD Professor Chief of Head and Neck Surgery and Oncology Lenox Hill Hospital New York, New York, USA Michael S Harris MD Ear, Nose and Throat Indianapolis, Indiana, USA

John Heaphy MD Otolaryngology Cleveland, Ohio, USA Yolanda D Heman-Ackah MD Associate Professor Department of Otolaryngology Drexel University College of Medicine Philadelphia, Pennsylvania, USA Christian T Herbst Postdoctoral Research Fellow Voice Research Lab Department of Biophysics Faculty of Science Palacký University Olomouc Olomouc, Czech Republic Markus M Hess MD Professor Department of Voice, Speech and Hearing Disorders University Medical Center Hamburg-Eppendorf Hamburg, Germany Douglas M Hicks PhD F-CCC-S Founding Director, The Voice Center Head, Speech-Language Pathology Head and Neck Institute The Cleveland Clinic Cleveland, Ohio, USA Shigeru Hirano MD PhD Associate Professor Department of Otolaryngology Kyoto University Kyoto, Japan

Norman D Hogikyan MD FACS Professor and Associate Chairman Department of Otolaryngology— Head and Neck Surgery University of Michigan Ann Arbor, Michigan, USA Rebecca J Howell MD George Washington University Washington, DC, USA Anne F Hseu MD Head and Neck Institute The Cleveland Clinic Foundation Cleveland, Ohio, USA Amanda Hu MD FRCSC Assistant Professor Department of Otolaryngology— Head and Neck Surgery Drexel University College of Medicine Philadelphia, Pennsylvania, USA Barbara H Jacobson PhD Assistant Professor Department of Hearing and Speech Sciences Vanderbilt University Nashville, Tennessee, USA Seema Jeswani MD Ear, Nose and Throat New York, New York, USA Jack J Jiang MD PhD Professor Department of Surgery Division of Otolaryngology— Head and Neck Surgery University of Wisconsin—Madison Madison, Wisconsin, USA

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Michael M Johns III MD Director, Emory Voice Center Associate Professor Department of Otolaryngology Emory University Atlanta, Georgia, USA Nikki Johnston PhD Associate Professor Department of Otolaryngology and Communication Sciences Medical College of Wisconsin Milwaukee, Wisconsin, USA Ramya Konnai PhD CCC-SLP Speech Language Pathologist Department of Neurology Henry Ford Health System West Bloomfield, Michigan, USA Gwen S Korovin MD ENT—Otolaryngologist Lenox Hill Hospital New York, New York, USA Karen M Kost MDCM FRCS Associate Professor Otolaryngology— Head and Neck Surgery Director of the Voice and Dysphagia Laboratory McGill University Montreal, Quebec, Canada Paul Krakovitz MD FACS Associate Professor Head and Neck Institute The Cleveland Clinic Cleveland, Ohio, USA Maggie A Kuhn MD Assistant Professor Department of Otolaryngology University of California Davis Health System Sacramento, California, USA Robbi A Kupfer MD Assistant Professor Department of Otolaryngology— Head and Neck Surgery University of Michigan Ann Arbor, Michigan, USA

Jeffrey T Laitman PhD DMedSc (hon) FAAAS FAAA FALA

Distinguished Professor Professor and Director of Anatomy and Functional Morphology Professor of Otolaryngology Professor of Medical Education Director of Gross Anatomy Center for Anatomy and Functional Morphology Icahn School of Medicine at Mount Sinai New York, New York, USA Yuna Choi Larrabee MD Resident Department of Otolaryngology— Head and Neck Surgery Weill Cornell Medical College New York, New York, USA Pierre Lavertu MD Professor Department of Otolaryngology— Head and Neck Surgery University Hospitals Case Medical Center Cleveland, Ohio, USA Gregory Lenczner Federation Nationale des Medecins Radiologues Paris, France Catherine Rees Lintzenich MD Riverside Ear, Nose, and Throat Physicians Williamsburg, Virginia, USA Robert R Lorenz Associate Professor Head and Neck Institute The Cleveland Clinic Cleveland, Ohio, USA David G Lott MD Assistant Professor Department of Otolaryngology— Head and Neck Surgery Mayo Clinic Arizona Phoenix, Arizona, USA Christy L Ludlow PhD Professor Department of Communication Sciences and Disorder James Madison University Harrisonburg, Virginia, USA

Hans F Mahieu MD PhD Professor Department of Otorhinolaryngology— Head and Neck Surgery Meander Medical Centre Amersfoort, The Netherlands Steven Mandel MD Clinical Professor of Neurology Thomas Jefferson Medical College Philadelphia, Pennsylvania, USA Ramon Mañon-Espaillat MD Clinical Professor Department of Neurology Thomas Jefferson University Hospitals Philadelphia, Pennsylvania, USA Jean-Paul Maria MD PhD Professor Department of Otolaryngology— Head and Neck Surgery University Hospital of Rouen Rouen, France Lesley Mathieson MD British Voice Association London, England Ted Mau MD PhD Associate Professor Department of Otolaryngology— Head and Neck Surgery University of Texas Southwestern Medical Center Dallas, Texas, USA Albert L Merati MD Professor Chief of Laryngology Department of Otolaryngology— Head and Neck Surgery University of Washington Medical Center Seattle, Washington, USA Claudio F Milstein PhD Director, The Voice Center Head and Neck Institute The Cleveland Clinic Cleveland, Ohio, USA Stephanie Misono MD MPH Assistant Professor Department of Otolaryngology University of Minnesota Minneapolis, Minnesota, USA

Contributors Jaime Eaglin Moore MD Assistant Professor Department of Otolaryngology Virginia Commonwealth University Richmond, Virginia, USA Thomas Murry PhD Professor Department of Otolaryngology— Head and Neck Surgery Weill Cornell Medical College New York, New York, USA Robert F Orlikoff PhD Professor Chair of the Department of Communication Sciences and Disorders Director of Graduate Study in Audiology West Virginia University Morgantown, West Virginia, USA Kyra Osborne MD Associate Staff Head and Neck Institute The Cleveland Clinic Cleveland, Ohio, USA Robert H Ossoff DMD MD Maness Professor of Laryngology and Voice Department of Otolaryngology Vanderbilt University Medical Center Nashville, Tennessee, USA Rita R Patel PhD CCC-SLP Assistant Professor, Speech Sciences Indiana University Bloomington, Indiana, USA Michael J Pitman MD Director, Division of Laryngology Director, The Voice and Swallowing Institute Department of Otolaryngology— Head and Neck Surgery New York Eye and Ear Infirmary of Mount Sinai New York, New York, USA Aron Z Pollack MD Chief Resident Department of Otolaryngology— Head and Neck Surgery New York University New York, New York, USA

Greg Postma MD Director, MCG Center for Voice and Swallowing Disorders Department of Otolaryngology— Head and Neck Surgery Georgia Regents University Augusta, Georgia, USA Rod Rezaee MD Director, Head and Neck Reconstructive Surgery University Hospitals Case Medical Center Assistant Professor Department of Otolaryngology Case Western Reserve University School of Medicine Cleveland, Ohio, USA Joy S Reidenberg PhD Professor Center for Anatomy and Functional Morphology Department of Medical Education Icahn School of Medicine at Mount Sinai New York, New York, USA Lou Reinisch PhD Dean and Professor of Physics School of Arts and Sciences Farmingdale State College (SUNY) Farmingdale, New York, USA Amanda L Richards MBBS FRACS Fellow in Laryngology Department of Otolaryngology— Head and Neck Surgery Icahn School of Medicine Mount Sinai Hospital New York, New York, USA William D Riley MM Voice Trainer Private Practice New York, New York, USA Mike Roizen MD Preventive Medicine The Cleveland Clinic Cleveland, Ohio, USA Bryan N Rolfes MD Otolaryngology Resident Head and Neck Institute The Cleveland Clinic Cleveland, Ohio, USA

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Clark A Rosen MD Professor Department of Otolaryngology University of Pittsburgh Pittsburgh, PA, USA Laura H Swibel Rosenthal MD Assistant Professor Department of Otolaryngology— Head and Neck Surgery Loyola University Chicago, Stritch School of Medicine Maywood, Illinois, USA Adam D Rubin MD Director, Lakeshore Professional Voice Center Clinical Associate Professor Michigan State University Assistant Professor Oakland University William Beaumont School of Medicine Adjunct Assistant Professor University of Michigan Ann Arbor, Michigan, USA John S Rubin MD FRCS FACS Senior Lecturer (Honorary) University College London Hospitals London, England Jonathon O Russell MD Chief Resident Head and Neck Institute The Cleveland Clinic Cleveland, Ohio, USA Amy L Rutt MD Department of Otolaryngology— Head and Neck Surgery Detroit Medical Center/Michigan State University Anna Arbor, Michigan, USA Michael J Rutter MBChB FRACS Professor Department of Otolaryngology— Head and Neck Surgery University of Cincinnati College of Medicine Cincinnati, Ohio, USA Babak Sadoughi MD Assistant Professor Department of Otolaryngology— Head and Neck Surgery Icahn School of Medicine at Mount Sinai New York, New York, USA

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Johnathan B Sataloff MD Amherst College Amherst, Massachusetts, USA Robert T Sataloff MD DMA FACS Professor and Chairman Department of Otolaryngology— Head and Neck Surgery Drexel University College of Medicine Philadelphia, Pennsylvania, USA Joseph Scharpf MD FACS Director of Head and Neck Endocrine Surgery Head and Neck Institute The Cleveland Clinic Cleveland, Ohio, USA Ronald C Scherer PhD Distinguished Research Professor Department of Communication Sciences and Disorders Bowling Green State University Bowling Green, Ohio, USA Michael Seidman MD FACS Director, Otologic/Neurotologic Skull Base Surgery Department of Otolaryngology— Head and Neck Surgery Henry Ford Health System Detroit, Michigan, USA Sonali Sethi MD FCCP Respiratory Institute— Interventional Pulmonary The Cleveland Clinic Cleveland, Ohio, USA Rupali N Shah MD Assistant Professor Department of Otolaryngology Division of Voice and Swallowing Disorders University of North Carolina Chapel Hill Chapel Hill, North Carolina, USA Rahul Shrivastav PhD Professor Department of Communicative Sciences and Disorders Michigan State University East Lansing, Michigan, USA C Blake Simpson MD Department of Otolaryngology— Head and Neck Surgery School of Medicine University of Texas Health Science Center San Antonio, Texas, USA

John T Sinacori MD FACS Assistant Professor Department of Otolaryngology Head and Neck Surgery Eastern Virginia Medical School Norfolk, Virginia, USA Jessica E Southwood MD Division of Laryngology and Professional Voice Department of Otolaryngology and Communication Sciences Medical College of Wisconsin Madison, Wisconsin, USA Shaum S Sridharan MD Clinical Instructor Department of Otolaryngology University of Pittsburgh Pittsburgh, Pennsylvania, USA Michael G Stewart MD MPH Professor and Chairman Department of Otolaryngology— Head and Neck Surgery Weill Cornell Medical College New York, New York, USA Marshall Strome MD FACS Emeritus Professor and Chair Head and Neck Institute The Cleveland Clinic Cleveland, Ohio, USA Lucian Sulica MD Sean Parker Professor of Laryngology Department of Otolaryngology— Head and Neck Surgery Weill Cornell Medical College New York, New York, USA Johan Sundberg Professor Department of Speech, Music, Hearing School of Computer Science and Communication KTH and University College of Music Education Stockholm, Sweden Jan G Švec Department of Biophysics Faculty of Sciences Palacky University Olomouc, Czech Republic Adam Szymanowski MD Drexel University College of Medicine Philadelphia, Pennsylvania, USA

Melin Tan MD Assistant Professor Department of Otolaryngology— Head and Neck Surgery Albert Einstein College of Medicine Montefiore Medical Center Bronx, New York, USA Susan L Thibeault PhD CCC-SLP Associate Professor Division of Otolaryngology— Head and Neck Surgery Department of Surgery University of Wisconsin School of Medicine and Public Health University of Wisconsin Madison, Wisconsin, USA Tjoson Tjoa MD Department of Otolaryngology— Head and Neck Surgery Medical School Virginia Commonwealth University School of Medicine Richmond, Virginia, USA Scott H Troob MD Clinical Instructor Department of Otolaryngology— Head and Neck Surgery Oregon Health and Science University Portland, Oregon, USA Sunil P Verma MD Assistant Professor Department of Otolaryngology University of California, Irvine Irvine, California, USA Peak Woo MD Clinical Professor Department of Otolaryngology Icahn School of Medicine at Mt. Sinai New York, New York, USA Gayle Woodson MD Professor Emeritus Division of Otolaryngology Southern Illinois University Springfield, Illinois, USA Rachael M Wu Medical Student Graduate Entry Medical School University of Limerick Limerick, Ireland

Foreword Sataloff’s Comprehensive Textbook of Otolaryngology: Head and Neck Surgery is a component of the most extensive compilation of information in otolaryngology—head and neck surgery to date. The six volumes of the comprehensive textbook are part of a 12-volume, encyclopedic compendium that also includes a six-volume set of detailed, extensively illustrated atlases of otolaryngologic surgical techniques. The vision for the Comprehensive Textbook was realized with the invaluable, expert collaboration of eight world-class volume editors. Chapter authors include many of the most prominent otolaryngologists in the world, and coverage of each subspecialty is extensive, detailed and scholarly. Anil K Lalwani, MD edited the volume on otology/neurotology/skull base surgery. Like all six of the volumes in the Comprehensive Textbook, the otology/neurotology/skull base surgery volume is designed not only as part of the multivolume book, but also to stand alone or in combination with the atlas of otological surgery. Dr Lalwani’s volume covers anatomy and physiology of hearing and balance, temporal bone radiology, medical and surgical treatment of common and rare disorders of the ear and related structures, occupational hearing loss, aural rehabilitation, cochlear and brainstem implantation, disorders of the facial nerve, and other topics. Each chapter is not only replete with the latest scientific information, but also accessible and practical for clinicians. The rhinology/allergy and immunology volume by Marvin P Fried and Abtin Tabaee is the most elegant and inclusive book on the topic to date. Drs Fried and Tabaee start with a history of rhinology beginning in ancient times. The chapters on evolution of the nose and sinuses, embryology, sinonasal anatomy and physiology, and rhinological assessment are exceptional. The volume includes discussions of virtually all sinonasal disorders and allergy, including not only traditional medical and surgical therapy but also complementary and integrative medicine. The information is state-of-the-art. Anthony P Sclafani’s volume on facial plastic and reconstructive surgery is unique in its thoroughness and practicality. The volume covers skin anatomy and physiology, principles of wound healing, physiology of grafts and flaps, lasers in facial plastic surgery, aesthetic analysis of the face and other basic topics. There are extensive discussions on essentially all problems and procedures in facial plastic and reconstructive surgery contributed by many of the most respected experts in the field. The volume includes not only cosmetic and reconstructive surgery, but also information on diagnosis and treatment of facial trauma. The volume on laryngology edited by Dr Michael S Benninger incorporates the most current information on virtually every aspect of laryngology. The authors constitute a who’s who of world experts in voice and swallowing. After extensive and practical discussions of science and genetics, the volume reviews diagnosis and treatment (traditional and complementary) of laryngological disorders. Chapters on laser physics and use, voice therapy, laryngeal dystonia, cough, vocal aging and many other topics provide invaluable “pearls” for clinicians. The volume also includes extensive discussion of surgery for airway disorders, office-based laryngeal surgery, laryngeal transplantation and other topics. For the volume on head and neck surgery, Drs Patrick J Gullane and David P Goldstein have recruited an extra­ ordinary group of contributors who have compiled the latest information on molecular biology of head and neck cancer, principles of radiation, immunobiology, medical oncology, common and rare head and neck malignancies, endocrine neoplasms, lymphoma, deep neck space infections and other maladies. The surgical discussions are thorough and richly illustrated, and they include definitive discussions of free flap surgery, facial transplantation and other subjects. Dr Christopher J Hartnick’s vision for the volume on pediatric otolaryngology was expansive, elegantly scholarly and invaluable clinically. The volume begins with information on embryology, anatomy, genetics, syndromes and other complex topics. Dr Hartnick’s contributors include basic discussions of otolaryngologic examination in a pediatric patient, imaging, hearing screening and aural rehabilitation, and diagnosis and treatment of diseases of the ear, nose, larynx, oral cavity, neck and airway. Congenital, syndromic and acquired disorders are covered in detail, as are special, particularly vexing problems such as chronic cough in pediatric patients, breathing and obstructive sleep apnea in children, pediatric voice disorders, and many other subjects. This volume will be invaluable to any otolaryngologist who treats children.

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Laryngology

All of us who have been involved with the creation of the six-volume Sataloff’s Comprehensive Textbook of Otolaryngology: Head and Neck Surgery and its companion six-volume set of surgical atlases hope and believe that our colleagues will find this new offering to be not only the most extensive and convenient compilation of information in our field, but also the most clinically practical and up-to-date resource in otolaryngology. We are indebted to Mr Jitendar P Vij (Group Chairman) and Mr Ankit Vij (Group President) of M/s Jaypee Brothers Medical Publishers (P) Ltd., New Delhi, India, for their commitment to this project, and for their promise to keep this work available not only online but also in print. We are indebted also to the many otolaryngologists who have contributed to this work not only by editing volumes and writing chapters, but also by asking questions that inspired many of us to seek the answers found on these pages. We also thank especially the great academic otolaryngologists who trained us and inspired us to spend our nights, weekends and vacations writing chapters and books. We hope that our colleagues and their patients find this book useful. Robert T Sataloff MD DMA FACS Professor and Chairman Department of Otolaryngology—Head and Neck Surgery Senior Associate Dean for Clinical Academic Specialties Drexel University College of Medicine Philadelphia, Pennsylvania, USA

Preface One of the fastest growing specialties in otolaryngology—head and neck surgery is the field of laryngology and voice. There are multiple reasons for this. There is growing, significant basic science research that is allowing us to understand basic principles of laryngeal genetics, causes of injury and mechanisms of repair, and fundamentals of voice production and vocal fold vibration. A major innovation that has been in large part the driving force for advances in laryngology has been the development of better microscopes and rigid and flexible laryngoscopes. Dramatically improved optics and recording capabilities have taken this somewhat hidden organ into the light. This not only allows for better diagnostic capabilities and refinements of preventive, medical and surgical techniques, it has created an easy way to share pathology and treatment successes with patients and with the academic laryngeal community, thereby expanding the application of new and better techniques and technologies. The advent of microsurgical instrumentation that can be used safely through both a rigid laryngoscope under directed microscopic guidance or through flexible laryngoscopes with distal-tip cameras providing remarkable optics, affords precision that prior was a limiting factor in laryngeal surgery. There have also been advances in laser and other coagulation and ablation technologies that have further added to the capabilities of the laryngologist. These innovations have led to a dramatic shift in the location of laryngeal procedures so that many of them, such as injections, biopsies and laser surgery, are now done safely in the office setting. This is not only more convenient to the patient but a notable decrease in healthcare resources. When I was asked to edit this volume of Sataloff’s Comprehensive Textbook of Otolaryngology: Head and Neck Surgery, I was challenged to not think of this as a part of a general textbook. Rather, I was charged to bring together the most highly recognized and innovative laryngologists, scientists, speech-language pathologists, and associated healthcare professionals in the world to develop the best and most comprehensive textbook ever written in the field of laryngology. I believe strongly that we have done this. The author list is the virtual international Who’s Who of the preeminent and most innovative names in our specialty. We cover the breadth of laryngology from the basic to the futuristic, providing not only core principles that could be used for the foundation of any laryngology or voice practice but also true cutting-edge techniques and details so that can serve as a great resource even for the most senior and experienced voice specialist or laryngologist. Editing this volume was not only a source of inspiration to me, it has greatly expanded my own knowledge of laryngology and the voice and has reassured me that our calling to be dedicated to care of the “greatest human instrument” is based on a strong foundation and will continue to improve and mature in the future. I am very proud of the work herein and I would graciously like to thank the multiple authors, JP Press, and of course Robert T. Sataloff for allowing me to spearhead this remarkable undertaking. Lastly I would like to thank my colleagues at The Cleveland Clinic and of course my wife, Kathy, and our family for supporting me as I spent countless hours engrossed in the efforts to create this remarkable book. Enjoy! Michael S Benninger MD

Acknowledgments The editor would like to thank Joseph Rusko, Marco Ulloa, Carol Rogers Field, Bridget Meyer, Thomas Gibbons and the rest of the Jaypee Brothers team. Without their perseverance and hard work, this volume would not have been possible. Special thanks are offered to the authors, who have shared their expertise and experience in order to improve the care of the Laryngology patients. I would also like to thank Mr Jitendar P Vij (Group Chairman), Mr Ankit Vij (Group President), Ms Chetna Malhotra Vohra (Associate Director), Mr Umar Rashid (Development Editor) and Production team of Jaypee Brothers Medical Publishers (P) Ltd., New Delhi, India.

Contents Section 1: Anatomy and Physiology 1. The Evolution of the Human Voice and Speech: Key Components in the Story of Our Uniqueness

3

Jeffrey T Laitman, Joy S Reidenberg

2. History of Laryngology

15

Tjoson Tjoa, Sunil P Verma

3. Gross Anatomy of the Larynx

23

Gerhard Friedrich, Georg P Hammer

4. Microanatomy of the Vocal Folds

45

Shigeru Hirano

5. Biomechanics, Fundamentals of Vibration, and Flow

51

Jack J Jiang, Matthew R Hoffman

6. Basics of Voice Acoustics–A Tutorial

63

Christian T Herbst, Jan G Švec

7. Whisper

81

Ronald C Scherer, Johan Sundberg, Ramya Konnai

8. Nervous System, Proprioception, and Reflexes

89

Christy L Ludlow

9. Genetics and Voice

99

Elizabeth Erickson-DiRenzo, Susan L Thibeault

Section 2: Evaluation of the Voice and Larynx 10. Multidisciplinary Evaluation and Voice Lab

113

Douglas M Hicks

11. The Voice History

119

Jaime Eaglin Moore, Amanda Hu

12. Wellness, Health and Voice

129

Mike Roizen

13. The Head and Neck Evaluation of a Vocalist

139

Brian B Burkey, Kyra Osborne

14. Voice Sound Perception

145

Rahul Shrivastav, Katherine Verdolini Abbott

15. Objective Voice Assessment

155

Rita R Patel, Michael S Harris, Stacey L Halum

16. Measuring Voice-Related Quality of Life Michael S Benninger, Barbara H Jacobson

169

xviii

Laryngology

17. Visualizing the Larynx

181

Simon RA Best, Lee M Akst

18. Stroboscopy and High-Speed Video Examination of the Larynx  



193

Peak Woo

19. CT Scan for Voice Disorders: Virtual Endoscopy—Virtual Dissection

235

Jean Abitbol, Albert Castro, Gregory Lenczner, Patrick Abitbol

20. Laryngeal Electromyography

263

Robert T Sataloff, Steven Mandel, Ramon Mañon~Espaillat, Yolanda D Heman-Ackah, Mona Abaza

21. Image Storage and Retrieval: The Present and the Future

287

Philip Goetz, Michael S Benninger

Section 3: General Principles of Treatment 22. Principles of Voice Therapy

311

Thomas Murry, Lise Crevier-Buchman

23. Treating the Singing Voice

319

William D Riley, Linda M Carroll

24. Medical Therapy, Medication and the Voice

335

Karen M Kost

25. Complementary and Alternative Medicines and Voice

349

Michael Seidman

26. Assessing Outcomes of Voice Treatment

363

Yuna Choi Larrabee, Michael G Stewart

27. Perioperative Management for Phonomicrosurgery

375

Stephanie Misono, Albert L Merati

28. Anesthesiology and Clinical Airway Management: A Brief Introduction for Laryngologists

385

D John Doyle

29. Phonomicrosurgery Setup and Instrumentation

403

Paul C Bryson, Danielle L Gainor

30. Principles of Phonomicrosurgery

415

Daniel S Fink, Mark S Courey

31. Laser Physics and Principles

429

Robert H Ossoff, Lou Reinisch

32. Voice Rest

435

Gwen S Korovin, Linda M Carroll

33. Care of the Professional Voice

443

Robert T Sataloff, Johnathan B Sataloff, Mary J Hawkshaw

Section 4: Voice Disorders 34. Etiology, Incidence, and Prevalence of Laryngeal Disorders Laura H Swibel Rosenthal

459

Contents 35. Dynamical Disorders of Voice

xix 471

Ronald J Baken, Robert F Orlikoff

36. Functional Dysphonia  

487

Danielle L Gainor, Bryan N Rolfes, Claudio F Milstein

37. Posture and Muscle Tension

497

John S Rubin, Lesley Mathieson, Edward Blake

38. Neurologic Disorders of the Voice

505

Lucian Sulica, Babak Sadoughi

39. Spasmodic Dysphonia

519

Gayle Woodson, Michael S Benninger

40. Surgical Management of Spasmodic Dysphonia

527

Gerald S Berke, Natalie Edmondson, Jennifer L Bergeron

41. Environment and Allergies  

533

R Eugenia Chavez

42. Acute Laryngitis

543

Aron Z Pollack, Milan R Amin

43. Chronic Laryngitis

553

Jason Chesney, Adam D Rubin

43A. Autoimmune Disorders of the Larynx: Common Conditions, Symptoms, and Treatments

565

Adam Szymanowski, Amy L Rutt, Robert T Sataloff

44. Laryngopharyngeal Reflux

573

Jessica E Southwood, Joel H Blumin, Nikki Johnston

45. Dysphagia in Esophageal Disorders

587

Greg Postma, Rebecca J Howell

46. Cough

599

Kenneth W Altman, Amanda L Richards, Rupali N Shah

47. Pulmonary Disorders and Voice

613

Amanda I Gillespie, Seema Jeswani, Ryan C Branski

48. Diagnosis and Treatment of Pediatric Voice Disorders

623

Anne F Hseu, Paul Krakovitz

49. The Aging Voice

635

Joseph P Bradley, Michael M Johns III

50. Hormones and the Female Voice

641

Jean Abitbol, Patrick Abitbol

51. Laryngeal Trauma

659

Gregory R Dion, Robert L Eller

Section 5: Benign Lesions and Masses of the Larynx 52. Nomenclature of Laryngeal Lesions Shaum S Sridharan, Clark A Rosen

679

xx

Laryngology

53. Nodules and Polyps: Assessment and Treatment

687

C Blake Simpson, Jeanne L Hatcher

54. Laryngeal Cysts  



697

55. Laryngeal Granulomas

705

James A Burns Thomas E Havas, Rachael M Wu

56. Vocal Fold Scar

715

Robert T Sataloff

57. Reinke’s Edema/Polypoid Corditis  

723

Melin Tan, Marvin P Fried

58. Laryngoceles and Saccular Cysts

729

Robbi A Kupfer, Norman D Hogikyan

59. Laryngeal Papilloma

739

Craig Berzofsky, Michael J Pitman

60. Benign Tumors of the Larynx

757

John T Sinacori, Craig S Derkay

Section 6: Vocal Fold Paralysis/Paresis 61. Principles and Timing of Treatment—Unilateral

773

Joel H Blumin

62. Classification of Laryngoplasty

777

Hans F Mahieu

63. Vocal Fold Injection

791

Paul C Bryson, Conor Devine

64. Medialization Laryngoplasty (Thyroplasty) and Arytenoid Rotation/Adduction

805

Michael S Benninger

65. Reinnervation

813

Robert R Lorenz, Roger L Crumley

66. Surgery for Bilateral Vocal Fold Immobility

821

Mona Abaza

67. Reinnervation for Bilateral Vocal Fold Paralysis

831

Jean-Paul Marie

Section 7: Airway Obstruction and Stenosis 68. Laryngotracheal Stenosis—Definitions and Pathogenesis

843

Alessandro de Alarcón, Aliza P Cohen, Michael J Rutter

69. Tracheostomy

849

John Heaphy, Rod Rezaee, Pierre Lavertu

70. Managing Glottic Stenosis Glendon M Gardner

859

Contents 71. Subglottic Stenosis

xxi 877

Robert R Lorenz

72. Tracheal Stenosis

887

Sonali Sethi, Thomas R Gildea

Section 8: Premalignant and Early Laryngeal Cancers 73. Leukoplakia  



901

Michael P Gailey, Harry T Hoffman

74. Premalignant and Early Malignant Lesions of the Larynx

915

Jonathon O Russell, Joseph Scharpf

75. Classification of Transoral Laser Microsurgery

931

Scott Troob, Gady Har-El

Section 9: Office Laryngeal Surgery 76. Setup and Safety in Office Procedures

941

Steven A Bielamowicz

77. Anesthesia for Office-Based Laryngology

947

Catherine Rees Lintzenich

78. Excisions of Laryngeal Masses

951

Markus M Hess, Susanne Fleischer

79. Office-Based Laryngeal Laser Surgery

959

Christopher M Bingcang, Seth H Dailey

80. Office-Based Esophagology

971

Maggie A Kuhn, Peter C Belafsky

Section 10: Voice Practice and New Innovations 81. New and Emerging Technology

985

Diane M Bless, Charles N Ford

82. Developing a Voice Practice

997

Ted Mau, C Gaelyn Garrett

83. Laryngeal Transplantation

1005

David G Lott, Marshall Strome Index 1015

SECTION Anatomy and Physiology

1

Chapter 1: The Evolution of the Human Voice and Speech: Key Components in the Story of Our Uniqueness

The Evolution of the Human Voice and Speech: Key Components in the Story of Our Uniqueness

3

CHAPTER

1

Jeffrey T Laitman, Joy S Reidenberg

INTRODUCTION Our planet is about 4.5 billion years old. Life has been around since the Archean era, some 3.8 billion years ago. The great dinosaurs ruled in the Triassic, Jurassic, and Cretaceous Periods from 248 to 65 million years. Our furry mammalian kin crept in during the demise of the dinosaurs and came to prominence in the Paleocene epoch. Some 60 million years ago, our own siblings, members of the order Primates (the “Firsts”) crept quietly along their little branches or out of their nocturnal caves as mammals came to prominence. From these relatives a host of lemurs, monkeys, apes, and eventually our ilk, came to the fore. Depending on how you define us, our own species, Homo sapiens, arrived maybe a few hundred thousand years ago. We are, literally, a blink in the timeline of our planet’s history. Since we, Homo sapiens, arrived, however, we have become the unquestioned masters of this world. Yes, it was tricky at first, as we possessed neither the great strength of mammoths nor the speed of gazelles. We lacked distinctive dentition, such as massive canines, that could frighten away competitors. We had no claws or even a quill or two. We could not swim very well. We could not climb very well. Neither our vision nor our hearing was particularly impressive. Physically, by mammalian standards, we just “were not all that”, as our kids would say today. We did accrue, however, something very special along the path of our evolution: a remarkable ability that no other animal on our planet either now or in our long history has had. We have a unique voice – and the ability to use that voice to produce articulate speech. Together, this duo has

enabled the panoply of our multilinguistic abilities and has given us our unique, species-specific, language. With these, we have dominated our planet.

WHAT ARE VOICE, SPEECH, AND LANGUAGE? These are topics for treatises by philosophes, linguists, and others of deep thought. They clearly overlap in meaning, and one can argue until the next phase of our evolution regarding how such terms may or may not apply to dif­ ferent species. Do bees have language? Can a dolphin speak? Does a parrot have cognitive abilities? What is a cat “thinking” when it looks at the moon? It is, however, necessary to have general, working, definitions for oto­ laryngologists so we are on the same page. Such is offered below. Voice, sometimes called “vocalization”, usually refers to sounds that are produced at the laryngeal vocal folds, mostly through air from the lungs. In humans, vocalizations comprise the fundamental components of speech (vide infra), but not all vocal sounds are part of the speech spectrum. Indeed, we utter many involuntary sounds— from coughs to an infant’s babble—that are generated at the vocal folds but not morphed into articulated sounds of speech. “Phonation” is the term that describes the production of the voice via vocal fold modifications. The essence of voice is, thus, its tie to vocal fold anatomy, physiology, and neuromuscular control. Of course, “voice” has also come to have a variety of societal, literary, and even philosophical meanings that go far beyond the con­ fines of the larynx.1

4

Section 1: Anatomy and Physiology

Speech is more complex than voice to define. For humans, we can consider speech as the verbal–vocal com­ munication system regularly used by all living people. By this definition nonhuman species would thus not have speech. As many species arguably have advanced vocal systems, they are often referred to as having “speech”, e.g. “ape-speech” or “the speech of prehumans”. Accordingly, what we produce is often given the modifier, “human”, and our speech indicated as “human speech” to distinguish what we do from other vocal utterances. For our purposes here, speech will be defined as what we do, and other species vocal communication considered and referred to as just that, vocal communication. Whales and apes may call to complain (please leave a vocal message if you can). Returning to our species, speech is the product of both the central (brain) and peripheral nervous systems and the aerodigestive tract (ADT), particularly that compo­ nent of it known as the “vocal tract”. Of particular interest to the otolaryngologist is the supralaryngeal component of the vocal tract, the region that is responsible for the modification of the fundamental sounds (voice) produced at the vocal folds. As will be emphasized below, it is important to always keep in mind that there is not an anatomically or physiologically separate “vocal tract” that functions solely for this purpose, rather the components are inherent parts of a complex, multifunctional ADT that evolved for primary purposes other than speech (a point often overlooked by our linguistic colleagues). Lastly, there is language, the most complex concept of them all.2,3 To define language in a few words would do it injustice, but as a working definition for us we can view it as the global expression of human communication either spoken, written, or gestural, consisting of words in a structured, ordered, and conventional manner. Inherent components of human language include brain (mental) functions of cognition, grammar, and syntax, among others. The crucial peripheral components of the input systems (i.e. auditory, visual) and output (voice, speech) are, obviously, inextricable elements.

THE ANATOMY OF VOICE AND SPEECH PRODUCTION: PART OF A LARGER SYSTEM WITH A LARGER ROLE What is often lost in discussions of voice or speech—or the conceptualizations regarding how these abilities arose in humans or our relatives – is that the anatomical mecha­ nisms for sound generation and/or modification did not

evolve for the purposes of making or modifying sounds. While the larynx – the central element in sound generation – is better known to those outside the medical world by its pseudonym, “voice box”, it emphatically did not come on the scene so that we could chat about the weather. That majestic conglomeration of cartilages, membranes, nerves, blood vessels, and an assortment of internal plica came about for three primary biophysiological functions: (1) regulation of air to and from the lungs, (2) protection of the airway, and (3) maintenance of intrathoracic and intra-abdominal pressure. That is the “Big Three”, and there are NO more important baseline functions for our body. We are air-breathing mammals and control, regulation, and protection of our airway is paramount.4,5

THE LARYNX: THE HOLY TEMPLE OF OUR BODY The larynx is the guardian of our lungs and thus has evolved as a special and protected structure. Although we have ascended the evolutionary ladder, the primary function of our larynx remains true to its origins: it is still essentially a valve, regulating and guarding the airway. As mammals morphed from their amphibian and reptilian ancestors their larynx also accrued added importance in new acti­ vities such as effectuating intra-abdominal pressure con­ trol during the transition from egg laying to birthing, and control of intrathoracic stabilization as movement of the upper limb required rib stabilization during climbing. Although the larynx of diverse mammalian species shares many homologous components, the specifics of structure for larynges of species that inhabit often vastly differing environments have been modified extensively during the course of evolution.5-8 The anatomical mechanisms for these controls and protections are the internal membranes, their folds, and controlling intrinsic muscles. While a detailed histology of the folds is beyond the scope of this essay, the basic composition of the structure has been divided by Hirano9 into five layers: squamous epithelium, superficial lamina propria (SLP), intermediate lamina propria (ILP), deep lamina propria (DLP), and vocalis muscle. These layers essentially function in mechanically “decoupled” groupings of the layers to form: the “Cover” or mucosa (epithelium and SLP); the “Transition area”, the vocal ligament itself (ILP and DLP); and the “Body” of the fold produced by the vocalis muscle. Although comparative and descriptive histology of the larynx, in general, and vocal folds, in particular, have

Chapter 1: The Evolution of the Human Voice and Speech: Key Components in the Story of Our Uniqueness been done, many aspects still remain unclear, particularly as concerns the direct relationship to functions.6 Indeed, the relatively new field of “Voice Science”, and how specific structures/layers of the folds directly relate to normal or abnormal function, and medical or surgical treatment is in its nascent stages. Furthermore, what remains largely unstudied and unknown is how the different compart­ ments of the vocal folds morphed and changed over the millennia to accommodate the evolutionary forces compelling their protective and pressure control roles. While the initial roles of the larynx and its internal membranes of mammals, in general, and primates (prosi­ mians, monkeys, apes, humans, and all of their ancestors), in particular, were sphincteric and protective, phonatory importance may well have played a part, though to what extent is unclear. Certainly, as we came to a hominid (direct human ancestors) grade of evolution, phonation/ vocal communication, and even singing (as an important part of social communication) would have begun to take on increasing importance. Such importance would have had a selective advantage in evolutionary terms, working to select for vocal fold histology in ways conducive to sound production, distinct, and with possibly greater ranges than our closest relatives. Some studies are already pointing to this. For example, only humans seem to pos­ sess a deep layer of the lamina propria, which may account for species-level differences between humans and our nonhuman primate relatives.10 Along similar lines, it has been shown that the human thyroarytenoid muscle (the muscle within the body of the vocal folds; the most medial fibers are often named the “vocalis”) may uniquely exhibit slow tonic muscle fibers with rare contraction properties, such as contractions that are prolonged, stable, precisely controlled, and fatigue resistant. Such properties have been suggested to be a unique specialization (called an “auta­ pomorphy”, or uniquely derived characteristic, in anthro­ pological terms) that may underlie our unique “voice” and help effectuate speech.11 It should be noted that while our field is collectively trying to identify that which is special or comparatively distinct about the anatomy/histology of human vocal folds, there remains much we do not know about developmental changes in this regard. Indeed, we humans go through a remarkable developmental scenario, particularly in the changes to the aerodigestive region (vide infra). Corres­ ponding, and perhaps cotemporaneous, developmen­ tal changes may well occur in the internal laryngeal environment. Indeed, recent studies have shown that

5

significant histological differences may exist in vocal fold development, for example, the deep layer of the lamina propria is not present at birth and not fully developed until the age of 11 or 12 years.10,12 While the functional and clinical implications of such observations are not yet fully clear, these may well have major implications for laryngeal functions, ranging from protection to voice production and speech attainment.

SETTING THE STAGE: THE AERODIGESTIVE TRACT AMONG MAMMALS While mammals exhibit great variation in body plan, the general template for their throat regions is remarkably similar.13,14 Most mammals are characterized by having an epiglottis that can make contact with, or overlap, the soft palate during both normal respiration and deglutition (Figs. 1.1A to D). This is accomplished in most species by a larynx positioned, at all stages of postnatal development, relatively “high” in the neck when related to the basicranium and/or cervical vertebrae. Its position, measured from the cranial aspect of the epiglottis to the caudal border of the cricoid cartilage, corresponds to the level of the basiocciput or first cervical vertebra (C1) to the third or fourth cervical vertebrae (C3 or C4) in most terrestrial mammals. Concomitantly, the hyoid bone and associated suprahyoid and infrahyoid muscles (i.e. muscles largely responsible for raising or lowering the larynx) are also relatively high. The tongue at rest lies almost entirely within the oral cavity, with no portion of it forming part of the anterior pharyngeal wall. Because of this high position of the larynx, the supralaryngeal region of the pharynx is noticeably small; the pharynx has little or no oral portion and significantly reduced nasal and laryngeal segments. Inferiorly, the striated muscle fibers of the pharynx blend with the longitudinal striated fibers of the esophagus to form a continuous functional unit. The high position of the larynx enables the epiglottis to pass upward behind the soft palate and “lock” the larynx directly into the nasopharynx. This configuration provides a direct air channel from the external nares through the nasal cavities, nasopharynx, larynx, and trachea to the lungs. Liquids, and in some species even chewed or solid material, can pass on either side of the interlocked larynx and nasopharynx by way of the isthmus faucium, through the piriform sinuses to the esophagus, following the so-called “lateral food channels.” This anatomic configuration

6

Section 1: Anatomy and Physiology

A

B

C

D

Figs. 1.1A to D: Midsagittal sections of the head and neck regions of: (A) adult dog, Canis familiaris; (B) adult goat, Capra aegagrus; (C) juvenile hog (pig), Sus scrofa; (D) adult spider monkey, Ateles paniscus. (E: Epiglottis; S: Soft palate).

permits the patency of the laryngeal airway while streams of liquid or semisolid food are transmitted around each side of the larynx during swallowing. Two largely separate pathways are created: a respiratory tract from the nose to the lungs and a digestive tract from the oral cavity to the esophagus. This arrangement confers on mammals the ability to use these two pathways simultaneously, including enabling: (1) nursing young to suckle while breathing, (2) ruminants to breathe while regurgitating cud, (3) carni­ vores to breathe while their mouth is clamped tightly closed around the neck of their prey, and (4) a variety of animals to breathe when the mouth is used as a tool (e.g. beavers gnawing trees, felines, or rodents grasping and carrying young). In addition, as many mammals are macrosmatic (i.e. largely dependent on olfaction for com­ munication with their environment), the two-tube system

is particularly valuable as this arrangement allows, for example, grazing or drinking herbivores to simultaneously detect the scent of a predator. While the larynx is consistently high in most mam­ mals, its exact position and the extent of its placement in the nasopharynx can vary considerably among species. Studies of cetaceans (i.e. whales, dolphins, porpoises), for example, have shown that the larynx in some species is positioned so high (rostral) that it is no longer in the neck but rather lies largely within the head.15 In many odontocetes (toothed whales), the larynx, from the tip of the epiglottis to the lower border of the cricoid carti­ lage, corresponds to the level of the presphenoidal syn­ chondrosis to the caudal border of the basiocciput. The larynx thus usually never reaches as far caudally as the compressed cervical vertebrae characteristic of these

Chapter 1: The Evolution of the Human Voice and Speech: Key Components in the Story of Our Uniqueness mammals. The epiglottis and corniculate cartilages form the anterior portion of an elongated larynx, which is encircled by a strong palatopharyngeal sphincter muscle (homologous to the soft palate and palatopharyngeal arch in humans). This sphincter grips the top of the larynx and keeps its aditus intranarial, thus effectively sealing the respiratory tract from the digestive route. Although exhibiting the basic mammalian pattern of a high larynx, odontocetes appear to have exaggerated it by placing the larynx even higher (or more rostral) than their terrestrial relatives. This extrahigh position ensures these mammals of a larynx fitted snugly into the nasopharynx and indeed may make it habitually intranarial, that is, it is not usually retracted from its position behind the soft palate. This arrangement may allow them to swallow whole fish while communicating with each other or while echolocating to orient themselves in their environment. Although cetaceans demonstrate an example of laryn­ges that have both migrated cranially and elongated their rostral cartilages, some terrestrial species have larynges that have expanded their caudal components (e.g. thyroid cartilage) so that they appear to extend con­ si­der­ably into the neck. For example, some male artio­ dactyls (red and fallow deer, Mongolian gazelle) exhibit particularly large larynges that seem to be located more caudally in the neck compared with other related species.16 However, although the larynges of these animals are elongated, they still retain roughly the same position opposite the cervical vertebrae as most other terrestrial mammals (extending from the basiocciput to C2–C3). Maintenance of this typical mam­malian position is due to concomitant elongation of the cervical vertebrae. These animals also exhibit an elongated and elastic velum (red and fallow deer) and an elongated epiglottis (Mongolian gazelle) that appear to assist in epiglottic/palatal contact and, therefore, the maintenance of the “two-tube” system. Thus, while larynges differ con­siderably in position, the basic, ancestral two-tube con­figuration is essentially main­ tained. These animals have modified a basic plan; they have not changed it. Postmortem dissections, and a range of imaging stu­ dies, including cineradiography, computed tomography, and magnetic resonance imaging, of our closest relatives, the nonhuman primates, show that their upper respira­ tory anatomy is also similar to the general mammalian pattern.4,17-19 As in other mammals, nonhuman primates exhibit a larynx positioned high in the neck, usually cor­ responding to the first to third cervical vertebrae. This position allows for epiglottic-soft palate apposition and

7

the possibility of an intranarial larynx, thus providing for a direct airway from the nose to the lungs, whereas the alimentary tract passes around the larynx en route to the esophagus (Figs. 1.2A to C). Cineradiographic stu­ dies have confirmed that nonhuman primates exhibit mostly separate respiratory and digestive routes and the ability to breathe and swallow almost simultaneously.17,20 Because of this configuration, nonhuman primates, like other mammals, appear strongly, if not totally, dependent on nasal breathing. As occurs in many mammals, the connection between the epiglottis and the soft palate can be broken, as the larynx exhibits extensive mobility and can be transiently lowered. This can occur for a number of reasons, including some vocalizations, swallowing certain foods (e.g. a large bolus of meat), or due to disease. Although this anatomic arrangement may enable almost simultaneous breathing and swallowing, it severely limits the array of sounds an animal can produce. The high position of the larynx means that only a small supralaryngeal portion of the pharynx exists. In turn, only a very reduced area is available to modify the initial sounds generated at the vocal folds. Due to this limitation, most mammals therefore depend primarily on altering the shape of the oral cavity and lips to modify laryngeal sounds. Although some animals can approximate some human speech sounds, they are anatomically incapable of producing the range of sounds necessary for human speech.21,22

THE DEVELOPMENT OF THE HUMAN AERODIGESTIVE TRACT: THE BASIS FOR OUR SPEECH ABILITIES One of the most distinguishing features of humans is the anatomy and inherent functions of our ADT. Our specia­­lized anatomy underlies our distinctive modes of breathing and swallowing, and our unique ability for speech. Indeed, the highly derived characteristics of the adult human ADT reflect both a distinctive develop­men­tal path as well as an evolutionary one. The human ADT, particularly the larynx and its posi­ tional relationships to contiguous structures, undergoes dramatic changes during development. The major morphologic events in embryonic develop­ ment (0–8 weeks) of the human larynx have been well documented and new data from homeobox genes are shedding further light on the mechanisms of early spatial establishment in the head and neck.23,24 The proper

8

Section 1: Anatomy and Physiology

A

B

C

Figs. 1.2A to C: Midsagittal sections and images of the human head and neck of: (A) 24-week fetus; (B) newborn infant; (C) magnetic resonance imaging of an adult. Note the apposition of the epiglottis and soft palate in A and B, and the descent of the larynx away from the soft palate in C. (E: Epiglottis; S: Soft palate).

development of the larynx during the embryonic period is obviously crucial to its later normal function, with miscues during this phase of development resulting in a range of serious congenital, often life-incompatible, anomalies. Although aspects of laryngeal development during the embryonic period have been well studied, changes dur­ ing the fetal period (eight weeks to birth) have not been as extensively explored. To elucidate the latter, studies by our laboratory and others have investigated fetal laryngeal development both through postmortem study employing precise means of age determination and ultrasonography of fetuses in utero.25-27 These studies have shown that the fetal period is a time of extensive laryngeal growth and of significant changes in the positional relationships of the larynx. The second trimester (13–26 weeks), in particular, is an active period for laryngeal development. By week 15, earlier than was previously reported, the epiglottis is already present, indicating that the epiglottic primordium may appear earlier in development than classically beli­ eved. Throughout this period, the larynx is found high

in the neck, generally corresponding, from the epiglottic tip to the inferior border of the cricoid, to the level of the basioccipital bone to the third cervical vertebra. By week 21, the epiglottis is found to be almost in apposition to the uvula of the soft palate. Between weeks 23 and 25, the epiglottis and soft palate overlap for the first time, providing the anatomical “interlocking” of the larynx into the nasopharynx characteristic of mammals previously described. The attainment of larynx–nasopharynx interlocking is a significant maturational horizon in the development of the aerodigestive region. Establishment of this anatomic relationship allows the creation of essentially separate respiratory and digestive routes that will function as such in the newborn infant (vide infra). Our ultrasound investigations have shown upper respiratory activity patterns that strongly suggest an operational two-tube system is beginning to function prenatally, in which the larynx remains highly positioned and intranarial during fetal swallowing movements. A critical time in the

Chapter 1: The Evolution of the Human Voice and Speech: Key Components in the Story of Our Uniqueness development of the entire upper respiratory region may take place during the period between weeks 23 and 25. Not only does the larynx attain a position that places it intranarially, but contiguous portions of the skull base— the de facto roof of the upper respiratory tract (vide infra)— also appear to be undergoing remodeling at this time. As portions of the cranial base are intimately related to the larynx and its contiguous musculature, cranial shape development and laryngeal/ADT positions may also be linked, although the precise extent and relationships are still unclear. What may be beginning during this period is a remodeling and refinement of the positional anatomy of the entire aerodigestive region—soft tissue and cartilaginous structures, such as the larynx, and bony skeletal parameters, such as the skull base—to provide the anatomical framework for the newborn’s upper respiratory and digestive tract. It should be noted that while these laryngeal and basicranial modifications are occurring in the upper respiratory region, concomitant changes are also occurring in the lower respiratory tract. For example, the period from weeks 23 to 25 corresponds to the maturation of the pulmonary glandular epithelium. This alveolar epithelium is responsible for the production of fetal lung surfactant, a substance that is essential for independent respiratory function. The contemporaneous development of the fetal larynx to permit soft palate– epiglottic overlap with increasing levels of lung surfactant

A

9

suggests that the time frame for the maturation of the upper and lower respiratory tracts are closely related. Normal fetal maturation of the larynx may be an essential factor in determining the beginnings of respiratory independence and overall fetal viability. The morphologic pattern of high laryngeal position established during fetal life continues past the perinatal period and into infancy. Indeed, the newborn/young infant period may more accurately be seen as an extension of the pattern established during the late second and early third fetal trimesters rather than as a distinct entity. Postmortem dissections and imaging studies have shown that the positional relationships in the aerodigestive region of human newborns and young infants closely resemble the basic primate and mammalian pattern. In newborns and infants until approximately 1½ to 2 years of age, the larynx remains high in the neck.4,14,28-32 Its position corresponds to the level of the basiocciput/C1, extends to the superior border of C4 in newborns, and descends slightly to the level between C2 and C5 by approximately 2 years of age. The tongue at rest can be found entirely within the oral cavity, with no portion of it forming the upper anterior wall of the pharynx. Largely separate respiratory and digestive pathways, similar to those described in most other terrestrial mam­ mals, are effectuated by the high laryngeal position in newborns and young infants (Figs. 1.3A and B). This

B

Figs. 1.3A and B: (A) The ADT of a newborn human during suckling and (B) the aerodigestive region in an adult human. Green arrows = Respiratory route, Blue arrows = Digestive route. Note that the high laryngeal position in the infant effectuates largely distinct pathways, whereas the lowered position of the larynx and tongue in the adult mandates the crossing of pathways.

10

Section 1: Anatomy and Physiology

arrangement prevents the mixing of ingested food and inhaled air, thereby enabling the baby to breathe and swal­ low liquids almost simultaneously in a manner similar to that of monkeys. Thus the baby can breathe through the nose with only minimal, if any, cessations as liquid flows from the oral cavity around the larynx into the esophagus. Because of this high laryngeal position, newborns are essentially, if not obligatorily, nose breathers. As with non­ human primates, the connection between the epiglottis and the soft palate is usually constant but may be inter­ rupted during the swallowing of a particularly large or dense bolus of food or liquid, during vocalization or crying, or because of disease as noted above. Although the high position of the larynx in a human newborn or young infant effectuates the dual-pathway system, it severely limits the array of sounds babies pro­ duce. Many studies have shown that the high position of the larynx greatly restricts the supralaryngeal portion of the pharynx/tongue available to modify the initial, or fundamental, sounds produced at the vocal folds. Thus, an individual with a larynx situated high in the neck, as is found in a newborn human or monkey, would have a more restricted range of vocalizations available than would individuals with larynges and tongues placed lower in the neck. Indeed, linguistic analyses have identified the quantal vowels [i], [u], and [a] as sounds that human infants or nonhuman primates cannot produce. As these vowels are the limiting articulations of a vowel triangle that is language universal, their absence considerably restricts speech capabilities. Although the larynx remains high in the neck until around the second year, functional changes, such as the first occasional instances of oral respiration, have been noted to occur considerably earlier, indeed within the first six months of life.29 The period between four and six months, in particular, may represent a crucial stage in upper respiratory activity. At this time, neuromuscular control mechanisms of the larynx and extralaryngeal pharyngeal control are beginning to change even before true structural “descent” of the larynx has occurred. This changeover period may also indicate a time of potential respiratory instability because of the transition from one respiratory pattern to another. The time and manifestation of both prenatal and postnatal maturation within the central nervous system relates directly to normal and abnormal upper respiratory and swallowing functions. For example, studies from our laboratory have suggested that there are crucial prenatal

periods for the development of mammalian upper res­ piratory motor nuclei in the brainstem and that insults in utero could affect postnatal functions.33,34 The combi­ nation of subsequent, postnatal central nervous sys­tem maturation and developmental changes in respiratory patterns may predispose the infant to several deve­ lopmentally related problems. The sudden infant death syndrome, SIDS, for example, may be related to these first postnatal upper respiratory changes and to the subtle changes in laryngeal position or central and peripheral neuromotor control of the larynx.33,35 The precise time of the shifts that occur in breathing patterns, their relationship to laryngeal changes, and the neurophysiologic mechanisms that accompany them are obviously crucial questions that are still poorly understood and require more specific and detailed study. The larynx of human infants may remain high in the neck until approximately 1½ to 2 years of age. Our studies and others have confirmed that around the second year, children begin to show positional rearrangements of the ADT that differ sharply from the condition in newborns and early infants. Around this period the larynx begins its permanent, structural descent into the neck. Although minor topographic changes in laryngeal position continue until puberty and beyond, the major qualitative change probably occurs between the second to third years of life. Although the exact timing of laryngeal descent has yet to be fully determined, imaging and postmortem observations indicate that by the third year the position of the larynx has been significantly lowered. Although the internal nature of the larynx changes relatively little after the third year (except for normal maturational changes at puberty), positional changes relative to contiguous upper respiratory structures are considerable. The tongue no longer lies entirely within the oral cavity at rest, as in the newborn infant or nonhuman primate. The posterior portion of the tongue, from the foramen cecum caudally, has descended into the neck and now forms the upper anterior wall of the pharynx. The larynx is now situated considerably lower in the neck. For example, in a seven-year-old child, the larynx—from the tip of the epiglottis to the inferior border of the cricoid carti­ lage—corresponds to the level between the upper border of C3 and the lower border of C5. In the adult, the larynx has further descended, lying between the lower border of C3/upper part of C4 to the upper border of C7. Concomi­ tantly, the hyoid bone and its associated suprahyoid and infrahyoid muscles are relatively lower in the neck.

Chapter 1: The Evolution of the Human Voice and Speech: Key Components in the Story of Our Uniqueness Due to the descent of the larynx, tongue, and hyoid apparatus in children after the second to third year, the epiglottis can no longer approximate the soft palate, even during maximal laryngeal elevation. As the larynx cannot lock into the nasopharynx, there no longer exists the possibility of a continuous, tube-like airway from the external nares to the lungs. The lower position of the larynx alters dramatically the way humans, after the early years of life, breathe and swallow. The loss of the ability of the epiglottis to make contact with the soft palate means that the possibility of having two separate pathways, one for air and one for liquid—the basic ancient terrestrial template—no longer exists. Unlike this general mammalian pattern, the respiratory and digestive tracts now cross each other in the area of the pharynx. This low position of the larynx also results in a large supralaryngeal portion of the pharynx. A permanently enlarged oropharynx is now present even during maximal laryngeal elevation. These changes have pronounced effects upon our respiratory behavior. For example, we are habitual nose breathers but, unlike newborn infants, adults have a greater ability for oral respiration and do so more frequently. Loss of the two-pathway system has now made it imperative that the respiratory tract be sealed off during swallowing. The permanent intersection of the respiratory and digestive pathways has created a de novo “aerodigestive” tract, a first of its kind in mammals. This has created many problems, which, if not unique to us, are certainly accen­ tuated in our kind. A major problem is that a bolus of food can easily become lodged in the laryngeal aditus leading to the common occurrence of food “going down the wrong pipe”; however, if the bolus is large or not expelled rapidly enough one may choke to death. This event is often referred to as a “cafe coronary”, because it frequently occurs in restaurants and may be mistaken for a heart attack. Similarly, another disadvantage of the crossed pathways is the relative ease with which vomitus can be aspirated into the larynx and trachea and passed to the lungs. Not only has a permanently lowered larynx proven to be a danger in the ingestion of material, but it may serve as the anatomic basis allowing for gastroesophageal reflux of stomach contents to enter the pharyngeal or oral cavities.36,37 The human ADT has clearly not been evolutionarily selec­ ted for the purpose of efficiently dealing with constant, retrograde emissions into the supraesophagus. Indeed, our ADT appears to be particularly poorly designed to handle any esophageal or gastroesophageal reflux. This is most clearly demonstrated by two features: (1) our uniquely

11

low laryngeal position and (2) the relatively unprotected posterior larynx. Low laryngeal position, by creating a permanent oropharynx, has by definition created a greatly expanded supraesophageal region. It should also be noted that as the larynx has migrated caudally, so too has the location of the cricopharyngeal sphincter (i.e. the upper esophageal sphincter) at the caudal-most extent of the pharynx. Thus by definition, adult humans have a relatively shorter esophagus and relatively longer supraesophagus than most other mammals. At the very least, then, the highly acidic contents of human gastroesophageal reflux have gained access to a proportionally greater surface area of pharyngeal mucosa with which they may interact. Laryngeal descent in humans has altered consider­ ably the way we breathe and swallow. From a comparative perspective, we have lost the basic mammalian ability to breathe and swallow simultaneously or almost simul­ taneously. We have also accrued a number of most unwan­ted guests, including the relative ease of lodging material in the airway or refluxing contents to the supraesopha­ gus and other portals. A litany of other diseases and/or incoordination clinicopathologies, ranging from otitis media and frequent rhinosinusitis38 to SIDS and aspects of obstructive sleep apnea39 may also be a price we pay for peripheral and central neuromuscular rearrangements that accompany ADT modifications. The lowered position of our larynx has, however, provided one major positive aspect: a greatly expanded supralaryngeal portion of the pharynx. This enlarged supralaryngeal pharynx has “liberated” the tongue from the oral cavity confinement, now having its posterior portion form the movable ante­ rior aspect of this enlarged chamber. This configuration allows for enhanced oral tidal respiration, which may have occurred in temperate environments for our early ancestors. In addition, pharyngeal/lingual modification of sounds produced at the vocal folds is considerably greater than that possible for newborns, early infants, or any nonhuman mammal. In essence, it is the unique marked descent of the larynx and the resultant expansion of the pharynx and liberation of the posterior tongue that gives us the anatomic ability to produce fully articulate speech.

WHEN DID WE GAIN OUR VOICE AND OUR ABILITY TO SPEAK? When, how, and why the unquestionably unique ADT that we exhibit today came about during the course of our evolution is an ongoing topic of often-heated (and vocal)

12

Section 1: Anatomy and Physiology

debate. The reason for the intensity, of course, is that it speaks to the centrality of what makes us “human” and what separates us from both other living animals and from our own nonhuman ancestors. While fossilized throats do not remain, some research­ ers, our lab included, have developed methods to recons­ truct the structure of the region through the use of remnant portions of the cranial base, the de facto “roof” of the ADT, as a guide.40-43 Reconstruction of the ADT of fossil human ancestors – ranging in age from our earliest direct relatives known as australopiths (who can be traced to over four million years before the present) to early members of our own genus, Homo (appearing over a million and a half years ago), to our own species, Homo sapiens (arriving perhaps 200,000 to 300,000 years before the present)—have enabled us to trace the changes in the region through our history. For example, our reconstructions have suggested that the earliest hominids likely exhibited an ADT largely similar to those of the extant apes, with the larynx positioned high in the throat and the epiglottis able to contact the soft palate during normal tidal respiration. These early ancestors likely breathed and swallowed essentially as do our living monkey and ape relatives, being essentially nasal breathers with a modified two-tube system. The high position of their larynx would, by necessity, limit the supralaryngeal area of the pharynx and the freedom of the tongue to modify sounds as extensively as modern adult humans can. This suggests that they were restricted in the types of sounds that they could make, probably being incapable of producing a number of the universal vowel sounds found in human speech patterns.4,41,42 What the internal anatomy/microanatomy of their vocal folds was exactly like, and whether changes toward the human condition were occurring in the distribution, structure or innervation patterns of the intrinsic musculature, remains unknown. If the global reconstructions given above for their ADT are correct and they were indeed very similar to living apes, then it is reasonable to hypothesize that their vocal fold anatomy would also not be very different from those of the living apes and monkeys. They may well, for example, have lacked a deep layer of the lamina propria, again a feature suggested to be found only in living humans and not in other primates (Fig. 1.4). If our earliest relatives were still “ape-like” in their ADT/ vocal tract component, when did things change en route to us? This is a key question of our evolution and while definitive answers in evolution are rare, clues are beginning to appear. Our fossil data—and by extension reconstruc­ tions—suggest that the region was starting to change with

Fig. 1.4: Reconstruction of the head and neck anatomy of Australopithecus africanus, an early human ancestor, during quiet nasal respiration (based upon the fossil Sts 5 from Sterkfontein, South Africa; for discussion see text and reference 42). As with living monkeys and apes, we hypothesize that the earliest hominids would exhibit a highly positioned, intranarial larynx during nasal breathing, as well as during ingestion of some foods. The high larynx would also have limited the supralaryngeal area and thus the ability to modify laryngeal sounds compared to living humans.

the first members of our own genus, Homo, some million— plus years before the present on the plains of Africa. It was at this time that the ancient, two-tube system in place for millennia was evolving into something different. The basicranium was changing, indicating that the larynx was changing in position, likely becoming disengaged from the nasopharynx. Such a shift would have radically altered the way our ancestors breathed (e.g. increasing oral respiration possibilities) and how they swallowed. Indeed, as we have previously hypothesized,4 the reason behind the advent of such changes may have been linked to increased need for oxygen due to lifestyle demands such as running on the African plains. In addition, such ancestors would also no longer have had the ability to breathe and swallow almost simultaneously. A new paradigm would have come in place. Such a shift would have required not only obvious anatomical uncoupling and rearrangements, but also a “rewiring” of central and peripheral neural processing. As with developmental shifts noted previously, change has its costs, and many of our early ancestors likely paid the ultimate price. Scenarios such as increased choking and other upper respiratory and upper digestive maladies probably evolved along with our laryngeal shifts. While breathing and swallowing abilities were chang­ ing, so too were vocal and speech capabilities. On the one hand, the brain size in our early Homo ancestors was

Chapter 1: The Evolution of the Human Voice and Speech: Key Components in the Story of Our Uniqueness increasing over that found in earlier australopith-level hominids. Concomitant with that were indications that the internal complexity of the brain was changing as well. Together with the ADT changes noted above, the stage was set for vocal tract and intrinsic laryngeal change. A watershed level of change was beginning with the advent of a new genus, one more advanced linguistically and cognitively than any that had preceded it. If, indeed, such changes were now becoming widespread, it is likely that the vocal component was taking on an ever-increasing communication role. Accordingly, microanatomical changes in vocal fold anatomy and function were also beginning to occur, as would have been alterations in intrinsic laryngeal muscle fiber type. While en route to the modern condition, our early Homo ancestors were probably not yet there. It is difficult, yet intriguing, to envision relatives who had an anatomical/physiological substrate different from either ourselves or our ape-like, earliest ancestors. The early members of our genus were remarkable in their own way, neither ape, nor australopith, nor us, humans, as we are today. While changes may have begun with early members of our genus, it was not until the appearance of early members our own species, Homo sapiens, some 200,000 to 300,000 years before the present (or even much later depending on who one sees as worthy of H. sapiens desig­ nation) that our reconstructions indicate an ADT similar to ours appeared.42 These early H. sapiens, probably func­ tioned much as we do today as regards their breathing, swallowing, and communicative parameters. Certainly, their extensive vocal tract component would have allowed for the production of the sounds of extant speech. We can also hypothesize that their internal laryngeal milieu was very similar to ours, but exactly when the type of muscle fibers, or presence of a lamina propria such as those shown today, actually appeared remains to be determined. Could there have been stages of change even within the timeframe of our own species? Could some of the answers to the late appearance of advances in the archeological record that point to highly advanced cognitive abilities44 be reflective of subtle, yet seminal, changes in our voice or speech capabilities? Clearly, as we uncover more of the secrets buried within our unique structures for voice and speech, so too will be able to uncover their deeply entwined role with the story of how we came to be.

REFERENCES 1. Abitbol J. The Odyssey of the voice. San Diego, CA: Plural Publishing;2006.

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2. Lieberman P. The biology of language. Cambridge, MA: Harvard University Press;1984. 3. Chompsky N. Reflections on language. New York: Pantheon Press; 1976. 4. Laitman JT, Reidenberg JS. Evolution of the human larynx: nature’s great experiment. In: Fried M, Ferlito A (eds), The larynx, 3rd edn. San Diego, CA: Plural; 2009:19-38. 5. Laitman JT, Reidenberg JS. The evolution and development of human swallowing: the most important function we least appreciate. Otol Clin N Am. 2013;46(6):923-36. 6. Harrison DFN. The anatomy and physiology of the mam­ malian larynx. Cambridge, UK: Cambridge University Press; 1995. 7. Reidenberg JS, Laitman JT. Morphophysiology of the larynx. In: Van De Water T, Staecker H (eds), Basic science review for otolaryngology. New York, NY: Thieme;2005:505-15. 8. Kirchner JA. The vertebrate larynx: adaptations and aber­ rations. Laryngoscope. 1993;103:1197-201. 9. Hirano M. Morphological structure of the vocal cord as a vibrator and its variations. Folia Phoniatrica Logopaedica. 1974;26:89-94. 10. Benninger MS. The human voice: evolution and per­ formance. Music Med. 2010;2(2):104-8. 11. Han Y, Wang J, Fischman DA, et al. Slow tonic muscle fibers in the thyroarytenoid muscles of human vocal folds: a possible specialization for speech. Anat Rec. 1999;256(2): 146-57. 12. Hartnick CJ, Rebhar R, Prasad V. Development and matu­ ration of the pediatric human vocal fold lamina propria. Laryngoscope. 2005;115:4-15. 13. Laitman JT, Reidenberg JS. Specializations of the human upper respiratory and upper digestive systems as seen through comparative and developmental anatomy. Dys­ phagia. 1993;8:318-25. 14. Laitman JT, Reidenberg JS. Comparative and developmental anatomy of human laryngeal position. In: Bailey B (ed), Head and neck surgery – otolaryngology, 2nd edn, vol. 1. Philadelphia, PA: Lippincott Company;1998:45-52. 15. Reidenberg JS, Laitman JT. The position of the larynx in Odontoceti (toothed whales). Anat Rec. 1987;218:98-106. 16. Frey R, Gebler A. The highly specialized vocal tract of the male Mongolian gazelle (Procapra gutturosa Pallas, 1777Mammalia, Bovidae). J Anat. 2003;203(5):451-71. 17. Laitman JT, Crelin ES, Conlogue GJ. The function of the epiglottis in monkey and man. Yale J Biol Med. 1977;50: 43-9. 18. Laitman JT, Crelin ES. Tantalum markers as an aid in identifying the upper respiratory structures of experimental animals. Lab Anim Sci. 1980;30(2):245-8. 19. Flugel C, Rohen JW. The craniofacial proportions and laryngeal position in monkeys and man of different ages. (A morphometric study based on CT scans and radiographs.) Mech Ageing Develop. 1991;61:65-83. 20. German RZ, Crompton AW. Integration of swallowing and respiration in infant macaques (Macaca fascicularis). Am J Phys Anthropol. 1993;(Suppl 16):94. 21. Laitman JT. The evolution of the hominid upper respiratory system and implications for the origins of speech. In:

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22.

23.

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25. 26. 27. 28. 29. 30. 31. 32.

33.

Section 1: Anatomy and Physiology de Grolier E (ed.), Glossogenetics: the origin and evolution of language. Paris, France: Harwood Academic Press;1983: 63-90. Lieberman P, Laitman JT, Reidenberg JS, et al. The anatomy, physiology, acoustics and perception of speech: essential elements in analysis of the evolution of human speech. J Hum Evol. 1992;23:447-67. Som PM, Smoker WR, Reidenberg JS, et al. Embryology and anatomy of the neck. In: Som PM, Curtin HD (eds), Head and neck imaging, 5th edn. New York, NY: Mosby; 2011:2117-64 Laitman JT, Noden DM, Van De Water TR. Formation of the larynx: from homeobox genes to critical periods. In: Rubin JS, Sataloff RT, Korovin GS, Gould WJ (eds), Diagnosis and treatment of voice disorders, 4th edn. San Diego, CA: Plural Publishing;2014. Magriples U, Laitman JT. Developmental change in the position of the fetal human larynx. Am J Phys Anthropol. 1987;72:463-72. Wolfson VP, Laitman JT. Ultrasound investigation of fetal human upper respiratory anatomy. Anat Rec. 1990;227: 363-72. Isaacson G, Birnholz JC. Human fetal upper respiratory tract function as revealed by ultrasonography. Ann Otol Rhinol Laryngol. 1991;100:743-7. Laitman JT, Crelin ES. Developmental change in the upper respiratory system of human infants. Perinatol Neonatol. 1980;4:15-22. Sasaki CT, Levine PA, Laitman JT, et al. Postnatal descent of the epiglottis in man: a preliminary report. Arch Oto­ laryngol. 1977;103:169-71. Westhorpe RN. The position of the larynx in children and its relationship to the ease of intubation. Anaesth Intensive Care. 1987;15:384-8. Schwartz D, Keller M. Maturational descent of the epiglottis. Arch Otolaryngol Head Neck Surg. 1997;123:627-8. Vorperian HK, Kent RD, Linstrom MJ, et al. Development of vocal tract length during early childhood: a magnetic resonance imaging study. J Acoust Soc Am. 2005;117: 338-50. Friedland DR, Eden AR, Laitman JT. Naturally occurring motoneuron cell death in rat upper respiratory tract motor

nuclei: a histological, Fast-DiI and immunocytochemical study in the nucleus ambiguus. J Neurobiol. 1995;26: 563-78. 34. Friedland DR, Eden AR, Laitman JT. Naturally occurring motoneuron cell death in rat upper respiratory tract motor nuclei: a histological, fast-DiI and immunocytochemical study in the hypoglossal nucleus. J Neurobiol. 1995;27: 520-34. 35. Tonkin SL, Gunn TR, Bennet L, et al. A review of the ana­ tomy of the upper airway in early infancy and its possible relevance to SIDS. Early Hum Dev. 2002;66:107-21. 36. Laitman JT, Reidenberg JS. The human aerodigestive tract and gastroesophageal reflux: an evolutionary perspective. Am J Med. 1998;103:3-11. 37. Lipan M, Reidenberg JS, Laitman JT. The anatomy of reflux: a growing health problem affecting structures of the head and neck. Anat Rec. B: the new anatomist. 2006;289B: 261-70. 38. Bluestone CD, Pagano AS, Swarts JD, et al. Consequences of evolution: is rhinosinusitis, like otitis media, a unique disease of humans? Otol Head Neck Surg. 2012;147: 986-91. 39. Davidson T. The great leap forward: the anatomic basis for the acquisition of speech and obstructive sleep apnea. Sleep Med. 2003;4:185-94. 40. Laitman JT, Heimbuch RC, Crelin ES. Developmental change in a basicranial line and its relationship to the upper respiratory system in living primates. Am J Anat. 1978; 152:467-83. 41. Laitman JT, Heimbuch RH, Crelin ES. The basicranium of fossil hominids as an indicator of their upper respiratory systems. Am J Phys Anthropol. 1979;51:15-34. 42. Laitman JT, Heimbuch RC. The basicranium of Plio-Plei­ stocene hominids as an indicator of their upper respiratory systems. Am J Phys Anthropol. 1982;59:323-44. 43. Reidenberg JS, Laitman JT. Effect of basicranial flexion on larynx and hyoid position in rats: an experimental study of skull and soft tissue interactions. Anat Rec. 1991;220: 557-69. 44. Tattersall I. The human odyssey: four million years of human evolution. New York: Prentice Hall;1993.

Chapter 2: History of Laryngology

15

CHAPTER History of Laryngology

2

Tjoson Tjoa, Sunil P Verma This work would not have been possible if not for the diligent work by the historians before us, including Colin Karmody, Steven Zeitels, Peter Alberti, and Matthew Clary.

INTRODUCTION Modern-day laryngology revolves around the ability to exa­mine the larynx in both awake and anesthetized patients. This ability developed through a stepwise prog­ ression of tools and methods to visualize the larynx. Curiosity about the production of voice, coupled with the need to treat diseases of the throat, provided the impetus for the pioneers of laryngeal instrumentation. This chap­ter reviews the high­lights in the evolution of this cons­tantly changing field. The earliest evidence documenting surgical treatment of the throat dates back to ancient Egypt. A drawing on the wall of the Step Pyramids, dated around 3600 BC, depicts what is thought to be a tracheostomy.1 The first use of the word “larynx” dates back to 350 BC. Aristotle states in his Historia Animalium, “The neck is the part between face and trunk (the front of this is the larynx and the back is the gullet). The front part of this is of gristle and through it speech and respiration take place; it is known as the windpipe”.2 In Roman society, the physician-philosopher Galen first discussed the functions of the larynx and provided names for the epiglottis and recurrent laryngeal nerves in the second century AD.3 He also described the three cartilages of the larynx and explained how it functions in breathing and voice production.4 For centuries thereafter, Byzantine physicians con­ tri­buted considerably to the advancement of surgery by

docu­menting operations and postoperative care for procedures such as tracheostomies, foreign body removals, and uvulectomies.3 These had a major influence on European surgeons. However, it was not until anatomic textbooks by Vesalius of Belgium in 1555 and Morgagni of Italy in 1719 that detailed anatomic descriptions of the larynx re-emerged.5 The terms “Vocal cords” and “Vocal folds” were eventually described and named in the 18th century by Ferrein and Bertin.1 Prior to the 18th century, much of the study on the larynx had been theoretical, elucidating its function as the organ of voice and lower airway protection. However, the increase in diphtheria, tuberculosis, and syphilis in the late 18th and early 19th century provided the impetus to create instruments that could be used to examine the larynx for the purpose of characterizing these pathologic conditions. Until that time, the laryngeal physical exami­ na­tion consis­ted primarily of external digital palpation.

INDIRECT LARYNGOSCOPY: EARLY DEVELOPMENT Phillip Bozzini (1773–1809) is credited with the creation of the first endoscopic instrument.6 His Lichtleiter, or light conductor, coupled an angled speculum and mirror insert to a candlelight source (Fig. 2.1). Using cannulae of vary­ ing shapes and sizes, he attempted to visualize various body cavities, including the rectum, urethra, and throat.

16

Section 1: Anatomy and Physiology

Fig. 2.1: Bozzini’s lichtleiter.

Fig. 2.2: Babington’s glottiscope.

Though there is no documentation that he was able to visualize the larynx, his instruments paved the way for modern endoscopy. Benjamin Guy Babington developed what is consi­ dered the first successful laryngoscope. Called the “glottiscope” at the time, it was a three-bladed device with a retracting spatula to displace the tongue and a mirror to direct external sunlight toward the larynx (Fig. 2.2). In 1837, Liston introduced the concept of heating the mirror portion of the glottiscope in order to avoid condensation.7 The first head mirror was used in 1844 by John Avery, who used a perforated concave reflective surface to reflect light from the source into the oropharynx in conjunction with Babington’s glottiscope. He later attached this mirror to a headband in 1855 to allow for two-handed examination of the patient. Though he never published, it is thought that he visualized the larynx with this apparatus.8 These early advancements in visualizing the larynx eventually led to the development of laryngology as a subspeciality. Horace Green (1802–1866), the first American throat and respiratory specialist, pioneered the transoral application of caustics to treat laryngeal membranes in the 1850s.6 He was a physician who studied in Paris, immigrated to United States, and brought the field of laryngo­ logy with him. He is credited with performing the first ever direct laryngoscopy in 1852 on an 11-year-old girl who suffered from persistent obstructive sleep apnea after tonsillectomy. She was found to have a ball-valving fibroepithelial polyp, which Green excised using a spatula and a curved tenaculum.9,35 Though his contributions were not immediately recognized, he would eventually be named the “Father of American Laryngo­logy” at the first meeting of the American Laryngological Association in 1879.

Around this same time, Manuel Garcia, a Spanish-born voice teacher practicing in France, separately developed a method of visualizing the larynx. He was reportedly walking on a street in Paris and noticed the flashing of sun on the window panes of a house and separately came up with the idea of reflecting light off mirrors to observe the movements of vocal cords. In his Observations on the Human Voice, he first described “autolaryngoscopy”, using the reflection of the sun to illuminate his own larynx.10 It is thought that he was able to tolerate this even without anesthesia due to his ability to suppress his own gag reflex.11 He detailed vocal fold motion as the rhythmic pulsation of expiratory airstream and also detailed the generation of human voice from vocal cords.10 His technique was widely circulated in Europe and he is credited for inspiring the widespread use of mirror laryngoscopy. In 1857, Ludwig Turck experimented with Garcia’s method of clinical laryngoscopy, but was unable to obtain consistent results due to reliance on external direct sun­ light as the light source.12 Around that same time, his col­ league, Czermak, began to use artificial light with mirrors that he borrowed from Turck.13 In addition to an attachment held between his teeth to stabilize the mirror, he used external laryngeal pressure on the patient, and he was able to obtain consistent visualization.6,13 Because Czermak initially used his mirrors, Turck felt as though his idea had been stolen, and a feud developed between the two. Both convened clinics to demonstrate laryngoscopy, which fueled interest in their techniques throughout Europe and the United States.14 Turck established the first textbook concerning pathology of the larynx, which he published in 1866 in Clinic on the Diseases of the Larynx and Trachea, along with an accompanying atlas that became the standard for several years.15,16

Chapter 2: History of Laryngology

Fig. 2.3: Oertel’s laryngostroboscope.

The fact that Green, Turck, Czermak, and other laryn­ go­logists of the mid-19th century were able to perform mani­pulations of the vocal cords is astonishing given the lack of anesthetic techniques available at the time. Turck attempted using a combination of morphine, chloroform, and alcohol, but his patients became intoxicated. Others, such as Schrotter, who in 1870 opened the first ambula­ tory laryngoscopy clinic in Vienna, trained his patients to reduce their gag reflex over a period of weeks. After doing so, he was able to remove polyps from the vocal cords.11 One of Czermak’s students, Morrell Mackenzie, introduced laryngoscopy to Great Britain, where he opened the first hospital dedicated to treating diseases of the larynx, developed improved instruments to examine and mani­ pulate the larynx, and authored a textbook on diseases of the throat.17,18 He is also credited as the first to coin the term “laryngoscope” (referring to the hand-held mirror at the time),8 and was one of the founders of the Journal of Laryngology and Otology, which is still in existence.11 Perhaps the most famous anecdote of early laryngology involved Mackenzie’s role in the misdiagnosis and death of Prince Frederick William of Prussia. After performing a biopsy of a laryngeal tumor for the Crown Prince, the specimen was read by Rudolph Virchow as benign. After continued hoarseness 9 months later, repeat biop­ sies found malignant tissue, and the Crown Prince, now Emperor, died shortly thereafter.1 In addition to wides­ pread political ramifica tions throughout Europe due to the replacement of the liberal Prince Frederick with a

17

more militaristic regime, this mistake contributed to the abolition of biopsy as a way to diagnose laryngeal cancer for the next 40 years.3 Two other students of Czermak, Louis Elsberg, an inter­ nal medicine physician, and Jacob Da Silva Solis-Cohen, a surgeon, were responsible for bringing the technique of mirror laryngoscopy to the United States. In 1863, Elsberg, in New York, established the first clinic for throat diseases in the United States.11,37 In 1867, Solis-Cohen performed the first hemilaryngectomy to cure laryngeal cancer. The two of them founded the American Laryngological Association in 1878 and served as the first and second presidents. Solis-Cohen’s book, Diseases of the Throat: A guide to diagnosis and treatment, was the standard textbook for laryngology for decades.6 The physiology of the vocal folds was initially described by Oertel in 1878, who used a cumbersome mechanical stroboscope for observation of the vibration of the vocal folds. He undertook his first investigations between 1876 and 1878 but published them in greater detail in 1895. His laryngostroboscope consisted of a rotating perforated disk interspersed between a light source and the exami­ ner’s head mirror (Fig. 2.3). By rotating it at various speeds, light would shine in pulses.1,6 He even fitted the scope to a magnifying telescope and described the use of electricity to power the wheel.

DIRECT ENDOSCOPY As mentioned, Horace Green studied in Paris and even­ tually brought the knowledge and methods to the United States. His direct laryngoscopy technique was not widely accepted initially due to the lack of anesthesia that would allow patients to tolerate it while awake. This was despite the fact that open approaches to the larynx and trachea, such as thyrotomies, tracheostomies, and even cancer resections, were already being performed either under no anesthesia or using ether for general anesthesia. Every­ thing changed in 1884, when Koller discovered the use of cocaine for ophthalmic topical anesthesia. Jelinek was the first to apply this to the larynx to remove a polyp.11,19 Coupled with the development of the incandescent light bulb by Thomas Edison in 1879 these developments paved the way for more widespread use of direct laryn­ goscopy.17 Alfred Kirstein, unaware of Green’s method, developed the first direct laryngoscope with electric lighting in 1895. The first volume of the Laryngoscope journal, in 1896, contains a review of a book by Kirstein on “autoscopy”, the

18

Section 1: Anatomy and Physiology

Fig. 2.4: Chevalier Jackson demonstrating sitting laryngoscopy with an assistant supporting the head.

term he first applied to direct laryngoscopy.20 He described the optimal position for this examination, known as the Kirstein position, with the patient in the sitting position, the neck flexed at the chest, and the head extended at the occipital-altoid joint (Fig. 2.4). At the same time, in Berlin, Gustav Killian was experimenting with an apparatus used to suspend a direct laryngoscope on a patient’s chest so that he could use both hands to perform laryngeal proce­ dures. He was the first to demonstrate that airways could be safely explored by passing a 9 mm tube beyond the carina. He introduced the supine position and coined the term “Bronchoscopy”17. In North America, direct laryngoscopy was advanced greatly by Chevalier Jackson, who was influenced by Kirstein. In teaching others the usage of the instruments he developed and techniques he pioneered to others, his knowledge slowly spread throughout the country. His first laryngoscope, designed in 1903, consisted of a distal spatula and a proximal tube. He subsequently developed various tubed designs for viewing the esophagus and bronchi as well. The tubed design allowed entry in a more lateral position, providing easier exposure. When coupled with his later innovations of distal lighting and distal suction, his laryngoscopes, bronchoscopes, and eso­phagoscopes are the basis for the instruments that are used today. He applied the Kirstein position, with the head extended, to the supine position, which eventually led to the surgical direct laryngoscopy positioning used today21 (Figs. 2.5A to D).

With the development of these instruments and techniques, laryngoscopy transitioned from a sitting proce­ dure in the clinic to a supine procedure in the operating room (Figs. 2.5A to D). Several design modifications by others such as Killian and Brünings paved the way for the instru­ments that are still used in the operating room today. Killian modified the laryngoscope blade into an invertedV shape to more closely conform to the shape of the vocal folds, and was the first to introduce the concept of suspension laryngoscopy, which is the basis of the “Boston” suspension technique used today.11,22 To further enhance the view of the larynx, Brünings, of Germany, produced a device with a pressure applicator on the larynx to increase exposure of the anterior commissure.23 It was Brünings who described the first vocal fold injection laryngoplasty performed in the office setting through a transoral app­ roach in 1911.24 In the 1950s and early 1960s, microscopic endoscopy, which had been developed for procedures on the uterine cervix, was applied to the larynx. Albrecht of East Germany and Kleinsasser of Austria are credited with development of this technology; however, parallel studies were pursued in the United States by Geza Jako. Albrecht used a colposcope for magnified vocal cord examination.25 In 1960, Scalco described the use of the Zeiss microscope with the Lynch suspension laryngoscope, which allowed for a leap in precision with regard to surgery of the vocal cords.26 Jako introduced the first set of microlaryngeal hand instruments27 and Kleinsasser designed further instrumentation, educated other surgeons in microlaryngoscopic technique, and introduced the 400-mm lens.28 The latter innovation increased the working distance bet­ ween the microscope lens and the laryngoscope, allowing for the usage of long-shafted laryngeal instruments.29 In the 1960s, general anesthesia was in widespread use and was applied to direct laryngoscopy. Deep anesthesia and muscle paralysis allowed for large caliber laryngoscopes to be inserted into mouth to optimize visualization.30 The precision afforded by magnification and illumina­tion, coupled with general anesthesia, revolutionized laryngeal surgery.20 Shortly after the invention of lasers in 1958, the carbon dioxide laser was coupled to a microscopic attachment, developed by Michael Polanyi, and was used by Jako in the late 1960s and early 1970s to evaporate discrete areas of tissue on the vocal cord surface in a rapid and bloodless manner.31,32 The development of their “stereo microscope attachment”, now more commonly known as the micromanipulator, was a landmark development that allowed

Chapter 2: History of Laryngology

A

C

B

D

19

Figs. 2.5A to D: Jackson’s illustration of Kirstein’s laryngoscopy position, modified for the supine patient.

for microscopic precision on the vocal cord target with a no-touch technique, the other hand being free to grasp the pathology and/or suction the operative field free of secretions or debris.33 The development of the concurrent use of CO2 laser with microlaryngoscopy by Polanyi, Jako, and Strong has greatly facilitated the now common practice of endoscopic excision of papillomas and early carcinomas.11 Additionally, microlaryngeal instrumentation is now designed with small distal, functional portions that allow precise manipulation at the level of the vocal fold while avoiding injury to deeper layers.34

OFFICE-BASED LARYNGOLOGY: A NEW FRONTIER After the development of general anesthesia, many advan­ cements within laryngology centered on improvements in operative techniques. However, developments within the office setting allowed for improvements in abi­lity to diagnose and treat diseases as well. The field of laryngeal surgery has undergone a full circle of development since its inception in 1855.10 Mirror laryngoscopy initially allowed for evaluation of the larynx and pharynx and later became the tool that enabled office-based laryngeal surgery (OBLS).8,36 While general anesthesia allowed for the migration of these surgical pro­ cedures to the operating room, recent trends have been back towards office-based surgery on awake patients. The most important change that led to the proliferation of OBLS was development of the flexible transnasal endoscope in 1968. The design of this fiberoptic laryngoscope

was based on the previously described flexible gastric endoscope38 and bronchoscope.39 The fiberoptic laryngoscope, which was designed to be passed transnasally, ushered in an entirely new method of evaluating and treating laryngopharyngeal diseases.40 This was certainly one of the landmark events that led to OBLS as it is known today.17 Primarily used to evaluate the vocal folds, fiberoptic endoscopes were used to facilitate unsedated tracheobronchoscopy,41,42 esophagoscopy,43 laryngopharyngeal biopsies, and even vocal fold injections.44 In fact, as unsedated endoscopic techniques improved there was discussion questioning the need for traditional panendoscopy for staging of head and neck cancer.41,45 “Distal-chip endoscopy” in which the image seen on the distal end of an endoscope was digitalized and transmitted to a monitor, markedly improved the quality of images able to be obtained through a flexible endoscope. Soon thereafter the transnasal esophagoscope was deve­ loped46,47 and commercialized, allowing an otolaryngologist to view the entire upper aerodigestive tract of an unsedated patient.

OFFICE-BASED VOCAL CORD INJECTIONS As mentioned, the first laryngeal interventions inclu­ ding biopsies and vocal fold injections were performed in the late 19th century and early 20th century prior to the development of local or general anesthesia. The resurgence of “office-based” laryngology took place in the mid to late 20th century as the ability to deliver local anesthesia to

20

Section 1: Anatomy and Physiology

the larynx improved. Even then, techniques for unsedated vocal cord injection laryngoplasty continued to develop using a laryngeal mirror to guide the procedure. Later, fiberoptic laryngoscopes and rigid angled telescopes48,49 were used to guide transoral vocal fold injections. Transcutaneous approaches were also developed, including tran­scricothyroid44 membrane and transthyrohyoid membrane approaches50,51 in which a flexible transnasal endoscope guided the placement of injectate. In the 1980s, Blitzer and Brin used botulinum toxin for the treatment of spasmodic dysphonia.52 It was later used beyond the management of neurolaryngologic diseases for bilateral vocal fold immobility,53 vocal fold granu­ loma,54 and dysphagia.55

OFFICE-BASED LASER LARYNGEAL SURGERY As mentioned, the introduction of the carbon dioxide laser by Strong and Jako in the 1970s transformed the field of laryngology.56 The line-of-sight laser was championed for its precise cutting capabilities and ability to coagulate vasculature in a defocused mode. However, though this laser was used in the office for palate surgery, its use in the larynx was not possible due to its line-of-sight nature. The advent of fiber-based lasers, combined with imp­ rovements in office endoscopy and laryngopharyngeal anesthesia, allowed for OBLS. The first laser commonly used was the pulsed dye laser.57-61 First discussed in 2004, the laser was touted for its affinity for oxyhemoglobin and ability to treat lesions such as papilloma, dysplasia, and other benign vocal fold lesions.57 Other lasers used commonly within the office setting have included the 532-nm KTP laser,62,63 the thulium laser,59,64,65 and the gold laser.66 Regardless of laser used, topical anesthesia is typically achieved with lidocaine. A laser fiber is threaded through the channel of an endoscope. The endoscope is passed into the patient through the nose and laser energy is applied to areas of interest in the laryngopharynx. Simultaneou­ sly transoral laser approaches have been developed for use in the office.67 Like other office-based laryngologic surgery, use of lasers has been demonstrated to be safe, well tolerated, and cost less than similar procedures in the operating room.68,69 In its current form, OBLS envelopes advanced techniques of laryngopharyngeal endoscopy including tracheobronchoscopy and esophagoscopy, and intervention, including biopsy, vocal fold injection, and laser surgery.

OBLS is performed as an outpatient procedure without the need for intravenous medication or cardiopulmonary monitoring. With a lack of prolonged operating room “turnover” time between surgical cases, physicians have been able to introduce increased efficiency into their practices. An additional advantage of OBLS includes decreased cost as there are no fees with operating room time and anesthesiology.69-71 The field of laryngology has been one of constant evolution, spurred by advancements in technology, instrumentation and anesthesia. While the methods have changed over time, many of the diseases that are treated remain the same, from polyps to papillomas to laryngeal cancer. The efficiency and precision with which these pathologies are treated continuously improves, as does our knowledge about them. The trajectory of the field is such that we can only expect that exciting treatments and solutions to current problems are on their way.

REFERENCES 1. Karmody CS. The history of laryngology In: Fried ME (ed.), The Larynx: A Multidisciplinary Approach. Boston: Little, Brown; 1988. 2. Aristotle (384-322 B.C.) Historia Animalium. 3. Assimakopoulos D, Patrikakos G, Lascaratos J. Highlights in the evolution of diagnosis and treatment of laryngeal cancer. Laryngoscope. 2003;113(3):557-62. 4. Galen CP (AD 130-200): De Usu Partium Corporis Humani. On the usefulness of parts of the body I, NY 1968. Cornell University Press (Translated by MT May). 5. Morgagni G: Adversaria Anatomica Prima. Padua. 1709. 6. Zeitels SM. Atlas of Phonomicrosurgery and Other Endo­ laryngeal Procedures for Benign and Malignant Disease. San Diego, CA: Singular; 2001. 7. Liston R. Practical Surgery. London, UK: J&A Churchill; 1837. p. 350. 8. Mackenzie M. The Use of the Laryngoscope in Diseases of the Throat with an Appendix on Rhinoscopy. London: J & A Churchill; 1865. 9. Green H. Morbid growths within the larynx. In: On the Surgical Treatment of Polyps of the Larynx and Oedema of the Glottis. New York, NY: GP Putnam; 1852. pp. 56-65. 10. Garcia M. Observations on the human voice. Proc Royal Soc London. 1855;7:397-410. 11. Alberti PW. The history of laryngology: a centennial cele­ bration. Otolaryngol Head Neck Surg. 1996;114(3):345-54. 12. Turck L. On the laryngeal mirror and its mode of employ­ ment, with engravings on wood. Zeitschrifi der Gesellschaft der Aertze ze Wein 1858;26:401-9. 13. Czermak JN. Du Laryngoscope et Son Emploi En Physiologie et Nen Medicine, Paris; 1860. 14. Majer EH, Skopec M. Zur geschichte der otorhinolaryngo­ logie in Osterreich. Vienna: Christian Brandstatter Verlag; 1985.

Chapter 2: History of Laryngology 15. Turck L. Atlas zur Klinik der Kehlkopfkrankheiten. Vienna: Wilhelm Braumuller; 1860. 16. Turck L. Klinik der Krankheiten des Kehlkopfes und der luftrohre. Vienna: Vorrede; 1866. 17. Clary MS, Courey MS. Development of procedures and tech­niques for the office. Otolaryngol Clin North Am. 2013; 46(1):1-11. 18. Rosenberg PJ. Total laryngectomy and cancer of the larynx. A historical review. Arch Otolaryngol. 1971;94(4):313-6. 19. Jelinek E. Das Cocain als anastheticum und analgeticum fur den pharynx und larynx. Wein Med Wochenschr. 1884; 34:1334-7, 1364-7. 20. Woodson GE. The history of laryngology in the United States. Laryngoscope. 1996;106(6):677-9. 21. Jackson C. Tracheo-bronchoscopy, esophagoscopy and gastroscopy. St. Louis, MO: The Laryngoscope Co; 1907. 22. Killian G. Die schwebelaryngoskopie. Arch Laryngol Rhinol (Berlin). 1912;26:277. 23. Brünings W, Howarth WG, trans. Direct laryngoscopy, bron­ choscopy, and oesophagoscopy. London: Bailliere, Tindall and Cox; 1912. 24. Brünings W. Über eine neue Behandlungsmethode der Rekurrenslähmung. Verhandl Deutsch Laryngol. 1911;18:93. 25. Albrecht R. Uber den Wert kolokopischer Untersuchung­ smethoden bei Leukoplakien und Carcinomen des Mundes und Kehlkopes. Arch fur Ohren Nasen und Kehlkopfhei­ lkunde. 1954;15:459-63. 26. Scalco AN, Shipman WF, Tabb HG. Microscopic suspension laryngoscopy. Ann Otol Rhinol Laryngol. 1960;69:1134-8. 27. Zeitels SM. Premalignant epithelium and microinvasive cancer of the vocal fold: the evolution of phonomicrosurgical management. Laryngoscope. 1995;105(3 Pt 2):1-51. 28. Kleinsasser O. Weitere technische Entwicklung und erste Ergebnisse der endolaryngealen Mikrochirurgie. Z Laryng Rhinol. 1965;44:711-27. 29. Zeitels SM. Universal modular glottiscope system: the evo­ lution of a century of design and technique for direct laryn­ goscopy. Ann Otol Rhinol Laryngol Suppl. 1999;179:2-24. 30. Priest RE, Wesolowski S. Direct laryngoscopy under general anesthesia. Trans Am Acad Ophthalmol Otolaryngol. 1960; 64:639-48. 31. Jako GJ. Laser surgery of the vocal cords. An experimental study with carbon dioxide lasers on dogs. Laryngoscope. 1972;82(12):2204-16. 32. Polanyi TG, Bredemeier HC, Davis TW, Jr. A CO2 laser for surgical research. Med Biol Eng. 1970;8(6):541-8. 33. Shapshay SM. Jako: “Laser surgery of the vocal cords; an experimental study with carbon dioxide lasers on dogs.” (Laryngoscope, 1972; 82:2204-2216). Laryngoscope. 1996; 106(8):935-8. 34. Benninger MS. Laryngeal microinstrumentation: a novel design to reduce movement. Otolaryngol Head Neck Surg. 2003;129(3):280-83. 35. Green H. Observations of the human voice. Proc R soc Lond. 1855;7:397-410. 36. Elsberg L. Laryngoscopal Medication or the Local Treatment of the Diseases of the Throat, Larynx, and Neighbroing Organs, Under Sight. New York, NY: William Wood & Co.; 1864.

21

37. Elsberg L. Laryngoscopal Surgery Illustrated in the Treat­ ment of Morbid Growths within the Larynx. Philadelphia, PA: Collins; 1866. 38. Hirschowitz BI, Curtiss LE, Peters CW, et al. Demonstration of a new gastroscope, the fiberscope. Gastroenterology. 1958;35(1):50; discussion 51-53. 39. Ikeda S. The flexible bronchofiberscope. Keio J Med 1968; 17:1-16. 40. Sawashima M, Hirose H. New laryngoscopic technique by use of fiber optics. J Acoust Soc Am. 1968;43(1):168-9. 41. Bastian RW, Collins SL, Kaniff T, et al. Indirect video laryngoscopy versus direct endoscopy for larynx and pharynx cancer staging. Toward elimination of preliminary direct laryngoscopy. Ann Otol Rhinol Laryngol. 1989;98(9): 693-8. 42. Hogikyan ND. Transnasal endoscopic examination of the subglottis and trachea using topical anesthesia in the otolaryngology clinic. Laryngoscope. 1999;109(7 Pt 1):1170-73. 43. Shaker R. Unsedated transnasal pharyngoesophagogas­ troduodenoscopy (T-EGD): technique. Gastrointest Endosc. 1994;40(3):346-8. 44. Ward PH, Hanson DG, Abemayor E. Transcutaneous Teflon injection of the paralyzed vocal cord: a new technique. Laryngoscope. 1985;95(6):644-9. 45. Bastian RW, Delsupehe KG. Indirect larynx and pharynx surgery: a replacement for direct laryngoscopy. Laryngo­ scope. 1996;106(10):1280-86. 46. Aviv JE, Takoudes TG, Ma G, et al. Office-based esophago­ scopy: a preliminary report. Otolaryngol Head Neck Surg. 2001;125(3):170-75. 47. Belafsky PC, Postma GN, Daniel E, et al. Trans­nasal esophagoscopy. Otolaryngol Head Neck Surg. 2001; 125(6):588-9. 48. Ford CN, Bless DM, Lowery JD. Indirect laryngoscopic approach for injection of botulinum toxin in spasmodic dysphonia. Otolaryngol Head Neck Surg. 1990;103(5 (Pt 1)):752-8. 49. Ford CN, Roy N, Sandage M, et al. Rigid endoscopy for monitoring indirect vocal fold injection. Laryngoscope. 1998;108(10):1584-6. 50. Getz AE, Scharf J, Amin MR. Thyrohyoid approach to cidofovir injection: a case study. J Voice. 2005;19(3):501-3. 51. Amin MR. Thyrohyoid approach for vocal fold augmentation. Ann Otol Rhinol Laryngol. 2006;115(9):699-702. 52. Blitzer A, Brin MF, Fahn S, et al. Botulinum toxin (BOTOX) for the treatment of “spastic dysphonia” as part of a trial of toxin injections for the treatment of other cranial dystonias. Laryngoscope. 1986;96(11):1300-1301. 53. Cohen SR, Thompson JW. Use of botulinum toxin to lateralize true vocal cords: a biochemical method to relieve bilateral abductor vocal cord paralysis. Ann Otol Rhinol Laryngol. 1987;96(5):534-41. 54. Nasri S, Sercarz JA, McAlpin T, et al. Treatment of vocal fold granuloma using botulinum toxin type A. Laryngoscope. 1995;105(6):585-8. 55. Schneider I, Thumfart WF, Pototschnig C, et al. Treatment of dysfunction of the cricopharyngeal muscle with botulinum A toxin: introduction of a new, noninvasive method. Ann Otol Rhinol Laryngol. 1994;103(1):31-5.

22

Section 1: Anatomy and Physiology

56. Strong MS, Jako GJ. Laser surgery in the larynx. Early clinical experience with continuous CO2 laser. Ann Otol Rhinol Laryngol. 1972;81(6):791-8. 57. Zeitels SM, Franco RA, Jr, Dailey SH, et al. Office-based treatment of glottal dysplasia and papillomatosis with the 585-nm pulsed dye laser and local anesthesia. Ann Otol Rhinol Laryngol. 2004;113(4):265-76. 58. Postma GN, Goins MR, Koufman JA. Office-based laser procedures for the upper aerodigestive tract: emerging tech­nology. Ear Nose Throat J. 2004;83(7 Suppl 2):22-4. 59. Koufman JA, Rees CJ, Frazier WD, et al. Office-based laryngeal laser surgery: a review of 443 cases using three wavelengths. Otolaryngol Head Neck Surg. 2007;137(1):146-51. 60. Mouadeb DA, Belafsky PC. In-office laryngeal surgery with the 585 nm pulsed dye laser (PDL). Otolaryngol Head Neck Surg. 2007;137(3):477-81. 61. Rees CJ, Halum SL, Wijewickrama RC, et al. Patient tole­ rance of in-office pulsed dye laser treatments to the upper aerodigestive tract. Otolaryngol Head Neck Surg. 2006; 134(6):1023-7. 62. Zeitels SM, Akst LM, Burns JA, et al. Office-based 532-nm pulsed KTP laser treatment of glottal papillomatosis and dysplasia. Ann Otol Rhinol Laryngol. 2006;115(9):679-85. 63. Koufman J. Office-based 532-nm pulsed KTP laser treatment of glottal papillomatosis and dysplasia. Ann Otol Rhinol Laryngol. 2007;116(4):317.

64. Zeitels SM, Burns JA, Akst LM, et al. Office-based and microlaryngeal applications of a fiber-based thulium laser. Ann Otol Rhinol Laryngol. 2006;115(12):891-6. 65. Zeitels SM, Burns JA. Office-based laryngeal laser surgery with local anesthesia. Curr Opin Otolaryngol Head Neck Surg. 2007;15(3):141-7. 66. Rees CJ, Allen J, Postma GN, et al. Effects of Gold laser on the avian chorioallantoic membrane. Ann Otol Rhinol Laryngol. 2010;119(1):50-53. 67. Verma SP, Dailey SH. Overcoming nasal discomfort—a novel method for office-based laser surgery. Laryngoscope. 2011;121(11):2396-8. 68. Kuo CY, Halum SL. Office-based laser surgery of the larynx: cost-effective treatment at the office’s expense. Otolaryngol Head Neck Surg. 2012;146(5):769-73. 69. Rees CJ, Postma GN, Koufman JA. Cost savings of unsedated office-based laser surgery for laryngeal papillomas. Ann Otol Rhinol Laryngol. 2007;116(1):45-8. 70. Andrade Filho PA, Carrau RL, Buckmire RA. Safety and cost-effectiveness of intra-office flexible video laryngoscopy with transoral vocal fold injection in dysphagic patients. Am J Otolaryngol. 2006;27(5):319-22. 71. Bove MJ, Jabbour N, Krishna P, et al. Operating room versus office-based injection laryngoplasty: a comparative ana­ lysis of reimbursement. Laryngoscope. 2007;117(2):226-30.

Chapter 3: Gross Anatomy of the Larynx

23

CHAPTER

Gross Anatomy of the Larynx

3

Gerhard Friedrich, Georg P Hammer

INTRODUCTION The human larynx is a complex organ composed of a skeletomembranous framework with a series of surro­und­ ing muscles, all together with the purpose of varying the position, shape, and tension of the vocal folds during the major laryngeal functions: respiration, deglutition, and phonation. Furthermore, laryngeal closure enables an effective cough, clearing the airway passage and allowing increased abdominal pressure necessary for the Toynbee/ Valsalva maneuver. Respiration and deglutition are phylogenetically old, vital, or so-called primary functions. Phonation is an evolutionary relatively young, secondary function for the human ability of oral communication.1,2 Nevertheless, this new function has substantial consequences in the evolu­ tion of the unique anatomical structure of the human larynx and vocal tract compared with our mammalian relatives. In deglutition and phonation, the sphincteric closure function of the larynx is a prerequisite, whereas in respira­ tion a wide lumen with abducted vocal folds is required. One of the major challenges the laryngeal surgeon is confronted with is to respect those different and very often conflicting requirements and to keep a balance between the primary and secondary functions. In this chapter, we will not go into detail with all basic anatomic laryngeal structures but want to focus on functional aspects in particular for the (phono-) surgeon.

PHYLOGENETIC ASPECTS Substantial works concerning the evolution of the whole aerodigestive tract, comparative anatomy, and the specific

role of the larynx and its precursors in premammalian vertebrates were published already by Sir Victor Negus3 and Sir Donald Harrison.4 The larynx of air-breathing individuals is responsible for maintaining a patent air channel to and from the lungs while also blocking incur­ sions from the digestive tract. Those functional challenges are the same in different vertebrate groups, although fundamental differences of laryngeal structure between the groups are evident. According to the laryngeal func­ tion, the prime assignment in all of these vertebrates is sphincteric to avoid aspiration. In many air-breathers, the larynx develops into a phonatory organ for soundwave based communication.5 According to Laitman,6 the basic laryngeal features such as the skeletal framework (including cartilages homologous to those found in humans) exist in most mammalian species, though they are often substantially modified to accumulate individual requirements. The primary function of the mammalian larynx remains true to its heritage: regulating and guarding the airway as a valve. Therefore, it is not surprising that the majority of the laryngeal musculature is responsible for laryngeal closure, predominantly by vocal fold adduction.7 Also, the position in relation to the skull base is essential for its function. A high position in the neck enables the epiglottis to pass upward behind the soft palatinal velum and lock the larynx directly into the nasopharynx. This anatomic configuration provides a direct conduit for air from the nose through the nasopharynx, larynx, and trachea into both lungs; it also permits the patency of the laryngeal airway while a stream of food is transmitted around each side of the larynx during swallowing. Some mammalian species (e.g. tooth whales) even exhibit an anatomic

24

Section 1: Anatomy and Physiology

Fig. 3.1: Position of the larynx in the neck (arrows regard to the lower rim of the cricoid cartilage) and comparison of the phylogenetic71 and ontogenetic72 development. The different angulations of the cranial basis according to Laitman6 are highlighted.

connation of the epiglottic tip to parts of the basicranium, thus sealing the respiratory tract from the digestive route completely.6 Our closest relatives among all mammals, the non­ human primates (apes, prosimians), show that their upper aerodigestive anatomy is similar to the before mentio­ ned general mammalian pattern. The laryngeal position related to the cervical vertebrae is high in the neck with a remarkable tendency of descensus along the evolutionary ladder (Fig. 3.1). This high position protects from aspiration, but it also implies that only a small supralaryngeal portion of the pharynx exists. Consequently, the sound generated at the vocal folds resonates directly into the epipharynx and nasal cavity. This is the reason for the restricted ability of primates to produce a large variety of sounds by articulatory movements, which is a precondition of human speech. To compensate for the lack of resonatory cavities, some species have evolved modifications in pharyngeal and/or laryngeal anatomic structures, such as laryngeal air sacs, which can increase the intensity and quality of the prime laryngeal sound. Laitman’s extraordinary studies of basicrania of fossil human ancestors (“hominids”) established a statistically significant, direct biomechanical link between the contour of the skull base and the laryngeal position in the neck. The basic pattern that has emerged from these studies is that basicrania that are essentially flat relate to the larynx positioned high in the neck, whereas basicrania that are markedly flexed correspond to larynges and associated structures positioned much lower in the neck as compared with the vertebrae. Nonhuman primates,

including the monkeys and apes, exhibit essentially the former, whereas adult humans exhibit the latter (Fig. 3.1).6 In the human species, speech is the outstanding elabora­ tion associated with the respiratory system. Human speech is characterized by rapid, precise movements of vocal tract articulators (lips, tongue, jaw, velum, larynx). The resulting changes in the shape of the supralaryngeal vocal tract lead to the dynamic pattern of formant variation that is exceptional for human vocal communication. However, recent studies show that the larynx in some nonhuman mammals (e.g. dogs and deer) is distinctively lowered during loud vocalizations as a “dynamic descent” to enhance vocal resonance.5 The human larynx is used for phonation continuously starting with the first cry of a newborn. The elaboration of laryngeal musculature and its subtle neural control, integrating laryngeal sound production with movements of respiratory, pharyngeal, palatal, lingual, and labial mus­ cles during the complex articulation of speech, provides mankind with a unique ability.6,8

DEVELOPMENTAL ASPECTS Embryology In humans, the rudiment respiratory system arises in the fourth week as an outgrowth of the digestive tract, the so-called laryngotracheal groove. The larynx itself develops from two parts: the supraglottis from the buccopharyngeal bud (fourth arch of the branchial system) and the glottis and subglottis from the tracheobronchial bud (fifth and sixth arch); as a consequence, also the lymphatic drainage occurs on two different ways (superior and inferior), which has a major impact on oncologic treatment. An exception is the epiglottis, which appears to be a unique mammalian addition unrelated to the ancestral branchial arches. The intrinsic musculature of the larynx is derived from the branchial arch mesenchyme of the fourth through sixth arches. Accordingly, the superior and recurrent laryngeal innervation to these muscles is related to this arch system either. Congenital anomalies (e.g. webs, atresia, laryngeal clefts, or stenosis) can be the result of irregularities in this early phase of embryonic development (0–8 weeks). The positional relationships of the larynx to contiguous structures undergo dramatic changes during development. The descensus from the skull base to its position at birth happens slightly; especially, weeks 23 to 25 seem to be a critical period of development, as portions of the cranial base are intimately related to the larynx and its contiguous

Chapter 3: Gross Anatomy of the Larynx musculature, cranial shape development, and laryngeal/ aerodigestive tract positions may also be linked (Fig. 3.1). As previously described, characteristic of mammals in those weeks the epiglottis and soft palate overlap for the first time, providing the anatomical “interlocking” of the larynx into the nasopharynx. Remodeling and refinement of the positional anatomy of the upper aerodigestive tract including cartilaginous structures and soft tissue (such as the larynx) and bony skeletal parameters (such as skull base) begins during this period, generating the anatomical framework for the newborn’s entire respiratory and digestive region.6,8,9

The Infant Larynx The anatomy of the pediatric airway differs remarkably from that of the adult—more than can be accounted for by size alone. By comparing the ontogenetic development in humans to the situation in primates, a strong parallelism to Haeckel’s Biogenetic law—ontogeny recapitulates phylo­ geny—is obvious. As shown in Figure 3.1, the topographic position of the infant larynx lies much more cranial than in adults and causes an overlap of the uvula and the epiglottis. In projection to the vertebral column, the cricoid of a fetus or newborn projects lies anterior to the third to fourth cervical vertebral body, whereas the adult larynx descends over the years to the sixth cervical vertebra, and in senility it projects down to the seventh vertebral body of the neck.2,10-12 A normal finding in the infant larynx is an overlap of the hyoid bone and the thyroid cartilage. This situation can persist as an atavistic residuum in adults and predisposes to laryngeal dysfunction (Fig. 3.3D).13,14 The thyroid cartilage, which is prominent in adolescents and adults, is much more difficult to palpate in the infant neck; the hyoid bone itself can be located externally by palpation almost in the submental region. A palpating finger moving from the hyoid bone caudally falls into a depression upon arrival at the thyroid cartilage—quite in contrary to its prominence in the adult. In infants, the prominent midline ridge of the thyroid cartilage, which begins at the thyroid notch, is not present. Instead, the anterior surface is rather flat and slightly rounded. Following further inferiorly the cricothyroid space with its membrane is rather palpable as a small slit, not a depression as in older humans. This fact has to be considered when performing a cricothyroid puncture or related surgical procedures in a pediatric larynx. With the descensus of the larynx and its enlargement also the major externally palpable structures of the laryngeal framework (hyoid bone, thyroid

25

and cricoid cartilage) separate and distance themselves, hereby forming the preliminarily described thyrohyoid and cricothyroid membranes. Consecutively, with this laryngeal descensus also the oropharynx develops and widens up. Endolaryngeally the elevated tip and curvature of the epiglottis is striking. This curved form increases from birth until the age of 3 years and slabs constantly over the years to its typical paddle-like configuration in the adult. The folded epiglottis and the thick and short aryepiglottic folds are one reason for the frequently seen supraglottic instability or so-called laryngomalacia in newborns. The arytenoid humps are disproportionally prominent and obscure a portion of the vocal folds. At birth, the arytenoids are very large in comparison to the dimensions of the other laryngeal structures and the length of the cartilaginous glottis accounts for about two-third of the whole glottis length (Fig. 3.10). During laryngeal maturation, a proportional diminution of the arytenoids can be observed and at about an age of 2.5 years the length between the cartilaginous and membranous glottis equalizes to result in an inverse relationship of roughly two-third membranous and one-third cartilaginous after the end of the growth period.15-17 Adult humans have the longest membranous glottis compared with animals; this is obviously a result of the evolutionary adaptation of the larynx as a phonatory organ. Negus described in animals the arytenoids forming more than the half of the entire glottis length, especially in those that need large air volumes for running (e.g. horses): “Present day man has a choked airway: He is in the position of a powerful motor car equipped with a good engine and efficient transmission, but with a choked air inlet to the carburetor.”3 Additionally, the laryngeal aditus becomes more triangular in adolescents and adults as a consequence of the proportional diminution of the arytenoids and the lengthening of the vocal folds. Also, the angulation of the folds varies as they insert onto the posterior surface of the thyroid’s midline. In the pediatric larynx, the vocal folds tend to slope inferiorly from posterior to anterior. This glottis angulation decreases with age, and they finally lie within the axial plane at adulthood. The subglottis is a nearly rounded airspace that rapidly increases in size during the first 2 years of life (from 13 to 28 mm2 in the means).9,16,17 The most caudal part of the upper pediatric airway, the trachea, measures approximately 0.5 cm in diameter in full-term newborns. Maximal internal diameter of the trachea in children aged less than 1 year ranges from 0.6 to 0.9 cm. The subglottis bounded completely by

26

Section 1: Anatomy and Physiology

the cricoid ring is the narrowest part of the infant larynx, especially because of its relatively thick mucosa.16 In conclusion, the pediatric larynx is not like an adult but more like a mammalian larynx and is primarily an organ for respiration and deglutition—it is not a “minilarynx” but a special organ.

Gender-Related Differences Up to puberty the female and male larynges vary marginally in shape and size. Thereafter, while the female larynx grows slightly, the male larynx enlarges under the influence of testosterone and growth hormone in all dimensions with the consequence of deepening the male voice around one octave. Although the larynx and the voice are secondary sexual characteristics, and even though the sex-related distribution of laryngeal disorders and lesions is striking, the evidence of hormonal receptors in laryngeal tissue is inconclusive.18-22 Essential gender-related differences are particularly pronounced in the thyroid cartilage (especi­ ally in the sagittal diameters) and in the thyroid angle, forming a prominence at its upper end, the so-called Adam´s apple (Fig. 3.2). The rapid and strong growth especially of the thyroid cartilage during maturation can lead to asymmetric developments that consequently are more frequent in men. A different development of the thyroid lamina leads to an asymmetric and tilted configuration of the endolaryngeal structures. A typical configuration can be observed: the aryepiglottic fold is situated more posteriorly on the side of the longer thyroid plate giving the clinical impression of a so-called arytenoid crossing or adduction asymmetry; the laryngeal prominence is shifted extramedian to the side of the shorter plate accordingly the interarytenoid region is tilted toward the longer side both resulting in an oblique course of the glottis. A strong growth of one thyroid plate very often leads to an inward buckling of the lamina in the anterior part moving the ventricular fold medially, mimick­ ing a ventricular fold hyperplasia (Figs. 3.3A to D).23-25 Furthermore an underdevelopment of the laryngeal dimen­ sions is not uncommon.24 It could be demonstrated that in clinically diagnosed functional mutational voice dis­ orders presenting with an abnormal high pitched pho­ nation, a larynx hypoplasia was the underlying cause.26 In general the female and male larynges differ signifi­ cantly not only in nearly in all dimensions but also in several biomechanically properties, so they almost can be considered as two different organs.17,26-32 Interestingly, in

contrast to the absolute dimensions, the relative propor­ tions are much more constant and are not gender-specific and therefore can be used as landmarks in laryngeal surgery (Fig. 3.4).17,33 Further details in gender-related differences will be provided in the corresponding chapters. Physiologic ossification of the laryngeal cartilages in females starts at the age of 50. In males this process begins much earlier between the ages of 18 and 20, although individual differences are evident. The thyroid´s ossification is much more distinctive in men, but a fully ossified thyroid is rare before the age of 50, in females even before the age of 75; there is no relation between the age and the degree of ossification. The cricoid cartilages ossification starts in accordance with the thyroid, but it does not occur completely. The arytenoids follow a few years after the other laryngeal cartilages, but they ossify completely in senility except the vocal processes, which stay cartilaginous throughout life.

THE ADULT LARYNX Skeletal Framework A series of cartilages connected by fibrous membranes and ligamental structures form the laryngeal framework. Although the thyroid cartilage, the cricoid cartilage and the epiglottis are single cartilages, the arytenoid cartilages are paired. Additionally, three paired small cartilages (corniculate or Santorini´s cartilage on the apex of each arytenoid; cuneiform or Wrisberg´s cartilage within the free margin of the aryepiglottic fold; triticeal cartilage within the thyrohyoid ligament) can be variably found.10-12,34-40 The thyroid, the cricoid, and the major portion of the arytenoid cartilages are composed of hyaline cartilage, whereas the vocal processes of the arytenoids, the epiglottis and the small variable cartilages (cuneiform, corniculate, triticeal) are composed of elastic fibrocartilage. From approximately the age of 25 the thyroid cartilage undergoes advanced calcification, but cases of congenital premature calcifications have been also described. Hematopoietic marrow can be present in senility. All these cartilaginous structures move in relationship to each other by forces generated by musculature external and internal to this skeletal framework and by recoil from elastic membranes and ligaments. The hyoid bone is the only bone of the human body that is not connected to other bones by articular joints; it is a U-shaped, backwards open bone that consists of a body (corpus) and two horns (major and minor) on each side.

Chapter 3: Gross Anatomy of the Larynx

27

Fig. 3.2: Thyroid angles, transverse, and sagittal diameters of the thyroid cartilage in different horizontal planes in females and males. The thyroid angle given in each plane refers to a reference point at the anterior quarter of the median sagittal diameter. At the glottis level additionally the angle between the median sagittal line and the posterior end of the thyroid cartilage is given.17 Given are each mean with standard deviation and significant levels on comparing the corresponding gender-related values (*p10% a week



12. Decrease patch size by one-third every 2 months



13. Decrease to one bupropion in the evening after 4 months and eliminate that one at 6 months

Number 2 of the Big 4 plus 2 is physical activity. Recent data from The National Health and Nutrition Examination Survey studies show that while America’s weight gain from 1983 to 1994 was due to an increased calorie consumption of 2% a year, compounded, or approximately 500 calories per day by 1995. That calorie increase is still sustained. But the recent increase in obesity relates to a decrease of approximately 1% per year since 1994 in physical activity. Thus, food choices and portion size, as well as lack of physical activity, are important in promoting sleep apnea and the upper respiratory and voice changes that occur consequent to obesity.17 While it is generally not thought that obesity affects voice—picture the large opera singer—it is clear that obesity affects lung function in the long term and that the simple physical activity of using voice the musculature can condition better voice. Improved voice performance would also be affected by a decrease in sleep apnea and better sleep patterns.18



Physical Activity

Some people exercise to lose weight and some exercise because it allows them to feel good, to reduce stress, or to win races, but of all the reasons to be physically active we think the one that trumps all others is to do it to live younger. While a pack per day smoking habit causes you to age (combination of increased risk for death and disability) about 12 years at age 55, that is your body is the equivalent of a 67 year old—physical activity—the three components of it that matter to rate of aging—give men about a 8.1-year slower rate of aging and women about a 9-year slower rate of aging. At age 55 the woman who does all three components of physical activity with an approach to do the minimum for maximum health would have the effective age—what we call Real Age—of a 46 year old.19 The primary questions we seek relating to exercise are: 1. What type of exercise do you do? Walking, strength or resistance training, cardiovascular exercise, such as swimming, biking, or running, or using exercise machines raise heart rate. We probe at questions 2 to 4 for each exercise done with some regularity. 2. Do you monitor your heart rate and how high do you usually get your heart rate and do you do intervals? All

data on obesity indicate this problem is accelerating due to reduced physical activity, we approach that next with our staff and our patients.





14. Carry one bupropion tablet with you at all times to take if you feel a craving

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contribute to lessened aging of your body when done in moderation and done for 35 for women and > 39 for men is associated with accelerated aging and adds the equiva lent of 2 years of age independent of blood pressure, low-density lipoprotein (LDL) cholesterol, TMAO (trime thylamine oxide), or hs-CRP (highly specific C-reactive protein, a measure of inflammation) levels, and other risk factors for chronic disease. It greatly accelerates aging by about 6 years independent of those factors if the waist is > 39 (for women) and > 43 (for men) (your waist is the inches around your body—your circumference— at your belly button with you sucking in as measured by a tape measure). Thus while blood pressure, normal LDL cholesterol, normal fasting blood sugar or hemoglobin A1C can be measured, we approach all wellness items including these in Food Choices and Portion Size by questioning areas that can lead to action steps that the patient can alter. These wellness questions and discussions are posed in ways that allow the patient to be motivated by the question and to change behavior with food choices, portion size, and physical activity to get healthier. ­

 

 

­





those benefits.25–30 No matter when you start exercising, as long as you are capable of doing so and are not at critical (dangerous to your heart muscle) blood flow levels before you start, decreases your disability substantially. In the Bay Areas Running Club studies27 the runners (who started at roughly 58 years old) time to 15% disability was 19 years versus 7 years for the control book reader only (nonexercisers) group. In the Cooper Clinic studies the quintile that was most fit averaged 14 mets in men, 11 mets in women. That most fit quintile had 45% of the chance of developing a chronic disease during their Medicare years in comparison to the least fit (which averaged a maximum tolerable exercise during stress test of 8.5 mets for men and 6.4 for women).29 If you extrapolate that data plus the Cleveland Clinic data30 if everyone in America who could make themselves 4 mets more fit did so, the USA would save over $100 billion a year in Medicare costs 15 years later. In the Jerusalem longevity studies28 the changes in disability from 70 to 85 years with people who first began physical activity at age 70 or 78 were examined. If the individual had high physical activity at the start, or inc reased that activity, there was an associated increase survival rate of over 80% for the 8-year period (from age 70 to 78, or age 78 to 85). Doing physical activity appears to have increased benefits the older you are. Unfortunately, only one in five Americans gets enough exercise to get even the 10,000 step a day minimum for general physical activity.31 The most disturbing part of the recent statistics is that our youth are becoming less and less fit, and by age 18 < 50% of boys and < 35% of women are doing even 30 minutes of any physical activity a day and cannot meet even the minimum physical activity standards for adults.32

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We have shown in our process for motivating behavior change that our Cleveland Clinic employees have lost a median of a little over 12 pounds per person—445,000 pounds in 5 years for the 37,000 employees we have tracked (unpublished data). Thus, as we will describe below, we believe that asking questions combined with programs and incentives help to motivate sustained healthier popu­ lations.

Managing Stress The fourth of the Big 4 plus 2 we assess and motivate for wellness is managing stress. The Interheart study38 assessed 30,000 patients in 52 countries to find that unmanaged stress was as great a risk for heart attack as was smoking, diabetes, or hypertension. Unmanaged stress is really the greatest factor increasing arterial aging, heart attacks, strokes, memory loss, impo­tence, decaying orgasm quality, and wrinkling of the skin. It increases immune aging such as cancer and infection risks, and increases accidents and other causes of disability. Unmanaged stress makes the RealAge the equivalent of 32 years older if there are three major life events in 1 year that are unmanaged or two major life events and chronic stress.19 We use a modification of the perceived stress scale to assess (and motivate doing something about) unmanaged stress in an individual. Using a scale of 1–10 where 1 means you have literally no stress and 10 means you have a great deal of stress, we ask: 1. How would you rate your average stress during the past month? 2. In the last month how often have you felt you were unable to control important things in your life? 3. In the last month how often have you felt confident about your ability to handle your personal problems? 4. In the last month how often have you felt that things were going your way? 5. In the last month how often have you felt difficulties were piling up so high you could not overcome them? These questions allow us to quickly assess stress, and then we ask questions to determine if they have learned techniques to manage their stress and if they use such techniques regularly. The key component is that events that cause stress, whether nagging unfinished tasks or one of the 13 major life events such as a close relative or spouse dying or being seriously ill, being sued, experiencing major financial problems, or taking a new job, do not cause massive aging unless they are unmanaged.39,40 Unmanaged stress can lead to premature aging. Another key point is that except for

those 13 major life events, what stresses one person is not the same as what causes stress for others around them.39-41 That is, it is the perception of the event that leads to stress. Because it is a perception, you can learn to manage this perception such that you have virtually no aging from the events that occur. The stress response was very useful in days when a woolly mammoth attacked as the norepinephrine and epinephrine and cortisol secretions mobilized sugar and mobilized muscles, energy, and heart function to help with escape or fight with more success. But now those res­ ponses are dysfunctional since most of us do not punch the doc in the face when a family member gets ill, or run to escape a family member’s death, or even a boss’s added task assignments at 4:45 on a Friday. These responses to the event now increase atherosclerosis, shrink connections in the brain and cause muscle wasting, inflammation, and abdominal fat buildup.41,43 Thus, managing the response to stress with one of 8 different techniques has been shown in randomized controlled trials to help patients as well as caregivers live productively, with more vitality, less burn­ out, and less feelings of anxiety and other components of stress.42,44

The Other 2 of the Big 4 Plus 2 The other 2 may be the hardest and may be the easiest to assess and change. We ascertain from medical records and questioning: 1. Have you gotten a flu shot every year for the last ten? 2. Are your immunizations up to date? and 3. Have you received an HPV vaccination? That vaccination may decrease sexually transmitted diseases and decrease cervical and throat cancer.45 Since most people we find do not know their immuni­ zation status, access to their primary care Electronic Medi­ cal Record (EMR) is key. We educate that getting a flu shot yearly decreases cardiovascular events such as heart attacks and strokes by 25% if done for 10 years in a row.45,46 This extra benefit of flu shots may be important in the perioperative period presumably because of the decreased inflammation and plaque rupture that is prevented by reducing the severity of flu and the flu in general. The EMR also allows the more difficult assessments to make sure that pneumonia, varicella, diphtheria, pertussis, and tetanus immunization status are current to reduce who­ oping cough and other diseases that may affect vocal strength, inflammation, and function.47

Chapter 12: Wellness, Health and Voice







Little interest or pleasure in doing things?



fatigue, mood, ability to function at work/daily chores, concentration, memory, mood, etc.) CURRENTLY? One good physical measurement that can be used to assess the likelihood of sleep apnea is neck circumference: a neck circumference >17 inches substantially increases the risk of sleep apnea. Online programs such as Go! to Sleep48 can help your patients assess and improve their sleep efficiency and quality of sleep. GO! to Sleep uses a combination of cognitive behavioral therapy and restrictive sleep practices as well as teaches sleep hygiene. In addition to improving sleep efficiency (time asleep divided by time in bed), it improves the ability to get into rapid eye movement sleep and get the restorative sleep needed for brain function and getting rid of brain waste.49



Sleep is one of the toughest to assess and to modify, partially because to get at pure sleep problems, you need to exclude depression and pain as causes of sleep problems. So we, of necessity, assess depression, pain, and sleep together. We use questions modified from the PDQ2 and 9 scales as well as the Insomnia Severity Index, and Pittsburgh and other Insomnia scales: 1. In past 2 weeks, have you been bothered by little interest or pleasure in doing things? 2. In the past 2 weeks, have you been bothered by feeling down, depressed, or hopeless? 3. Over the last 2 weeks, how often have you been bothered by any of the following problems:

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Feeling down, depressed, or hopeless?

MOTIVATING AND SUSTAINING BEHAVIOR CHANGE

Trouble falling or staying asleep, or sleeping too much? Feeling tired or having little energy?

Moving or speaking so slowly that other people could have noticed? Or the opposite – being so fidgety or restless that you have been moving around a lot more than usual? Thoughts that you would be better off dead, or of hurting yourself?





















If you checked off any problems, we pose question number 4: 4. How difficult have these problems made it for you to do your work, take care of things at home, or get along with other people? After those answers are tabulated, we then go to questions that specifically address sleep related issues: 5. Do you have difficulty falling asleep? 6. Do you have difficulty staying asleep? 7. Do you have problems waking up too early? 8. How SATISFIED/DISSATISFIED are you with your CURRENT sleep pattern? 9. How NOTICEABLE to others do you think your sleep problem is in terms of impairing the quality of your life? 10. How WORRIED/DISTRESSED are you about your current sleep problem? 11. To what extent do you consider your sleep problem to INTERFERE with your daily functioning (e.g. daytime



Trouble concentrating on things, such as reading the newspaper or watching television?

At Cleveland Clinic the process for motivating behavior change for employees and dependents involves five components. Experience with our own employees and other employee populations we have worked with and either failed or succeeded indicates all five components are needed to both get the change and sustain changes in the Big 4 plus 2.17 These five components are: 1. Ah Ha moments and culture change. The first step, and probably the most important, is to change the culture (or reinforce it) to a culture of health. The imperative for seeking wellness—the Big 4 plus 2—both in your life, and motivating it in your employees is that well-being is a huge cost saver, and also increases productivity and competitiveness. That point has to be and is made repeatedly by our CEO, Toby Cosgrove, and by the CEO of every company that we have worked with that succeeds in getting its employees to embrace and sustain wellness. Each employee’s job includes a responsibility to all other employees to be healthy, because the corporation’s ability to survive, compete, and have jobs is dependent on each employee’s well-being. (And by the way, your health status is the biggest influence on outcome—how long you’ll be disabled and how much suffering you’ll have—after medical procedures, illnesses, and events.) It is important to give examples of employees at various job sites with either live or on video on the web testimonials who have gotten a health “Do-Over”. And similar examples of Do-Over’s are repeated monthly in

Feeling bad about yourself or that you are a failure or have let yourself or your family down?



Poor appetite or overeating?

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Section 2: Evaluation of the Voice and Larynx

a 3-minute vignette so each employee knows that “If that guy can get healthy and feel great again, I can too”. The “Do-Over” is repeated so that employees realize almost all can get a do-over, and almost all can feel better for the long run. Establishing a “culture of health” is the most important of the five steps for a healthy, productive workforce that loves their work and their employer. 2. The second is to change the environment such that it expects, supports, and sustains well-being. The box of “Chip Ahoys” is too strong an addictive force to have in your home or office. If you have it nearby you will be tempted by it and the additive components of saturated fats, salt and sugar will lead you to consume it and overwhelm any hope of discipline sooner or later. 3. It takes socialization buddies, spouses, or coaching programs and other programs like Stress Free Now and Go to Sleep as well as social media to help people who are ready to make the change and to sustain the changes they have made. 4. You need a care program that is medically adjudicated— someplace you can refer the person and the patient to help those with chronic disease get to what we call 5 normals plus 2. The five normals include: a. Normal blood pressure b. Normal waist for height (the waist should be half of the height or  66% of the frames of the glottal cycle is in the open position. Closed-phase predominates is rated when > two thirds of the frames of the glottal cycle is in the closed position.

Phase symmetry is defined as whether the each vocal fold is a mirror image of the other. Normal vocal folds should vibrate together with a mirror image between the right and the left vocal folds. When the vocal folds are not vibrating in phase, it results in a less efficient flow converter and oscillator and will result in an open-phase relationship. When this happens, the vocal folds are said to lack phase symmetry. Phase symmetry is easy to detect when one vocal fold seems to open before the other. Figure 18.16 shows the left vocal fold is opening while the opposite has not yet opened. Later, the opposite vocal fold is opening while the right fold is already closing (Fig. 18.17). This gives the vocal folds a snake dance lateral to medial oscillation to vocal fold motion. Normal phase symmetry is when both vocal folds open and close together and are vibrating with the middle

Chapter 18: Stroboscopy and High-Speed Video Examination of the Larynx

213

Fig. 18.16: Example of lateral to medial phase shift asymmetry. This photograph in this illustration show left vocal fold opening with a prominent mucosal wave. The right vocal fold has not yet opened.

Fig. 18.17: This is the same patient as shown in Figure 18.16. The glottal aperture has shifted to the right as the right side is now opening while the left is closing. This phase shift is occurring in the lateral to medial direction.

of the vocal fold as having the greatest amplitude. Out-ofphase vibration is when one vocal fold is in the open phase while the other is in the closing or closed phase. Lateral to medial phase shift is most commonly seen in tension and mass effects oscillation, phase shifts can occur in the lateral to medial, anterior to posterior, or superior to inferior directions. Phase asymmetry or phase shift abnormality refers to vocal fold vibrations that are not in keeping with expected vibratory behavior of the normal. This creates inefficiencies in the vibratory pattern that may contribute to subtle complaints such as a veiled voice, vocal fatigue, and lack of projection. These changes should be systematically evaluated. They all contribute to an open-phase pattern with a short closed phase. The most obvious phase asymmetry is the patient with a lateral to medial phase shift. In this pattern, the vocal folds are not mirror images of the other. The vocal folds vibrate with a phase lag. While one fold is opening, the other is closing. This can occur in patients with vocal fold paresis, scar or stiffness. Usually, the side that is more pliable will open first while the stiffer or more massive vocal fold will follow. Phase abnormalities can occur in the lateral/medial direction or the anterior/posterior or superior/inferior directions. In the lateral to medial phase shift, the opening and closing will result in the vocal fold shifting from side to side like a snake dance. When one vocal fold is in the open phase while the other is in the closing or closed phase, it creates an impression of the fold opening shifting from side to side. Anterior to posterior phase shift occurs when

the vocal folds open from back to front as if peeling open as in a zipper opening. Usually, there is a posterior chink associated with this finding. This is the posterior to anterior phase shift pattern. In the final phase asymmetry pattern, the vocal fold on opening or closing will appear erratic. The vocal folds will appear to jerk open and close. The smooth opening and closing of the folds will be lost. The fold may even open, pause, and then open again, giving the impression of an alternating pattern of opening and closing. This is usually associated with edema, or stiffness of the folds. Configuration of Glottis Closure: Vocal folds are judged at their most closed phase. The seven most common types of vocal fold confi­gurations will be discussed. Normal complete closure is present in males and females. At the most closed, the vocal folds come into contact along the membranous portion of the vocal fold. Some subjects have a small posterior glottis chink present between the vocal processes of the arytenoids and a glottis chink may be present between the arytenoids. This should still be rated as complete closure as its presence is common in males and females. Figure 18.18 is a mon­ tage of a normal female phonation. Notice there is a small gap between the vocal processes. Midcord gap is the glottis configuration if there is incomplete closure at the midmembranous fold. This is also sometimes noted as vocal fold bowing. The folds never come into complete contact in the midmembranous portion. This pattern is seen most often in presbypho­nia

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Section 2: Evaluation of the Voice and Larynx

Fig. 18.18: This shows normal glottal configuration of complete closure in a female. Despite a small posterior gap between the vocal process, membranous vocal folds are in contact and this is considered completely closed.

or vocal fold paralysis or paresis but may be present in patients with vocal scarring. Figure 18.19 is a montage of a patient with vocal fold bowing showing midcord gap. An anterior gap is different than a mid cord gap by being more anterior. This type of gap is often limited to just a small portion of the anterior membranous vocal fold and implies involvement of a limited portion of the vocal fold. The small gap may have a spindle-shaped appearance or may be elliptical in shape. This configuration is seen often in patients with sulcus vocalis, vocal scarring, or occasionally in patients with vocal fold paresis. Figure 18.20 is a male with scarring or sulcus on the left notice the very small anterior gap present on the montage of the glottal cycle. When there is only mid portion of vocal folds in con­ tact, the configuration is rated as hourglass, or mid­cord

contact. There is only midfold contact with a gap both anterior and posterior to the midfold contact area. The hour-glass appearance will be more pronounced if the midmembranous area is thicker and irregular. Hourglass configuration is usually symmetric, but sometimes the hourglass is more pronounced on one side. When the area is not thickened, there is no hourglass appearance, only the presence of midfold contact. Sometimes, only a small bridge of mucous is present at the midmembranous area. When the hourglass is very obvious, it is the typical appearance of vocal fold nodules. Figure 18.21 shows the configuration of a midcord contact pattern. When the hourglass is asymmetric, this may imply the presence of a polyp with a contralateral reactive nodule. The curvature of the hourglass can give one a hint as to the degree of vocal fold thickening. In some subjects, early formation

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Fig. 18.19: This is a video montage of an elderly male with vocal fold bowing and atrophy. The glottis configuration shows a midcord gap at the most closed frame.

of nodules is shown by the midcord contact pattern but without the actual nodules being present. This has been called prenodules or a nodular diathesis configuration. When the closure shows an irregular line of the glottis during maximal closure with incomplete contact, the rating on configuration is irregular. Masses of the vocal fold are the most common cause of irregular contact. The irregular edge may be smooth as in polyps and cysts or may be rough due to cancer, leukoplakia, or papilloma. Figure 18.12 is a montage of the irregular closure with one side smooth and the other irregular. The irregular side is due to cancer. 18.11 is the video showing the irregular closing pattern. The closure has an irregular appearance with the side that is irregular touching the normal vocal fold only briefly. Irregular contact can also be present when the vocal fold is not straight due to an absence of

vocal fold tissue. This can occur if there is a notch in an otherwise straight vocal folds after biopsy or vocal fold stripping. The important aspect is the unpredictable and nonlinear shape of the vocal margin during contact. If there is a larger posterior glottal gap between the vocal processes or extension anterior of the gap to involve portions of the membranous vocal folds, this is called a posterior gap. Figure 18.22 is an example of a posterior glottal gap that is abnormal. A small posterior gap is often present in normal subjects, but the gap usually does not extend beyond the vocal process. When there is a significant triangular gap in between the membranous vocal folds that extends to approximately one third the length of the vocal folds during complete closure, this is rated as a posterior gap configuration. A posterior gap is often symmetric and common in patients with

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Fig. 18.20: This photo montage is of a male with left vocal fold bowing and stiffness suspected to be due to a sulcus formation. Notice the spindle-shaped anterior glottis gap.

Fig. 18.21: This photograph shows the vocal fold of a female with early vocal fold nodules. The configuration is an hourglass appearance.

muscle tension dysphonia. It may be present in patients with glottal incompetence due to vocal fold paresis or paralysis. When vocal folds never come into contact, the rating of glottis configuration is rated as incomplete. Figure 18.11 is a glottal cycle that never closes and come into contact. This is a patient with vocal fold paralysis. The vocal folds are incompletely approximated and the air escape is usually large with a breathy voice quality. Usually, the gap is present along the entire membranous vocal fold. The vocal folds never contact along the entire length of the vocal fold. Usually, the gap is large and the gap extends across the span of the glottis. This is seen in patients with high vagus nerve paralysis and in patients after iatrogenic trauma due to intubation or after laryngeal fracture. Amplitude of vocal fold oscillation is rated at modal pitch and loudness. It is rated for each vocal fold. The

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Fig. 18.22: This female has an excessively large posterior glottal gap with short closed phase. This was attributed to muscle tension dysphonia.

amplitude of vocal fold vibration is the degree in which each vocal fold moves laterally in response to subglottic driving pressure. The greater the driving pressure, the greater should be the degree of lateral excursion of each vocal fold. If the vocal fold has different stiffness, mass, or tension, each vocal fold will respond differently to the driving pressure and may show asymmetry of the vocal fold vibration. The amplitude of vocal fold motion of each vocal fold should be the same as the other. When there is an abnormal loss or increase in amplitude, it is evalua­ ted as to whether it is unilateral or bilateral. Unilateral loss in amplitude suggests isolated stiffness or mass effect. Bilateral involvement suggests diffuse stiffness, inflamma­ tion or an increased in effort resulting from excessive muscle tension. Figure 18.23 is a female singer with acute laryngitis. There is reduced amplitude of vibration from

both folds due to acute edema and erythema. Figure 18.24 is a patient with unilateral cyst, and it shows loss of ampli­ tude unilaterally on the side of the cyst. Normal amplitude of vocal fold vibration depends on the driving pressure of the lungs and the loudness. With modal phonation, approximately one half to two thirds of the width of the midmembranous vocal fold should lateralize. With loud phonation, the degree of lateral movement should become greater. Reduced vibratory amplitude is when there is less than the expected degree of lateral excursion. This is more obvious if one side is normal and the other is reduced. Reduced amplitude can occur with patients with mass or stiffness of the vocal folds. Zero amplitude of movement is when there is no visible movement with any effort. This usually implies a board like vocal fold edge seen in severe scar or tumor.

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Fig. 18.23: Acute laryngitis resulting in bilateral reduction in vibratory amplitude.

Fig. 18.25: Soft vocal fold fusiform polyp on the right fold shows us as a reduction in mucosal wave propagation.

The traveling mucosal wave is rated next. Mucosal wave is rated for each side. The mucosal wave is generated by deformation of the superficial layer of the lamina propria (SLP) and depends on its propagation on the water like properties of the SLP. It starts from under the vocal fold edge and propagates across the curved surface of the vocal fold. It is usually propagated across the membranous vocal fold at the same time as the vocal fold is beginning to open and lasts through the opening and closing phase of the vocal fold. Therefore, it is different from the amplitude of the vocal fold oscillation. The mucosal wave is the most subtle and most sensitive of indicators for subtle dysphonia. The mucosal wave is an indicator of

Fig. 18.24: Unilateral mucous cyst on the right fold has caused reduction in amplitude of vocal fold vibration compared with the patients' left fold.

the pliability of the superficial and intermediate layer of the lamina propria while the amplitude is reflective of the entire vocal fold cover and even the vocalis. Normal mucosal wave should look sharp and linear along the membranous vocal fold. It will propagate from below the vocal fold edge across the superior surface. In the female the mucosal wave may be less obvious than the male. A reduced mucosal wave may be present in only one part of the vocal fold. This will result in the wave going around the area of localized absence of the wave much as a traveling tide or wave will go around a rock in the ocean. When the vocal folds are swollen there may be loss in mucosal wave along the entire edge involving both sides. This may make the vocal fold vibration look erratic with a rocking motion. The fine crisp details of the edge of the wave are often absent. Mucosal wave proper­ ties change with the rheology of the vocal fold cover. The stiffer the mucosa, the less marked the wave. The greater the subglottic pressure, the more marked the mucosal wave. This is useful in study of patients with vocal fold scar. Figure 18.25 shows the difference in mucosal wave pro­pagation in a singer. Her left fold is normal and one can see the crisp light on the edge of the fold indicating the mucosal wave. The opposite fold has a soft polyp and the mucosal wave is indistinct. Figure 18.26 is a video montage of a patient with vocal fold scar. The normal side clearly shows a beautiful propagating wave across the superior surface of the vocal fold. The scarred side is red and devoid of a mucosal wave. By using a loud glottal sound, any mucosal wave differences will be accentuated.

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Fig. 18.26: Video montage of a patient with vocal fold scar. The mucosal wave is absent and is accompanied by loss of amplitude, poor closure, and open-phase dominant pattern.

Mucosal wave is a very good indicator mucosal health. When there is dryness or mucosal injury, the surface mucosa is the first to show changes. The mucosal wave propagation is uneven and sluggish. Nonvibrating segment does not always need to be noted but should be evaluated if the patient has a rough voice quality and scar or stiffness is suspected from the rating of the vibratory amplitude and wave. A nonvibrating segment of the vocal fold is an area of vocal fold that fails to show oscillation. This is rated as present or absent. The normal vocal fold should show event vibration along the length of each fold. Areas of scar and stiffness or mass may show areas of isolated vibratory amplitude and mucosal wave. 18.13 shows an example of a nonvibrating segment after cancer resection.

Interpretation and Synthesis of the Voice Disorder Based on Videostroboscopy Interpretation of the vibratory characteristics of the vocal fold is often the basis for understanding the vocal behavior. From this, one can often deduce the cause of the voice disorder. In this regard, some observations of vocal fold vibration are more clinically relevant than others. This will be discussed next. Organic dysfunction of the vocal folds that result in stiffness, mass, or tension may affect the vocal fold on one side or both sides. The observation of symmetric loss versus asymmetric loss in amplitude and mucosal wave often serves as a key differential in the diagnosis. Symmetric loss of mucosal wave and amplitude may occur in inflammatory

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Section 2: Evaluation of the Voice and Larynx

and infiltrative conditions that affect both folds while unilateral loss brings on a different list of differential dia­ gnosis. Symmetric loss due to mass or stiffness may be due to edema, infection, radiation, or reflux related scarring. Asymmetric loss in amplitude and mucosal wave implies a more localized abnormality affecting the side with the loss in amplitude or wave. A mass inside the fold or on the fold will result in loss in amplitude of vocal fold vibration and propagation of the mucosal wave. Stiffness due to isolated scarring after surgery or vocal fold injury will result in asymmetric loss of amplitude and mucosal wave. Asymmetric tension due to unilateral recurrent nerve or superior laryngeal nerve paresis or paralysis may result in differences in amplitude and mucosal wave. This may be seen on stroboscopy as a flaccid fold or as chaotic vibration. One of the more subtle findings of vibratory asymmetry in patients with vocal fold paresis is the lateral to medial phase shift. This can occur if the vocal folds have asymmetric tension or if the paretic vocal fold is on a lower plane. 18.14 is a video segment of a patient with paresis. The lateral to medial phase shift results in an open-phase dominant pattern with short closing time and a lateral to medial phase. Asymmetric phase shift results in an openphase dominant pattern with short closing time. When vocal fold vibration breaks down, it is remark­ able how they follow similar patterns. The common path­ ways of vocal efficiency breakdown can be summarized by noting the changes in configuration, closure, phase, phase asymmetry, amplitude, and mucosal wave. These are features that can be rated by examination using stro­ boscopy. Pathological changes in vocal fold vibration results often in incomplete closure with abnormal glottis configuration, unilateral or bilateral loss in amplitude, open-phase dominant pattern, and irregular vibration that makes tracking of the fundamental frequency difficult. These features are most important. Additional details that could be analyzed are more subtle and may contribute to voice insufficiency symptoms such as vocal fatigue, effortful phonation, and lack of vocal brilliance. More subtle and perhaps more challenging for the beginner to evaluate on stroboscopy include the findings of phase asymmetry, crispness of the mucosal wave, and a presence or absence of a nonvibrating segment. It is usual for the surgeon in performing phonosurgery to be able to re-establish the major features of better function such as improved glottis configuration, closure, better amplitude, and better closed phase. It may not be possible to establish all the features of a normal stroboscopy with surgery such as perfect mucosal wave propagation and phase symmetry.

Synthesis of the cause of voice disorder is based on the history, the physical examination, and radiographic and operating room findings. Stroboscopy is only one aspect of the physical examination that gives some insight into the vocal fold vibratory behavior. From the physical examination, evaluation of the moving visual image of the vocal folds obtained from videostroboscopy is increasingly the key to making a diagnosis. In general, patients with voice abnormalities will present with vibratory abnormalities. For example, patients with organic voice disorders such as carcinoma, laryngeal papilloma, and scar will have discreet tissue abnormalities that interfere with vocal vibratory function. Patients with abnormal voice production secon­ dary to functional voice disorders will present with abnor­ malities of vocal vibratory function but may look normal on constant light examination of the larynx. Patients with muscle tension dysphonia, phonasthenia, and voice abuse will also present with abnormalities in their vocal vibratory function. The expert laryngologist will know what to elicit in the stroboscopic examination. Because both organic and functional causes can affect vibratory behavior, it is logical to expect interactions between the two and to expect component of both in most patients with voice disorders. Thus, patients with vocal fold scar will often exhibit muscle tension dysphonia pattern with pres­ sed phonation and false vocal fold squeezing. Similarly, patients who habitually abuse their voice may result in mucosal lesions that may be classified as organic in nature. Polyps, nodules, and vocal fold granulomas are just some of the organic lesions seen on the vocal fold that may have as a basis functional voice disturbance. The clinician must weigh the evidence for each component and have a plan to manage both components to be successful. In many cases, both functional and organic lesions may present simultaneously. It is the role of the clinician to tease out the multiple issues and determine the primary and secondary diagnosis. By incorporating the visual evidence with perceptual and acoustic aerodynamic data, the clinician can better synthesize the cause of the voice disorder. By the careful assessment of vibratory function before and after treatment, the clinician has a powerful tool in assessing function before and after treatment and gaining information on the effect of treatment on vibratory function. By direct observation, the presence or absence of lesions will decrease the uncertainty about the diagnosis. Observation of vocal fold closure will lead to improved understanding of phonatory pathophysiology. Independent verification of the diagnosis and judging the

Chapter 18: Stroboscopy and High-Speed Video Examination of the Larynx results of medical and phoniatric therapy is easily done by clinicians. For the surgeon, the visual feedback of vib­ ratory function restoration will reduce the learning curve in doing better microlaryngeal surgery. Stroboscopy observation alone is not a substitute for clinical knowledge. The limits of stroboscopy should be realized. Because stroboscopy depends on a quasiperiodic source, not all dysphonic patients are good candidates and can benefit. In general, stroboscopy should be consi­ dered for the professional voice user with mild dysphonia. The patient with mild to moderately veiled, breathy, or rough voice will usually demonstrate good information from the stroboscopic examination. The patient with low gag and a > 5 seconds of phonation time will be more easily examined. Finally, the patient should have some insight to follow commands to generate voice at the requested frequency and amplitude for approximately 5 seconds so the stroboscopy effect can be recorded. The poor candidate for stroboscopy will be the patient with severe dysphonia where the lesion may obscure the vocal fold. In the elderly patient and the very young patient with poor insight or cooperation, a stroboscopic examination may not yield great dividend. Finally, the patient suspected of having neurological diseases such as vocal tremor, spasmodic dysphonia, or movement disorders may need fiberoptic examination with stroboscopy rather than focusing on the vibration alone to establish the appropriate diagnosis. On Table 18.9 is listed the specific assessments that are easier using stroboscopy. Stroboscopic examination should be done in patients with prior surgery, where the patients history does not fit with the referred diagnosis, in those patients with failed speech therapy when applied faithfully, where visual documentation is needed before or after surgery or other treatments, and when there are multiple diagnoses being considered in the differential. Table 18.9: Specific assessments made easier by stroboscopy

•  Mucosal hygiene •  Stiffness and mass of vocal fold cover •  Areas of nonvibration/scar •  Mature versus early nodule •  Nodular diathesis •  Understand vocal fatigue •  Hyper- and hypo-function •  Return of vocal fold pliability after surgery, voice rest •  Detection of lesions previously missed

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While stroboscopy is the most practical tool for clinical evaluation of vocal fold vibration, the standardization of the interpretation continues to be difficult. Not all raters will have the same criteria. Judgments on stroboscopy features continue to be subjective. Interpretive bias is possible and may be common. What is relevant and what is not from the stroboscopic examination need more inves­ tigation. For some, the videostroboscopic examination is easy to perform but difficult to interpret. This is because there is a wide variety of phonation gestures that may be recorded. While standardization of the token is helpful, it is difficult to do in the moderate to severely dysphonic patient. Therefore, the interpretation of videostroboscopic examinations continues to be qualitative and based on the experience of the examiner. This will not be likely to change soon unless standardization of the recording token can take into consideration the subglottic pressure, air­ flow rate, phonatory register, loudness, and frequency. It would be highly doubtful whether pathologic larynxes can be forced into a standardized protocol that is based on normal phonation. In the absence of such uniform, objective, measures, qualitative interpretation of the stro­ boscopic examination will continue to be the standard.

AVOIDING THE PITFALLS OF STROBOSCOPY It probably takes several hundred examinations and inter­ pretations over years of practice in order for the experien­ ced videostroboscopy rater to consistently evaluate more complex videostroboscopic examinations. Complex stro­ boscopic examinations usually involve patients with subtle dysphonia with possible inconsistent findings. Unless the endoscopist has had multiple years of experience interpreting the results of videostroboscopy, the problem of over interpretation and under interpretation of the stroboscopic findings is common. Lack of experience in the interpretation of stroboscopy can affect the results even in large centers where there may be a variety of examiners doing the interpretation. One method to overcome this inconsistency is to use a rating tape for training. Test and retest for consistency of interpretation before and after the training can be used to ensure consistency of inter­ pretation. Over-interpretation of abnormalities may be done if a stroboscopy feature may be a normal variant. A good example of such is the presence or absence of small posterior gaps. The wrong position of the scope or inter­ pretation of a wrong token can also generate an erroneous

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impression of abnormal function. For example, if the scope is not centered over the larynx, one vocal fold will appear to be higher than the opposite vocal fold and the phase shift abnormality may be present if the vocal fold is being visualized from one side. The range of normal vocal behavior is quite wide. This can result in a normal larynx exhibiting pathologically abnormal vocal fold vibration. This may be interpreted as abnormal only if a small token of abnormality is captured for analysis. When presented with brief tokens of pathologic vocal fold vibration, the interpreter may be tempted to call such examinations abnormal if the full range of vibration is not sampled. A good example is the rating of a falsetto voice as being open-phase dominant pattern. A careful clinician will then tell the subject to change register and evaluate the modal voice and not base the interpretation on a high falsetto voice. Under interpretation of the videostroboscopic exami­ nation can occur if only standardized tokens are used to explore the larynx. Since some patients with very subtle abnormalities will exhibit phonatory abnormalities only at soft phonation or specific pitch range transitions, full exploration of the entire phonatory range is mandatory prior to a conclusion that the phonatory apparatus is normal. One example where more in-depth exploration is necessary is in the patient with a veiled voice quality that is not accompanied by any gross abnormality of the vocal fold edge. In these cases, exploration of the phase of vocal fold vibration must be performed in relationship to the phonatory frequency and loudness. A subject that is using great effort and still has the vocal folds in openphase dominant pattern is probably experiencing glottal incompetence. A female subject with a fundamental fre­quency of 190 Hz may not be abnormal if that is her habitual pitch; it would be pathological if it is a sudden change due to masculine hormone intake. To avoid error, the examination should be repeatable and be consistent. Since videostroboscopy is an optical illusion created from fusion of multiple flashes of light distributed over many glottal cycles, data regarding the opening and closing patterns can be considered to be representative of the vibrating vocal folds if they can be repeated from cycle-to-cycle. In the interpretation of vibratory abnormalities, the same vibratory abnormality should be present over many glottal cycles at the same frequency and amplitude. If these abnormalities cannot be observed consistently, the interpretation of the data should be considered suspect. When the vibratory pattern

is very chaotic due to a severely disordered voice, inter­ pretation of stroboscopy may not be possible as steadystate oscillation cannot be accomplished by the subject. In these cases, it may be better to simply note the presence of severely disordered voice that prevents stroboscopy interpretation. Vibratory abnormalities that are transient in nature will be difficult to capture using stroboscopy. The ear may pick up an abnormal sound, but the videostroboscopy may not show a vibratory abnormality. This may be one of the advantages of high-speed video. Recording the patient using the wrong register will result in a not very useful stroboscopic examination. The recording of modal voice should always be performed first. It is by convention the most common register during sustained speech. It also demonstrates the body and cover of the vocal fold during vocal fold vibration at its best. If the patient habitually phonates at a falsetto, the patient should be instructed to change his phonation mode to a chest register for the examination. This is because inter­ pretation of phonation produced during falsetto will be always abnormal relative to the standards used for inter­ pretation of modal phonation. Therefore, if the strobo­ scopic examination is performed while the patient is producing vocal fry or falsetto, very limited information can be derived as to the vibratory capability of the vocal fold relative to normal. Other than stating that the voice is habitually produced at falsetto or vocal fry, the inter­ pretation as to stiffness or mass effect cannot be performed if the interpretation is based on phonation tokens done using vocal fry or falsetto gesture. The simplest tokens used for stroboscopy is the four token samples of modal phonation, high phonation, low phonation, and loud phonation. However, in vocal exploration using imaging, there are other aspects that may be necessary. The examiner may need to do fiberoptic laryngoscopy with the stroboscopy light. Fiberoptic laryn­ goscopy using stroboscopic light has become much better with the advent of the distal chip scopes. In some explorations of the voice, flexible laryngoscopy exami­ nations using strobe light is preferable to rigid endoscopes. Voice exploration with stroboscopy does not force the patient to produce the expected token but looks at the naturalistic methods of the patient for voice production. In this way, functional abnormalities and compensatory adaptive changes of the vocal tract may be identified easier than with rigid endoscope imaging. Flexible fiberscope imaging should be considered for identification of muscle

Chapter 18: Stroboscopy and High-Speed Video Examination of the Larynx tension dysphonia, investigation of vocal fold paresis, and evaluation of hyper- or hypofunctional aspects of voice production. Specific evidence of muscle tension dys­pho­ nia is suggested by the presence of Coup de Glotte where there is prephonatory closure of the false vocal folds before voicing, isometric muscle tension with midcord contact in patients with early nodules and excessive false vocal fold compression with short vocal folds. Incomplete closure with a large posterior glottis gap is another sign of functional vocal function. Paradoxical vocal fold shor­ tening with pitch elevation, abnormal laryngeal posturing with pitch and amplitude adjustment, large posterior chink, hourglass configuration with short thick vocal folds are other configuration changes in patients with muscle tension dysphonia. Hypophonia with poor breath support is suggested by the presence of a long open phase with a glottis gap.

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Figure 18.27 is a video montage of the glottal cycle of a patient with vocal fold nodules. The glottal cycle shows poor closure with and open phase. The open phase may be associated with vibration breaks with aperiodicity. This may be most obvious during register transition in singers (glide through the passage). Hypophonia due to vocal fold paresis may manifest as asymmetric tension showing up as a phase shift in the lateral direction or in the poste­ rior to anterior direction. Patients with vocal nodules are a good example of where functional voice disorder may produce organic changes in the vocal folds. Differentiating between polyps with reactive nodule versus vocal fold nodules are helpful to the clinician as vocal fold polyps are more likely to respond to surgery followed by therapy while patients with vocal fold nodules are best treated by therapy alone. Patients with small vocal fold cysts are also sometimes confused

Fig. 18.27: Video montage of poor closing and hypophonia due to isometric muscle tension dysphonia. Notice the subject has bilateral vocal fold masses.

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Fig. 18.28: Bilateral keratosis with midfold redness is associated with voice abuse and overuse in this patient with poor vocal hygiene, muscle tension dysphonia, and hyperkeratosis. There is severe redness with loss of vibration, amplitude, and mucosal wave over the midfold swelling.

with vocal fold nodules when viewed by stroboscopy. 18.15 is a video of a left vocal fold cyst. The glottal configuration suggests vocal fold nodules due to midfold contact. The amplitude on the patient’s right shows a mass effect with reduced amplitude and wave. This patient has a mucous cyst. Figure 18.28 shows a patient with severe laryngitis with bilateral keratosis on the both vocal folds in a patient with habitual voice abuse and overuse. The stroboscopy findings show loss in amplitude and mucosal wave along with redness and stiffness over the red swollen vocal folds. Vocal fold nodule in its earliest form will have midcord contact pattern with little thickening. There may be only a persistent collection of mucous at midmembranous vocal fold. There may be isolated sym­ metric loss of amplitude and wave with localized edema at the nodal point. The nodal point being the point of maximal vocal fold oscillation. While soft nodules have excellent amplitude and may be the voice may sound normal, the glottis configuration suggests inefficiency as there is incomplete closure with an open-phase dominant pattern. Hard nodules have a thicker keratin thickening at the nodal point and look like an hourglass during maximal closure. The vocal folds do not vibrate well at the nodule site. When the lesions are fibrotic, they have a mass effect and the amplitude and mucosal wave will be lost. The fibrotic nodules may still show some vibration, but the mass will rock back and forth much like a ship will roll on an ocean with a traveling wave underneath the mass.

Surface lesions such as nodules and hyperkeratosis or leukoplakia should be differentiated from mass lesions deeper to the epithelium. This is because the surgical aspects of treatment differ as is the differential diagnosis. Deeper lesions such as cysts, sulcus vocalis, and fibrovascular deposits have different surgical approach and are most often treated by cordotomy and microflap excision. Vocal fold cyst presents with the patient complaining of a husky veiled voice quality. The high notes and register transition are most affected. When viewed with constant light, the larynx and vocal folds may appear normal when the cyst is small. When they are larger the differential diagnosis includes vocal fold nodules, vocal fold polyp, and vocal fold edema. The key stroboscopy sign is asym­ metric loss in mucosal wave and asymmetric loss in vibra­tory amplitude ( 18.17). The white epithelial lined keratin cyst and the yellow mucous cyst have a ‘pea in a pod’ appearance with a mass effect that causes rocking of the affected fold. The site of vocal fold involvement is in the superficial and intermediate layer of the lamina propria. In the subepithelial plane, the result of the cyst and reaction may result loss of layered vocal folds with fibrosis with inflammation. Occasionally, there is a dimple or cyst opening that raises the question of a sulcus. Cysts that are small or may have ruptures can also have reactive nodule on the opposite side and may be difficult to differentiate from nodules. Figure 18.29 shows a video image of a patient with a left-sided cyst and a right-sided nodule. The nodule is on the surface while the cyst swelling is on the superior surface of the vocal fold and is deep inside the fold causing a fullness of the affected vocal fold. Sulcus vocalis is another condition that results in loss in amplitude and mucosal wave. The histopathology of sulcus is that of a vocal fold groove with loss in layered structure of the vocal fold. Frequently, the vocal ligament is attached to epithelium. Figure 18.30 is a still photo of a sulcus formation on the right vocal fold. The depression on the right is clearly different than the sulcus formation. Sulcus can be difficult to detect even with stroboscopy and sometimes are only found at the time of microlaryngoscopy. The lining may show focal keratosis, acanthosis, and dyskeratosis. The thickening involves all layers of vocal cover. The patient presents with a rough, stained, and sometimes breathy voice loss. The classic description of the configuration of sulcus vocal is a spindle-shaped glottis closure pattern. The groove may not be visible but suspicious findings for a sulcus include a spindle-shaped vocal fold closure, asymmetric loss of vibratory capability, and loss of mucosal wave. There is

Chapter 18: Stroboscopy and High-Speed Video Examination of the Larynx

Fig. 18.29: Vocal fold nodule is present on the patient’s right vocal fold. The left vocal fold shows fullness with a white cyst in the midmembranous fold.

reduced vibratory amplitude and wave over the site of the sulcus. The asymmetric loss with loss of amplitude and wave on side of sulcus should make the clinician suspect a sulcus or scar. Sometimes sulcus can only be definitely identified at the time of surgery by palpation.

SUMMARY Videostroboscopy has become a tool most clinicians can apply in their evaluation of their patients. From a practical perspective, today, the dysphonic patient can have a high-quality video examination of the vocal fold vibratory function that can be stored and compared across time. The challenge is no longer how one can get a sample of the patient’s phonatory behavior but what does this sample mean in the interpretation and synthesis of the voice disorder. By systematic study of the normal vibratory function and by standardization of the token for study, the beginner has a powerful tool in understanding of vocal pathology. Stroboscopy is now the standard of care and no longer the state of the art in the management of the patient with voice disorders. By systematic study of disordered function, the practitioner will come to a wellbalanced qualitative assessment of vocal function based on experience that does neither over nor under rate the pathological condition from the normal. By using the stroboscopy data with the history, physical examination and the added information from radiography and operative examination, the clinician can better synthesize the cause of the voice disorder and formulate appropriate treatment.

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Fig. 18.30: Right vocal fold sulcus is seen on this video still. The sulcus can only be seen when the upper lip of the fold is in the open position while the lower lip is closing. This is best shown by having the patient phonate in a low loud chest register.

HIGH-SPEED VIDEO IMAGING Compared to clinical applications of stroboscopy, highspeed imaging in clinical applications can be considered to be still novel. It is still uncommon in most practice to see high-speed video in the clinic. It is, however, a viable and exciting new technology that can be used to investi­ gate voice disorders. Prior to high-speed video technology, observation of high-speed images of vocal vibratory behavior was only available by using cinematography techniques. The high-speed imaging technique allowed the investigator to look at each individual glottal cycle by using frame capture rates that are high enough to look at all the details of the vibratory behavior of the fast vibrating vocal folds. The use of high-speed image by cinematogra­ phy was already published in 1936.5,6 Moore published multiple papers on investigation of vibratory function of the normal vocal folds starting in 1937.7,8 These were based on laborious work of frame-by-frame analysis of the highspeed cinematography images. From their investigation, much of the understanding of the normal glottal cycle was able to be understood. Investigation of abnormal vocal fold vibration was limited.74,75 These studies showed that vibratory abnormalities occur as asynchronous vibrations between the two folds and chaotic vibrations can result as a result of interactions between the two folds. The clinical applications using high-speed imaging were not applied due to cost and lack of perceived advantages in the clinical care of patients. It was not until the 1980s that high-speed imaging was again considered. The lower cost and rapid

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improvement in CCD in digital imaging systems have made the digital cameras practical for laryngeal imaging. The development of a clinical commercial system based on high-speed image acquisition camera coupled to an endoscope has made high-speed imaging available to all clinicians interested in recording high-speed vibration of vocal fold function. Today, commercial systems can be obtained color high-speed images of 2000 frames per second at 512 × 512 resolution. The sampling of the vocal fold images have increased with technology such that eight seconds of high-speed images can be stored for analysis. High-speed imaging of vocal fold vibration and clinical applications is now readily available within the time and cost constraints of a clinical practice.16,17 High-speed imaging devices depend on digital capture and writing of data to disc using a CCD. The frame rate sufficient to resolve vocal fold vibration is typically 2000 to 4000 frames per second. The resolution per pixel has increased from 8 bit to 12 bit to some 16 bit resolution. Such high resolution rates and video rates come at a cost of large amount of data with massive amounts of data written to disk. The better the resolution, the larger the amount of data for the same amount of time recording of the vocal folds. With high frame rates, the sampling time of the phonatory token must be limited. Typically, four to eight seconds of sampling time is done. Since recording is usually done to a frame buffer, the video data are first recorded, then reviewed to see if the high-speed capture is representative of the vibration of the vocal fold of interest and then stored to disk. Analysis is laborious as playback is done at 20 to 30 frames per second while capture is done at 4000 frames. Thus, to review a two-second video done in high speed captured at 2000 frames per second, a reviewer will take100 second to review the video just once! Practically, in the clinical situation, there must be some compromise as to who should receive high-speed video examination and what parameters are worth reviewing. Despite excellent systems available for clinical recordings, a consensus for the parameters for clinical indications and interpretation of high speed imaging are still lacking. The following discussion is just one view of practical applications of high-speed video in clinical applications by the author over the last 13 years. The deficiencies of using a videostroboscopy for imag­ ing of vocal fold vibration are outlined in Table 18.10. Stroboscopy is based on the assumption that the vibra­ tion of the vocal folds is stable and regular. Irregular vibrations, which are common in voice pathology, cannot

Table 18.10: Features of vocal fold behavior not able to be imaged with stroboscopy

•  Voice breaks •  Diplophonia •  Vocal function during voice onset and voice offset •  Vocal tremor and spasms •  Extremely rough voice quality •  Alternate laryngeal and pharyngeal sources of oscillation

easily be studied and described in a reliable way. Because video­stroboscopy depends on quasiperiodic vocal fold oscilla­tion, many features of the phonatory gesture cannot be visualized. High-speed video overcomes some of the problems with stroboscopy. High speed imaging allows thousands of pictures to be taken of the vibrating vocal folds per second. Rigid endoscopes are normally used for highspeed video. After clinical investigation of the patient, kymography analysis from the video can be carried out off-line. In one clinical model, up to 8000 gray scale images of 256 × 256 pixels can be stored by the Wolf HS Endocam 5560. A maximum of 4000 images/s can be taken by the high-speed camera.76 Observations about laryngeal physiology using high-speed video was able to show that combining high-speed video with other measures such as electroglottography is very helpful in visualization of voice onset and offset, singing gestures, and extremely high phonation. Furthermore, analysis of various singing styles could be realized.77,78 Clinical report of high-speed video to identify diplophonia pattern consistent with vocal fold paresis was also reported as being important in identification of a patient with previously undiagnosed vocal fold paresis.79 Using kymography techniques, patho­ logical vocal fold motion after laryngectomy was com­ pared to the normal side.80 Voice onset differences in different glottal attacks as well as diplophonia could be clearly displayed on the digital kymogram. Furthermore, multislice kymography could be defined and displayed to check for phase differences between the sides.81 Review of the high-speed images can be done manually by looking at the high-speed video and slowing it down to 20 frames per second. This is tedious and brief breaks in steady phonation can be noted but is difficult to document. To compensate for this, the use of digital kymogram is usually used to display asynchronous anomalies as a display of the high-speed video.

Chapter 18: Stroboscopy and High-Speed Video Examination of the Larynx The initial application videokymography was the use of a line scanning camera.12 This used a line scanning camera scanning one line instead of the entire 256 lines of a video camera. This allowed high-speed sampling of a single video line. The initial impetus for videokymography is the same realization of the deficiencies of videostrobo­ scopy. Vocal fold vibration was observed with the aid of videokymography, during which images from a single transverse line can be recorded. Successive line images were shown in real time on a monitor, with the time dimension displayed in the vertical direction.13 Videoky­ mography, using a modified CCD-video camera, works in two modes: standard and high speed. In standard mode the vocal folds are displayed on a video monitor in the usual way, providing 50 images per second (or 60 in the National Television Standards Committee system). This is used for routine laryngoscopy and stroboscopic exami­ nation of the larynx. In high-speed mode (nearly 8000 images per second) only one line from the whole image is selected and displayed on the x-axis of the monitor; the y-axis represents the time dimension. This system enabled the assessment of left-right asymmetries, open quotient, propagation of mucosal waves, scanning camera using a single line can be placed on the area of interest of the laryngeal image and line scanning of that line is able to be achieved at high speed. This was initially reported by Svec and Schutte12 This was reported for routine laryngoscopic and stroboscopic examination of the larynx in clinical applications. In high-speed mode (nearly 8000 images per second) only one line from the whole image is selected and displayed on the x-axis of the monitor; the y-axis represents the time dimension. They reported that all vocal fold vibrations, including those leading to pathological rough, breathy, hoarse, or diplophonic voice productions can be observed.13 Videokymography was able to detect small left-right asymmetries, open quotient differences along the glottis, lateral propagation of mucosal waves, and movements of the upper margin. This method for data reduction from high-speed motion is to use multiple line kymography lines. In this technique, the video is acquired and high-speed mode. The line of interest across the midmembranous vocal fold at several sites is selected for DKG extraction and a video­ kymography plot is generated. This technique is more practical than the line scanning camera since the line of interest can be defined after the high-speed images have been acquired.82 Using multislice kymography, asymmetry and breaks can be compared and measured.81

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The images obtained by high speed can be analyzed in the same way as the stroboscopy image. The major advantage of high-speed images is that the images are real time and not based on a montage. Because the images are acquired in such brief period with steady light illumi­ nation, the images are very stable for image analysis. Our current applications of high-speed video is for: (a) evaluation of diplophonia and voice breaks, (b) assess­ ment of multiple oscillators in the airway, (c) study of voice onset in muscle tension dysphonia and spasmodic dysphonia, (d) study of tremor rate, and (e) understand­ ing of voice onset and offset problems in scar and stiffness.

Voice Onset and Offset Laryngeal movements and adjustments are seen before and after steady-state vocal fold oscillation. This may be a rich area of investigation and understanding of voice production. By studying the prephonatory vocal tract adjust­ments and the oscillatory behaviors of the folds before steady-state vibration, one can see many differences in normal and abnormal states. In the normal onset of voice from the abducted position of the vocal fold, there are several stages of voice onset that can be analyzed. First, there is vocal fold adduction with symmetric medial movements inward. The vocal pro­ cesses are adducted gently. This is followed by vocal fold oscillation. The events from the adduction of the folds into the phonatory position and before the beginning of vocal fold are termed the prephonatory set. The prepho­ natory set has a variable degree of movement, duration, and approximation. This is dependent on the loudness, the frequency, and the phonatory effort of the glottal attack. For example, a soft phonatory gesture is associated with onset of vocal fold vibration well before there is approximation of the folds. A loud phonation is associa­ted with more adductor effort, closer vocal fold approxima­tion, and supraglottic closure. At higher phonation, the folds are adducted in a thinner configuration with more sinusoi­ dal oscillation of the edges. An example of 18.16 shows phonation at 105 Hz and 79 db, whereas 18.17 shows the same subject phonating at 195 Hz and 83 db. The kymography analysis can demonstrate these changes better. This can be demonstrated on the DKG plot shown in Figure 18.31. On this figure, one can appreciate the edges of the vocal fold coming together and being approximated. The prephonatory set is the movement of the larynx into the position for the production of vocal fold vibration, while the phonatory position is the vocal folds

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Fig. 18.31: Digital kymography shows the midmembranous fold during voice onset of a patient with vocal fold paresis.

during the sustained phonation. The prephonatory set and the actual onset of vibration of the vocal folds may occur in an overlapping manner. With soft to easy onset of vocal fold gestures, there is no contact of the vocal folds before oscillation begins. Thus while the vocal fold is still being adducted and the vocal process is being placed into position, vocal fold oscilla­ tion has already started. Oscillation occurs with small oscillations and build to larger oscillations until a set configuration of vocal fold oscillation has been achieved. The number of cycles from just noticeable vocal fold vib­ ration to full steady state of vocal fold vibration can be called the voice onset phase of the voice token. Once the vocal fold oscillation is steady, quasi-pe­riodic vibra­ tions can be seen and one glottal cycle resembles the other. Thus, the events of sustained vocal fold oscillation from approximation of the vocal folds together to the achievement of steady-state phonation can be divided further into two parts. The first part being the appro­ ximation of the folds into the phonatory position to allow the vocal fold oscillation to begin, this is the pre-phonatory set portion of voicing. The second part being the number of cycles between when there is observed vocal fold

oscillation to a steady-state amplitude and phase that is quasiperiodic. This is the voice onset portion. When the steady state of vocal fold oscillation has been achieved, the phonatory cycle shows definable open and closed period with well-defined vibratory amplitude, mucosal wave, and open and closed quotient. The number of cycles of vocal fold oscillation, which is necessary before the achievement of full vocal fold oscillation is variable and appears dependent on factors such as frequency, loudness, and glottal attack effort. This will need to be better quantified. 18.18 shows the typical finding of onset of vocal fold oscillation during a vowel ‘ee’ for a chest voice in a male speaker. The phonation token is 105 Hz and the amplitude is 79 db recorded 6 inches from the lip. Notice the adduction occurs symmetrically, the slow ramp up of vocal fold vibration starts to occur before complete closure of the vocal folds. It usually takes 3–7 cycles of vibration before full steady state of vibration. During this voice onset time, the open phase is dominant and the amplitude is small. With each subsequent vibration, the amplitude becomes larger, and the closed phase is better defined. 18.19 shows the voice onset for a high-phonation token. Notice the vocal folds are thinner and vibrate as in a sinusoidal pattern.

Voice Offset At the end of the voice gesture, the vocal folds stop oscil­ lating slowly. The number of glottal cycles for this to occur is also variable. This slow declination of vocal fold oscillation is dependent on the stiffness and the mass of the vocal folds for the gesture and seems less dependent on cessation of flow by abduction. The declination of vocal fold vibration that occurs when the steady state is lost to complete cessation of vocal fold vibration can be termed the voice offset phase of that vocal fold gesture. 18.18 shows a male phonation from 105 Hz and 79 db to voice cessation. The number of cycles, which vocal folds take to stop vibration is greater in low loud phonation than in high soft phonation. This is due to mass and stiffness differences between the gestures.

Voice Breaks, Diplophonia, and Chaotic Oscillations A good clinical application of high-speed imaging is for investigation of voice breaks and vocal transients. Aperiodic vibrations of the vocal folds can result in voice breaks and if they occur in a repetitive cycle, is perceived by the ear as

Chapter 18: Stroboscopy and High-Speed Video Examination of the Larynx having a diplophonic quality. Aperiodic breaks can occur with either one fold showing failure or with both vocal folds showing loss of periodicity. This will be of interest to the clinician interested in stiffness or tension differences between the folds. The following will give some clinical examples of such. When the vocal folds are vibrating in phase, but the regular beats are interrupted by aberrant beats at a regular interval of every second, third, or fourth beat. This can occur with both vocal folds moving symmetrically as simu­lated diplophonia or in muscle tension dysphonia pattern. An example is shown in 18.19. In this example, the subject is simulating diplophonia and has achieved a subharmonic of vocal fold vibration by a repeating cycle every fourth cycle of a prolonged pause. This symmetric subharmonic of diplophonia is typical of the muscle tension dysphonia pattern. A second type of diplophonic vibration pattern can occur when there are two distinct frequencies of vibration from each fold. If the folds are vibration at slightly different frequencies, each vocal fold will vibrate at times in phase and at times out of phase to the other. This in and then out of phase vibration results in distinct subharmonic of vibration below the two vocal fold fundamental frequen­­ cies and is perceived as a lower frequency diplophonic sound. This is most commonly seen in patients with uni­ lateral vocal fold paralysis. 18.20 is a patient with left vocal fold paralysis. When the vocal folds vibrate each has a distinct frequency and this can be appreciated as two distinct vibrations. If a stroboscope was used to evaluate this pattern, only one frequency will be tracked and the opposite side will appear as a blur. These two distinct frequencies of vocal fold oscillation are due to different innervation resulting in different mass characteristics of the folds. The patients left fold appears flaccid and has a different frequency of vocal fold oscillation despite the same subglottic pressure. Sometimes, irregular vibration may be present with no steady frequency. This source of vibration may be from the opposite fold with a mass lesion, a stiff inelastic vocal fold or from other structures being moved in the air stream such as the arytenoid mucosa or the false vocal fold. Occasionally, the source is periodic and usually of lower frequency. This can be identified on high-speed imaging as another vibratory source. Subharmonics are created when there is regularly recurring acoustic spectral energy lower than fundamental frequency. Subharmonic vibrations can occur due to vib­ ration of vocal folds vibrating initially in and then out of

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phase with each other, thereby creating a amplification of the sound when the folds are vibrating in phase and then damping the sound when the folds are vibrating out of phase to each other low frequency vibration of masses other than vocal folds can create alternate sources of sound. The false vocal folds, the arytenoid mucosa or the pharyngeal mucosa may be sources of vibration that can generate either periodic or aperiodic sources of oscillation that can generate acoustic signals that dampen or amplify the glottis signal, creating noise or subharmonics. These changes all create a lower than fundamental frequency in vibration that contribute to the acoustic signature of subharmonics. 18.21 is the high-speed video show­ing the right vocal fold as normal while the left fold is stiff and vibrating at a lower frequency. As the folds vibrate, they come in and then out of phase to each other creating a subharmonic that is perceived as diplophonia.

Vocal Cord Paralysis Tension pattern is best seen in the patient with vocal cord paralysis. The vocal fold, which has greater tension, will tend to vibrate faster than the vocal fold, which is not innervated and therefore flaccid. The intrinsic coupling of the vibration between the vocal folds may result in each vocal fold vibrating in synchrony but this system may fall apart with inadequate breath support or adjustments of the supraglottic articulators. This will then result in two different frequencies of the vocal folds vibrating with the same subglottic pressure. The net effect of two different vocal folds vibrating at different frequencies is the creation of phase shifts as the vocal folds vibrate in and then out of phase at a predictable rates. Tension differences between two sides can result in two oscillators with different frequencies. As the folds vibrate, the fold may vibrate in and out of phase to the opposite fold resulting in diplophonia. Because of flaccid nature of the paralyzed side, the paralyzed side lags behind the normal innervated side in onset. The ramp up of the paralyzed side lags one or two cycle longer than the normal side. As the paralyzed side has lower tone, it may seem to be more flaccid and does not vibrate as a unit. The paralyzed side may have larger amplitude. There may be false vocal fold oscillation. In patients with vocal fold paralysis, the vibration may be too short or chaotic to visualize using stroboscopy. This can occur if the phonation time is short and sustained vibration is not possible. Some patients with vocal cord paralysis will present with aphonia or with perceptual

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Fig. 18.32: Digital kymography on this patient with vocal folds paresis shows contact with a phase asymmetry. There is short contact and open-phase dominant pattern.

diplophonia. High-speed digital imaging may show two separate frequencies of vibration for each vocal fold. 18.22 is a high-speed video of the voice onset and steadystate oscillation of a patient with left vocal fold paralysis. The vocal fold, which was innervated, vibrates normally while the paralyzed vocal fold follows the normal fold. This resulted in the vocal folds vibrating in and then out of phase. A good way to track this is by using DKG. When vocal fold recovers from paralysis, vocal fold paresis may still show the less innervated fold to have a phase delay. This is seen on the DKG in Figure 18.32. The phase shift can be better seen on the DKG. It also shows brief contact with open-phase dominant pattern.

Stiffness due to Scarring Stiffness pattern is seen in patients with laryngitis, scarr­ ing, and other inflammatory effects of the vocal fold cover. In this pattern the patient may be speaking in vocal fry with a predominantly rough voice quality. This is seen as aperiodic vibrations interspersed with. Thus large glottal opening are followed by small glottal opening in an alternating manner. The key difference between the stiffness versus the tension pattern is that both vocal folds participate in the alternation of glottal cycle. The subharmonics, which are created, may be every other beat, every third beat, or every fourth beat of the fundamental frequency. In general, the stiffer side starts vibration later than the normal side. The stiff side has reduced amplitude. The stiff side lags behind the normal side during each glottal cycle. During vibration, chaotic breakdown is common. Vocal fold stiffness can cause vibratory anomalies that are difficult to track by stroboscopy. 18.23 shows the high-speed video of voice onset in a male with right vocal fold stiffness. There is prephonatory pressed phonation

with prolonged delay before phonation starts. When the phonation starts, the left side is more pliable with the right side following. Short time later, chaotic vibration starts with the anterior to posterior portion of the membranous fold vibrating alternately from the front to back and vice versa. The vocal folds then seems go into a cycle of two normal beats followed by four chaotic beats. Although the stiffness with differences in the vocal fold tissue is probably contributing to the voice disorder, there is also evidence of muscle tension dysphonia. The high-speed imaging can help resolve severely chaotic vibrations due to a purely stiffness pattern with only unilateral involvement and differentiate them from those with combined stiffness and functional components. This is unique to high-speed imaging.

Mass Lesions Mass pattern is seen when there is another mass, which must be moved on as an oscillatory structure by the air stream. This may be unilateral as in a polyp or cyst, or bilateral as in patients with polypoid corditis. When the mass is on the vocal folds, it may interfere with the affected vocal fold by alteration of the glottal cycle. 18.24 shows the voice onset of a female with a unilateral soft polyp on the right fold. The normal side will lead the opposite fold in starting of vocal fold oscillation. The mass may have a rocking motion. As in stroboscopy, there may be a less distinct amplitude and mucosal wave on the mass affected side. 18.25 shows the pattern in a deeper layer, the mass effect shows sluggish movement on the affects side more than the superficial mass from the polyp shown in 18.26. The deeper lesion results in more amplitude and mucosal wave impairment than the more superficial mass on the edge of the fold.

Chapter 18: Stroboscopy and High-Speed Video Examination of the Larynx Cysts, nodules, and small polyps may be associated with diplophonia. The affected vocal fold clearly has a reduced amplitude. In addition, every other beat of the affected vocal fold is smaller than the one previously. This results in incomplete glottal closure, which is alternating with one before which is better. The net result is a pattern of vocal fold vibration, which has a subharmonic exactly half that of the fundamental frequency.

High-Speed Video Use in Functional and Neurogenic Dysphonia Spasmodic dysphonia, vocal fold tremor, and presbylarynx can have frequent voice breaks and laryngeal spasms that resulted in a breakdown of the vibration of the periodic vibration of the vocal folds. High-speed video can show important features that are not previously studied. One example of where high-speed can uniquely contribute to evaluation of neurogenic disorders can be seen in a sub-ject with phonation spasms due to spasmodic dysphonia. 18.26 is a high-speed video of a patient with spas­modic dysphonia and 18.27 is of the same patient after treatment with botulinum toxin injection to the vocal folds. The pretreatment video shows the distinct laryngeal spasm with prolonged phonation break and delay in phonation after a long prephonatory set. After treatment, the vocal folds now vibrate nicely with gentle adduction of the folds. Other application of high-speed video can show the prephonatory set of patients with muscle tension dysphonia before and after treatment.

CONCLUSION While stroboscopy is still the most practical for evaluation of vocal fold vibration in patients with dysphonia, highspeed imaging is now possible for analysis of normal and pathologic vocal fold vibration. High speed in color is suitable for all vibratory abnormalities and not just quasiperiodic vibration. Because of the nature of highspeed imaging, high speed is suitable for quantification. It is however, quite labor intensive in its acquisition and review. It should be considered in patients where stro­ boscopy deficiencies fail to resolve the vibratory abnorma­ lities in the patient under study. The clinical potential for high-speed video in voice disordered patients still needs to be validated.

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VIDEO LEGENDS Video 18.1: Stroboscopy video of normal female phonation at modal pitch and loudness. This video is the video used to extract the video montage for Figure 18.1. Video 18.2: Stroboscopy video demonstrating four dif­ ferent tokens of phonation from a male speaker. The four tokens are: modal phonation at comfortable pitch and loudness, high pitch, low pitch, and loud phonation at comfortable pitch. Video 18.3: This is a video of a female smoker with complaints of rough voice and low voice. The video examination shows the rough voice quality with very poor frequency tracking by the stroboscope. There is a lower than normal fundamental frequency with large amplitude and mucosal wave. Video 18.4: This is a female patient with a right-sided keratin cyst. The stroboscopy examination shows redu­ced amplitude and loss of the mucosal wave compared to the normal left side. Video 18.5: This is a subject with complete paralysis on the left. The stroboscopy examination shows flaccid fold on the side of paralysis with greater than normal amplitude. Video 18.6: This is an elderly male with breathy dys­phonia after cancer resection for early stage car­ cinoma. Glottal gap is present on the left. The vocal folds do not come into contact during the glot­tal cycle. The gap is in the midmembranous por­tion of the fold. Video 18.7: Open-phase dominant pattern exist in this video. The vocal fold has short contact and spends its entire glottal cycle opening and closing. Video 18.8: This singer has a small left fusiform polyp with dysphonia. The stroboscopy video shows the vocal folds to have a prominent posterior chink with the vocal folds opening from the back to the front. Video 18.9: In this video of a patient with vocal fold paralysis, the vocal folds aperture shift from side to side as it vibrates. This is an example of a lateral to medial phase shift. The result is an open-phase domi­ nant pattern with loss of rapid vocal fold opening and closing necessary for generation of a loud glottal sound source. Video 18.10: Glottis closure insufficiency is seen in this video of a patient with early vocal nodules. This is an example of failure of closure along the entire length. The vocal fold vibrates but with only the middle third coming into contact.

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Video 18.11: Video of Figure 18.12. A patient with cancer involving the left vocal fold. There is almost complete loss of amplitude and mucosal wave with an irregular edge. Video 18.12: Right vocal fold hemorrhage in an elderly male singer. The voice is rough and stroboscopy track­ing failed to show periodic vibration. Video 18.13: Video of a patient with stiff left vocal fold after prior surgery for cancer. The left fold shows reduced amplitude and wave. There is a nonvibrating segment on the left scarred fold. Video 18.14: Video of a patient with immobile left vocal fold. The out-of-phase vibration results in complete closure but short closed phase. The voice is lacking in brilliance and loud phonation is difficult. Video 18.15: Video of a patient with a left vocal fold mass. This was a mucous cyst and has resulted in contralateral vocal fold nodular swelling. The mass effect from the cyst causes reduced amplitude, mucosal wave, and a mass effect from the left fold. Video 18.16: High-speed video of voice onset of a target frequency of 105 Hz and at 79 db. The vocal folds come together and begin oscillation before full closure. Video 18.17: High-speed video of voice onset of high phonation. Note the configuration of the folds is thinner and has a sinusoidal oscillation even at the onset of phonation. Video 18.18: High-speed video of voice offset from 105 Hz, 79 db to cessation of vocal fold oscillation. Video 18.19: Vocal fry with diplophonia is shown in this example where the vocal folds show pauses every 4th beat. This is a simulated vocal fry and can be seen in muscle tension dysphonia. Video 18.20: Vocal fold paralysis with two distinct oscillators. The patient has diplophonia and the folds vibrate at two different frequencies. Video 18.21: This is the high-speed video showing the right vocal fold as normal while the left fold is stiff and vibrating at a lower frequency. Video 18.22: Left vocal fold paralysis is present in this subject. The paralyzed fold follows the innervated right fold. The folds vibrate out of phase with a glottal gap. Video 18.23: This video shows the high-speed video of a patient with right vocal fold stiffness and dip­lophonia. Video 18.24: This shows the high-speed video of a patient with right-sided soft polyp. Video 18.25: This shows the high-speed video of a patient with deep mass on the left fold. The high-speed video

should be compared with video 26 as this shows a deep lesion while video 26 shows a superficial mass lesion. Video 18.26: This shows the high-speed video of a patient with spasmodic dysphonia. The prephonatory spasm results in prolonged prephonatory spasm with delay in vibration after prephonatory set. Video 18.27: This shows the high-speed video of the same patient as 18.26 after injection of botulinum toxin injection into the thyroarytenoid muscle. The voice onset is smooth and phonation starts with gently adduction of the vocal folds.

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38. Schade G, Hess M, Muller Fet, et al. Physical and technical elements of short-interval, color-filtered double strobe flash-stroboscopy. HNO. 2002;50:1079-83. 39. Mora R, Jankowska B, Guastini Let, et al. Computerized voice therapy in hypofunctional dysphonia. J Otolaryngol Head Neck Surg. 2010;39:615-21. 40. Eller R, Ginsburg M, Lurie D, et al. Flexible laryngoscopy: a comparison of fiber optic and distal chip technologies. Part 1: vocal fold masses. J Voice. 2008;22:746-50. 41. Kawaida M, Fukuda H, Kohno N. Electronic videoendoscopic laryngostroboscopy. ORL J Otorhinolaryngol Relat Spec. 2004;66:267-74. 42. van den Berg JW. Myoelastic aerodynamic theory of voice production. J Speech Hear Res. 1958;1:227-44. 43. Story BH, Titze IR. Voice simulation with a body-cover model of the vocal folds. J Acoust Soc Am. 1995;97:1249-60. 44. Jiang J, Lin E, Hanson DG. Vocal fold physiology. Otola­ ryngol Clin North Am. 2000;33:699-718. 45. Kusuyama T, Fukuda H, Shiotani A, et al. Analysis of vocal fold vibration by x-ray stroboscopy with multiple markers. Otolaryngol Head Neck Surg. 2001;124:317-322. 46. Qin X, Wu L, Jiang H, et al. Measuring body-cover vibration of vocal folds based on high frame rate ultrasonic imaging and high-speed video. IEEE Trans Biomed Eng. 2011. 47. Hirano M, Koike Y, Hirose S, et al. Structure of the vocal cord as a vibrator. J Otolaryngol Jpn. 1973;76,:1341-8. 48. Hirano M. Morphological structure of the vocal cord as a vibrator and its variations. Folia Phoniatrica, 1974;26:89-94. 49. Hirano M. Clinical examination of voice. New York: Springer-Verlag. 1981. 50. Gray SD, Pignatari SS, Harding P. Morphologic ultrastruc­ ture of anchoring fibers in normal vocal fold basement mem­brane zone. J Voice. 1994;8:48-52. 51. Hirano M, Kakita Y. Cover-body theory of vocal fold vibration. In: Daniloff RG (ed) Speech science. San Diego: College-Hill Press. 1985;1-46. 52. Kadota Y. Pliability of vocal fold mucosa in relation to the location of subglottic mucosal upheaval during phonation. Nippon Jibiinkoka Gakkai Kaiho. 1994;97:1423-36. 53. Yumoto E, Kadota Y, Mori T. Vocal fold vibration viewed from the tracheal side in living human beings. Otolaryngol Head Neck Surg. 1996;115:329-34. 54. Hirose H. High-speed digital imaging of vocal fold vibration. Acta Oto-laryngologica. 1988;458:151-3. 55. Koster O, Marx B, Gemmar P, et al. Qualitative and quan­titative analysis of voice onset by means of a multi­ dimensional voice analysis system (MVAS) using highspeed imaging. J Voice. 1999;13:355-74. 56. Woo P. Quantification of videostrobolaryngoscopic find­ ings–measurements of the normal glottal cycle. Laryn­ goscope.1996;106:1-27. 57. Timcke R, von Leden H, Moore P. Laryngeal vibrations: measurements of the glottic wave. Part 1. The normal vibratory cycle. Arch Otolaryngol. 1958;68:1-19. 58. Timcke R, von Leden H, Moore P. Laryngeal vibrations: II. Physiologic vibrations. Arch Otolaryngol. 1959;69,: 438-44.

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59. von Leden HV, Moore P, Timcke R. Laryngeal vibrations: Measurements of the glottic wave. Arch Otolaryngol. 1960;71:16-35. 60. Moore GP, White FD, von Leden H. Ultra high speed photo­ graphy in laryngeal physiology. J Sp Hear Dis. 1962;27:165-71. 61. Moore P, Von Leden H. Dynamic variation of the vibratory pattern in normal larynx. Folia Phoniartrica (Basel). 1958; 10:205-38. 62. Krausert CR, Olszewski AE, Taylor LN, et al. Mucosal wave measurement and visualization techniques. J Voice. 2011;25:395-405. 63. Hirano M, Vennard, W, and Ohala, J Regulation of register, pitch, and intensity of voice: An electromyographic investigation of intrinsic laryngeal muscles. Folia Phoniatrica. 1970;22:1-20. 64. Kitzing P. Photo- and electroglottographical recording of the laryngeal vibratory pattern during different registers. Folia Phoniatr. 1982;34:234-41. 65. Silverman PM, Korobkin M. High-resolution computed tomography of the normal larynx. AJR Am J Roentgenol. 1983;140:875-9. 66. Baer T. Measurement of vibration patterns of excised larynxes. QPR. 1973;110:169-75. 67. Portmann G. The physiology of phonation. J Laryngol Otol. 1957;71:1-15. 68. Isshiki N, Ohkawa M, Goto M. Stiffness of the vocal cord in dysphonia-its assessment and treatment. Acta Otolaryngol Suppl. 1985;419 (supplement):167-74. 69. Isshiki N, Tanabe M, Ishizaka K, et al. Clinical significance of asymmetrical vocal cord tension. Ann Otol Rhinol Laryngol. 1977;86:58-66.

70. Bless DM, Hirano M, Feder R. Videostroboscopic exa­mi­­ nation of the larynx. Ear Nose Throat J. 1987;66:289-96. 71. Woo P, Casper J, Colton R, et al. Aerodynamic and stro­ boscopic findings before and after microlaryngeal pho­ nosurgery. J Voice. 1994;8:186-94. 72. von Leden HV, Moore P and Timcke R. Laryngeal vibra­tions: Ill. The pathologic larynx. Arch Otol Rhinol Laryngol. 1960; 71:1232-50. 73. von Leden H, Moore P. Vibratory pattern of the vocal cords in unilateral laryngeal paralysis. Acta Otolaryngol. 1961; 53:493-506. 74. Schade G, Muller F. High speed glottographic diagnostics in laryngology. HNO. 2005;53:1085-86,1088-91. 75. Hertegard S, Larsson H, Wittenberg T. High-speed imaging: applications and development. Logoped Phoniatr Vocol. 2003;28:133-9. 76. Hertegard S. What have we learned about laryngeal physiology from high-speed digital videoendoscopy? Curr Opin Otolaryngol Head Neck Surg. 2005;13:152-6. 77. Mortensen M, Woo P. High-speed imaging used to detect vocal fold paresis: a case report. Ann Otol Rhinol Laryngol. 2008;117:684-7. 78. Verdonck-de Leeuw IM, Festen JM, Mahieu HF. Deviant vocal fold vibration as observed during videokymography: the effect on voice quality. J Voice. 2001;15:313-22. 79. Wittenberg T, Tigges M, Mergell P, et al. Functional imaging of vocal fold vibration: digital multislice high-speed kymography. J Voice. 2000;14:422-442. 80. Tigges M, Wittenberg T, Mergell P, et al. Imaging of vocal fold vibration by digital multi-plane kymography. Comput Med Imaging Graph. 1999;23:323-30.

CHAPTER CT Scan for Voice Disorders: Virtual Endoscopy—Virtual Dissection

19

Jean Abitbol, Albert Castro, Gregory Lenczner, Patrick Abitbol

HISTORY X-Ray Radiology developed as a result of both the understand­ ing of electricity and the ability to create a vacuum lamp. Sir Wilhelm Croobes, a physician, and a president of the Royal Society of Medicine in London, performed the first experiment to create the cathodic ray tube in 1856.1 He found that a few particles of gas remained in vacuum tube when used as a vehicle of electricity. The molecules of radiation matter in front of the cathode that escape and bombard the surfaces they meet are the cathodic rays. It was the experiment known as the “Shadow of the Maltese Cross”, by Professor W Goodspeed, from the University of Pennsylvania in Philadelphia2 in 1890, that is considered the embryology of radiology.3 The English photographer, William Jennings, performed the first “ray photography” with a Crookes tube.4 William C Roentgen, considered the “father of radiology”, performed the first X-ray for medical purposes in 1895 when he X-rayed his wife’s hand. He gave his name to the process of X-ray of the photonic emission. The medical applications of Roentgen rays (X-rays) began in 1896 and WC Roentgen was awarded the Nobel Prize in 1901 for his pioneering work.5-7 By the end of the 19th century, Otto Glasser reported on the works of 23 pioneers in radiology in the United States alone.8,9 For example, in Chicago, in 1896, the surgeon James Burry successfully X-rayed his hands, assisted by an engineer, Charles Ezra Scribner. At the 1896 Medical Society of Philadelphia Meeting, Henry Ware Cattell presented the first communication on radiology. Follow­ing this meeting, WW Keen and EP Davies published

“Medical Applications of X-rays or Roentgen Rays” in the American Journal of Medical Sciences, in March of 1896. Thus, the principles and applications of X-rays were established.10

Kymography Kymography was first described by Kaestle, Riedor, and Rosenthal in 1909 in Munich.11 They used a number of plates running at a speed of 5 cm/s producing an illusion of a movement: it was also called the radio cinema. Thus, the Roentgen cinema developed and allowed the study of the movements of organs inside the body with X-rays.12 Mosher, in 1927, studied the movements of the tongue, the epiglottis, and the hyoid bone during speech and swallowing, which was the first cineradiography of the vocal tract. In September 1945, Henny and Boone pub­ lished in the American Journal of Roentgenology, “electrokymography for heart”.12 They studied the paral­le­ lism between the electrocardiogram and the radiographic movements while recording their data.12

Tomography The radiograph is a projection of an organ on a film called summation. Tomography is a slice by slice image of the organ. Laryngeal radiotomography, developed by André Bocage in 1921,13 was the first to image “slice the body” with slice-thickness from 1 mm to 10 mm. The principle was to move synchronously the plate and the tube, with the patient being immobile, so the synchronous motion of these parameters would print a specific and precise area of the organ to be studied.

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In 1935, Georges Massiot and his son, Jean, made the first recorded tomography collecting all their data on film.12-14 Until the early 1960s, the radiograph was merely a view of one plane. Tomography of the lungs or the larynx was interesting and very useful for diagnosis, but it had shortcomings. The density of the tissue was useful in distinguishing a tumor from normal tissue. Air is used as a differentiating contrast medium within soft tissues when processing radiographs of the vocal tract.15 However, the overlapping cervical spine disturbs the anterior–posterior views. To avoid this disturbance, high-kilovolt (120 kV) filtered radiographs and tomo­ graphs have been used with a copper filter placed in front of the X-ray tube to enhance the air–soft tissue interface by obscuring bone shadows.16,17 There are series of anterior– posterior views at 5-mm intervals from the cervical spine to the thyroid cartilage. The images may be acquired dur­ ing respiration or sustained phonation on /i/. The radia­tion exposure will be very high if multiple slices are taken. The most helpful tomography of the larynx is the anterior–posterior view or frontal view avoiding the cervi­cal spine shadow. The lateral plane yields very little additional information. Tomography shows the laryngeal surface and is useful in examination of any soft tissue, benign or malignant mass, laryngocele, or thickening of the mucosa. However, the anterior commissure, the pos­terior wall of the glottic space, the cricoarytenoid and cricothyroid joints are poorly visualized. This new tech­nology using multiple and complex movements of the X-ray tube and the receptor substantially improved image quality.18-22 In the 21st century, this technique has been repla­ced by the volumic computerized tomography (CT) scan.

CONVENTIONAL AND NUMERIZED RADIOLOGY Today, conventional diagnostic X-ray technology utilizes a numerized technique, both direct and indirect. The direct technique uses an X-ray tube instead of a film as its receptor. This receptor sends the data to a computer, and the result is an image summation. It is then possible to analyze, to magnify, and to distinguish bone from soft tissue, but it is limited to one plane. The indirect technique instead of a receptor uses a support, which can be digitalized in a computer and analyzed in the same way as the direct technique. It is no longer used clinically.

Computerized Tomography Scanning Volumic (CT) Scan In 1967, Hounsfield studied a new concept with the EMI Corporation, the analysis of X-ray data with appropriate software.23 This idea occurred to him when he was asked by EMI to perform research on the shape of blood cells. He studied all angles of these structures, first in two dimensions and later in three dimensions, and found the computer to be crucial in his work. Hounsfield had the idea to take multiple radiographs, with frames being computerized with a specific program. This process was the birth of CT. Hounsfield published his first manu­ script on this subject, “Computerized Transverse Axial Scanning”, in 1973 in the British Journal of Radiology with J Ambrose, who developed the clinical applications.24 Allan MacLeod Cormack, a South African American physicist won the 1979 Nobel Prize in Physiology and Medicine along with Godfrey Hounsfield for his work on X-ray computed tomography. Initially, axial transverse tomography was the only possible connection to the computer. Thus, it was named CT. In 1990, spiral CT was available with one detector, in 1993 it was used with two detectors, and in 1999, it became a technique utilizing multiple detectors. At the same time, important computer advances occurred. In 1995, the first work station with multiplane imaging became available, and in 1999, volume-rendering and transparency techni­ ques became practical.

Magnetic Resonance Imaging (MRI) In 1946, 51 years after Roentgen created the X-ray, Edward Purcell and Felix Bloch developed MRI, and in 1952 were awarded the Nobel prize for their work. Instead of using X-rays, which bombard the body and the plate and after having been excited by a magnetic system, they analyzed the behavior of the body’s own protons on a magnetic field. The protons are oriented with an accurate spin. Raymond Vahan Damadian, an American medical practi­ tioner and inventor of the first MR (magnetic resonance) Scanning Machine, was the first to perform a full body scan of a human being in 1977 to diagnose cancer. Damadian invented an apparatus and method to scan the human body, a method now well known as MRI. This technique had the capability of distinguishing tumor mass from normal tissue by analysis of the tissue density. This imaging is often called “protonic imaging” because it uses the variations of the magnetic field or

Chapter 19: CT Scan for Voice Disorders: Virtual Endoscopy—Virtual Dissection gradient. The X-rays are called “calcic imaging” because they use the photonic transmission of X-rays that are strongly absorbed by the human body because of its high percentage of calcium. MRI is capable of multiplanar, high-resolution imaging and may be superior or more accurate for soft tissue definition compared to the CT scan.25-28 There is no exposure to irradiation with MRI; how­ever, artifacts are numerous because of the respira­ tory movements and the pulsatile flow of the carotid and other arteries. These artifacts may be reduced by using fast-spin echo techniques. The sections may be 3–5 mm, parallel to the vocal folds and perpendicular to the vocal folds. Fatty tissue yields a high signal and gives a very satisfactory anatomic analysis of the paraglottic space. The ossified cartilage yields a bright signal, the nonossified cartilage, a low signal. MRI must never be used if a patient has surgical clips (after thyroïd surgery), pacemakers, or cochlear implants.

Xeroradiography Xeroradiography is performed with wider latitude of exposure with edge enhancement; thus, images have a higher resolution with a better contrast.29 It has provided a large amount of information on laryngeal cartilages, on the soft tissues, and a precise analysis of the ventricles. It has proven accurate when looking for foreign bodies and in distinguishing a subglottic mass not always visible on stroboscopy. It is also a technique that the author (JA) has used to analyze vocal tract behavior during sustained vowels “a,” “i,” “u”. Today, xeroradiography is no longer available because of the high exposure to radiation required, which, compared to numerized radiology and CT scan, is five times higher (Fig. 19.1).30

Fluoroscopy—Laryngography Fluoroscopy is rarely used to study the voice. It is per­ formed for swallowing analysis. It creates a high radiation exposure. Pharyngolaryngography with barium contrast is commonly used for the visualization of the poste­ rior wall of the tongue, the vallecula, the piriform sinu­ ses, and the posterior wall of the hypopharynx, since the 1980s.31

Positron Emission Tomography (PET) Scan Positron emission tomography or PET scan is a relatively new and interesting imaging technique based on the

237

Fig. 19.1: Xeroradiography (left) versus tomography (right).

difference in the uptake and metabolism of glucose, H2O3, or fluorine 18-FDG. PET scans should prove very useful in future laryngeal research for voice fatigue and can be compared with the other techniques.32

ANATOMY RELATED TO RADIOGRAPHY Phylogenetically The larynx is an organ that functions as a constrictor– dilator mechanism in the airway. From amphibians to mammals, the larynx develops as a complex structure of cartilages, muscles, and mucosa primarily from branchial arches in utero. At six weeks, the epiglottis is seen at the base of the third and fourth pharyngeal arches. At eight weeks, the thyroid, the cricoid, and the arytenoid cartilages are formed. Around 10–12 weeks, the vocal folds are individualized. At seven months, the larynx is ana­ tomically and functionally a sketch of an adult larynx. An understanding of the skeletal elements and articulations of the vocal tract is necessary to avoid mis­ diagnosis when interpreting imaging of the larynx.

Cartilages of the Larynx The cartilages of the larynx, including the thyroid, cricoid, arytenoid, and corniculates, consist of three components: nonossified hyaline cartilage, a cortical bone marrow cavity containing fatty tissue, and scattered bony trabeculae. Enchondral (such as thyroid cartilage) ossification starts around 30 years of age. The ossification process follows specific patterns in each cartilage.33,34 The epiglottis and the arytenoids are composed of yellow fibrocartilage

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Section 2: Evaluation of the Voice and Larynx

that does not usually ossify. However, in our series, on helical CT scan at around 60–70 years of age, the authors have seen numerous ossified arytenoids.35 It is very diffi­ cult to observe the cricoarytenoid joint before 60 years of age; a good imaging is possible with a specific algorithm with the vocal scan from a specific scale of color used in the lung exploration scale. Over the age of 60, the arytenoids become ossified cartilage, with a high-alternating, outer and inner cortex, and a central, low-alternating medullary space. Nonossified hyaline cartilage and nonossified fibro­ elastic cartilages have the same attenuation values of soft tissue.36-43 The angle of the two laminae of the thyroid or “shield of the folds” is approximately 110° in children, 120° in females, and 90° in males.44 The cricoarytenoid joint depends on the articular surface, as described by Lampert in 1926.45 The facets of the cricoid are cylindrically curved with an axis sharply inclined horizontally. The angles between the horizontal plane and the cricoarytenoid joint axis are primate speci­ fic: 25° for the Mycetes, 55° for the Macacas, and 55–60° for Homo sapiens. These facets do not exist in non­ primates.46,47 The cricoid cartilage is a complete ring with a height of 2.5 cm at the posterior arch and 0.75 cm at the ante­ rior arch. The arytenoids measure around 1.2 cm in height and are mobile and symmetric. The corniculate cartilages are at the apices of the arytenoids. The virtual dissection used in helical CT scanning by the authors shows the facet of the arytenoids. The cricothyroid joint lies between the convex articu­ lar facet of the thyroid inferior horn and the flat articular facet of the posterolateral surface of the cricoids carti­ lage. The cricoarytenoid joint is a saddle-shaped synovial joint with a strong capsular ligament. The arytenoid joints have complex sliding, rocking, and tilting movements de­s­cribed for decades by the observations gained through indirect and direct laryngoscopy but never by a CT scan “virtual arthroscopy” in vivo. Because of their low mass, they allow abduction–adduction in  0.5 mm must be ablated. In most clinical applications, surgeons use the

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Section 3: General Principles of Treatment

PDL or pulsed KTP laser to induce enough heat damage so that the surrounding tissues become immediately necrotic and can be removed by wiping or suctioning the treated area. Tissue interaction with the KTP or PDL laser is often reported as selective photothermolysis and is inaccurately likened to antiangiogenic tumor therapy as it is supposed to affect only the tumor vasculature.31 Yet, in the same articles the authors show figures of tumor ablation with carbon debris indicative of thermal damage to the surrounding tissue. The damage to surrounding tissue was again noted by Burns et al. in a chick chorioal­ lantoic membrane model. In this study, settings required to ablate 80% of vessels caused 0.18 mm2 of thermal injury, and settings required to ablate 100% of vessels caused 0.41 mm2 of thermal injury.32 As such, it appears that the photoangiolytic lasers operate at least in part through tissue ablation. When used as an ablative tool, KTP laser energy has been shown to cause a significant reduction in size in multiple benign vocal fold lesions as well as to cause a significant improvement in voice handicap index scores in patients with vocal polyps.33,34 Since the early 1990s, the CO2 laser in pulsed mode has been utilized based on the principle of controlled tissue ablation. With all lasers, the energy is delivered and absorbed by a chromophore. In order to achieve a clinical effect, the tissue must be ablated or damaged to a nonrepairable state. While it is appealing to believe that using a laser in some way is similar to inhibiting tumor angiogenesis, there is no scientific background to support this claim. Therefore, the surgeon should choose the laser with which he or she is most comfortable. In our experience, the CO2 laser with a pulsed delivery structure and a computerized pattern generator provides the highest level of control and precision in the operative setting under direct suspension microlaryngoscopy. However, we continue to find optimal results in phonomicrosurgery are achieved with cold steel dissection.

TECHNIQUES OF MICRODISSECTION WITH NONLASER INTSRUMENTATION Medial Microflap The medial microflap technique is our preferred technique for phonomicrosurgical resection of vocal fold nodules, vocal fold polyps, pseudocysts, or any lesion in which the lesion and surrounding cover separate easily from the underlying vocal ligament. Lesions that separate easily from the underlying ligament will likely have relatively

intact vibratory parameters on preoperative stroboscopy. However, the final approach, medial or lateral, depends on findings from intraoperative palpation. Under suspension laryngoscopy, the vocal fold changes are retracted with an open-ended suction tip or tissue-grasping forceps. If the lesion and cover separate freely from the underlying ligament and body than a medial approach can be used. If the lesion does not separate easily—ideally with palpation with a 3 French suction—then an incision over the lesion will make it difficult to identify the normal planes and the identification of normal surrounding tissue to be preserved will be hampered. An incision is made over the lesion with a sickle knife (Fig. 30.2A). The authors prefer to visualize the superficial portion of the mucosa being tented by the blade in order to ascertain that the lesion remains undisturbed. If needed, the incision length and depth can be enlarged and deepened with up angled scissors. A blunt, right-angled flap elevator is then inserted through the incision into the superficial aspect of the SLLP. The superficial mucosa is elevated laterally outward from the incision. Again, the mucosa should be thin enough to see the flap elevator through it. This will ensure that the appropriate plane of dissection is achieved. Once the superior mucosal flap has been raised, the flap elevator is reinserted facing medially and the lesion and covering mucosa are separated from the underlying vocal ligament (Fig. 30.2B). This may require traction on the flap or the undersurface of the lesion itself with 1 mm cup forceps or Boucheyer forceps if they are not too large. Once the plane is started a whistle tip microsuction may be placed within the flap for gentle retraction (Fig. 30.2C). Most often the lesion will separate with blunt dissection; however, occasionally sharp dissection with a scissors is indicated. The surgeon must take care to remain immediately lateral to the lesion, preserving the maximal amount of SLLP. As is discussed elsewhere in the text, vocal fold nodules and polyps are generally found within the superficial portion of the SLLP. As such, SLLP preservation by shallow dissec­ tion is a priority throughout this procedure. The elevator is then used to separate the lesion from the inferior most portion of the inferiorly based flap (Fig. 30.2D). Finally, up angled scissors are used to incise the mucosa to be sacrificed with the lesion (Fig. 30.2E). The epithelial flaps are then carefully redraped. Suturing of the flaps is unnecessary. This technique permits excision of the lesion without excessive de-epithelialization of the medial surface of the vocal fold. In addition, it increases the possibility of saving uninvolved SLLP (Figs. 30.3A and B).

Chapter 30: Principles of Phonomicrosurgery

421

A

B

C

D

E

Figs. 30.2A to E: (A) Sickle knife incision in vocal fold epithelium. Note knife tip visualized under epithelium ensuring appropriate depth of incision. (B) Extension of incision with lower tine of microscissors. (C) Flap elevator used to define depth of lesion and separate lesion from healthy lamina propria. (D) Flap elevator lifting subepithelial disease from healthy inferior flap epithelium. (E) Microscissors used to remove lesion while preserving epithelium.

A modification of the microflap technique may be used for pedunculated polyps with minimal involvement of the medial surface of the vocal fold. In this techni­ que, a sickle knife is used to incise the mucosa over the polyp stalk. The incision is next extended with an

up-cutting scissors. A flap elevator is then used to sepa­ rate the poly­ poid change from the normal SLLP with the lesion retrac­ted medially. Finally, the inferior mucosal and epithelial attachments are cut with an up-cutting scissors.

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Section 3: General Principles of Treatment

A

B

Figs. 30.3A and B: (A) Zero-degree Hopkins rod telescope visualization after microflap excision of a left true vocal fold polyp. (B) Seventy-degree Hopkins rod telescope visualization after microflap excision of a left true vocal fold polyp demonstrating the minimal epithelial defect with minimal trauma to subepithelial tissues.

Some surgeons favor a subepithelial infusion of saline with or without epinephrine prior to incision in order to assist in maintaining hemostasis and attempt to elevate the lesion away from the vocal ligament by increasing the size of the SLLP.35 In the authors’ experience this technique obscures the true tissue planes, making appropriate dis­ section more difficult.

LATERAL MICROFLAP TECHNIQUE When the lesion is more adherent to the vocal ligament, a lateral microflap approach may be required. The purpose of the lateral approach is to facilitate identification the vocal ligament and appropriate plane of dissection in the SLLP in a region that is relatively free of disease. Adherence to the vocal ligament is suggested by preoperative strobo­ scopic parameters that demonstrate reduction or absence of the normal vibratory patterns. Adherence is then confirmed by intraoperative palpation, which reveals that the lesion and cover do not lift off the deeper layers of the lamina propria to a significant depth, binding the cover to the body. Incising too near these changes does not allow identification of the normal tissue planes for dissection. However, the dorsolateral surface of the vocal fold is usually relatively spared. Therefore a lateral incision allows identification of the normal vocal ligament. The authors recommend making an incision slightly longer than the lesion to ensure adequate exposure under the flap. Dissection can then take place within the SLLP.36 A sickle knife is used to make an incision on the superior surface of the vocal fold laterally, near the ventricle. This

place is chosen for the incision site for two reasons. First, the normal anatomy is relatively well preserved, facilitating identification of the vocal ligament, and second, scarring and contracture on the lateral superior vocal fold have minimal effect on laryngeal vibratory patterns. The incision is finished with the up-cutting microscissors. A blunt elevator is then inserted and used to separate SLLPs and epithelial cover from the underlying intermediate and deep layers of the lamina propria. The flap can be retracted medially with a whistle-tip microsuction. Once the lesion is encountered, the dissection continues between the lesion and vocal fold ligament. In the lateral approach, sharp dissection is more often required than during the medial microflap approach. This is consistent with the lesion being adherent to the vocal ligament and interfering with the normal vibratory parameters. Care is taken not to evacuate the contents of the cyst. Once the lesion is free from the vocal fold ligament, blunt and sharp dissection are used to develop a plane between the lesion and the vocal fold cover. Occasionally these steps can be reversed. The key to surgical success, however, is preservation of the vocal fold ligament and uninvolved SLLP. Thin epithelium may be sacrificed with acceptable results, while vocal ligament and excess SLLP sacrifice will lead to unacceptable voice results. Once the lesion is removed, the operative field is inspected for secondary lesions. If none is found then corticosteroids are placed into the newly created pocket and the flap is redraped.

Chapter 30: Principles of Phonomicrosurgery

TECHNIQUES OF MICRODISSECTION WITH LASER INTSRUMENTATION As noted above, the CO2 laser with attached pattern generator can be used to make incisions by rapidly sweeping the laser beam across a given surface.27 Both a straight line, mimicking a straight scissor, and a curved line, mimicking the Bouchayer curved scissor incision, can be generated. As such once appropriate laser precautions have been taken, the laser may be used in lieu of the sharp technique described above to make an incision in conjunction with a tradition microflap technique.

Truncation The laser may also be used for truncation vocal fold nodules and polyps. In this technique, the lesion is grasped with a microcups forceps or a Bouchayer forceps and retracted medially. This allows visualization of the plane of the vocal ligament. The laser is then used to make an incision over the lesion in order to preserve epithelium lateral to the incision.25 The lesion is then grasped again, allowing for preservation of the epithelium lateral to the incision. As the lesion is then retracted further medially, a series of laser cuts are made immediately on the lesion’s lateral aspect. This technique may then be used to dissect out the lesion while minimizing trauma to the SLLP. While this is not the authors’ favored approach, there is limited data to suggest comparable functional outcomes.21 The authors would consider this approach for pedunculated polyps with a narrow stalk or lesions too small for a microflap to be practicable.

ABLATION For lesions located within the vocal fold epithelium, such as respiratory papillomatosis, ablation of the lesion with minimal damage to the underlying SLLP is the preferred technique. The authors prefer using the pulsed CO2 laser in conjunction with the operating microscope, micromanipulator, and computerized pattern generator to maximize efficiency and minimize depth of penetration. Exposure is achieved as noted above (Fig. 30.4A). Appro­ priate laser precautions must be taken, as is reviewed elsewhere in the text (Fig. 30.4B). The laser, on a lowpowered setting, is then used to ablate the lesion, one pass at a time (Fig. 30.4C). After each pass, the lesion is wiped with a saline-soaked cottonoid and char removed with a microsuction (Fig. 30.4D). This serves to remove debris

423

that can absorb laser energy and assess depth. The authors have found that removal of the epithelium without damage to the SLLP allows preservation of vocal fold vibration with minimal or no scarring (Fig. 30.4E). Some surgeons have advocated use of the microdebrider for the ablation of epithelial disease, and in the pediatric literature there are some data suggesting improved voice outcomes with use of microdebrider in ablating respiratory papillomtosis.37,38 The authors have found that using the carbon dioxide laser with the pattern generator, the bulk can be removed efficiently and cleanly. The line pattern is used to incise through the papilloma parallel to the medial edge of the true vocal fold while the platform suction is used to retract the papilloma medially away from the vocal fold (Fig. 30.5A). Care is taken to incise through the papilloma only to avoid injuring the lamina propria. The platform suction is used to retract the papilloma further from the vocal fold and the laser is used to achieve complete separation (Fig. 30.5B). With limited papilloma remaining, the single pass technique can be used to meticulously remove the remaining papilloma safely. If disease extends to the anterior commissure, the vocal folds may be sepa­ rated by placing a rolled cottonoid in the posterior aspect of the field to separate the vocal folds, allowing for improved visualization of bilateral medial edges (Fig. 30.6). In order to avoid webbing, the authors recom­ mend avoiding ablation of disease at the anterior com­ mis­sure on both vocal folds in the same procedure. Some authors have also reported using the coblator to perform cordotomies or reduce Teflon granulomas.39,40 While these devices may be useful for bulky disease, the authors do not find them useful in performing phonomicrosur­gical procedures due to a lack of control.

Dissection Remacle et al. have described using the pulsed CO2 laser with Accu Blade attachment as both cutting and dissecting instrument in the setting of scar or sulcus vocalis, conditions in which the plane of dissection within the SLLP has been altered by the disease process.25 In this technique, the laser is used to make an incision in the epithelium lateral to the lesion. The lesion is then grasped with a Bouchayer forceps and retracted. The laser is then used to dissect the lesion from the healthy SLLP. Care is taken to stay immediately lateral to the lesion for maximal mucosal preservation. The laser allows for hemostasis and smoother dissection in what may be a difficult plane of dissection. Once the lesion

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Section 3: General Principles of Treatment

A

B

C

D

E

Figs. 30.4A to E: (A) Papilloma exposed. (B) A cottonoid is placed over the endotracheal tube for laser safety. (C) Papilloma ablated superficially, preserving the deeper vocal fold. (D) The ablated papilloma is cleaned from the superior surface of the vocal fold using a saline-soaked cottonoid. (E) True vocal folds after papilloma excision. Note superficial removal.

has been dissected from healthy SLLP, it is rotated using forceps to assess the length of the lesion and ensure that it has been dissected to its full extent. Then, the lesion may be retracted medially and excised with the laser.

POSTOPERATIVE MANAGEMENT Current recommendations regarding the use of voice rest among contemporary laryngologists show considerable

Chapter 30: Principles of Phonomicrosurgery

A

425

B

Figs. 30.5A and B: (A) Platform suction used to retract papilloma medially away from substance of vocal fold while laser incision used to cut through bulk of papilloma. (B) The bulk of the papilloma has been separated from the vocal fold and the plane is demonstrated using medial retraction.

Fig. 30.6: The anterior commissure has been exposed by placing a rolled cottonoid into the posterior aspect of the vocal folds, gently and atraumatically retracted the vocal edges laterally.

variation. Recommendations range from zero to 14 days postoperatively.1,2 As in orthopedic surgery, immobilization (voice rest) was long considered mandatory. However, more recently, orthopedic surgeons have discovered in rehabilitating joints that early and controlled remobilization allows for superior healing of the soft tissues around the joint.44 Immobilization in the orthopedic literature has been shown to lead to more disorganized extracellular matrix arrangements and a slowdown in turnover of extracellular matrix constituents.42,43 Remobilization has been shown to stimulate production of ground substance and help deposition of collagen fibers in the direction of movement.44 In examining human vocal fold fibroblasts

placed under biaxial cyclic tensile strain, Titze et al. noted expression levels of matrix protein gene products and proteoglycans/hyaluronic acid gene products were significantly increased with a combination of strain and vibration.13 Bransky et al. found that applying cyclic tensile strain to rabbit vocal fold fibroblasts in the setting of proinflammatory IL-1β decreased proinflammatory gene induction and upregulated collagen synthesis.12 However, in comparing the healing of dog larynges with or without recurrent laryngeal nerve (RLN) section, Cho et al. found the RLN group to have more rapid restitution of the basement membrane.45 The surgeon must weigh the potential for improved alignment of collagen fibers using appropriate tension against the potential for hypertrophic scarring from excess use.46 We present our protocol here in the absence of clinical data comparing voice rest outcomes. Recovery is divided into four phases. Phase 1 consists of 1–2 weeks of complete voice rest. Based on studies of vocal fold remucosalization and wound healing in general, 1–2 weeks seems most appropriate.4 This allows adequate time for the majority of remucosalization to occur. In addition, collagen cross-linking for wound healing is at a point of steady incline. Some surgeons opposed to such lengthy periods of voice rest indicate potential vocal fold atrophy as their reason against use. No objective evidence, however, exists to support this view. In addition, examination of multiple patients after two-week periods of complete voice rest does not show atrophy. During phase 1, pharmacotherapy may include the use of antibiotics secondary to the presence of a contaminated

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Section 3: General Principles of Treatment

surgical wound, pain medication, mucolytic agents, and control of hyperacidity if indicated. Postoperative phase 2 includes postoperative weeks two through four and begins with an examination includ­ ing videostroboscopy. If a microflap technique has been utilized, the operated vocal fold is edematous and stiff. Some evidence of return of the vertical phase difference and mucosal wave exists. The patient is allowed to phonate for five minutes the first day off voice rest. The time is then doubled to 10 minutes the second day, then 20 minutes, 40 minutes, 1.5 hours, three hours, and so forth. In this manner the patient is back to nearly full conversational speech by the midpoint of the fourth postoperative week. Good vocal hygiene measures are continued. These include increased water uptake, mucolytic agents, and reflux control if appropriate.47 The patient is instructed on easy-onset phonation and asked to observe frequent 10-minute periods of vocal rest. Vocal fatigue and strain are signs of overactivity, and the patient is asked to use biofeedback methods for regulating activity Postoperative phase 3 includes postoperative weeks 5 through 12 and consists of continued behavior modifi­ cation and vocal hygiene. Physical examination should show continued resolution of edema with return of the vertical phase difference and the mucosal wave. Frequent examinations and videostroboscopy are performed to assess the effect of continued and increased function on the glottis. Vocal coaching for the singing voice is instituted during phase 3. The vertical phase difference, mucosal wave, and glottic closure should continue to improve with each examination. Should evidence of worsening of these factors develop, then vocal activity is decreased or halted. Finally, phase 4 consists of weeks 13 and beyond and represents a return to full vocal activity with observation every 8–12 weeks. This is carried on for approximately 24 months from the time of surgery. Healing and changes in appearance of mucosal wave and glottic function will continue for up to two years postoperatively. Patients will continue to make improvement in their vocal technique and capability. Intermittent vocal re-education or reha­ bilitation enhances continued vocal hygiene and proper vocal function.

SUMMARY The surgical management of benign voice disorders relies on accurate history and examination. Videostroboscopy is essential for the examination of glottic vibratory behavior and vocal fold closure. With these tools, the accuracy

of diagnosis of vocal fold abnormalities is enhanced.3 However, it is often still not possible to diagnose the exact nature of a vocal fold lesion on the initial examination. In this instance, serial or interval examination is helpful. In addition, behavior modification with vocal abuse reduction and correction of misuses may help to resolve surrounding vocal fold edema and further identify the true lesion. This principle of exhaustive behavioral and medical management before surgical intervention is essential for good surgical results. It is equivalent to the use of physical therapy by the orthopedic surgeon or neurosurgeon prior to definitive joint or disk surgery. If surgical intervention is deemed necessary, then precise excision of the lesion with minimal disturbance to the surrounding normal tissue is crucial for the return of glottic function postoperatively. Patients who have had overaggressive resection of benign glottic lesions show altered mucosal wave formation and impaired glottic func­­ tion on postoperative videostroboscopy. These patients have decreased vocal capabilities. To attain this goal of minimal disturbance to the surrounding normal tissues, the surgeon must time the surgical intervention with regard to treatment of the surrounding edema and use precise surgical techniques. Surgeons operating on benign vocal fold lesions should be well-versed in glottic anatomy, histology, and physiology. They should feel comfortable with the use of microlaryngeal instrumentation and in viewing the glottis under high magnification. Currently, these techniques are not a standard practice in most residency programs. After surgical intervention, postoperative rehabilita­ tion with continued behavioral modification and improved vocal hygiene is important for adequate postoperative results. Preoperative physical or speech therapy is benefi­ cial in establishing adequate vocal hygiene habits that can then be applied to the postoperative rehabilitation. Post­ o­peratively patients should expect a 7- to 14-day period of complete voice rest followed by 2.5 months of reha­ bilitation. Overuse of edematous or stiff vocal fold(s) may result in the acquisition of functional disorders. There­ fore, the patient’s progress postoperatively needs to be monitored closely with repeat examination and video­ endostroboscopy. Activity can be liberalized as the characteristics of vocal fold vibration improve.

REFERENCES 1. Gould WJ. Surgery in professional singers. Ear Nose Throat J. 1987;66:327-32.

Chapter 30: Principles of Phonomicrosurgery 2. Bouchayer M, Cornut G. Microsurgery for benign lesions of the vocal folds. Ear Nose Throat J. 1988;67:446-66. 3. Rosen CA, Gartner-Schmidt J, Hathaway B, et al. A nomenclature paradigm for benign midmembranous vocal fold lesions. Laryngoscope. 2012;122:1335-41. 4. Gray SD. Benign pathologic responses of the larynx. Curr Opin Otolaryngol Head Neck Surg. 1997;5:129-32. 5. Garrett CG, Coleman JR, Reinisch L. Comparative histology and vibration of the vocal folds: implications for experimental studies in microlaryngeal surgery. Laryngo­ scope. 2000;110:814-24. 6. Durkin GE, Duncavage JA, Toohil RJ, et al. Wound healing of true vocal cord squamous epithelium following CO2 laser ablation and cup forceps stripping. Otolaryngol Head Neck Surg. 1986;95:273-7. 7. Bastian RW. Factors leading to successful evaluation and management of patients with voice disorders. Ear Nose Throat J. 1988;67(6):411-20. 8. Cohen SM, Garrett CG. Utility of voice therapy in the management of vocal fold polyps and cysts. Otolaryngol Head Neck Surg. 2007;136:742-6. 9. McFarlane SC. Treatment of benign laryngeal disorders with traditional methods and techniques of voice therapy. Ear Nose Throat J. 1988;67(6):425-35. 10. Lancer JM, Syder D, Jones AS, et al. Vocal cord nodules: a review. Clin Otolaryngol. 1988;13:43-51. 11. Lancer JM, Syder D, Jones AS, et al. The outcome of different management patterns for vocal cord nodules. J Laryngol Otol. 1988;102:423-7. 12. Bransky RC, Perera P, Verdolini K, et al. Dynamic biomechanical strain inhibits IL-b1-induced inflammation in vocal fold fibroblasts. J Voice. 2007;21(6):651-60. 13. Titze IR, Hitchcock RW, Broadhead K, et al. Design and validation of a bioreactor for engineering vocal fold tissues under combined tensile and vibrational stresses. J Biomech. 2004;37(10):1521-9. 14. Kutty JK, Webb K. Vibration stimulates vocal mucosa-like matrix expression by hydrogel-encapsulated fibroblasts. J Tissue Eng Regen Med. 2010;4:62-72. 15. Remakle M, Eckel H (Eds). Surgery of Larynx and Trachea. Heidelberg: Springer; 2010. p. 46. 16. Hochman II, Zeitels SM, Heaton JT. Analysis of the forces and position required for optimal exposure of the anterior vocal folds. Ann Otol Rhinol Laryngol. 1999;108:715-24. 17. Kantor E, Berci G, Partlow E, et al. A completely new approach to microlaryngeal surgery. Laryngoscope. 1991; 101:676-9. 18. Bouchayer M, Cornut G, Loire R, et al. Epidermoid cysts, sulci, and mucosal bridges of the true vocal cord: a report of 157 cases. Laryngoscope. 1984;95:1087-94. 19. Werkhaven J, Ossoff RH. Surgery for benign lesions of the glottis. Otolaryngol Clin North Am. 1991;24:1179-99. 20. Shapshay SM, Healy GB. New microlaryngeal instruments for phonatory surgery and pediatric applications. Ann Otol Rhinol Laryngol. 1989;98:821-3.

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21. Beninger MS. Microdissection or microspot CO2 laser for limited vocal fold benign lesions: a prospective randomized trial. Laryngoscope. 2000;110:1-17. 22. Reinisch L. Laser physics and tissue interactions. Otolaryngol Clin North Am. 1996;29:893-914. 23. Reinisch L, Ossoff RH. Laser applications in otolaryngology. Otolaryngol Clin North Am. 1996;29:891-2. 24. Garrett CG, Reinisch L. New-generation pulsed carbon dioxide laser: comparative effects on vocal fold wound healing. Ann Otol Rhinol Laryngol. 2002;111:471-6. 25. Remacle M, Lawson G, Nollevaux MC, et al. Current state of scanning micromanipulator applications with the carbon dioxide laser. Ann Otol Rhinol Laryngol. 2008;117:239-44. 26. Ossoff RH, Werkhaven JA, Raif J, et al. Advanced microspot microslad for the CO2 laser. Otolaryngol Head Neck Surg. 1991;105(3):411-4. 27. Remacle M, Hassan F, Cohen D, et al. New computer-guided scanner for improving CO2 laser-assisted microdissection. Eur Arch Otorhinolaryngol. 2005;262(2):113-9. 28. Mouadeb DA, Belafsky PC. In-office laryngeal surgery with the 585 nm pulsed dye laser (PDL). Otolaryngol Head Neck Surg. 2007;137:477-81. 29. Zeitels SM, Askt LM, Burns JA, et al. Office-based 532-nm pulsed KTP laser treatment of glottal papillomatosis and dysplasia. Ann Otol Rhinol Laryngol. 2006;115(9):679-85. 30. Altshuler GB, Anderson RR, Manstein D, et al. Extended theory of selective photothermolysis. Lasers Surg Med. 2001;29(5):416-32. 31. Zeitels SM, Burns JA, Lopez-Guerra G, et al. Photoangiolytic laser treatment of early glottic cancer: a new management strategy. Ann Otol Rhinol Laryngol Suppl. 2008;199:3-24. 32. Burns JA, Kobler JB, Heaton JT, et al. Predicting clinical efficacy of photoangiolytic and cutting/ablating lasers using the chick chorioallantoic membrane model: implications for endoscopic voice surgery. Laryngo­scope. 2008;118(6):1109-24. 33. Mallur PS, Tajudeen BA, Aaronson N, et al. Quantification of benign lesion regression as a function of 532-nm pulsed potassium titanyl phosphate laser parameter selection. Laryngoscope. 2011;121:590-95. 34. Sridharan S, Achlatis S, Ruiz R, et al. Patient-based out­ comes of in-office KTP ablation of vocal fold polyps. Laryngoscope. 2014;124(5):1176-9. 35. Zeitels SM. Phonomicrosurgery I: principles and equip­ ment. Otolaryngol Clin North Am. 2000; 33(5):1047-62. 36. Garrett CG, Coleman JR, Reinisch L. Comparative histo­ logy and biration of the vocal folds: implications for experimental studies in microlaryngeal surgery. Laryngo­ scope. 2000;110:814-24. 37. El-Bitar MA, Zalzal GH. Powered instrumentation in the treatment of recurrent respiratory papillomatosis: an alternative to the carbon dioxide laser. Arch Otolaryngol Head Neck Surg. 2002;128:425-8. 38. Holler T, Allegro J, Chadha NK, et al. Voice outcomes fol­ lowing repeated surgical resection of laryngeal papillomata in children. Otolaryngol Head Neck Surg. 2009;141:522-6.

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39. Osborne KM, Bryson PC, Benninger MS. Cordotomy by coblation in bilateral vocal fold immobility. Otolaryngol Head Neck Surg. 2012;147(2):190. 40. Meslemani D, Benninger MS. Coblation removal of laryngeal Teflon granulomas. Laryngoscope. 2010;120(10):2018-21. 41. Ishikawa K, Thibeault S. Voice rest versus exercise: a review of the literature. J Voice. 2010;24(4):379-87. 42. Buckwalter JA, Grodzinsky AJ. Loading of healing bone, fibrous tissue, and muscle: implications of orthopaedic practice. J Am Acad Orthop Surg. 1999;7(5):291-9. 43. Amiel D, Woo SL, Harwood FL, Akeson WH. The effect of immobilization on collagen turnover in connective tissue: a biochemical-biomechanical correlation. Acta Orthop Scan. 1982;53(3):325-32.

44. Cantu RI, Steffe JA. Soft tissue healing considerations after surgery. In: Maxey LMJ (Ed). Rehabilitation for Post­ surgical Orthopedic Patient, 2nd edition. St Louis, MO: Mosby; 2006. 45. Cho SH, Kim HT, Lee IJ, et al. Influence of phonation on basement membrane zone recovery after phonomicrosur­ gery: a canine model. Ann Otol Rhinol Laryngol. 2000; 109(7):658-66. 46. Culav EM, Clark CH, Merrilees MJ. Connective tissues: matrix composition and its relevance to physical therapy. Phys Ther. 1999;79(3):308-19. 47. Emerich KA, Spiegel JR, Sataloff RT. Phonomicrosurgery III: pre-and postoperative care. Otolaryngol Clin North Am. 2000;33(5):1071-80.

Chapter 31: Laser Physics and Principles

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CHAPTER

Laser Physics and Principles

31

Robert H Ossoff, Lou Reinisch

HISTORY Laser is an acronym for Light Amplification by the Stimulated Emission of Radiation. This acronym was coined by Gordon Gould, the inventor of the laser. Although many people believe that laser concept was invented by Charles Townes, after 30 years of legal challenges Gould proved to be the legal patent owner of the laser. To understand the David and Goliath battle over the invention of the laser, it is appropriate to start are the beginning. In 1916, Einstein postulated the concept of stimulated emission in his publication Strahlungs-emission und— ab­sorption nach der Quantentheorie.1 When an object, typically an atom or molecule, is in an excited state, it can spontaneously decay down to the ground state. During this process, energy is released, typically as a packet of light—a photon, in a random direction. However, when this object in the excited state interacts with an external photon of the same energy, it is prompted to decay to the ground state and emit its photon in the same direction as the original photon. The two photons have matched phase, frequency, polarization, and direction of travel. This esoteric physics concept had little significance until 1953 when Townes, Gordon, and Zeiger at Columbia University built the first ammonia maser.2,3 The maser, which stands for Microwave Amplifi­cation by the Stimula­ ted Emission of Radiation, followed the principle of stimula­ ted emission established by Eins­ tein, but worked with microwaves or low energy photons in the microwave region of the electromagnetic spectrum. Thus, it demonstrated the stimulated emission concept and how it could be used to create a relatively intense parallel beam of radiation.

A few years later, starting in 1957, Townes and his brother-in-law, Arthur Schawlow, began to postulate how the maser might work in the infrared and quickly moved to the visible portion of the spectrum. In 1958, they filed for a patent on the laser and then published their work in Physical Review.4 It should be pointed out that Townes and Schawlow did not call their device a “laser”. Instead they used the phrase “infrared and optical maser”. In 1960 the patent was granted to Townes and Schawlow, and for many decades they were credited with inventing the idea of the laser. However, working independently of Townes and Schawlow was Gordon Gould. Gould was a graduate student in physics at Columbia University and he spoke to Townes, who was a professor at Columbia, about his ideas in 1956. In 1957, Gould dropped out of school; sitting at the table of his girlfriend’s apartment in New York, he wrote his notes on the laser. These notes contain the first use of the word LASER: light amplification by the stimulated emission of radiation. Gould discussed applications of the laser, including surgery. He was once told if he thought the notes were important that he should get them notarized. He took his notes to a local candy store where the owner was a Notary Public. On 13 November 1957, the notes were notarized by Jack Gould. This was three months before Townes and Schawlow devised their plans for a laser. Gould, working with the company TRG, applied for a patent on the laser in April 1959. This was after Townes and Schawlow applied in July 1958. At the time, US patent law stated that the patent would be granted to the first to demonstrate they conceived the idea, not the first to file. Even though Gould had his notarized notes, as a drop-out

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Section 3: General Principles of Treatment

Fig. 31.1: A simplified laser with a ruby crystal shown as the lasing medium. There are mirrors on either end of crystal to provide optical feedback and two flash lamps are located above and below the crystal. If one of the mirrors is made partially reflecting and partially transmitting, the laser light will be emitted as a nearly parallel light beam from that mirror.

student living, unmarried, with a girlfriend (she was also a member of the Communist Party), he just did not have the credentials to compare to a professor at Columbia University. The notarized notes were dismissed because it was assumed that they were notarized by a relative of Gould. In reality, the Notary Public, Jack Gould, was not a relative. It was simply a coincidence that he happened to have the same last name. This started a 30-year fight in the courts that Gordon Gould finally won. In 1987, a federal judge ordered the US Patent Office to issue patents to Gould for optically pumped and gas discharge lasers. It was on 16 May 1960 that Theodore Maiman, working at Hughes Research Laboratories, created the first laser using a synthetic ruby crystal and a flash lamp.5 Although the otolaryngologist showed an interest in using the laser during the early years, it was not until 1964 that the carbon dioxide laser was invented.6 This laser, emitting infrared light at 10.6 µm, was the first laser to have high enough absorption by hydrated tissue to be really useful for surgical applications. After the laser was invented and then carbon dioxide was used to create strongly absorbed 10.6 µm light, the mechanism for the delivery of the light from the laser to the patient at the appropriate location had to be solved. In 1968, Polanyi developed the articulated arm.7 Greza Jako was the first to use it as a new tool in laryngology.

PRINCIPLES OF OPERATION There are three main elements to the laser: (1) the lasing medium, (2) the excitation source, and (3) optical feedback. In Maiman’s laser, the lasing medium was crystalline ruby. It was synthetic ruby, manufactured free of flaws.

The excitation source was a flash lamp, similar to the flash on a camera. The optical feedback was provided by two mirrors. A simplified setup of the laser is shown in Figure 31.1. In this ruby laser, the light from the flash lamps would be absorbed by the chromium ions in the ruby crystal. It is the violet and yellow-green light absorption of chromium ions that give ruby its red color with bluish overtones. If a greater number of chromium ions are in the excited state than the number of chromium ions in the ground state, it is said that a population inversion is created. Some of the excited chromium ions will spontaneously decay to the ground state. This decay will be accompanied by the emission of a photon in a random direction. This is termed spontaneous emission. If one of these randomly emitted photons happens to be along the optical axis of the crystal (and eventually, one photon will be along the optical axis), then it will be reflected by the mirror back into the crystal. While in the crystal, the photon can interact with the chromium ions in the crystal. For instance, if the photon interacts with a chromium ion in the ground state, it can be absorbed by the chromium ion and put the chromium ion into the excited state. If the photon interacts with a chromium ion in the excited state, it can stimulate that excited chromium ion to decay to the ground state and emit its energy as light that completely matches the incident light is direction, polarization, and phase. This is called stimulated emission. Recall that the ruby crystal has a population inversion; there are more chromium ions in the excited state than the number of atoms in the ground state. Therefore, there will be more stimulated emission than absorption in the crystal. This leads to a net increase or amplification of the light in the optical cavity. Thus, we have the laser acronym, light amplification by the stimulated emission of radiation. The two mirrors will keep this process going as long as there is a population inversion. To allow the beam to exit the laser cavity, one of the mirrors is made to be partially reflecting and partially transparent. This allows a fraction of the light to escape from the optical cavity and a fraction of the light to remain in the cavity to keep the lasing process going.

LASER PROPERTIES Laser light has several characteristics that distinguish it from light emitted by a conventional light bulb. First, the laser light is monochromatic. This means the light is emitted at a single wave to a few single wavelengths. Light from a conventional light bulb is emitted over a range of wavelengths (Fig. 31.2).

Chapter 31: Laser Physics and Principles

431

Fig. 31.2: The spectrum of visible light from the violets near 400 nm to the reds near 700 nm. The lighter line shows a typical lamp spectrum spanning the entire spectrum. The darker lines would be emission from a laser with three distinct laser wavelengths.

Fig. 31.3: A plot of several of the more popular lasers as a function of the wavelength of the emitted light from the laser.

The importance of monochromatic light from lasers as applied to medicine is often overestimated. It is important that lasers can target the absorption of hemoglobin when targeting vascular lesions. In fact, this has been termed selective photothermalysis when particular chromophores are targeted.8 Yet the narrow-band, single-wavelength emis­ sion of the laser, is much more narrow than the broader absorption peaks in tissue. This has led, for instance, to discussions about the relative merits of 532 nm versus 585 nm when treating vascular lesions on the vocal folds. Also, there are few natural chromophores to target besides hemoglobin, melanin, and water. Photodynamic therapy (PDT) has also been developed to exploit the specific wavelengths of laser. In PDT, the patient is given a dye that preferentially remains in the

tissue that the physician wants to destroy. The particular dye is selected to absorb the laser light at a wavelength where untreated tissue has little absorption. Thus, one is able to preferentially treat the tissue retaining the dye. Photodynamic therapy (PDT) has been used for many different kinds of cancer. 9-11 This has also been used to treat other conditions, including papillomas.12 A laser can be found to operate at nearly any in the inf­rared, visible, and ultraviolet parts of the electromagnetic spectrum. There are tunable lasers that span regions of the spectrum. Some of the more common lasers in the infrared, visible, and ultraviolet portions of the spectrum are shown in Figure 31.3. This figure does not include the free-electron laser, which is generally tunable throughout the infrared portion of the spectrum. It also does not

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Section 3: General Principles of Treatment

A

B

C Figs. 31.4A to C: When a lens is placed close to a conventional lamp (A) to collect a large fraction of the light emitted by the lamp, the image of the lamp is larger than the original source. When the lens is placed far away from the conventional lamp (B) and collects only a small fraction of light emitted by the lamp, the image created is smaller than the source. However, when light is collimated, like the light emitted from a laser (C), no matter where the lens is placed; the light is focused to a diffraction limited small spot.

include dye lasers that can be tuned throughout the visible and most of the ultraviolet portions of the spectrum. With this array of lasers, nearly any chromophore could be targeted by the appropriate laser. The second characteristic of laser light that distin­ guishes it from light emitted by a conventional lamp is that laser light is coherent. That means that all the light waves go up and down at the same time. This is a direct result of the stimulated emission that is important in the creation of laser light. The coherence of laser light is the reason that laser light seems to sparkle. The coherence of laser light has not been utilized in medicine. There have been studies to use coherence to measure the backward and forward motion of the tympanic membrane.13 However, this work remains experimental and it is really not a clinical application. The third cha­ racteristic of laser light is that the light is emitted nearly parallel. Again, this is due to the stimulated emission that is used to create laser light. Gordon Gould, in his original notes on the laser, recognized the importance of having collimated light. Collimated light is the reason that the light can be focused down to a very small spot diameter. If we take the light from a conventional lamp and try to focus that light to a very small spot, we soon discover that when the

lens is close to the lamp, the focused image of the light is an inverted image of the original light. Not only is it not focused to a spot but also the image of the bulb is larger than the original bulb. As we move the lens away from the bulb, the image decreases in size. As we get infinitely far away, then the image start to approach a spot. However, if we move further away from a lamp with a lens, we capture less and less light from the lamp. It does not matter how “clever” we are or how many lenses we use; the limitations of focusing the light from a lamp persist. However, if we take light that is collimated, we can use a lens to focus the light to a diffraction limited spot, the smallest spot size possible. Since the light is collimated, it does not matter how far the lens is away from the laser, we still capture all the light and it is focused to a tight spot (Figs. 31.4A to C). It is the collimated beam of light that is emitted from a laser that makes it such an important tool in medicine. It is the simple fact that 10 watts of light emitted by a laser can be focused down to a spot less than 0.1 mm in diameter to produce irradiance (intensity/area) greater than 100,000 W/cm2 that makes this useful in medicine. The last characteristic that is normally associated with laser light is the high intensity of the laser light. In reality, the intensity of laser light is not very significant. Most medical lasers operate with an output of a few watts or tens of watts. This is not very different than the light emitted from conventional light bulbs. What makes the laser light significant is the irradiance that can be achieved. Irradiance is the intensity of the laser light divided by the area over which the laser light is distributed. The units of irradiance are often given in watts/cm2. A related quantity, the fluence of laser light, is the energy delivered divided by the area. Fluence is irradiance × time and is typically reported in Joules/cm2. Intensity Watts = Area cm 2 = Irradiance × time



Irradiance =



Fluence



=

Intensity × time Watts × s = Area cm 2

MODES OF OPERATION Laser light can be delivered either as a continuous wave (CW) or pulsed. If we have a 5W CW laser, then every second it delivers 5 J of light energy to the target (5 W × 1 s = 5 J). However, if we use a 1-Hz pulsed laser, and each pulse is 1 µs long with an intensity of 5 MW, we can also deliver 5 J of energy to the target (5 MW × 1 µs = 5 J). Of

Chapter 31: Laser Physics and Principles

A

433

B

Figs. 31.5A and B: In the figure, 1 J of laser energy at 532 nm (KTP laser) is delivered to the tissue through a 600 µm optical fiber that ends 1 mm away from the tissue surface. In figure (A), the energy is delivered over 1.0 s. In image (B), the energy is delivered in 10 ms. Each contour in the simulation is an increase in temperature of 2°C (the red color at the center of the profile in figure B indicates 20°C temperature increase).

course, we would expect tissue to behave very differently between having the intensity delivered over the full second (CW) and having all the energy dumped into the tissue in one-millionth of a second. When equivalent amounts of energy are delivered slowly over time, the increase in tissue temperature is much less compared with the same energy being dumped into the tissue over a short time. This is termed “thermal confinement” when short pulses are used to prevent the heat from spreading during the pulse. In Figures 31.5A and B, we show temperature profiles for two different laser pulses. In Figure 31.5A, the laser energy is 1 J and delivered over one second. The simulation was made using the technique reported in Reinisch.14 In this simulation, normal tissue parameters are used and the laser light is 532 nm light from a KTP laser. The light is delivered from a 600 µm diameter optical fiber that is held 1 mm above the tissue surface. In Figure 31.5B, the same delivery parameters are used, but now the energy of 1 J is delivered over 10 ms. Immediately after the laser pulse, the tissue temperatures are much higher with the shorter pulse. The pulsed laser is also important for a concept of photothermalysis.8 It is mentioned above that one uses photothermalysis when targeting particular chromopho­ res. The chromophore that is more often targeted in medicine is hemoglobin. Thus, lasers that emit light, which is strongly absorbed by the red hemoglobin protein, can be used to target blood vessels. To achieve photothermalysis, one must not only match the wavelength of the laser to the absorption of the target but also deliver the energy in a sufficiently short pulse to achieve thermal confinement.

It is sometimes convenient to know or to be able to calculate the optimal pulse duration to achieve thermal confinement. The length of the laser pulse must be less than the thermal relaxation time. The thermal relaxation time is the amount of time for a hot spot to cool down to 50% of its peak temperature. So, if you had a laser with an infinitely short pulse and the wavelength of the laser was only absorbed by hemoglobin, then you could irradiate the tissue and put all of the heat into the blood vessels. Since laser pulses are not infinitely short, but exist for a finite duration, you want that laser pulse duration to be shorter than the time it takes for the heat to be diffused away from the blood vessels (to be diffused away from where you are trying to localize the heat). You want the laser pulse duration to be shorter than the thermal relaxation time. Thermal relaxation times are often quoted for different types of tissues. This is a mistake. Thermal relaxation time does depend on the tissue type. Different tissue types have different thermal diffusivities. Thermal diffusivity is how fast heat diffuses through the material. We all have experienced that heat diffuses through metal faster than it diffuses through Styrofoam. In the body, heat transfers through bone faster than soft tissue. In soft tissue, most measurements find the thermal diffusivities of tissue to be close to the thermal diffusivity of water (0.14 mm2/s).15 Thermal diffusivity is normally written as the Greek letter alpha (α). Thermal relaxation times are very dependent on the target volume and shape. Since a focused laser normally

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heats up a more-or-less spherical volume of tissue, the thermal relaxation time (tr) for a sphere is given as follows: t1, ≅ d2 , 27α where d is the diameter of the volume of tissue heated. Thus, thermal relaxation times are mainly dependent on the volume of tissue heated, and the volume heated is largely related to the focal spot size of the laser in addition to the size of the target. To give some idea of thermal relaxation times, if we use the thermal diffusivity of water, we find for d = 10 µm, tr = 30 µs, for d = 0.1 mm, tr = 3 ms and for d = 1 mm, tr = 0.3 s. Therefore, when the diameter of the heated spot is increased by a factor of 100 from 10 µm to 1000 µm, the thermal relaxation time changes by a factor of 10,000 from 30 µs to 0.3 s.

CONCLUSION Lasers are common and useful tools in medicine. The collimated beam of the laser allows the physician to focus it to a tight spot and to achieve fluences large enough to have a therapeutic value. It is incumbent on the physician to understand how the light interacts with the tissue and how that can affect the outcomes. This brief introduction to the laser and the physics behind the operation of the laser is to convey what a laser is capable of doing and the limitations when using a laser. Better outcomes can be obtained when the laser user questions and tries to understand these basic concepts.

REFERENCES 1. Einstein A. Strahlungs-emission und—absorption nach der Quantentheorie. Verhandlungen der Deutschen Physika­ lischen Gesellschaft. 1916;18:318-23.

2. Gordon JP, Zeiger HJ, Townes CH. Molecular microwave oscillator and new hyperfine structure in the microwave spectrum of NH3. Phys Rev. 1954;95:282-4. 3. Gordon JP, Zeiger HJ, Townes CH. The maser—new type of microwave amplifier, frequency standard and spectrometer. Phys Rev. 1955;99:1264-74. 4. Schawlow AL, Townes CH. Infrared and optical masers. Phys Rev. 1958;112:1940-49. 5. Maiman TH. Stimulated optical radiation in ruby. Nature. 1960;187:493-4. 6. Patel CKN. Continuous—wave laser action on vibrationalrotational transitions of CO2. Phys Rev. 1964;136:A1187-93. 7. Simpson GT, Polanyi TG. History of the carbon dioxide laser in otolaryngologic surgery. Otolaryngol Clin North Am. 1983;16:739-52. 8. Anderson RR, Parrish JA. Selective photothermolysis: precise microsurgery by selective absorption of pulsed radiation. Science. 1983;220:524-27. 9. Okunaka T, Kato H, Conaka C, et al. Photodynamic therapy of esophageal carcinoma. Sug Endosc. 1990;4:150-53. 10. Rausch PC, Rolfs F, Winkler MR, et al. Pulsed versus continuous wave excitation mechanisms in photodynamic therapy of differently graded squamous cell carcinomas in tumor-implanted nude mice. Eur Arch Otorhinolaryngol. 1993;250:82-7. 11. Wening BL, Kurtzman DM, Grossweiner LI, et al. Photodynamic therapy in the treatment of squamous cell carcinoma of the head and neck. Arch Otolaryngol Head Neck Surg. 1990;116:1267-70. 12. Shikowitz MJ. Comparison of pulsed and continuous wave light in photodynamic therapy of papillomas: an experimental study. Laryngoscope. 1992;102:300-310. 13. Decraemer WF, Direckx JJ, Funnell WR. Shape and derived geometrical parameters of the adult, human tympanic membrane measured with a phase-shift moiré interferometer. Hear Res. 1991;51:107-121. 14. Reinisch, L. Scatter-limited phototherapy: a model for laser treatment of skin. Lasers Surg Med. 2002;30:381-8. 15. Valvano JW, Cochran JR, Diller KR. Thermal conductivity and diffusivity of biomaterials measured with self-heating thermistors. Int J Thermophys. 1985;6:301-11.

Chapter 32: Voice Rest

435

CHAPTER Voice Rest

32

Gwen S Korovin, Linda M Carroll “Wisdom is made up of ten parts—nine of which are silence, and the tenth is brevity of language”.1 Ergo, voice rest may have wisdom. None other than William Shakespeare stated “Give every man thy ear but few thy voice”,2 implying that Shakespeare may have realized the importance of voice conservation. According to Merriam-Webster,3 “rest” means to cease work or movement in order to relax, refresh oneself, or recover strength. Wikipedia4 defines voice rest as “Vocal rest is the process of resting the vocal folds by not speak­ ing or singing, … in an effort to hasten recovery time”. Total voice rest refers to absolute avoidance of phonation. Modi­ fied voice rest refers to limited voice use, either amount of voice use, vocal loudness, or situational voice abstine­­ nce. Merriam-Webster defines conservation as planned man­­ agement of a natural resource to prevent exploita­tion, des­truction, or neglect. Therefore, voice con­ serva­tion would entail limited voice use. Modified voice rest and voice conservation vary by the physician and the patient.

HISTORY AND RATIONALE OF VOICE REST The importance of voice rest has been proposed for centuries, but the extent of voice rest and the conditions when voice rest is warranted remain controversial. There is a paucity of evidence-based literature on this topic. Voice rest requires a behavioral change. Rest may be difficult to implement but could be ultimately beneficial for select situations. In the professional voice user, rest can be of even greater importance for career longevity. Punt

admonished performers, and advised they should not say an unnecessary word unless they are paid for it.5 The physiology of phonation is related to the frequency of vocal fold contact and the potential for phonotrauma during adduction. Phonotrauma can occur from an inter­ ruption of microcirculation, thus leading to temporary ischemia and a disruption of capillaries with increased permeability. This can then lead to a rapid reorganization of tissue, which can then lead to edema or the formation of a fibrous mass. Regions of microtrauma were identified by Gray et al.6 These regions include the basement mem­ brane zone (BMZ) and the superficial layer of the lamina propria. Even with an intact BMZ there can be a relative absence of structural glycoproteins and fibrous proteins in the superficial layer of the lamina propria. These struc­ tural changes coupled with the frequency and amplitude of vibration form the basis of phonotrauma. The phases of healing are (1) inflammation involving migration, recruitment and activation of cells to repair the wound; (2) proliferation involving mitosis to expand cell population to fill tissue deficits; and (3) remodeling, which is maturation of the restoration of tissue structure and function.7 Early events set the stage for long-term healing. Tissue repair occurs on a daily basis, and voice rest, or voice conservation, is often necessary following exten­ sive voice use to permit healing, thereby restoring normal vibratory function. However, voice rest does not neces­ sarily address the underlying problem, and excessive voice rest may lead to atrophy. Dysphonia can arise from continued voice use in the presence of voice fatigue or medical illness affecting the larynx. Voice rest is believed to hasten recovery time, and

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allows a reduction of mechanical stress. The theory behind voice rest is to prevent the vocal fold edges from approximating, thereby decreasing or eliminating the possibility of friction or irritation. The vocal folds remain in a partially adducted position during respiration, and move to adduction/abduction during phonatory tasks. Some occupations are at greater risk for dysphonia due to voice use demands in the workplace. Professional singers, teachers, salesmen, telemarketers, stockbrokers, and canvassers have reduced ability to implement voice pacing and moments of voice rest in the workplace, thereby increasing the risk for phonotrauma. Politicians have higher risk during campaigns when added stress, increased travel, and urgency of communication are placed upon them. Enflo et al.8 found increased phonotrauma with voice use among nonsingers, but that trained singers were at reduced risk for phonotrauma. This may be due to tonal placement, vocal range of motion and breath manage­­ment in the trained population. Reduction of phono­ trauma may be improved with voice training and has been advo­ cated for teachers as well as politicians. Research has been published on voice use in teachers, and the impact of inadequate voice rest in that population. Titze et al.9 found that school teachers had 1800 occurrences of voicing (onset followed by offset) per hour at work and 1200 occurrences per hour while not at work. This study helped lay the groundwork for understanding vocal fati­ gue in terms of repetitive motion and collision of tissue, as well as recovery from such mechanical stress. Most reco­ very from mechanical stress of the vocal folds occurs after 4–6 h, with full recovery after 12–18 h.10 This suggests the potential for chronic wound trauma if the voice is not rested adequately after extended voice use. Changes in tissue morphology have been found after 17 min of continuous vocalization or 35 min of continuous reading.11 Hydration and gene expression can affect energy dissipation through modification of strain. Vibrational strain may also affect the extracellular matrix gene expres­ sion.12 Since voice rest can reduce vibrational strain, it can then play an important role in short-term and long-term vocal health. Tissue trauma from vibrational strain is influenced by systemic hydration and/or local viscosity changes. Verdolini et al.13 found increased phonation threshold pressures (PTP) with increased voice use and presence of dehydration. PTP is significantly increased for elevated lesions and scar conditions on the vocal folds, and may serve as an indicator of voice injury.

The extent of voice use vs amount of voice rest can be measured through voice dosimetry. Research on voice dosi­ metry yields information on vocal loading and can be used to examine the impact of mechanical stress and energy dissi­ pation.14 The extracellular matrix may be affected by vocal dosimetry, including distance dose and energy dissipation. Distance dose relates to the total distance traveled by the vocal folds in an oscillatory path, while the energy dissipa­ tion dose is related to the total amount of heat energy dissipated in the vocal folds. Titze et al.11 posited that internal vibrational forces could affect molecular bonds, leading to inertial “whiplash”. Blood circulation within the vocal fold has a role in heat dissipation, but Griffin15 hypothesized that prolonged phonation could be linked to a change in circulation. Despite these studies, there remains a paucity of evid­ e­nce-based research on the necessary, amount and proper circumstances for voice rest and voice conservation. Cho et al.16 examined BMZ recovery using laminin stain­ ing following phonomicrosurgery (bilateral removal of a segment of the mucosa) in 20 canines. The process of wound healing in the BMZ was examined at regular intervals within the three-month post-op period, comparing animals permitted and induced to phonate (10 min every 6 h) and animals who had recurrent laryngeal nerve resection (to create an artificial voice rest condition). Results found delayed healing for animal permitted to phonate, while the basement membrane was completely reformed after two weeks in animals who were in the voice rest group. At four weeks, post-op, the voice rest group was found to have anchoring fibers and collagen type III fibers in the superficial layer of the lamina propria. Complete recovery of the vocal fold cover (epithelium BMZ and superficial layer of the lamina propria) was present by eight weeks in the voice rest group. The phonation group was character­i­ zed by a “delayed healing process and BMZ changes” with attenuation, interruption, or loss of basement membrane observed in underlying hemidesmosomes, including a separation of the basal cell layer.17 This study recommended voice rest of at least two weeks postoperatively. Photochemical repair of wounds was examined in animal models, examining BMZ recovery at zero, two weeks and eight weeks post-trauma.18 Use of an Nd:YAG laser for ex vivo sheep treatment was compared to in vivo canine treatment. Results suggested the potential for improved healing using photochemical tissue bonding. Human vocal folds are similar, but not parallel, to animal models. Other studies have examined wound healing

Chapter 32: Voice Rest in human skin and discussed BMZ healing. Human skin re-epithelializes rapidly after injury, with keratinocytes in the basal cell layer present at one day postinjury and comp­ lete restoration of the BMZ (collagen type IV observed along the epithelial–stromal interface) between four days to as much as five weeks after injury.19–21 Recent studies by Rousseau et al.22 showed evidence of voice rest for 3–5 days and that prolonged avoidance of vocal fold activity beyond 5 days may be more harmful than good, based on necessary cell behavior to reduce scar effects and inflammatory res­ ponse. In wound repair, there is an inflammatory response from day 2–5 postinjury, and a pro­liferation phase from day 2–21 postinjury. Unique repair conditions can affect the normal continuous state of repair by the vocal folds, critical markers of repair at 8 h and 72 h. Voice rest, however, does not ensure a return to healthy voice use patterns. Therapy is still warranted for many patients. Other studies on humans have shown good healing with use of a laryngeal suture to close the wound bed following excision of a vocal fold lesion to “afford the surgeon an opportunity for primary repair with improved functional result”.23 Woo et al. found voice and healing near normal at 10-day post-op, and return of mucosal wave often complete by day 14.23 More recently, a randomi­ zed prospective trial on microsuture24 in adult humans showed microsuture of the vocal defect sped the recovery in the study group compared to the control group. Use of microsuture was felt to be of benefit, particularly in the professional voice user, because of the possibility of more rapid return to voice function. Wang and Huang25 examined outcome in voice rest, vocal hygiene and a direct voice therapy group following phonosurgery. They found benefits of postsurgical voice rehabilitation program lasting 3–6 months. Voice rest should not generally include whispering. In many instances, whispering results in the approximation of the anterior third of the vocal folds. There has been ample clinical experience to support the clinical prescrip­ tion of no whispering when voice rest is advised. It is believed that whispering may result in unwanted vocal fold adduction, extreme glottal friction, and/or drying of the laryngeal mucosa.26 Whispering can involve supraglottic and glottal compression, whether attempted at low effort (quiet whisper) or high effort (stage whisper), and has high intersubject variability.27–28 Stage whisper was found to be highly variable by subject, but was observed to be associated with a larger glottal size (less constriction) despite perceptions of a smaller glottis

437

posture. Colton and Casper felt that “Because the high effort forced whisper tends to suggest increased tension and effort somewhere in the system, and because tension and force are precisely the behaviors that most patients need to reduce or eliminate, it seem to us that the use of a forced whisper could be counterproductive”.26 Increased subglottal pressure has been found in males using a loud (stage) whisper, as well as increased airflow compared to normal phonation.29 Rubin et al.30 examined 100 patients with no reported dysphonia, comparing vocal fold function in normal voice vs. whisper. Findings during whisper included 69% supraglottic hyperfunction, 18% no change from baseline normal voice, and 12% absence of vocal fold contact during whispered speech. They concluded that although whispering involved more severe hyperfunction in most patients, it does not in all patients. The most common glottal configuration during whisper was an inverted “y” that resulted in a compression of the anterior and middle thirds of the vocal folds. Type of glottal shape during whisper may be related to type of whisper, effort involved in the whisper, and/or phonetic context. In clinical terms, extremely soft whispering without actual vocal fold contact may be safe. Hufnagle and Hufnagel31 found a quiet whisper may not result in injury. Unfortunately, few patients can actually maintain a healthy whisper posture. Most resort to using a forced whisper so that they can actually be heard. Benninger et al.32 found a potential for harmful effects during whispering, particu­ larly in the previously traumatized larynx. Therefore, patients should be cautioned against using a whisper when they should be on vocal rest. Patients may assume whistling to be a safe communi­ ca­tion during voice rest. The definition of a whistle is to produce a clear musical sound by forcing air through the teeth or through an aperture formed by pursing the lips. Whistling is therefore a production of high-pitched sound by rapid movement of air through an opening or past an obstruction. Whistling may be accomplished through lip compression or lingual-alveolar compression. Whistling through the lips is believed to require vocal fold motion, but there is inadequate research on the precise laryngeal behaviors during whistles. Use of forceful air movement may be contraindicated in the patient who needs to use smooth airflow patterns and reduce laryngeal workload. Benninger et al.32 did find vocal fold approximation during whistling was similar to speech. Therefore, whistling is also contraindicated during voice rest.

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Crying increases subglottal pressure and upper tho­­ racic tension. At the glottal level, there is a rapid vocal fold closure and prolonged closed phase. Murry and Rosen33 described crying as continuous or a series of inter­ rupted phonation consisting of excessive glottis closu­res followed by increa­­ sed subglottic pressure. Crying is a traumatic action in child­ren and adults due to the vocal intensity of the crying, perceived hard glottal onset, strai­ ned voice quality, and irregular brea­thing pattern during the cry gestures. Cough and throat clearing involve sudden vocal fold abrasion in an effort to clear or protect the respiratory sys­ tem. Cough behaviors are associated with a greater number of repetitive pressurizations and a more vigorous upper esophageal sphincter contraction compared with  throat clearing.34 Cough may be triggered by dryness at the laryn­ geal level or excessive mucus collecting during periods of voice rest. Throat clearing may be excessive mucus, dry­ness, or may be triggered by gastroesophageal reflux disease (GERD), which can be exacerbated by the stress of voice rest. Chronic cough and frequent throat clear­ing are often felt to be a behavioral issue, rather than actual need, and are traumatic to the laryngeal tissues. As a result, these behaviors should be avoided during periods of vocal rest. Grunting is forced exhalation against a closed glottis, and can occur with medical states or in association with certain types of exercise or activity (tennis, weight lifting). Grunting is a form of vocal vio­lence, which can increase fundamental frequency, achieved through increased laryn­geal tension. It is an attempt to incr­ease upper body strength35 and achieve forceful exertion­. There is a tight compression of the vocal folds that may result in vocal fold swelling. Grunting should therefore also be discouraged when someone is on voice rest. Loud, hard, abusive laughing also involves the rapid, forced expulsion of air. This usually occurs from the elastic vocal folds snapping open and closed. This reflexive vocalism could be phonotraumatic and is contraindicated during vocal rest. Although initiation of a laugh with air pulsing and gradual voicing may be used to reduce phonotrauma for some lesions, laughing remains contraindicated during voice rest due to the laryngeal adduction requirements. Yelling and screaming are certainly never an allowable vocal gesture when one is on voice rest or vocal conserva­ tion. The same is the case with excessive talking, and certainly the avoidance of talking in noisy environments is essential with voice rest.

Subvocalization, snoring, and talking during sleep also involve vocal fold movement, but are difficult to control in the voice rest or voice conservation patient. The degree of vibration during these events is not fully explored. Playing of woodwind and brass instruments may also be contraindicated during voice rest. Woodwind playing was associated with increased lateral tension in the larynx and constriction of the vocal tract, with the larynx actively involved with regulation of airflow.36–37 There is an increased risk for individuals with existing voice disorders who persist in playing their instruments. Vocal output was studied in 63 wind instrumentalists. After one hour, 19 subjects exhi­ bited a perceptually worse voice.38

VOICE REST IN ISOLATION TO MANAGE DYSPHONIA Voice rest is necessary when it is essential for rapid, proper healing. This is the case with a mucosal tear on the vibratory margin when any voice use increases the risk for scarring. Acute vocal fold hemorrhage is another condi­tion that requires complete vocal rest in order to maximize resorption of blood to avoid scarring, stiffness, or development of a vocal fold polyp. There are certain types of acute laryngitis that also warrant complete voice rest, such as presence of active infection and edema of the membranous vocal fold.

VOICE REST IN COMBINATION WITH MEDICAL MANAGEMENT TO MANAGE DYSPHONIA A combination of voice rest and medical management is warranted in certain situations. This could include initial treatment with antibiotics, antifungals, or antivirals for cer­ tain types of infectious lesions. It could also include a course of steroids if acute inflammation or an inflammatory is observed. This may be needed if the patient is in prepara­tion for a show or a voice use event and found to have inflam­ mation without mucosal disruption.

POSTOPERATIVE VOICE REST FOR PHONOSURGERY Use of voice rest following phonosurgery is a combina­ tion of tradition and belief that voice rest is needed to acco­mplish initial healing. The amount of time needed to accomplish this is variable, and may be adjusted based on

Chapter 32: Voice Rest the amount of tissue resection. However, the true amount of voice rest postoperatively has not been thoroughly studied. Some believe 5–8 days of absolute voice rest are needed, while others advocate a period of three weeks. Longer periods of absolute voice rest may be necessary with extensive surgical dissections, whereas smaller, more superficial lesions may heal well following a very short period of voice rest. Phonosurgery is accomplished most often through the use of cold knife technique. Voice rest recommendations may be dependent upon extent of surgery, extent of result­ ing defect or deficit, and location of dissection. The use of laryngeal suture has been recommended as a method to speed healing and therefore reduce the extent of voice rest necessary when a large vocal fold mass is excised. Use of laser during surgery may impact the extent of recommended vocal rest. Early studies using the CO2 laser in dogs found evidence of delayed healing. Durkin et al.39 found granulation response (fibroblasts and new vessel formation) at three days post cup forceps, and at five days post CO2 laser treatment in dogs. Jako40 and Strong and Jako41 found CO2 laser delayed healing, and recommended controlling power and duration settings to reduce depth of destruction. PDL and KTP lasers do permit change in wavelength, allowing reduced tissue destruction and more precise treatment of lesions. The canine larynx has similarities to the human larynx. However, the canine larynx has a rudimentary vocal ligament, thicker lamina propria but similar BMZ when compared to humans. Newer lasers used on humans may allow for less tissue destruction due to their ability to preserve mucosal tissue while focusing the laser to a specific depth in the vocal fold and specific wavelength. Depending on the laser type and laser use, healing may be shorter or longer than traditional cold knife dissection. Use of voice rest with laser is therefore dependent on many factors that continue to change as newer laser technologies emerge. In-office procedures that include injections, use of the PDL or KTP laser and cup or brush biopsy also carry considerations for voice rest. Recommendations will depend on the extent and location of the procedure, and vary by the surgeon’s preference. Other factors to consider in the postoperative patient that could affect the amount and extent of voice rest to be advised include other medical conditions (including diabetes, immunosuppression, etc.) that can slow the heal­ ing process, thereby necessitating a longer period of voice rest. In addition, the capacity for patient cooperation and com­ pliance impacts the voice rest recommendations.

439

Table 32.1: General length of voice rest recommended

Condition

Amount and type of voice rest

Postlaryngeal mucosal surgery

Complete voice rest 2–7 days

Postnonlaryngeal surgery

Relative voice rest 3–7 days

Vocal fold hemorrhage

Complete voice rest 2–5 days

Acute laryngitis: • Minimal edema, mucus • Active infection, edema

Relative voice rest Complete voice rest 2–5 days

Patients who have a history of excessive voice use due to lifestyle demands may require more extensive voice rest.

VOICE REST POSTOPERATIVE FOR NONLARYNGEAL SURGERY OR OTHER PROCEDURES Voice rest may be suggested following surgery or medical procedures on nonlaryngeal structures because they may sub­sequently affect function of the larynx and ease of voice production. This may include such procedures as cervical spine surgery, thyroid surgery, parathyroid sur­ gery, ton­sillectomy, adenoidectomy, nasal/sinus surgery, oral sur­gery, and abdominal surgery (Table 32.1).

PRACTICAL CONSIDERATIONS FOR VOICE REST VS VOICE CONSERVATION Cessation of all oral communication can be challenging for any patient. The emotional effects of voice rest must be considered in determining the amount of voice rest or conservation necessary to optimize healing. Rosen and Sataloff42 suggested that feelings of insecurity, helplessness, and dissociation from the verbal world can occur with prolonged voice rest. Methods of communication as alternatives during voice rest include pen and paper, erase boards, texting, unvoiced noises (hand clap, finger snap, unvoiced pho­ nemes), elec­ trolarynx, email, and text messaging. New applications to produce synthetic voice in patients who cannot, or should not, use oral com­munication have made methods of com­ munication easier for those placed on voice rest. Prolonged voice rest may result in atrophy. Opinions vary, but some believe that atrophy can occur after two weeks of total voice rest. A steady incline of collagen

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cross-linking is present with voice rest, but the amount of necessary cross-linking for initial voice use is unknown. Voice rest may be influenced by exposure to low levels of hydration (environmental, medication, medical condi­ tion, airline travel).43 Karaoke singers given hydration and periods of vocal rest were found to be able to sing longer and not experience loss of upper range access when compared to other karaoke singers. This suggests improved attention to hydration in combination with voice rest as a method to preserve voice function and quality.44

SUMMARY Voice rest is a necessary part of voice care. Clinically, it has proven to be a successful adjunct to promote healing in cases of mucosal disruption due to either inflammation, injury, or surgery. There is a paucity of research to help establish parameters of voice rest. It is known that phonotrauma can exist with excessive voice use, but it is not known how much rest is necessary to recover normal vocal function. Future research is needed on both voice rest and voice conservation.

REFERENCES 1. Wortabet J. Arabian Wisdom. London: J Murry; 1913. p. 35. 2. Wells S, Taylor G. William Shakespeare: the Complete Works. New York, NY: Oxford University Press; 1988. p. 659. 3. www.merriam-webster.com 4. www.wikipedia.org 5. Punt NA. Applied laryngology-singers and actors. Proc R Soc Med. 1968:61:1152-6. 6. Gray SD, Pignatari SS, Harding P. Morphologic ultrastructure of anchoring fibers in normal vocal fold basement membrane zone. J Voice. 1994:8(1):48-52. 7. Branski R, Perera P, Verdolini K, et al. Dynamic biomechanical strain inhibits IL-1β-induced inflammation in vocal fold fibroblasts. J Voice. 2007;21(6):651-60. 8. Enflo L, Sundberg J, McAllister A. Collision and phonation threshold pressures before and after loud, prolonged voca­ li­zation in trained and untrained voiced. J Voice. 2013; 27(5):527-30. 9. Titze IR, Hunter EJ, Svec JG. Voicing and silence periods in daily and weekly vocalizations of teachers. J Acoust Soc Am. 2007;121(1):469-78. 10. Hunter EJ, Titze IR. Quantifying vocal fatigue recovery: dynamic vocal recovery trajectories after a vocal loading exercise. Ann Otol Rhinol Laryngol. 2009;118(6):449-60. 11. Titze IR, Svec JG, Popolo PS. Vocal dose measures: quanti­ fying accumulated vibration exposure in vocal fold tissues. J Speech Lang Hear Res. 2003;46(4):919-32. 12. Titze IR, Hitchcock RW, Broadhead K, et al. Design and validation of a bioreactor for engineering vocal fold tissues under combined tensile and vibrational stresses. J Biomech. 2004;37(10):1521-9.

13. Verdolini K, Min Y, Titze IR, et al. Biological mechanisms underlying voice changes due to dehydration. J Speech Lang Hear Res. 2002;45(2):268-81. 14. Svec JG, Popolo PS, Titze IR. Measurement of vocal does in speech: experimental procedure and signal processing. Logoped Phoniatr Vocol. 2003;28(4):181-92. 15. Griffin MJ. Handbook of human vibration. New York: Academic Press;1990. 16. Cho SH, Kim HT, Lee IJ, et al. Influence of phonation on basement membrane zone recovery after phonomicro­ surgery: a canine model. Ann Otol Rhinol Laryngol. 2000; 109(7):658-66. 17. Cho SH, Kim HT, Lee IJ, et al. Influence of phonation on basement membrane zone recovery after phonomicro­ surgery: a canine model. Ann Otol Rhinol Laryngol. 2000; 109:658-66. 18. Franco RA, Dowdall JR, Bujold K, et al. Photochemical repair of vocal fold microflap defects. Laryngoscope. 2011; 121(6):1244-51. 19. Betz P, Nerlich A, Wilske J, et al. Time-dependent pericellular expression of collagen type IV, laminin, and heparin sulfate proteoglycan in myofibroblasts. Int J Legal Med. 1992;105:169-72. 20. McGrath JA, Leigh JM, Eady RA. Intracellular expression of type VII collagen during wound healing in severe recessive dystrophic epidermolysis bullosa and normal human skin. Br J Dermatol. 1992;127:312-7. 21. Mommaas AM, Teepe RG, Leigh IM, et al. Ontogenesis of the basement membrane zone after grafting cultured human epithelium: a morphologic and immunielectron microscope study. J Invest Dermatol. 1992;99:71-7. 22. Rousseau B, Ge P, Ohno T, et al. Investigation of experimental induced phonation on gene expression of the vocal fold 48 hours after injury. The Voice Foundation’s 37th Annual Symposium: Care of the Professional Voice, Philadelphia, PA, May 29, 2008. 23. Woo P, Casper J, Griffin B, et al. Endoscopic microsuture repair of vocal fold defects. J Voice. 1995;9(3):332-9. 24. Yilmaz T, Sözen T. Microsuture after benign vocal fold lesion removal: a randomized trial. Am J Otolaryngol. 2012;33(6):702-7. 25. Wang NM, Huang TS. A vocal treatment plan for voice disorders after phonosurgery—a preliminary study. Chang­ geng Yi Xue Za Zhi. 1994;17(2):144-8. 26. Colton RH, Casper JK. Understanding voice problems: a physiological perspective for diagnosis and treatment, 2nd edn. Philadelphia, PA: Lippincott Williams & Wilkins; 1996, pp. 313-14. 27. Solomon NP, McCall GN, trosset MW, et al. Laryngeal configuration and construction during two types of whispering. J Speech Hear Res. 1989;32(1):161-74. 28. Fleischer S, Kothe C, Hess M. Glottal and supraglottal configuration during whispering. Laryngorhinootologie. 2007;86(4):271-5. 29. Konnai R, Scherer RC. Whisper and phonation: aerodynamic comparisons across adduction and loudness levels. The Voice Foundation’s 41st Annual Symposium: Care of the Professional Voice, Philadelphia, PA, May 31, 2012.

Chapter 32: Voice Rest 30. Rubin AD, Praneet Vetakul V, Gherson S, et al. Laryngeal hyperfunction during whispering: reality of myth. J Voice. 2006;20(1):121-7. 31. Hufnagel J, Hufnagle K. Is quiet whisper harmful to the vocal mechanism? A Research note. Percept Mot Skills. 1983;57 (3 Pt 1):735-7. 32. Benninger MS, Finnegan EM, Kraus DH, et al. The whisper and whistle: the role in vocal trauma. Med Prob Perf Art. 1988;3:151-4. 33. Murry T, Rosen CA. Phonotrauma associated with crying. J Voice. 2000;14(4):575-80. 34. Xiao Y, Carson D, Boris L, et al. The acoustic cough monitoring and manometric profile of cough and throat clearing. Dis Esophagus. 2014;27(1):5-12. 35. Johnson AF. In: Benninger MS, Jacobson BH, Johnson AF (eds.), Vocal arts medicine: the care and prevention of professional voice disorders. New York: Thieme Medical Publishers;1994. p. 157. 36. Eckley CA. Glottic configuration in wind instrument pla­ yers. Braz J Otorhinolaryngol. 2006;72(1):45-7. 37. Weikert M, Schlomicher-Their J. Laryngeal movement in saxophone playing: video-endoscopic investigations with saxophone players: a pilot study. J Voice. 1999;13(2):265-73.

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38. Ocker C, Poshei W, Rohrs M, et al. Voice Disorders among players of wind instrumentalists. Folia Phoniatr. 1990;42: 24-30. 39. Durkin GE, Duncavage JA, Toohill RJ, et al. Wound healing of true vocal cord squamous epithelium after CO2 laser ablation and cup forceps stripping. Otolaryngol Head Neck Surg. 1986;95(3 Pt 1):273-7. 40. Jako GJ. Laser surgery of the vocal cords: an experimental study with carbon dioxide lasers on dogs. Laryngoscope. 1972;82(12):2204-16. 41. Strong MS, Jako GJ. Laser safety in the larynx: early clinical experience with continuous CO2 laser. Ann Otolaryngol Rhinol Laryngol. 1972;81:791-8. 42. Rosen DC, Sataloff RT. Psychology of Voice Disorders. San Diego, CA: Singular Publishing Group; 1997. 43. Solomon NP, DiMattia MS. Effects of a vocally fatiguing task and systemic hydration on phonation threshold pressure. J Voice. 2000;14(3):341-62. 44. Yiu EM, Chan RM. Effect of hydration and vocal rest on the vocal fatigue in amateur karaoke singers. J Voice. 2003; 17(2):216-27.

Chapter 33: Care of the Professional Voice

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Care of the Professional Voice

33

Robert T Sataloff, Johnathan B Sataloff, Mary J Hawkshaw Although singers and actors inspired many of the advances that have altered the standard of care for all patients with voice disorders, many other patients also are professional voice users. Clergy, attorneys, politicians, physicians, teachers, telephone receptionists, sports coaches, factory supervisors, and many others depend on vocal quality, volume, and endurance for their livelihoods. Because voice quality is essential for transmitting information and establishing credibility in our society, the majority of our patients are voice professionals; and all patients should be treated as such. In many ways, singers are the most demanding voice patients because they require outcomes that are not just “normal” but that approach “perfect”, especially classical operatic singers. However, they do not necessarily have the greatest demands for endurance among our many groups of voice professionals. An operatic singer typically performs once or twice a week. Rock singers may perform six nights a week; Broadway singers perform eight shows a week; and elementary and middle school teachers have voice demands that are even greater, in some cases. So, it is important for us to understand not only the skills required to recognize subtle problems with singers but also the vocal demands of professionals in any voice-intensive endeavor. This subject is extensive and has filled entire books.1-4 Because of space limitations, this chapter will be brief and limited to selected topics relevant to professional voice users, not covered elsewhere in this book; and it will focus primarily on singers because when otolaryngologists are skilled at caring for these especially challenging patients they usually are able to care for nearly all voice professionals.

PATIENT HISTORY Obtaining extensive historical background information is necessary for thorough evaluation of the voice patient, and the otolaryngologist who sees professional voice patients (especially singers and actors). A history questionnaire can be extremely helpful in documenting all the necessary information, helping the patient sort out and articulate his or her problems, and saving the clinician time recording information5,6 (see Sataloff RT. Professional Voice: The Science and Art of Clinical Care, 3rd edition. San Diego, CA: Plural Publishing, Inc. 2005). Additional useful quality of life information also can be obtained from validated instruments such as the Vocal Health Index (VHI),7 the VHI-10,8 and the VHI-S.9 No history questionnaire is a substitute for direct, penetrating questioning by the physician; however, the direction of most useful inquiry can be determined from a glance at a questionnaire. This obviates the need for extensive writing, which permits the physician greater eye contact with the patient and facili­ tates rapid establishment of the close rapport and confi­ dence that are vital in treating voice patients. The physician is also able to supplement initial impressions and histori­ cal information from the question­naire with seemingly leisurely conversation during the physical examination. The use of the history questionnaire adds substantially to the efficiency, consistent thorough­ness, and ease of managing these delightful, but often complex, patients.

How Old are You? Serious vocal endeavor may start in childhood and con­ tinue throughout a lifetime. As the vocal mechanism

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undergoes normal maturation, the voice changes. Agerelated vocal training is controversial, especially training of children and pubescent voices. Nevertheless, performers and other voice professionals include patients of all ages; and otolaryngologists and their voice teams should acquire the special knowledge and skills required to treat voice professionals of any age. This complex topic is beyond the scope of this chapter. The clinical effects of aging in older adults seem more pronounced in female singers, although vocal fold histologic changes may be more prominent in males.10,11 Nevertheless, excellent male singers occasionally extend their careers into their 70s or beyond. However, some degree of breathiness, decreased range, and other evi­ dence of aging should be expected in elderly voices. Nevertheless, many of the changes we typically associate with elderly singers (wobble, flat pitch) are due to lack of conditioning, rather than inevitable changes of biological aging. These aesthetically undesirable concomitants of aging often can be reversed.

What is Your Voice Problem? Careful questioning as to the onset of vocal problems is needed to separate acute from chronic dysfunction. Often an upper respiratory tract infection will send a patient to the physician’s office; but penetrating inquiry, especially in singers and actors, may reveal a chronic vocal problem that is the patient’s real concern. Identifying acute and chronic problems before beginning therapy is important so that both patient and physician may have realistic expectations and make optimal therapeutic selections. The specific nature of the vocal complaint can provide a great deal of information. Hoarseness is a coarse or scratchy sound that is most often associated with abnor­ malities of the leading edge of the vocal folds such as laryngitis or mass lesions. Breathiness is a vocal quality characterized by excessive loss of air during vocalization. Any condition that prevents full approximation of the vocal folds can be responsible. Possible causes include vocal fold paralysis, a mass lesion separating the leading edges of the vocal folds, arthritis of the cricoarytenoid joint, arytenoid dislocation, scarring of the vibratory margin, senile vocal fold atrophy (presbyphonia), psycho­ genic dysphonia, malingering, and other conditions. Fatigue of the voice is inability to continue to speak or sing for extended periods without change in vocal quality and/or control. The voice may show fatigue by becoming hoarse, losing range, changing timbre, breaking

into different registers, or exhibiting other uncontrolled aberrations. A well-trained singer should be able to sing for several hours without vocal fatigue. Fatigue is often caused by misuse of abdominal and neck musculature, oversinging, singing too loudly, or too long. However, we must remember that vocal fatigue may be a sign not only of general tiredness or vocal abuse (sometimes secondary to structural lesions or glottal closure problems) but also of serious illnesses such as myasthenia gravis. So, the importance of this complaint should not be understated. Volume disturbance may manifest as inability to sing loudly or inability to sing softly. Each voice has its own dynamic range. Within the course of training, singers learn to sing more loudly by singing more efficiently. They also learn to sing softly, a more difficult task, through years of laborious practice. Actors and other trained speakers go through similar training. Most volume problems are secondary to intrinsic limitations of the voice or technical errors in voice use, although hormonal changes, aging, and neurologic disease are other causes. Superior laryngeal nerve paralysis also impairs the ability to speak or sing loudly. Most highly trained singers require only about 10 minutes to half an hour to “warm up the voice”. Prolon­ ged warm-up time, especially in the morning, is most often caused by reflux laryngitis. Tickling or choking dur­ ing singing is most often a symptom of an abnormality of the vocal fold’s leading edge. The symptom of tickling or choking should contraindicate singing until the vocal folds have been examined. Pain while singing can indicate vocal fold lesions, laryngeal joint arthritis, laryngeal tendonitis, infection, or gastric acid reflux irritation of the arytenoid region. However, pain is much more commonly caused by voice abuse with excessive muscular activity in the neck rather than an acute abnormality on the leading edge of a vocal fold. Sudden onset of pain (usually sharp pain) while singing may be associated with a mucosal tear or a vocal fold hemorrhage and warrants voice conservation pending laryngeal examination.

Do You have any Pressing Voice Commitments? If a singer or professional speaker (e.g. actor and politician) seeks treatment at the end of a busy performance season and has no pressing engagements, management of the voice problem should be relatively conservative and designed to ensure long-term protection of the larynx, the most delicate part of the vocal mechanism. However, the

Chapter 33: Care of the Professional Voice physician and patient rarely have this luxury. Most often, the voice professional needs treatment within a week of an important engagement and sometimes within less than a day. Caring for voice complaints in these situations requi­res highly skilled judgment and bold management.

Tell Me about your Vocal Career, Long-term Goals, and the Importance of your Voice Quality and Upcoming Commitments To choose a treatment program, the physician must understand the importance of the patient’s voice and his or her long-term career plans, the importance of the upcoming vocal commitment, and the consequences of canceling the engagement. Injudicious prescription of voice rest can be almost as damaging to a vocal career as injudicious performance. For example, canceling a concert at the last minute may seriously damage a performer’s reputation. Although a singer’s voice is usually his or her most important commodity, other factors distinguish the few successful artists from the multitude of less success­ ful singers with equally good voices. These include musi­ cian­ship, reliability, and “professionalism”. Reliability is especially critical early in a singer’s career. Moreover, an expert singer often can modify a performance to decrease the strain on his or her voice. No singer, actor, or speaker should be allowed to perform in a manner that will permit serious injury to the vocal folds; but in the frequent borderline cases, the condition of the larynx must be weighed against other factors affecting the singer or actor as an artist. Similar considerations apply to all professional voice users such as teachers, politicians, attorneys, clergy, motivational speakers, and others.

How Much Voice Training Have You Had? Establishing how long a singer or actor has been perform­ ing seriously is important, especially if his or her active performance career predates the beginning of vocal train­ ing. Active untrained singers and actors frequently develop undesirable techniques that are difficult to modify. Exten­ sive voice use without training or premature training with inappropriate repertoire may underlie persistent vocal difficulties later in life. The number of years a performer has been training his or her voice and the number of teachers during that time may be fair indices of vocal proficiency, but other factors also must be considered.

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Under what kinds of Conditions Do you use your Voice? The Lombard effect is the tendency to increase vocal intensity in response to increased background noise. A well-trained singer learns to compensate for this tendency and to avoid singing at unsafe volumes. Singers of classical music usually have such training and frequently perform with only a piano, a situation in which the balance can be controlled well. However, singers performing in large halls, with orchestras, or in operas early in their careers tend to oversing and strain their voices. Similar problems occur during outdoor concerts because of the lack of auditory feedback. This phenomenon is seen even more among “pop” singers. Often, despite little vocal training, they enjoy great artistic and financial success and endure extremely stressful demands on their time and voices. They are required to sing in large halls or outdoor arenas not designed for musical performance, amid smoke and other environmental irritants, accompanied by extremely loud background music. One frequently neglected key to survival for these singers is the proper use of monitor speakers. These direct the sound of the singer’s voice toward the singer on the stage and provide auditory feedback. Determining whether the pop singer uses monitor speakers and whether they are loud enough for the singer to hear is important. Amateur singers are often no less serious about their music than are professionals, but generally they have less ability to compensate technically for illness or other physi­ cal impairment. Rarely does an amateur suffer a great loss from postponing a performance or permitting someone to sing in his or her place. In most cases, the amateur singer’s best interest is served through conservative management directed at long-term maintenance of good vocal health. A great many of the singers who seek physicians’ advice are primarily choral singers. They often are enthusiastic amateurs, untrained but dedicated to their musical recrea­ tion. They should be handled as amateur solo singers, edu­ cated specifically about the Lombard effect, and cautioned to avoid the excessive volume so common in a choral environment. Like singers, actors require superior vocal quality, flexibility, and endurance; and they often have to work under very challenging circumstances. Understanding the performance and rehearsal environment for actors is as important to providing informed laryngological care as it is for singers. For both, it is also important for physicians to determine whether the professional voice

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user is also engaged in a “day job”. Some such endeavors required to earn money are very vocally demanding. These may include positions as waiters, receptionists, tour guides, sales personnel, babysitters, part-time teachers, and others. In evaluating actors, the physician needs to know whether the person works on stage (proscenium or in-the-round), camera (television and/or film), in nightclubs, comedy clubs, or other venues. Each has its own special vocal demands and hazards. Inquiries also should include information about the length of the working day and associated vocal demands, travel, special voice requirements (character voices, voice-overs, aging during the course of a play, etc.), special voice gestures required (screaming, sobbing, laughing), costumes that affect the voice (heavy hats or helmets, corsets that limit breathing and others), makeup that causes allergies or limits facial motion, stage fog or smoke and many other factors. More information on this topic is available elsewhere.12

How Much Do You Practice and Exercise Your Voice? Vocal exercise is as essential to the vocalist as exercise and conditioning of other muscle systems is to the athlete­. Proper vocal practice incorporates scales and other specifi­c exercises designed to maintain and develop the voca­l apparatus. Simply acting or singing songs and giving performances without routine studious concentration on voca­l technique are not adequate for the vocal performer.

How, When, and Where Do You Use Your Voice? The physician should be aware of common habits and environments that are often associated with abusive voice behavior and should ask about them routinely. Screaming at sports events and at children is among the most common. Extensive voice use in noisy environments also tends to be abusive. These include noisy rooms, cars, airplanes, sports facilities, and other locations where background noise or acoustic design impairs auditory feed­back. Dry, dusty surroundings may alter vocal fold secretions through dehydration or contact irritation, altering voice function. Activities such as cheerleading, teaching, choral conducting, amateur singing, and fre­quent communication with hearing-impaired persons are likely to be associated with voice abuse, as is extensive profes­ sional voice use without formal training.

Are You Aware of Misusing or Abusing Your Voice During Speaking or Singing? Voice abuse and/or misuse should be suspected parti­ cularly in patients who complain of voice fatigue associa­ ted with voice use, whose voices are worse at the end of a working day or week, and in any patient who is chronically hoarse. Technical errors in voice use may be the primary etiology of a voice complaint, or they may develop second­ arily due to a patient’s effort to compensate for voice distur­ bance from another cause. Often, they are correctable through expert therapy and training.13

What Kind of Physical Condition Are You In? Phonation is an athletic activity that requires good condi­ tioning and coordinated interaction of numerous physical functions. Maladies of any part of the body may be reflected in the voice. Failure to maintain good abdominal muscle tone and respiratory endurance through exercise is particularly harmful because deficiencies in these areas undermine the power source of the voice. Patients gen­ erally attempt to compensate for such weaknesses by using inappropriate muscle groups, particularly in the neck, causing vocal dysfunction. Similar problems may occur in the well-conditioned vocalist in states of generalized fatigue. These are compounded by mucosal changes that accompany excessively long hours of hard work. Such problems may be seen even in the well-trained voice professionals shortly before important engagements.

Have You Noted Voice or Bodily Weakness, Tremor, Fatigue, or Loss of Control? Even minor neurological disorders may be extremely disruptive to vocal function. Specific questions should be asked to rule out neuromuscular and neurological diseases such as myasthenia gravis, Parkinson’s disease, tremors, other movement disorders, spasmodic dysphonia, multiple sclerosis, central nervous system neoplasm, and other serious maladies that may be present with voice complaints.

Do You Have Allergy or Cold Symptoms? Acute upper respiratory tract infection causes inflamma­ tion of the mucosa, alters mucosal secretions, and makes

Chapter 33: Care of the Professional Voice the mucosa more vulnerable to injury. Coughing and throat clearing are particularly traumatic vocal activi­ ties and may worsen or provoke hoarseness associate­d with a cold. Postnasal drip and allergy may produce the same response. Infectious sinusitis associated with dis­ charge and diffuse mucosal inflammation results in similar problems, and may actually alter the sound of a voice, especially the patient’s own perception of his or her voice. Futile attempts to compensate for disease of the supraglottic vocal tract, in an effort to return the sound to normal, frequently result in laryngeal strain. The expert singer or speaker should compensate by monitoring technique by tactile rather than by auditory feedback or singing “by feel” rather than “by ear”.

Do You Have Breathing Problems, Especially After Exercise? Respiratory problems are especially important in voice patients. Mild respiratory dysfunction may adversely affect the power source of the voice.14 Likewise, more severe respiratory dysfunction such as occult asthma may be particularly troublesome.15 A complete respiratory history should be obtained in most patients with voice complaints, and pulmonary function testing is often advisable.

Have You Been Exposed to Environmental Irritants? Environmental pollution is responsible for the presence of toxic substances and conditions encountered daily. Inhala­ tion of toxic pollutants may affect the voice adversely by direct laryngeal injury, by causing pulmonary dysfunction that results in voice maladies, or through impairments elsewhere in the vocal tract. Ingested substances, especially those that have neurolaryngologic effects, may also adver­ sely affect the voice. Nonchemical environmental pollu­ tants such as noise can cause voice abnormalities, as well. Otolaryngologists should be familiar with the laryngologic effects of the numerous potentially irritating substances and conditions found in the environment, as well as special pollution problems encountered by performers. Numerous materials used by artists to create sculptures, drawings, and theatrical sets are toxic and have adverse voice effects. In addition, performers are exposed routinely to chemicals encountered through stage smoke, and pyrotechnic effects, as discussed elsewhere.16-18 Although it is clear that some of the “special effects” result in serious

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laryngologic consequences, much additional study is need to clarify the nature and scope of these occupational problems. Mucosal irritants can disrupt the delicate vocal mecha­ nism in almost any setting; but performers are often in high-risk environments even in the absence of stage fogs and pyrotechnics. Allergies to dust and mold are aggravated commonly during rehearsals and performances in concert halls, especially older theaters and concert halls, because of numerous curtains, backstage trappings, and dressing room facilities that are rarely cleaned thoroughly. A history of recent travel suggests other sources of mucosal irritation. The air in airplanes is extremely dry, and airplanes are noisy, and one must be careful to avoid talking loudly and to maintain good hydration and nasal breathing dur­ ing air travel.

Do You Smoke, Live With a Smoker, or Work Around Smoke? The deleterious effects of primary and secondary exposure to smoke are well known and should be considered in evaluation of the professional voice user.

Do Any Foods Seem to Affect Your Voice? Various foods may affect the voice. Traditionally, many singers avoid milk products before performances. In many people, these foods seem to increase the amount and viscosity of mucosal secretions. Allergy and casein have been implicated. In some cases, restriction of these foods from the diet before a voice performance may be helpful. Chocolate and other foods (mint, eucalyptus, alcohol, fatty foods and others) may have the same effect on some individuals and should be viewed similarly. Eating foods that cause or aggravate reflux prior to a performance may cause symptoms that interfere with the voice, as discussed later in this chapter. Such behaviors may explain symptoms in some voice professionals, especially the many who are unaware that they have laryngopharyngeal reflux (LPR) and have a need to control their diets.

Do You Have Morning Hoarseness, Bad Breath, Excessive Phlegm, a Lump in Your Throat, or Heartburn? LPR is especially common among singers and trained speakers because of lifestyle and the high intra-abdominal

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pressure associated with proper support. Singers frequently perform at night, and many vocalists refrain from eating before performances because a full stomach can compromise effective abdominal support. They typically compensate by eating heartily at postperformance gatherings late at night and then go to bed with a full stomach. Although LPR typically occurs while the patient is upright, nocturnal reflux may be precipitated by large meals prior to bedtime. Chronic irritation of arytenoid and vocal fold mucosa by reflux of gastric secretions may be associated occasionally with dyspepsia or heartburn. However, the key features of this malady are bitter taste and halitosis on awakening in the morning, a dry or “coated” mouth, often a scratchy sore throat or a feeling of a “lump in the throat”, hoarseness, and the need for prolonged vocal warm up. LPR occurs typically while patients are upright. So, symptoms are noted during the day rather than predominantly at night. The physician must be alert to these symptoms and ask about them routinely; otherwise, the diagnosis will often be overlooked; because people who have had this problem for many years or a lifetime do not even realize it is abnormal.

Do You Have Problems Controlling Your Weight? Are You Excessively Tired? Are You Cold When Other People are Warm? Endocrine problems warrant special attention. The human voice is extremely sensitive to endocrinological changes. Many of these are reflected in alterations of fluid content of the lamina propria just beneath the laryngeal mucosa. This causes alterations in the bulk and shape of the vocal folds and results in voice change. Hypothyroidism is a wellrecognized cause of such voice disorders. Hoarseness, vocal fatigue, muffling of the voice, loss of range, and a sensation of a lump in the throat may be present even with mild hypothyroidism.

Do You Have Menstrual Irregularity, Cyclical Voice Changes Associated With Menses, Recent Menopause, or Other Hormonal Changes or Problems?

Any condition that alters abdominal function, such as mus­ cle spasm, constipation, or diarrhea, interferes with support and may result in a voice complaint. These symptoms may accompany infection, anxiety, various gastroenterological diseases, and other maladies, and they are common in performers who travel to numerous countries.

Voice changes associated with sex hormones are enco­ un­tered commonly in clinical practice and have been investigated more thoroughly than have other hormonal changes. Although a correlation appears to exist between sex hormone levels and depth of male voices (higher testosterone and lower estradiol levels in basses than in tenors),20 the most important hormonal considerations in males occur during or are related to puberty. Voice problems related to sex hormones are more common in female singers.

Are You Under Particular Stress or in Therapy?

Do You Have Jaw Joint or Other Dental Problems?

The human voice is an exquisitely sensitive messenger of emotion. Highly trained voice professionals learn to control the effects of anxiety and other emotional stress on their voices under ordinary circumstances. However, in some instances, this training may break down or a performer may be inadequately prepared to control the voice under specific stressful conditions. Preperformance anxiety is the most common example; but insecurity, depression, and other emotional disturbances are also generally reflected in the voice. Other publications have highlighted the complexity and importance of psychological factors associated with voice disorders.19

Dental disease, especially temporomandibular joint (TMJ) dysfunction, introduces muscle tension in the head and neck, which is transmitted to the larynx directly through the muscular attachments between the mandible and the hyoid bone and indirectly as generalized increased muscle tension. These problems often result in decreased range, vocal fatigue, and change in the quality or placement of a voice. Such tension often is accompanied by excess tongue muscle activity, especially pulling of the tongue posteriorly. This hyperfunctional behavior acts through hyoid attachments to disrupt the balance between the intrinsic and extrinsic laryngeal musculature.

Do You Have Trouble with Your Bowels or Belly?

Chapter 33: Care of the Professional Voice

Do You or Your Blood Relatives Have Hearing Loss? Hearing loss is often overlooked as a source of vocal problems. Auditory feedback is fundamental to speaking and singing. Interference with this control mechanism may result in altered vocal production, particularly if the person is unaware of the hearing loss. Distortion, particularly pitch distortion (diplacusis), may also pose serious problems for the singer. This appears to be due not only to aesthetic difficulties in matching pitch but also to vocal strain that accompanies pitch shifts.21 In addition to determining whether the patient has hearing loss, inquiry should also be made about hearing impairment occurring in family members, roommates, and other close associates. Speaking loudly to people who are hard-of-hearing can cause substantial, chronic vocal strain. This possibility should be investigated routinely when evaluating voice patients.

Have You Suffered Whiplash or Other Bodily Injury? Various bodily injuries outside the confines of the vocal tract may have profound effects on the voice. Whiplash, e.g., commonly causes changes in technique, with con­ sequent voice fatigue, loss of range, difficulty singing softly, and other problems. These problems derive from the neck muscle spasm, abnormal neck posturing secondary to pain, and consequent hyperfunctional voice use. Lumbar, abdominal, head, chest, supraglottic, and extremity injuries may also affect vocal technique and be responsible for the dysphonia that prompted the voice patient to seek medical attention.

Did You Undergo Any Surgery Prior to the Onset of Your Voice Problems? A history of laryngeal surgery in a voice patient is a matter of great concern. It is important to establish exactly why the surgery was done, by whom it was done, whether intubation was necessary, and whether voice therapy was instituted pre- or postoperatively if the lesion was asso­ ciated with voice abuse (vocal nodules). If the vocal dys­ function that sent the patient to the physician’s office dates from the immediate postoperative period, surgical trauma must be suspected. Other operations also may cause voice dysfunction even without laryngeal incision,

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including tonsillectomy, surgery of the neck such as thyroi­ dectomy, thoracic and abdominal surgery and other sur­ gical procedures.

What Medications and Other Substances Do You Use? A history of alcohol abuse suggests the probability of poor vocal technique. Intoxication results in incoordination and decreased awareness, which undermine vocal discipline designed to optimize and protect the voice. The effect of small amounts of alcohol is controversial. Patients fre­qu­ ently acquire antihistamines to help control ‘postnasal drip’ or other symptoms. The drying effect of antihistamines may result in decreased vocal fold lubrication, increased throat clearing, and irritability leading to frequent coughing. Antihistamines may be helpful to some voice patients, but they must be used with caution. A history of using any medications is important in evaluating voice professionals including antibiotics, diuretics, hormones, cocaine, pain medications (including aspirin and ibupro­ fen), psychotro­pic medications, and others.22

PHYSICAL EXAMINATION Physical examination of any voice patient must include a thorough ear, nose and throat evaluation, and assessment of general physical condition. The physician must remember that maladies of almost any body system may result in voice dysfunction, and the doctor must remain alert for conditions outside the head and neck. If the patient uses his or her voice professionally for singing, acting, or other vocally demanding professions, physical examination also should include assessment of the patient during typical professional vocal tasks; e.g. a singer should be asked to sing, or a member of the clergy should be asked to deliver part of a sermon.

General Ear, Nose, and Throat Examination Examination of the ears must include assessment of hearing acuity. Hearing loss in a spouse or significant other may be problematic as well if the voice professional strains vocally to communicate. The conjunctivae and sclerae should be observed routinely for erythema that suggests allergy or irritation, for pallor that suggests anemia, and for other abnormalities such as jaundice. These observations may reveal the problem reflected in the vocal tract even before the larynx is visualized. The nose should be

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Section 3: General Principles of Treatment

assessed for patency of the nasal airway, character of the nasal mucosa, and nature of secretions, if any. A patient who is unable to breathe through the nose because of anatomic obstruction is forced to breathe unfiltered, unhumidified air through the mouth. Examination of the oral cavity should be complete. Xerostomia is particularly important because dryness of the oral and laryngeal mucosa is very disturbing to voice professionals; and often the etiology can be identified and the problem, resolved. The presence of scalloping of the lateral aspects of the tongue should be noted. This finding is caused commonly by tongue thrust and may be associated with inappropriate tongue tension and muscle tension dysphonia. Dental examination should focus not only on oral hygiene but also on the presence of wear facets suggestive of bruxism. This suggests bruxism is a clue to excessive tension and may be associated with dysfunction of the TMJs, which also should be assessed routinely. Thinning of the enamel of the central incisors in a normal or underweight patient may be due to bulimia. However, it also may result from excessive ingestion of lemons, which some singers eat to help thin their secretions. The neck should be examined for masses, restriction of movement, excess muscle tension and/or spasm, and scars from prior neck surgery or trauma. Laryngeal vertical mobility is also important. For example, tilting of the larynx produced by partial fixation of cervical muscles cut during previous surgery may produce voice dysfunction, as may fixation of the trachea to overlying neck skin. Examina­ tion of posterior neck muscles and range of motion should not be neglected. The cranial nerve function also should be assessed.

Laryngeal Examination Examination of the larynx begins when the singer or other voice patient enters the physician’s office. The range, ease, volume, and quality of the speaking voice should be noted. If the examination is not being conducted in the patient’s native language, the physician should be sure to listen to a sample of the patient’s mother tongue, as well. Voice use is often different under the strain or habits of foreign language use. Rating scales used to describe the speaking voice more consistently may be helpful.23,24 The classification proposed by the Japanese Society of Logopedics and Phoniatrics is one of the most widely used. It is known commonly as the GRBAS Voice Rating Scale.25 Physicians are not usually experts in voice classifica­ tion. However, the physicians should at least be able to

discrimi­nate substantial differences in range and timbre, such as between bass and tenor, or alto and soprano. Although the correlation between speaking and singing voices is not perfect, a speaker with a low, comfortable bass voice who reports that he is a tenor may be misclassified and singing inappropriate roles with consequent voice strain. This judgment should be deferred to an expert, but the obser­vation should lead the physician to make the appropriate referral. Any patient with a voice complaint should be examined by indirect laryngoscopy at a minimum. Stroboscopic examination adds substantially to diagnostic abilities allowing visualization of small mucosal disruptions and hemorrhages that may be significant but overlooked otherwise. This technique also allows photography of the larynx. This author evaluates all new voice patients with both flexible and rigid (telescope) laryngoscopy for optimal assessment of laryngeal dynamics and vibratory margin structure and function. In some patients, videokymography or high-speed video is valuable, as well. Rigid endoscopy under general anesthesia may be reserved for the rare patient whose vocal folds cannot be assessed adequately by other means or for patients who need surgical procedures to remove or biopsy laryngeal lesions.

Objective Tests Reliable, valid, objective analysis of the voice is extremely important and is an essential part of a comprehensive physical examination. It is as valuable to the laryngologist as audiometry is to the otologist. Familiarity with some of the measures and technological advances currently avail­ able is helpful. This information is covered elsewhere.26

Laryngeal Electromyography Electromyography (EMG) requires an electrode system, an amplifier, an oscilloscope, a loudspeaker, and a record­ ing system.27 Electrodes are placed transcutaneously into laryngeal muscles. EMG can be extremely valuable in confirming cases of vocal fold paresis, in differentiating paralysis from arytenoid dislocation, distinguishing recurrent laryngeal nerve paralysis from combined recurrent and superior nerve paralysis, diagnosing other more subtle neurolaryngological pathology, and documenting functional voice disorders and malingering. It is also recom­mended for needle localization when using Botulinum toxin for the treatment of spasmodic dysphonia and other conditions.

Chapter 33: Care of the Professional Voice

Outcomes Assessment Measuring the impact of a voice disorder has always been challenging. However, recent advances have begun to address this problem. Validated instruments such as the Voice Handicap Index (VHI)7-9 are helpful in assessing the impact of the patient’s voice disorder on the quality of life.

Voice Impairment and Disability Quantifying voice impairment and assigning a disability rating (percentage of whole person) remain controversial. This subject is still not addressed comprehensively even in the most recent edition (2008, 6th Edition) of the American Medical Association’s Guidelines for the Evaluation of Impairment and Disability (The Guides).28 The Guides still do not take into account the person’s profession when calculating disability. Alternative approaches have been proposed, and advances in this complex arena are anti­ cipated over the next few years.29

Evaluation of the Singing Voice The physician must be careful not to exceed the limits of his or her expertise especially in caring for singers. However, if voice abuse or technical error is suspected, or if a difficult judgment must be reached on whether to allow a sick singer to perform, a brief observation of the patient’s singing may provide invaluable information. This is accomplished best by asking the singer to stand and sing scales either in the examining room or in the soundproof audiology booth. Similar maneuvers may be used for professional speakers, including actors (who can vocalize and recite lines), clergy and politicians (who can deliver sermons and speeches), and virtually all other voice patients. The singer’s stance should be balanced, with the weight slightly forward (Figs. 33.1A and B and 33.2A and B). The knees should be bent slightly and the shoulders, torso, and neck should be relaxed. The singer should inhale through the nose whenever possible allowing filtration, warming, and humidification of inspired air. In general, the chest should be expanded, but most of the active breathing is abdominal. The chest should not rise substantially with each inspiration, and the supra­­ cla­vicular musculature should not be involved obviously in inspiration. Shoulders and neck muscles should not be tensed even with deep inspiration (Figs. 33.3A and B). Abdominal musculature should be contracted shortly before the initiation of the tone. This may be evaluated

451

visually or by palpation (Fig. 33.4). Muscles of the neck and face should be relaxed (Figs. 33.5A and B). Economy is a basic principle of all art forms. Wasted energy and motion and muscle tension are incorrect and usually deleterious. The singer should be instructed to sing a scale (a five-note scale is usually sufficient) on the vowel /Y/, beginning on any comfortable note. Technical errors are usually most obvious as contraction of muscles in the neck and chin, retraction of the lower lip, retraction of the tongue, or tightening of the muscles of mastication. The singer’s mouth should be open widely but comfort­ ably. When singing /Y/, the singer’s tongue should rest in a neutral position with the tip of the tongue lying against the back of the singer’s mandibular incisors (Figs. 33.6A). If the tongue pulls back or demonstrates obvious muscular activity as the singer performs the scales, improper voice use can be confirmed on the basis of positive evidence (Figs. 33.6B to D). The position of the larynx should not vary substantially with pitch changes. Rising of the larynx with ascending pitch is evidence of technical dysfunction. This examination also gives the physician an opportunity to observe any dramatic differences between the qualities and ranges of the patient’s speaking voice and the singing voice. Remembering the admonition not to exceed his or her expertise, the physician who examines many singers can often glean valuable information from a brief attempt to modify an obvious technical error. For example, deciding whether to allow a singer with mild or moderate laryngitis to perform is often difficult. However, an expert singer has technical skills that allow him or her to compensate safely. However, if a singer does not sing with correct technique and does not have the discipline to modify volume, technique, and repertoire as necessary, the risk of vocal injury may be increased substantially even by mild inflammation of the vocal folds. In borderline circumstances, observation of the singer’s technique may greatly help the physician in making a judgment. Details of appropriate observations and cautious therapeutic interventions may be found in other literature.30

ADDITIONAL EXAMINATIONS A general physical examination should be performed whenever the patient’s systemic health is questionable. Debilitating conditions such as mononucleosis may be noticed first by the singer as vocal fatigue. Neurologic and pulmonary assessments may be particularly revealing.

452

Section 3: General Principles of Treatment

A

B

Figs. 33.1A and B: (A) Proper stance with weight balanced over metatarsal heads and knees slightly bent. It is close to a standard, athletic “ready” posture. (B) Incorrect stance with weight unbalanced.

A

B

Figs. 33.2A and B: (A) Correct, forward-leaning posture, with weight over metatarsal heads and knees bent. (B) Incorrect position with weight over heels and knees locked. Abdominal support is less effective in this position.

Laryngologic manifestations of systemic disease, and common diagnoses and treatments in voice professionals, are beyond the scope of this brief chapter and are reviewed elsewhere in this book and in other literature.1,2

It is extremely valuable for the laryngologist to assemble an arts-medicine team that includes not only a speech-language pathologist, singing voice specialist, acting voice specialist, and voice scientist, but also medical

Chapter 33: Care of the Professional Voice

A

453

B

Figs. 33.3A and B: (A) Inspiration without excessive muscle effort. (B) Inspiration with excessive use of shoulder and neck musculature.

Fig. 33.4: Bimanual palpation of the support mechanism. The singer should expand posteriorly and anteriorly with inspiration. Muscles should tighten prior to onset of the sung tone.

colleagues in other disciplines. Collaboration with an expert neuro­logist, pulmonologist, endocrinologist, psychologist, psychiatrist, internist, physiatrist, and others with special knowledge of, and interest in, voice disorders is invaluable in caring for patients with voice disorders and provide

expanded history and physical examination expertise that is outside the scope of otolaryngology but essential to the comprehensive “team” assessment of professional voice users. Such interdisciplinary teams have not only elevated the standard of care in voice evaluation and

454

Section 3: General Principles of Treatment

A

B

Figs. 33.5A and B: (A) Relative relaxation of facial, neck, and shoulder muscles while singing /a/. (B) Excessive, extraneous muscle use during singing /a/.

A

B

C

D

Figs. 33.6A to D: Proper relaxed position of the anterior (A) and posterior (B) portions of the tongue while singing /a/. Common improper use of the tongue pulled back from the teeth (C) and raised posteriorly (D).

Chapter 33: Care of the Professional Voice treatment, but they are also largely responsible for the rapid and productive growth of voice as a subspecialty.

REFERENCES 1. Sataloff RT. Professional Voice: The Science and Art of Clinical Care, 3rd edition. San Diego, CA: Plural Publishing, Inc.; 2005. 2. Rubin J, Sataloff RT, Korovin G. Diagnosis and Treatment of Voice Disorders, 3rd edition. San Diego, CA: Plural Publishing, Inc.; 2006. 3. Benninger MS, Jacobson BH, Johnson AF (Eds). Vocal Arts Medicine: The Care and Prevention of Professional Voice Disorders. New York: Thieme Medical Publishers; 1994. 4. Fried MP, Ferlito A (Eds). The Larynx, 3rd edition, Volume I. San Diego, CA: Plural Publishing Inc.; 2009. 5. Sataloff RT, Hawkshaw MJ, Anticaglia J. Patient history. In: Sataloff RT. Professional Voice: The Science and Art of Clinical Care, 3rd edition. San Diego, CA: Plural Publishing, Inc.; 2005. pp. 323-38. 6. Sataloff RT. Professional Voice: The Science and Art of Clinical Care, 3rd edition. San Diego, CA: Plural Publishing, Inc.; 2005. pp. 1537-1732. 7. Jacobson BH, Johnson A, Grywalski C, et al. The Voice Handi­ cap Index (VHI). Am J Speech Lang Pathol. 1997;6:66-70. 8. Rosen CA, Lee AS, Osborne J, et al. Development and validation of the Voice Handicap Index-10. The Laryn­ goscope. 2004;114(9):1549-56. 9. Rosen CA, Murry T. Voice handicap index in singers. J Voice. 2000;14(3):370-7. 10. Sataloff RT, Linville SE. The effects of age on the voice. In: Sataloff RT (ed.), Professional Voice: The Science and Art of Clinical Care, 3rd edition. San Diego, CA: Plural Publishing, Inc.; 2005. pp. 497-512. 11. Benninger MS, Abitbol J. The aging voice. In: Chalian AA (ed.), Primary Care Otolaryngology for the Geriatric Patient. Washington: American Academy of Otolaryngology Head and Neck Surgery; 2006. pp. 66-85. 12. Raphael BN. Special considerations relating to members of the acting profession. In: Sataloff RT. Professional Voice: The Science and Art of Clinical Care, 3rd edition. San Diego, CA: Plural Publishing, Inc.; 2005. pp. 339-41. 13. Sataloff RT. Professional Voice: The Science and Art of Clinical Care, 3rd edition. San Diego, CA: Plural Publishing, Inc.; pp. 961-1060. 14. Spiegel JR, Cohn JR, Sataloff RT, et al. Respiratory function in singers: medical assessment, diagnoses, treatments. J Voice. 1988;2:40-50. 15. Cohn JR, Sataloff RT, Spiegel JR, et al. Airway reactivityinduced asthma in singers (ARIAS). J Voice. 1991;5:332-7.

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16. Sataloff RT. Pollution and its effect on the voice. In: Sataloff RT. Professional Voice: The Science and Art of Clinical Care, 3rd edition. San Diego, CA: Plural Publishing, Inc.; 2005. pp. 729-36. 17. Opperman D. Pyrotechnics in the entertainment industry: an overview. In: Sataloff RT. Professional Voice: The Science and Art of Clinical Care, 3rd edition. San Diego, CA: Plural Publishing, Inc.; 2005. pp. 737-50. 18. Rossol M. Pyrotechnics: Health Effects. In: Sataloff RT. Professional Voice: The Science and Art of Clinical Care, 3rd edition. San Diego, CA: Plural Publishing, Inc.; 2005. pp. 751-6. 19. Rosen DC, Sataloff RT. Psychology of Voice Disorders. San Diego, CA: Singular Publishing Group; 1997. 639-42. 20. Meuser W, Nieschlag E. Sex hormones and depth of voice in the mail. Dtsch Med Wochenschr. 1967;102:261-4. 21. Sundberg J, Prame E, Iwarsson J. Replicability and accuracy of pitch patterns in professional singers. In: Davis PJ, Fletcher NH (eds), Vocal Fold Physiology: Controlling Chaos and Complexity. San Diego, CA: Singular Publishing Group Inc; 1996. pp. 291-306. 22. Sataloff RT, Hawkshaw MJ, Anticaglia J. Medications and the voice. In: Sataloff RT. Professional Voice: The Science and Art of Clinical Care, 3rd edition. San Diego, CA: Plural Publishing, Inc.; 2005. pp. 905-24. 23. Fuazawa T, Blaugrund SM, El-Assuooty A, Could WJ. Acoustic analysis of hoarse voice: a preliminary report. J Voice. 1988;2(2):127-31. 24. Gelfer M. Perceptual attributes of voice: development and use of rating scales. J Voice. 1988;2(4):320-26. 25. Hirano M. Clinical Examination of the Voice. New York, NY: Springer Verlag; 1918. pp. 83-4. 26. Heuer RJ, Hawkshaw MJ, Sataloff RT. The clinical voice laboratory. In: Sataloff RT. Professional Voice: The Science and Art of Clinical Care, 3rd edition. San Diego, CA: Plural Publishing, Inc.; 2005. pp. 355-94. 27. Sataloff RT, Mandel S, Heman-Ackah YD, Manon-Espaillat R, Abaza M. Laryngeal Electromyography, 2nd edition. San Diego, CA: Plural Publishing, Inc.; 2006. 28. Rondinelli R (Ed.). Guides to the Evaluation of Permanent Impairment, 6th edition. American Medical Association; 2008. 29. Sataloff RT. Voice impairment, disability, handicap, and medical-legal evaluation. In: Sataloff RT. Professio­ nal Voice: The Science and Art of Clinical Care, 3rd edition. San Diego, CA: Plural Publishing, Inc.; 2005. pp. 1427-32. 30. Sataloff RT. Physical examination. In: Sataloff RT. Profes­ sional Voice: The Science and Art of Clinical Care, 3rd edition. San Diego, CA: Plural Publishing, Inc.; 2005: 343-54.

SECTION Voice Disorders

4

Chapter 34: Etiology, Incidence, and Prevalence of Laryngeal Disorders

459

CHAPTER

34

Etiology, Incidence, and Prevalence of Laryngeal Disorders Laura H Swibel Rosenthal

INTRODUCTION The larynx is a complex organ with a prominent role and intricate anatomy. The larynx is essential to the most basi­c functions in life, including breathing and eating, and com­ municating. Pathology of the larynx can be intrinsic or associated with pulmonary disease, muscle disorders, or central or peripheral neuropathy. The larynx is also suscep­ tible to systemic disease, infectious disease, iatrogenic disease, inhaled or other toxins, and trauma, including iatrogenic injury. With four critical joints, common and rare arthropathies, such as degenerative disease and rheu­ matoid arthritis, can affect the larynx. As with any organ, the larynx is susceptible to malformations during development that range from complete atresia, requiring immediate tracheotomy at birth, to more common problems such as subglottic narrowing. Nearly everyone experiences a disorder of the larynx at some point, whether the etiology is intrinsic or extra­laryn­ geal. For example, cough is the most common presentin­g complaint in adults seeking medical treatment in an ambulatory setting,1 and it is one of the most common chief complaints, overall, responsible for 30 million clinician visits annually in the United States.2 Over-the-counter self-medication estimated expenses for acute and chronic cough are in excess of $3.6 billion annually, in the United States.3 Hoarseness is estimated to cost approximately $2.5 billion in lost wages.4 However, only 6% of those with hoarseness seek medical treatment. The underlying etiology of dysphonia may be as simple as an acute viral laryngitis or a concerning malignancy. The common cold can frequently involve the larynx and is one of the most

common medical problems, with an estimated cost of $40 billion annually.5 Children get 6–10 upper respiratory infections (URI) annually, and adults 2-4. URIs account 20 million days lost from work, 21 million lost school days in children, and more than $10 billion in costs for medical care.6 Determining the etiology, incidence, and prevalence of the most common laryngeal problems can often be difficult because definitions may vary across studies and patients may not always seek treatment. Etiology and prevalence of most laryngeal disorders have changed and will continue to change over time. Genetic disorders tend to have a stable prevalence; however, these are rare in the larynx. Furthermore, prenatal diagnosis can have an impact on incidence and prevalence. When the environment plays a significant role, such as those secondary to infection or smoking, incidence and prevalence are most susceptible to change. The prevalence of smoking decreased 42.5% bet­ ween 1965 and 2010 to about 19% among working adults,7 and this has resulted in fewer laryngeal malignancies.

CHIEF AND/OR SECONDARY COMPLAINTS Hoarseness Overview and Impact Hoarseness may be due to a wide variety of etiologies. When considering primary care and otolaryngology visits, the most common etiologies diagnosed are acute laryngi­tis (42.1%), nonspecific dysphonia (31.2%), benign

460

Section 4: Voice Disorders

vocal fold pathology (10.7%), chronic laryngitis (9.7%), laryngeal cancer (2.2%), laryngeal spasm (2.2%), unilateral vocal fold paralysis (2.0%), other speech disorder (1.5%), vocal fold paresis (0.7%), and bilateral vocal fold paralysis (0.1%).8 Orolaryngologists have a higher proportion of chronic laryngitis diagnoses, and primary care physicians have higher proportions of acute laryngitis diagnoses. In addition to these more common diagnoses, inflammation may be secondary to allergies, lichen planus, other auto­ immune disorders (such as sarcoidosis, systemic lupus erythematosus, pemphigus, or relapsing polychondritis), reflux, or smoking. Reduced volume of the vocal folds alone may limit their approximation, as in patients with presbylarynges, central or peripheral nervous system dis­ease, or neuromuscular disease. There may be adduc­tor spasmodic dysphonia or functional etiologies of dyspho­ nia. Important elements of the patient history may help establish a diagnosis such as a history of radiation to the neck or intubation. The overall lifetime prevalence of hoarseness is nearly 30% in adults, with a point-prevalence of 6.6%.9 The overall prevalence of hoarseness is 50% in elderly patients, with a point-prevalence of 29%. It is chronic (lasting more than 4 weeks) in nearly one-third of the 29%. Causes of dyspho­ nia in these patients may be vocal hygiene, decreased res­pira­tory support, medication effects, and other medical prob­l­ems.10 Hoarseness is more common in women and among certain professions such as those with significant voice use, including telemarketers, aerobics instructors, and teachers, with prevalence reaching 60%.

Difficulty Swallowing Overview and Impact Dysphagia occurs in about 16–22% of the adult population, with those over 50 being the most commonly studied.11 As with dysphonia, problems can be laryngeal or extralaryn­ geal. It is important to rule out malignancy. Other structural problems include pharyngeal pouch, pharyngeal stenosis, cricopharyngeal bar, pharyngeal web, and extrinsic com­ pression.

Difficulty Breathing Overview and Impact Patients with difficulty breathing can present in ambulatory settings, acute care settings, perioperatively for problems unrelated to the larynx, or in other specialty clinics as a result

of extralaryngeal or systemic diseases. Cardiovascula­r dis­ ease, pulmonary disease, and trauma are commo­n causes. Otolaryngologists are familiar with many extralaryngeal etiologies of difficulty breathing, such as nasal obstruction, obstructive sleep apnea, and tracheal stenosis. For the patient who presents to the otolaryngo­logist with difficulty breathing, most laryngeal etiologies will also cause symp­ toms of hoarseness, difficulty swallow­ing, chronic cough or other problems, which are addressed below.

Specific Etiologies of Hoarseness, Difficulty Swallowing, and Difficulty Breathing Vocal Fold Dysfunction Dysphonia and aspiration are among the usual presenting complaints for patients with vocal fold dysfunction. Between 1985 and 1995, extralaryngeal malignancies and surgeryrelated injuries were the most common causes of vocal fold immobility (excluding primary laryngeal malignancies). In the following 10 years, extralaryngeal malignancy became a less likely cause of vocal fold immobility (from 24.7% to 13.5% of unilateral cases and 17% to 9.7% of bilateral cases) with a rise in surgical causes (from 23.9% to 46.3% for unilateral cases and 25.7% to 55.5% for bilateral cases). Nonthyroid surgeries represent a growing etiology of unilateral vocal fold immobility (30.6%), causing more unilateral vocal fold immobility than thyroid surgery (15.7%).12 Surgeries with risk to the recurrent laryngeal nerve include those of the cervical spine, carotid artery, lung, aorta, heart, or skull base. Unilateral immobility (85%) is much more common than bilateral immobility (15%). Bilateral surgical injury occurs in total thyroidectomy, parathyroidectomy, bilateral carotid endarterectomy, and, rarely, heart surgery, with thyroid surgery being the most common cause (48.6%). The absolute number of traumatic and intubation injuries are declining. Overall, however, intubation has remained a significant cause of bilateral vocal fold immobility, along with extralaryngeal malignancy (Table 34.1). Over onethird of patients with vocal cord palsy will have positive CT findings that correlate with the cause for immobility, most of them being suspicious for malignancy in the lung or mediastinum.13 In cases of mild vocal fold hypomobility, 84% were found to have imaging or laboratory findings that could explain the hypomobility. Thyroid abnormalities were the presumed cause in 43%. The cause was idiopathic in 16%,

Chapter 34: Etiology, Incidence, and Prevalence of Laryngeal Disorders

461

Table 34.1: Etiology of vocal fold immobility

Unilateral immobility

Bilateral immobility

Surgery

46%

Surgery

56%

Idiopathic

18%

Intubation

10%

Extralaryngeal malignancy

13%

Extralaryngeal malignancy

10%

Other

8%

Idiopathic

8%

Intubation

4%

Central nervous system

7%

Infection

4%

Stenosis

3%

Central nervous system

3%

Inflammation

1%

Trauma

2%

Infection

1%

Inflammation

2%

Radiation

1%

Trauma

1%

Other

1%

viral in 10%, associated with a central nervous system abnormality in 8%, neural tumor in 6%, joint dysfunction in 6%, iatrogenic nerve injury in 4%, myopathy in 4%, and noniatrogenic traumatic nerve injury in 2%.14

Central Nervous System Pathology Diseases of the central nervous system can cause voice and/or swallowing disorders, often by means of vocal fold dysfunction. More than one-third of patients with idiopathic Parkinson’s disease (IPD) report problems with dysphonia and describe them as the most debilitating defi­ cit related to their disease.15 At least 500,000 Americans have Parkinson’s disease and about 50,000 new cases are diagnosed annually.16 On examination patients have a typical bowed appearance. 17 The voice is classically mono­ pitch with a harsh and breathy vocal quality and articula­ tory imprecision. The speech may seem rushed at times and then have inappropriate silence. Fifty percent of patients with multiple sclerosis (MS) demonstrate dyspho­ nia as a result of damage to the myelin sheaths in multi­ ple motor and sensory pathways in the central nervous syste­m. MS affects more than one million people in the Unite­d States. The prevalence of MS varies from about 50–200 per 100,000 in the United States depending on geo­ gra­phic location.18 Stroke rarely causes vocal fold paralysis, possibly occurring in about 20% of patients, and recovery is similar to motor recovery in general in stroke patients. Most stroke patients with vocal cord paralysis had involvement at the level of the brainstem, lateral medullary syndrome, Wallenberg syndrome, or Bernard-Horner syndrom­e affec­ tin­ g the recurrent laryngeal nerve.19 Lateral medulla lesion­s resulted in ipsilateral vocal fold paralysis 80% of

the time. About 11.4% of lacunar infarcts and 16.4% of cortical and large subcortical groups had vocal paralysis on the contralateral side.20

Iatrogenic Vocal Fold Disorders Aside from iatrogenic injuries previously addressed, such as surgery and radiation therapy, intubation can also be a cause of throat discomfort or hoarseness. Prolonged intubation increases risk of laryngeal injury. In those intubated for more than one day, 97% of patients will have some form of laryngeal injury, which can include vocal fold granulomas or granulation tissue (44–52%), immobility (20–39%), subglottic edema or narrowing (13%), vocal process ulceration (34%), or other problems. Duration of intubation and endotracheal tube and size did not correlate with immobility or degree of laryngeal injury.21 Vocal fold scarring can occur from intubation, caustic or thermal burns, after radiation, or vocal fold surgery. Injury to the cords that would require multiple surgeries and/or healing by secondary intention (as in cases of recurrent leukoplakia or papilloma) can be expected to heal with poorer results. Anterior commissure surgery, vocal ligament injury, and bilateral injury increase the risk of scar development. Patients with chronic inflammation of the larynx are also at increased risk.22

Inflammatory/Autoimmune Autoimmune disease is common in the population and can present in unusual ways. Patients may present with “atypical” asthma, chronic cough, chronic inflammation, or an unusual tumor. Growths are sometimes suspicious

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Section 4: Voice Disorders

for chondrosarcoma, until the underlying autoimmune disease is identified.23 The autoimmune disease can be especially difficult to diagnose in patients whose laryngeal disease is the only manifestation of their autoimmune disease. Classically, rheumatoid arthritis can cause crico­ arytenoid joint fixation. Rheumatoid nodules may form in the larynx, but biopsy may demonstrate nonspecific inflammation rather than the classic central fibrinoid necrosis surroun­ded by palisading epithelioid macropha­ ges, which is comm­only seen in rheumatoid nodules. Rheumatoid arthritis is the most common autoimmune disease, affecting about 3% of the adult population. The prevalence in children is about 15–35 per 100,000. Wegener’s granulo­matosis typically causes bronchial, renal, and upper airway necrotizing granulomatous inflammation. Head and neck manifestations are the initial present­ ing symptoms in 73% of patients.24 Ninety percent of patients will present with upper and lower airway prob­ lems. Head and neck manifestations can include ear, sinus, oral and salivary gland, or airway disease. Subglottic and tracheal stenosis occur in about 16% of patients, and can present as progressive shortness of breath, or less com­monly acute stridor. Wegener’s granulomatosis affects about 3 per 100,000 in the United States. (About 90% of patients are white). Positive antineutrophil cytoplasmic antibody (ANCA) is indicative of the disease. Sarcoidosis presents with laryngeal involvement in 0.5–1.4% of patients with sarcoidosis. The supraglottis is most commonly infec­ ted, in 80–85% of patients; however, subglottic (15–20%) or true vocal fold (1%) involvement can occur. The sino­ nasal tract or salivary glands can also be affected. Laryngeal symptoms can include hoarseness (in 70–85%), dyspho­nia (10–40%), dyspnea (47–60%), stridor (8–10%, cough (10–13%), or laryngeal involvement can be asympto­ matic (8-18%). The incidence of sarcoidosis is about 16.5/100,000 men and 19/100,000 women worldwide.25 Other autoimmune diseases that can, but rarely, affect the larynx include cica­tricial pemphigoid, systemic lupus erythematosus, and Churg–Strauss syndrome.

Infection As part of the upper respiratory system, infection of the larynx is quite common, but prevalence and etiologies of certain pathogens have changed significantly with medical progress, including developments in treatment and pre­ vention. Problems such as diphtheria and epiglottitis, which were common and potentially devastating, have become rare in most countries. Diphtheria can cause one

of the most impressive infectious diseases of the larynx. Diphtheria was responsible for 15,520 deaths in 1921, prior to vaccination programs, after which rates quickly dropped. From 2004 to 2008, there were no diphtheria cases reported in the United States. The case-fatality rate once at 50% has now been stable at about 5–10% since antibiotic treatment has been available. (The case-fatality rate may be as high as 20% in children less than five years and adults over 40 years).26 In a study in Sweden, Haemophilus influenzae vaccination programs for children reduced the incidence of epiglottitis from 4.5/100,000 to 1/100,000 (including children and adults).27 Epiglottitis is now more common in adults and usually secondary to Streptococcus pneumoniae, which could also usually be preventable by vaccine. Vaccination programs have changed the incid­ ence of these and other diseases and may continue to decrease the prevalence of diseases such as recurrent respiratory papillomatosis (RRP) or head and neck malign­ ancies associated with human papilloma virus (HPV) in the future.

Laryngeal Masses and Neoplasms Benign laryngeal masses typically include polyps, nodules, Reinke’s edema, and cysts. The incidence of each can be difficult to quantify as there is no histological or clinical fea­ ture that can reliably distinguish between types, aside from cysts, which are lined by epithelium. Even expert otolaryn­ gologists may not always agree as to the type of lesion.28 The estimated number of new laryngeal malignancies every year is declining, with a more significant decline between 1988 and 2010 as compared with 1975–1988, according to the National Cancer Institute.29 The mortality rate from laryngeal malignancy continues to decline as well. It was estimated that 12,260 men and women would be diagnosed with a new laryngeal malignancy in 2013 (9680 men and 2850 women). Malignancies in the head and neck are usually second­ ary to long-term exposure to carcinogens that cause genetic changes. Alcohol use is associated with malignancy as well, and, in particular, the combination of alcohol and tobacco use has a multiplicative effect. From about 1995 to 2010, the overall incidence of head and neck squamous cell carcinoma (HNSCC) was stable, but there was an increase in oropharyngeal squamous cell carcinoma, partly secondary to HPV.30 HPV malignancy has greater association in the tonsils than the larynx,31 but is still an important pathogen in the larynx, more commonly causing recurrent respiratory papilloma than malignancy.

Chapter 34: Etiology, Incidence, and Prevalence of Laryngeal Disorders Recurrent papilloma affects about 2 per 100,000 adults.32 The implications of HPV-associated malignancy in the larynx is not as well known as in the oropharynx where it is associated with improved outcomes compared with non-HPV SCC. HPV is estimated to infect 85% of humans and is present in about 25% of HNSCC specimens. In one study, HNSCC patients had a 30% prevalence of HPV 16 compared with 5% in the control group.33 HPV types 16, 18, 31, and 33 are the most common high-risk types. Types 6 and 11 are the most common low-risk types, associated with lesions such as benign papilloma.

Other Etiologies of Dysphonia or Difficulty Swallowing There are several other causes of laryngeal disease inclu­ ding trauma (penetrating and blunt trauma causing edema or arytenoids dislocation), functional disorders of the larynx, and laryngospasm (which can occur during induction of anesthesia, upon awakening from anesthesia, or unrelated to surgery). As with most medical problems, in addition to developing the differential diagnoses, a good history and physical examination can help narrow the workup.

Cough Overview and Impact Otolaryngologists see only a portion of the quarter billion of outpatient visits for cough, and should be reminded that congestive heart failure, pulmonary disease, and other systemic diseases can be a serious cause of cough. In otolaryngology practices, asthma and gastroesophageal reflux disease (GERD) are considered the most common causes of chronic cough. In a pulmonary practice in the United States, the most common causes of chronic cough were postnasal drip (PND) (41%), asthma (24%), and GERD (21%). Chronic cough was the sole symptom of asthma 28% of the time and the sole symptom of GERD 43% of the time.34 In a British pulmonary practice, additional causes of chronic cough were postviral (8%), and primary pulmonary disease (16%), the latter being more common in those with a productive cough and an abnormal radiograph.35 A multidisciplinary approach is often necessary to treat cough. The concept of the unified airway is especially important in this regard. Allergy and asthma may play significant roles in a patient’s disease process. Identifying and treating these issues should result in improved patient outcomes.36

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The etiology, incidence, and prevalence of chronic cough can vary significantly by how the chronic cough is defined, how the etiologies are defined, and the population being studied. For example, infectious etiologies of laryn­ geal disease vary significantly depending on acuity and the population being studied. (These are beyond the scope of this chapter). Etiology and incidence may also change with increasing medical knowledge, new disease entities, and increased awareness of certain problems. For example, laryngopharyngeal reflux, nonasthmatic eosinophilic bron­ chitis, and immune deficiencies are increasingly rec­ognized as causes of chronic cough. It is also important to recognize that there is significant overlap between causes of dysphonia, dysphagia, and chronic cough. For example, vocal fold para­ lysis can cause any of these symptoms, including cough, especially if there is aspiration.

Specific Etiologies of Chronic Cough Postnasal Drip PND has been described as one of the most common causes of chronic cough, mostly in pulmonary and allergy practices, whereas GERD is more frequently described as the most common etiology (in patients without asthma) in the otolaryngology literature. Otolaryngologists are more likely to diagnose the underlying etiology of PND as allergic rhinitis, vasomotor rhinitis, acute nasopharyngitis, and sinusitis. PND syndrome can also be called upper airway cough syndrome. There is no objective testing for PND and symptoms significantly overlap with LPR. Although reflux disease is not a direct cause of CRS, GERD is associated with worse nasal symptoms scores.37 Furthermore, there is a decrease in sensation of PND in patients on protonpump inhibitor therapy.

Laryngopharyngeal Reflux and Gastroesophageal Reflux Disease The criteria for diagnosis of reflux disease vary between studies making measurements of prevalence difficult. Furthermore, patients with signs of reflux on examination or pH evidence of episodes of laryngopharyngeal reflux may be asymptomatic,38 and many patients with symptoms may never seek treatment. Laryngopharyngeal reflux com­ monly appears in the literature beginning in the 1990s and helps characterize the laryngeal symptoms of reflux. However, even distal GERD may cause a chronic cough via many mechanisms, such as a vagal-mediated cough

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reflex, increased intra-abdominal pressure creating lower esophageal feedback loops, sensory neuropathy, or other mechanisms. In a series of patients with chronic cough of sudden-onset (after excluding reflux, asthma, and PND), symptomatic relief was achieved in 68% with gabapentin treatment.39

Table 34.2: Etiology of laryngeal disease in children

Infection Laryngomalacia Laryngopharyngeal reflux Laryngeal stenosis (webs) Benign lesions of the vocal folds (nodules, granulomas)

Malignancy

Recurrent respiratory papillomatosis

Laryngeal malignancies typically present with hoarseness or shortness of breath. Cancers presenting with a cough are more likely to originate in the large central airways, where cough receptors are common.40

Vocal fold immobility

Iatrogenic and Environmental When considering the workup of chronic cough in an adult, it is important to consider iatrogenic and environmental causes as well. Angiotensin converting enzyme (ACE) inhibi­­ tors are common antihypertensive medications and are notorious for causing chronic cough and, in many patients, more worrisome angioedema. Other medications that can cause GERD include anticholinergics, beta-agonists, bis­ phosphonates, calcium channel blockers, corticosteroids, benzodiazepines, estrogens, opiates, progesterone, prosta­ glandins, and theophylline.41 Sicca syndrome can cause a chronic cough. It can often result from radiation therapy or other medical problems such as autoimmune disease. Chronic cough without any of the above causes or other explanation can be referred to as chronic bronchitis. Most patients with chronic bronchitis are smokers, but there can be exposure to other airway irritants, especially in certain work environments. These patients do not usually seek treatment and are thus not a significant part of the cases in most epidemiologic studies.

Immune System Disease and Autoimmune Disease Autoimmune disease can cause chronic cough, typically as a result of another process such as sinusitis or bron­ chi­tis. Certain autoimmune diseases, such as Sjögren’s syndrome, can present more commonly with symptoms of laryngopharyngeal reflux than inflammatory lesions in the airway, as in rheumatoid arthritis, which are more likely to present with dysphonia or difficulty breathing. Eosinophilic eso­phagitis is commonly diagnosed in children, but can be diagnosed in adulthood. When looking for this disease in a series of 20 patients with no clear cause for their cough, 80% were found to have eosinophilic bronchitis.42

• Idiopathic • Neurological • Heart malformations/cardiac surgery • Prolonged intubation/difficulty delivery • Functional dysphonia Subglottic stenosis Vascular anomalies (hemangiomas) Laryngeal cleft Trauma (blunt, penetrating, alkali ingestion) Malignancy

Common variable immune deficiency (CVID) can present in adulthood, typically between 20 and 40 years old. It usually presents with recurrent infections rather than cough; however, cough can often be a manifestation of the recurrent pulmonary or sinonasal infections in these patients. CVID affects about 1/25,000 people and is, therefore, important to consider in patients with recurrent infections or “atypical asthma”.

PEDIATRIC LARYNGOLOGY Laryngeal disorders in children include many of the same problems as adults, although malignancy is rare (Table 34.2). Additional considerations are made for congenital anomalies and a careful history is important. Anatomic differences (and environmental factors) in the vocal folds of children may partially be responsible for different disease pattern. The larynx of the newborn is significantly smaller and the layers of the vocal folds are not well defined. Differentiation into two layers starts at about 2 months of age. The tri-layered lamina propria develops by about 7 years of age, but the differential composition of elastin and collagen fibers within the layers is not present until 13 years of age.43 The overall shape of the larynx is different in children and the narrowest region is the subglottis, making children susceptible to subglottic pathology. It is important to keep in mind that the epiglottis is omega

Chapter 34: Etiology, Incidence, and Prevalence of Laryngeal Disorders shaped in about 50% of the pediatric population and is not always indicative of laryngomalacia, one of the most common causes of stridor in infants.44 Of course, the larynx will naturally grow and change during child­ hood resulting in voice changes. This typically occurs without any issues.

Difficulty Breathing and Stridor Overview and Impact Stridor is the most common presenting symptom in infants with congenital laryngeal disease. In one study of infants in 2007, congenital anomalies accounted for 84% of stridor (78% were laryngeal and 6% tracheal). The most common laryngeal anomaly was laryngomalacia (94%). Twenty-first percent of children had at least one other anomaly and half of the patients were diagnosed with laryngopharyngeal reflux.45 Compared with results from the same institution 27 years earlier with all patients under 2.5 years of age, laryngeal anomalies were previously less frequent and tracheal anomalies more frequent. Laryngeal anomalies accounted for 60% of stridor, tracheal anomalies 16%, bronchial anomalies 5%, infection 5.5%, internal laryngeal trauma 5.5%, and other causes in 7%. Seven percent of patients with vascular anomalies were classified according to the area in which the vascular anomaly occurred. There was more than one anomaly in 45% of patients.46 These results demonstrate the significant prevalence of laryngomalacia in infants who present with stridor and the need to consider a second lesion in pediatric patients if given a finding of laryngomalacia or other anomaly on examination. As with adults, breathing difficulty can necessitate a tracheotomy. Most children who require a tracheotomy are those needing prolonged ventilation. Other common reasons for pediatric tracheotomies include subglottic and tracheal stenosis, respiratory papillomatosis, caustic alkali ingestion, and craniofacial syndromes.47 In any child with difficulty breathing, one must also consider the presence of a foreign body, although this is rare in the true larynx and may not necessarily produce stridor. Foreign bodies of the airway can also present as wheezing, difficulty breathing, or asthma. In the nose, they are more likely to cause nasal obstruction and drainage. Foreign bodies in the head and neck are more likely to present in the esophagus or ear than in the airway, but cause significant morbidity and mortality when present in the airway. In 2000, airway foreign bodies were

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res­ponsible for greater than 17,000 emergency department visits in children less than 14 years old in the United States.48

Dysphonia Overview and Impact Prevalence studies of hoarseness vary widely in children, from about 3.9% to 23.4%. As with difficulty breathing or stridor, dysphonia may also be a presenting symptom of a pediatric laryngeal disorder. The type of pathological phonation may help determine the cause of the dysphonia, as described in a Hungarian study. “Hoarseness” may be caused by inflammation or tumor of the vocal folds. A “hollow” voice may be indicative of tracheal stenosis. A “shrill” may be suggesting central nervous system damage. “Bleating” is pathognostic of Down syndrome. A “faint” voice may occur with myogenic disease. The “mewing cry” is pathognostic of cri-du-chat syndrome. Other hyper­ functional or hypofunctional forms may be a result of immature innervation and gradually improve and/or resolve.49 As in adults, functional disorders of the larynx can occur and are associated with emotionally traumatic events, anxiety, and depression. Muscle tension dysphonia may present with a strained, easily tired voice. Paradoxical vocal fold motion can be psychogenic and is often confu­ sed with or be present with asthma.

Specific Etiologies of Difficulty Breathing or Dysphonia Vocal Fold Dysfunction Vocal fold paralysis is commonly diagnosed in neonates with hoarseness or difficulty breathing. In one study, unilateral immobility was slightly more common than bilateral paralysis. Forty-two out of one-hundred thirteen (37%) cases were idiopathic, 29 (26%) were associated with neurological disorders, 6 (5%) were associated with heart malformations, and 15 (13%) were associated with difficult delivery. Most newborns with unilateral paralysis will have spontaneous recovery (73% of those with an abnormal delivery, 70% of those with a neurological disorder, 74% of those with an idiopathic etiology). Spontaneous recovery is less likely with bilateral paralysis, with only 52% recovery in those with either neurological disorders or idiopathic etiologies.50

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In children of all ages with unilateral vocal fold paraly­ sis, causes are similar to adults (excluding malignant etiolo­ gies in adults). Paralysis is usually left-sided (approximately 88%). The most common causes of unilateral vocal fold immobility are cardiac surgery (28.5%) and prolonged intubation/prematurity (16.7%).51 Additional surgeries causing vocal fold paralysis in children include thyroide­ ctomy and tra­ cheoesophageal fistula repair. Neurolo­ gic abnormalities associated with vocal fold paralysis include Arnold-Chiari malformation, posterior fossa tumor, menin­ gomyelocele, cerebral agenesis, and hydrocephalus.

Benign Lesions and Tumors of the Larynx Vocal fold nodules are most common in school-aged boys, but can occur in males and females of any age.52 Polyps are rare in children. Vocal fold granulomas can occur from intubation, reflux, vocal misuse or other forms of trauma. Other benign tumors include papillomas (most common tumor), cystic hygromas, neurofibromas, and hemangiomas. Infantile hemangiomas are a common tumor in the head and neck with cutaneous, salivary gland, and airway locations; however, they are a rare cause of stridor, 0.6% of patients with laryngeal anomalies causing stridor.53 Most patients with subglottic hemangiomas present in the larynx will have cutaneous hemangiomas,54 but most patients with cutaneous hemangiomas will not have hemangiomas of the larynx. PHACE syndrome is charac­ terized by abnormal posterior fossa anatomy, heman­gioma in a beard distribution, arterial abnormalities intracrani­ ally, cardiac abnormalities, and eye problems. The cause of the syndrome is unknown. About half of children with this syndrome will have airway hemangiomas, usually subglottic (83%).55 It is important for patients with large facial hemangiomas to have intracranial imaging. Other vascular malformations of the airway can occur, but are less common.56 The mean presentation is older than those of infantile hemangiomas, 11.3 months compared with three months. Vascular malformations are more likely to cause hemoptysis or dysphagia and present postcricoid or epig­lottic. CT angiogram can be helpful in distinguishing between hemangiomas and other vascular mal­ formations.

Recurrent Respiratory Papillomatosis Papillomas are caused by the HPV and are likely passed to children during birth, but the exact mechanism is not

completely understood. Vaginal delivery is associated with increased risk (4.6-fold greater); however, children born by cesarean section can also acquire RRP. Other risk factors include being the first child (1.6-fold greater), having a mother less than 20 years old (2.6-fold greater) and having a mother with genital condylomata (231 times more likely to develop RRP, 95% CI: 135–396).57 (Of note, the parity effect is largely mediated by maternal age.) These increased risk factors are not significant in adultonset RRP. HPV is prevalent in the population and most children do not develop RRP. The risk of RRP in children born to mothers with a history of condylomata is less than one percent. RRP in children is most commonly caused by HPV6 and HPV11. HPV 16, 18, and other subsets are less commonly observed and may be associated with increased risk of malignancy.58 Papillomas are usually diagnosed in childhood, most before five years old. In 2006, the incidence was about 3.5 per million person-years, with a prevalence of 4 in 100,000. Treatment accounted for an estimated 109 million annual expenditure in the United States.59 The RRP Task Force reported results from twenty tertiary-care pediatric otol­aryngology centers throughout the United States. Of children with RRP, 52% were male, 63% white, 28% black, 11% Hispanic ethnicity, and 9% other or unknown race. The mean age at diagnosis was 3.8 years. Children with RRP had an average of 4.4 surgeries per year, with children diagnosed at younger ages being more likely to need more frequent surgery.60

Infection Children have frequent respiratory infections, and because they have small airways, can be more suscep­ tible to inflammation. Children less than five years old are most likely to develop laryngotracheitis (or croup), which is characterized by a “barking” cough and subglottic edema and inflammation. Croup is most commonly caused by the parainfluenz­a virus, but can have other viral etiologies. If children have chronic laryngitis, it is important to consider other infectiou­s and non-infectious etiologies, similar to those of adults. Croup is frequently diagnosed but other laryngeal disease can exacerbate symptoms of croup. Croup is the most common cause of stridor in children over six months. It is most common in children between 6 and 36 months old.61 At two years of age, 5% of children will have had an episode of croup.62 In one study of children with atypical croup, significant laryngeal disease was often found. Over

Chapter 34: Etiology, Incidence, and Prevalence of Laryngeal Disorders one-third (39%) of patients had laryngeal pathology, including subglottic stenosis (33% of those with laryngeal pathology), laryngeal cleft (22.5%), subglottic hemangioma (19%), tracheomalacia (13%), and laryngomalacia (10%). Esophagitis was diagnosed in 45% of the children, a portion of which had eosinophilic esophagitis (14%). Forty-four percent of children had an atopic condition such as asthma, allergic rhinitis, eosinophilic esophagitis, and food allergies.63 It is important to evaluate the airway and the esophagus in children with recurrent croup-like episodes, typically involving cough and difficulty breathing.

Other Causes of Acute and Chronic Laryngitis Chronic laryngitis can be from an environmental exposure (airborne chemicals or allergies), chronic sinusitis with PND, medications, dehydration, reflux, or systemic disease (such as amyloidosis, autoimmune disease, or hypothyroidism). It is important to consider inhalation or ingestion injury in the child with acute (or chronic) onset of difficulty brea­ thing or dysphonia. Acute neck trauma may also cause difficulty breathing and dysphonia. A history of a moto­r vehicle accident or sports-related injury is usually easy to obtain. Malignancies can occur in the pediatric larynx, however, rare, and are usually rhabdomyosarcomas. Other sarcomas are the second most common malignancy. Other malignancies, such as squamous cell carcinomas, which are the overwhelming majority of malignancies of the larynx in adults, are rare in children. Additional rare malignancies in children include chondrosarcoma, lymphoma, plas­ma­cytoma, mucoepidermoid carcinoma, metastatic carci­noma, and neuroectodermal tumors.

Chronic Cough and Reflux Cough is a common complaint in 45% of preschool children and 9% of 7–11 year olds.64 The child with a chronic cough can be one of the most challenging problems in pediatric otolaryngology. The usual etiology of chronic cough is similar to that of adults although congenital anomalies such as laryngeal cleft are higher in the differential. Any process causing laryngeal incompetence can cause cough and/or aspiration. As with adults, asthma and reflux are among the most common causes of cough in childhood. However, other etiologies include nasal and sinus problems and other extralaryngeal problems, such as eosinophilic esophagitis, food allergies, immune disorders, and pulmonary diseases. The symptoms of these disorders usually overlap so signifi­ cantly with each other and with upper respiratory or other

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infections that the underlying disorder can be elusive. A multidisciplinary approach is helpful. Increasing medical knowledge and awareness of these issues can help make an earlier diagnosis. Patients are often cared for by multiple specialists. GERD in children is common, especially in infancy. It is commonly cared for by pediatricians or pediatric gastroenterologists, especially when presenting as regurgi­ tation or vomiting. Otolaryngologists are more likely to see children presenting with laryngeal symptoms, such as chronic cough, globus sensation, hoarseness, or sore throat. Laryngopharyngeal reflux is associated with asthma in children. In patients with asthma who were evaluated by 24-hour pharyngeal pH monitoring, LPR was diagnosed in 61.9% of children. The reflux symptoms scores were twice as high in those with LPR than those without.65

Specific Extralaryngeal Etiologies of Chronic Cough and Reflux Eosinophilic Esophagitis Since its description in 1983, Eosinophilic esophagitis has become widely recognized. Increasing incidence and prevalence may be due to a true increase in disease and/or increased awareness and therefore increasing num­bers of EGDs with biopsy confirming the diagnosis (histologic evidence of eosinophil-predominant inflam­ mation, with more then 15 eosinophils per high power field). The population incidence and prevalence vary by study, from 0.7 to 10 per 100,000 person-years. Prevalence ranges from 0.2 to 43 per 100,000.66 Clinical signs of eosi­ nophilic esophagitis include feeding difficulties, failure to thrive, GERD, nause­ a, vomiting, chest or epigastric pain, food impaction, and dysphagia. Atopy is common. Patients may have allergic rhinitis, asthma, eczema, and IgE-mediated food allergies.

Systemic Disease Pulmonary disease and cardiac disease can cause a chronic cough in children, as in adults. Immune deficiencies can evade diagnosis as healthy children can have upper respira­ tory problems very frequently. Recurrent pneumonia is often a sign of a more serious condition. Recurrent pneumo­ nia can be indicative of pulmonary disease. In children, especially with chronic sinonasal disease, cystic fibrosis should be considered. As of 2010 cystic fibrosis screening has been mandatory in all states in the United States, with

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many states screening long before that. The overall birth prevalence of cystic fibrosis in the United States is 1 in 3,700,67 and while present in nearly every race and around the world, the prevalence varies in different populations.

Congenital and Genetic Anomalies Congenital structural anomalies of the vocal fold are rare, but include webs, cysts, clefts, and laryngeal agenesis. Some congenital lesions are associated with other abnormalities. Ten percent of patients with webs have other anomalies, usually of the upper respiratory tract, such as subglottic stenosis or submucous cleft palate.68,68a Laryngeal clefts are associated with Opitz GBBB syndrome but can also occur in nonsyndromic patients. Laryngeal webs can occur as part of the 22q11 deletion syndromes (DiGeorge and velocardiofacial syndrome). Cri du chat is caused by a deletion on the short arm of chromosome 5 and has a prevalence of 1 in 50,000 live births. In addition to a high pitched cry, children have receptive and expressive language deficits.69 The etiology of sulcus vocalis is often unknown, but it may be congenital and possibly congenital, in some cases, as a result of failure of development of the 4th and 6th branchial arches. There are adult patients diagno­sed with sulcus vocalis who have had a history of dysphonia since childhood. Sulcus vocalis has also been reported in families, although no known gene has been identified. Sulcus vocalis may, alternatively, be a result of include chronic inflammation or atrophy of the vocal folds.70

Difficulty Swallowing Overview and Impact Children with difficulty swallowing can present in a variety of ways. They can have chronic problems that are followed in ambulatory settings or acutely in the emergency depart­ ment. The etiologies in these settings vary. The differential changes based on patient age as well. For the patient who presents to the otolaryngologist with difficulty swallowing, ensuring normal laryngeal anatomy and function is critical. Most laryngeal etiologies will also cause symptoms of hoarseness, difficulty swallowing, chronic cough or other problems, and are addressed above.

CONCLUSION The etiology of laryngeal disorders includes disease pro­ cesses of all kinds, including those intrinsic to the larynx

and important extralaryngeal diseases. The differentials discussed are not exhaustive of the types of problems that individual patients may have, but problems that are either important because they are ubiquitous, uphold classic principles of epidemiology, or have unique epidemiology. Common complaints are addressed, such as hoarseness, cough, and difficulty breathing. Rare complications of common problems, which ultimately result in relatively high patient volumes, are addressed. Additional etiologies, incidence, and prevalence information are available in other chapters.

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Chapter 34: Etiology, Incidence, and Prevalence of Laryngeal Disorders 15. Hartelius L, Svensson P. Speech and swallowing symptoms associated with Parkinson’s disease and multiple sclerosis: a survey. Folia Phoniatrica Logopedica. 1994;46:9-17. 16. National Institute of Neurological Disorders and Stroke. Parkinson’s Disease Backgrounder, Retrieved June 24, 2013 from http://www.ninds.nih.gov/disorders/parkinsons_ disease/parkinsons_disease_backgrounder.htm 17. Berke GS, Gerratt B, Kreiman J, Jackson K. Treatment of Parkinson hypophonia with percutaneous collagen aug­ men­tation. Laryngoscope. 1999;109:1295-9. 18. Noonan CW, Williamson DM, Henry JP, et al. The preva­ lence of multiple sclerosis in 3 US communities. Prev Chronic Dis. 2010;7(1)A12. Accessed on June 24, 2013 at http://www.cdc.gov/pcd/issues/2010/jan/08_0241.htm. 19. Rigueiro-Veloso MT, Pego-Reigosa R, Branas-Fernandez F, et al. Wallenberg syndrome: a review of 25 cases. Rev Neurol. 1997;25(146):1561-4. 20. Venketasubramanian N, Seshadri R, Chee N. Vocal cord paresis in acute ischemic stroke. Cerebrovasc Dis. 1999;9 (3):157-62. 21. House JC, Noordzij JP, Murgia B, Langmore S. Laryngeal injury from prolonged intubation: a prospective analysis of contributing factors. Laryngoscope. 2011;121(3):596-600. 22. Benninger MS, Alessi D, Archer S, et al. Vocal fold scarring: current concepts and management. Otolaryngol Head Neck Surg. 1996;115:474-82. 23. Haben CM, Chagnog FP, Zakhary K. Laryngeal manifesta­tions of autoimmune disease. J Otolaryngol. 2005;34(3):203-6. 24. Erickson VR, Hwang PH. Wegener’s granulomatosis: cur­ rent trends in diagnosis and management. Curr Opin Oto­ laryngol Head Neck Surg. 2007;15:170-6. 25. Mrowka-Kata K, Kata D, Lange D, et al. Sarcoidosis and its otolaryngological implications. Eur Arch Otorhinolaryngol. 2010;267:1507-14. 26. CDC. (2103). Diphtheria. Retrieved June 21, 2013, from http://www.cdc.gov/diphtheria/clinicians.html 27. Isakson M, Hugosson S. Acute epiglottitis: epidemiology and Streptococcus pneumoniae serotype distribution in adults. J Laryngol Otol. 2011;125(4):390-3. Epub 2010 Nov 25. 28. Cipriani NA, Martin DE, Corey JP, et al. The clinicopathologic spectrum of benign mass lesions of the vocal fold due to vocal abuse. Int J Surg Path. 2011;19(5):583-7. 29. Howlader N, Noone AM, Krapcho M, et al. SEER Cancer Statistics Review, 1975-2010, National Cancer Institute. Bethesda, MD, http://seer.cancer.gov/csr/1975_2010/,  based on November 2012 SEER data submission, posted to the SEER web site, 2013. 30. Allen CT, Lewis JS Jr, El-Mofty SK, et al. Human papil­ lomavirus and oropharynx cancer: biology, detection and clinical implications. Laryngoscope. 2010;120:1756-72. 31. Hobbs CG, Sterne JA, Bailey M, et al. Human papillomavirus and head and neck cancer: a systematic review and metaanalysis. Clin Otolaryngol. 2006;31(4):259-66. 32. Derkay CS. Task force on recurrent respiratory papilloma. Arch Otolaryngol Head Neck Surg. 1995;121(!2):1386-91. 33. Chen KM, Stephen JK, Ghanem T, et al. Human papilloma virus prevalence in a multiethnic screening population. Otolaryngol Head Neck Surg. 2013;148(3):436-42.

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34. Irwin RS, Curley FJ, French CL. Chronic cough. The spe­ ctrum and frequency of causes, key components of the diagnostic evaluation, and outcome of specific therapy. Am Rev Respir Dis. 1990;141(3):640. 35. Kastelik JA, Aziz I, Ojoo JC, et al. Investigation and man­ agement of chronic cough using a probability-based algorithm. Eur Respir J. 2005;25(2):235. 36. Krouse JH, Brwon RW, Fineman SM, et al. Asthma and the unified airway. Otolaryngol Head Neck Surg. 2007;136(5 Suppl):S75-106. 37. Hanna BC, Wormald PJ. Gastroesophageal reflux and chronic rhinosinusitis. Curr Opin Otolaryngol Head Neck Surg. 2012;20(1):15-8. 38. Hicks DM, Ours TM, Abelson TI, et al. The prevalence of hypopharynx findings associated with gastroesophageal reflux in normal volunteers. J Voice. 2002;16(4):564-79 39. Lee B, Woo P. Chronic cough as a sign of laryngeal sensory neuropathy: diagnosis and treatment. Ann Otol Rhinol Laryngol. 2005;114(4):253-7. 40. Hyde L, Hyde CI. Clinical manifestations of lung cancer. Chest. 1974;65(3):299. 41. Chandra KM, Harding SM. Therapy insight: treatment of gastroesophageal reflux in adults with chronic cough. Nat Clin Pract Gastroenterol Hepatol. 2007;4(11):604-13. 42. Brightling CE, Ward R, Woltmann G, et al. Induced sputum inflammatory mediator concentrations in eosinophilic bronchitis and asthma. Am J Respir Crit Care Med. 2000; 162(3 Pt 1):878. 43. Hartnick CJ, Rehbar R, Prasad V. Development and maturation of the pediatric human vocal fold lamina propria. Laryngoscope. 2005;115:4-15 44. Zoumalan R, Maddalozzo J, Holinger L. Etiology of stridor in infants. Ann Otol Rhinol Laryngol. 2007;116(5):329-34. 45. Zoumalan R, Maddalozzo J, Holinger LD. Etiology of stri­ dor in infants. Ann Otol Rhinol Laryngol. 2007;116(5): 329-34. 46. Holinger LD. Etiology of stridor in the neonate, infant and child. Ann Otol Rhinol Laryngol. 1980;89(5 Pt 1):397-400. 47. Hadfield PJ, Lloyd-Faulconbridge RV, Almeyda J, et al. The changing indications for pediatric trach­ eostomy. Int J Pediatr Otorhinolaryngol. 2003;67(1):7-10. 48. Centers for Disease Control and Prevention (CDC). Nonfatal choking-related episodes among children—United States, 2001. MMWR Morb Mortal Wkly Rep. 2002;51(42):945. 49. Hirschberg J. Dysphonia in infants. Int J Pediatr Otorhinol­ aryngol. 1999;49:S293-6. 50. de Gaudemar I, Roudaire M, François M, et al. Outcome of laryngeal paralysis in neonates: a long term retrospective study of 113 cases. Int J Pediatr Otorhinolaryngol. 1996;34 (1-2):101. 51. Shah RK, Harvey-Woodnorth G, Glynn A, et al. Perceptual voice characteristics in pediatric unilateral vocal fold paralysis. Otolaryngol Head Neck Surg. 2006;134 (4):618. 52. Cornut G, Troillet-Cornut A. Childhood dysphonia: clinical and therapeutic considerations. J Voice. 1995;4:70. 53. Zoumalan R, Maddalozzo J, Holinger LD. Etiology of stri­ dor in infants. Ann Otol Rhinol Laryngol. 2007;116(5): 329-34.

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54. Parhizkar N, Manning SC, Ingalis AF Jr, et al. How airway venous malformations differ from airway infantile heman­ giomas. Arch Otolaryngol Head Neck Surg. 1022;137 (4)352:7. 55. Durr ML, Meyer AK, Huoh KC, et al. Airway hemangiomas in PHACE syndrome. Laryngoscope. 2102;122(10):2323-9. 56. Parhizkar N, Manning SC, Inlis AF Jr, et al. How airway venous malformations differ from airway hemangiomas. Arch Otolaryngol Head Neck Surg. 2011;147(4):352-7. 57. Shah KV, Stern WF, Shah FK, et al. Risk factors for juvenile onset recurrent respiratory papillomatosis. Pediatr Infect Dis J. 1998;17(5):372-6. 58. Joos B, Joos N, Bumpous J, et al. Laryngeal squamous cell carcinoma in a 13-year-old child associated with human papillomaviruses 16 and 18: a case report and review of the literature. Head Neck Pathol. 2009;2:37-41. 59. Tasca RA, Clarke RW. Recurrent respiratory papillomatosis. Arch Dis Child. 2006;91(8):689. 60. Armstrong LR, Derkay CS, Reeves WC. Initial results from the national registry for juvenile-onset recurrent respiratory papillomatosis. RRP Task Force. Arch Otolaryngol Head Neck Surg. 1999;125(7):743. 61. Choi J, Lee GL. Common pediatric respiratory emergencies. Emergency Med Clin North Am. 2012;30(2);529-63. 62. Cherry J. Clinical practice. Croup. N Engl J Med. 2008;358 (4):384-91.

63. Cooper T, Kuruvilla G, Persad R, et al. Atypical croup: association with airway lesions, atopy, and esophagitis. Otolaryngol Head Neck Surg. 2012;147(2):209-14. 64. Palmer R, Anon J, Gallagher P. Pediatric cough: what the otolaryngologist needs to know. Curr Opin Otolaryngol Head Neck Surg. 2011;19:204-9. 65. Banaskiewicz A, Dembinski L, Zawadzka-Krajewska A, et al. Evaluation of laryngopharyngeal reflux in pediatric patients with asthma using a new technique of pharyngeal pH-monitoring. Adv Exp Med Biol. 2013;755:89-95. 66. Soon IS, Butzner JD, Kaplan GG, et al. Incidence and prevalence of eosinophilic esophagitis in children. JPGN. 2013;57:72-80. 67. Centers for Disease Control and Prevention. Newborn screening for cystic fibrosis. MMWR. 2004;53(RR13):1-36. 68. McHutgh HE, Loch WE. Congenital webs of the larynx. Laryngoscope. 1942;52:43. 68a. Benjamin B. Chevalier Jackson lecture. Congenital laryn­ geal webs. Ann Otol Rhinol Laryngol. 1983;92(4 Pt 1):317. 69. Virbalas JM, Palma G, Tan M. Obstacles to communication in children with cri du chat syndrome. J Voice. 2012;26(6): 821.e1-3 70. Martins RH, Silva R, Ferreira DM, et al. Sulcus vocalis: probable genetic etiology. Report of four cases in close relatives. Braz J Otorhinolaryngol. 2007;73(4):573.

Chapter 35: Dynamical Disorders of Voice

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CHAPTER

Dynamical Disorders of Voice

35

Ronald J Baken, Robert F Orlikoff The modern era of voice research might fairly be said to have begun about 60 years ago, with the elaboration of a crucial understanding: phonation results from and is governed by the biomechanical characteristics of vocal fold tissue interacting with glottal aerodynamics. That insight was the heart of the myoelastic–aerodynamic theory of phonation,1-3 a construct that physiologic observation of vocal fold behavior has amply validated. Numerous mathematical models of vocal fold function that were founded upon it4-5 have generally had extraordinarily impressive predictive and explanatory power. As a result, the process of normal phonation is quite well understood. Unfortunately, despite very serious efforts by many of our best researchers over a significant period of time, there are still large gaps in our comprehension of laryngeal phonatory behavior. Nowhere are these lacunae wider than in our understanding of many of the anomalies encountered in abnormal vocal function, and (when one actually looks for them) even in the normal voice.6 The increase in frequency and amplitude perturbation that is so characteristic of dysphonia, e.g. remains only poorly explained, despite several hypotheses of varying attractive­ ness.7-13 The “pitch breaks” of the adolescent also lack a coherent explanatory model, as does the “biphonation” of the infant’s cry.14-15 Even less well explained is the kind of situation illu­ strated in Figure 35.1A, which shows the fundamental frequency (F0) of successive periods during a sustained vowel by an 81-year-old female with a diagnosis of spas­ modic dysphonia. Her F0 undergoes a relatively slow cyclic variation at a rate of about four cycles per second, perhaps

caused by tremor of the laryngeal muscles. There is also, however, a much faster frequency variation that is some­ times observable at the peaks of the slower oscillations. This is harder to explain. However, most striking are the outbreaks of “diplophonia”—more properly, subharmonic oscillation—that occur in the “valleys” of the F0 pattern and that persist halfway up the next peak. We have had no easy explanation for this kind of behavior. Even less have we been able to offer coherent and parsimonious expla­ nations for the more complex patterns of F0 change, like that of Figure 35.1B, that are not uncommon in dysphonic voices. While we have developed a fairly clear picture of the mechanisms of the phonationally regular, we have not done nearly as well in elucidating the vocally complex or erratic. Our measurement techniques and our taxonomies of vocal pathology are mutually interactive and interde­ pendent. Testing and measurement methods are deve­ loped according to our conceptions of how disorders are categorized, and abnormal voices are categorized largely by the types of data obtained. Yet there may be something missing, whose need grows in proportion to the increas­ ing sophistication of the remedial methods at our disposal. Intervention strategies are becoming ever more refined, more precisely targeted, and more physiologically based. On the medicosurgical plane, remediation methods include, e.g. more refined surgical approaches to resto­ ration or optimization of vocal fold morphology, as, e.g. in cases of vocal fold scarring or sulcus vocalis16-19 and optimization of regional biomechanics by implantation of many different endogenous and exogenous materials of

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A

B

Figs. 35.1A and B: (A) Fundamental frequency of successive glottal cycles (blue circles) by an 81-year-old woman with spasmodic dysphonia. There is a pattern of cyclic and subcyclic variation in fundamental frequency and intervals of subharmonic oscillation when the fundamental frequency drops below a certain level; (B) Fundamental frequency of successive cycle of a dysphonic voice. There is the sudden appearance of frequency “quadruplets”.

widely varying rheological properties,20-26 either to restore tissue contours or improve structural rheology. On the be­ havioral front, new therapies are being developed that take advantage of the anatomic or physiologic phenomena at the heart of phonatory mechanisms. The alteration of airway impedance as a means to altering glottal aerody­ namics and vocal tract acoustics is one example of such a physiologically based approach to correction of appropri­ ately chosen cases of dysphonia.27-30 On the relatively near horizon is the application of tissue engineering techniques that operate on the cellular and molecular level to alter unacceptable vocal fold pro­ perties or to replace defective vocal tract components.31-36 Successful implementation of the methods being devel­ oped by cell biologists will require a deep understanding of the ways in which biomechanical properties deter­ mine the characteristics of vocal fold oscillation in a given case. As progress is made in all these domains, it will be increasingly necessary to have a better characterization of acoustic output, aerodynamics, tissue properties, and biomechanics. But more importantly, we will require a meaningful and interpretable description that can charac­ terize and categorize what happens as all of the parts work together, with all their interactions and mutual influences taken into account. As interventions get closer and closer to the structural and functional level, it will be especially necessary to understand the dynamics of the phonation process that is to be addressed therapeutically. Our current diagnostic test armamentarium is not equipped to extend to this deeper level. All too few of

the tools currently at our disposal allow for sufficiently fine-grained and unambiguous dynamical descriptions. Yet dynamical analysis is likely to prove extraordinarily helpful in establishing the goals—at the rheological level— of surgical, cytological, or behavioral intervention. It also offers the possibility of deeper insight into clinical and theoretical situations that are clinically not unusual but are not well explained or characterized or categorized with the methods and taxonomies more commonly available at this time. Call them “misbehavior of apparently intact systems”. They include abnormal phonation by healthylooking vocal folds, sudden pitch breaks without apparent physiologic origins, transient intrusion of aphonia or of complex patterns of oscillation into ongoing phonation, and abnormalities of voice initiation. It is our contention that voice research and vocal rehabilitation will benefit from a new and parallel taxo­ nomy of dysfunction that is grounded in the science of nonlinear dynamics. While it seems clear that the diagnostic categories that have traditionally been used are likely to be valid and have proven their worth with respect to observable organ and tissue abnormalities— and more or less demonstrably valuable in the service of medicosurgical intervention—it is nonetheless possible that they do not offer a complete picture and may not be reflective of some important natural categories of phona­ tory behavior. The present purpose is not to promulgate a new theory of diagnosis, and most certainly not to unveil a new taxonomy. The necessary science for that is nowhere near sufficiently developed. At present, one can

Chapter 35: Dynamical Disorders of Voice make no pretense to the definitive because it may be too soon even for the tentative. Rather, the objective in what follows is to point out and encourage a novel perspective, a conceptual approach that has the potential to provide a much better understanding of the dysfunctions of patients’ vocal systems and to offer a more complete guide to rehabilitation. The outlook improved dramatically about 25 years ago with the recognition of the pivotal importance, broad applicability, and enormous explanatory power of a radi­ cally different way of considering natural phenomena. The new discipline is formally known as the theory of nonlinear dynamics, but it is more popularly called chaos theory. It offers a different way of looking at life func­ tion37-39 that has begun to have a significant impact in the biomedical world. Cochlear function,40 abnormal motor behavior,41 cardiac electrical instability,42-46 Cheyne–Stokes respiration,47 cerebral electrophysiology,48 and even men­ opausal hot flashes49 have been explored with the new tools—both qualitative and quantitative—that it provides. The application of chaos theory to voice production is now well under way.50-66 It holds the promise of important breakthroughs in understanding those erratic phenomena of voice, normal and disordered, that have thus far proved so intractable. Recent years have seen a rising tide of publications suggesting the applicability of the theoretical concepts of nonlinear dynamical systems theory to vocal dysfunction. With only a few exceptions, most have focused on the detection of chaotic phenomena in the vocal signal,67-78 but nonlinear dynamics theory is more than just chaos. It is concerned with irregularity of every sort, and has much to offer to the elucidation of the origins of vocal productions of all signal types.79-83 There have been only a few attempts to apply the broader principles of nonlinear dynamical theory to clinical assessment of dysphonia, yet it is clear that the basic theoretical position and the analytic methods it offers are potentially of enormous value, since to analyze the dynamics of a system is to characterize it at a deeper level, a level where the influences of all the contributing influences are accounted for, but the distractions of the particular background phenomena are themselves removed. The science of nonlinear dynamics is unfamiliar territory to most professionals, and it is mathematically complex. Understanding its foundational concepts, while not particularly difficult, does require that its students adopt a certain amount of conceptual reorganization and

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develop a relaxed acceptance of principles that violate many of the assumptions inherent in more traditional physical sciences and mathematics. The purpose of this chapter is to consider a few of the most basic concepts of chaos theory, and to show how they might profitably be applied to problems of vocal dysfunction. The theory itself is intensely mathe­ matical, and the mathematics can be quite difficult and counterintuitive. It is, therefore, useful to take a very informal concept-oriented approach even though doing so greatly circumscribes the extent to which important areas can be developed. The objective is not to provide a tutorial introduction to applied chaos theory so much as to suggest something of the flavor of this relatively new branch of science and to suggest why it holds such promise. To do this, some conjectures will be proposed that might explain the sudden appearance of phona­ tory anomalies that are so characteristic of disordered voices. Insofar as possible, we will proceed in a completely nonmathematical (and consequently nonrigorous) way, because it seems likely that doing so will meet the needs of most readers who would like to understand the general tenor of what is involved, but who are unlikely to want to tackle nonlinear dynamical analyses themselves (at least not yet). Numerophiles and those who wish really to explore the area should consult a good general text.

CHAOS DEFINED The very term “chaos” has become almost trendy, a fashionable buzzword that is too often dropped into discussions as a synonym for “erratic”, “unpredictable”, or “very complex”. But, in the dynamical context, the word chaos has, in fact, a very specific definition. If it is to be a useful concept, it is important to specify exactly what “chaos” really means. Basically, behavior can be said to be chaotic if and only if: • It is the product of a deterministic system. “Determi­ nistic” means that the observed behavior is not ran­ dom but is governed by a rule. We may not understand what that rule is but we must know that it does, in fact, exist and that it is controlling the system. The fact that there is a governing rule is the sine qua non of a chaotic system • The system that generates the behavior is nonlinear. In the algebraic sense, a linear system is one whose function can be plotted as a straight line on a graph, as on the left side of Figure 35.2A, which idealizes the relationship between the length of a spring and the

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load acting on it. In contrast, a nonlinear function— the relationship between lung pressure and lung volume—is shown on the right side of Figure 35.2A. (Most physiologic relationships are, in fact, nonlinear). From the physical point of view, a linear system is one that is purely “feed-forward”. That is, each part of the system feeds its output into the following stage, and no element provides any feedback to an earlier stage. A very simple model of the vocal tract, on the left of Figure 35.2B, represents voice production as a linear system: the signal produced by the larynx is processed by the vocal tract that radiates its output as a sound wave. But in reality voice production involves signi­ ficant nonlinearity, schematized on the right of Figure 35.2B: the vocal tract properties, e.g. do affect the vocal folds as does auditory feedback (among other factors) • Despite the determinism (rule-based operation) of the generating system, the output is nonetheless

unpredictable. This requirement needs to be under­ stood carefully. It does, of course, imply that the be­ havior might be random-looking. But it also allows, e.g. for the system to produce a number of different patterns of response (within each of which a succes­ sion of output states might be completely predictable). If one is not able to specify, to any arbitrarily specified level of precision, which pattern will be produced at any given time, the system may validly be described as chaotic (provided, of course, that the other require­ ments are met). • The system must have a relatively small number of parameters. That is, it must be controlled by only a few factors. Put another way, a chaotic system, however much it behaves in complex ways, must nonetheless be a fairly simple system. For reasons that will shortly become clear, it is described as a “low dimensional” system.

A

B

Figs. 35.2A and B: In a linear system, one variable can be represented as a straight-line function of another variable, as in the relationship between the length of a spring and the load it is carrying (A, left). However, relationships in a nonlinear system can be represented only by something other than a straight-line plot: the relationship between lung pressure and lung volume (A, right) is an example. In a linear combination of elements each component influences only the component that follows it (purely feed-forward) as in the (overlysimple) model of phonation on of B, left. In a real vocal tract (B, right), there are numerous instances of a feedback: each element tends to modify the function of the component that feeds into it.

Chapter 35: Dynamical Disorders of Voice • Finally, the behavior of the system must be “exquisitely sensitive to initial conditions”. What this means is that extremely small differences in some controlling parameter can have dramatically large effects on the qualitative aspects of the system’s behavior. In fact, radical shifts in the output of a chaotic system can be produced by changes that are infinitesimally small. “Infinitesimal” is used here in its literal mathematical sense. Therefore, we can never have enough decimal places in our specification of the controlling variable to be able to predict the resultant behavior of the system with absolute certainty. Furthermore, an infini­ tesimally small difference is, from a practical point of view, a difference of zero. This implies that a chaotic system can change its behavior for no measurable reason at all.

THE INFLUENCE OF NONLINEARITY Nonlinearity is a useful property in a system, but it must be kept under control. Too little may limit the system’s flexibility—its ability to adapt to changing demands and conditions. However, excessive nonlinearity may cause the system to be unstable, difficult to control, and, in fact, to be subject to sudden catastrophic failure. An experiment using a simple model of the vocal folds is sufficient to suggest the possible phonatory effects that even a limited amount of nonlinearity might engender.84 Reasonable values were selected for the various parameters of the Ishizaka-Flanagan two-mass model85 of the vocal folds, including the tension of the upper and lower vocal fold masses. The proportion of tension of the lower part of the vocal fold that behaves nonlinearly was varied from 0.1% to 0.9% and the behavior of the model was studied. Figures 35.3A to D demonstrate that a small amount of nonlinearity has a significant influence on phonation. Increasing the influence of nonlinearity causes the vocal F0 and glottal airflow to change very significantly and (of potentially great interest to the clinician) results in large and unpredictable variations in both jitter and shimmer. It is therefore reasonable to suppose that Conjecture 1: The extent to which operating nonlinear­ ity is constrained is a vital characteristic of a given phona­ tory system. There are some ways in which one might begin to use phonatory acoustic and physiologic waveforms to assess the importance of nonlinearity in a given vocal system. The task of applying them is likely to be neither simple nor free of compromises. But it is important to begin, because

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Conjecture 2: Vocal pathologies will be reliably classifi­ able in terms of the degree of system nonlinearity.

EVALUATING THE DYNAMICS OF A SYSTEM Trajectories in State Space How can one describe the dynamics (the behavior) of a system? One of the common ways is to plot its behavior in state space (often called phase space). It is easier to understand what this means from an example than from a definition, and an example will prove useful in developing some further concepts. Consider a pendulum—like one that hangs from a clock. Give it, for the sake of example, the rather special property that it is not subject to friction so that, once started, it swings forever. It turns out that the dynamics of this extraordinarily simple system can be fully described in terms of the position and velocity of the pendulum. We can show their relationship graphically, as in Figure 35.4. The position of the pendulum (in degrees) to the left or right of midline is plotted on the horizontal axis, while its speed (in degrees per second, toward the left or right) is plotted on the vertical axis. The (two-dimensional) space that these axes create is one example of a state space (also called a phase space). The circle that results is a trajectory that passes through all the points in this space that are possible for a simple pendulum. It, therefore, demarcates all the combinations of position and speed that this uncomplicated dynamic system can have. As it happens, the pendulum is so simple that a two-variable state space is enough to define its dynamics completely. That is, there is nothing else that we need to know (or would have to derive) about this system to understand all its operation.

Attractors Real pendulums, of course, are subject to friction. Move a pendulum to one side, let it go, and with each oscillation a little energy is lost and the width of the swing decreases, until finally the pendulum hangs at rest. This is represented by the phase-space trajectory in Figure 35.5A. Having been pulled to the right (indicated by the black square) and let go, the pendulum swings in ever-diminishing arcs (the spiral in the velocity vs position phase space) until it comes to rest, hanging vertically, motionless. To counter this tendency to “wind down”, pendulum clocks have a mechanism that provides a little “kick” when the

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A

B

C

D

Figs. 35.3A to D: Changes in four characteristics of the behavior of the Ishizaka-Flanagan two-mass model as nonlinearity of the “tension” of the vocal fold is increased. F0 and mean peak flow change in a relatively smooth way, but jitter and shimmer vary unpredictably.

Fig. 35.4: The trajectory of a swinging pendulum in a velocity/ position phase space.

pendulum passes a given point, once in each swing cycle, adding back the energy that was lost during the previous oscillation. Now, the amount of energy added by each kick is constant, and is just enough to keep the pendulum’s arc at a given width. Suppose, therefore, that the pendulum is started by pulling it far from the midline, to a position much further out than it would normally swing. Remembering that the once-per-cycle kick only provides enough energy for a swing of moderate width, it is clear that the amount of energy lost to friction on the initial relatively huge swing will not be fully made up by the kick. Therefore, the next swing will be a little less energetic, and a little less wide. In fact, more energy is lost during each wider-than-normal swing than is restored by the kick, and so the swings will constantly become less wide until the arc is just the right size—the size at which the energy lost is exactly made up

Chapter 35: Dynamical Disorders of Voice

477

A

B

C

Figs. 35.5A to C: Trajectories in a phase space of a pendulum under different conditions. In image (A), there is no restoration of the energy lost on each swing. It will ultimately come to rest. But if energy losses are made up for by giving the pendulum a “boost” on each swing (B and C), then no matter where it is started from, it will ultimately settle into and remain on a final and stable trajectory, called an attractor.

by the energy that the kick adds. Because, at this arc width, the energy loss and addition are exactly balanced, the pendulum will continue to oscillate in an arc of that width (for as long as the clock is kept wound up). In phase space, the pendulum system will then follow the heavy circular path forever. The situation is illustrated in Figure 35.5B. A similar situation prevails, in reverse, if the pendulum is started from just a little bit off the vertical midline (Fig. 35.5C). If the energy provided by the kick is the same as in the previous example, then it will be just a little more than the pendulum loses during its initial small swing. Hence, the width of the swing will grow wider (it will spiral out in phase space) until, as before, the energy put in by the kick is equal to the energy lost to friction. Thus, it will follow this very same circular path around phase space forever, as long as none of the conditions changes. The final trajectory, then, has an important property. Starting the pendulum from almost anywhere in the

state space—with however much displacement from the midline, and with however strong a push one might give it— it will always end up swinging with the same frequency and arc width. The path of the trajectory seems to be compelled to head for the same final trajectory, which is therefore called an attractor. Whatever else they might be, from the dynamics point of view, the vocal folds, just like a pendulum, constitute an oscillator, and their behavior can also be represented in an appropriately constructed phase space. Figure 35.6 offers an example using the electroglottographic (Lx) record of phonatory initiation by a normal speaker. The phase-space axes are the instantaneous magnitude of the Lx signal and the magnitude of the same signal some time later, the “lagged EGG”. (More about the validity of doing this will be offered later.) Vocal fold oscillation is enormously more complex than the swing of a simple pendulum, and it is nowhere near as neat and regular. Nonetheless, their

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Fig. 35.6: Trajectory in phase space of the electroglottogram at the start of phonation (small circle in center) by a normal speaker. The trajectory spirals out to a (somewhat messy) attractor.

phase-space trajectories have some features in common. The phonation trajectory begins in the region of the black circle in the middle of the phase space, but close inspection (especially of the lower-right quadrant) shows that it “spirals out” to a final orbit, an attractor. The “EGG attractor” is clearly not neat and orderly like the pendu­ lum attractor: it is a tangle of not-quite-identical traces clumped messily together in phase space. That fact tells us some important things about the dynamics of phona­ tion, and points to the need for a phase space of more than two dimensions.

Dimension If a simple pendulum was free to swing not only from side to side but also front to back (so that its path through real space describes not an arc, but a horizontal circle), then we would need another phase-space axis to account for and describe its motion. Adding an axis creates a threedimensional space, which is the minimum that would be necessary to completely describe this system. Hence, it could be called a three-dimensional dynamical system. “Dimension” is the way in which we specify the number of axes, each representing an independent variable that is necessary to completely describe the dynamics of a system, and to account for all of its governing factors.

It is obvious that three variables (i.e. three axes) are still not going to depict all of the information that is available in a complex vocal signal. More variables (more signals, more axes) will be needed. Although there is no way to depict them on a single graph in our threedimensional world, at least from a mathematical point of view adding a fourth axis, or a fifth, or a tenth, will be no more difficult than was adding a third one. There will ultimately come a point in this axis-adding process when all of the information present in the voice signal will have been accounted for. The minimum number of axes—and hence, the minimum number of dimensions— needed to fully account for its behavior is a measure of the complexity of a signal. Each axis that is added to the data plot defines a dimension of the phase- or state space that is created. So saying that complete characterization of a voice requires n variables (n axes) is to say that all the information it contains requires a plotting area, or state space, of at least n “dimensions”. To determine, therefore, that a given phonation can only be fully depicted in an n-dimensional state space is to say that n factors are needed to tell us everything that there is to know about it. The process for estimating how many dimensions are needed involves, not surprisingly, moderately complex mathematical considerations* One crucial, amazing, and eminently useful element in that mathematical back­ ground is the fact that it can be proven that all of the relevant factors do not have to be known at all. The Takens Embedding Theorem90 assures us that we can construct new axes—provide new dimensions—out of the data that are already available by using one of the data sets with a fixed “lag”—that is, by plotting (to take a very simple case) datum Xn against datum Xn+lag. (Finding the optimal lag is not a simple matter, however.) So to increase the number of dimensions in which we are plotting the system’s dynamical trajectory we do not have to measure anything new at all. There are, in addition, well-established ways of determining when we have all the dimensions that are needed to completely “fit” the trajectory of the system’s behavior.91-93 Thus, it is possible—and usual—to determine how many dimensions a given dynamical sys­ tem’s behavior occupies without knowing what those dimensions specifically represent or what they are called.

* The underlying logic is not particularly daunting, but it requires a certain amount of rethinking of long-held assumptions and biases. A very elementary outline of what is involved can be found in Baken,86 a somewhat more technical discussion is provided by Kakita and Okamoto,87 and much more compact considerations are available in Berhman and Baken88 or Tokuda et al.89

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How, in the everyday world of clinical practice, is a dimensional categorization likely to be different from our present taxonomy? The standard superior endoscopic views of two larynges in Figure 35.7 suggest one possible example. The two sets of vocal folds share a common diagnosis: ordinary vocal fold polyps. To the eye, there is not much apparent difference between the two cases. Yet there is an important distinction. The polyps shown in Figure 35.7A are found, on stroboscopic observation, to be relatively firmly attached to the deeper tissue. Although they intrude on the glottis, they move together with the vocal fold margins. Thus, they do not radically change the basic dynamical pattern of vocal fold oscillation. Although not apparent on visual inspection of a single frame, as in the figure, the situation is quite different in the case of Figure 35.7B. Here, the polyps are only loosely attached, and hence, as the vocal fold margin moves, the polyp tissue flops about with some degree of independence, behaving as partially independent pendulum like oscilla­ tors in their own right. The result is that the two larynges are almost certain to produce glottal waves (vocal source signals) that differ in some discernible ways. From the dynamical point of view, the polyps of Figure 35.7B are likely to contribute additional participating degrees of freedom (i.e. to require a higher dimensional state space) to this vocal system. If so, the dynamics of this larynx’s behavior would likely be hyperdimensional. In contrast, the movement of the polyps of Figure 35.7A is more or less completely governed by the motion of the vocal folds to



The value of dimensionality is that each dimension represents a degree of freedom in the system. A degree of freedom, with respect to phonation, is a variable factor that is actually participating in the creation of the vocal product. While it may be true that there is an uncountable number of different kinds of potential adjustments that could be made to the many players in the phonatory system, the fact is that the overwhelming majority of them are held constant for any given voice production, and hence, in a dynamical sense, are not participating and do not need to be modulated or dynamically controlled. The number of active degrees of freedom, and hence the number of dimensions required to accommodate the dynamical trajectory, is thus very much less than the number of potential degrees of freedom. Common sense decrees that it must be so: the number of degrees of freedom that must be actively controlled at any one time must of necessity be limited or the control mechanisms will be overwhelmed. Vocal stability requires that the number of active degrees of freedom be minimized, whereas vocal adaptability is enhanced when they are maximized. Phonation involves an ever varying compromise between these two require­ ments. One therefore surmises that a failure to achieve an adequate compromise in dimensionality will characterize many vocal disorders, and that Conjecture 3: Vocal dysfunction may be reasonably classified into three categories: 1. Hypodimensional (too few degrees of freedom) 2. Eudimensional (normal number of degrees of freedom) 3. Hyperdimensional (too many degrees of freedom).

Figs. 35.7A and B: Two examples of vocal fold polyps. Judged visually, they seem very similar. But in image (A), the polyp is firmly attached to the deeper tissues, while in image (B) the polyp is free to oscillate with some independence. There is a significant difference in their dynamics.

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Figs. 35.8A and B: A typical case of sulcus vocalis. Histological examination shows a region (white hemi-ellipse) of thinned and adherent epithelium that is likely to alter vocal fold oscillatory dynamics.

which they are attached, and hence they have essentially no degrees of freedom of their own. All other things being equal, the dynamics of this larynx’s behavior, despite the morphological abnormality, may well be eudimensional. (It is also possible, of course, that these polyps severely restrict the motion of the vocal fold margin, in which case hypodimensionality might result). A classic case of sulcus vocalis (Figs. 35.8A and B) provides yet another example. The histological section of one of these vocal folds shows an area (demarcated by the hemi-elliptical white margin) of abnormally thinned epithelium that is undoubtedly more adherent to the subjacent tissue than is normal. There is thus, in this particular case, an area of the vocal fold that is less free to participate in the vocal folds’ oscillatory displacement. Glottographic waveform analysis, one might conjecture, would show a hypodimensional dysfunction. (It is entirely possible that other sulci, because of structural differences, would behave differently, and thus would be differently classified in terms of dimensionality). A reasonable hypothesis is that dimensionality will discriminate, e.g. between vocal fold paralysis and crico­ arytenoid joint ankylosis or between stiffness of the vocal fold cover and hyperfunction-associated stiffness of the vocal fold body. Dimensional analysis might differentiate between the effects of copious mucus on the surface of the vocal fold and disturbed movement of the vocal fold cover itself, and it might well have the potential to dis­ tinguish functional from organic dysfunction.

BASIN OF ATTRACTION: THE ATTRACTOR’S REALM It is worthwhile to consider the dynamics of a pendulum once again. Recall that it gets a fixed amount of “boost” whenever it passes a given point in its swing, and this little boost is sufficient to replace the energy lost to friction, but no more. Therefore, if the pendulum is started from a position either more or less than its usual displacement, oscillations either diminish or enlarge until their amplitude represents an equilibrium between the energy gain and loss. So, depending on where the pendulum is started from, its trajectory in the position-velocity phase space will either spiral out or spiral in to an endlessly repeated path. The final trajectory that represents this equilibrium state is called an attractor, because the dynamics of the system seem to be drawn to it. Let’s call it the “cycle attractor”. The position-velocity state space includes all the possible combinations of position and velocity that, in principle, a pendulum could have. A reasonable question is “Which starting combinations of position and velocity (i.e. which starting positions in the state space) will produce a trajectory that ends up on the attractor? Are there any regions (starting combinations of position and velocity) that will not lead to the attractor?” It might seem that all positions in the space are equally subject to the attractor’s lure, but that is not the case. The reason lies in the fact that the pendulum gets “a little “kick” when the pendulum passes a certain point, once in each swing cycle”. If the pendulum fails to get this once-percycle boost frictional losses will cause it to come to rest.

Chapter 35: Dynamical Disorders of Voice

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Figs. 35.9A to C: Basins of attraction of a pendulum in the velocity/ position phase space.

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outcomes for the dynamics of the system. There is a zone within which starting points lead to a “point attractor” (the rest position). There is also a zone (shaded blue) that occupies all the rest of the plane, and within which all starting points lead ultimately to the cycle attractor. Each zone is the basin of attraction for its attractor.

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A Phonatory Basin of Attraction Voice specialists have used the concept of a basin of attraction, even if unknowingly, for quite some time. The voice range profile (VRP, Figure 35.10) is considered an important evaluative tool. What it depicts is the region in a vocal intensity vocal frequency “state space” in which periodic oscillation of the vocal folds (i.e. phonation) is possible. Outside the VRP’s polygon, vocal fold motion (if there is any) is not periodic, and, hence, is not phonation. Since vocal intensity is largely a function of subglottal -

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Assume that the “boost” occurs when the pendulum passes a point slightly to the right of fully vertical, and mark that position in the pendulum’s state space, as in Figures 35.9A to C. If the pendulum’s starting swing is not wide enough to pass this point, as in Figure 35.9A, it gets no push and, therefore, its lost energy will not be returned. Absent the replacement of frictional losses, the pendulum’s swing grows even more feeble. Rather than reaching the attractor, it will end up hanging, absolutely still, at the 0 position/0 velocity locus in the state space. In fact, that point is itself a “point attractor” for all starting positions that do not take the pendulum past the boost point in its swing. However, if the initial position is such that the first swing takes the pendulum through its boost delivery position, as in Figure 35.9B, its swings will increase in size until it reaches—and then remains on—the attractor. The state space of Figures 35.9A to C is thus composed of two different regions that, so to speak, dictate different

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pressure, and since vocal F0 is largely governed by vocal fold tension, the VRP polygon might usefully be viewed as the boundary of a “phonation basin of attraction” in a pressure-tension phase space. In the case of an ideal pendulum the boundary between the basins of attraction is neat, precise and sharply defined. But this is not usually the case in more complex real-world systems. In fact, it is not really the case for the VRP because, if the patient’s voice were to be tested at every possible vocal frequency—every fraction of a hertz – instead of simply at sample frequencies, minor variations in maximal and minimal vocal intensity would make the

Fig. 35.10: A typical voice range profile. If vocal intensity is equated with driving pressure and vocal frequency with vocal fold tension, then the polygon encloses all combinations of pressure and tension that lead to stable phonation.

boundary lines very much more irregular. Suppose one were to take a very small segment of the VRP boundary, perhaps the segment in the box of Figure 35.10, and magnify it. The enlarged version of the boundary separat­ ing the “phonation” from the “not phonation” basins of attraction might have the appearance of Figure 35.11A.** Even when viewed at this relatively low magnification, the boundary looks extremely irregular. If one then magnifies just the little bit of the basin boundary encompassed by the very small rectangle of Figure 35.11A, one sees yet more detail (Fig. 35.11B). The “phonation” basin is “invaded” by fine projections of the “not phonation” basin that were not observable at the lower magnification. Again enlarging a rectangular zone shows (Fig. 35.11C) even deeper and finer intrusions of the not-phonation basin into the phonation basin of attraction. In fact if, in some ideal world, one could get enough measurements to allow an unlimited number of magnifications of the boundary each enlargement would reveal the boundary to have everfiner levels of similar complexity. The boundary is “self similar at all scales”, or, in the terminology of mathematics, it is “fractal”.# What the fractal nature of the basin boundary implies is that, as one looks with ever more powerful magnification at the boundary one finds that the phonation basin of attraction is riddled with ever-finer regions of nonphonation basin of attraction. In fact, as the (fractional) dimension of the basin boundary grows it becomes increasing likely that a point in the phonation basin might be separated from a point in the not-phonation basin by an infinitesimal distance. In other words, in the case of

Fig. 35.11: Successive (hypothetical) enlargements of a small region of the boundary of the voice range profile “basin of attraction”. **  Note that the boundary in this figure is hypothetical, and is not drawn from any real vocal sample. # This means that the structure has a dimension that is not integer. In the present case, the boundary is more than a line but less than a plane or surface. Hence, its dimension is fractional, i.e. greater than 1 but less than 2. Fractal basin boundaries are characteristic of chaotic systems.

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REFERENCES



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Phonatory rehabilitation entered a new era with the development of surgical interventions (most prominently by Isshiki94 97) whose purpose is the modification of the laryngeal framework to alter intralaryngeal, and in particular vocal fold, biomechanical properties. We are now at the inception of a period in which the tools and techniques of “vocal fold engineering” are available clinically. We are on the verge of learning to use materials science and molecular biology to alter the rheological properties of a malfunctioning glottal region.98 109 The new era and its novel capabilities call for a different approach to conceptualizing and evaluating dysphonia. Voice disorders, at base, are disorders of glottal dyna­ mics. As is true of other organic dysfunctions, many dys­ phonias are “dynamical diseases”.110 A nonlinear dynamical perspective, and the methods that nonlinear dynamical systems theory provides, gives us the perspective and the means to better understand glottal function and to disentangle the behavior of the glottis from aberrations of morphology and histology. It permits exploration at a more abstract level that is closer to pure “function”.111 114 We stand at the inception of a period in which the tools of “vocal fold engineering” will play an important role in vocal rehabilitation.115 120 A nonlinear dynamical approach offers a means of better specifying what vocal fold engineering needs to accomplish in a particular case. And it holds the promise of explaining much of what today remains obscure.121





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58. Steinecke I, Herzel H. Bifurcations in an asymmetric vocal fold model. J Acoust Soc Am. 1995;97:1874 84. 59. Herzel H, Berry D, Titze IR, Steinecke I. Nonlinear dynamics of the voice: signal analysis and biomechanical modeling. Chaos. 1995;5:30 34. 60. Berry DA, Herzel H, Titze IR, et al. Bifurcations in excised larynx experiments. J Voice. 1996:10;129 38. 61. Fletcher, NH. Nonlinearity, complexity, and control in vocal systems: In: Davis PJ, Fletcher NH (eds), Vocal Fold Physiology: Controlling Complexity and Chaos. San Diego, CA: Singular Publishing; 1996:3 16. 62. Herzel H. Possible mechanisms of vocal instabilities. In: Davis PJ, Fletcher NH (eds), Vocal Fold Physiology: Controlling Complexity and Chaos. San Diego, CA: Singular Publishing; 1996. pp. 63 75. 63. Kumar A, Mullick SK. Nonlinear dynamical analysis of speech. J Acoust Soc Am. 1996;100. pp. 615 29. 64. Behrman A, Baken RJ. Correlation dimension of electro­ glottographic data from healthy and pathologic subjects. J Acoust Soc Am. 1997;102:2371 9. 65. Ouaknine M, Giovanni A, Guelfucci B, et al. Nonlinear behavior of vocal fold vibration in an experimental model of asymmetric larynx: role of coupling between the two folds. Revue de Laryngologie, Otologie, et Rhinologie. 1998;119:249 52. 66. Behrman A. Global and local dimensions of vocal dyna­ mics. J Acoust Soc Am. 1999;106:432 43. 67. Titze IR, Baken RJ, Herzel H. Evidence of chaos in vocal fold vibration, In Titze IR (ed.), Vocal fold physiology: Frontiers in Basic Science. San Diego, CA: Singular; 1993, pp. 143 88. 68. Herzel H. Possible mechanisms of vocal instabilities. In Davis PJ, Fletcher NH (eds), Vocal Fold Physiology: Con­ trolling Complexity and Chaos. San Diego, CA: Singular; 1996, pp. 63 75. 69. Steinecke I, Herzel H. Bifurcations in an asymmetric vocal fold model. J Acoust Soc Am. 1995;97:1874 84. 70. Neubauer J, Mergell P, Eysholdt U, et al. Spatio temporal analysis of irregular vocal fold oscillations: biphonation due to desynchronization of spatial modes. J Acoust Soc Am. 2001;110:3179 92. 71. Giovanni A, Ouaknine M, Guellfucci B, et al. Nonlinear behavior of vocal fold vibration: the role of coupling between the vocal folds. J Voice. 1999;13:465 76. 72. Yu P, Ouaknine M, Revis J, et al. Objective voice analysis for dysphonic patients: a multiparametric protocol including acoustic and aerodynamic measurements. J Voice. 2001; 15:529 42. 73. Giovanni A, Ouaknine M, Triglia JM. Determination of largest Lyapunov exponents of vocal signal: application to unilateral laryngeal paralysis. J Voice. 1999;13:341 54. 74. Jiang JJ, Zhang Y, Stern J. Modeling of chaotic vibrations in symmetric vocal folds. J Acoust Soc Am. 2001;110:2120 28. 75. Menzer F, Buchli J, Howard DM, et al. Nonlinear modeling of double and triple period pitch breaks in vocal fold vibration. Logoped Phoniat Vocol. 2006;31:36 42.

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98. Gray SD. Cellular physiology of the vocal folds. Otolaryngol Clin North Am. 2000;33:679-98. 99. Hammond TH, Gray SD, Butler JE. Age and gender-related collagen distribution in human vocal folds. Ann Otol Rhinol Laryngol. 2000;109:913-20. 100. Thibeault SL, Gray SD, Bless DM, et al. Histologic and rheologic characterization of vocal fold scarring. J Voice. 2002;16:96-104. 101. Ding H, Gray SD. Senescent expression of genes coding collagens, collagen-degrading metalloproteinases, and tissue inhibitors of metalloproteinase’s in rat vocal folds: comparison with skin and lungs. J Gerontol A: Biol Sci Med Sci. 2001;56:B145-B152. 102. Tsunoda K, Kondou K, Kaga K, et al. Autologous trans­ plantation of fascia into the vocal fold: long-term result of type-1 transplantation and the future. Laryngoscope. 2005;115(Suppl 108):1-10. 103. Duflo S, Thibeault SL, Li W, et al. Effect of a synthetic extra­ cellular matrix on vocal fold lamina propria gene expres­ sion in early wound healing. Tissue Eng. 2006;12:3201-07. 104. Luo Y, Kobler JB, Zeitels SM, et al. Effects of growth fac­ tors on extracellular matrix production by vocal fold fibroblasts in 3-dimensional culture. Tissue Eng. 2006;12: 3365-74. 105. Thibeault SL, Klemuk SA, Chen X, Quinchia Johnson BH. In vivo engineering of the vocal fold ECM with injectable HA hydrogels—late effects on tissue repair and biomechanics in a rabbit model. J Voice. 2011;25:249-53. 106. Xu CC, Chan RW, Weinberger DG, et al. Pawlowski KS. Controlled release of hepatocyte growth factor from a bovine acellular scaffold for vocal fold reconstruction. J Biomed Mater Res A. 2010;93:1335-47. 107. Xu CC, Chan RW, Tirunagari N. A biodegradable, acellular xenogeneic scaffold for regeneration of the vocal fold lamina propria. Tissue Eng. 2007;13:551-66. 108. Chhetri DK, Mendelsohn AH. Hyaluronic acid for the treatment of vocal fold scars. Curr Opin Otolaryngol Head Neck Surg. 2010;18:498-502.

109. Ohno S, Hirano S, Tateya I, et al. Atelocollagen sponge as a stem cell implantation scaffold for the treatment of scarred vocal folds. Ann Otol Rhinol Laryngol. 2009;118:805-10. 110. Glass L, Mackey MC. From Clocks to Chaos: The Rhythms of Life. Princeton, NJ: Princeton University; 1988. 111. Matassini L, Hegger R, Kantz H, et al. Analysis of vocal disorders in a feature space. Med Eng Phys. 2000;22: 413-8. 112. Jiang JJ, Zhang Y, McGilligan C. Chaos in voice, from mode­ ling to measurement. J Voice. 2006;20:2-17. 113. Jiang JJ, Zhang Y. Nonlinear dynamic analysis of speech from pathological subjects. Electron Lett. 2002;38:294-5. 114. Titze IR, Baken R, Herzel H. Evidence of chaos in vocal fold vibration. In: Titze IR (ed.), Vocal Fold Physiology: New Frontiers in Basic Science. San Diego, CA: Singular; 1993, pp. 143-188. 115. Baiguera S, Gonfiotti A, Jaus M, et al. Development of bioengineered human larynx. Biomaterials. 2011;32: 4433-42. 116. Chen X, Thibeault SL. Biocompatibility of a synthetic extra­ cellular matrix on immortalized vocal fold fibroblasts in 3-D culture. Acta Biomater. 2010;6:2940-48. 117. Finck CL, Harmegnies B, Remacle A, et al. Implan­tation of esterified hyaluronic acid in microdissected Reinke’s space after vocal fold microsurgery: short- and long-term results. J Voice. 2010;24:626-35. 118. Kanemaru S, Nakamura T, Omori K, et al. Regeneration of the vocal fold using autologous mesenchymal stem cells. Ann Otol Rhinol Laryngol. 2003;112:915-20. 119. Kishimoto Y, Hirano S, Kojima T, et al. Implan­tation of an atelocollagen sheet for the treatment of vocal fold scarring and sulcus vocalis. Ann Otol Rhinol Laryngol. 2009;118:613-20. 120. Long JL. Tissue engineering for treatment of vocal fold scar. Curr Opin Otolaryngol Head Neck Surg. 2010;18: 521-5. 121. Baken RJ. Dynamical disorders of voice: a chaotic perspec­ tive on vocal irregularities. In Rubin JS, Sataloff RT, Korovin GS (eds), Diagnosis and Treatment of Voice Disorders, 2nd edition. Clifton Park, NY: Thomson; 2003.

Chapter 36: Functional Dysphonia

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CHAPTER

36

Functional Dysphonia Danielle L Gainor, Bryan N Rolfes, Claudio F Milstein



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Functional dysphonia is a fascinating but poorly under­ stood disorder. It is unclear why a patient with normal laryngeal structures and a previously unremarkable voice suddenly loses the ability to control the larynx. Despite the increasing awareness of the condition over the past two decades, the precise pathophysiology of this disorder remains poorly characterized. By definition, functional dysphonia is a condition of change in voice quality in the absence of structural abnormality or neurogenic dysfunction of the larynx. These changes are often a result of an imbalance in tension of the muscles that control voice production. The imbalance can be either excessive or diminished contraction of the intrinsic and/or extrinsic laryngeal muscles. At times it can involve other accessory voicing muscles such as respiratory muscles and those in the neck, jaw, shoulders, and back. In functional dysphonia, the muscle tension imbalance disrupts the complex and delicate coordination of structures that regulate voice production. The muscles seem to get “locked” in this abnormal posturing, preventing the generation of a normal voice. The harder the patient tries, the worse the voice becomes. This results in increasing frustration that only exacerbates the pathological process. Functional dysphonia is often a diagnosis of exclusion, based on history, laryngoscopic examination, perceptual acoustic examination, musculoskeletal features, and response to treatment. Chronic dysphonia is defined as any voice change that persists for over four weeks. Cohen found in a large

epidemiologic study that the lifetime prevalence of chronic dysphonia of any cause is approximately 4.3%.1 It is estimated that 35% of patients with chronic dysphonia do not seek treatment partly because they are unaware of available treatment options. Dysphonia has been shown to significantly impact patient quality of life and leads to lost work productivity or work related dysfunction. Cohen found that 2% of employed participants had missed four or more days of work due to voice related health issues. The true prevalence of functional dysphonia is unclear given the relative rarity of the condition and the incon­ sistency in defining its population. The historical lack of consensus on terminology used to describe functional voice disorders has led to confusion among clinicians. Psychogenic, psychosomatic, hysterical, conversion, muscle misuse, tension dysphonia, and non­ organic dysphonia, along with many others, have been used synonymously to describe functional dysphonia.2 There is more than one functional voice presentation, and nonorganic dysphonia should not be equated with one of psychogenic etiology. The absence of psychopathology in a large proportion of patients on routine psychiatric evaluations such as the MMPI has also been recorded.3 It is not uncommon that these patients will admit to symptoms of depression or anxiety that have developed as a result of, and not necessarily as a predecessor to, their voice handicap. Functional dysphonia has many diverse presentations. The onset can be either gradual or sudden. It can follow an upper respiratory infection, illness, trauma, stress, or have no identifiable triggers. The most common symptoms include generalized throat tightness, tension and strain,

THE VOICE CENTER, HEAD AND NECK INSTITUTE—CLEVELAND CLINIC

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lack of vocal projection, changes in pitch and volume, globus sensation, complete aphonia, and sore throat. In addition, patients with functional dysphonia will often complain of vague-associated symptoms including difficulty swallowing, headaches, light headedness or dizziness, referred otalgia or ear congestion, headaches, shortness of breath, and in more severe cases, atypical dysarthrias. Similar to muscle tension dysphonia (MTD), patients may demonstrate physical examination findings such as significant hyperfunction of the strap musculature, laryngeal tenderness to palpation, a displacement of the larynx in the vertical plane in the neck, and a decrease in the thyrohyoid membrane space due to muscle tension imbalance.4 Functional dysphonia’s chameleon-like resemblance to a number of conditions can make it difficult to diagnose. It can present with a wide range of vocal qualities and endoscopic findings, and there is no one type of voice quality that is characteristic of functional dysphonia. The most well-known form of the disorder is a sudden-onset of complete voice loss, or aphonia, typically described as a whisper-type vocal quality, but with normal vocal fold mobility and no evident pathology.5 However, other presentations include voices that may sound strained and forced, weak and soft, choppy, or abnormally low or high in pitch. The voice quality can also sound raspy, gravelly, harsh, or diplophonic. Some patients may have a relatively normal sounding voice but a sensation of extreme tightness, possibly associated with only a mild pitch change. The vocal changes may be sustained or intermittent. In some cases, supraglottic compression can be so severe that it interrupts airflow through the glottis resulting in the complete inability to produce even a whisper. As a result, these patients will try to communicate by mouthing words. In addition, cases have been observed in which the strain is severe enough to result in a variety of atypical dysarthrias, often leading to a misdiagnosis of a neurogenic condition. The presentation of functional dysphonia can also mimic that of spasmodic dysphonia. Despite the degree of vocal dysfunction, the vegetative functions such as laughing, crying, throat clearing, or cough are generally intact. Patients are usually not aware that these involve “voicing”, or sound produced by the vocal folds. The role of stroboscopy in diagnosis of functional dysphonia is limited by the fact that the vocal characteristics observed in these patients are not unique to functional dysphonia.6 It has a tendency to mimic a number of other

conditions, making it difficult to diagnose at times. By definition, the endoscopic examination should reveal an absence of structural abnormalities; however, the muscle tension imbalance can result in a number of physical findings that may complicate diagnosis. These findings can be separated to categories to better characterize them (Flowchart 36.1). The first division is between those patients who despite the hoarseness and irregular vocal fold vibration maintain a normal laryngeal pos­ture (Fig. 36.1), and those that demonstrate identifiable laryn­geal posturing such as supraglottic compression, inappro­priate glottic closure, or atypical laryngeal positioning during voice production. The laryngeal posturing group can be clas­sified as hyper­adducted, hypoadducted, or mixed, a com­bination of both hyper and hypoadduction. Variations in the hyperadducted group can include: • Glottic hyperfunction with tightly adducted aryte­­noids and vocal folds, with a predominantly closed phase of vibration (Fig. 36.2). • Supraglottic hyperfunction, with varying degrees of lateral compression, anteroposterior compression, or both, ranging from mild to severe to complete (Figs. 36.3 to 36.5). Most hyperadducted cases will present with increased stiffness of the vocal folds during phonation, with increa­ sed closing velocities and increased collision forces. The hypoadducted group can present as follows: • Glottic adduction with a predominantly open phase of vocal fold vibration. • Adduction of the vocal folds, but no vibration during attempted phonation. • Incomplete glottic closure with varying degrees of glottic gaps (Fig. 36.6). • Vocal fold pseudobowing (Fig. 36.7). • Vocal fold pseudoflaccidity (Fig. 36.8). Most hypoadducted cases will present with increased subglottic pressures, a predominant open phase of the vibratory cycle, with decreased closing velocities and col­ lision forces. At times, the vocal folds can appear weak or flaccid and mimic a hypofunctional neurologic disorder such as myasthenia gravis. The mixed group can show components of both hyper and hypofunction, such as an incomplete glottic closure with significant supraglottic compression (Fig. 36.9). For all groups, vocal fold vibration and phase symmetry can be regular or irregular. In some cases, there is muscle tension imbalance between the right and left sides of the larynx, leading to a decreased range or speed of

Chapter 36: Functional Dysphonia

489

Flowchart 36.1: Functional dysphonia diagram: Findings can be separated to categories to be better characterized.

Fig. 36.1: Irregular VF vibration: Despite the hoarseness and irregular vocal fold vibration, some patients maintain a normal laryngeal posture.

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Section 4: Voice Disorders

Fig. 36.3: Predominantly lateral compression.

Fig. 36.2: Glottic hyperfunction: With tightly adducted vocal folds, with a predominantly closed phase of vibration.

Fig. 36.5: Mixed lateral and anterior-posterior compression.

Fig. 36.4: Predominantly anterior-posterior compression.

motion of one vocal fold, mimicking a vocal fold paresis or paralysis. Other atypical presentations can show abnor­ mal torque­ing or inward rotation of the arytenoids dur­ing phonation. Voice specialists will often interchange the terms func­ tional dysphonia and MTD. It is important to distinguish the difference between these terms. MTD is a feature that

can be present in most voice disorders, whether a result of vocal fold pathology, benign or malignant lesions, neurologically based disorders, postsurgical, or voice overuse. It usually refers to a compensatory voicing stra­ tegy for conditions that affect laryngeal function. Other terms for MTD found in the literature include hyper­ functional dysphonia, muscle misuse dysphonia, hyper­ kinetic dys­ phonia, musculoskeletal tension dysphonia, mechanical voice disorder, and laryngeal tension–fatigue syndrome. MTD can be recognized as both a primary and secondary feature of voice disorders.3 In cases of “primary” MTD, excessive phonatory effort can be the initial cause. Secondary MTD is defined as MTD that has developed in an attempt to compensate for an underlying organic abnormality such as a vocal paresis, bowing, or vocal fold lesion.

Chapter 36: Functional Dysphonia

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Fig. 36.6: Hypoadduction: incomplete glottic closure with varying degrees of glottic gaps.

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Primary MTD is commonly seen in younger to middle aged women with high voice demands, particularly in stressful occupations such as teaching, telemarketing, or cheerleading.4 This results in excessive phonatory effort and a chronic pathological state of hypercontraction in the paralaryngeal and suprahyoid muscles. The etiology is likely multifactorial, including factors such as postinfection habituation, high risk occupation, psychosocial, and inadequate vocal skills. Over time, patients may develop phonotraumatic lesions, such as vocal nodules, or a diffuse “chronic laryngitis”. At this stage, it may become difficult to determine if the organic abnormalities are either a consequence of, or a precursor to, their MTD.5 By definition, primary MTD can be considered a functional voice disorder. However, the authors feel this particular subset of functional dysphonia tends to have different treatment requirements than other patients considered to

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Fig. 36.7: Pseudo-bowing.



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have “classic” functional dysphonia. MTD tends to respond effectively to well established traditional voice therapy techniques such as vocal hygiene, respiratory training, relaxation techniques, and other approaches such as resonant voice therapy, flow phonation, and frontal focus, among others. These behavior modification therapies often take between several weeks to several months to produce the intended changes. These approaches require slow progression over time until the patient can success­ fully utilize the newly established vocal behavior during conversational speech. The strategies used to treat MTD often prove ineffective in those with “classic” functional dysphonia. In contrast to MTD, functional dysphonia patients tend to have a low recurrence rate if they are provided with the necessary tools to intervene early in case of a recurrence of their symptoms. In some cases, the presentation of functional dyspho­ nia can mimic that of spasmodic dysphonia. In general, functional dysphonias are rarely intermittent, there are no obvious differences between voice and voiceless con­ texts, and there is no improvement with falsetto voice production or singing. Performing a series of vocal tasks, including whistling, coughing, yawning, humm­ ing, high pitched voicing, singing, and speaking sentences with all voiced segments, and sentences with voiceless and voiced segments can help the clinician with the differential diagnosis. In spasmodic dysphonia, voice tends to improve with high pitched phonation, laughing, crying, and singing. Patients with spasmodic dysphonia may have islands of normal speech, and there is a tendency to perform worse depending on speech context. Despite these general differences, at times it can be quite

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Section 4: Voice Disorders

Fig. 36.8: Pseudoflaccid.

Fig. 36.9: Mixed supraglottic compression and incomplete glottic closure.

challenging to distinguish between these two conditions, and it may require extensive interactions with the patient, or a few sessions of diagnostic therapy, to reach the correct diagnosis. Many authors have described the potential for psycho­ pathology in playing a role with the onset of functional dysphonia.2 Because the vast majority of patients respond very well to treatment, have relatively infrequent relapses, and in our experience usually lack a psychiatric history, the true impact of psychogenic disorders on this process is in question. The authors recommend reserving psychogenic diagnoses for those muscle misuse voice disorders that clearly have a primary psychoemotional etiology as deter­ mined through a formal psychiatric evaluation.6

Attempts have been made to develop diagnostic clinical features to assist in the differentiation of functional dysphonia from other types of dysphonia. The MorrisonRammage classification (see Flowchart 36.1) and Van Lawrence descriptors6,7 are two examples. These features were analy­zed in 2001 by a prospective control-blinded study comprised of 51 patients with functional dysphonia and 52 nondysphonic control subjects. During the study, the authors found that 60% of control subjects demon­ strated one or more of the 12 features described. None of the features revealed a statistical difference in the prevalence among functional dysphonia patients and control subjects. About one-third of patients with functional dysphonia were judged to have a normal laryngoscopy. They conclu­ded

Chapter 36: Functional Dysphonia

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This process can be lengthy, prolonging the patient’s dis­ ability, until the patient is seen by a voice specialist who can correctly identify the condition (Flowchart 36.2). The American Academy of Otolaryngology has recently acknowledged that there are inaccuracies in the diagno­ sis of voice disorders in general, and recognized the need to improve diagnostic accuracy for hoarseness.9 It was reported that, on average, it takes about three months to correctly diagnose patients who present with hoarseness of any etiology. In the authors’ experience, patients with functional dysphonia take longer, with a median time to diagnosis of six months, with about one third of patients going one year or longer from onset of symptoms to dia­ gnosis. This delay in diagnosis results in unnecessary referrals, tests, procedures, prescription medications, and a significant waste of health care dollars. In addition, we believe that functional dysphonia patients present a unique challenge as a subgroup of voice disorders. Even when diagnosis is correct, traditional voice treatment is not always effective. Some patients can remain vocally impaired for years after unsuccessful

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that functional dysphonia is a “complex process and is unlikely to be made from visual examination only”.8 Due to the variety of presentations and physical findings, the diagnosis often remains in question until treatment has been attempted by an experienced speech language pathologist. The diagnosis is confirmed when the patient shows a rapid response to appropriate therapy. Stroboscopy should be performed when available in patients with sig­ nificant vocal complaints; however, its role in patients with functional dysphonia is to rule out organic forms of dysphonia rather than to confirm the ultimate diagnosis. A common scenario seen by the voice specialist is that of a patient who initially presents to the primary care phy­ sician with prolonged dysphonia. Typically, the patient will be treated with rounds of antibiotics, allergy, asthma, and reflux medications with no response. Subsequently, the patient is referred to a variety of subspecialists, including general otolaryngology, pulmonary, allergy, gastroenterology, neurology, and sometimes psychiatry, who will typically, in turn, do more diagnostic testing and prescribe more medication trials, often ine ective.

493

Flowchart 36.2: Treatment diagram: This process can be lengthy, prolonging the patient’s disability, until the patient is seen by a voice specialist who can correctly identify the condition.

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Section 4: Voice Disorders

treatment. The voice handicap not only impacts the patient but also the family, work, and close friends and the social environment. The inability to communicate effectively can lead not only to loss of working days and income but also to substantial disability, frustration, social isolation, and depression. Once functional dysphonia is correctly identified, the treatment of choice is specialized voice therapy performed by a speech pathologist with expertise in functional voice disorders. Treatment is not a “one size fits all” approach and not all modalities work for every patient. As stated previously, functional dysphonia does not tend to respond to conventional voice therapies such as vocal hygiene, breathing training, relaxation, head rolls, and easy onset. These most commonly used techniques in voice therapy are ineffective in the modification of the well-established laryngeal and paralaryngeal musculoskeletal imbalance characteristic of this disorder. Other vocal therapies such as resonant voice therapy, flow phonation, and frontal focus tend to fail when implemented as a first approach to functional dysphonia. However, these approaches can be invaluable for training once the basic voicing behavior has been re-established. The goal of traditional voice therapy is to facilitate learning of a new motor skill. To achieve correct acquisition of the new behavior, the therapist must provide feedback on the target performance, require context-specific repetitions of target behaviors, and provide frequent reinforcement. The treatment of functional dys­ phonia is different, in that the patient does not have to learn a new skill and there are no required target behaviors. This therapy is often “done to the patient”, as opposed to the more traditional model. In this therapeutic modality, the patient has a more passive role, until normal voicing is established. Successful treatment is often multimodal and utilizes several possible techniques at once, honing in on those that seem to work for each individual patient. Not all patients will respond to the same treatment modality, which is why it is important to have a large armamentarium of therapeutic probes and voicing techniques to attempt to elicit voice when treating these functional cases. A successful approach often starts with implementation of digital laryngeal manipulation10-12 or laryngeal reposi­ tioning. These include: 1. Manual lengthening and stretching of the cervical spine region and strap, upper trapezius, and sternocleido­ mastoid muscles. 2. Lateral displacement of the larynx to improve joint mobility.

3. Exertion of downward pressure on the thyroid carti­ lage to increase the thyrohyoid space. These techniques will be performed initially with no sound production. Subsequently, the patient is asked to sustain a sound, as the laryngeal manipulation conti­nues. Manipulation of the head, shoulders, neck, and spine is also performed as part of this specialized treatment. These approaches appear to be most effective when employed in conjunction with other voicing strategies, such as vegetative voicing tasks (laughing, crying, throat clearing, and coughing), gargling, humming, chanting, and distracting techniques to prevent maladaptive muscle posturing. The goal of therapy is to restore the prior natural resting position of the larynx in the neck and reduce over­ all muscle tension and vocal hyperfunction, thus allow­ ing normal adduction and vibratory function of the vocal folds. Once these biomechanical changes take place voice will rapidly return to normal. Initially, the voice is restored within a nonspeech context, such as production of sus­ tained vowels or humming. Once this is established, the patient must be guided through a slow and gradual prog­ ression into conversational speech. If conversational speech is introduced too early in the treatment session, the patient will likely revert to the maladaptive laryngeal posture and experience a return of the dysphonia. One of the key elements of successful treatment and prevention of recurrence is to provide the patient with the necessary tools to self-treat in the event that they experience dysphonia again. In the authors’ clinic, patients are provided with a series of exercises based on the treatment that was successful in their initial voice therapy session. Patients are instructed to perform these exercises multiple times daily for several days and immediately if there is any sign of recurrence of hoarseness in the future. This self-correcting treatment regimen has resulted in a 95% cure rate at the authors’ institution. Eighty-five per­ cent of patients require only one intervention, with the remaining patients requiring one or two additional treat­ ment sessions. Immediately following treatment, patients report com­p­lete resolution of hoarseness, a significant decrease in vocal effort, and resolution of associated symptoms, such as throat tightness, effort, and fatigue. Patients can resume normal activities right away and report a signi­ ficant improvement in quality of life. With this complete approach to treatment, most patients receive prompt and permanent relief from the exhaustion, stress, and discom­ fort that uniformly accompany functional dysphonia.

Chapter 36: Functional Dysphonia

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• Traditional voice therapy techniques are less effective • Individualized and specialized treatment by SLP with expertise in voice disorders very effective within short period of time • When patients are trained in self correcting tech­ niques, the rate of recurrence is low.

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1. Cohen SM. Self reported impact of dysphonia in a primary care population: an epidemiological study. Laryngoscope. 2010;2022 32. 2. Gerritsma, EJ. An investigation into some personality characteristics of patients with psychogenic aphonia and dysphonia. Folia Phoniatrica. 1991;43:177 80. 3. Altman KW, Atkinson C, Lazarus C. Current and emerging concepts in muscle tension dysphonia: a 30 month review. J Voice. 2005;19:261 7. 4. Morrison MD, Rammage LA. Muscle misuse voice dis­ order: description and classification. Acta Otolaryngol. 1993;113:428 34. 5. Koufman JA, Blalock PD. Functional voice disorders. Otolaryngol Clin North Am. 1991;24:1059 73. 6. Rammage L, Murray M, Hamish N. Management of the voice and it’s disorders. Canada: Thompson Learning Singular; 2000. p. 35. 7. Van Lawrence L. Suggested criteria for fibre optic diag­ nosis of vocal hyperfunction. Presentation at Care of the Professional Voice Symposium. The British Voice Asso­ ciation, London; 1987. 8. Sama A, Carding PN, Price S, et al. The clinical features of functional dysphonia. The Laryngoscope. 2001;111:458 63. 9. Schwartz SR, Cohen SM, Daily SH, et al. Clinic Practice Guideline: hoarseness (dysphonia). Otolaryngol Head Neck Surg. 2009;141:S1 S31. 10. Mathieson L. The evidence of laryngeal manual therapies in the treatment of muscle tension dysphonia. Curr Opin Otolarynogol Head Neck Surg. 2011;19:1 5. 11. Roy N, Bless DM, Heisey D, et al. Manual circumlaryngeal therapy for functional dysphonia: an evaluation of short and long term treatment outcomes. J Voice. 1997;11(3):321 31. 12. Roy N, Leeper HA. Effects of the manual laryngeal mus­ culoskeletal reduction technique as a treatment for func­ tional voice disorders: perceptual and acoustic measures. J Voice. 1993;7(3):242 9. -





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• Pathophysiology of FD poorly understood • In most cases it is a physiological disorder of muscle imbalance, and not a psychogenic disorder • Presents with a wide range of voice qualities and endoscopic findings – more diverse than clinicians assume • Requires a broader differential diagnostic perspective in order to avoid misdiagnoses and poor clinical outcomes • Suspect FD if: ° Larynx appears normal or relatively normal but voice is poor or disproportionately poor compared to laryngeal findings ° The patient presents with significant dysphonia on conversational speech but better sounding voice when yawning, coughing, throat clearing, or laughing ° There is no response to traditional voice therapy despite the absence of laryngeal pathology • Delays in diagnosis and effective voice therapy result in waste of health care dollars °

REFERENCES

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KEY POINTS

Video 36.1: Samples of pre treatment laryngeal endo­ scopic examinations of patients with confirmed func­ tional dysphonia. Video 36.2: Samples of pre and post treatment voice qualities of patients with functional dysphonia.







For those voice patients who seem to be refractory to traditional voice therapy and have failed to improve voice within a few sessions, the authors recommend reassessment and potentially altering therapeutic modalities. If still unsuccessful, a referral to a speech language pathologist with a specialized interest and expertise in treatment of functional dysphonia is recommended. In summary, functional dysphonia is an under recognized and frequently misdiagnosed condition with a variety of presentations. The diagnosis is unlikely to be made based solely on visual examination of the larynx. The true prevalence and pathophysiology remain unclear and require further clarification. Functional dysphonia should not be assumed to be psychogenic. Suspicion should be high in patients who demonstrate an absence of laryngeal pathology, but have altered vocal function that is unresponsive to traditional voice therapy. The standard treatment includes a multimodal approach with digital laryngeal manipulation in conjunction with several other voicing techniques. Treatment must be tailored to each individual patient. If appropriately treated, patients have a quick response to therapy and a low recurrence rate.

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Chapter 37: Posture and Muscle Tension

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Posture and Muscle Tension

37

John S Rubin, Lesley Mathieson, Edward Blake

This chapter is dedicated to Ida Pauline Rolf, PhD (1896–1979), a scientist and innovator in the field of structural integration.

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Efficiency is a “buzzword” often used in relation to ergo­ nomics, and vocal efficiency to vocal performance. It is our view that vocal efficiency can best be obtained/pre­ served in the background of postural efficiency. Rolf coined the phrase “equipoise” for such posture whereby the head is vertically positioned over a perpendicular shoulder girdle, a forward facing pelvis, hip joints, and feet. With the eye plane horizontal, a plumb line through a coronal plane (formed by a line through the ears) passes directly over this shoulder–hip joint plane.1,2 However, such posture is uncommon. As Aronson noted over 30 years ago, contraction of the internal and external laryngeal musculature is commonplace, caused by issues such as stress,3 5 and laryngeal musculature imbalance needs to be considered in the backdrop of more general imbalance of the deep flexors and extensors of the neck and upper torso as caused by behavioral predi­ lections or structural abnormalities. When considering posture, the requirements and move­ ment habits of a 21st century Western lifestyle will to a large extent dictate the body positions we adopt. These range from car seats and more frequent air travel with often little concern given to ergonomics, to the use of desktop computers, tablets, and smart phones that are essential in today’s world of communication. Performance related

postures, repetitive choreographic demands, and costume requirements are clearly integral to head, neck, and trunk position. Raked stages, heavy wigs, or head costumes and microphone pack position are all potentially implicated. The mechanical advantage provided to certain muscle groups through these regular and suboptimal positions may lead over time to a gradual shortening of muscle tissue and a localized muscular imbalance. Preferential adoption of these positions or postures can occur even when away from the direct tasks that may have initiated the process. This is one of the fundamental reasons why disciplines such as Pilates, Yoga, and Tai Chi have become so popular and often promoted by health practitioners. They specifically target the less commonly used muscles in day to day life. With regular compliance patients can attempt to achieve equipoise in spite of their subopti­ mal professional postural requirements. However, these attempts may not always be successful and professional medical intervention may be required. Furthermore, emotions and posture are interrelated. It has been known for centuries that the psyche can affect posture, and that posture can have an effect on psyche. Aristotle summed up this metaphysical relationship nicely when he stated that a change in the shape of the body produces a change in the state of the soul, and a change in the state of the soul produces a change in the shape of the body. To speak about vocal efficiency we believe

VOCAL EFFICIENCY

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strongly that one needs to speak about upper torso postural efficiency. Ohashi,6 a Shiatsu practitioner, notes that the neck mirrors the body’s health; also, that abnormal stiff­ ness or pain in the neck may indicate an unhealthy body. Positional factors related to voicing primarily encom­ pass the head, neck, and upper back. Whether or not this is a further compensation for lumbar spine positional issues or even foot position could also be argued (but will not be within the context of this short chapter). The primary postural problem that we have observed is a forward protrusion of the head and neck away from the central plumb-line as envisioned by Rolf (see above and ref. 1) (Fig. 37.1). To understand the muscular consequences of this, one must have a basic understanding of muscle physiology and force production. In essence, any slight shortening of muscle tissue will provide a mechanical advantage to that muscle or group of muscles; such a mechanical advantage then can lead to a vicious cycle of further muscular shortening, with a corresponding weakness to the opposing or antagonistic muscle group. A “tug of war” is a useful analogy with one side slightly stronger initially but becoming increasingly powerful as the momentum of their efforts increases. As this process continues, force production levels within each muscle group are affected (increased and conversely compromi­ sed) thereby influencing function. In the case of the peri­ laryngeal muscles, this may have serious effects on their role in laryngeal and vocal fold movement.7 Mechanisms involved in “righting” oneself, in standing erect, are predominantly under control of the medial component of the somatic motor system. The function of the medial component is maintenance of erect posture (antigravity movements), integration of body and limbs, synergy of the whole limb, and orientation of body and head. Even in humans, although there is a corticospinal component taking part in this medial component, impor­ tant structures of the medial component are located in the brain stem.8,9 The newborn has a straight cervical and thoracic spine. But as soon as he tries to raise his head up to look out upon the world, the cervical spine begins to take on the natural curve that all adults have; as soon as he sits up the thoracic spine begins to take on the characteristic curve seen in all “normal” adults. Thus, the nerves associated with the righting behavior, the act of seeing, of sitting, of preparing to stand and walk, become integrated at an extraordinarily early stage in our lives. They become embedded in and part of our nervous system long before we even say our first word.1

Fig. 37.1: Exaggerated example of forward protrusion of the cervical spine with the coronal plane passing downwards from the ear in the forward position in relation to the shoulder.

These nerve pathways are basic to concept of self. Any subtle alteration will also quickly become a “part” of us. Thus, according to Rolf,1 abnormal behavioral patterns may become fixed and elemental. They will seem natural. However, on a long-term basis such behavioral patterns, once developed, are likely to have the sequelae of chronic pain. This is particularly seen about the head and neck. Until recently, in the Western world, there has been relatively little research into the area of postural causes of neck pain. In modern times, the importance of posture to well being and to spirituality has become popularized through the works of authors such as Rolf, Alexander, Pilates, and Feldenkrais.1,10-12 Posture could, in one sense, be considered to be a constant battleground between the deep extensor and flexor groups of muscles.7 The long bones and pelvis, the skull, and the spine are the obvious targets and (in many cases) the origins and/or insertions of these muscle groups. There are groups of muscles that attach to all of the long bones and work in antagonism across joints, thereby permitting controlled movement. Some flex and some extend. For body harmony, these groups need to work together. Often in 21st century day-to day activities, this harmony is abrogated as noted above. Robinson et al.10 in their Pilates manual have identified the following problems to be associated with prolonged

Chapter 37: Posture and Muscle Tension



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facet approximation. The longus colli (cervicis) muscle attaches directly to each vertebra throughout its anatomical length (C2 to T3) and is therefore ideally located to perform this stabilizing role (EB personal comment 2013). “Mobility” muscles are the prime movers of the head, neck, and shoulder girdle. They also serve to provide a substitute stability mechanism in the event of reduced muscular support from the longus colli (cervicis). Examples of mobility muscles include the sternocleidomastoid, trapezius, and levator scapulae. For example, the sterno­ cleidomastoid arises by two heads from the clavicle and manubrium sterni and inserts into the lateral surface of the mastoid process and the superior nuchal line of the occipital bone, thereby bypassing the cervical spine from an attachment perspective completely. Stage direction that involves singing to the dress circle, often on a raked stage (a stage sloped upward away from the audience), will not infrequently position the upper and mid cervical spine in a substantial degree of extension. Less specifically but more commonly, shorter individuals have a tendency to head tilt upward when in the presence of taller; taller individuals have a tendency to stoop, with one postural element including a forward head and neck. The potential loss of anterior muscular stability in this position will result in increased shearing forces through the intervertebral joints and facet joint compression. With the chronic positional changes that can occur with persistent postural compromise, the force output of these specific muscles alters to the point whereby the cervical spine can no longer be stabilized effectively by the longus colli (cervicis) (which is lengthened and weakened) and hence the sternocleidomastoid must adopt a stabilizing role. This is necessary from a functional perspective but is a substitute action nonetheless. It is therefore often considered a “suspect” in contributing to cervical spine articular pathology by promoting chronic facet joint com­ pression and intersegmental shearing, in addition to the changes in laryngeal position that are associated with its shortened length. This situation further enhances the cycle of imbalance and movement related problems.7 This likely accounts for some of the benefit accrued by Mathieson’s interventions in individuals with muscle tension dyspho­ nia (“MTD”).14 We postulate that the resultant increased cross bridge overlap and consequent improved force production levels from the sternocleidomastoid, levator scapulae, and upper fibers of the trapezius serve to pull the upper cervical spine into further extension. This positional dominance results in

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sitting: weak transversus abdominis; tight upper rectus abdominis; tight dominant hip flexors; rounded thoracic spine; tight pectorals; medially rotated scapulae; tight levator scapulae (elevating the scapulae); head forward, leading to weak deep neck flexors and tight neck extensors; tight adductors and medial rotators of the hip; weak gluteals; and a “rotated twisted spine”. One can immediately identify several effects on the neck. Rolf adds that chronic shortening and flexion of the rectus abdominis strains the entire body. Neck and cervical spine are inevitably included in the compensation. The myofascial structures of the cervical spine become anteriorly shortened and therefore the head comes forward.’1 This problem may then be augmented by exercises such as weight lifting, sit ups, and abdominal crunches. These activities, if performed inaccurately, can lead to further muscular imbalance, with further advantage given to the flexors. Further abdominal compression can occur, as well as compression and strain of the three or four upper­ most ribs. This may impact deleteriously on the function of the upper intercostals, this function being important in singing. In turn, continued ventral sag of the first and sec­ ond ribs displaces and raises the first dorsal vertebra in the back. Anterior displacement of the entire group of lumbar vertebrae is also a not infrequent spinal aberration. In the neck, which may already be held “forward”, the muscle masses of the semispinalis can become (per Rolf) “amor­ phous, solid, unyielding”,1 thereby “crowding” the cervical vertebrae into a shortened arc. Some of the segments are forced into spaces anterior or posterior to the position of good function. A physiological consequence is what Lieber­ man calls a cervical dorsal shelf.13 An associated consequence of positional change is the alteration of the role of an individual muscle in terms of movement and control. Certain muscle groups are earmar­ ked to stabilize the spine to allow for a stable platform on which controlled movement can occur. The muscles or muscle groups that provide movement at various articula­ tions do not have the same anatomical attachments as those that provide segmental stability. The point of muscle­ controlled stability, in addition to providing a stable platform for movement, is to protect the delicate noncon­ tractile stabilizers such as ligamentous tissue and inter­ vertebral discs that have a far more limited deformation range, prior to the onset of injury.7 “Stability” muscles control the head and neck in a “neutral” position, thereby minimizing the loads placed on the stability mechanisms provided by annular fibers and

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continued overactivity and eventual adaptive shortening (chronic contraction). This, in turn, maintains the cervical spine in some degree of extension (hyperlordosis) at rest (EB, personal comment, 2013). The consequence of this, from a muscular perspective, is an imbalance between the activity and force production of the designed stability mechanism and that of the prime movers of the neck and shoulder girdle, which are now unopposed in pulling the spine in the direction of their anatomical pull. The severity of the imbalance is directly linked to the amount of extension in which the cervical spine is held. These loads are often too great to be tolerated by the more delicate structures of the cervical spine, and are a common cause of facet and annular injury. Due to space limitation, we cannot review individual muscle anatomy and physiology. We suggest references 15-18 for further review.

POSTURE-RELATED VOICE DISORDERS Having established the primary muscular imbalances that can occur in relation to the cervical spine as a result of postural changes, attention can now be focused on the impact at a laryngeal/perilaryngeal level. The larynx is a very complex structure from a biomechanical perspective. It consists of a series of cartilages, muscles, and ligaments and is suspended from the basicranium, not by direct bony attachment, but by a series of muscles and ligaments. It could be viewed as a hapless victim in the constant flexor/ extensor muscular struggle described above, in part due to its location in the anterior neck, in part due to its dense muscular attachments to the prevertebral fascia, and in part due to its attachments to the basicranium above and the trachea below. The cervical spine itself is clearly more mobile in a healthy subject than the dorsal or thoracic spine, primarily as a result of the absence of the rib cage. Referring back to the anatomical pathway and attachments of the sterno­ cleidomastoid, any changes in muscle length (shortening) will affect the position of the cervical spine and cranium, ahead of the thoracic spine, as a result of this increased mobility. The cranium is tilted back and the cervical spine pulled into a position of extension. This has huge cons­ equences for the perilaryngeal muscle groups (both agonist and antagonist) as the changes seen in the balance of cervical spine musculature are reflected at a perilaryngeal level. Sharing identical or neighboring attachments to the sternocleidomastoid are the strap muscles that elevate

and retract the larynx, namely the stylopharyngeus, diga­ stric, stylohyoid, and styloglossus. All of these now enjoy a mechanical advantage over their antagonists as a shortened length secondary to a change in cervical spine and cranium position will lead to improved cross-bridge attachments in comparison to the muscles that lower or depress the larynx. The result is that the larynx is effectively pulled into a superior and posterior position at rest influencing cri­ cothyroid joint rotation and therefore vocal fold length as well as reducing the size and shape of the pharynx.7 This is still speculative, but is consistent with the common clinical report of reduced access to the upper register, inconsistent pitch, alterations in resonant quality and fatigue. It could be argued at this point that repetitive attempts to elongate the vocal folds through anterior cricothyroid joint rotation against the restriction of the stylopharyngeus result in frequent microtrauma to the epithelium of the folds. However, a note of caution is required. It has become the accepted view that the thyrohyoid space is reduced in size in cases of hyperfunctional aphonia. However, a recent MRI study by Lowell et al.19 involving 20 participants, 10 with primary MTD and 10 without voice disorders, found that although hyoid and laryngeal positions were higher in people with primary MTD as compared with people without voice disorders, the hyolaryngeal space during phonation did not show differences between the groups. Clearly the last word on this mechanism has not been written. Lieberman et al. believe that shortening (chronic contraction) of the cricothyroid muscle may occur.13,20,21 This could be posited to occur in response to the abovedescribed laryngeal elevation, or even to the forward translation of the larynx in relation to the hyperlordotic cervical spine. Often the anterior cricoid ring is noted to be positioned in a plane anterior to the inferior thyroid cartilage in this clinical scenario (JR, personal observa­ tion, 2013). As a correlate, Lieberman et al. often note the resting anatomical relationship of the anterior cricoid ring/infe­ rior rim of thyroid cartilage complex (which they desig­nate the “cricothyroid visor”) to be narrowed with little discer­ nible space.13,20,21 Furthermore, they often identify, in this clinical scenario, a decreased range of motion of the “cri­ cothyroid visor” as the individual changes vocal pitch from vocal fry to falsetto,13,20,21 presumably, in association with diminished cricothyroid muscle activity or efficiency. We have noted some affected individuals to recruit exter­nal muscles, particularly the suprahyoid muscles but also the

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Chapter 37: Posture and Muscle Tension strap muscles, and even at times other muscles of the 1st and 2nd branchial arch origin, to assist in pitch elevation. The physical consequence is that of an “elevated” larynx, in this situation, and also of tightened suprahyoid and perilaryngeal muscles.20

PHONATION AND PAIN

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If the answer to one of these questions is “not so good”, then consideration could be given to a referral to a physiotherapist. Figure 37.1 shows a postural position (viewed from the side) that would fall into the “not so good” category. Figure 37.2 shows a postural position (viewed from the side) more in accord with the equipoise concept (see above).

TREATMENT

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There have been various techniques developed that can help alleviate neck discomfort. These vary from treatments well accepted in western medicine, such as physiotherapy, osteopathy, and chiropractory, to a range of complemen­ tary medicines. The complementary medicines can be arranged into the following groupings: aromatherapy, Ayurvedic medicine, bodywork and somatic practices (including Alexander technique, Aston Patterning, Cra­ nioSacral therapy, Feldenkrais Method, Hellerwork, massage therapies, Oriental bodywork therapy, polarity therapy, re exology, reiki, rolfing, shiatsu, therapeutic touch, Trager approach, trigger point myotherapy), herbal therapy, homeopathy, hydrotherapy, nutrition and supple­ mentation, traditional Chinese medicine (acupuncture, acupressure, Chinese herbal therapy), yoga and meditation, and others.12 ­





It could be asked, “How can the untrained clinician safely determine when a patient/client is out of equipoise?” While we do not advocate laryngeal manipulation by such a clinician, we do believe that there are relatively simple evaluator techniques to aid in this determination. A. Viewing—this can be done with little to no training: • When viewed from in front, is the head centered (good) or tilted (not so good)? • Are the shoulders at equal level (good) or at different levels (not so good)? • When seen from the side, is the highest point of the head toward the vertex (good) or front (not so good)? • Is the ear approximately in the same vertical axis as the shoulder (good) or substantially in front of it (not so good)? Are the shoulders held in a neutral position (good) or held in a “slumped forward” position (not so good)? B. Palpating—this should not be done by the untrained clinician: • When the larynx is gently moved from side to side, does it move easily (good), or not so easily (not so good)? • When the back of the neck is felt from below up, does it have a smooth gentle bow shaped curve (good) or is it irregular with an area where it indents (not so good)?

Fig. 37.2: The cervical spine in a more normative position with the coronal plane passing downwards from the ear, directly through the shoulder.



ASSESSMENT BY THE CLINICIAN

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The issue of pain/discomfort in relation to muscular imbalance should perhaps be mentioned. The sense of discomfort commonly arises when muscles are not used appropriately. Further discomfort may occur as phonation is attempted while the anatomically related muscles are unduly tense. This can result in a cycle of muscle tension and pain, and further reinforce the behavioral muscular “holding” pattern.22,23 Mathieson et al. have devised a validated questionnaire in their laryngeal manual therapy (LMT) protocol whereby laryngeal pain and discomfort are key questions, and relief thereof key markers of success.14

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Section 4: Voice Disorders

From the standpoint of voice care, we tend to limit ourselves to the following physical techniques for use in our patients: • Release of tension/contraction of involved suprah­ yoid musculature and the sternocleidomastoid. Such techniques have been championed by workers in the field such as Nelson Roy and Lesley Mathieson14,24-26 • Release/stretch of the cricothyroid mechanism. Such techniques have been championed by Jacob Lieberman20,21 • Reposition of the forward (hyperlordotic) cervical spine, including release of restriction of the cervical facet joints, release of contraction of the sternocleidomas­ toid and trapezius, stretch of the upper fibers of the erector spinae. Such techniques are commonly used in physiotherapy, osteopathy, and to a lesser degree in massage. For voice patients, they have been cham­ pioned by Ed Blake7,27 • Release of tight strap muscles. Such techniques have been championed by Jacob Lieberman13 • For neck discomfort with characteristic pressure points, use of acupressure in an in-office setting6,28-30 (not uncommonly used by the author JR) Lieberman et al.13 have described techniques for work­ ing directly on the cricothyroid joint and muscle, and on the ligamentous and muscular attachments of the hyoid in such scenarios. They have identified rapid improve­ ment of voicing in certain individuals. We have noted this as well, but should note that LMT may only become pos­ sible when other fundamental issues of posture have been addressed. Mathieson, in her extensive work combining voice therapy with LMT, has often found vocal improvement to occur immediately upon working on the muscular and tendinous attachments to the hyoid bone.22,23 Roy has had similar experience.24,25 Mathieson posits that vocal improvement may occur when a muscle status is achieved that allows the larynx to respond easily to lateral digital pressure. This passive lateral laryngeal movement may well be an indicator that excessive tension has been eliminated or significantly reduced. As a result, vocal stra­tegies can then be introduced in therapy, whereas previously they would have been counterproductive (LM, personal obser­ vation, 2001). It has been recorded by teachers and per­formers, through the ages, that lateral movement of the laryngeal cartilages is associated with improved sense of freedom of the voice.2

Underlying psychological issues and chronic tension may be related to persistent vocal postural behavior. For example, we find that many “driven” persons who present with voice disorders to the voice clinic are found to have a tightly bound, lowered larynx.31 Our group has also found an association between individuals presenting with high degrees of anxiety and a high held larynx with tender supra hyoid musculature.20,27 Thus, although this chapter has focused on the physical manifestations and management for voice disorders, there may, in certain instances, be a role for consideration of seeking psychological management. Psychosomatic psychotherapy, in the form of Gestalt the­rapy, has proven particularly helpful to many affected people; other branches of the behavioral science are as well. Perhaps case reports (fictitious but based on our clinical experience) will help elucidate our current man­ agement approach.

CASE REPORT 1: PHYSIOTHERAPEUTIC INTERVENTION, ACUTE A 45-year-old professional female singer and dancer presents to the otolaryngologist on the day of an evening performance with a two- or three-week history of throat pain and increasing difficulty with the upper register of the voice. A few months earlier she had suffered from a back injury for which she has received intermittent physical therapy. On laryngeal examination, there is a satisfactory mucosal wave on stroboscopy with no definitive mucosal pathology, but the neck is found to be “held” in extension, and the anterior neck musculature is tight and tender to palpation. An urgent referral is then made to the physiotherapist who identifies several musculoskeletal abnormalities, including resting extension of the upper cervical spine, deficits in force production of the deep neck flexor stability mechanism, and stiffness in the upper and mid thoracic spine. Palpation of the C 2/3 facet joint demonstrates restriction of movement and duplicates the discomfort noted by the patient. There are also trigger points found in the upper trapezius and levator scapulae, spasm of the sternocleidomastoid, and the lower trapezius is found to be inefficient, with difficulty initiating contraction. Initial therapy focuses on altering the resting position of the larynx. Specific technical aspects are outside of the purview of this chapter, but this is accomplished through direct manipulation and mobilization of the upper cervical

Chapter 37: Posture and Muscle Tension

This chapter reviewed issues related to posture and muscle tension. Pain syndromes were also looked at as they are clinically intertwined with voice complaints and relief of one often leads to relief of the other. Case studies were provided to summarize and explain the management pro­ tocol. It is our hope that this leads the reader to his/her own journey into this fertile area of research and clinical study.

REFERENCES



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1. Rolf IP. Rolfing: Reestablishing the Natural Alignment and Structural Integration of the Human Body for Vitality and Well being. Rochester, VT: Healing Arts Press; 1989. 2. Rubin JS, Epstein R. Care for the professional voice. In: Rubin JS, Sataloff RT, Korovin G (eds), Diagnosis and Treatment of Voice Disorders, 2nd edition. Buffalo, New York: Thomson Learning Group;2003. 3. Aronson AE, Peterson HN, Litin EM. Psychiatric symptoma­ tology in functional dysphonia and aphonia. J Speech Hear Disord. 1966;31(2):115 27. 4. Aronson AE, Peterson HN, Litin EM. Voice symptomatology in functional dysphonia and aphonia. J Speech Hear Res. 1964;34:801 11. 5. Aronson A. Clinical Voice Disorders, 3d edition. New York, NY: Thieme Medical Publishers; 1990. pp. 117 45. 6. Ohashi W. Do It Yourself Shiatsu: How to Perform the Ancient Art of Acupressure. New York, NY: Penguin Compass, Penguin Group New York; 2001. 7. Rubin JS, Blake E, Mathieson L. The Effects of Posture on Voice. In: Sataloff RT (ed.), Professional Voice: The Science and Art of Clinical Care, 3rd edition, Vol II. San Diego, CA: Plural Publishing Inc; 2005. pp. 1079 86. 8. Holstege G. Emotional innervation of facial musculature. Movement Disorders. 2002;17Suppl 2:S12 S16. 9. Kuypers HGJM. Anatomy of the descending pathways. In: Burke RE (ed.), Handbook of Physiology, Section I, The Nervous System, Vol. II, Motor Systems. Washington, DC: Washington American Physiological Society; 1981. pp. 597 666. 10. Robinson L, Fisher H, Knox J, Thomson. The Official Body Control Pilates Manual. London, UK: Macmillan Publishers Ltd; 2000. 11. Harvey P. Yoga for Every Body. Pleasantville NY: Reader’s Digest Publishers Inc.; 2001.



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A 55 year old male fund manager is referred for voice therapy for the treatment of his severe dysphonia; video­ stroboscopic laryngeal examination reveals no structural or biomechanical abnormalities. His vocal profile is char­ acterized by marked vocal creak, lowered fundamental frequency, limited pitch range, reduced loudness, and vocal fatigue. Patient self rating on the Vocal Tract Dis­ comfort Scale (VTDS)14 indicates high levels of aching and tightness of the perilaryngeal musculature. The Palpatory Evaluation Protocol17 reveals extremely resistant sterno­ cleidomastoid and supralaryngeal muscles, and a forced lowered larynx that is highly resistant to lateral digital pressure. His chin is held in a markedly depressed posi­ tion and his head is retracted. (This is not the typical head posture or laryngeal position of individuals with MTD but clinical experience indicates that these positions are typi­ cal of a significant sub set of MTD cases.) LMT,14 a form of perilaryngeal manual therapy within the knowledge base and skill set of speech language path­ ologists who specialize in voice disorders, reduces the perilaryngeal tension using circular massage along the length of the sternocleidomastoid muscles, and kneading and stretching of the supralaryngeal area. Following inter­ vention, the patient’s chin is released to a more normal position and all acoustic parameters normalized. In parti­ cular, vocal creak is virtually eliminated and pitch range extended into the upper part of his potential range. He notes that phonation is no longer accompanied by discomfort. The improvements obtained at the initial consultation have been largely maintained when the patient is seen again, 1 week later. Further LMT at two subsequent appointments, in combination with phonatory function strategies, stabilizes the changes and he is discharged. One key issue, perhaps, in discussing aspects of therapeutic intervention is that changes in the resting position of the

SUMMARY



CASE REPORT 2: LARYNGEAL MANUAL THERAPY

larynx often appear to be secondary to changes in the resting position of the cervical spine. These in turn may well be secondary to fundamental postural changes elsewhere in the body. Such postural issues require address if local treatment of laryngeal position is to provide more than temporary relief of vocal symptoms.





and thoracic vertebrae, and through soft tissue work on the affected muscles. The performer is able to perform that evening. Intermediate therapy is designed to continue releasing the restricted muscular and arthrogenic structures. An exercise plan is also developed to strengthen the deep neck flexors and lower fibers of the trapezius. Following a further three or four sessions, the performer feels that she is back to normal voicing.

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12. Pressman AH, Shelley D. Integrative Medicine: The Patient’s Essential Guide to Conventional and Complementary Treat­ ments for more than 300 Common Disorders. New York, NY: The Philip Lief Group Inc., St. Martin’s Press; 2000. 13. Lieberman J. Principles and techniques of manual therapy. In: Harris T, Harris S, Rubin JS, Howard D (eds), The Voice Clinic Handbook. London: Whurr Publishers; 1998. pp. 91-138. 14. Mathieson L, Hirani, SP, Epstein R, et al. Laryngeal Manual Therapy: A Preliminary Study to Examine Its Treatment Effects in the Management of Muscle Tension Dysphonia. J Voice. 2009;23:353-66 15. Lumley JSP, Craven JL, Aitken JT. Essential Anatomy. Edinburgh: Churchill Livingstone; 1973. 16. Ger R, Abrahams P, Olson TR. Essential Clinical Anatomy, 2nd edition. New York: Parthenon Publishing Group; 1996. 17. Boileu Grant JC, Basmajian JV. Grant’s Method of Anatomy, 7th edition. Baltimore: Williams and Wilkins; 1965. 18. Williams PL. Gray’s Anatomy, 38th edition. New York: Churchill Livingstone; 1995. 19. Lowell SY, Kelley RT, Colton RH, et al. Position of the hyoid and larynx in people with muscle tension dysphonia. Laryngoscope. 2012;122:370-77. 20. Rubin JS, Lieberman J, Harris TM. Laryngeal manipulation. Otolaryngol Clin North Am. 2000;33(5):1017-34. 21. Lieberman J, Rubin JS, Harris TM, et al. Laryngeal Mani­ pulation in Diagnosis and Treatment of Voice Disorders, 3d edition. Rubin JS, Sataloff RT, Korovin GK (Eds). San Diego CA: Plural publishers; 2005.

22. Mathieson L. Vocal tract discomfort in hyperfunctional dysphonia. J Voice. 1993;2:40-48. 23. Mathieson L. Greene and Mathieson’s The Voice and Its Disorders, 6th edition. London, England: Whurr Publishers Limited; 2001. 24. Roy N, Leeper HA. Effects of the manual laryngeal musculo­ skeletal tension reduction technique as a treatment for functional voice disorders: perceptual and acoustic meas­ ures. J Voice. 1993;7:242-9. 25. Roy N, Bless DM, Heisey D, et al. Manual circum­laryn­ geal therapy for functional dysphonia: an evaluation of short- and long-term treatment outcomes. J Voice. 1997; 11:321-31. 26. Mathieson L The evidence for laryngeal manual therapies in the treatment of muscle tension dysphonia. Curr Opin Otolaryngol Head Neck Surg. 2011;19:171-6. 27. Rubin JS, Blake E, Mathieson L. Musculoskeletal patterns in patients with voice disorders. J Voice. 2007;21(4):477-84. 28. Starlanyl D, Copeland ME. Fibromyalgia and Chronic Myofascial Pain: A Survival Manual, 2nd edition. Oakland, CA: New Harbinger Publications Inc.; 2001. 29. Beresford-Cooke C. Acupressure: A Practical Introduction to the Benefits of this Therapy. New York: Macmillan; 1996. 30. Chaitow L. Soft Tissue Manipulation: A Practitioner’s Guide to the Diagnosis and Treatment of Soft Tissue Dysfunction and Reflex Activity. Rochester, VT: Healing Arts Press; 1988. 31. Koufman J, Blalock O. Functional voice disorders. Otolaryn­ gol Clin North Am. 1991;24:1059-73.

Chapter 38: Neurologic Disorders of the Voice

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CHAPTER

38

Neurologic Disorders of the Voice Lucian Sulica, Babak Sadoughi

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NEUROLARYNGOLOGIC EVALUATION



Because of their expertise in laryngeal examination, it frequently falls to otolaryngologists to identify signs and symptoms of systemic neurologic illness. Although the fundamentals remain the same, the task of neurolaryn­ gologic diagnosis differs in several important ways from the standard laryngeal evaluation. Because neurologic disorders are by definition disorders of laryngeal motion, examination must be dynamic and performed across a variety of laryngeal tasks; sustained phonation alone, the mainstay of evaluation for benign vocal fold lesions, frequently will not reveal all relevant findings. The spasms of spasmodic dysphonia, for instance, may only be evident in connected speech. Subtle cases of paresis may remain obscure until repetitive motion has



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The larynx is a biological valve at the confluence of the respiratory and digestive tracts, of which the main role is airway protection. For this, it depends on a sensitive neural system, which responds to a wide variety of mechanical and chemical stimuli to trigger laryngeal closure. Its function as a phonatory organ depends on a still more sophisticated interaction between afferent and efferent neural systems to produce precise and finely modulated glottic closure. As a consequence, the larynx is exquisitely sensitive to neurologic derangements, and is involved in a wide variety of neurologic disorders. In fact, compromise of laryngeal function—alterations in respiration, deglutition, and phonation—may sometimes be the earliest sign of such disease.

fatigued the laryngeal muscles. An extended examination also helps to distinguish incidental asymmetries in laryn­ geal motion, occasionally observed in the normal larynx from significant findings, which are typically more consis­ tent. Sensory abnormalities may go unappreciated until a swallowing trial is undertaken. Tasks that may be helpful in the assessment include quiet and forceful expiration, swallowing, sustained and connected speech, rapid alter­ nating tasks, and occasionally singing and other special forms of phonation. The larynx is probably best examined using a flexible endoscope, as rigid peroral endoscopy or mirror examina­ tion renders many laryngeal tasks other than sustained phonation impossible, and forces the patient into a non­ physiologic posture that may mask or attenuate charac­ teristic laryngeal findings. Rigid laryngoscopy should be considered an adjunctive study in cases of neurologic disease; e.g. it can be helpful in characterizing the confi­ guration of glottic insufficiency more precisely. Because neurologic disease often is not restricted to the larynx, a broader neurologic assessment is also essential. This need not be exhaustive and time consuming; a cra­ nial nerve examination should already be a routine part of the otolaryngologic assessment, and an assessment of strength, rigidity, tremor, and coordination in the upper extremities and an evaluation of gait adds considerable information in exchange for only minutes of time. Special note should be made of articulation impediments, often confused with voice disorders by patients and their physi­ cians, and velopharyngeal insufficiency, which frequently occurs together with vocal fold dysfunction in the context of neurologic illness.

INTRODUCTION

506

Section 4: Voice Disorders

Fig. 38.1: This EMG recording of the thyroarytenoid muscle of a patient with essential voice tremor during sustained /i/ phonation clearly reveals the perfectly rhythmic waxing and waning activation of the muscle typical of tremor, in this case at a rate of 5 Hz. Normally, muscle activation should be continuous during this activity (each horizontal division = 100 ms; each vertical division = 100 μV).

For many neurologic diseases, particularly movement disorders, there is no known biologic marker, so there is no definitive laboratory or radiologic study to confirm diagnosis. Spasmodic dysphonia, essential tremor, and Parkinson disease (PD) are all cases in point. Diagnosis rests on judicious interpretation of the features of the clinical examination. This redoubles the importance of this element of the evaluation. Finally, most otolaryngologists do not often diagnose and treat neurologic disease, and appropriate training is frequently sparse. In the evaluation of a patient suspected to have neurologic disease, cooperation with an interested neurologist is almost always informative, often stimulating, and usually indispensable for optimal patient management. Laryngeal electromyography (LEMG) continues to occupy an ill-defined place in the evaluation of neurologic laryngeal disorders. It is important to understand that, apart from amyotrophic lateral sclerosis (ALS), in which EMG (typically of the tongue) may be diagnostic, EMG findings are not definitive. Nevertheless, LEMG can be extremely helpful in (1) identifying laryngeal pareses that are part of a systemic neurologic disorder, (2) distinguishing these from innocent asymmetries of laryngeal motion, and (3) characterizing laryngeal motions, as in tremor (Fig. 38.1). The utility and limitations of LEMG are fully discussed elsewhere in this volume. The inventory of neurologic disease reviewed in this chapter is by no means exhaustive. We have focused on disorders that the otolaryngologist must recognize because patients may present without antecedent diagnosis or with erroneous diagnosis and disorders for which adept otolaryngologic management may achieve meaningful

improvements for the patient or, conversely, uninformed intervention may create difficulties.

STROKE Vocal fold paralysis may appear in the wake of a stroke. The close proximity of the nucleus ambiguus to other cranial nerve nuclei dictates that it is virtually never an isolated finding; it is almost always found in conjunction with other deficits, a circumstance that adds to its morbidity. Significant dysphagia is found in 30–50% of stroke patients, and aspiration is a leading cause of death.1-3 Vocal fold paralysis may follow lacunar or cortical strokes, but is most common after medullary infarcts.4 Lateral medullary infarct (Wallenberg syndrome) is a well-known complex of neural injury from posterior inferior cerebellar artery thrombosis that features vocal fold paralysis, dysphagia, vertigo, ataxia, Horner syndrome, and hemifacial sensory deficit and/or pain. Patients with dysphagia or vocal fold motion deficits following stroke should be investigated promptly and thoroughly. Although many cases of vocal fold paralysis recover or improve over weeks to months, all necessary measures should be taken in the short term to prevent aspiration.5

MULTIPLE SCLEROSIS Multiple sclerosis (MS) is characterized by relapsing and remitting, usually progressive, neurologic symptoms due to immune-mediated destruction of myelin in the central nervous system. The cause is unknown, but genetic and

Chapter 38: Neurologic Disorders of the Voice

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by asking the patient to walk three or four paces and turn 180°. Affected patients will not be able to pivot, but instead will take several steps to rotate their body. The underlying pathology is neuronal loss in the substantia nigra and consequent loss of dopamine in the basal ganglia. The mainstay of treatment remains dopa­ mine replacement, augmented by agents to boost transit of levodopa across the blood–brain barrier and other dopamine receptor agonists that have been developed in recent years. The aim is symptomatic relief, and the under­ lying disease remains relentlessly progressive. Stimulation of deep brain nuclei by means of a surgically implanted electrode is gaining popularity in incapacitating cases of parkinsonism that resist medical management.

Parkinson Hypophonia

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The characteristic low intensity monotone voice of patients with PD has been termed Parkinson hypophonia. The laryngoscopic correlates of Parkinson hypophonia include vocal fold bowing (spindle shaped glottic insufficiency) (Figs. 38.2A and B), vocal fold bradykinesia, and tremor.7 9 These laryngeal abnormalities usually coexist with oral motor articulatory difficulties and poor respiratory function and coordination, both reflections of underlying rigidity and bradykinesia. These are not infrequently accompanied by cognitive dysfunction.10 14 In addition, underestimation of own speech volume is a perceptual anomaly that has been found consistently in patients with Parkinson hypophonia, and may be a critical derangement in this type of dysphonia.15,16 Standard medical treatment with levodopa generally improves speech and voice difficulties in PD.17 19 Early enthusiasm for vocal fold augmentation to remedy the observed glottic insufficiency20,21 has been tempered by an understanding for the broader range of abnormalities involved in Parkinson hypophonia; only in the carefully selected patient without severe respiratory or articulatory dysfunction is augmentation likely to offer appreciable benefit. Deep brain stimulation (DBS) has been shown to be most effective in tremor suppression, but evidence of practical voice and speech benefit from this procedure remains equivocal. Selective improvement in speech related functions has been feasible at the expense of limb motor control improvement in a recent study, using less aggressive electrical stimulation parameters.22 The most effective intervention, apart from systemic medication, may be behavioral therapy. Lee Silverman Voice Treatment (LSVT) is an intensive course of behavioral -

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environmental factors appear to play a role. The notion of viral transmission has also been considered, but no convincing evidence has been uncovered. The peak incid­ ence is between ages 20 and 40, and women are affected approximately twice as often as men. Paresthesias, dip­ lopia, gait abnormalities, or loss of strength in the upper extremities are common presenting symptoms. Within the domain of otolaryngology, imbalance and vertigo are probably the most common complaints. Diagnosis rests on the finding of oligoclonal bands in cerebrospinal fluid (CSF) electrophoresis and/or increased CSF IgG, one attack of symptoms, and evidence of two separate central nervous system lesions. Acute episodes are treated with anti inflammatory agents, principally steroids. Immune modulators (interferon β, glatiramer acetate) and immuno­ suppressive drugs are used to ameliorate the progress of the disease over the long term with variable success. So called “scanning speech” is held to be typical in patients with MS. This is a dysarthric rather than dysphonic phenomenon of abnormal pauses and dropped sounds. Patients may also complain of dysphagia, which appears to be due to disturbed coordination of pharyngeal activity and weakness of the constrictor muscles;6 gross vocal fold motion abnormalities are conspicuous by their absence in the MS literature.

507

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Parkinsonism (including its primary or idiopathic variant PD) is a neurodegenerative syndrome characterized by four cardinal signs: resting tremor, rigidity, bradykinesia, and postural instability. At least two must be present for the diagnosis to be entertained. Most commonly, parkinsonism is idiopathic, although there are genetic, postencephalitic, drug induced (following metoclopramide, neuroleptics, and other dopamine antagonists) and traumatic variants (as in boxers). Asymmetry in the physical examination is typical; the most common presenting symptom is unilateral extremity tremor. Parkinsonian tremor typically improves on finger to nose tasks and is more evident when the limb is at rest and supported. Cogwheel rigidity describes a ratchet like sensation felt during passive flexion extension of the upper limb or neck. Bradykinesia refers to slowness of voluntary movement. When this affects the muscles of facial expression, it yields a characteristic lack of facial affect described in the medical literature as “mask like”. The integrity of postural reflexes can be easily evaluated



Parkinsonism



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MOVEMENT DISORDERS

508

Section 4: Voice Disorders

A

B

Figs. 38.2A and B: Best phonatory glottal closure is shown at right in this 56-year-old attorney with Parkinson disease. Glottic insufficiency is exacerbated by early vocal fold atrophy. Symptoms were typical of Parkinson hypophonia, and the patient improved with voice therapy.

therapy that aims to increase phonatory effort to overcome the impaired self-perception of loudness and appears to result in improved neuromuscular control of the entire upper aerodigestive tract. The mechanism for this effect remains unclear. Benefit has been demonstrated in placebocontrolled trials and appears to be sustained over time.23-26

Multiple System Atrophy Multiple system atrophy (MSA) is a neurodegenerative syndrome that features parkinsonism and autonomic and cerebellar dysfunction. When symptoms of autonomic dysfunction—typically postural hypotension—are promi­ nent, it is known as Shy-Drager syndrome. When cerebel­ lar dysfunction—gait ataxia, severe intention tremor, and dysarthria—predominates, it is known as olivopontocellu­ lar atrophy. Many cases are initially diagnosed as PD until the appearance of additional symptoms makes the nature of the disease clear. MSA is usually lethal, with a mean sur­ vival of 8–10 years.27 Laryngeal problems may contribute to the mortality of MSA—nighttime respiratory dysfunction appears to be a leading cause of death. Nocturnal stridor is present in some 13% of patients, and is a poor prognostic sign.27,28 Both bilateral vocal fold paralysis and paradoxical vocal fold adduction during inspiration have been amply documented in MSA and appear to account for this symptom.29-34 Early identification of either of these abnormalities followed by tracheotomy may prevent or delay some deaths,27,35 although there is evidence that central respiratory dysfun­ ction is substantial in these patients, independent of

laryngeal findings.36 Of additional concern, misdiagnosis of patients with MSA may prompt the otolaryngologist to consider vocal fold medialization, as in PD, which stands likely to exacerbate respiratory problems, possibly to a lifethreatening degree.

SPASMODIC DYSPHONIA (FOCAL LARYNGEAL DYSTONIA) Spasmodic dysphonia is a form of dystonia, a chronic neurologic disorder of central motor processing charac­ terized by task-specific action-induced muscle spasms. Its clinical features, epidemiology, and treatment are presen­ ted in detail in another chapter; it is mentioned here for completeness and to draw attention to similarities with essential voice tremor, which may cause diagnostic confu­ sion. Sometimes, the involuntary vocal fold adduction or abduction of spasmodic dysphonia will occur with rhy­ thmic or near-rhythmic regularity, creating a pattern of phonatory breaks nearly indistinguishable from that of severe essential tremor.37,38 Dystonic tremor has been noted in up to one-third of spasmodic dysphonia patients,39 a feature spasmodic dysphonia shares with other focal or segmental dystonias, such as torticollis and writer’s cramp.40,41 Like dystonic activity as a whole and unlike essential tremor, dystonic tremor is often task specific and may decrease with a sensory trick (a method of touching an affected body part to reduce the severity of the involuntary motion).40 In the larynx, a dystonic tremor may be more evident during connected speech than during singing or

509

Chapter 38: Neurologic Disorders of the Voice -



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The phonatory apparatus may be involved in 25–30% of patients with essential tremor.47 Voice tremor may be the only manifestation of essential tremor,48 but usually it is associated with tremor in other parts of the body, including the upper extremities or head. Essential tremor, when it affects the voice, is usually not restricted to the intrinsic muscles of the larynx; extrinsic laryngeal muscles, pharyngeal and palatal muscles, the muscles of articulatory structures, as well as muscles of the diaphragm, chest wall, and abdomen, which affect phonatory expiration,



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Essential Voice Tremor

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Essential tremor is an age related disease of involuntary movement. Although generally acknowledged to be the most common adult onset movement disorder, it is difficult to fix a precise incidence because essential tremor may be mild enough to go unnoticed in 50% or more of affected people.42,43 In many instances, the disease is familial, and it can be inherited in an autosomal dominant fashion; the remainder of cases appear to be sporadic.42 44 Absence of a family history of tremor does not preclude a diagnosis of essential tremor. The diagnosis of essential tremor is clinical. The tremor begins insidiously and progresses at a variable rate,45 although generally slowly. Most commonly, the tremor begins in the upper extremities, and it is usually mildly asymmetric.46 In contrast to tremor in PD, essential tremor is an action induced tremor that occurs during voluntary movement and posture holding through the oscillation between agonist and antagonist muscle group activity, without task specific characteristics.40 In general, it occurs at a rate of 4–10 Hz (Fig. 38.1), whereas enhanced physiologic tremor occurs at a rate of 8–12 Hz. Intention (“cerebellar”) tremor is slower, occurring at a rate of 2–5 Hz.40,42 As is evident, there is considerable overlap in the frequencies of different tremors and, as a result, clinical circumstance (resting versus action) is a more useful diagnostic than is tremor frequency.



Essential Tremor

are often variably involved.49 51 The term “essential voice tremor” thus describes the clinical situation better and is more apt than “essential laryngeal tremor”. Because of this broad involvement of different muscle groups, a patient with essential voice tremor may present with variability in frequency as well as (or in place of ) intensity. Most often, though, patients complain of intensity fluctuations associated with a perception of increased phonatory effort. Muscular discomfort and fatigue may result from efforts to stabilize the vocal tract. Symptoms are usually present across all phonatory activity. Usually there is no dysphagia or dyspnea. Occasional patients complain of dyspnea, probably representing a perception of breathlessness during voicing resulting from glottic insufficiency, similar to that experienced by patients with unilateral vocal fold paralysis. Patients with essential voice tremor generally report slowly deteriorating symptoms over months to years. Voicing worsens with anxiety or stress—although this can apply to any central movement disorder,52 and is especially troublesome under more demanding acoustic conditions, such as speaking against background noise, addressing a classroom or conference, or using the telephone. In common with other manifestations of essential tremor, alcohol may effect a voice improvement. Similar features are found in spasmodic dysphonia, which can be a source of diagnostic confusion. Rhythmic, oscillatory motion of the palate, pharynx, and/ or vocal folds is diagnostic. Vocal fold tremor is bilateral and grossly symmetric. Tremor may be present across all laryngeal tasks, including quiet respiration as well as phonation; the traditional distinction between rest and activity appears unhelpful in the larynx, as the larynx rarely finds itself in a true resting mode and its primary physiologic functions constantly take turns to maintain some form of activity in the laryngeal valve system. Instrumental measures of voice have revealed (1) elevated jitter and shimmer and (2) decreased harmonic to noise ratio, s/z ratio, and maximum phonation time, which are abnormalities shared with other conditions of glottic insufficiency.53 If both history and examination are characteristic, further investigation is unnecessary. If findings are atypi­ cal or ambiguous, and especially if onset of symptoms is rapid, it is prudent to consult a neurologist, as tremor may often be associated to other movement disorders, or an indirect manifestation of an underlying neurologic pathology.54 Ruling out thyrotoxicosis and drug induced

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sustained vowel phonation, and may be suppressed by insertion of a flexible fiberoptic laryngoscope. Dystonic tremor is usually somewhat aperiodic, although this may be extremely hard to appreciate. Ultimately, a therapeutic trial of botulinum toxin chemodenervation may be requi­ red to distinguish essential voice tremor from laryngeal dystonia.

510

Section 4: Voice Disorders

tremor—in the otolaryngologic pharmacopeia, adrenergic decongestants are the most common source—will prevent an unnecessary referral.

Treatment First-line treatment of essential tremor is pharmacologic. Propranolol and primidone are mainstays of treatment, with proven efficacy in controlled clinical trials. Proprano­ lol is a b-adrenergic blocker that reduces tremor ampli­ tude by means of peripheral modulation of b-adrenergic receptors in skeletal muscle, resulting in symptomatic relief in up to 50% of patients.55 Primidone is an anti­ convulsant that is effective in the control of tremor symp­ toms in about 50% of patients; the mechanism is not fully understood but it may involve enhancement of g-aminobutyric acid neurotransmission in the central nervous system.55 Neither primidone56 nor propranolol57 has been shown to improve voice tremor in studies of small numbers of patients. Methazolamide, a carbonic-anhydrase inhi­ bitor, appeared to improve vocal symptoms in more than half of patients (16 of 28) treated in an open trial,58 results not supported by a subsequent blinded investigation.59 A case of effective treatment with gabapentin has been

reported.60 These few reports notwithstanding, pharma­ cologic treat­ment of voice tremor has been sparsely studied; further investigation is needed. Botulinum toxin treatment of essential voice tremor is predicated on the assumption that vocal fold tremor and resulting inappropriate glottal aperture account for the greater part of the symptoms of essential tremor of the phonatory tract. Generally, botulinum toxin is injected into one or both thyroarytenoid muscles55,61-64 in the manner of treatment of adductor spasmodic dysphonia and in comparable doses (Table 38.1). According to patient selfperception of vocal quality, botulinum toxin injections were useful to 67–80% of cases. Acoustic measures docu­mented benefit less often, leading investigators to hypothesize that much of the perceived improvement resulted from decreased phonatory effort. The reader is referred to the primary reports for details of treatment and results. Thalamic DBS by means of implanted electrodes is an evolving method of treating disabling, medicationresistant essential tremor. Initial reports of postoperative dysarthria, particularly after bilateral procedures, created reservations regarding the utility of DBS in the treatment

Table 38.1: Botulinum toxin treatment of essential voice tremor: Summary of studies

Outcome Study

Type of study

Number of Dose subjects Muscles injected used

Hertegard et al.61

Open trial

15

Warrick et al.62,63

Patient subjective Blinded percepevaluation tual evaluation

Acoustic analysis

Bilateral TA, 0.6–5 U 10 of 15 (67%) occasionally per side reported benefit thyrohyoid, and (TA) cricothyroid

Significant mean improvement on VAS

Significant decrease in F0 and F0 variation

Open trial 10 with crossover (unilateral vs bilateral injec­ tion)

Bilateral TA

2.5 U 8 of 10 (80%) per side wished to be treated again 15 U

No statistically significant improvement

No statisti­ cally significant change

Koller et al.55

Open trial

?

Bilateral TA

1.0– Significant mean 2.5 U improvement on per side 0- to-100 scale of function

Not reported

Not reported

Adler et al.64

Dose-rand­ omized open trial

13

Bilateral TA

1.25 U, 2.5 U, or 3.75 U per side

Significant mean improvement on 5-point tremor severity scale

Significant mean improvement in F0 variation

Unilateral TA

Significant mean improvement on 5-point tremor severity scale

(U: Units of botulinum toxin type A; TA: Thyroarytenoid; VAS, 100 mm visual analog scale; F0: Fundamental frequency). Source: From Sulica L, Louis E. Essential voice tremor. In: Merati A, Bielamowicz S (eds), Textbook of Laryngology. San Diego, CA: Plural Publishing; 2006. pp. 245-53.

Chapter 38: Neurologic Disorders of the Voice

The primary disease process remains untreatable, and interventions are usually supportive and symptomatic. Drooling may occur early in the course of the disease, and affected patients may benefit from anticholinergic medication. Dysphagia is a common complaint in mid to late stage disease secondary to involvement of bulbar motor neurons. The deficit involves poor oral pharyngeal coordination and decreased pharyngeal contraction, but not upper esophageal sphincter function, which appears relatively well preserved even in advanced disease.75 Vocal fold movement abnormalities are occasionally seen, but do not appear to be central to dysphagia in ALS.76,77 Velo­ pharyngeal insufficiency from palatal weakness is relatively common, however, and may benefit from a prosthesis or a palatal adhesion procedure.3 Timely placement of a gastrostomy tube prevents malnutrition and minimizes the risk of aspiration. Optimally, gastrostomy tube place­ ment, like the creation of a tracheotomy for ventilatory support, is discussed with the patient and family as part of end of life planning, well in advance of clinical need. -

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of essential voice tremor, as both speech and voice are tightly time gated activities requiring a high degree of coordination. However, mounting evidence suggests that DBS may be efficacious in the treatment of voice tremor.65 69

511

MOTOR NEURON DISORDERS Amyotrophic Lateral Sclerosis ALS is a degenerative disorder of unknown cause affecting both upper and lower motor neurons. Loss of the former results in hyperreflexia and spasticity, and loss of the latter results in weakness and muscle wasting. The disease incidence typically peaks after the age of 50, and slightly more men than women are affected. Patients may present to the otolaryngologist with dysarthria, typically caused by tongue muscle involvement. Tongue fasciculations are distinctive and virtually pathognomonic. Relentlessly progressive, ALS has a 50% rate of mortality at four years, usually related to respiratory muscle failure.74

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Poliomyelitis and Postpolio Syndrome

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Poliomyelitis is a viral disease that resolves without sequ­ elae following a nonspecific febrile illness in the majority of patients. About 1–5% develop the paralytic form, featur­ ing motor symptoms involving respiratory, bulbar, and/or limb weakness that are in some cases permanent. Sensory symptoms are absent. Largely eradicated in developed countries, poliomye­ litis remains relevant because some 25% of patients will experience a reactivation of neurologic symptoms 20–30 years after their acute episode, probably due to age related loss of anterior motor horn cells from a population already depleted by the primary disease. Existing neurologic deficits may worsen, and new weakness may affect previ­ ously uninvolved muscle groups. This phenomenon, termed postpolio syndrome, affects swallowing in a high proportion of patients. Vocal fold paresis and paralysis in these patients are well documented.78 80 These appear to be amenable to standard techniques to maintain the airway and improve phonatory glottal closure. -

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Tics are abrupt, purposeless movements or vocalizations that interrupt normal motor activity. Motor tics can assume almost any form, from simple twitches or blink­ ing to complex patterned motions like grimacing or hand gestures. Vocal tics can also be simple, such as grunting, or complex, such as meaningful phrases. In the context of otolaryngology practice, tics should remain a considera­ tion in cases of particularly persistent throat clearing or coughing. Tics are usually suppressible to some degree, and occur along a broad clinical spectrum from mild and barely noticeable to severely disruptive and, thus, crippling to the patient in his or her daily activity. Often, they are associated with behavioral abnormalities like obsessive compulsive disorder or attention deficit hyperactivity disorder. Gilles de la Tourette’s syndrome is diagnosed when multiple motor tics and at least one vocal tic are present for at least one year, beginning under the age of 21. Coprolalia, the best known feature of Gilles de la Tourette syndrome, is rare, occurring in fewer than 10% of cases.41 Treatment is aimed at controlling symptoms. Dopamine antagonists (haloperidol, clozapine, and others) appear to be especially effective. Unilateral and bilateral botulinum toxin injections of the thyroarytenoid muscles, as for adductor spasmodic dysphonia, have been successful in controlling vocal tics, including coprolalia.70 73

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TICS AND GILLES DE LA TOURETTE’S SYNDROME

PERIPHERAL NERVE DISORDERS Idiopathic Vagal or Recurrent Laryngeal Nerve Neuropathy Most cases of vocal fold paralysis or paresis of unknown cause are peripheral neuropathies that do not form part of

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a systemic neurologic illness. Based on serologies, cases of unknown cause have been attributed to neurotropic infections caused by Lyme borreliosis,81 herpes zoster,82-85 herpes simplex,86,87 Epstein-Barr virus,88 West Nile virus,89 and cytomegalovirus in the immunocompromised pati­ent.90 In addition, a transient increase in the number of cases of idiopathic vocal fold paralysis was recorded in the wake of the Hong Kong flu in the winter of 1969 to 1970 both in Europe and Japan.91-93 Although these clinical relationships are convincing, the majority of cases of idiopathic vocal fold paralysis, which present with normal serologies and no antecedent history of viral disease, remain unexplained. Of further note, some cases of vocal fold paralysis may serve as early signs of neurologic disease; in a recent review, 20% of patients with idiopathic laryngeal paralysis developed subsequent neurologic symptoms and disorders, including postpolio syndrome, stroke, and paraneoplastic neuropathy.94 Most series suggest that some 20–40% of patients with idiopathic vocal fold paralysis recover full mobility (Table 38.2) and an additional percentage regain acceptable voice. Occasionally, both figures are much higher.95-97 No features of these latter reports suggest an explanation for the discrepancy. The delay in diagnosis, typically four weeks or more, probably dooms anti-inflammatory treat­ ment, as used for Bell’s palsy or sudden sensorineural hearing loss, to ineffectiveness. Recovery generally takes place between one and nine months after onset, with rare cases returning after one year. Postma and Shockley have pointed out even more short-lived paralyses, and it is likely that some cases resolve before the patient seeks medical attention.98

Guillain-Barré Syndrome Guillain-Barré syndrome, also known as acute inflammatory polyneuropathy, is an idiopathic demyelinating dis­ order that causes rapidly progressive weakness. In about half of cases, it follows an infectious illness, sometimes as trivial as an upper respiratory infection. The motor deficits evolve over hours to days and usually resolve completely, although this may take months. Treatment in the meantime is supportive, and may include mechanical ventilation. Steroids are not helpful, but plasmapheresis may be effec­ tive in reducing the duration of the disorder if used early. Bilateral vocal fold paralysis may develop rapidly in patients with Guillain-Barré syndrome, and occasionally may be the initial sign.107-109 Because the deficit is likely to

Table 38.2: Idiopathic vocal fold paralysis

Study Laccourreye et al., 2003

99

N

Recovery of Recovery of voice without motion motion

40

35%

Loughran et al., 2002

9

44%

León et al., 200197

50

14%

72%

36

75%

14%

100

Havas et al., 1999

96

Benninger et al., 1998

50

24%

Ramadan et al., 1998102

16

19%

6%

Verhulst et al., 1997

67

39%

15%

Willat and Stell, 1989

28

22%

25%

Fex and Elmqvist, 1973*93

16

31%

Blau and Kapadia, 1972105

21

48%

Williams, 195995

29

83%

Work, 1941

8

25%

101

103 104

106

*Combined unilateral and bilateral cases. Source: Adapted from Sulica L, Blitzer A, eds. Vocal Fold Paraly­ sis. New York, NY: Springer-Verlag; 2006.

be temporary, no destructive airway widening procedure should be contemplated until neurologic recovery is comp­ l­ete. Tracheotomy, on the other hand, may be neces­sary for safety and to permit ventilation.

Hereditary Motor and Sensory Neuropathy Hereditary motor and sensory neuropathy (HMSN), also known as Charcot-Marie-Tooth neuropathy or peroneal muscular atrophy, is a genetic disorder that has weakness and sensory loss in the distal limbs as its most prominent features. It accounts for 80–90% of all genetic neuropa­ thies, which in turn make up about 20% of all neuropa­ thies. In the United States, this amounts to an incidence of 42 per 100,000, or more than 250,000 cases.110 HMSN results from mutations in a number of genes, and has variable modes of inheritance. The most common forms are transmitted in an autosomal dominant manner, causing extensive demyelination impairing nerve conduc­ tion velocity. In the majority of cases, the disease begins to manifest in the first or second decade and progresses slowl­y. In general, life expectancy is not markedly dim­ inished, except for the infrequent variants affecting laryngeal and respiratory function.111,112 Characteristic clinical features include distal muscle weakness and atrophy of the legs with bone changes, resulting in pes cavus, hammer toe, and talipes equina

Chapter 38: Neurologic Disorders of the Voice

A

For reasons that are not clear, affected children appear to be more likely to develop acute respiratory compromise and may need more urgent intervention.

DISORDERS OF THE NEUROMUSCULAR JUNCTION Myasthenia Gravis

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Myasthenia gravis is an autoimmune disorder of fluctu­ ating weakness and fatigue of cranial, limb, and trunk musculature caused by antibodies to postjunctional ace­ tylcholine receptors. Although remissions and relapses are typical, the disease is, overall, slowly progressive. The diagnosis is suggested by fatigability of muscle with repeti­ tive or sustained contraction (typically, the development of ptosis or diplopia with sustained upward gaze). Three tests are used to confirm clinical suspicion: administration of intravenous edrophonium should correct signs of muscle weakness attributed to myasthenia; antiacetylcholine receptor (AChR) antibodies are found in the serum; and repetitive stimulation of peripheral nerves should yield a decreased number of muscle twitches. It is not necessary for all tests to be positive for diagnosis. In fact, some 10–20% of patients do not have AChR antibodies. Antibodies to muscle specific kinase are found in some of these; others remain seronegative. Steroids and other immune modulating drugs, and plasmapheresis for severe cases, are mainstays of treat­



varus. Upper extremity findings are similar and patients may have claw hands. Sensory loss is often subtle, and most often affects vibration. Peripheral nerves are palpa­ bly enlarged in about half of patients with HMSN types 1 and 3.112 An affected greater auricular nerve is particu­ larly helpful to the examining otolaryngologist. The dis­ order is slowly progressive, and treatment is supportive. It was once held as axiomatic that HMSN nearly always spares the cranial nerves, and that the finding of vocal fold paresis was considered exclusive to HMSN type 2C. Numerous reports have made it plain that neither of these observations hold true, and the pathologic process can affect the laryngeal nerves to produce vocal fold paresis.113 It is not clear how many HMSN patients have laryngeal involvement, and it is possible that many cases go unnoticed. Paresis is usually bilateral, although the degree of vocal fold hypomobility is typically asymmetric (Figs. 38.3A and B). In this respect, laryngeal abnormalities are consistent with other clinical findings of HMSN. Because of the slow progression of the disease, patients can sometimes tolerate surprising degrees of glottic restriction; many are stridulous at presentation, but accept this as a matter of course, having been so for months or years. Despite this, the treating physician should have no hesitation in intervening when clinical criteria indicate that the potential for airway difficulties is high. Patients with milder impairment should be followed carefully, and efforts should be made to examine other patients from the same kinship to identify evolving laryngeal abnormalities.

513

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Figs. 38.3A and B: The range of motion of the vocal folds of a 44-year-old truck driver with HMSN is markedly restricted, producing inspiratory noise during conversation and dyspnea on exertion. Maximum abduction is shown on the left. Laryngeal EMG confirmed bilateral vocal fold paresis, more dense on the left than the right. One year after this examination, vocal fold abduction deteriorated further and a surgical procedure was required.

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Section 4: Voice Disorders

ment. Some 10% of myasthenia patients have thymomas, but most are thought to benefit from a thymectomy. Anti­ cholinesterase drugs, which potentiate the acetylcholine effect by inhibiting its breakdown, are used for additional symptomatic relief, but are no longer regarded as firstline agents as the autoimmune nature of the disease has become fully appreciated.74 One practical problem has been that patients may become refractory to anticholinesterases during disease flares, leading to overdose. Vocal fold paresis, typically bilateral, may occur in myasthenia gravis, contributing to respiratory difficulties; occasionally, it may be the presenting symptom.114-118 Despite the availability of medical treatment, most repor­ ted patients ultimately underwent tracheotomy, for the vocal fold paresis was not identified until dangerously symptomatic. Conceivably, anticipation and early identifi­ cation of laryngeal involvement might make nonsurgical management possible. Recently, Mao and colleagues have proposed a form of antibody-negative myasthenia gravis, which is largely limited to the larynx, to account for asymmetries in laryngeal motion and dysphonia in certain patients.119 In contrast to most series of myasthenic patients, only 1 of the 40 patients reported (2.5%) had AChR antibodies, and diagnosis in their series was based on edrophonium testing and repetitive stimulation. To date, these observations remain unduplicated.

Botulism Classic botulism results from ingestion of a clostridial neurotoxin, which blocks acetylcholine release from the nerve terminal. Clinically, the disease manifests as rapidly evolving weakness and autonomic dysfunction, marked by diplopia, dysphagia, dysphonia, dry mouth, and postural hypotension. Death results from respiratory failure. Recent outbreaks have been associated with improperly canned fish products and honey, although the disease was initially observed after sausage ingestion (botulus [Latin] = sausage). Because botulinum toxin is used therapeutically in otolaryngology, one is more likely to see local effects from intramuscular overdose than systemic toxicity from inges­ tion. Symptoms depend on the muscle treated. Adductor muscle overdose will result in incomplete glottic closure, breathy dysphonia, and in the worst case, dysphagia to liquids. Frank aspiration is extremely rare. Abductor muscle overdose will result in an immobile vocal fold; if bilateral, airway narrowing may be significant and even dangerous. The effect of the toxin is temporary, so treatment

is aimed at avoiding complications until function returns; the duration of effect of botulinum toxin is app­roximately 90 days.

Organophosphate Toxicity Organophosphates found in chemical warfare agents (“nerve gas”, e.g. tabun and sarin) and commercially available pesticides inhibit acetylcholinesterase, causing massive parasympathetic discharge and muscle weakness in acute toxicity. Low or intermediate-dose exposure may produce a more subtle muscle weakness and bilateral vocal fold paralysis, which contributes to the distress caused by dysfunction of respiratory muscles.120-122 Vocal fold paralysis tends to be reversible, although intubation is occasionally necessary to secure the airway. Atropine, which is given to counteract parasympathetic effects, is generally not helpful in reversing paralysis; pralidoxime, a cholinesterase activator, is used for this purpose.

DISORDERS OF MUSCLE Oculopharyngeal Muscular Dystrophy Oculopharyngeal dystrophy is a late onset autosomal dominant, slowly progressive myopathy whose most pro­ minent findings are eyelid ptosis and dysphagia. Other cranial muscle and limb muscle weakness may also occur, but are extremely variable. Clusters of disease, a reflection of immigration of affected individuals—a so called “foun­ der effect”—exist in Quebec and among Bukharan Jews in Israel; in Quebec, the family who imported the disease from Europe in 1648 has actually been identified.123 Treat­ ment is supportive and features surgical correction of ptosis as well as cricopharyngeal myotomy for dysphagia. Both interventions have been shown to effect meaningful improvements in daily function and quality of life.124,125

Inclusion Body Myositis Inclusion body myositis (IBM) is the most common prog­ ressive muscle disease in persons over 50.126 It is an inflam­ matory myopathy of uncertain cause, and distinct from immune disorders like dermatomyositis and polymyositis. Most forms are sporadic, although a hereditary form has been described. The “inclusion body” of the name refers to accumulations of proteinaceous material within muscle fibers that are similar to those in the Alzheimer brain, including amyloid-b, phosphorylated tau protein, and 20 other proteins.127 In addition, there is a pronounced

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13. Tzelepis GE, McCool FD, Friedman JH, et al. Respiratory muscle dysfunction in Parkinson’s disease. Am Rev Respir Dis. 1988;138:266 71. 14. Forrest K, Weismer G, Turner GS. Kinematic, acoustic, and perceptual analyses of connected speech produced by parkinsonian and normal geriatric adults. J Acoust Soc Am. 1989;85:2608 22. 15. Fox CM, Ramig LO. Vocal sound pressure level and self perception of speech and voice in men and women with idiopathic Parkinson disease. Am J Speech Language Pathol. 1997;6:85 94. 16. Ho AK, Bradshaw JL, Iansek T. Volume perception in parkinsonian speech. Mov Disord. 2000;15:1125 31. 17. Jiang J, Lin E, Wang J, Hanson DG. Glottographic measures before and after levodopa treatment in Parkinson’s disease. Laryngoscope. 1999;109:1287 94. 18. Gallena S, Smith PJ, Zeffiro T, et al. Effects of levodopa on laryngeal muscle activity for voice onset and offset in Parkinson disease. J Speech Lang Hear Res. 2001;44:1284 99. 19. Sanabria J, Ruiz PG, Gutierrez R, et al. The effect of levodopa on vocal function in Parkinson’s disease. Clin Neuropharmacol. 2001;24:99 102. 20. Berke GS, Gerratt B, Kreiman J, et al. Treatment of Parkin­ son hypophonia with percutaneous collagen augmenta­ tion. Laryngoscope. 1999;109:1295 9. 21. Kim SH, Kearney JJ, Atkins JP. Percutaneous laryngeal collagen augmentation for treatment of parkinsonian hypo­ phonia. Otolaryngol—Head Neck Surg. 2002;126:653 6. 22. Hammer MJ, Barlow SM, Lyons KE, et al. Subthalamic nucleus deep brain stimulation changes speech respiratory and laryngeal control in Parkinson’s disease. J Neurol. 2010;257:1692 1702. 23. Ramig LO, Countryman S, O’Brien C, et al. Intensive speech treatment for patients with Parkinson’s disease: short and long term comparison of two techniques. Neurology. 1996;47:1496 1504. 24. Ramig LO, Sapir S, Countryman S. et al. Intensive voice treatment (LSVT) for patients with Parkinson’s disease: a 2 year follow up. J Neurol Neurosurg Psychiatry. 2001;71:493 8. 25. Ramig LO, Sapir S, Fox C, Countryman S. Changes in vocal loudness following intensive voice treatment (LSVT) in individuals with Parkinson’s disease: a comparison with untreated patients and normal age matched controls. Mov Disord. 2001;16:79 83. 26. El Sharkawi A, Ramig L, Logemann JA, et al. Swallowing and voice effects of Lee Silverman Voice Treatment (LSVT): a pilot study. J Neurol Neurosurg Psychiatry. 2002;72:31 6. 27. Silber MH, Levine S. Stridor and death in multiple system atrophy. Mov Disord. 2000;15:699 704. 28. Wenning GK, Geser F, Stampfer Kountchev M, et al. Multiple system atrophy: an update. Mov Disord. 2003;18 Suppl 6:S34 42. 29. Bannister R, Gibson W, Michaels L, et al. Laryngeal abductor paralysis in multiple system atrophy. A report on three necropsied cases, with observations on the laryngeal muscles and the nuclei ambigui. Brain. 1981;104:351 68. -



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Chapter 39: Spasmodic Dysphonia

519

CHAPTER

39

Spasmodic Dysphonia Gayle Woodson, Michael S Benninger

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In the majority of SD patients, spasms occur in adductor muscles, so that the larynx closes too tightly during speech. This is termed adductor SD. Less than 20% of SD patients have an abductor variant of SD, with breathy voice breaks.7 These patients have spasms in laryngeal abductor mus­ cles, but also have simultaneous suppression of adductor activity, consistent with a complex deficit in control, rather than simple over activation of abductor muscles. Occasional patients have mixed SD, with both strained and breathy voice symptoms. Patients with adductor SD have maximal difficulty with the onset of words beginning with a vowel, such as “eat” or “eggs”. Abductor voice breaks are characteristically observed when a vowel follows an unvoiced consonant, as in “puppy” or “happy”. The diagnosis of SD is often difficult, as there is signifi­ cant variation in speech and voice manifestations. Although the fundamental pathophysiology is muscle spasm, the voice that we hear is greatly impacted by the patient’s effort to compensate for the voice breaks.8 Some patients may adopt a breathy voice to diminish the disruptions caused by adductor spasms and may even appear to have abductor SD. More often, patients compensate with hyperfunction that can seem indistinguishable from muscle tension dysphonia (MTD). The distinguishing sign of SD is the occurrence of voice breaks, best documented by acoustic and aerodynamic assessment, as the laryngeal spasms seen in SD cause sudden cessation or distortion of phonation and airflow. Voice breaks are much less prevalent in MTD.9 Support for the key significance of ­

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Spasmodic dysphonia (SD) is a rare speech disorder, characterized by a strained voice with frequent breaks. Spasmodic dysphonia is much more common in women than in men. The onset is generally in the fifth decade, but it is has been reported to occur from adolescence through old age. Symptoms usually develop gradually, increasing over 1–2 years, and then stabilizing. The first documented account of this problem was in 1871, when Traube described a patient with “nervous hoarseness”, which he named “spastic dysphonia”. In 1936, Critchley reported three patients who sounded as though they were “trying to talk while being choked”.1 For many years, SD was regarded as a psychogenic or functional disorder, as vocal disruption occurs predominantly during speech. Other phonatory functions, such as laughter, whispering, shouting, and often even singing, are relatively normal.2 The first firm indication that SD is an organic disease came in 1975, when Dr Herbert Dedo documented that surgical transection of the recurrent laryngeal nerve (RLN) produced significant vocal improvement in SD patients.3 Subsequent research documented multiple neurologic abnormalities in SD patients, and it became clear that the disorder did not involve spasticity, and was more properly termed “spasmodic” dysphonia.4 Spasmodic dysphonia is currently regarded as a focal dystonia, with involuntary spasms that occur in laryngeal muscles during speech.5 This is based on the observation of speech dysfunction similar to SD in some patients with generalized dystonias, as well as the occurrence of other focal dystonias, such as blepharospasm or writer’s cramp, in patients with SD. However, most patients with SD only exhibit speech symptoms.6

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voice breaks is the observation that a dramatic decrease in voice breaks correlates with symptomatic improvement in patients who have been treated with botulinum toxin injections.10 A major diagnostic characteristic of SD is task speci­ ficity, with maximal symptoms during spontaneous speech. Task specificity is not characteristic of patients with MTD, as their vocal strain is constant across speech and nonspeech tasks. Recently, Roy et al. used auto­ mated Cepstral Spectral Index to quantify dysphonia in patients with SD and MTD. In SD patients, severity was significantly greater for vowels during speech than sustained phonation. There was no significant difference for patients with MTD.11 In 2005, an NIH Research Planning Conference esta­ blished criteria for diagnosis of SD. The voice symptoms should be present > 3 months. The voice is strained and strangled during speech but should be normal during some nonspeech tasks, such as shouting, crying, whisper­ ing, sighing, or laughing. Tremor is observed in up to 30% of SD patients, and some SD patients may have other associated dystonias, such as blepharospasm or writer’s cramp, but there should be no other neurological signs. Laryngeal examination is recommended to rule out any other patho­logy or motion deficits.2 However, a recent report suggests that the diagnosis can be made with a high degree of certainty by just listening to the voice and that laryngeal examination rarely changes the diagnosis.11a

ETIOLOGY The cause and mechanism of SD are unknown. SD is generally assumed to be a focal dystonia, as the signs and symptoms are essentially identical to the speech dys­ function seen in some patients with segmental or genera­ lized dystonia. This suggests a common mechanism. There is an increasing body of information regarding the gene­ tic basis of familial dystonias. Specific genetic mutations have been identified for each of 17 different forms of dys­ tonia (DYY 1–17).12 The most common dystonia, DTY-1, is caused by a defect in the TOR1A gene, which encodes the protein torsin A. Polymorphism in this gene has been identified in segmental dystonias, including some cases of SD. There is less evidence for a genetic cause in SD than for generalized dystonia. Most cases of SD appear to be sporadic, as only 12% of patients have a family history of a similar voice disorder.13 Thus, there could be at least two populations of SD patients—those with a genetic

basis, and those which have other causes. However, the mechanisms involved in genetic cases of SD could be very similar to those in patients with nonfamilial SD. There is scant evidence linking the genes associated with dystonia to SD. The most common dystonia gene, DTY-1, codes for a protein, torsin. A mutation in TUBB4 that has been found in an Australian family with “whispering dysphonia”, a DTY4 dystonia. TUBB4 is a tubulin, expressed in neurons. Thus, at least this form of SD could be caused by micro­ tubule dysfunction.14 DTY6 dystonia typically affects cra­ nial nerves. The defective gene in DTY6 is THAP-1, which encodes a DNA binding protein. Mutations in THAP 1 have been seen in patients with early-onset generalized dys­tonia some of whom also have SD.15 Research indicates that SD and other dystonias are due to central neurological dysfunction. Anatomic and imaging studies have identified lesions and altered func­ tion in the brains of patients with SD.16 Functional mag­ netic resonance imaging studies in patients with SD have found decreased activation of sensorimotor cortex dur­ ing speech. This would be consistent with a theory that laryngeal response to sensory input is dysfunctional in patients with SD.17 However, another study found increa­ sed activation of sensorimotor cortex in SD patients, and this activity normalized after successful treatment with botulinum toxin injection.18 It should be noted that any observed abnormalities in sensory activity could be attri­ buted to the patient’s sensation of the disorder, rather than the underlying pathophysiology. The neural pathways of vocalization offer a potential mechanism for the differential performance of speech and nonspeech tasks in patients with SD. Electrophysiologic studies in primates document that spontaneous vocali­ zation can be triggered by stimulation of the cingulate cortex and the periaquaductal gray, which activate central pattern generators in the pons and brainstem.19 Humans also have this pathway but in addition have a second pathway, which directly connects the laryngeal motor cortex to the nucleus ambiguous. This pathway is not found in any other animal and is implicated in speech control.20 Thus, it seems logical that the symptom manifestations, which are specific to speech, should involve this tract but not the brainstem structures that are common to both learned and unlearned vocalization.

TREATMENT OF ADDUCTOR SD There is currently no “cure” for SD. Speech therapy and medications to relax muscles and reduce seizure activity

Chapter 39: Spasmodic Dysphonia

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Botulinum toxin: This is currently the most widely used treatment for SD. It reduces symptoms in the vast majority of patients with adductor SD. Botulinum toxin, produ­ ced by Clostridium bacteria, is the most potently lethal known biologic toxin, and is the causative agent of botu­ lism. The toxin blocks the release of acetylcholine in all cholinergic synapses in the peripheral nervous system, including motor endplates, but does not affect conduc­ tion along axons. The lethal effect of systemic toxin results from paralysis of respiratory muscles. Therapeutic use of the toxin is achieved by focal injection of small amounts of toxin directly into target tissue. It is used to diminish many cholinergic actions, including muscle contraction, vasospasm, salivary secretion, and sweating. There are seven types of botulinum toxin. A through E are produced by Clostridium botulinum, whereas F and G are produced by Clostridium baratii and butyricum, respec­ tively. Four forms of botulinum toxin are commercially available: three include type A (Botox, Dysport, and Xeomin) and one (MyoBloc) contains type B. Type A is the type used most often in the treatment of SD. Its site of action is the SNAP 25 protein, which is required for the fusion of acetylcholine vesicles with the cell wall of the nerve terminal.28 The most commonly used preparation in the United States is Botox, and this is the type that will be discussed in this section of the chapter. It was approved by the Food and Drug Administration in 1989 for use in strabismus, hemifacial spasm, and blepharospasm.29 SD is an off label, literature supported use of this drug. In a preliminary study of the use of botulinum toxin, 30 units were injected into one thyroarytenoid muscle in each of three patients with adductor SD, with the intent of causing unilateral paralysis, similar to that achieved by RLN resection.30 Before and after injection, intrathoracic pressure was monitored with an esophageal probe, to quantify expiratory effort during phonation. The toxin injec­ tion resulted in unilateral vocal fold weakness, not total paralysis. Nevertheless, patients noted marked improve­ ment in speech, with relief of the high intrathoracic -



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Surgery: RLN transection was the first treatment found to have any therapeutic effect on SD.3 Its immediate benefit was dramatic; however, there were some adverse effects. Some patients struggled with a weak or breathy voice. Injection augmentation (at that time Teflon was the preferred injectate) could strengthen a breathy voice, but too much injection would result in a recurrence of vocal strain. Recurrence of symptoms after augmentation could be reduced by removing the injected material.21 In many patients who had an initial good response to nerve section, the symptoms recurred after a period of time.22 Surgical re exploration in patients with recurrent spasms indicated that the nerve had regenerated, even though the vocal fold remained immobile: spasms but not useful function recurred. Avulsion of the nerve was used in an attempt to prevent regrowth of the nerve, but this proved to be no more effective than transection.23 Because vocal fold augmentation to improve glottic closure could result in recurrence of spasms, it seemed that glottic closing pressure, rather than innervation status alone, was a key determinant of the recurrence of spasms after RLN section. Thyroarytenoidmyectomy has been reported as a poten­ tial treatment, with some benefit reported.24 However, it is difficult to determine how much muscle should be removed, and excessive removal can cause unacceptable breathiness. Thus, this approach has not gained wide use. Berke has reported selective denervation of the thyro­ arytenoid muscles to abolish spasms in patients with adductor SD. This is performed in combination with reinnervation of the stumps of the transected nerves using branches of the ansa cervicalis, to provide muscle bulk and tone to the vocal folds and to prevent subsequent reinnervation by fibers from the RLN. In addition, por­ tions of the lateral cricoarytenoid muscle (LCA) are also resected, as thyroarytenoid denervation alone does not provide adequate relief. LCA resection must be performed cautiously to prevent breathy dysphonia and aspiration. Patients have about 6 months of significant breathiness or aphonia until the nerve fibers from the ansa grow back into the thyroarytenoid muscle. After this period of dis­ ability, patients have been reported to enjoy stable function, with reduction of spasm. The level of function has been found comparable to that achieved with botulinum toxin injection, but without the fluctuations in symptoms that occur in botulinum toxin therapy.25

Electrical stimulation: In a single case report, an RLN stimulator was implanted into a patient with adductor SD, with dramatic improvement.26 The author did not pursue this approach further, as botulinum toxin therapy became available and seemed to be highly effective. However, a recently reported preliminary study has provided further evidence that electrical stimulation could be effective.27 With increasing sophistication of implantable stimula­ tors, this is an approach that may be explored further in the future.



have not been shown to have any benefit in patients with SD. However, a number of approaches have been used to mitigate symptoms and improve speech function and quality of life.

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Section 4: Voice Disorders

pressure generated during phonation. In addition, it was noted, as had also been noted with RLN transection, that unilateral denervation also reduced adductor activity in the opposite, noninjected side. It has been suggested that botulinum toxin may be transported centrally via the axon, since unilateral injection suppresses spasms in the noninjected larynx. However, reduction of contralateral hyperactivity also occurs after unilateral resection of the RLN or myoectomy, and so a central transport of the toxin is not necessary to explain this effect. Blitzer et al. approached botulinum therapy of adduc­ tor SD with bilateral injections, using smaller bilateral doses intended to weaken the muscles, similar to the stra­ tegy that had been used to treat other dystonias.31 This also pro­duces dramatic improvement. A crossover study compared bilateral and unilateral injections in 32 patients with adductor SD. Eight patients were best controlled with unilateral injections, as bilateral injection resulted in excess breathiness. These patients who preferred unila­ teral injection presented with mild SD and were well controlled with an average dose of 5 units. Fourteen patients were more satisfied with their voice after bilateral injection. These patients had moderate or severe SD and required an average of 1.25 units per side, for a total of 2.5 units (Table 39.1). In all patients, unilateral injection required a higher dose to control spasms. For example, a patient who could be managed with a bilateral injection of 2.5 units per side required 25 units in a unilateral injec­ tion.32 Currently, the most common practice is to use small bilateral injections for moderate to severe SD and unilateral for mild or intermittent SD. The onset of action of botulinum toxin is not imme­ diate. The toxin must be taken up by the nerve terminal and cleaved to release the active chain of the molecule. After a few days, the toxin effects reach maximum, as nerve terminal can no longer release acetylcholine; however, new sprouts form to produce a small amount of synaptic activity. Thus, patients generally note effects within 24 hours. This is followed by a 1–2 week period of “overshoot” when breathiness is maximal, and patients may report a Table 39.1: Equivalency doses for unilateral in comparison to bilateral vocal fold injections for spasmodic dysphonia

Unilateral

Bilateral

1.25–2.5 units

No equivalence

5 units

0.625 units

10–15 units

1.25 units

25–30 units

2.5 units

sensation of dysphagia. This corresponds to the period during which the nerve terminals form small temporary sprouts. After 2–4 weeks, the effect stabilizes. The origi­nal terminal recovers from the toxin in about three months. Patients will note return of symptoms at variable intervals, ranging from 3 to 6, since atrophic muscles require some time to regain strength as neural activation resumes.

Techniques of Botulinum Toxin Injections for Adductor SD Botulinum toxin therapy for SD is often injected with electromyographic (EMG) guidance, to confirm location of the injection within the muscle. However, experienced physicians can achieve accurate placement and compar­ able results using percutaneous injection without EMG guidance.33 The toxin can also be injected transorally, with indirect or flexible laryngoscopic guidance, or via direct laryngoscopy.34 The keys to successful management are consistent placement of the injection and individual titration of the dose.

Injection through the Cricothyroid Membrane (Fig. 39.1) This injection can be performed either with EMG locali­ zation or observing the vocal folds from above with a flexible scope. In many cases, it is simpler and quicker to use EMG localization. The injection can be performed in either a sitting or supine position. A small amount of xylocaine can be injected into the cricothyroid space and then into the tracheal lumen. A hollow bore electromyographic needle is passed through the cricothyroid space and directed super­ iorly and laterally into the vocal fold until muscle motor potentials are identified. Position is confirmed by seeing an increase in motor unit potentials and the Botox is injected. The needle can then be directed superiorly and laterally into the other vocal without withdrawing the needle from the neck. The entire procedure typically can be performed in less than a minute or two. The thyroarytenoid muscle can be accessed per­cu­ taneously without entering the airway. The needle is intro­ duced through the cricothyroid membrane, 5–10 mm from the midline, and then directed superiorly to enter the muscle. The upward vector must be greater in males than in females, because the caudal extent of the thyroid carti­ lage below the vocal fold is greater in males. When EMG guidance is used, action potentials indicate placement in the muscle, whereas 60 cycle interference noise indicates

Chapter 39: Spasmodic Dysphonia

Fig. 39.1: Botulinum toxin injection through the cricothyroid space. Source: Reproduced with permission of the Cleveland Clinic.

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Fig. 39.2: Botulinum toxin injection through the thyrohyoid membrane. Source: Reproduced with permission of the Cleveland Clinic.

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that the needle has entered the air space. Experienced injectors report confidence in placement without EMG guidance. In the “point touch” technique reported by Berke et al., the needle is introduced through the thyroid cartilage. The needle can become blocked by cartilage fragments during this approach.

Injections through the Thyrohyoid Space (Fig. 39.2) Similar to the technique above, this can be performed either with EMG guidance or with direct visualization above with a flexible scope, although the angles make it simpler to use a flexible endoscope to visualize the needle. Local anesthesia can be performed by injection into the skin just above the thyroid notch and into the deeper tissues. The needle is then passed in the midline just above the thyroid notch, directed inferiorly and visualized as it enters into the larynx. It can be directed inferiorly to one side until it can be seen entering the vocal fold and the injection can be made. Similarly, the needle is directed to the opposite side and the injection can be made.

Injections from Above (Figs. 39.2 and 39.3) There are two approaches to injecting Botox from above (Fig. 39.3). The first is to have the patient hold their own tongue and a rigid endoscope can be passed through

Fig. 39.3: Botulinum toxin injection transorally. This can be guided either with flexible or rigid laryngoscopy. Source: Reproduced with permission of the Cleveland Clinic.

the mouth. A curved needle can then be passed into the vocal fold and injection made into the vocal folds. A similar approach can be made using a flexible scope. Since these are longer needles the volume of the needle needs to be taken into consideration. To access the thyro­ arytenoid muscle percutaneously, another option is to use a flexible endoscope to direct the needle into the vocal fold under visual guidance. The needle is inserted

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through the cricothyroid space in the midline, and then directed laterally to the vocal fold. The disadvantage of this approach is that the needle crosses airway mucosa twice, including sensitive vocal fold mucosa. This can stimulate vigorous coughing or gagging, unless the airway is anesthetized. Efficacy of botulinum toxin has been reported using a number of metrics, including patient diaries and voice satisfaction questionnaires.35 Acoustic and aerodynamic effects have documented objective changes after treat­ ment. Acoustic parameters such as jitter and shimmer are not significantly altered. Satisfactory improvement of adductor SD correlates with reduction or elimination of breaks in the acoustic voice signal.36,37 This is consistent with observations that perceived effort of speaking is more improved than the quality of voice. Phonatory airflow, which is below normal in patients with adductor SD, is increased as adductor muscles are weakened; however, airflow significantly above normal results in a breathy voice. The goal of therapy is a sufficient decrease in glottic closing pressure to reduce the effort of speaking and elimi­ nate breaks, without causing significant breathiness of the voice. The treatment does not restore normal function, and often the satisfactory result is a compromise between decreased vocal effort and reduced vocal power. As men­ tioned above, the dose should be individualized to the patient and may require trial and error titration.

abolished. However, not all patients with abductor SD obtain adequate relief with botulinum toxin therapy. The pathophysiology of abductor SD is not limited to PCA spasm. Patient with abductor SD also have decreased adductor muscle activity during phonation.41 Conse­ quently, if the PCA activity is suppressed, glottic closure may still be inadequate. Thyroplasty can compensate for lack of TA muscle activation.38,42

Techniques of Botulinum Toxin Injections for Abductor SD Accessing the PCA muscle for injection is technically more difficult than injecting the TA muscle, as the PCA muscle is located on the posterior aspect of the larynx. There are different options and selection of the optimal route depends on patient’s anatomy and physician’s preference. Lateral approach (Fig. 39.4): The larynx is rotated away from the side to be injected. This author does so by depressing soft tissue just medial to the sternocleido­ mastoid muscle and using the finger tips to engage the thyroid ala. The larynx can also be rotated by grasping the thyroid cartilage. A hollow EMG needle is inserted through the skin 5–10 mm caudal to the cricoid and then directed upward and medially to contact the posterior cricoid. This upward trajectory avoids the posterior extension of the thyroid ala.

ABDUCTOR SPASMODIC DYSPHONIA Abductor SD is a more complex clinical problem than adductor SD and is more difficult to treat. In abductor SD, patients have breathy voice breaks and/or a conti­n­ uously breathy voice. These symptoms can be mitigated by weakening the posterior cricoarytenoid muscle (PCA), the only abductor muscle in the larynx. But reduction of abductor spasm also weakens respiratory opening of the larynx, which limits the amount of PCA weakening that can be used clinically. Unilateral injection is not often adequate to improve the voice, but cautious bilateral injection can produce significant improvement in symptoms.38-40 A dose escalation protocol, with asymmetric bilateral injections, has been shown to be effective in many patients with SD.39 Flexible laryngoscopy is used to identify the side with dominant abductor activity. Then PCA injection is per­ formed, using 10 units on the dominant side and 1.25 units on the other side. If this is inadequate, then additional toxin is injected into the dominant PCA until the spasms are suppressed, or abductor activity with inspiration is

Fig. 39.4: Botulinum toxin injection for abductor spasmodic dysphonia. Lateral approach. Source: Reproduced with permission of the Cleveland Clinic.

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Chapter 39: Spasmodic Dysphonia

REFERENCES

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Current therapies reduce symptoms in patients with SD but do not restore a normal voice or correct the underly­ ing cause, which is still unknown. Research into neural mechanisms and the molecular biology of the disorder may guide improved therapy or even a cure in the future.



FUTURE DIRECTIONS





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The PCA can be injected by an anterior approach (Fig. 39.5), by passing the needle through the cricothyroid membrane, into the subglottic airspace, and then through the posterior cricoid cartilage so that the tip of the needle is in the body of the PCA. A more lateral approach has also been used, passing the needle posteriorly along inner surface of the cricoid without entering the airspace. With a unilateral injection five units is a good starting dose. Although most people note some improvement, a good response is seen in about 20% of patients.43 They will usually require a second injection a month or so later and are often done in a staged fashion, with another five units injected at that time. The larynx should be examined at the time of the second injection to confirm the side of the prior injection and to assure that the subsequent injection can be performed on the more active side. The safety of simultaneous, symmetric, bilateral injec­ tions has been reported.40 In these cases, the initial dose is approximately 2.5 units injected into each side.





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Fig. 39.5: Botulinum toxin injection for abductor spasmodic dysphonia. Anterior approach. Source: Reproduced with permission of the Cleveland Clinic.





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1. Critchley M. “Spastic dysphonia” inspiratory speech. Brain. 1939;62(1):96 103. 2. Ludlow CL, Adler CH, Berke GS, et al. Research priorities in spasmodic dysphonia. Otolaryngol Head Neck Surg. 2008;139(4):495 505. 3. Dedo HH. Recurrent laryngeal nerve section for spastic dysphonia. Ann Otol Rhinol Laryngol. 1976;85(4 Pt 1): 451 9. 4. Schaeffer S. Neuropathology of spasmodic dysphonia. Laryngoscope. 1983;93(9):1183 204. 5. Blitzer A, Lovelace RE, Brin MF, et al. Electromyographic findings in focal laryngeal dystonia (spastic dysphonia). Ann Otol Rhinol Laryngol. 1985;94(6 Pt 1):591 4. 6. Schweinfurth JM, Billante M, Courey MS. Risk factors and demographics in patients with spasmodic dysphonia. Laryngoscope. 2002;112:220 3. 7. Blitzer A. Spasmodic dysphonia and botulinum toxin: experience from the largest treatment series. Eur J Neurol. 2010;17(Suppl 1):28 30. 8. Woodson GE, Zwirner P, Murry T, et al. Use of flexible fiberoptic laryngoscopy to assess patients with spasmodic dysphonia. J Voice. 1991;5:85 91. 9. Sapienza CM, Walton S, Murry T. Adductor spasmodic dysphonia and muscular tension dysphonia: acoustic analysis of sustained phonation and reading. J Voice. 2000; 14(4):502 20. 10. Zwirner P, Murry T, Swenson M, et al. Effects of botulinum toxin therapy in patients with adductor spasmodic dyspho­ nia: acoustic, aerodynamic and videoendoscopic findings. Laryngoscope. 1992;102:400 6. 11. Roy N, Mazin A, Awan SN. Automated acoustic analysis of task dependency in adductor spasmodic dysphonia vs. muscle tension dysphonia. Laryngoscope. 2014;124(3):718 24. Epub 2013 Aug. 11a. Daraei P, Villari CR, Rubin AD, et al. The role of laryngoscopy in the diagnosis of spasmodic dysphonia. JAMA Otolaryngol Head Neck Surg. 2014;140(3):228 32. 12. Sharma N, Franco R. Consideration of genetic contributions to the risk for spasmodic dysphonia. Otolaryngol Head Neck Surg. 2011;145(3):369 70. 13. Blitzer A. Spasmodic dysphonia and botulinum toxin: experience from the largest treatment series. Eur J Neurol. 2010;17(Suppl 1):28 30. 14. Lohmann K, Wilcox RA, Winkler S, et al. Whispering dysphonia (DYT4 dystonia) is caused by a mutation in the TUBB4 gene. Ann Neurol. 2013;73(4):537 45. 15. Djarmati A, Schneider SA, Lohmann K. Mutations in THAP1 (DYT6) and generalised dystonia with prominent spasmodic dysphonia: a genetic screening study. Lancet. 2009;8(5):447 52. 16. Ludlow C. Spasmodic dysphonia: a laryngeal control dis­ order specific to speech. J Neurosci. 2011;31(3):793 7. 17. Haslinger B, Erhard P, Dresel C, et al. “Silent event related” fMRI reveals reduced sensorimotor activation in laryngeal dystonia. Neurology. 2005;65(10):1562 9.

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18. Ali SO, Thomassen M, Schulz GM, et al. Alterationsin CNS activity induced by botulinum toxin treatment in spas­ modic dysphonia: an H215O PET study. J Speech Lang Hear Res. 2006;49:1127–46. 19. Jurgens U. Neural pathways underlying vocal control. Neurosci Biobehav Rev. 2002; 26(2):235-58. 20. Kuypers HG. Cortico-bulbar connections to the pons and lower brainstem in man. Anatomical study. Brain. 1958;81:364–88. 21. Dedo HH, Behlau MS. Recurrent laryngeal nerve section for spastic dysphonia: 5- to 14-year preliminary results in the first 300 patients. Ann Otol Rhinol Laryngol. 1991;100 (4 Pt 1):274-9. 22. Aronson AE, De Santo LW Adductor spastic dysphonia: three years after recurrent laryngeal nerve resection. Laryngoscope. 1983;93(1):1-8. 23. Weed DT, Jewett BS, Rainey C, et al. Long-term follow-up of recurrent laryngeal nerve avulsion for the treatment of spastic dysphonia. Ann Otol Rhinol Laryngol. 1996;105(8): 592-601. 24. Koufman JA, Rees CJ, Halum SL, et al. Treatment of adduc­ tor-type spasmodic dysphonia by surgical myectomy: a preliminary report. Ann Otol Rhinol Laryngol. 2006;115(2): 97-102. 25. Friedman M, Toriumi DM, Grybauskas VT, Applebaum EL. Implantation of a recurrent laryngeal nerve stimulator for the treatment of spastic dysphonia. Ann Otol Rhinol Laryngol. 1989;98(2):130-4. 26. Mendelsohn AH, Berke GS. Surgery or botulinum toxin for adductor spasmodic dysphonia: a comparative study. Ann Otol Rhinol Laryngol. 2012;121(4):231-8. 27. Pitman MJ. Neuromodulation of the muscle spindle gamma loop for the treatment of spasmodic dysphonia. Presented at the 2013 Meeting of the Fall Voice Conference Atlanta Georgia, October 19, 2003. 28. Jankovic J. Properties botulinum toxin in clinical practice. J Neurol Neurosurg Psychiatry. 2004;75:951-7. 29. Schantz EJ, Johnson EA. Properties and use of botulinum toxin and other microbial neurotoxins in medicine. Microbiol Rev. 1992;56(1):80-99. 30. Miller RH, Woodson GE, Jankovic J. Botulinum toxin injec­ tion of the vocal fold for spasmodic dysphonia. A prelimi­ nary report. Arch Otolaryngol Head Neck Surg. 1987;113(6): 603-5.

31. Blitzer A, Brin MF, Fahn S, et al. Localized injections of botulinum toxin for the treatment of focal laryngeal dystonia (spastic dysphonia). Laryngoscope. 1988;98(2):193-7. 32. Woodson GE. Determining the optimal dose for botuli­ num toxin in spasmodic dysphonia. In: Isshiki N (ed.). The Third International Symposium on Phonosurgery: Proce­ edings. IAP, Kyoto; 1994: 155-7. 33. Susan L. Fulmer MD, Albert L. et al. Efficacy of laryngeal botulinum toxin injection: comparison of two techniques. Laryngoscope. 2011;121(9):1924-8. 34. Ford CN, Bless DM, Lowery JD. Indirect laryngoscopic approach for injection of botulinum toxin in spasmodic dysphonia. Laryngoscope. 2011;121(9):1924-8. doi: 10.1002/ lary.21966. 35. Benninger MS, Gardner G, Grywalski C. Outcomes of botulinum toxin treatment for patients with spasmodic dysphonia. Arch Otolaryngol Head Neck Surg. 2001;127(9): 1083-5. 36. Ludlow CL, Naunton RF, Sedory SE, et al. Effects of botu­ linum toxin injections on speech in adductor spasmodic dysphonia. Neurology. 1988;38(8):1220-5. 37. Zwirner P, Murry T, Swenson M, et al. Effects of botuli­ num toxin therapy in patients with adductor spasmodic dys­ phonia: acoustic, aerodynamc, and videoendoscopic findings. Laryngoscope. 1992;102:40116. 38. Blitzer A, Brin MF, Stewart C, et al. Abductor laryngeal dys­ tonia: a series treated with botulinum toxin. Laryngoscope. 1992;102(2):163-7. 39. Woodson, GE, Hochstetler H, Murry T. Botulinum toxin therapy for abductor spasmodic dysphonia. J Voice. 2006; 20:137-3. 40. Klein AM, Stong BC, Wise J, et al. Vocal outcome measures after bilateral posterior cricoarytenoid muscle botulinum toxin injections for abductor spasmodic dysphonia. Oto­ laryngol Head Neck Surg. 2008;139(3):421-3. 41. Cyrus CB, Bielamowicz S, Evans FJ, et al. Adductor muscle activity abnormalities in abductor spasmodic dysphonia. Otolaryngol Head Neck Surg. 2001;124(1):23-30. 42. Shaw GY, Sechtem PR, Rideout B. Posterior cricoarytenoid­ myoplasty with medialization thyroplasty in the manage­ ment of refractory abductor spasmodic dysphonia. Ann Otol Rhinol Laryngol. 2003;112(4):303-6. 43. Blitzer A, Brin MF, Stewart CF. Botulinum toxin manage­ ment of spasmodic dysphonia (laryngeal dystonia): a 12-year experience in more than 900 patients. Laryngo­ scope.1998;108:1435-41.

Chapter 40: Surgical Management of Spasmodic Dysphonia

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CHAPTER

40

Surgical Management of Spasmodic Dysphonia Gerald S Berke, Natalie Edmondson, Jennifer L Bergeron

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ADDUCTOR SPASMODIC DYSPHONIA Selective Laryngeal Adductor Denervation–Reinnervation

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Selective laryngeal adductor denervation—reinnervation (SLAD R) is a surgical procedure designed to treat ADSD. The patients who typically undergo SLAD R surgery are those with a clear diagnosis of ADSD and who are either unhappy with or cannot tolerate Botox injections and would like a long lasting solution.5 The most important consideration for long term success of the SLAD R surgery is that an accurate diagnosis of ADSD be made preoperatively. There are no objective diagnostic tests for ADSD. However, experienced clinicians can diag­ nose it by its typical voice breaks during connected speech and normal voice during emotional vocalizations, such as laughing and crying. Botox therapy can be both diagnostic and therapeutic, and we often suggest that patients try Botox and experience the “Botox lifestyle” prior to surgery. Patients with concomitant tremor are advised that surgery may control the SD symptoms but may be less effective for the tremor.2 ­

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Spasmodic dysphonia (SD) is an idiopathic focal dystonia of the larynx characterized by involuntary spasms of laryngeal muscles resulting in breaks in speech. These spasms are task specific occurring only during connected speech and not during laughter, crying, singing, coughing, or swallowing. The three subtypes of SD are abductor, adductor, and mixed. In abductor spasmodic dysphonia (ABSD), spasms of the posterior cricoarytenoid (PCA) muscle result in voice breaks that produce a breathy voice quality. In adductor spasmodic dysphonia (ADSD), spasms of the laryngeal adductors result in strangled voice breaks and a strained or tight voice quality. Patients may also have a mixed variant affecting both abductors and addu­ ctors. In addition, a laryngeal tremor may be present along with the above voice changes.1,2 Historically, ADSD was managed unsuccessfully with psychotherapy and speech therapy, as it was believed to be a psychogenic disorder. Subsequently, systemic medi­ cations were attempted, but again without success.3 Currently, the standard of care for ADSD is injection of botulinum toxin (Botox) into the laryngeal adductor muscles, which was initiated in the 1980s by Blitzer et al.4 Botox injections, if successful, will result in breathy dys­ phonia for days to weeks, followed by fluent speech for weeks to months. The patient’s symptoms typically return in 4–5 months requiring repeat injection. While Botox is effective for many, it is limited by the need for repeat injections, the on off phenomenon described by cyclic initial breathiness and eventual return of symptoms, and dose variability.2

Through the years, several surgical procedures have been proposed and developed for the management of SD. Depending on the subtype of SD present, different surgical targets have been identified, including the adductor mus­ culature, the PCA muscle, and the various branches of the recurrent laryngeal nerve (RLN). A discussion of these surgical options is presented here.



INTRODUCTION

528

Section 4: Voice Disorders

Fig. 40.1: Intraoperative SLAD-R showing the intralaryngeal portion of the procedure. Through a laryngotomy window, the recurrent nerve has been isolated.

Surgical Technique SLAD-R is performed under general anesthesia with an endotracheal tube that allows electromyographic monito­ ring of the RLNs (NIM-Response System, Medtronic Xomed, Inc., Jacksonville, FL, USA). A skin incision is placed in a skin crease along the inferior border of the thyroid lamina. The incision should extend bilaterally to the midpoint of the carotid triangle, which is bordered by the sternocleidomastoid and the omohyoid muscles, to obtain adequate exposure for identification of the ansa cervicalis nerves.2 The ansa cervicalis nerve is an excellent choice for use in laryngeal reinnervation because of its proximity to the larynx and its activity during phonation.6 It is a cervical motor nerve formed by the junction of two main nerve roots derived entirely from ventral cervical rami, which innervates the infrahyoid strap muscles. The superior (anterior) root is derived from C1, which joins the hypoglossal nerve for a short distance before branching off from this nerve at the level of the origin of the occipital artery, and descends on the lateral surface of the internal jugular vein. The inferior (posterior) root usually arises from the junction of two primary ventral cervical rami, most commonly C2 and C3, and travels posterior and deep to the internal jugular vein. A loop is formed at the point of anastomosis of the superior and inferior roots, usually on the lateral surface of the internal jugular vein.6 The ansa cervicalis nerve is exposed from the level of the superior border of the thyroid lamina and followed distally until a length needed for easy rotation into the larynx is exposed.

After fully exposing the thyroid cartilage by freeing the attached musculature and rotating the larynx medially, an inferiorly based, rectangular, cartilaginous laryngotomy window is cut in the thyroid lamina. Attention is given to preserve the external branch of the superior laryngeal nerve, which runs along the superior border of the cri­ cothyroid muscle. The intralaryngeal portion of the operation (Fig. 40.1) is performed with microinstruments and magnification. The adductor branch is typically identified running an oblique course from the posteroinferior corner of the window toward the mid-belly of the thyroarytenoid muscle anterosuperiorly and divided. The branch to the lateral cricoarytenoid (LCA) muscle is typically seen during this maneuver and is divided as well. The severed end of the proximal adductor branch is then sewn outside the larynx to the posterior lamina to prevent reanastomosis. Partial LCA myotomy is then performed at the mid-belly using microscissors. We typically cut less than 50% of the thickness of the LCA muscle. The previously identified ansa cervicalis nerve is cut distally and passed under the strap muscles to reach the laryngotomy window. Typically, the nerve to the sterno­ hyoid or sternothyroid is used. Epineurial anastomosis is performed using 8-0 nonabsorbable sutures between the ansa cervicalis and the distal stump of the adductor nerve branch. The cartilaginous laryngotomy window is replaced after a small entryway in the cartilage is made to accom­ modate the ansa cervicalis nerve, and the skin incision is closed. The postoperative laryngoscopic exam should reveal normal abduction. Near complete adduction is observed at the vocal processes, but a large glottal gap is seen midcord. Breathiness lasts between 3–6 months, at which time glottic closure is complete and reinnervation presumably occurs. Further improvement in vocal strength occurs between 9 and 12 months. Patients are strongly advised to observe good vocal hygiene and maintain control of any laryngopharyngeal reflux, if present, during the post­ operative period.2

Complications and Follow-Up There have been no documented cases of airway compro­ mise postoperatively, but all patients will experience voca­l fold bowing and breathiness in the early postoperative period. Documented complications of the SLAD-R proce­ dure include wound seroma, glottal insufficiency, dyspha­gi­a, aspiration, and surgical failure. To prevent a seroma,

Chapter 40: Surgical Management of Spasmodic Dysphonia

only provides bulk to the vocal cord but also prevents reinnervation of the adductors by fibers from the RLN, which may result in recurrent ADSD symptoms.5

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SLAD R is not the first or the only proposed surgical treatment of ADSD. In 1976, Dedo described RLN section for ADSD. The procedure appeared to be promising in the short term.8 However, in 1983, Aronson and De Santo reported that within three years 64% of patients had voice failure.9 RLN section, avulsion, or resection is therefore no longer performed for ADSD. In 1981, Carpenter et al. proposed the selective section of the adductor branch of the RLN for ADSD.10 While this procedure is similar to the SLAD R, it does not include the important step of reinnervation with the ansa cervicalis. Reinnervation not

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First proposed in an animal model in 1993, Genack et al. showed a potential new treatment by partially excising thyroarytenoid muscle tissue accessed by a cartilaginous window. Through this study involving ten rabbits, the weakened adductor function of the treated vocal fold was able to maintain glottal competence suggesting a potential therapeutic role for ADSD patients.11 In 2006, Koufman et al. proposed a transcervical thyroarytenoid myomectomy for the treatment of ADSD.12 Under local anesthesia, a unilateral laryngotomy window is made, and fibers of the thyroarytenoid and LCA muscles are removed until breathiness occurs in the patient’s voice. The surgery is repeated on the contralateral side in 3–6 months if necessary. Early data in this study of five patients showed improved fluency at 5–19 months after treatment.12 There might also be a role for this procedure as a salvage for patients who fail SLAD R surgery and who are not candidates for additional Botox therapy. Studies with larger sample sizes and long term follow up will be needed to better evaluate the optimal timing and indications for this operation. Transoral laser thyroarytenoid myoneurectomy was introduced by Su et al. in 2007.13 In this operation, a sus­ pension direct microlaryngoscopy is performed, and the carbon dioxide laser is used to vaporize the bilateral ven­ tricular folds and the middle and posterior thirds of the bilateral thyroarytenoid muscles. If terminal nerve fibers are found, these are also vaporized.13 Long term follow up appears optimistic for this surgery; however, a significant number of patients required revision surgery for residual or recurrent dysphonia.14 Other smaller studies have corroborated the potential of this procedure as a possible long term option for some ADSD patients.15,16 -

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Recurrent Nerve Section

Thyroarytenoid Myomectomy and Transoral Procedures



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a Penrose drain is placed, and the patient is kept in the hospital until the drain output is minimal. If a seroma does occur, needle aspiration is typically sufficient management.5 While breathiness is expected for up to six months post­ operatively, prolonged moderate to severe postoperative breathiness may occur in up to 20% of patients.7 Patients typically describe their immediate postoperative voice as similar to the greatest effect ever experienced following bilateral Botox injection. A few patients may not reinner­ vate and may have permanent adductor paralysis. This is thought to be due to overaggressive LCA myotomy. If a patient has prolonged breathiness and/or permanent adductor paralysis, we may consider injection thyroplasty or type I thyroplasty to improve vocal strength.5 Dysphagia is common in the first postoperative day, with most difficulty swallowing liquids. Due to vocal cord bowing and poor glottic closure, postoperative patients are also at risk of aspiration. One case of aspiration pneumonia requiring hospitalization has been reported.5 To prevent aspiration and ease swallowing, a soft diet with thickened liquids is recommended, and the patient is taught supraglottic swallow techniques. These measures are typically only needed short term. Most patients improve their swallowing by the second postoperative day allowing discharge from the hospital at that time.5 Lastly, recurrent dystonia or true failure of the ope­ ration was found to occur 10–12% of the time.5,7 The mechanism for recurrence of symptoms is still unknown, but it is suggested that failure of reinnervation by the ansa cervicalis nerve, regrowth of the RLN axons into the laryngeal adductors, and residual SD of the interaryte­ noid muscles, which are not addressed with the SLAD R surgery, may all play a role. Rarely, patients with recurrent ADSD following SLAD R have been managed with Botox injections.5,7

529

Type II Thyroplasty Type II thyroplasty consists of laryngeal framework surgery in order to lateralize the vocal folds. Under local anesthesia, the thyroid cartilage is cut vertically at the midline, and the two sides are separated by 2–6 mm and secured in position with one or two titanium bridges or silicone wedges. The distance is determined by the patient’s sensation and

530

Section 4: Voice Disorders

phonation. Isshiki et al. in 2000 reported a successful result with this procedure for the treatment of ADSD. Since that time, several studies have also identified this procedure as a potential effective long-term option.17-19 Opponents of this surgical option argue that Botox injection becomes much more difficult for postoperative patients who still require injection. Second, there is controversy regarding whether these conclusions of studies of Japanese patients with SD can be fully applied to American SD patients.

ABDUCTOR SPASMODIC DYSPHONIA Bilateral Type I Thyroplasty for Abductor Spasmodic Dysphonia As Botox injections are less reliable and technically more difficult to perform for patients with the abductor subtype of SD, a more permanent surgical treatment would be especially desirable. A potential surgical answer to this problem was suggested by Postma et al. in 1998. This study proposed bilateral type I thyroplasties (Fig. 40.2) for ABSD patients who cannot be adequately treated with Botox injection. In this way, the vocal folds cannot fully abduct during spasms improving vocal quality.20 This is a viable option for ABSD patients whose disease proves difficult to treat.

PCA Section for Abductor Spasmodic Dysphonia Shaw et al. described a small study of three patients with ABSD, who demonstrated improvement following a uni­ lateral or staged bilateral disinsertion of the PCA muscle from the muscular process of the arytenoid in conjunction with a medialization thyroplasty.21 Similar to the idea of performing a thyroarytenoid myomectomy for ADSD, it seems surgically weakening the PCA muscle may have some therapeutic benefit for ABSD patients. Access to this muscle is much more technically difficult, however, and it is unclear how much of the observed improvement was due to the medialization procedure and not due to weakness of the PCA. Also, determining the end point intraoperatively is very difficult and achieving consistent results may prove to be problematic. Third, the PCA muscle is made up of two anatomic bellies, known as the horizontal and vertical bellies, and it is unclear which belly is the optimal surgical target. Despite these limitations, the PCA muscle and nerve may remain a viable surgical option for ABSD intervention.

Fig. 40.2: Bilateral type I thyroplasty window placement for abductor spasmodic dysphonia.

CONCLUSION Although the majority of SD patients can be maintained with regular Botox injection therapy, several possible surgical treatments have emerged for those unable to tolerate Botox or those unsatisfactorily treated by Botox. Currently, our most commonly performed options include selective laryngeal denervation–reinnervation surgery, thyroarytenoid myomectomy or myoneurectomy, type II thyroplasty for ADSD, and bilateral type I thyroplasty for ABSD. The true limitation to these procedures absolutely lies in the experience of the surgeon. All of these surgeries can be very technically and conceptually challenging and should only be attempted by experienced surgeons who are comfortable with the techniques in order to ensure optimal benefit for SD patients.

REFERENCES 1. Sulica, L. Contemporary management of spasmodic dys­ phonia. Curr Opin Otolaryngol Head Neck Surg. 2004;12(6): 543-8. 2. Chhetri DK, Berke GS. Treatment of adductor spasmodic dysphonia with selective laryngeal adductor denervation and reinnervation surgery. Otolaryngo Clin North Am. 2006; 39:101-9. 3. Klotz DA, Maronian NC, Waugh PF, et al. Findings of multiple muscle involvement in a study of 214 patients with laryngeal dystonia using fine-wire electromyography. Ann Otol Rhinol Laryngol. 2004;113:602-12.

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Chapter 40: Surgical Management of Spasmodic Dysphonia

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13. Su CY, Chuang HC, Tsai SS, et al. Transoral approach to laser thyroarytenoid myoneurectomy for treatment of adductor spasmodic dysphonia: Short term results. Ann Otol Rhino Laryngol. 2007;116:11 8. 14. Su CY, Lai CC, Wu PY, et al. Transoral laser ventricular fold resection and thyroarytenoid myoneurectomy for adductor spasmodic dysphonia: long term outcome. Laryngoscope. 2009;120:313 8. 15. Hussain H, Shakeel M. Selective lateral laser thyroarytenoid myotomy for adductor spasmodic dysphonia. J Laryngol Otol. 2010;124:886 91. 16. Tsuji DH, Takahashi MT, Imamura R, et al. Endoscopic laser thyroarytenoid myoneurectomy in patients with adductor spasmodic dysphonia: a pilot study on long term outcome in voice quality. J Voice. 2012;26 (5):666.e7 12. 17. Isshiki N, Tsuji DH, Yamamoto Y, et al. Midline lateraliza­ tion thyroplasty for adductor spasmodic dysphonia. Ann Otol Rhinol Laryngol. 2000;109:187 93. 18. Isshiki N, Sanuki T. Surgical tips for type II thyroplasty for adductor spasmodic dysphonia: modified technique after reviewing unsatisfactory cases. Acta Oto Laryngologica. 2010;130:275 80. 19. Sanuki T, Yumoto E, Minoda R, et al. Effects of type II thyroplasty on adductor spasmodic dysphonia. Otolaryngol Head Neck Surg. 2010;42:540 6. 20. Postma GN, Blalock PD, Koufman JA. Bilateral medialization laryngoplasty. Laryngoscope. 1998;108:1429 34. 21. Shaw GY, Sechtem PR, Rideout B. Posterior cricoarytenoid myoplasty with medialization thyroplasty in the manage­ ment of refractory abductor spasmodic dysphonia. Ann Otol Rhinol Laryngol. 2003;112(4):303 6.



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4. Blitzer A, Brin MF, Fahn S, et al. Botulinum toxin (BOTOX) for the treatment of “spastic dysphonia” as part of a trial of toxin injections for the treatment of other cranial dystonias. Laryngoscope. 1986;96(11):1300 1. 5. Berke GS, Blackwell KE, Gerratt BR, et al. Selective laryn­ geal adductor denervation reinnervation: a new surgical treatment for adductor spasmodic dysphonia. Ann Otol Rhinol Laryngol. 1999;108(3):227 31. 6. Chhetri DK, Berke GS. Ansa cervicalis nerve: review of the topographic anatomy and morphology. Laryngoscope. 1997;107(10):1366 72. 7. Chhetri DK, Mendelsohn AH, Blumin JH, et al. Long term follow up results of selective laryngeal adductor denerva­ tion reinnervation surgery for adductor spasmodic dys­ phonia. Laryngoscope. 2006;116:635 42. 8. Dedo HH. Recurrent laryngeal nerve section for spastic dysphonia. Ann Otol Rhinol Laryngol. 1976;85:451 9. 9. Aronson AE, DeSanto LW. Adductor spastic dysphonia: three years after recurrent laryngeal nerve resection. Laryngoscope. 1983; 93:1 8. 10. Carpenter RJ, Snyder GG, Henley Cohn JL. Selective section of the recurrent laryngeal nerve for the treatment of spastic dysphonia: An experimental study and preliminary clinical report. Otolaryngol Head Neck Surg. 1981;89:986 91. 11. Genack SH, Woo P, Colton RH, et al. Partial thyroary­ tenoid myomectomy: an animal study investigating a proposed new treatment for adductor spasmodic dyspho­ nia. Otolaryngol Head Neck Surg. 1993;108(3):256 64. 12. Koufman JA, Rees CJ, Halum SL, et al. Treatment of adduc­ tor type spasmodic dysphonia by surgical myectomy: A pre­ liminary report. Ann Otol Rhino Laryngol. 2006;115:97 102.

CHAPTER Environment and Allergies

41

R Eugenia Chavez Meteorological factors such as wind direction, relative humidity, altitude, and local geographical factors influence the outdoor air pollution (Table 41.1). The main gases present in outdoor air that negatively affect its quality are ozone, nitrogen dioxide, sulfur dioxide, and carbon monoxide. There are as well microscopic particles from indust­ rial dust, pollens, yeasts, parts of animals, and mites; these particles are responsible for the allergic reaction in our respiratory system. A certain level of each pollutant is considered permissible for good air quality. The concentration during one hour is presented in Table 41.2. The concentration can be calculated in parts per million (ppm) or in micrograms per cubic meter (mg/m3). The presence of ozone in a polluted area during sunny weather is responsible for photochemical smog; its presence is due to automobiles and industries. The tolerated concentration is 0.11 ppm or 120 mg/m3 in eight hours. It produces dryness and irritation in the nasal, pharyngeal, and laryngeal mucosa, changes in mucus transportation, and irritation in the airway system, and the voice can lose flexibility for speaking and singing. The concentration of carbon monoxide recommen­ ded is 0.11 ppm; the main causative agents of carbon

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Table 41.1: Meteorological factors  

1. Relative humidity  

2. Geographical aspects  

3. Wind direction and speed 4. Altitude  

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The environment is defined as the various factors sur­ rounding an object. For human civilization, the study and knowledge of the natural environment are transcendental. In the modern world, the interaction between the physical, chemical, biological, social, and industrial factors occurs all the time. The epigenetic studies show the changes in the genetic code due to the external hazards.1–3 Physically, the atmosphere has different layers. The first one (troposphere) is related directly to the human activities. In this layer, the different physical, chemical, and biological substances that human beings are breathing are found. If the environment has harmful effects on the air, we call it pollution. Gases, fumes, dust, and different sizes of particles are present in the air all over the world.4,5 Air pollution is considered to be the presence of con­ taminants in the air that change the natural environment and affect human beings. There are outdoor and/or indoor pollution. Also, there are other forms of air pollution such as noise, heat, and light. In this chapter, chemical and biological pollutants are discussed. Another phenomenon of hypersensitivity toward air content is allergic response from our airway system. Air pollutants are found in small or middle size towns, cities, megalopolis, and urban or rural areas.6,7 Local and regional characteristics are important in order to under­ stand the presence and type of outdoor air pollution.8,9 Air pollution leads to atmospheric changes like ozone depletion and global warming, constituting a complica­ ted combination of harmful effects on the quality of the air.



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INTRODUCTION

534

Section 4: Voice Disorders

Table 41.2: Concentration and effects of air pollutants

Chemical

Value

Source

Effect

Ozone

0.11 ppm

Cars and industry

Dryness

Carbon monoxide

0.11 ppm

Tobacco and cars

Dryness

Sulfur dioxide

0.13 ppm

Combustion of coal

Inflammation

Nitrogen dioxide

0.053 ppm

Heating industry

Inflammation

Lead (Pb)

0.1 μ/m

Cars and fuels

Inflammation, alterations in nervous system

Particles

10 μm

3

20 μ/m

Irritation

Particles

2.5 μm

10 μ/m3

Irritation

3

monoxide are tobacco, emission of air pollutants from cars, and industrial pollutants. Sulfur dioxide concen­ tration is 0.13 ppm or 20 mg/m3 in 24 hours. Its presence is due to chemicals produced by combustion of coal or other biological fuels; it causes inflammation in the eyes and the respiratory system, producing itching and sore throat. When sulfur dioxide is mixed with water, the resulting acid rain causes large-scale damage and deforestation Heating, power generation, and industries produce nitrogen dioxide. The acceptable concentration annu­ally is 0.053 ppm and 40 mg/m3; nitrogen dioxide causes hoarseness due to mucosa irritation of the vocal folds. Lead (Pb) causes damage to the nervous system; the concentration that is considered safe for human beings is 0.1 mg/m3. Particles of 10 mm can be tolerated in a concentration of 20 mg/m3 per 24 hours; particles of 2.5 mm can be tolerated in a concen­tration of 10 mg/m3 in 24 hours. The particles can have sulfate, nitrates, mineral dust, ammonia, sodium chloride, carbon, biological elements (botanical and animal), and water. Many of them cause hyper-reactivity the airway system, provoking irritation, itching, and sometimes allergic reactions.10,11 Industrialization and the concentration of popu­ lation have changed the environment, causing different catastrophes such as in London in 1952 when natural processes were unable to clean the air. Mainly, the gaseous discharges of industries and the use of cars contribute more pollution to the natural environment. It is well known that the physiology of the upper and lower airways can change because of air pollution6,9,10 and help increase symp­ tomatology due to a personal allergic response. The airway system has two protective mechanisms: (1) lubrication mechanism through mucus with certain elas­ ti­­city and viscosity with a balanced chemical compo­sition

and (2) transportation of mucus due to the ciliary move­ ment with chronometrical beating.12,13 Respiratory symptoms caused by outdoor air pollu­ tion are dryness of the mucosa, changes in the viscosity of secretions, retardation of secretion transport, irritation, and/or inflammation of the mucosa. The nose serves to filter, humidify, and warm the air. A humid pharynx provides flexibility for the voice in speaking and helps to avoid infections. Lubrication and hydration are important in optimal vocal fold physiology. Many hydration studies (e.g. Hilton in 1837, Moore in 1922, Kirchner in 1968, Norman in 1974, Chavez since 1992, Verdolini in 1995, Hiroto and Vilkman since 1996) have shown that without lubrication subglottal pressure is higher and there are mucosal wave disorders due to dry air. It is known that the humidity phases of lubrication and cooling can be affected in diffe­ rent degrees due to air pollution.12-15 Changes in lung elasticity and bron­chial hyper­sen­ sitivity due to the pollution substances are recognized, and they affect the quality of respiratory function and voice production. The most frequent vocal symptoms caused by outdoor air pollution are dryness in the nasal, pharyngeal, or laryngeal mucosa; constantly clearing the throat because of the presence of secretions; and a nasal timbre. Inflammation in the pharynx provokes a slight sore throat, and the viscosity of the secretions is thicker, which also causes coughing. Endoscopic examination of the vocal folds reveals a slight edema that causes dysphonia or changes in vocal flexibility.15,16 Phonasthenia can also be present in professional voice users and performers (Table 41.3). In the artistic voice, such as singers who must work in high-pollution conditions, minimal changes in their phonatory system can be uncomfortable, while secretions

Chapter 41: Environment and Allergies

535

Table 41.3: Signs and symptoms due to outdoor air pollution

Signs

Symptoms

Dryness

Clearing throat Cough Slight dysphonia

Irritation

Pharyngeal itching Nasal itching

Edema

Nasal timbre Sore throat

Edema in vocal folds

Dysphonia Lack of flexibility

Fig. 41.1: Throat disorders in 100 professional singers.

Fig. 41.2: Nose disorders in 100 professional singers.

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Fig. 41.3: Singing voice disorders in 100 professional singers.

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in a group of 100 professional singers without bacterial or viral infection, allergy, or esophageal reflux. Forty percent of performers had symptoms such as sneezing at the beginning of rehearsal; 10% experienced them in performance. Nasal and pharyngeal dryness was present all the time in 55%. Nasal and pharyngea itching was cited by 35% of the singers, causing lack of vocal flexibility and slight hoarseness in 30%. Mineral oil smoke was present in 20% of the performances, provoking throat dryness in 40% for a few minutes (Fig. 41.4). In a study of occupational voice pathology, two groups of teachers were compared (Figs. 41.5 to 41.7).16 Both groups (80 teachers) worked in schools in the same city, one in the north and the other in the south. Due to the geographical factors such as the presence of large



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on the vocal folds, slight dysphonia, and phonasthenia change the quality of the timbre and make pitch and volume uncontrolled. The treatment for voice pathology due to air pollu­ tion is mainly directed toward balancing hydration and lubrication with mucolytics, such as guaifenesin, carbo­ cisteine, ambroxol, to decrease the viscosity of the mucus. Through inhalotherapy with a nebulizer, hydration can improve. For some patients, artificial nasal and pharyngeal lubrication with mineral oil and glycerin with water can help avoid more dryness. When the vocal mechanism changes, speaking or singing voice therapy sometimes is necessary. There are different studies of high risk groups and the effects on the voice due to air pollution. Figures 41.1 to 41.3 show the harmful effects caused by outdoor air pollution

536

Section 4: Voice Disorders

Fig. 41.4: Symptoms during performance due to dust presence.

Fig. 41.5: Symptom complaints in hot (30–35°C) and cold weather (5–10°C).

Fig. 41.6: Symptoms in two groups of teachers.

Fig. 41.7: Dysphonia in both groups by cold weather.

mountains in the south part of the city and the wind direction from north to south, pollution was higher in the south area from the higher industrial activity in the north.16 Symptoms caused by outdoor air pollution are treated. It is possible to improve dryness with humidifica­tion of the environment such as with humidifiers or vaporizers in a bedroom, studio, or office. Mucosa dryness needs lubrication and humidification. It is possible to improve this symptom by using personal nebulizers, gargles, and increasing warm water intake. The use of mucolytics improves the thinning of secre­tions. Anti-inflammatory drugs are prescribed when the vocal folds are inflamed. It is advised to use enzy­ matic preparates. Although there are few possibilities for

an indi­vidual to change outdoor air pollution, cooperat­ ing with laws and regulations is important. For indoor air pollution, it is recommended to use high-efficiency particulate air filter (HEPA) air purifier with the capacity to filter the air of a bedroom, studio or a closed area. A central purifying system is not appropriate due to the lack of tube cleaning; it is easier to have a separate purifier for each space and to be able to open win­dows to exchange air. To have less impact on the airway system due to the outdoor exposures, the person needs to avoid exercis­ ing in the open air during high concentrations of ozone or other pollutants. Exposition to cigarette smoke or other kind of smoke damages the mucosa. The chemical irritants

Chapter 41: Environment and Allergies Table 41.4: Vocal symptoms due to respiratory allergies

Nose and sinuses Nasal timbre and changes in high tones sensitivity

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Pharynx

Obstruction sensation or by speaking or singing

Larynx

Lack of flexibility, phonasthenia, and high tones difficulty

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liliopsida, and magnoliopsida). Climate change influences the reaction of the allergic population, and because of air pollution the respiratory pathology worsens. In the voice, production needs a healthy vocal fold mucosa that permits a good mucosal wave. The most frequent allergic signs in the nose are edema and paleness in the mucosa and hypertrophy in the inferior and medial turbinates. Computed tomography (CT) reveals sinusitis, mainly in the anterior and posterior ethmoidal groups. In the pharynx, erythema, edema, and hyaline secretions can be found. The larynx shows edema of epiglottis, hyaline secre­ tions, and changes in mucus transportation and in the viscosity.27,28 The endostroboscopic examination shows edema in the bony edges and sublottic region of the vocal folds (phonatory inspiration). An increase in mucus with higher viscosity and the anterior commissura with polyploid inflammation can be observed. Allergic symptoms that can affect the voice occur in the nose and sinuses, producing a nasal timbre and sensi­ tivity to high tones.21 In the pharynx, the patient can expe­ rience a sensation of obstruction while speaking or singing. The larynx shows lack of flexibility, phonasthenia, and difficulty with high tones. Professional voice users complain of disorders in vocal projection, nasal obstruc­ tion, phonasthenia, and lower volume.20 Symptoms in the singing or acting voice include nasal obstruction, a sensation of pharyngolaryngeal obstruction, diminished auditory perception, lack of vocal endurance, lack of brilliance, and use of resonators in high tones and changes in pitch quality23 25 (Table 41.4). Personal auditory feedback can also be changed. It is important to know exactly to which allergen and how intense is the allergy level by measuring the IgE reaction or the skin inflammation by intradermal tests. In 1911, Prof. Noon created the first allergen extract to make the endpoint treatment. He created the Noon unit, which is equal to 0.001 mg from pollen. Hansel, in 1930, and Rinkel, in 1937, defined the skin endpoint titration test using a dilution of 1:5.31

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in the workplace, at home, or in personal products increase the pathological personal load. Sometimes it is necessary to avoid rush hours to avoid being exposed to high concentration of pollutants. There are personal conditions that can increase the risks during environmental exposure to polluted areas, such as genetic personal predisposition due to respiratory hyper­ sensitivity, a high load of chemical exposures at home or in personal care, and frequent respiratory pathologies. If the person presents with an allergic reaction of the airway system, the exposure to a highly polluted area increases the inflammatory allergic response. Tobacco use also increases the damage to respiratory tissues when the airway is allergic and at the same time exposed to outdoor pollution. It is important to be careful with weather changes, extreme emotional arousal and intake of aspirin, non­ steroidal medications or beta blockers. Treatment for air pollution signs is merely symptomatic and helps prevent more damage in the respiratory system. The human immune system has innate barriers such as epithelium as a mucosa barrier, a phagocytic system that employs monocytes and macrophages, and a com­ plement system to inactivate the foreign bodies.17,18 It also has adaptive barriers such as a specific immune response through cellular components B and T and the presence of lymphocytes with mediators such as cytokines that initiate a specific response that attempts to defend against and eliminate foreign antigens. In the 1960s, Johansson and Ishizaka demonstrated the presence of IgE.26 There are several mechanisms to recognize the antigens stimulating an immune response. The presence of antibodies initiates a cascade of immune events provoking an allergic inflammation. The first aller­ gic patient was described in 1819 by Prof. Bostock. An allergen enters through the nose or mouth; in response, the mast cells release chemicals or histamines that irritate and inflame the respiratory membranes, causing an allergic reaction. The allergic response of the airways provokes inflammation of the respiratory mucosa. Nose, sinuses, pharynx, larynx, trachea, bronchi, and lungs can be affected by this phenomenon.19,20 Some allergies are seasonal (experienced only part of the year), whereas others are independent of seasons.27 29 Persons with genetic hypersensitivity to general innocuous substances can present an allergic reaction. The different kinds of allergens are inhalant aller­ gens: dust, mites, fungi (ascomycota and basidiomycota), yeasts, animals (animalia arthropoda and Chordata), and pollens from the different families (plantae coniferopsida,

537

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Section 4: Voice Disorders

Two different tests that are recommended for voice patients: (1) multiple dilution test with optimal skin end point titration and (2) in vitro mRAST radioimmunoas­ say (modified radioallergosorbent test) without risk.18,29 Another modern test with fluoroenzyme immunoassay is ImmunoCap, which is used to measure the presence of IgE for each allergen.30 Desensitization treatments are based on these tests. Desensitization treatment helps control the symp­ toms and the signs diminish. Continuously increasing desen­sitization with personal vaccines does not provoke side effects and is relatively simple due to the possi­bility of subcutaneous or sublingual intake.29 The duration of the treatments depends on the level of the allergies. It must last at least one year (four climate seasons) and sometimes as long as three years; also, it is sometimes necessary to be reinforced every year at a specific time.25 There are different treatments for controlling the aller­gic response to environmental allergens. For vocal users, antihistamines’ side effects (mucosal dryness, changes in the viscosity of secretions, and esophageal-gastric reflux) are contraindicated for good hydration; if they are needed, desloratadine, ebastine, and levocetirizine have fewer side effects. Other types of pharmacotherapy inc­lude decongestants and topical mucolytics (guaifene­ sin, car­bocisteine, ambroxol). Immunoregulators such as anti­leu­cotriens and monoclo­nal antibody are helpful for stabilization of the immune response. Transfer factor is also a new treatment for allergic pathologies.30 Inhalational therapy includes the use of hydration, water, steam, or nebulizers. The use of an HEPA-filter puri­ fier helps to create a better environment for sleep. There are chemical allergens that can produce neuro­ logical pathology. The relationship between respiratory airway unity and the digestive system is very close due to the anatomi­cal vicinity, the vagal reflexes, and the influ­ ences from reflux from both esophageal sphincters. Some medications used to treat allergy, mainly bronchodilators, can cause changes in the lower esophageal sphincter. Food allergens cause digestive symptoms and can increase acid production, causing indirect voice dis­tur­ bances if the patient has pathology in the esophagus, hiatus, stomach, or colon. Food allergies present to our clinic in the following frequencies: milk 20%, chocolate 20%, coffee 15%, wheat 10%, and tomatoes 10%. Rotating the diet helps avoid reactions from food, and it is also necessary to have a desensitization treatment. Grass pollen allergens cross-react with food allergy proteins in

vegetables such as onions, lettuce, carrots, celery, and corn. Recent studies have identified miRNA profiles in multiple allergic inflammatory diseases; miRNAs play an important role in regulating homeostatic immune architecture and acquired immunity. In a phoniatrical voice group from 269 patients, 80% were artistic voice users. Seventy-five percent of these patients were tested by skin end titration and multiple dilu­tion tests (Fig. 41.8). Twenty-five percent were tested by RAST. At the beginning of desensitization, 20% needed the support of 5 mg desloratadine at 65% for 2-3 months, and used antileucotriens 10 mg constantly during the first year once a day (Figs. 41.14 and 41.15). All patients used a daily purifier (Fig. 41.9). In the most recent study, a group of 567 patients32 showed the results seen in Figures 41.10 to 41.13. The artistic voice patient cannot be treated in the same way as other patients. To diminish the allergen load it is important to use fewer house cleaning chemicals, avoid passive smoking and dust in closed spaces, have as few food chemicals as possible, have good ventilation and good eating habits, keep a quantitative, qualitative schedule and restrict drinking to one to two daily glasses.22 Adverse emotional factors worsen the allergic reaction; a good night’s sleep helps stabilize the immune system. The differential diagnosis for allergic laryngitis in­cludes functional disorders, occupational voice disorders, esophageal-gastric or pharyngeal–laryngeal reflux symp­ toms, and medication side effects. See Cases A to I for illustrations of allergic symptoms (Figs. 41. 14 to 41.23).

Fig. 41.8: Tests in respiratory allergies in voice patients.

Chapter 41: Environment and Allergies

Fig. 41.9: Treatments for respiratory allergies.

Fig. 41.11: Distribution of allergies to grass pollens in 567 patients (89%).

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Fig. 41.10: Distribution of allergies to tree pollens in 567 patients (93%).

Fig. 41.12: Distribution of allergies to yeasts in 567 patients (87%).

Fig. 41.13: Distribution of allergies to inhalants such as tobacco in 567 patients (87%).

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Fig. 41.14: Case A . Photo 1. A 35-year-old woman with dysphonia mainly during cold weather with problems singing in high tones and lack of brilliance before allergy treatment.

Fig. 41.15: Case A. Photo 2. RAST for respiratory allergens and frequent food allergies after vaccines for three-month allergy treatment.

Fig. 41.16: Case B. A 50-year-old man, elementary school teacher, with phonasthenia, sore throat, and discomfort in speaking. He required skin end point titration tests and vaccine allergy treatment.

Fig. 41.17: Case C. A 35-year-old woman, high school teacher, with respiratory and food allergies. She required phonosurgery.

Fig. 41.18: Case D. A 20-year-old woman, singing student, has lack of tonal flexibility and difficulty with high tones. She required allergy treatment for respiratory allergens and air pollution irritation.

Fig. 41.19: Case E. An 18-year-old theater student with food allergies and respiratory allergies.

Chapter 41: Environment and Allergies

541

Fig. 41.20: Case F. A 7-year-old child with allergies to food and respiratory allergens.

Fig. 41.21: Case G. Computed tomography scan of a patient with rhinitis and sinusitis due to respiratory allergy and air pollution irritation.

Fig. 41.22: Case H. Computed tomography scan of a patient’s nose and sinuses affected by respiratory allergies and exposure to air pollution.

Fig. 41.23: Case I. Endoscopic image of an allergic nose.

VIDEO LEGENDS Video 41.1: Slight edema, severe secretions in middle of the body of the vocal folds, small hemangiomatous polyp in middle third of the right vocal fold. Video 41.2: Edema in body and edges of the vocal folds, nodular inflammation with incomplete closure. Video 41.3: Edema in body and edge of the vocal folds, complete closure. Video 41.4: Singer with allergic reaction, vocal fold edges with inflammation, incomplete smoothness of the vocal fold body, complete glottal closure, secretions, medial turbinate hypertrophic with edema. Video 41.5: Singer with general respiratory allergies, vocal folds with incomplete closure, vertical wave irregularities,

irregular periodicity, general edema with nodular edema in the middle third, secretions. Video 41.6: Allergic response with bleeding and small ectasia, edematous. Inferior turbinate. After treatment there was no bleeding but ectasia remained. In the third examination there was still edema but no bleeding. Video 41.7: Soprano with slight edema. Video 41.8: Allergy with edema and incomplete closure before treatment in the first examination. Video 41.9: Patient from Video 41.8 after allergy desensitization, recovery of smoothness, complete closure. Video 41.10: Mezzosoprano with allergy in the nose and sinuses, severe general edema with middle third polypoid degeneration and incomplete closure.

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Video 41.11: Lack of smoothness, edema in middle third provoking disturbances in glissando with incomplete closure and lack of flexibility. Video 41.12: Child with edema, nodules, incomplete closure. Video 41.13: Polypoid degeneration in middle third, edema in all parts of the vocal folds, incomplete closure. Video 41.14: No smoothness of vocal fold, bilateral nodular tendency, incomplete closure, hyperquinesis of ventricular folds. Video 41.15: General edema, small ectasia in middle third of left vocal fold.

REFERENCES 1. Clean Air Initiative. http://cleanairinitia­ tive.org/portal/ index.php. (Last accessed May 2, 2011.) 2. Cohen AJ, Ross Anderson H, Ostro B, et al. The global burden of disease due to outdoor air pollution. J Toxicol Environ Health, Part A. 2005;68:1301-7. 3. Air quality and health WHO fact sheet no 313 September 2011. 4. Gloxhuber C. Toxicology, 5th edn. Stuttgart, FRG: Thieme Verlag;1994. 5. Hofmann W. Lecture Script–Aerosol Physics; University of Salzburg; AUT; 2001. 6. Lutgens F, Tarbuck E. The atmosphere, 7th edn. Englewood Cliffs, NJ: Prentice Hall; 1998. 7. Reichl F. Taschenatlas der Toxikologie. Stuttgart Thieme Verlag; 1997. 8. Stockholm Convention on Persistent Organic Pollutants. United Nations treaties May 2004. treaties.un.org/pages. 9. European pollutant emission register eea.europa.eu eper. eceuropa.eu. 10. UNEP and WHO, Mage D. et al. Urban air pollution in megacities of the world. Atmos Environ. 1996;30(5):681-6; Elsevier Science, UK. 11. Brimblecombe P. Air composition and chemistry, 2nd edn. Cambridge Environmental Chemistry Series 6. Cambridge, UK: Cambridge University Press;1986. 12. O’Connell RM, Rao DS, Baltimore D. microRNA regulation of inflammatory responses. Annual Rev Immunol. 2012;30: 295-12. 13. Deitmer TK. Physiology and pathology of the mucociliary system. Advances Oto-Rhino-Laryngol. 1989;43. 14. Chávez RE. Environmental and respiratory allergies effects on the voice. Presentation at the Voice Foundation 36th Symposium, Philadelphia, PA, USA; 2007.

15. Chávez RE. Vocal pathology in singers and actors due to respiratory allergies and harmful environment. Presentation at 4th International Congress of World Voice Consortium. Seoul, Korea, 2010. 16. Chavez RE. Pollution. In: Dejonckere P (ed). Occupational voice disorders. Philadelphia, PA: Elsevier. 17. Marbry R. Skin endpoint titration. New York: Thieme Medical Publishers;1992. 18. Krouse J, Derebery J, Chadwick S. Managing the allergic patient. Philadelphia, PA: Elsevier;2008. 19. Chávez RE. Stimmaertzliche Betreung der Schauspieler und Saenger in Mexiko. Berlin; 2002. Stimmbildung Kurs. Charite KK.UnivA. von Humboldt. 20. Chávez RE. 3er curso básico de alergias en ORL .Factores alérgicos en la producción de la voz Xalapa, Ver. 2009. 21. Chávez RE. The effect of environmental conditions on voice. Istanbul 2006 3rd. World Voice Congress. 22. Chávez RE. Environment, smoking and voice. 4th World Voice Consortium World Voice Congress, Seoul, Korea, 2010. 23. Chávez RE. Allergies and environment conference In laser voice surgery and voice care 2010, 15th International Workshop, Paris, France, 2010. 24. Chávez RE. Alteraciones de la voz por patología alérgica, La influencia del ambiente en el Canto.VII Congreso Inter­ nacional de Alergia y Medicina Ambiental 2009 Mexico. 25. Chávez RE. Ambiente, alergia y voz. Congreso 52 SMORL y CCC CanCun 30 abril 2012. 26. Siow JK, Alshaikh NA, Balakrishnan A, et al. Ministry of Health Clinical Practice Guidelines: management of rhino­sinusitis and allergic rhinitis. Singapore Med J. 2010; 51(3):190. 27. World Allergy Organization 2011. worldallergy.org. 28. Silverstein A. History of immunology, 2nd edn. Burlington: Academic Press; 2009. 29. Passalacqua G. Update on the role of slit in tolerance induc­ tion to allergens safety and efficacy. Ircccs San Martino Hosp Univ. of Genoa WAO. 30. ARIA: Allergic Rhinitis and Its Impact on Asthma. www. whiar.org. 31. Burmester G. Taschen atlas der Immunologie. Stuttgart, New York: Thieme; 1998. 32. Chávez RE. Voice patients with respiratories allergies. New results. In preparation for publication.

Chapter 42: Acute Laryngitis

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CHAPTER

42

Acute Laryngitis Aron Z Pollack, Milan R Amin

PATHOPHYSIOLOGY



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Laryngitis refers to any acute or chronic, infectious or noninfectious, localized or systemic inflammatory process involving the mucous membrane of the larynx. Acute laryngitis represents a very common and self-limited inflammatory condition with abrupt onset whose course of illness typically lasts less than three weeks. Clinical pre sentation depends on several factors including etiology, the amount of tissue edema, the affected region of the larynx, and the patient’s age and immune system function. Patients may present with one or more of the following symptoms: dysphonia, dysphagia, odynophagia, cough, dyspnea, or stridor. Diagnosis is primarily based on symptomatology, detailed and directed history and physical examination, including laryngoscopy, when appropriate. The general appearance of the patient, the patency of the airway, as well as associated regional or systemic signs should be addressed. Vocal symptoms typically last 7–10 days; symptoms persisting longer than three weeks warrant a workup for chronic laryngitis. Anatomic differences in the pediatric and adult airway render children more susceptible to acute airway compromise. Acute laryngitis in children typically presents in more dramatic fashion with symptoms of hoarseness, anorexia, and noisy breathing. Acute laryngitis in adults, however, is usually less serious than that seen in children, as the anatomically larger adult larynx may accommodate swelling without obstructing as readily. Although there are many causes for acute laryngitis, it is most commonly due to a viral upper respiratory tract infection in both adults and children. Less frequently, acute phonotrauma or

exposure to noxious substances may be causative factors. Acute laryngitis is not amenable to voice therapy as its cause is usually not habitual or behavioral. In contrast, chronic laryngitis develops gradually and symptoms may wax and wane over protracted periods of time. Symptoms are generally present weeks before medical attention is sought. This separate entity will be discussed elsewhere in this text. The etiology of acute laryngitis is diverse and it may be broadly divided into two categories: infectious and noninfectious. Viruses, bacteria, and fungi may infect the larynx and cause acute laryngitis. Noninfectious causes include acute phonotrauma (a mechanical laryngitis) from vocal abuse, misuse, and overuse. In this condition, various violent vocal or laryngeal behaviors can result in an acute injury. Lastly, exposure to a potpourri of various laryngeal irritants and antigens, such as thermal, chemical, organic, or environmental, may acutely affect the larynx as well. Table 42.1 lists common causes of acute laryngitis.

BACKGROUND

Acute laryngitis represents inflammation of the vocal fold mucosa and larynx (supraglottic structures, including the epiglottis, aryepiglottic folds and arytenoid cartilages, or subglottis) that lasts less than three weeks. Although the duration of the acute response is relatively brief, the initial degree of the inflammation may be dramatic and profound. Indeed, in extreme situations, acute airway obstruction may develop. Inflamed tissues appear erythematous and edematous with associated pain; normal functions are frequently compromised or even lost. Not infrequently,

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Table 42.1: Common causes of acute laryngitis

Infectious Viral

Rhinovirus, parainfluenza viruses, respiratory syncytial virus, adenovirus, influenza virus, coronavirus, measles virus, human papillomavirus, varicella zoster, herpes simplex, cytomegalovirus

Bacterial

Hemophilus influenzae, Streptococcus pneumoniae, β-hemolytic Streptococcus, Klebsiella pneumoniae, Moraxella catarrhalis, Staphylococcus aureus, Mycobacterium

Fungal

Candida, Aspergillus, coccidioidomycosis, blastomycosis

Noninfectious Mechanical

Vocal abuse, misuse, and overuse

Traumatic

Direct injury from intubation or surgical endoscopy, internal or external blunt or penetrating trauma

Allergic

Various environmental antigens, foods, medications

Nonallergic

Hereditary or acquired angioedema, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers

Thermal

Hot liquids/foods, steam inhalation, proximity to fire, smoking certain illicit substances

Smoke, noxious fumes, occupational exposure

Smoking, pollutants, inhaled exposures, inhaled steroids

systemic markers of acute infectious inflammatory reac­ tions, such as fever, elevated white blood cell count, or lymphocyte counts, are present as well. Purulent exudate may be produced by dying neutrophils within the blood­ stream and necrosis of the afflicted tissues may occur in cases of severe acute inflammation.1 As such, patients usually complain of hoarseness, breathiness, voice changes, or throat pain. The vibratory properties of the edematous vocal folds are adversely affected; indeed, movements of the inflamed vocal folds show greater asymmetry and aperiodicity with incomplete vibratory closure. Propagation of the mucosal wave is reduced and is asymmetric. Due to the inflammatory changes to the layers of vocal fold, the vocal fold tissue becomes more viscous and difficult to mechanically move. The amount of pressure needed to set the vocal folds into vibration—the phonation threshold pressure—may become so large that it is difficult to produce sounds in a normal way, thus resulting in hoarse­ness. When phonation threshold pressure cannot be overcome, frank aphonia results. The irregular mucosal thickening along the entire length of the free edge of the vocal fold induces the production of a lower pitch in the voice of laryngitic patients. In a study describing the effects of acute laryngitis on various acoustic, aerodynamic, and perceptual measurements of the larynx, Ng et al. reported a significant lowering of speaking fundamental frequency across the five sustained vowels in patients with acute laryngitis. This was attributed to both thickening of the

vocal folds and an increase in the stiffness of the vocal fold mass contributing to incomplete glottal closure during phonation. Patients with acute laryngitis have an increased open quotient value—their vocal folds remain separated longer with less time spent in the closed position during a glottal cycle. This contributes to the hoarseness and breathiness. In these patients, there is a substantial increase in airflow rate due to the greater air escape dur­ing the glottal cycle; greater average airflow rate is signifi­can­ tly related to laryngeal hoarseness.2

EPIDEMIOLOGY Acute laryngitis is one of the most common laryngeal pathologies. The exact prevalence is not reported, however, as many patients often use conservative measures as treatment rather than seeking medical attention. Since symptoms of an upper respiratory tract infection (nasal congestion, rhinorrhea, cough, odynophagia) often precede or accompany the disease, patients feel comfortable man­ a­g­ing their own treatment while waiting for the disease to run its short-lived course. Generally, significant morbidity and mortality are not encountered with acute laryngitis. Patients with this condition, may, however, ultimately sustain vocal fold injury. The deficient voice production may result in appli­ cation of greater adduction forces to compensate for the glottal incompetence during an acute laryngitic episode. This additional tension further strains the vocal folds, often leading to mucosal injury.

Chapter 42: Acute Laryngitis

INFECTIOUS LARYNGITIS

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Acute laryngotracheal bronchitis, or croup, is a common entity seen in infants and young children from three months to three years of age. Affecting 3–5% of all children at least once, less than 10% of patients require hospitali zation, while 5% of hospitalized children develop respira tory failure requiring airway intervention. In croup, there is a circumferential mucosal inflammation of the subglottic larynx—the narrowest point in the child’s airway. This marginalizes an already small larynx, leading to labored dynamic breathing and potential airway compromise. In fact, only one millimeter of circumferential edema in the infant’s larynx reduces cross-sectional area by over 40%. The most prominent symptoms include hoarseness, dry barking cough, stridor, and fever. Parainfluenza viruses, respiratory syncytial virus, and influenza A are the most common causative agents.7 Other agents such as herpes simplex virus may infect the immunocompromised patient and herald acute respiratory failure with a fulminant disease process. Determining the degree of airway obstruction is the most important consideration when evaluating children with croup; indeed, as clinical status may abruptly deteriorate, cautious serial clinical assessment is essential. Treatment depends on the degree of airway obstruction; mild cases may be appropriately managed conservatively in an outpatient setting. Moderate-to-severe cases are managed in the hospital under monitored conditions. Treatment involves humidification and supplemental oxygen. Nebulized racemic epinephrine decreases airway edema via mucosal vasoconstriction; children who receive racemic epinephrine must be monitored for a minimum of three hours.8 Systemic and nebulized corticosteroids, once controversial, are now proven mainstays in treat ment, as two meta-analyses have shown a clinically signi ficant benefit in their use.9,10 The use of heliox has been shown to be favorable in isolated cases of severe croup;11 its properties allow for greater laminar airflow through the tracheobronchial tree and thus decrease airway resis tance through a narrow opening.

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ACUTE BACTERIAL LARYNGITIS Most often caused by inhalation of bacteria transmitted by an infected individual, signs and symptoms of acute bacterial laryngitis are similar to those of viral laryngitis, and include odynophagia, cough, sinusitis and facial pres sure, headache, lymphadenopathy, and laryngeal edema, and erythema. The presence of purulent secretions and ­

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Viral laryngitis is the most common cause of infectious laryngitis in both children and adults and is usually associated with a viral upper respiratory infection. Trans mitted by infected individuals via air droplets during exhalation, sneezing or coughing, patients present with a generalized viral syndrome and dysphonia characterized by hoarseness and lowering of the vocal pitch. Symptoms are self-limited with resolution usually within one week. Viral laryngitis is usually caused by the common cold, or rhinovirus, although many other viruses have been implicated, including influenza A, B and C, parainfluenza viruses, adenovirus, coronavirus, measles and varicella zoster, in addition to more obscure agents. Treatment involves supportive care, including anti-inflammatory medication, humidification, and hydration. Voice rest is imperative, as use while acutely inflamed may lead to vocal injury and ultimately scar. Various antiviral treat ments have no proven impact on the clinical course of acute laryngitis. A 2013 Cochrane Database Review concluded that antibiotics appear to have no benefit in treating uncomplicated acute laryngitis and will not objectively improve symptoms.5 In severe cases presenting with airway distress and potential impending obstruction, ensuring a secure airway is of paramount importance. Medical management involves steroids,6 antibiotics for secondary infections, proton pump inhibitors, humi dification, and nebulizers.

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Acute Viral Laryngitis

Croup

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In a 2012 retrospective analysis of a nationally repre sentative administrative US claims database of almost 55 million individuals examining annual direct costs asso ciated with the diagnosis and management of laryngeal disorders, the total annual direct costs averaged over $200 million, with mean costs per person averaging over $750. Acute laryngitis was by far the most common diagnosis of study participants (43.57%) and invariably represents a sizable portion of such costs and thus a significant economic burden on today’s market.3 A 2013 study utilizing the same database reported acute laryngitis as having the highest odds for prescription medication use compared with all other laryngeal pathology. Due to its self-limited nature where symptoms typically resolve on their own, there is real potential for overmedication. Though the above study did not address the specific issue of medication overuse in cases of acute laryngitis, it continues to have significant impact on public health due to cost.4

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A

B

Figs. 42.1A and B: Acute bacterial laryngitis. (A and B) Diffuse endolaryngeal erythema with bacterial exudates over the right arytenoid, interarytenoid region, left true vocal fold, and postcricoid area are observed. Source: Photo courtesy of Kenneth W. Altman MD, PhD.

exudative, membranous plaques within the endolarynx may be observed,1 as shown in Figures 42.1A and B. In addition to the above treatment of viral laryngitis, oral or IV antibiotics are administered. Diagnosis is confirmed through history, physical examination, and appropriate treatment response.

Supraglottitis Epiglottitis, or more correctly, supraglottitis, is a bacterial cellulitis of the supraglottic structures, most notably of the lingual surface of the epiglottis and the aryepiglottic folds. It represents a true airway emergency: as supraglottic edema increases, the epiglottis becomes more posteriorly displaced thus resulting in airway obstruction. Indeed, its presentation is often quite dramatic with an urgent call from the emergency room describing a drooling, febrile patient in respiratory distress. Although supraglottitis tends to occur in children aged two through seven, cases of patients younger than one year of age have been reported. Additionally, supraglottitis in the adult population is not infrequently seen. Heumophilus influenzae type B is the most commonly implicated organism, even though its incidence has greatly decreased since the initiation of childhood vaccination programs with Hib-conjugated vaccines in the late 1980s.12 Other common pathogens include Streptococcus pneumoniae, Staphylococcus aureus, β-hemolytic Streptococci, and Klebsiella pneumoniae.7 In children, the prodrome is typically very short with rapid progression (hours) that may be life threatening. The child is usually toxic appearing, with a muffled voice and

limited speech, assuming the classic “tripod” position. Stridor is a late finding, signaling near complete airway obstruction. Secondary infectious processes may be present, including meningitis, otitis media, and pneumonia. The epiglottis appears hyperemic and swollen and there is edema and erythema of surrounding pharyngeal mucosa. The aryepiglottic folds and false folds may be involved as well. Physical examination should be done with the utmost caution given the tenuous airway and all anxiety-provok­ ing maneuvers should be avoided. Sudden obstruction may be caused by mucus plugs, plugging of the swollen epiglottis and aryepiglottic fold during inspiration, or laryngospasm. As such, the optimal environment of direct laryngeal visualization is the operating room, where close communication with an anesthesiologist is paramount in ensuring a secure airway. Afterward, any further diag­ nostic and therapeutic interventions may be initiated. The child is observed in the ICU for 24–48 hours before extubation is attempted. Medical management includes broad-spectrum antibiotics against β-lactamase positive H influenzae such as second- or third-generation cepha­ losporins (cefuroxime or ceftriaxone) or ampicillin-sulbac­ tam,8 and systemic corticosteroids, despite the absence of supporting scientific evidence.13 Supraglottitis in adults tends to have a more benign course, with fewer patients presenting with drooling, stridor, and airway compromise and even fewer requiring elective or emergent intubation. Patients tend to present with dysphagia, odynophagia, and fever. Indirect laryngo­ scopy can usually be performed for airway assessment and diagnosis. Less severe cases are managed with serial

Chapter 42: Acute Laryngitis

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Laryngeal diphtheria should be within the differential diagnosis when treating an unimmunized child with travel to, or contact with, visitors from endemic areas, such as Afghanistan and Pakistan. A well-recognized but extremely uncommon manifestation, laryngeal diphtheria presents with hoarseness, dry barking cough, and progressive respiratory distress with characteristic adherent gray pseudomembranes over upper respiratory tract mucosa. Diagnosis is made with laryngoscopy and confirmatory cultures. Toxigenic strains of Corynebacterium diphtheriae produce a potent exotoxin that may damage the heart and central nervous system, causing palatal and pharyngeal paralysis. The airway must be secured and mainstay of treatment is the timely administration of diphtheria antitoxin and antibiotics (penicillin or macrolide).17 Pertussis, or whooping cough, is an acute respiratory infection caused by the gram-negative coccobacillus Bordetella pertussis. Despite routine childhood vaccination programs, pertussis remains endemic in the United States as the number of reported cases have steadily increa sed since the 1980s. Traditionally a childhood infection, pertussis has recently been emerging in vaccinated adults. It colonizes the ciliated upper respiratory epithelia of the host, suppresses ciliary motility, and begins production of cytotoxins. In adults, upper respiratory symptoms are milder than that in children, and they generally present with a prolonged, distressing cough. Children display fever and paroxysmal whooping cough. Due to the chronic cough associated with this condition, significant voice disturbances may occur and otolaryngologists must be aware of this entity as a possible cause of acute laryn gitis. Diagnosis is confirmed with sputum culture.18 In conjunction with supportive treatment, antibiotic treatment with a macrolide is recommended, as it may decrease time of infectivity. It does not, however, alter the course of disease.19



OTHER ACUTE BACTERIAL LARYNGITIS

Pasteurella multocida is a gram-negative coccobacillus that colonizes the upper aerodigestive tract of domestic, farm animals and wild mammals. Though the majority of human infections are soft tissue infections from animal bites or scratches, the upper or lower respiratory tract is the second most common site of infection, via inhalation of contaminated dust or infectious droplets by sneezing animals, which then colonize and invade the underlying mucosa. Pasteurella supraglottitis is a rare, but welldefined entity seen in immunocompetent individuals with a history of recent exposure to animals, especially to cats. Symptoms and laryngoscopic exam findings are identical to classic of bacterial supraglottitis. Penicillin, tetracycline, and trimethoprim-sulfamethoxazole are all effective antibacterial agents.20 Many other pathogenic bacterial species are known to cause well-described laryngeal pathology, but their presentation is not acute and they induce chronic granulo matous inflammatory changes; as such, they are not described in this chapter. Some notable examples include rhinoscleroma, mycobacterial laryngitis (tuberculosis and leprosy), syphilis, and actinomycosis.

Acute Fungal Laryngitis This section discusses laryngeal pathology from Candida species; several other pathogenic fungal species are well described including aspergillosis, histoplasmosis, blastomycosis, coccidioidomycosis, paracoccidioidomycosis and cryptococcosis, and are more appropriately reviewed in the chronic laryngitis chapter. Superficial fungal infection of the mucous membranes (thrush) of the larynx is neither widely reported nor well recognized. It may be seen in both immunocompromised and immunocompetent individuals and is often associated with prior ineffective treatment with antibacterials and even unnecessary surgical interventions due to suspicion for malignancy. Candida albicans is the most common organism associated with laryngeal candidiasis, as other Candida species are less commonly found in the larynx. Most importantly, though it is part of the normal oral and gastrointestinal flora, the ability for Candida species to cause mucosal infection depends on the presence of predisposing factors. These factors are highlighted in the two largest reviews on this clinical entity by Sulica in 2005 and Wong et al. in 2009. The presence of defective host immunity in the form of chronic steroid use, neutropenia, use of antibiotics altering natural upper aerodigestive tract flora, diabetes, prior radiotherapy or other tissue trauma,

fiberoptic examinations, a proven methodology in reducing the number of airway interventions without increasing mortality.14 If airway intervention is required, intubation in a controlled setting (operating room) is appropriate. Management requires admission to the ICU for close monitoring, broad-spectrum IV antibiotics, and steroids.15 Epiglottic abscess is an uncommon complication of supraglottitis, seen more frequently in adults, usually on the lingual surface of the epiglottis. Management includes immediate operative drainage.16

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Figs. 42.2A and B: Acute fungal laryngitis. (A) Erythematous mucosa with whitish yellow exudate over the endolarynx with hypopharyngeal involvement. (B) White fungal plaques over both true vocal folds.

and other forms of immune deficiency, most notably, AIDS are all noteworthy predispositions. Lastly, the use of inhaled steroids is a significant factor in both series as well.21,22 Laryngeal thrush appears to present most commonly in one of two typical patterns: one, as diffuse laryngeal mucosal involvement with associated pain and dysphagia, with laryngoscopy revealing erythematous, edematous mucosa with whitish yellow exudate, plaques or pseudo­ membrane over the entire larynx with extension into the hypopharynx (Figs. 42.2A and B); or two, as focal thick, white lesions isolated to one or both vocal folds with hoarseness as the only presenting symptom. Asthmatics on steroid inhalers typically present with the latter form. Diagnosis is made with history, laryngoscopy, and a prompt response to medical treatment; formal cultures are neither practical nor common. Oral fluconazole appears to be broadly effective in treating laryngeal thrush with rapid disease clearance.21

The Immunocompromised Patient Patients with compromised humoral or cell-mediated immunity are at risk of opportunistic airway infections and may present with symptoms and physical findings consistent with acute laryngitis. These infections may evolve rapidly with a fulminant disease course and elicit a massive localized inflammatory response, proving to be fatal in several hours’ time without intervention. These infections often become invasive and even necrotizing with resultant erosion of laryngeal structures. Patients with acquired immune deficiency syndrome (AIDS),

those immunosuppressed due to transplantation or from chemotherapy, those with aplastic anemia, agranulocytosis, or neutropenia are all at risk. Cytomegalovirus (CMV) is a common opportunistic viral infection in immuno­ compromised patients, specifically transplant recipients and AIDS patients. Though a rare manifestation, CMV may cause a necrotizing, ulcerative laryngitis, and signify the initial manifestation of disseminated disease in such patients.23 Causative bacterial pathogens, in addition to the classic organisms, include Staphylococcus aureus and various gram negatives, such as Pseudomonas aeruginosa,24 Serratia marcescens,25 and Escherichia coli.24 Candida is by far the most common fungal cause, though others have been reported including Aspergillosis and Mucormycosis.27 The management protocol for the immunocompromised patient with acute laryngitis includes early recognition with airway intervention, laryngoscopy, confirmatory cul­ tures and/or biopsy, debridement of infected/necrotic tissues, broad-spectrum antimicrobials, and aggressive supportive management. It is imperative that the otolaryn­ gologist be familiar with such entities so as to facilitate rapid treatment and avoid mortality.

NONINFECTIOUS ACUTE LARYNGITIS Phonotrauma Most commonly a result of excessive collision forces between the vocal folds, mechanical laryngitis is usually caused by very loud and prolonged vocalizations. Under these conditions of traumatic vibratory forces, the surface layers of the vocal folds experience intense friction, thermal

Chapter 42: Acute Laryngitis

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Figs. 42.3A and B: Acute traumatic laryngitis following prolonged coughing and throat clearing. (A) Erythematous true vocal fold mucosa with irregular shape and contour. (B) Glottal incompetence is illustrated during adduction of the acutely injured vocal fold.



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restore their homeostasis and reconstitute functionality, by regulating an array of proinflammatory and antiinflammatory mediators.28 In fact, Li et al. showed that vibratory stress from resonant voice augmented the antiinflammatory effects of certain cytokines. Furthermore, a marked decrease in proinflammatory mediators was shown following resonant voice exercises within 24 hours.29 Internal blunt laryngeal trauma, due to injurious intuba tion attempts, instrumentation during direct laryngoscopy or esophagoscopy and brief endotracheal intubation or use of laryngeal mask airway (LMA) commonly cause acute dysphonia, dysphagia and/or odynophagia.30 This is presumably due to local reactive edema from direct injury to the vocal folds, although anesthetic-related changes in pulmonary function and higher cortical control likely also contribute to postintubation dysphonia.31 Because direct trauma to the vocal folds by the LMA is not common, it is presumed that the cold and dry inspiratory gases that pass over the glottis may substantially contribute to transient voice changes following LMA use. Moreover, the inflated LMA cuff may increase hypopharyngeal sensitivity, as the calculated cuff pressure exerted on the surrounding tissue drastically exceed pharyngeal mucosal perfusion pressure. This likely contributes to reported discomfort with swallowing after LMA use.32 Symptoms related to postintubation mucosal injury typically resolve within 12–72 hours. ­



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irritation and molecular breakdown. Macroscopically, this may result in vocal fold mucosal hyperemia from dilated surface vessels, submucosal hemorrhage and edema. Other common causes of mechanical laryngitis include persistent coughing, habitual throat clearing behaviors, screaming, abrupt and strained voice usage and untrained, forceful singing. These activities induce diffuse inflamma tion and erythema of both true and false vocal fold mucosa. Symptoms include a hoarse or breathy, harsh, strained, low-pitched voice, varying in severity from mild to quite profound. These voice changes are a result of a combina tion of glottal insufficiency (due to changes in vocal fold shape) and alterations in mucosal pliability (which affects vibratory properties). Figures 43.3A and B show laryngo scopy of a patient with acute laryngitis due to phonotrauma. Examination should include a detailed history, fiberoptic laryngoscopy and video stroboscopy. This form of laryn gitis is self-limited and subsides with strict voice rest and humidification. In situations of continued, repetitive phonotrauma, traumatic tissue breakdown may lead to polyposis, nodules, hemorrhagic polyps, hyperkeratosis and scar formation. It is imperative that the patient be educated on vocal hygiene strategies and support exercises to avoid chronic laryngeal insult and permanent damage.1 A novel debate that has recently emerged is whether voice rest or tissue mobilization, in the form of resonant voice exercise, is a better intervention in patients with acute vocal fold injury. Though traditional wisdom suggests voice rest as the logical, ideal approach, recent data suggests that anabolic, biomechanical signals generated from resonant voice exercises might optimally assist stressed tissues to

Thermal Laryngitis Supraglottitis due to thermal damage to the larynx may occur after swallowing or aspirating scalding hot liquids or

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foods, from inhalation of hot steam, or from involvement in a fire. This type of injury is more common in children.33 An association between smoking crack cocaine and thermal supraglottitis is also well-recognized and occurs as a direct result from inhalation of crack cocaine vapors or heated particles from the smoking apparatus.34 Treatment involves laryngoscopy (to rule out presence of heated inhaled foreign bodies in addition to assessing the airway), humidification, corticosteroids, and airway observation or intubation, if necessary.

Allergic Laryngitis Though consistent anecdotal evidence in the medical literature has indicated a link between allergies and vocal dysfunction for at least 40 years, a clear causal relationship between antigen exposure and symptoms of laryngitis in the allergic, atopic patient is only recently beginning to be highlighted.35 Two primary forms of allergy-related laryngeal inflammation have been proposed: acute IgE mediated and chronic, recurrent non-IgE mediated.36 The former subtype occurs during anaphylaxis after exposure to certain foods, medications, insect bites and venoms. Symptoms evolve rapidly and may be severe due to edema of supraglottic, oropharyngeal, oral and/or facial struc­ tures with resultant airway compromise, stridor, globus, dysphonia and dysphagia. Recurring, cyclic laryngitis in the allergic, atopic patient has a gradual onset with mild symptoms. Patients may complain of increased mucus with associated throat clearing and coughing, odynophagia and strained, hoarse voice. Evaluation includes a detailed history paying close attention to any association of symptoms with antigen exposure. Laryngoscopy reveals mild to moderately thick endolaryngeal secretions and edema with polypoid mucosa. Examination may show the presence of boggy watery nasal mucosa, nasal polyposis or supratip crease, and the patient may endorse a history of allergic rhinitis or asthma, further suggesting an atopic etiology. The most common triggering agents are insecticides, phenol, petroleum-based compounds, formaldehyde, and various environmental allergens including certain plants and flowers.37 Treatment involves avoidance or removal of offending agents, use of nondehydrating antihistamine medi­cations, mucolytics, steroids, and immunotherapy. Hyd­ ration, avoidance of diuretics, and voice therapy targeting cessation of vocal abuse patterns are additional adjunctive treatments. The patient may be sent for skin testing or radioallergosorbent testing. Importantly, more

common causes of laryngitis such as laryngopharyngeal reflux (LPR) should be effectively ruled out prior to diagnosing primary allergic laryngitis. This may be difficult, as there is significant similarity in clinical signs and symptoms of vocal allergy and LPR; according to Roth et al., the four most commonly reported signs and symptoms are shared between the two entities: diffuse laryngeal edema, vocal fold edema, excessive mucus, and thick viscous mucus. Unlike allergic laryngitis, LPR causes posterior laryngeal edema and favors formation of granulomas.35

Smoke, Fumes, and Occupational Exposures Exposure to tobacco smoke or the smoke generated by noxious fumes of pollutants, engine exhaust pipes, certain chemicals, and occupational substances including freon gas, sulphuric acid, formaldehyde, herbicides and organic solvents may cause laryngeal mucosal contact inflam­ mation and irritative laryngitis.38 Although laryngeal symp­ toms typically develop gradually after sustained, long-standing exposures, in a minority of cases dysphonia may acutely develop with associated dryness of the laryngeal mucosa. Secondary cough reflexes may occur accompanied by complaints of globus or foreign body sensation. Due to inherent hygroscopic properties, inhaled pollutants desiccate the laryngeal mucosa. The resultant lack of mucosal viscosity contributes to high degrees of friction and heat generation on vocal fold vibration, heralding tissue breakdown and dysphonia.1 Treatment involves avoidance of the offending agents while increas­ ing systemic hydration and laryngeal humidification.

Angioedema Angioedema is a rare and potentially life-threatening con­ dition characterized by acute attacks of intense swelling of the skin and/or mucous membranes, usually involving the upper airway, face, abdomen, or extremities. The swelling is usually painless and nonpitting, with ill-defi­ ned margins, and results from an extravasation of fluid into interstitial tissues in response to a number of vasoactive mediators. Any number of mucosal subsites in the upper airway, from the lips to the larynx, may be involved; involvement is random, may be noncontiguous, and can cause airway compromise. Several studies have shown that specific sites of upper airway involvement correlate with increased likelihood of intubation or tracheotomy,

Chapter 42: Acute Laryngitis

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corticosteroids. Such treatments are typically ineffective for acute attacks of nonallergic, bradykinin-mediated angioedema. If airway obstruction develops, intubation or tracheotomy may be required.

REFERENCES









































1. Dworkin JP. Laryngitis: types, causes, and treatments. Otolaryngol Clin North Am. 2008;41:419-36. 2. Ng ML, Gilbert HR, Lerman JW. Some aerodynamic and acoustic characteristics of acute laryngitis. J Voice. 1997; 11(3):356-63. 3. Cohen SM, Kim J, Roy N, et al. Direct health care costs of laryngeal diseases and disorders. Laryngoscope. 2012;122(7):1582-8. 4. Cohen SM, Kim J, Roy N, et al. Assessing factors related to the pharmacologic management of laryngeal diseases and disorders. Laryngoscope. 2013;123(7):1763-9. 5. Reveiz L, Cardona AF. Antibiotics for acute laryngitis in adults. Cochrane Database Syst Rev. 2013;28:3. 6. Super DM, Cartelli NA, Brooks LJ, et al. A prospective randomized double-blind study to evaluate the effect of dexamethasone in acute laryngotracheitis. J Pediatr. 1989; 115:323-9. 7. Stroud RH, Friedman NR. An update on inflammatory disorders of the pediatric airway: epiglottitis, croup, and tracheitis. Am J Otolaryngol. 2001;22(4):268-75. 8. Tulunay OE. Laryngitis—diagnosis and management. Otolaryngol Clin North Am. 2008;41:437-51. 9. Kairys SW, Olmstead EM, O’Connor GT. Steroid treatment of laryngotracheitis: a meta-analysis of the evidence from randomized trials. Pediatrics. 1989;83(5):683-93. 10. Ausejo M, Saenz A, Pham B, et al. The effectiveness of glucocorticoids in treating croup: meta-analysis. BMJ. 1999;319(7210):595-600. 11. Beckmann KR, Brueggemann WM Jr. Heliox treatment of severe croup. Am J Emerg Med. 2000;18(6):735-6. 12. Wenger JD. Epidemiology of Hemophilus influenzae type b disease and impact of Hemophilus influenzae type b conjugate vaccines in the United States and Canada. Pediatr Infect Dis J. 1998;17(9 Suppl):S132-6. 13. Mayo-Smith MF, Spinale JW, Donskey CJ, et al. Acute epiglottitis: an 18-year experience in Rhode Island. Chest. 1995;108:1640-7. 14. Nakamura H, Tanaka H, Matsuda A, et al. Acute epiglottitis: a review of 80 patients. J Laryngol Otol. 2001;115(1):31-4. 15. Shah RK, Roberson DW, Jones DT. Epiglottitis in the Hemophilus influenzae type B vaccine era: changing trends. Laryngoscope. 2004;114:557-60. 16. Berger G, Landau T, Berger S, et al. The rising incidence of adult acute epiglottitis and epiglottic abscess. Am J Otol. 2003;24:374-83. 17. Ganeshalingham A, Murdoch I, Davies B, Menson E. Fatal laryngeal diphtheria in a UK child. Arch Dis Child. 2012;97:748-9. 18. Tornabene SV, Crose J, Cruz RM. Pertussis presenting as hoarseness in an adult. Ear Nose Throat J. 2012:91(2):E22-4.



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as does involvement of multiple sites.39 The exact mech anisms differ among its causes, which may include defects in C1 esterase inhibitor (hereditary and acquired angioedema), accumulation of bradykinin (angiotensinconverting enzyme inhibitor- and angiotensin receptor blocker-induced angioedema) or mast cell degranulation.40 Hereditary angioedema is an autosomally dominant disease characterized by either low levels of C1 esterase inhibitor (type I), reduced C1 esterase inhibitor function (type II) or mutations in factor XII (type III). Acquired angioedema may be caused by anti-C1 esterase inhibitor antibodies and tends to be associated with hematologic malignancy or autoimmune disease. In each of the above, however, angioedema results from the generation of increased levels of bradykinin, a potent vasoactive peptide that causes increased vascular permeability, vasodilation, and constriction of nonvascular smooth muscle. Roughly 50% of patients with hereditary angioedema have at least one episode of laryngeal swelling during their lifetime; if left untreated or undiagnosed, airway obstruction is associated with mortality rates as high as 30%. Common documented triggering factors attacks include trauma, stress, infection, menstruation, oral contraceptives, hormone replacement therapy, angiotensin-converting enzyme inhibitors, and angiotensin receptor blockers. However, it is important to note that many attacks do not have an identifiable trigger.41 A number of treatments are available for hereditary angioedema. For long-term prophylaxis of frequent attacks, oral therapies such as attenuated androgens or antifibrinolytics may be used. Regular IV infusions of C1 esterase inhibitor are an additional therapeutic option for prophylaxis. Treatment options for acute attacks include plasma-derived C1 inhibitors, recombinant C1 inhibitor, kallikrein inhibitor and bradykinin B2 receptor antago nist. In acquired angioedema, treatment of the underlying condition may result in improvement.42 Allergic angioedema is mediated by preformed IgE and histamine release from degranulating mast cells. In such cases, pruritus, overlying erythema, and urticaria may be present. In severe instances, the angioedema can be one of multiple components of anaphylaxis, such as hemodynamic instability and bronchoconstriction. Com mon causes include venom hypersensitivity, latex and various foods, and medications. In many instances, however, the offending agent is not known. Treatment is aggressive and includes supplemental oxygen, epine phrine, H1- and H2-histamine receptor antagonists, and

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19. Bass JW. Erythromycin for treatment and prevention of pertussis. Pediatr Infect Dis. 1986;5(1):154-7. 20. Wine N, Lim Y, Fierer J. Pasteurella multocida epiglottitis. Arch Otolaryngol Head Neck Surg. 1997;123:759-61. 21. Sulica L. Laryngeal thrush. Ann Otol Rhinol Laryngol. 2005;114(5):369-75. 22. Wong KH, Pace-Asciak P, Wu B, Morrison MD. Laryngeal candidiasis in the outpatient setting. J Otolaryngol Head Neck Surg. 2009;38(6):624-7. 23. López-Amado M, Yebra-Pimentel MT, García-Sarandeses A. Cytomegalovirus causing necrotizing laryngitis in a renal and cardiac transplant recipient. Head Neck. 1996;18 (5):455-8. 24. Connolly AA, Rowe-Jones J, Leighton SE,et al. Pseudomonal supraglottitis occurring in a patient with profound neu­ tropenia in an immunocompromised host. J Laryngol Otol. 1992;106(8):739-40. 25. Bower CM, Suen JY. Adult acute epiglottitis caused by Serratia marcescens. Otolaryngol Head Neck Surg. 1996; 115(1):156-9. 26. Goldsmith AJ, Schaeffer BT. Necrotizing epiglottitis in a patient with procainamide-induced neutropenia. Am J Otolaryngol. 1994;15(1):58-62. 27. Eckmann DM, Seligman I, Coté CJ, Hussong JW. Mucor­ mycosis supraglottitis on induction of anesthesia in an immu­ nocompromised host. Anesth Analg. 1998; 86(4):729-30. 28. Abbott KV, Li NY, Branski RC, et al. Vocal exercise may attenuate acute vocal fold inflammation. J Voice. 2012;26 (6):814.e1-13. 29. Li NYK, Vodovitz Y, Kim KH, et al. Biosimulation of acute phonotrauma: an extended model. Laryngoscope. 2011;121(11):2418-28. 30. Mendels EJ, Brunings JW, Hamaekers AEW, et al. Adverse laryngeal effects following short-term general anesthesia: a systematic review. Arch Otolaryngol Head Neck Surg. 2012;138(3):257-64.

31. Beckford N, Mayo R, Wilkinson A, et al. Effects of shortterm endotracheal intubation on vocal function. Laryngo­ scope. 1990;100(4):331-6. 32. Rieger A, Brunne B, Hass I, et al. Laryngo-pharyngeal complaints following laryngeal mask airway and endotracheal intubation. J Clin Anesth. 1997;9(1):42-7. 33. Deutsch ES. Traumatic supraglottitis. Int J Ped Otorhi­ nolaryngol. 2004;68(5):851-4. 34. Osborne R, Avitia S, Zandifar H, et al. Adult supraglottitis subsequent to smoking crack cocaine. Ear Nose Throat J. 2003;82(1):53-5. 35. Roth D, Ferguson BJ. Vocal allergy: recent advances in understanding the role of allergy in dysphonia. Curr Opin Otolaryngol Head Neck Surg. 2010; 18(3); 176-81. 36. Chadwick SJ. Allergy and the contemporary laryngologist Otolaryngol Clin North Am. 2003;36:957-88. 37. Perkner JJ, Fennelly KP, Balkissoon R, et al. Irritantassociated vocal cord dysfunction. J Occup Environ Med. 1998;40(2):136-43. 38. Williams NR. Occupational voice disorders due to work­ place exposure to irritants—a review of the literature. Occup Med. 2002; 52(2):99-101. 39. McCormick M, Folbe AJ, Lin HO, et al. Site involvement as a predictor of airway intervention in angioedema. Laryngoscope. 2011;121(2):262-6. 40. Tai S, Mascaro M, Goldstein NA. Angioedema: a review of 367 episodes presenting to three tertiary care hospitals. Ann Otol Rhinol Laryngol. 2010;119(12):836-41. 41. Banerji A. Hereditary angioedema: classification, patho­ genesis and diagnosis. Allergy Asthma Proc. 2011;32(6): 403-7. 42. Jolles S, Williams P, Carne E, et al. A UK national audit of hereditary and acquired angioedema. Clin Exp Immunol. 2014;175(1):59-67.

CHAPTER

43

Chronic Laryngitis Jason Chesney, Adam D Rubin

DIRECT IRRITATION Vocal Trauma

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Vocal trauma is one of the most common etiologies of vocal fold inflammation. Microscopically, several mecha­ nisms of laryngeal inflammation from trauma have been elucidated. Inflammatory mediators, such as interleukin 1 beta, transforming growth factor beta 1, and cyclooxy­ genase 2 2 have been shown to be involved.2 These media­ tors are the focus of further research regarding vocal fold healing after microflap surgery.3,4 When chronic or repetitive vocal abuse or misuse occurs this may prevent healing of acute trauma and result in persistent inflam­ mation to the vocal folds. Of course, other structural injuries may also occur, such as polyps or nodules. Expo­ sure to gastric contents may impair healing after an acute vocal fold injury resulting in persistent inflammation and symptoms.5 8 A complete discussion of vocal trauma is -



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Chronic “laryngitis” insinuates chronic inflammation of the vocal folds and can present diagnostic and therapeutic challenges for the otolaryngologist. Although inflamma­ tory changes to the larynx will almost always result in dysphonia, patients may also complain of throat pain, globus pharyngeus, and/or cough. Severe inflammation may also result in airway obstruction. These symptoms are not specific to “laryngitis” or to any one etiology of inflammation. Persistent hoarseness should never be dee­ med due to “laryngitis” until the vocal folds have been appropriately visualized. Although the duration of hoar­ seness qualifying symptoms as “chronic” is controversial, most would agree that symptoms persisting over two weeks warrant laryngeal imaging. It is up to the otolaryngolo­ gist to identify the cause of the symptoms and to rule out more ominous etiologies, such as laryngeal carcinoma. If laryngeal examination suggests inflammation as the primary cause, the otolaryngologist must identify the source of inflammation to direct appropriate treatment. Inflammation of the vocal folds will result in edema and erythema of the true vocal folds. Inflammation may impede mucosal wave propagation and result in dyspho­ nia. Increased stiffness of the vocal fold mucosa may increase the effort of voice production and increase the risk of additional injury. Increase in mass of the vocal folds will result in lowering of pitch. At a cellular level, macrophages, lymphocytes, fibroblasts, and collagen are seen during chronic inflammation. If there is an “acute on chronic” presentation, neutrophils and acute inflammatory mediators may also be present. Chronic inflammation

may ultimately lead to fibrosis, which can cause perma­ nent alteration of the vocal fold architecture and change in vocal quality.1 There are many potential etiologies of chronic laryn­ gitis, and the problem may be multifactorial. In this chapter, we divide the differential into four categories: direct irritation, infectious, autoimmune, and idiopathic. Vocal trauma and reflux are likely the two most common etiologies in patients presenting with chronic dysphonia caused by vocal fold inflammation. However, less common etiologies should be considered. This chapter provides an overview of potential etiologies of chronic laryngitis.

INTRODUCTION

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Section 4: Voice Disorders

beyond the scope of this chapter; however, one should recognize the likelihood of vocal trauma contributing to chronic laryngitis. This can often be addressed with voice therapy. Oral steroids may be helpful to expedite voice recovery, particularly when there is acute on chronic inflammation. A good history will often help determine if vocal trauma is the etiology of the inflammation, as well as if the inflammation is acute or chronic.

Laryngopharyngeal Reflux Laryngopharyngeal reflux (LPR) refers to the retrograde flow of gastric and duodenal contents into the upper aerodigestive tract resulting in symptoms, which may involve the throat, sinuses, middle ear, and lungs.9-14 It is felt to be one of the most common causes of chro­nic laryngitis. Aviv reports that 50% patients presenting with common throat complaints suffer from LPR.15 Koufman suggests up to 10% of patients that present to the otolaryn­ gologist have LPR.16 Reflux is thought to be predominantly due to transient relaxations of the lower esophageal sphincter (LES). Other mechanisms, such as lower LES resting pressure and increases in intra-abdominal pressure, have been repor­ ted as well17 Symptoms of classic gastroesophageal reflux disease (GERD), such as heartburn, reflect the effect of the refluxate on the distal esophagus, whereas extraeso­ phageal symptoms reflect the effect on the proximal aero­ digestive tract. Hanson and Jiang described the earliest symptoms of LPR to be the sensation of postnasal drip.18 A report from the American Bronchoesophagological Association des­ cribes the most common symptoms to be throat clearing (98%) followed closely by persistent cough (97%), globus (95%), and hoarseness (95%).19 The Reflux Symptom Index (RSI) was devised as a potential outcome measure of the severity of reflux symptoms. A score from 0–1 is assigned to the following symptoms by the patient: difficulty swallowing, hoarseness or voice problem, throat clearing, excess throat mucous or post­nasal drip, troublesome cough, breathing difficulties or choking, sensation of a lump in the throat, coughing after lying down or after eating, and heartburn/chest pain/ indigestion/acid coming up. A total score of > 13 is consi­ dered abnormal.20,21 A number of findings on laryngeal examination have been described as suggestive of LPR. Such findings include vocal fold erythema and edema, pachydermia of the poste­ rior glottis and interarytenoid area, leukoplakia,

Fig. 43.1: Laryngopharyngeal reflux. A number of findings consi­ dered positive for LPR are seen: posterior commissure hyper­ trophy, endolaryngeal mucus (in anterior commissure, appears like a web), vocal cord edema, and arytenoid hyperemia. This larynx would have a reflux finding score of approximately 9. Scoring is somewhat subjective, however.

ventricular obliteration, and pseudosulcus (edema of the subglottis).22-24 These findings are not specific, but in the absence of other potential inflammatory causes (e.g. smo­ king, inhalers) are highly suggestive of reflux. Pseudo­ sulcus has been suggested to have as high as a 90% positive predictive value.24 Belafsky et al. found pseudo­ sulcus in 70% of patients with pH probe—confirmed LPR and only 30% of controls.25 The Reflux Finding Score (RFS) was described as an outcome measure evalua­ting laryn­ geal findings of LPR. Eight findings on laryngeal examina­tion, including erythema, subglottic edema (pseu­ dosul­ cus), ventricular obliteration, posterior commis­ sure hyper­trophy, granuloma, thick endolaryngeal mucus, diffuse laryn­geal edema, and vocal fold edema are given a score on a severity scale of 0 to 4 (Fig. 43.1). A total score > 7 is supposed to be indicative of LPR with a 95% confi­ dence interval.20,26 In general, laryngeal findings do not resolve with treatment as rapidly as symptoms.23 A great deal of controversy still exists around the subject of LPR. The RSI and RFS are controversial and not universally applied. Much of this controversy stems from the fact that the symptoms described are not specific for reflux. For example, although globus pharyngeus is often caused by LPR, other potential etiologies exist, such as neuralgia, other inflammatory causes, upper esophageal sphincter spasm, and anxiety.27 Furthermore, signs felt to be specific for reflux have been found in healthy subjects. Although it has high sensitivity, the specificity for the RFS is reported as low 37.8%.28

Chapter 43: Chronic Laryngitis

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been shown to be beneficial for GERD in patients who are postgastrectomy; however, it has since been linked to severe cardiac adverse events.43 Baclofen, a GABA B agonist, has been shown to decrease transient LES relaxa­ tions and has potential for decreasing the number of reflux events.44 It has been demonstrated to be useful in treating the symptoms of GERD both on its own and with concurrent PPI management.45,46 Cossentino et al. perfor­ med a randomized, placebo controlled study and demon­ strated a significant decrease in pH probe documented reflux as well as overall symptom score in the upright posi­ tion with the use of baclofen.47 Recently, there has been investigation into alginate formulations for the treatment of GERD. Alginate formula­ tions precipitate in the presence of gastric acid forming a gel. The formulations also contain a bicarbonate com­ pound, which is converted to carbon dioxide and becomes trapped within the gel. The resulting foam floats on top of gastric contents and is thought to preferentially reflux into the esophagus as opposed to the gastric contents.48 These formulations have shown benefit in reducing GERD symptoms both over placebo49 and roughly equivalent to omeprazole.50 However, these products have not been formally investigated in the treatment of LPR. A number of surgical approaches are used to treat reflux. The objective of the majority of the procedures is to improve the efficacy of the LES to keep stomach contacts from refluxing into the esophagus. Although other proce­ dures have been described,51,52 Nissen fundoplication is still the most commonly performed. It is most effective in patients who respond to PPI management and has been shown in some studies to be effective for extraesophageal symptoms.53,54 One could postulate that if nonacidic reflux is the etiology of symptoms, or if pepsin is the major offending agent, then a Nissen would likely be the ideal treatment in patients who do not respond to medical therapy.55 Studies have demonstrated conflicting results.56 One should be cautious in the recommendation of sur­ gical intervention for the patient who does not respond to high dose PPI management, particularly if there is no concrete pH probe and impedance data to suggest reflux. All other potential etiologies should be ruled out. Despite the controversy involving LPR, extraesopha­ geal reflux symptoms have been shown to be prevalent in patients with Barrett’s esophagus and adenocarcinoma of the esophagus.57 Therefore, it is important to identify patients with reflux to avoid potential late sequelae. The use of transnasal esophagoscopy has made screening for Barrett’s esophagus safer and less expensive. This can be a useful adjunct in long term management of LPR.58

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Studies such as pH probe and impedance testing are used to investigate for the presence and severity of reflux. The importance of the proximal probe evaluation has been well established for diagnosing LPR.29,30 Impedance testing is useful to identify nonacidic reflux episodes. Unfortunately, the use of these studies is also contro­ versial31,32 as specific criteria for a positive study is yet to be agreed upon. Often, an empiric trial of reflux medications is the best way to confirm the diagnosis of LPR.33 Failure to respond to a three month trial of high dose proton pump inhibitor (PPI) management should lead the physician to consider other potential etiologies of inflammation and symptoms, as well as considering objective testing for reflux. Treatment for reflux includes dietary and behavioral modifications, medications (most commonly PPIs for LPR), and surgical intervention. Studies have demonstrated conflicting results in terms of the efficacy of PPI use. Many studies have failed to show a difference in improvement of symptoms or signs with the use of PPIs versus placebo,34,35 whereas others have shown improvement in certain symp­ toms.36,37 Steward et al. demonstrated an overall significant improvement in symptoms of LPR with behavioral modi­ fications such as avoidance of eating within two hours of lying down and head of bed elevation (p < 0.01) but found no significant difference for improvement in the use of PPI over placebo.34 Unfortunately, many of the studies published have fundamental design flaws. There are histological studies that have shown the potential detrimental effects of gastrointestinal contents on laryngeal mucosa.38,39 Laryngeal mucosa lacks inherent defense mechanisms present in esophageal mucosa such as E cadherin molecules, and sufficient levels of carbonic anhydrase.40,41 Further complicating the issue is the role of pepsin and its relation to the above mechanisms in LPR.41,42 Pepsin is the most significant proteolytic enzyme produced by the gastric mucosa. It has traditionally been thought of to be active only at pH < 4; however, there is evidence that this is not the case.42 Johnston et al. have demonstrated that pepsin remains stable (yet not active) at pH < 8. The pH of the laryngopharynx within a normal subject is approximately 6.8. Pepsin can be taken in via endocytosis by the laryngeal epithelium and be reactiva­ ted by later reflux events. In addition, it can be transpor­ ted to more acidic regions of the cell and cause significant damage.41,42 Theories on treatment of nonacidic reflux have focu­ sed mainly on the lifestyle modifications and potential surgical intervention. Prokinetics such as cisapride have

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B

Figs. 43.2A and B: Postnasal drainage. Many patients may complain of the sensation of postnasal drainage. However, if truly present it can be visualized on examination. (A) Presence of postnasal drainage within larynx. (B) Postnasal drainage visualized in nasal cavity.

Allergy Inhalation allergy is likely a potential etiology of chronic laryngeal irritation that may go unrecognized and be difficult to concern from reflux. It is currently believed that the late phase reaction of the allergic response, mostly in those with perennial allergies, is the prominent mecha­ nism affecting laryngeal mucosa.59 In addition to direct effects on the vocal folds, changes in resonance and vocal effort can occur due to nasal congestion. Allergy-related cough may result in inflammation from vocal fold trauma.60 Postnasal drainage may contribute to cough and direct irritation of the vocal folds. It is important to distinguish true postnasal drainage, however, from the sensation of postnasal drainage that one may have due to generalized irritation from other etiologies, such as LPR (Figs. 43.2A and B). Allergy testing should be considered in patients whose history suggests systemic allergies or with a seasonal com­ po­ nent to their hoarseness. If significant allergies are demonstrated, immunotherapy should be considered as antihistamines may have a drying effect on the vocal folds that may affect voice quality. In the absence of significant systemic symptoms and without positive allergy testing, it is difficult to attribute inflammation of the vocal folds to allergy. If treatment for reflux fails and there is no other clear-cut etiology such as vocal trauma or smoking, an empiric trial of allergy medication may prove useful.

Inhalants A number of inhalants can cause inflammation to the vocal folds. Smoking is likely the most common culprit.

Repeated exposure to external fumes can also irritate the vocal fold mucosa. Inhalers, particularly steroid inhalers and combination steroid/bronchodilators can be irritating to the laryngeal mucosa. Findings may include edema, hyperemia, and candidiasis.61,62 These changes may not resolve without discontinuation of the medication.62 Treat­ ment with fluconazole is warranted in patients with sus­ pected laryngeal candidiasis. Reinke’s polyposis or “smokers’ polyps”, is a result of chronic cigarette smoking. In 1982, Kleinsasser described telengiectatic and gelatinous polypoid changes of the true vocal folds at the site of maximum contact force during phonation. Histologically, increased permeability to blood vessels leads to extravasation of fibrin, edema fluid, and erythrocytes in a fashion similar to thrombus forma­ tion.63 More recently, Branski et al. have described both an increase in the expression of certain oxygenases (namely heme oxygenase-1) as well as the proliferation of inflam­ matory mediators (such as COX-2) from fibroblasts expo­sed to chronic cigarette smoke.64,65 They describe the former mechanism as a possible protective factor in targe­ting reactive oxygen species and a putative explanation for the extremely small portion of these patients that deve­lop car­ cinoma. Some have suggested that chronic vocal overuse predisposes female smokers to polyposis.66 Treatment includes smoking cessation and surgical intervention. Surgi­cal options include microlaryngeal surgery or awakepulsed potassium-titanyl-phosphate laser treatments for reduction of polyp size.67 Voice therapy may be useful in some cases.

Chapter 43: Chronic Laryngitis

A

557

B

Figs. 43.3A and B: Candidal laryngitis. (A) Candidal laryngitis can be subtle. Notice the subtle hyperemia and small plaques of white. (B) In this case, the plaques of white are plentiful and seen on the supraglottic structures.

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this disease quite common in the immunocompetent patient.95,96 Most commonly presenting with dysphonia, up to 89% of these patients are currently using inhaled steroids and the vast majority are cured with a course of oral fluconazole.97 White plaques are observed with surro­ unding inflammation in most cases; however, at times the inflammatory pattern is nonspecific (Figs. 43.3A and B). Increased magnification with rigid videostroboscopy can help identify a subtle lacy white appearance to inflamed vocal folds. Of note, laryngeal candidiasis has been conf­ used with laryngeal carcinoma.98,99 and may lead to unnecessary surgical procedures if not considered. Res­ ponse to fluconazole confirms the diagnosis. Close follow up is warranted to ensure complete eradication of the infection.

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Although many infectious causes of laryngitis lead to acute presentation of disease and are discussed elsewhere in this volume, a few entities warrant discussion here. Although a complete discussion of the pathogens that affect the larynx is beyond the scope of this chapter, a few are dis­ cussed below.

Candida albicans is ubiquitous in the environment. Once thought to be a disease mainly of the immunocompro­ mised host, the broad use of inhalational steroids has made

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Candida Albicans

Bacterial laryngitis should be expected when crusts are visualized on the vocal folds (Fig. 43.4). It is often preceded by a bacterial upper respiratory infection. Although viral laryngitis is the most common cause of acute infectious laryngitis, it is typically self limited and will resolve. Bacterial laryngitis will not resolve without appropriate antibiotic management. Often, this will require a longer treatment duration than other bacterial upper respiratory infections, which is why patients often present with a history of improving on antibiotics but recurring after treatment. Typical patho­ gens include Staphylococcus aureus, Hemophilus influenzae, Streptococcus pneumonia, beta-hemolytic -

INFECTIOUS LARYNGITIS

Bacterial Laryngitis

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Fig. 43.4: Bacterial laryngitis. The presence of crusts on the vocal folds is highly suggestive of bacterial laryngitis.

558

Section 4: Voice Disorders

streptococci, and Klebsiella pneumonia. In addition to antibiotics, hydration and voice rest are important. Corticosteroids may be useful to reduce inflammation. Response to antibiotics confirms the dia­gnosis, but if antibiotics are not effective, culture of the crusts may be warranted. Close follow-up is necessary to make sure the infection completely clears to avoid develo­ ping antibiotic resistance. Methicillin-resistant Staphylo­ coccus aureus laryngitis has been reported.100 If bacterial laryn­gitis is left untreated, sequelae such as scarring may occur. Airway obstruc­tion is also possible, particu­ larly if there is a concurrent tracheitis. Close follow-up is warranted to ensure eradication of the infection.

Blastomyces Dermatitidis Blastomycosis, caused by the saprophytic fungus Blasto­ myces dermatitidis, is an uncommon disease of the larynx and is endemic to the Ohio and Mississippi river valleys. The true vocal folds are the most common site affected, with hoarseness as the most common complaint.83 Fungal stains show the classic “broad-based buds”. Histologically, pseudoepitheliomatous hyperplasia is noted, which can lead to the misdiagnosis of squamous cell carcinoma.101 Misdiagnosis and even unnecessary radiation and laryn­ gectomy have been reported.102 Therefore, conside­ration of the disease is prudent.

Mycobacterium Tuberculosis Laryngeal tuberculosis causes granulomatous inflam­ ma­tory lesions, often in multiple sites. The disease most com­monly affects the true vocal folds with hoarseness being the most common symptom.103,104 Laryngoscopic findings vary and may include ulcerations, as well as white mucosal and granulomatous lesions.104 The vast majority of patients with laryngeal involvement also have pulmo­ nary disease.103,104 Tuberculosis also may be misdiagnosed as laryngeal carcinoma. Cervical lymphadenopathy and decreased vocal fold mobility can make for a confusing presentation.104 Medical therapy should be initiated imme­ diately with involvement of infectious disease specia­ lists. Vocal fold immobility, when present, has also been shown to improve with current therapies.104

AUTOIMMUNE LARYNGITIS Autoimmune inflammatory disorders can present with laryngeal manifestations. A brief discussion of the more common disorders is found below.

Wegener’s Granulomatosis Wegener’s granulomatosis is characterized by necrotiz­ ing granulomas of the upper and lower respiratory tract, small vessel vasculitis, and glomerulonephritis. An anti­ neu­trophil cytoplasmic antibody-positive vasculitis, it is thought to be due to T-cell-mediated hypersensitivity to what are as of now unknown antigens.68 Trimarchi et al. note laryngeal and tracheal ulcers being present in up to 25% of patients and more often than the classically associated subglottic stenosis (16%).69 When present, subglottic stenosis almost always presents 1.5–2.0 cm below the true vocal cords. The reason for this is not well understood; however, it is believed to be due to this area being a division between two embryologic growth centers, resulting in a junction of two separate microcirculations. Stenosis is often memb­ ranous and may also occur where other microcircula­ tions meet, such as between the trachea and main stem bronchi.70 Lebovics et al. found otolaryngological mani­fes­ tations of Wegener’s granulomatosis in 145/158 patients, with 16% having subglottic stenosis. Local manage­ment may include steroid injections, dilations, tracheostomy, and laryngotracheal reconstruction.71 Topical appli­ca­tion of mitomycin-C may be useful.72-74 Systemic immuno­ suppressive therapy may be warranted (Fig. 43.5).

Sarcoidosis In 1940, Poe described one of the first cases of laryngeal sarcoidosis in the literature.75 A granulomatous autoim­ mune disorder, sarcoidosis is known to primarily affect the pulmonary system (90%). Otolaryngologic involvement is seen in approximately 10–15% of cases.76 Schwartzbauer and Tami report laryngeal involvement from 0.5–8.3% of cases.77 The supraglottis is involved most frequently. Pallor and edema of the supraglottic structures, often with a nodular appearance, is typically seen (Fig. 43.6). The true vocal folds and subglottis may be involved. Hoarseness may be caused by compression of the superior surface of the vocal folds from supraglottic sarcoid, change in resonance due to change in the shape of the supraglottis, or from direct inflammation to the vocal folds. Airway obstruction is of paramount concern.78 Tissue biopsy is required for diagnosis. Classic noncaseating granulomas are seen. While frequently used to follow the clinical course of the disease, serum angiotensin-converting enzyme levels are not useful in the initial diagnosis of sarcoidosis as it is elevated in as little as 40% of those with active disease.79

Chapter 43: Chronic Laryngitis

559

Fig. 43.6: Sarcoidosis. The large outpouchings of tissue are from the ventricles. Notice the nodularity. The left vocal fold is visuali­ zed and inflamed. It is also involved.

Prednisone remains the most common drug used today for sarcoidosis. It is important to rule out tuberculosis prior to treatment, as steroid will suppress the immune response. Refractory cases are further treated with cyto­ toxic agents, most commonly methotrexate. In light of the well documented complications associated with prolon­ ged corticosteroid use many alternative options have been proposed, such as azathioprine, mycophenolate, thalidomide, minocycline, and the monoclonal antibody infliximab.80 Surgical excision of supraglottic lesions is often required. Local steroid injections may be useful.81

Systemic Lupus Erythematosus

Rheumatoid Arthritis

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Rheumatoid arthritis (RA) affects approximately 1% of the population and is the most common autoimmune arth­ ritis. Laryngeal involvement has been reported in 25–30% of cases.82,83 Symptoms may include dysphonia, dysphagia, throat pain, and airway obstruction.84 Involvement of the cricoarytenoid joints, specifically ankylosis and ultimately fixation, has been described as early as 1957.83,85,86 Direct involvement of the cricothyroid joint has been described as well.84 In 1975, Webb and Payne described nodular changes of the true vocal folds with pathologic findings (fibrinoid necrosis and palisading histocytes) classic for RA.87 These entities have been called “bamboo nodes”. Treatment often requires administration of systemic disease modifying antirheumatic medications, the most common of which is methotrexate.88 Bamboo nodes may be responsive to localized steroid injection.89

Systemic lupus erythematosus is a chronic autoimmune disease resulting from recurrent activation of the immune system with resultant inflammation. The pathogenesis is not well understood and is known to be multifactorial involving both environmental and genetic factors. It can be a disfiguring disease and has a staggering 9:1 female: male predominance.90 Laryngeal involvement can occur and range from mild epithelial ulcerations and edema to cricoarytenoid joint involvement and airway compro mise.91,92 Recurrent laryngeal nerve involvement resulting in vocal fold paralysis is possible.93,94 Immunosuppressive therapy is often required.90 Serologic studies confirm the diagnosis.

IDIOPATHIC Prolonged Ulcerative Laryngitis Prolonged ulcerative laryngitis (PUL) is a disease charac­ terized by ulceration and inflammation of the membranous vocal fold resulting in severe vibratory impairment and dysphonia. It has a prolonged course with an average time to resolution of approximately three months (Fig. 43.7). The cause of the disease is unknown, but it often occurs after an upper respiratory infection involving vigorous coughing. The disease is self limited and often resolves completely, although it may be slow to resolve. However, it can result in permanent scarring in some cases. No -

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Fig. 43.5: Wegner’s granulomatosis. This larynx demonstrates nonspecific inflammation of the vocal fold in a patient with limited Wegner’s granulomatosis. Notice the hyperemia, mild sicca appea­ rance with some crusting, and the fullness within the conus elas­ ticus, particularly on the left.

560

Section 4: Voice Disorders

A

B

Figs. 43.7A and B: Prolonged ulcerative laryngitis. (A) Notice the large ulceration of the left vocal fold. (B) Two months later, the ulcera­ tion has significantly improved.

medical treatment has been shown to be effective, but voice therapy may be useful to avoid additional vocal trauma during the time of severe impairment. It is most prevalent in females.105,106 Diffuse severe inflammatory process with ulceration of the vocal folds that does not respond to steroids or antifungals suggests PUL. There is often temptation to biopsy for fear of missing malig­ nancy. However, this should be resisted, as biopsy will likely result in permanent scarring given the likelihood of injuring the vocal ligament. Rather, close follow-up should be maintained to make sure there is no progressive nature, which might suggest another etiology. If one feels a biopsy is warranted, efforts should be made to avoid the medial edge of the vocal fold.

CONCLUSION Chronic “laryngitis” insinuates chronic inflammation of the vocal folds and can present diagnostic and therapeutic challenges for the otolaryngologist. Laryngeal imaging is critical for diagnosis and to rule out more ominous causes of dysphonia. When inflammation is determined to be the primary cause of chronic dysphonia, the otolaryngologist must determine the cause of the inflammation so appropriate treatment can be prescribed. The history and examination, particularly the appearance of the vocal folds, are often sufficient to determine the most likely source of inflammation. However, empiric trial of medication often is necessary to confirm the diagnosis. Occasionally, serologic studies and biopsy are warranted. There are many potential etiologies of chronic laryngitis, and the problem

may be multifactorial. We divide the differential into four categories: direct irritation, infectious, autoimmune, and idiopathic.

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62. DelGaudio JM. Steroid inhaler laryngitis: dysphonia caused by inhaled fluticasone therapy. Arch Otolaryngol Head Neck Surg. 2002;128(6):677-81. 63. Kleinsasser O. Pathogenesis of vocal cord polyps. Ann Otol Rhinol Laryngol. 1982;91(4):378-81. 64. Branski RC, Saltman B, Sulica L, et al. Cigarette smoke and reactive oxygen species metabolism: implications for the pathophysiology of Reinke’s edema. Laryngoscope. 2009; 119(10):2014-8. 65. Branski RC, Zhou H, Kraus DH, et al. The effects of cigarette smoke condensate on vocal fold transepithelial resistance and inflammatory signaling in vocal fold fibroblasts. Laryngo­ scope. 2011;121(3):601-5. 66. Bastian RW. Benign vocal fold mucosal disorders. In: Flint PW, Haughey BH, Lund VJ, et al. (eds), Cummings otolary­ ngology head and neck surgery, 5th edn. Philadelphia, PA: Mosby;2010. 67. Pitman MJ, Lebowitz-Cooper A, Iacob C, et al. Effect of the 532nm pulsed KTP laser in the treatment of Reinke’s edema. Laryngoscope. 2012;122(12):2786-92. 68. Schoen FJ. Blood vessels. In: Kumar V, Abbas AK, Fausto N (eds), Robbins and Cotran: pathologic basis of disease, 7th edn, Philadelphia, PA: Mosby;2005. 69. Trimarchi M, Sinico RA, Teggi R, et al. Otorhinolaryngo­ logical manifestations in granulomatosis with polyangiitis (Wegener’s). Autoimmun Rev. 2013;12(4):501-5. 70. Eliachar I, Chan J, Akst L. New approaches to the manage­ ment of subglottic stenosis in Wegener’s granulo­matosis. Clev Clin J Med. 2002;69(2):149-51. 71. Lebovics RS, Hoffman GS, Leavitt RY, et al. The management of subglottic stenosis in patients with Wegener’s granulo­ matosis. Laryngoscope. 1992;102(12):1341-5. 72. Simpson CB, James JC. The efficacy of mitomycin-C in the treatment of laryngotracheal stenosis. Laryngoscope. 2006; 116(10):1923-5. 73. Smith ME, Elstad M. Mitomycin C and the endoscopic treat­ ment of laryngotracheal stenosis: are two applications better than one? Laryngoscope. 2009;119(2):272-83. 74. Wolter NE, Ooi EH, Witterick IJ. Intralesional corticosteroid injection and dilatation provides effective management of subglottic stenosis in Wegener’s granulomatosis. Laryngo­ scope. 2010;120(12):2452-5. 75. Poe DL. Sarcoid of the larynx. Arch Otolaryngol. 1940;32(2): 315-20. 76. Shah UK, White JA, Gooey JE, et al. Otolaryngologic mani­ festations of sarcoidosis: presentation and diagnosis. Laryn­ goscope. 1997;107(1):67-75. 77. Schwartzbauer HR, Tami TA. Ear, nose, and throat mani­ festations of sarcoidosis. Otolaryngol Clin N Am. 2003;36(4): 673-84. 78. Ellison DE, Canalis RF. Sarcoidosis of the head and neck. Clin Dermatol. 1896;4(4):136-42. 79. Costabel U, Teschler H. Biochemical changes in sarcoidosis. Clin Chest Med. 1997;18(4):827-42. 80. Baughman RP, Costabel U, du Bois RM. Treatment of sarcoidosis. Clin Chest Med. 2008;29(3):533-48. 81. Butler CR, Nouraei SA, Mace AD, et al. Endoscopic airway management of laryngeal sarcoidosis. Arch Otolaryngol Head Neck Surg. 2010;136(3):251-5.

Chapter 43: Chronic Laryngitis

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94. Gordon T, Dunn EC. Systemic lupus erythematosus and right recurrent laryngeal nerve palsy. Br J Rheumatol. 1990; 29(4):308 9. 95. Sulica L. Laryngeal thrush. Ann Otol Rhinol Laryngol. 2005; 114(5):369 75. 96. Heman Ackah YD, Hawkshaw MJ, Lyons KM. Laryngeal thrush from asthma inhalers. Ear Nose Throat J. 2012;91(1): E24 25. 97. Wong KK, Pace Asciak P, Wu B, et al. Laryngeal candidiasis in the outpatient setting. J Otolaryngol Head Neck Surg. 2009;38(6):624 7. 98. Nunes FP, Bishop T, Prasad ML, et al. Laryngeal candi­ diasis mimicking malignancy. Laryngoscope. 2008;118(11): 1957 9. 99. Nair AB, Chaturvedi J, Venkatasubbareddy MB, et al. A case of isolated laryngeal candidiasis mimicking laryngeal carcinoma in an immunocompetent individual. Malays J Med Sci. 2011;18(3):75 8. 100. Liakos T, Kaye K, Rubin AD. Methicillin resistant Staphy­ lococcus aureus laryngitis. Ann Otol Rhino Laryngol. 2010; 119(9):590 3. 101. Vrabec DP. Fungal infections of the larynx. Otolaryngol Clin N Am. 1993;26(6):1091 114. 102. Hanson JM, Spector G, El Mofty SK. Laryngeal blasto­ mycosis: a commonly missed diagnosis. Report of two cases and review of the literature. Ann Otol Rhinol Laryn­ gol. 2000;109(3):281 6. 103. Bhat VK, Latha P, Upadhya D, et al. Clinicopathological review of tubercular laryngitis in 32 cases of pulmonary Kochs. Am J Otolaryngol. 2009;30(5):327 30. 104. Wang CC, Lin CC, Wang CP, et al. Laryngeal tuberculosis: a review of 26 cases. Otolaryngol Head Neck Surg. 2007; 137(4):582 8. 105. Hsiao TY. Prolonged ulcerative laryngitis: a new disease entity. J Voice. 2011;25(2):230 5. 106. Simpson CB, Sulica L, Postma GN, et al. Idiopathic ulcera­ tive laryngitis. Laryngoscope. 2011;121(5):1023 6.







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82. Lawry GV, Finerman ML, Hanafee WN, et al. Laryngeal invol­ vement in rheumatoid arthritis. A clinical, laryngoscopic, and computerized tomographic study. Arthritis Rheum. 1984;27 (8):873 82. 83. Leahy KP. Laryngeal and tracheal manifestations of syste­ mic disease. In: Flint PW, Haughey BH, Lund VJ, et al. (eds), Cummings otolaryngology head and neck surgery, 5th edn. Philadelphia, PA: Mosby;2010. 84. Berjawi G, Uthman I, Mahfoud L, et al. Cricothyroid joint abnormalities in patients with rheumatoid arthritis. J Voice. 2010;24(6):732 7. 85. Copeman WS. Rheumatoid arthritis of the cricoarytenoid joints. Br Med J. 1957;1(5032):1398 9. 86. Copeman WS, Elkin AC, Pearce R. A case of rheumatoid arthritis with ankylosis of the crico arytenoid joints. Br Med J. 1959;1(5137):1575. 87. Webb J, Payne WH. Rheumatoid nodules of the vocal folds. Ann Rheum Dis. 1972;31(2):122 5. 88. O’Dell JR. Treatment of rheumatoid arthritis. In: Firestein GS (ed.), Kelley’s textbook of rheumatology, 9th edn. Philadelphia, PA: Elsevier;2013. 89. Schwemmle C, Kreipe HH, Witte T, et al. Bamboo nodes associated with mixed connective tissue disease as a cause of hoarseness. Rheumatol Int. 2013;33(3):777 81. 90. Crow MK. Systemic lupus erythematosus and related synd­ romes. In: Firestein GS (ed.), Kelley’s textbook of rheuma­ tology, 9th edn. Philadelphia, PA: Elsevier;2013. 91. Ozcan KM, Bahar S, Ozcan I, et al. Laryngeal involvement in systemic lupus erythematosus: report of two cases. J Clin Rheumatol. 2007;13(5):278 9. 92. Martin L, Edworthy SM, Ryan JP, et al. Upper airway disease in systemic lupus erythematosus: a report of 4 cases and a review of the literature. J Rheumatol. 1992;19(8):1186 90. 93. Muniain MA, Toyos FJ, Girón JM, et al. Right recurrent laryngeal nerve palsy in a patient with systemic lupus erythematosus. Lupus. 1992;1(6):407 8.

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CHAPTER

Autoimmune Disorders of the Larynx: Common Conditions, Symptoms, and Treatments

43A

Adam Szymanowski, Amy L Rutt, Robert T Sataloff

INTRODUCTION A wide variety of occupations require the continuous use of high-intensity phonation. This group of professional voice users includes singers, actors, and teachers among other occupations. Professional voice users suffer disproportionately from voice disorders compared with their peers in less vocally taxing professions. A study of patients visiting the voice clinic at the University of Wisconsin found that over 40% of the clinical load was accounted for by teachers, singers, and salespeople. These data support the relationship between vocally taxing occupations and prevalence voice disorders.1 Voice disorders result from physiologic, anatomic, or functional changes that impair normal phonation and change voice production. These changes can affect professional voice users.2 While vocal dysfunction can result from regular use, a number of medical problems can lead to serious voice impairment. Specifically, autoimmune diseases can lead to serious and permanent vocal deterioration.3 Autoimmune diseases are a group of disorders that share a defect in the immune system leading to the body’s inability to differentiate between normal and foreign components. Immune system components, including anti­ bodies, identify normal tissue as foreign and incite an inflammatory response. The process of ‘autoreactivity’ is attributed to a number of factors, including genetic predi­ sposition, gender, and environmental exposure.

Between 3% and 9% of the general population are affected by autoimmune diseases, and the impact can be limited or systemic. Pathologic autoimmunity can lead to extensive damage to normal anatomy and potentially permanent loss of function.3 This review discusses the most common autoimmune diseases and their laryngeal sequelae, common signs and symptoms of vocal fold involvement, disease diagnosis, and effective treatment options. The information presen­ted is especially important for professional voice users with autoimmune diseases. Awareness of the signs and symptoms of voice involvement can potentially limit time from symptom onset to first physician visit.

METHODS A thorough literature search was conducted to gather data to complete this review. For each autoimmune disorder presented, the search term “laryngeal manifestations of” preceded the disorder name. The search term was run through the PubMed database. Table 43A.1 summarizes the search results found for each query. Initial filters were set between the years of 2000 and 2014. Additional criteria for inclusion in the review were specific discus­sion of laryngeal manifestation of the autoimmune disorder and text written in English. Following initial review of collected literature, selected cited references were added as sources for this review.

Modified in part from Szymanowski A, Rutt AL, Sataloff RT. Autoimmune disorders of the larynx: common conditions, symptoms, and treatments. J Singing. 2015; in press.

566

Section 4: Voice Disorders

Table 43A.1: Pubmed search results

Results produced from PubMed search

Autoimmune disorder Amyloidosis

19

Relapsing polychondritis

31

Sarcoidosis

27

Systemic lupus erythematosus

12

Rheumatoid arthritis

25

Scleroderma

6



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Amyloidosis is an autoimmune disease characterized by the unnecessary secretion of protein into the extracellular environment. The disease becomes clinically apparent usually during the fifth and sixth decades of life, affecting men and women equally. The deposited protein, amyloid, is an insoluble fibrillar substance that can occur locally or throughout the body.4 With the exception of laryngeal involvement, head and neck amyloidosis is often a sign of existing underlying malignancy. Laryngeal masses caused by amyloidosis makeup < 1% of all benign laryngeal masses5 (Fig. 43A.1). Laryngeal amyloidosis is rare and frequently occurs in the absence of systemic disease. The false vocal folds and ventricular space are affected most commonly follo wed by the true vocal folds.4 Amyloid collects beneath the surface layer of epithelial cells and elicits a chronic inflammatory response comprised of lymphocytes and plasma cells.4,6 The precise cause of amyloidosis is not known.4 A reaction to a self-antigen and the inability to clear protein produced by plasma cells are potential explanations.7 The most common presenting symptom is progressive hoarseness.6-10 Other complaints include dyspnea, stridor,

vocal fatigue, and dysphagia.6,7,9,10 The voice may sound high pitched, raspy, or coarse.11 Dedo et al. completed objective acoustic analysis on 10 patients with laryngeal amyloidosis revealing increased breathiness and friction, decreased total voice range, diminished loudness, and decreased maximum phonation time. The same study found that symptoms were more severe when amyloid was deposited bilaterally on the undersurface of the true vocal folds and when amyloid extended from the false vocal folds to the true vocal folds. Patients with significant laryngeal involvement may be limited to a whisper and may suffer other changes to the voice.8 Severe vocal impair ment can prohibit patients from a variety of activities.6 Laryngeal amyloidosis must always be considered in patients with progressive hoarseness and voice impair ment.11 Definitive diagnosis can be made with biopsy of the lesion, staining with Congo Red, and exposing the tissue to polarized light to visualize the classic applegreen birefringence.4 On electron microscopy, antiparallel beta pleated sheets can be observed.4,6 Laryngoscopy permits visualization of the lesions, which range from edematous glottic strictures to protruding nodules.9 The lesions may appear yellow, orange, or gray in color.10 With significant false vocal fold involvement, the true vocal folds can be partially or completely obscured.6,11 After diagnosing laryngeal amyloidosis, signs and symptoms of systemic involvement should be assessed. Traditionally, gastrointestinal and bone marrow biopsies are required to diagnose systemic amyloidosis.4 More recently, lessinvasive blood tests have become accepted to assess kidney, liver, and hematologic health.10 ­

AMYLOIDOSIS

Fig. 43A.1: Videostroboscopy shows the near-circumferential sub­glottic subepithelial infiltrate and the focal areas of nodularity typical of amyloidosis.



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Selected articles were organized subsequently into four groups. The groups included (1) articles that discussed disease development, pathogenesis, and mechanism of laryngeal insult; (2) signs and symptoms found on exam, including classic and rare presentations; (3) current diagnostic modalities, with an emphasis on gold standard diagnostic tools; (4) current treatments and their efficacy as well as potential future treatments. Articles including a broad discussion of a specific disorder were placed in more than one group. This algorithm permitted adequate organization of resources and facilitated the identifica tion of gaps in the literature.

Chapter 43A: Autoimmune Disorders of the Larynx: Common Conditions, Symptoms, and Treatments There is no cure for amyloidosis; however, disease control is usually possible, and treatment often leads to excellent outcomes. Surgery often is recommended regard­ less of presentation, but it is especially important for patients presenting with substantial vocal impairment or evidence of airway obstruction.8 Surgical extirpation followed by adjuvant radiotherapy can be used to treat isolated laryngeal amyloidosis.7,10,12 This method putatively eliminates the pathologic plasma cells responsible for depositing the amyloid into the extracellular space, an approach that resembles the concept of chemotherapy for B-cell malignancies.7 Truong et al. treated 10 patients with head and neck amyloidosis using low dose radiotherapy to limit the potential for disease recurrence and reported disease control in eight of the patients. The dose of radia­tion used was low compared to that used for cancer treatment, leading to a limited side effect profile.12 Further studies are needed to validate the true efficacy of radiation therapy for amyloidosis and the possible long-term adverse effects.7,11 Patients with recurrent disease, submucosal lesions, or polypoid lesions should be treated surgically.10 Although some authors believe that carbon dioxide laser excision is more precise and less traumatic to surrounding tissue compared with traditional surgical techniques,13 many other surgeons (including RTS) disagree and favor cold instruments especially for disease involving the true vocal folds. Surgical treatment is often vocally restorative.8,10 Regardless of treatment choice, patients should be follo­ wed up regularly with serial laryngoscopies to assess for disease recurrence, and serial imaging also is valuable.9,10

RELAPSING POLYCHONDRITIS Relapsing polychondritis (RP) is a rare autoimmune disease that leads to recurrent inflammatory episodes within cartilage.14 The disease can manifest locally or systemically. Onset occurs usually between the ages of 40 and 60;15 however, pediatric cases have been described.16 While the etiology is unknown, a strong genetic relationship has been found between RP and the HLA-DR415 and HLADR B1 alleles.17 Recent literature suggests that many RP patients have T inflammatory cells that react with type II collagen, the predominant protein in hyaline cartilage.17 Chronic intrachondral inflammation leads to weakened structures, including vocal and airway support structures. Advanced disease can lead to airway obstruction, which is responsible for 10% of all RP-related deaths.14,18

567

Table 43A.2: Summary of the McAdams criteria19

Bilateral auricular chondritis Nonerosive inflammatory polyarthritis Nasal chondritis Ocular inflammation (conjunctivitis, scleritis, uveitis) Respiratory tract chondritis (laryngeal and tracheal cartilages) Vestibulocochlear dysfunction (hearing loss, tinnitus, and vertigo)

Compared with healthy control subjects, T cells from patients with RP increased almost five times the original number when exposed to type II collagen.17 Navarro et al. recently published a pediatric case study in which a patient with RP was given exogenous type II collagen orally for 8 months apparently leading to complete disease remission. The authors propose that regular feedings with type II leads to induced tolerance.16 These data suggest that RP results from an inappropriate reaction by the body’s immune system to type II collagen. RP is diagnosed classically using the McAdams cri­teria, proposed in 1976. Table 43A.2 outlines the quali­ fying signs and symptoms for diagnosis. A patient requires three of the six manifestations for definitive diagnosis.19 While patients with RP may present with a variety of signs and symptoms associated with cartilage inflammation, a significant number of patients diagnosed with RP initially present with airway manifestations.18,20 Com­mon laryngotracheal symptoms include cough, dyspnea, hoar­seness, stridor, and wheezing.15,18,20 Over time these symp­ toms can lead to airway stenosis and collapse, most pronounced with inspiration.15 Vocal fold masses may develop with severe disease.20 Stenosis, perma­nent deformity, and pneumonia are sources of morbidity and mortality.18,19,21 More recent literature demonstrates the existence of type II collagen antibodies20 and T cells reac­ tive to type II collagen.17 As more literature becomes available, serological evidence of RP could lead to imp­ roved ability to diagnose the disease. RP is a progressive and fluctuating disease that often can be controlled with oral steroids and methotrexate.14,18 Nonsteroidal anti-inflammatory medications can be bene­ficial.15 Severe disease exacerbation, including airway obstruction, requires emergency tracheotomy or endo­tracheal tube placement. If the patient is not in res­ piratory distress, high dose pulsed intravenous steroids may be effective.14,18 Under certain circumstances, RP may be refractory to standard therapy. Childs et al. described a patient with laryngeal RP complaining of dysphonia

Section 4: Voice Disorders Definitively diagnosing sarcoidosis requires tissue biopsy to visualize noncaseating, nonnecrotic granulomas; however, a number of clinical manifestations can support the presence of laryngeal sarcoidosis.23 Hoarseness, dyspnea, dysphonia, and stridor are common presenting complaints.22-24,27 Mayerhoff et al. described four patients to demonstrate the highly variable presentation of laryn geal sarcoidosis. The four cases differed in age of onset, presenting symptom, and timing of disease onset. The four cases included one pediatric patient and a variety of different chief complaints including dysphonia, globus, progressive snoring, and dysphagia.28 A distinct “honking” vocal quality may be a diagnostic clue.25 A rapidly enlarging neck mass also may indicate the presence of disease.22,27 Any airway symptom occurring in a patient already diag nosed with sarcoidosis should elicit immediate laryn goscopy to identify airway disease and prevent respiratory distress.29 Pulmonary function testing can be helpful to identify extrapulmonary obstructive airway disease, the classic manifestation of laryngeal sarcoidosis.23,24 Patients with symptoms highly suspicious for laryn geal sarcoidosis should receive routine blood tests, a chest radiograph to identify evidence of pulmonary involve ment, and direct laryngeal visualization and biopsy when indicated. Biopsy is the gold standard for diag nosis. Laboratory and radiographic information serve a supportive role.23 Granulomas in the larynx are rare and may require multiple biopsies to confirm their nature when sarcoidosis is suspected.26 The appearance glottic structures during videolaryngoscopy can provide addi tional evidence suggestive of sarcoidosis. Turban-like supraglottic obstruction is often seen on endoscopic exam. Additionally, the true vocal folds and subglottis often appear nearly normal. Only with severe disease do these structures appear slightly erythematous and thickened. Vocal fold mobility is often normal.24,25 After establishing an open airway, the goal of treat ment is to preserve or restore voice quality.24 First-line treatment of laryngeal sarcoidosis involves oral steroids. More recent literature supports the potential use of topical or inhaled steroids to specifically treat laryngeal sarcoidosis.23 Dean et al. described a patient with longstanding, systemic sarcoidosis that presented with vocal manifestations. The patient was treated successfully with systemic steroids, but returned with isolated vocal mani festations. A trial of inhaled corticosteroids successfully led to sustained resolution of voice symptoms.23 Another patient with progressive dysphonia, neck pain, and

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Sarcoidosis is a chronic granulomatous disease that com monly manifests in the respiratory tract.22 In the United States, Hispanic and African American women are more often affected compared with other ethnicities and men.23 Laryngeal sarcoidosis is rare, and can lead to serious voice alterations especially concerning for professional voice users (Fig. 43A.2).24 Neel et al. studied over 2,000 patients with sarcoidosis between 1950 and 1981 and found laryngeal sarcoidosis in 8  mm Hg above gastric pressure) and (2) aperistalsis of the body of the esophagus characterized by simultaneous contractions of low amplitude (10% wet swallows and (2) mean simultaneous contraction amplitude > 30 mm Hg (Fig. 45.4). Radiographically, it appears by tertiary contractions of

Chapter 45: Dysphagia in Esophageal Disorders the esophagus or corkscrew appearance.33 Medical treat­ ment includes nitrates, calcium channel blockers, silde­ nafil, and tricyclic antidepressants, and sometimes Botox has been shown to be beneficial. Esophageal hypercontraction can best be described as “nutcracker esophagus”, originally described clinically as noncardiac chest pain and/or dysphagia. The manometric findings proposed for diagnosis include (1) mean distal peristaltic wave amplitude > 180 mmg Hg. Peristaltic con­ tractions often occur with longer duration, but it is not criteria for diagnosis. A diagnosis of isolated LES hyper­ contraction is a mean resting pressure > 45 mm Hg.33 Scleroderma is the best-known motility disorder described in the category of hypocontraction. The under­ ly­ing disease process of fibrosis affecting both muscle and its innervation weakens the LES predisposing to GERD. Scleroderma affects primarily the smooth muscle of the distal esophagus. Manometric findings are not specific for this disorder; in fact, they are similar in patients affected by other collagen vascular disorders, such as mixed connective tissue disease, rheumatoid arthritis, and lupus. Nonrheumatologic disorders, such as diabetes mellitus, amyloidosis, alcoholism, myxedema, and multiple sclero­ sis, also demonstrate hypocontraction of the esophagus resulting in ineffective motility. Manometric features pro­­posed for diagnosis include hypocontraction ( 30% of wet swallows.33 Inef­ ective motility is commonly seen in patients with GERD; antireflux medications are highly effective in most cases. Treatment includes prokinetic drugs, proton-pump inhibitors, and dietary modification. However, in refractory patients with GERD and ineffective esophageal motility, bethanechol has been proposed.36

Inflammatory/Infectious Esophagitis Esophagitis is inflammation of the esophagus. It can be acute or chronic, symptomatic, or incidental. Esophagitis can be caused by reflux, foreign body, allergy, infection, caustic injury, radiation, or idiopathic. Pill-induced eso­ phagitis results from local trauma and chemical contact to the surface epithelium of the esophagus caused by the retained pill. Reflux esophagitis is caused by an abnormal exposure of the esophageal mucosa to the gastroduodenal contents. Acute changes seen on endoscopy can be erythema or sloughing of the mucosa, whereas chronic inflammation can lead to scarring and stricture. Ambulatory pH moni­ toring can be helpful in the diagnosis of gastroesophageal

593

reflux, but the presence of esophagitis can only be con­ firmed on endoscopy. The Los Angeles classification is currently the most accepted system for endoscopic evalua­ tion of esophagitis, based on the extent of visible mucosal breaks. A mucosal break is defined as “an area of slough or erythema with a discrete line of demarcation from the adjacent, more normal looking mucosa”. The classification grades esophagitis A–D and correlates well with severity of acid exposure on pH testing.37

Eosinophilic Esophagitis Eosinophilic esophagitis is a clinicopathologic disease initially described in children, but it has emerged as a clinical disorder of adults as well. Symptoms in children vary by age: infants and toddlers have feeding difficulty, school-aged children have abdominal pain and vomiting, and adolescents present with adult findings. Typical present­ation in younger adults, more often male, will be solid food dysphagia or recalcitrant GERD. The etiology is still unknown; however, it has been associated with a TH-2 type allergic inflammatory response. The presence of allergic rhinitis or allergy to aeroallergens has been documented from 24% to 78% in adults and 42% to 93% in children. Sensitization to foods is common in children. Therefore, allergy testing is warranted according to 2011 updated consensus guidelines.38 Eosinophilic esophagitis is described histologically by a constellation of findings: thick epithelium with large numbers of intraepithelial eosinophils, abnormally long papillae, and fibrotic lamina propria also containing eosinophils. Eosinophilic esopha­ gitis is often patchy and highly variable; therefore, several biopsies must be procured (at least three specimens at two sites including distal and either mid or proximal esophagus). The most commonly used method is to count the number of intraepithelial eosinophils per highpowered field (HPF = 400x) this is called the peak number. A peak of 15/HPF is the threshold number of eosinophils to diagnose eosinophilic esophagitis.38 It is important to emphasize a clinical correlation as patients with GERD may also meet the same histopathologic criteria; therefore, a trial of proton-pump inhibitors is warranted to help differentiate the two.38,39 Several esophageal structural abnormalities have been associated with eosinophilic esophagitis and can suggest a diagnosis on endoscopy: small-caliber esophagus, corrugations or a series of rings (trachealization of the esophagus), proximal esophageal stenosis, and whitish vesicles or papules representing microabscesses (more commonly seen in children).40

594

Section 4: Voice Disorders

Treatment includes pharmacotherapy such as topical swallowed corticosteroids and/or dietary modifications; however, relapse rate is as high as 91% with cessation of medication.41 Esophageal dilation is an alternative treatment; however, due to the inflammatory nature and fragility of esophageal mucosa, several studies have repor­ ted mucosal tears, trauma, and even perforation (although rare). Furthermore, up to 86% of patients had relapse of symptoms within one year after dilation.40,41 Most agree that dilation should be reserved for select patients, usually those presenting with food impaction.

Esophageal Foreign Body Both otolaryngologists and gastroenterologists commonly see foreign bodies or food impaction. In children, coins are by far the most common foreign body. Spontaneous passage rate of 25% within 16 hours was observed in a prospective randomized trial. Observation and repeat imaging can be considered within the first 16 hours of presentation.42 Removal of an impacted foreign body, espe­ cially a suspected battery, is mandatory as the sequelae of nontreatment are severe: penetration or perforation of the esophageal wall with subsequent local, mediastinal, or generalized infection.

Caustic Ingestion Both accidental and intentional (suicide attempt) ingestion of caustic agents has increased in both adults and children likely second to an increased availability of household products both alkaline (drain cleaners, oven/grill cleaners, dishwasher powders, paint removers) and acidic (toilet cleaner, rust remover, kettle descaling) have increased.43,44 Timing of endoscopy is generally expected within the first 24–36  hours after caustic ingestion. Endoscopic grading initially classified by Di Costenzo describes mucosal damage: grade 0 no damage; grade 1 edema, erythema, or exudate; grade 2 moderate ulceration or hemorrhage; grade 3 extensive ulceration or hemorrhage.45 The degree of mucosal damage is more correlated with outcomes than type of substance ingested. A retrospective review of 179 caustic ingestions demonstrated that mortality rates after acidic ingestion, which are usually associated with suicide attempts, were up to 14% versus 2% alkaline, with most deaths occurring within the first 24–48 hours.46 The most important morbidity of caustic ingestion is esophageal stricture, typically presenting 6–12 weeks after ingestion and with increasing risk based on endoscopic

grade 2 (6.3%) or 3 (23.1%).43 The use of corticosteroids to prevent stricture formation has been controversial.43,44

Infectious Esophagitis Infectious esophagitis is an important diagnosis to consider, especially in the immunocompromised patient. Almost half of all HIV patients present with gastrointestinal (GI) symptoms and almost all will eventually develop GI complications. The most common esophageal lesions include candidiasis, cytomegalovirus (CMV), herpes sim­ plex virus (HSV), and idiopathic ulceration. Candidiasis appears as thick, creamy white plaques with surrounding erythema on otherwise normal appearing epithelium. Histopathologic features include pseudomembranes, neutrophilic infiltration, and budding yeast or pseudo­ hyphae. CMV is the most common opportunistic agent in HIV-infected patients, and while it can affect the entire GI tract, it most commonly affects the esophagus and the colon. CMV often presents with distal esophageal ulceration. Biopsy specimens should be taken from the base to demonstrate CMV inclusion bodies within the stromal and endothelial cells. Endoscopic features of HSV are vesiculation and ulceration, round, multiple, and better circumscribed compared with CMV. Histopathologic features of ground-glass nuclei, nuclear molding, multi­ nucleation, and rarely Cowdry A inclusion bodies are best identified on the ulcer edges. Mycobacterium avium intracellulare (MAI) is the most common mycobacterial infection in severely immunocompromised patients. MAI can be normal mucosa or multiple raised nodules with biopsy confirmed acid-fast bacilli. Gastric neoplasia can also be diagnosed on biopsy: Kaposi’s sarcoma (asymptomatic; submucosal violet red plaques) and nonHodgkin’s lymphoma (epigastric pain or obstruction; ulcerated mass lesion). Endoscopy with biopsy is the diagnostic test of choice in HIV-associated GI disorders.47

ESOPHAGEAL NEOPLASM Barrett’s Esophagus and Adenocarcinoma Over the last three decades, there has been a marked change in the biology and epidemiology of esophageal carcinoma. Where squamous cell carcinoma (SCC) prevailed in association with alcohol and tobacco use, now there is a shift toward EAC. In contrast to SCC, a meta­ plasia–dysplasia–carcinoma sequence has been delineated

Chapter 45: Dysphagia in Esophageal Disorders for EAC. Furthermore, Barrett’s esophagus as a conse­ quence of chronic GERD has been identified as a precancerous lesion to EAC.48 The definition of Barrett’s esophagus is the metaplastic replacement of the normal squamous epithelium by specialized columnar epithe­ lium at the GEJ. Endoscopically, Barrett’s esophagus looks like salmon-pink finger-like projections extending beyond the normal SCJ (Fig. 45.5).49 Histologically, Barrett’s is intestinal metaplasia with goblet cells. The risk of progression to cancer in low-grade dysplasia is variable; high-grade dysplasia progresses in up to 30% > five years.50 The incidence of adenocarcinoma in Barrett’s esophagus follow-up studies varies dramatically from 1:46 (patient:years) to 1:441 (patient:years).48 The American College of Gastroenterology has developed screening recommendations based on histologic diagnosis where Barrett’s nondysplastic metaplasia should be screened every three years, low-grade dysplasia every year, and high-grade dysplasia every three months.50 The five-year survival of adenocarcinoma was com­ monly reported at 20% until Portale et al. in 2006 docu­ mented a 10-year retrospective study on 263 patients undergoing esophagectomy for adenocarcinoma with five-year survival of 50%.51 Furthermore, patients presen­ ting with T1 lesions had increased over the 10-year study. The shift toward early detection of early stage cancers from Barrett’s surveillance programs is a direct result of the recognized relationship of esophageal adenocarcinoma and gastroesophageal reflux. However, surveillance endo­ scopy continues to be controversial due to a lack of ran­ domized controlled studies demonstrating decrea­ sed 50 mortality in EAC.

Surveillance in HNCA In patients treated for HNCA, regardless of modality (i.e. surgery versus chemoradiation), dysphagia is a very common symptom. In a prospective study of 100 HNCA patients post-treatment recruited from routine surveil­ lance program, only 22% did not complain of difficulty swallowing, and of those 22 patients, only 4 had normal esophagoscopy evaluations.52 HNCA patients may have symptoms of dysphagia for a variety of reasons, including decreased saliva, structural deformity of the oral cavity/ oropharynx/hypopharynx, neuromuscular dysfunction of the swallowing mechanism, and importantly, new or recurrent tumor.53 It is important, although sometimes difficult, to distin­ guish a functional/mechanical problem of swallow­ ing

595

Fig. 45.5: Endoscopic findings of classic Barrett’s esophagus.

and a newly developing or recurrent tumor. Since many post-treatment patients have trismus and/or stenosis, evaluation of dysphagia through endoscopic, fluoroscopic, or other imaging studies have been utilized. In another one-year prospective study of patients treated for HNCA with new onset dysphagia finding 16/33 patients diagnosed with either recurrence or second primary HNCA on trans­ nasal esophagoscopy (nine hypopharyngeal cancers, five esophageal cancers, one local hypopharynx recur­rence, one local neopharynx recurrence).53 Further advantages of TNE in HNCA patient are the in-office procedures: dilation of stenotic segments, secondary tracheoesopha­ geal puncture, excision, or ablation using flexible lasers through the channeled side port.54

Benign Esophageal Neoplasm Benign neoplasms of the esophagus are rare, typically slow growing and asymptomatic. Leiomyomas represent 60–70% of benign esophageal neoplasms. Most often, they are submucosal, diagnosed on endoscopy at the distal esophagus where smooth muscle predominates. Esophageal cysts are the second most common benign esophageal mass, usually congenital. On esophagoscopy, these appear blue, smooth, and round. Both lesions can be treated by enucleation and thoracotomy when symptomatic. Fibrovascular polyps are intramural, usually arising from the postcricoid space. Most are excised for fear of regurgitation, asphyxiation, and possible death.55 Inflammatory pseudotumors can be seen associated with mucosal ulcers, most commonly in the middistal esophagus. Lastly, single or multiple papillomas have been described throughout the aerodigestive tract, and are also treated with excision.

596

Section 4: Voice Disorders

COMPLICATIONS The most dreaded complication of esophagoscopy is per­ foration, a risk generally quoted between 0.1% and 1%. A retrospective review from 2002 to 2007 demonstrated 1.2% (7/546) overall perforation rate from esophagoscopy, including both rigid and flexible. However, all seven perforations occurred during rigid esophagoscopy alone, yielding a 2.6% incidence of perforation in rigid esophago­ scopy, specifically. Furthermore, it was suggested that the use of a rigid cervical esophagoscope, by junior residents, with junior faculty may be most predictive of perforation.56 A retrospective study by Eroglu demonstrated 27 of 44 patients with esophageal perforation were from instru­men­ tation, diagnosed within the first six hours of the procedure. Pain was the most common symptom, whereas subcuta­ neous emphysema was the most common sign.57 Vogel described 25 of 47 iatrogenic perforations, a 4.2% overall mortality, despite 32 patients treated nonoperatively with 100% survival.58 Treatment of esophageal perforation is medical or surgical depending on location; however, pri­­mary repair within 24 hours still remains the gold standard.57,58

SUMMARY With the advent of transnasal esophagoscopy, the otolaryngologist has a unique opportunity for in-office endoscopy that can be utilized in the evaluation of dysphagia. In addition to direct observation, cinefluoro­ scopy, multichannel intraluminal impedance-pH testing, and high-resolution manometry are just a few examples of other complementary tools available to the clinician that can be utilized in the diagnosis of esophageal disorders.

REFERENCES 1. Edwards HC. The technique of gastroscopy. Br Med J. 1936;1(3927):737-41. 2. Jackson C. New mechanical problems in the bronchoscopic extraction of foreign bodies from the lungs and oesophagus. Ann Surg. 1922;75(1):1-30. 3. Aviv JE,  Takoudes TG,  Ma G,  Close LG. Office-based eso­ pha­go­scopy: a preliminary report. Otolaryngol Head Neck Surg.  2001;125(3):170-5. 4. Shaker R. Unsedated trans-nasal pharyngoesophagogas­ troduodenoscopy (T-EGD): technique. Gastrointest Endosc. 1994;40(3):346-8. 5. Heeg P, Herrmann I. The new requirements of endoscopy. Ann N Y Acad Sci. 2011;1232:365-8. 6. Amin MR, Postma GN, Setzen M, Koufman JA. Transnasal esophagoscopy: a position statement from the American

Bronchoesophagological Association (ABEA). Otolaryngol Head Neck Surg. 2008;138(4):411-4. doi: 10.1016/j.otohns. 2007.12.032. 7. Postma GN, Bach KK, Belafsky PC, et al. The role of trans­ nasal esophagoscopy in head and neck oncology. Laryngoscope. 2002;112(12):2242-3. 8. Jobe BA, Hunter JG, Chang EY, et al. Office-based unsedated small-caliber endoscopy is equivalent to conventional sedated endoscopy in screening and surveillance for Barrett’s esophagus: a randomized and blinded comparison. Am J Gastroenterol. 2006;101(12):2693-703. 9. Dumortier J, Napoleon B, Hedelius F, et al. Unsedated transnasal EGD in daily practice: results with 1100 con­ secutive patients. Gastrointest Endosc. 2003;57(2):198-204. 10. Postma GN, Cohen JT, Belafsky PC, et al. Transnasal esophagoscopy: revisited (over 700 consecutive cases). Laryngoscope. 2005;115(2):321-3. 11. Wildi SM, Glenn TF, Woolson RF, et al. Is esophagoscopy alone sufficient for patients with reflux symptoms? Gastrointest Endosc. 2004;59(3):349-54. 12. Glaws WR, Etzkorn KP, Wenig BL, et al. Comparison of rigid and flexible esophagoscopy in the diagnosis of esophageal disease: diagnostic accuracy, complications, and cost. Ann Otol Rhinol Laryngol. 1996;105(4):262-6. 13. Tsao GJ, Damrose EJ. Complications of esophagoscopy in an academic training program. Otolaryngol Head Neck Surg. 2010;142(4):500-4. doi: 10.1016/j.otohns.2010.01.008. 14. Gmeiner D, von Rahden BH, Meco C, et al. Flexible versus rigid endoscopy for treatment of foreign body impaction in the esophagus. Surg Endosc. 2007;21(11):2026-9. Epub 2007 Mar 29. 15. Allen BC, Baker ME, Falk GW. Role of barium esophago­ graphy in evaluating dysphagia. Cleve Clin J Med. 2009; 76(2):105-11. doi: 10.3949/ccjm.76a.08032. 16. Hirano I, Richter JE; Practice Parameters Committee of the American College of Gastroenterology. ACG practice guidelines: esophageal reflux testing. Am J Gastroenterol. 2007;102(3):668-85. 17. Hila A, Agrawal A, Castell DO. Combined multichannel intraluminal impedance and pH esophageal testing compared to pH alone for diagnosing both acid and weakly acidic gastroesophageal reflux. Clin Gastroenterol Hepatol. 2007;5(2):172-7. 18. Spechler SJ, Castell DO. Classification of oesophageal motility abnormalities. Gut. 2001;49(1):145-51. Review. 19. Kahrilas PJ, Ghosh SK, Pandolfino JE. Esophageal motility disorders in terms of pressure topography: the Chicago Classification. J ClinGastroenterol. 2008;42(5):627-35. doi: 10.1097/MCG.0b013e31815ea291. Review. 20. Bredenoord AJ, Fox M, Kahrilas PJ, et al. Chicago classification criteria of esophageal motility disorders defined in high resolution esophageal pressure topography. Neurogastroenterol Motil. 2012;24 (Suppl 1): 57-65. doi: 10.1111/j.1365-2982.2011.01834.x. 21. Geng Z, Hoffman MR, Jones CA, et al. Three-dimensional analysis of pharyngeal high-resolution manometry data. Laryngoscope. 2013;123(7):1746-53. doi: 10.1002/lary. 23987. Epub 2013 Feb 16.

Chapter 45: Dysphagia in Esophageal Disorders 22. Achildi O, Grewal H. Congenital anomalies of the esophagus. Otolaryngol Clin North Am. 2007;40(1):219-44, viii. Review. 23. Cook IJ,  Gabb M,  Panagopoulos V,  et al. Pharyngeal (Zenker’s) diverticulum is a disorder of upper esophageal sphincter opening. Gastroenterology. 1992;103(4):1229-35. 24. van Overbeek JJ, Hoeksema PE. Endoscopic treatment of the hypopharyngeal diverticulum: 211 cases. Laryngoscope. 1982;92(1):88-91. 25. Weerda H, Ahrens KH, Schenter WW. Measures for reducing the rate of complications in endoscopic surgery of Zenker’s diverticulum. Laryngorhinootologie. 1989;68(12):675-7. 26. Collard JM, Otte JB, Kestens PJ. Endoscopic stapling technique of esophagodiverticulostomy for Zenker’s diverticulum. Ann Thorac Surg. 1993;56(3):573-6. 27. Leong SC, Wilkie MD, Webb CJ. Endoscopic stapling of Zenker’s diverticulum: establishing national baselines for auditing clinical outcomes in the United Kingdom. Eur Arch Otorhinolaryngol. 2012;269(8):1877-84. doi: 10.1007/ s00405-012-1945-3. Epub 2012 Feb 17. Review. 28. Altman JI, Genden EM, Moche J. Fiberoptic endoscopicassisted diverticulotomy: a novel technique for the management of Zenker’s diverticulum. Ann Otol Rhinol Laryngol. 2005;114(5):347-51. 29. Pitman M, Weissbrod P. Endoscopic CO2 laser cricopharyngeal myotomy. Laryngoscope. 2009;119(1):45-53. doi: 10.1002/lary.20032. Review. 30. Maune S. Carbon dioxide laser diverticulostomy: a new treatment for Zenker diverticulum. Am J Med. 2003;115 (Suppl 3A):172S-4S. Review. 31. Ho AS, Morzaria S, Damrose EJ. Carbon dioxide laserassisted endoscopic cricopharyngealmyotomy with primary mucosal closure. Ann Otol Rhinol Laryngol. 2011; 120(1):33-9. 32. Lawson G, Remacle M. Endoscopic cricopharyngealmyotomy: indications and technique. Curr Opin Otolaryngol Head Neck Surg. 2006;14(6):437-41. Review. 33. Spechler SJ, Castell DO. Classification of oesophageal motility abnormalities. Gut. 2001;49(1):145-51. Review. 34. Chuah SK, Hsu PI, Wu KL, et al. 2011 update on esophageal achalasia. World J Gastroenterol. 2012;18(14):1573-8. doi: 10.3748/wjg.v18.i14.1573. Review. 35. Lopushinsky SR, Urbach DR. Pneumatic dilatation and surgical myotomy for achalasia. JAMA. 2006;296(18): 2227-33. 36. Agrawal A, Hila A, Tutuian R, et al. Bethanechol improves smooth muscle function in patients with severe ineffective esophageal motility. J Clin Gastroenterol. 2007;41(4): 366-70. 37. Lundell LR, Dent J, Bennett JR, et al. Endoscopic assessment of oesophagitis: clinical and functional correlates and further validation of the Los Angeles classification. Gut. 1999;45(2):172-80. 38. Liacouras CA, Furuta GT, Hirano I, et al. Eosinophilic esophagitis: updated consensus recommendations for children and adults. J Allergy ClinImmunol. 2011;128(1): 3-20.e6; quiz 21-2. doi: 10.1016/j.jaci.2011.02.040. Epub 2011 Apr 7. Review.

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39. Collins MH. Histopathologic features of eosinophilic esophagitis. Gastrointest Endosc Clin N Am. 2008;18(1):5971; viii-ix. Review. 40. Potter JW, Saeian K, Staff D, et al. Eosinophilic esophagitis in adults: an emerging problem with unique esophageal features. Gastrointest Endosc. 2004.;59(3):355-61. 41. Enns R, Kazemi P, Chung W, et al. Eosinophilic esophagitis: clinical features, endoscopic findings and response to treatment. Can J Gastroenterol. 2010;24(9):547-51. 42. Waltzman ML, Baskin M, Wypij D, et al. A randomized clinical trial of the management of esophageal coins in children. Pediatrics. 2005;116(3):614-9. 43. Pelclová D, Navrátil T. Do corticosteroids prevent oesophageal stricture after corrosive ingestion? Toxicol Rev. 2005;24(2):125-9. Review. 44. Howell JM, Dalsey WC, Hartsell FW, et al. Steroids for the treatment of corrosive esophageal injury: a statistical analysis of past studies. Am J Emerg Med. 1992;10(5):421-5. 45. Di Costanzo J, Noirclerc M, Jouglard J, et al. New therapeutic approach to corrosive burns of the upper gastrointestinal tract. Gut. 1980;21(5):370-5. 46. Poley JW, Steyerberg EW, Kuipers EJ, et al. Ingestion of acid and alkaline agents: outcome and prognostic value of early upper endoscopy. Gastrointest Endosc. 2004;60(3):372-7. 47. Bhaijee F, Subramony C, Tang SJ, et al. Human immu­ nodeficiency virus-associated gastrointestinal disease: common endoscopic biopsy diagnoses. Patholog Res Int. 201126;2011:247923. doi: 10.4061/2011/247923. 48. Conio M, Blanchi S, Lapertosa G, et al. Long-term endoscopic surveillance of patients with Barrett’s esophagus. Incidence of dysplasia and adenocarcinoma: a prospective study. Am J Gastroenterol. 2003;98(9):1931-9. 49. Halum SL, Postma GN, Bates DD, et al. Incon­ gruence between histologic and endoscopic diagnoses of Barrett’s esophagus using transnasal esophagoscopy. Laryngoscope. 2006;116(2):303-6. 50. Wang KK, Sampliner RE; Practice Parameters Committee of the American College of Gastroenterology. Updated guidelines 2008 for the diagnosis, surveillance and therapy of Barrett’s esophagus. Am J Gastroenterol. 2008;103(3): 788-97. 51. Portale G, Hagen JA, Peters JH, et al. Modern 5-year survival of resectable esophageal adenocarcinoma: single institution experience with 263 patients. J Am Coll Surg. 2006;202(4):588-96; discussion 596-8. 52. Farwell DG, Rees CJ, Mouadeb DA, et al. Esophageal pathology in patients after treatment for head and neck cancer. Otolaryngol Head Neck Surg.2010;143(3):375-8. doi: 10.1016/j.otohns.2010.05.006. 53. Wang CP, Lee YC, Lou PJ, et al. Unsedated transnasal esophagogastroduodenoscopy for the evaluation of dys­ phagia following treatment for previous primary head neck cancer. Oral Oncol. 2009;45(7):615-20. doi: 10.1016/j. oraloncology.2008.08.013. Epub 2008 Nov 21. 54. Postma GN, Bach KK, Belafsky PC, et al. The role of transnasal esophagoscopy in head and neck oncology. Laryngoscope. 2002;112(12):2242-3.

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55. Carrick C, Collins KA, Lee CJ, et al. Sudden death due to asphyxia by esophageal polyp: two case reports and review of asphyxial deaths. Am J Forensic Med Pathol. 2005;26(3):275-81. 56. Tsao GJ, Damrose EJ. Complications of esophagoscopy in an academic training program. Otolaryngol Head Neck Surg. 2010;142(4):500-4. doi: 10.1016/j.otohns.2010.01.008.

57. Eroglu A, Turkyilmaz A, Aydin Y, et al. Current management of esophageal perforation: 20 years experience. Dis Esophagus. 2009;22(4):374-80. doi: 10.1111/j.1442-2050. 2008.00918.x. Epub 2009 Jan 9. 58. Vogel SB, Rout WR, Martin TD, et al. Esophageal perfora­ tion in adults: aggressive, conservative treatment lowers morbidity and mortality. Ann Surg. 2005;241(6):1016-21; discussion 1021-3.

Chapter 46: Cough

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CHAPTER

46

Cough Kenneth W Altman, Amanda L Richards, Rupali N Shah

INTRODUCTION Cough is a common problem that may significantly affect patients and pose a diagnostic challenge for physicians. An estimated 3% (27 million) of outpatient visits are attributable to acute and chronic cough. Prevalence has been estimated by surveys at 9–33% of the population. In 2006, US $3.6 billion was spent on over-the-counter cough and cold medications. Cough is an adaptive respiratory reflex that aids in respiratory clearance. It is stimulated by inflammation and irritation of the airway and mediated by sensory afferents of the vagus nerve. While cough may be a protective response in the short term, abnormal persistence is an indicator of underlying disease. As the concept of the uni­fied airway is consolidated and expanded, our under­ standing of the pathophysiology of cough mandates a true interdisciplinary approach. Cough affects patientsacross the generations and can be a manifestation of disease within otolaryngology, pulmonology medicine, allergy and immunology, gastroenterology, neurology, and psychia­ try. For patients, chronic cough can lead to significantly decreased physical and psychological quality of life.1 The cough reflex is protective, especially when the normal mucociliary transport mechanism is inadequate or overwhelmed.2 A coordinated release of air results in intrathoracic pressures as high as 300 mmHg and air velo­ cities up to 500 miles per hour. Patients often seek help secondary to the toll on the body after repeated vigorous coughing. Classification of cough, as determined by the duration of symptoms, includes acute cough ( 8 weeks). Patients with chronic cough seek medical attention more often. It is often multifactorial, and placing significant weight on one cause may lead to frustration for the patient and the physician. The otolaryngologist is often in a position to initiate and coordinate multidisciplinary care for these complex patients.1 The various disease contributions and interrelation of disciplines are shown in Figure 46.1. The concept of the unified airway is an integral com­ ponent to understanding and treating cough.3 The relation­ ship between the upper and lower airways is exemplified in allergy, with upper airway disease reflected in rhinitis and lower airway disease in exacerbation of asthma. Rhinosinusitis can also have the same result.4 Although not part of the airway per se, the gastrointestinal tract can markedly affect the local environment, leading to a direct inflammation or development of secondary edema.3 This chapter will focus on the care of patients with cough. It will highlight the pathophysiology of cough, history, and physical examination and delineate the differential diagnosis. It will also discuss the use of objec­ tive testing, interdisciplinary care, and treatment options.

PATHOPHYSIOLOGY OF COUGH A summary of the mechanisms involved in the normal cough reflex is important in understanding potential pathologic mechanisms. Figure 46.2 shows the interrelation of mechanisms inducing the cough reflex as a schematic of airway tissue.5 Multiple stimuli can be present, including topical airway infectious agents, inflammatory cytokines, the viscosity of the airway surface liquid and mucus,

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Fig. 46.1: Inter-relatedness of clinical disease relating to cough. Multiple mechanisms exist at both the local and systemic levels to account for synergy in exacerbation of disease processes. Note: systemic disease includes congestive heart failure, hypertension treated with angiotensin converting enzyme inhibitors, and cystic fibrosis. Tumor may have a direct effect on nerves triggering cough, particularly all branches of the vagus. It may also result in an indirect cause of cough through a postobstructive inflammatory/infectious process in the lung or paranasal sinuses. There are a number of mechanisms by which gastroesophageal reflux disease (GERD) may trigger cough, both directly related to gross or microspiration, as well as through neurologic reflex (see text). Aspiration may also occur independent of GERD. Source: Redrawn with permission from Altman and Irwin.1

Fig. 46.2: Interrelation of mechanisms inducing cough. Note: “•” denotes sensory receptor. Sensory receptors may include both cough receptors and C-fiber receptors in the lung. Although the latter communicates with slower conducting fibers to the brainstem, strong stimuli may result in an inhibitory effect. The transient receptor potential (TRP) family of ion channels and especially overexpression of TRPV1 (the capsaicin receptor) may also play a critical role on sensory triggers for cough. Also note that the cortex may have voluntary initiation of cough, as well as intended cough suppression. Source: Redrawn with permission from Altman and Irwin.1

gene-regulation pathologic mucus, and the temperature and pH of the airway surface. The starting point for neural activity begins with the sensory receptor.6 Different recep­ tors are activated from different stimuli to include: • TRPV1—transient receptor/ion channel potential vanil­loid 1, stimulated by acids, protons, and capsaicin • TRPA1—transient receptor potential ankyrin, stimu­ lated by cigarette smoke and toluene di-isocyanate • Cough receptors – myelinated nerves with a conduction velocity of 5 m/s • RAR—rapidly adapting receptors, functioning as mecha­noreceptors • SAR—slowly adapting receptors, responsible for sens­ing stretch • C-fiber afferents nerves—small diameter, slowly con­ ducting nerve with a velocity of 3% nonsqua­ mous sputum eosinophils).49 The etiology of asthma and NAEB is unknown but can be associated with exposure to inhaled aeroallergen or an occupational sensitizer.50

607

Microscopically, there are increased mast cells in the smooth muscle of asthmatic patients and in the mucosa of NAEB patients. The different pathways of immunologic airway inflammation for these two entities translate to their clinical manifestations. For most patients, the diagnosis of asthma has often already been made. Typical asthma is associated with wheezing, dyspnea, a reversible clinical nature, and some­times an identifiable trigger. CVA or cough as the initial presenting symptom for typical asthma, however, can have a limited history and non-diagnostic findings on examination and spirometry. It is recommended by the ACCP that these patients undergo methacholine inhalation challenge (MIC). Although a positive MIC is consistent with, but not diagnostic of CVA, a negative MIC essentially rules out asthma as the etiology of cough (i.e. high-negative predictive value).51 If MIC cannot be performed, then empiric treatment of asthma should be begun. Response to treatment without an MIC does not rule out NAEB.52 Partial response to an inhaled broncho­ dilator may be achieved initially, whereas complete reso­ lution may require up to eight weeks of treatment with inhaled corticosteroids.53,54 During the treatment, pulmo­ nology consultation should be considered. Bronchoscopy with bronchoalveolar lavage or induced sputum may identify patients who may benefit from more aggressive treatment. Refractory or severe symptoms may require stronger anti-inflammatory medications such as oral steroids. Patients with NAEB may present with cough as their sole presenting symptom. NAEB might be related to an allergen or occupational sensitizer. Often, they have a nondiagnostic examination and normal chest X-ray. Patients may not exhibit any objective evidence of variable airflow obstruction or airway hyper-responsiveness [MIC producing a 20% decrease in forced expiratory volume in one second (FEV1) of > 16 mg/mL].55 Pulmonology con­ sultation should be employed to aid in diagnosis. NAEB is confirmed by the presence of eosinophilia with sputum induction or bronchial wash fluid obtained with bronchoscopy. According to the ACCP, > 3% nonsquamous cell sputum eosinophil count is indicative of NAEB.55 Like other diagnoses for chronic cough, NAEB is confirmed with improvement with treatment. When an allergen or occupational sensitizer is elicited, avoidance is the best treatment. If no precipitant is identified, then an inhaled corticosteroid is first-line therapy. Currently, there are no data available that establish optimal dose and duration of

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inhaled steroid.55 If symptom control is not achieved, oral corticosteroids may be required; however, revisiting other potential causes of chronic cough is prudent.

Nonasthmatic Inflammatory Airway Disease in Adults Syndromes associated with chronic productive cough include chronic bronchitis, bronchiectasis, and bronchio­ litis. As previously mentioned, chronic bronchitis is a disease of bronchi characterized by an abnormal inflammatory response to gases and particles such as cigarette smoking. When there is airflow obstruction seen on spirometry, it is termed chronic obstructive pulmonary disease. Chronic sputum and cough occurs most days for three months of the year, for two years consecutively. In bronchiectasis, mucopurulent sputum is seen from chronic inflammation and infection. Bronchial wall damage and permanent destruction can occur, causing shortness of breath. Highresolution CT is the standard for diagnosis, classifying it as cylindrical, varicose, or cystic. It typically is recurrent and progressive. Goals of therapy are to mobilize secretions, to reduce inflammation, and to treat and prevent infection. A spectrum of processes can be at play in bronchiolitis. Small airways are affected by infectious, postinfectious, inflammatory, or idiopathic processes. Damage can be reversible or irreversible. Possible etiologies include, but are not limited to, Mycoplasma pneumoniae, Chlamydia pneumoniae, inhalation of organic or nonorganic material, systemic lupus erythematosus, rheumatoid arthritis, Sjogren’s syndrome, and radiation. Medications such as amiodarone, sulfasalazine, or cephalosporins may also contribute. Chest X-ray may show nonspecific findings, whereas high-resolution CT is most sensitive. Spirometry monitors severity and response to treatment. Management includes avoidance of exposures, discontinuation of any causative medications, and treatment with antimicrobial agents when infectious (Table 46.3).

NEUROGENIC COUGH Neurogenic cough is a chronic cough in the absence of typical external cough stimuli. Since it is far more common to have a direct medical cause for the cough, a neurogenic cough remains a diagnosis of exclusion. Although it can occur as a hypersensitization associated with other cough stimuli (e.g. the irritable larynx56), the neurogenic cough in isolation often has a characteristic presentation and is

Table 46.3: Nonasthmatic Inflammatory Airway Disease

Differential

Clinical Features

Objective Testing

Chronic Bronchitis

Cough and chronic sputum expectoration most days for at least 3 months for 2 consecutive years Expiratory flow limitation

Spirometry

Bronchiectasis Chronic cough and High-resolution mucopurulent sputum CT related to chronic inflammation and infection Leads to permanent destruction of bronchi Diffuse crackles or wheezes and coarse rhonchi Bronchiolitis

Spectrum of inflammatory processes that affect small airways Dry or productive cough with mucus particles, dyspnea, night sweats, fatigue, chest tightness Wheezing, inspiratory crackles, manifestations of systemic disorders

PFTs CXR High-resolution CT

thought to be related to sensory neuropathy.57 The paradox is, however, that although sensory neuropathy reduces nerve stimulation, the clinical presentation of neurogenic cough is that of hyper-excitability. Isolated idiopathic neurogenic cough often presents after a viral prodrome, so it is instructive to consider the evidence and mechanisms of viral-induced nerve injury in the larynx and elsewhere. There is evidence to support facial nerve palsy, sudden sensorineural hearing loss, vestibular neuronitis, and idiopathic vocal paresis/paraly­ sis to have viral causality. Associations with herpes simplex virus, varicella-zoster, Epstein–Barr virus, cytomegalovirus, and human immunodeficiency virus (HIV) have all been documented. A strong body of evidence was also recorded with vocal paralysis following the influenza epidemic 1969–1970.58 The pathophysiology of neuropathy in these and other conditions has been investigated and sheds insight into possible etiologies of neurogenic cough. The mechanism of nerve injury may be indirect through viral infection of its blood supply. For example, varicella zoster viralinduced optic neuropathy has been demonstrated to be related to temporal artery vasculitis.59 Similarly, hepatitis B virus-induced Guillain–Barré syndrome has been linked

Chapter 46: Cough to a systemic vasculitis-related mononeuritis multiplex.60 The viral infection may also have a direct effect on the nervous system, as with HIV peripheral neuropathy where viral RNA has been shown in the spinal cord.61 However, the diagnosis of infection-related neuro­ pathies can be challenging based on the pattern of deficits, geographic distribution of pathogens, length of time from infection to the development of the neuropathy, and variable mechanisms of nerve injury.62 The complexity of cough compared with the other conditions listed above also confounds defining a discrete mechanism of injury.63 In the situation of cough and neurogenic (or neuro­ adaptive) disease, the strongest scientific evidence sup­ ports multiple synergistic cough inputs sensitizing the brainstem, as well as a heightened brainstem reflex. The convergence of stimulatory inputs may have a paradoxical outcome, as in the case of vagal afferent nerve activation in one organ reflexively initiating changes in autonomic outflow to other organs.64,65 Also, while C-fiber activation is inconsistent at initiating cough in anesthetized animals, there appears to be a synergistic effect of C-fibers with cough receptor stimuli, similar to models of chronic pain.64,66 The inhibitory role at the brainstem of C-fiber activation from strong stimuli also presents an opportunity where a true sensory neuropathy may negate the negative control of the brainstem reflexes. The potential mechanisms of neurogenic cough are listed in Table 46.4, listed by site. This table also includes maladaptation with potential overlap of cough and res­ piratory nuclei at the brainstem, as well as neurologic and neuropsychiatric disease modulation of cough behavior at a cortical level. Understanding the pathophysiology empowers increased recognition of diagnosis and targets pathways for therapy for neurogenic cough.

RESPIRATORY DYSTONIA, COUGH, AND PVFM The brainstem nuclei responsible for cough in the nuc­ leus ambiguous are closely related to brainstem reflexes re­ sponsible for respiration. Consequently, there is an understandable overlap in the clinical presentation of patients with paroxysms of cough, and those with PVFM. The latter is a spectrum of disturbances that includes a group of patients with psychiatric disorders,67 but a significant portion of those patients with PVFM have true respiratory dystonia. Although the subject of PVFM is beyond the focus of this chapter, common treatments for cough and PVFM exist and are worthy of mention.

609

Table 46.4: Sites and proposed mechanisms for elements of neurogenic cough

Site

Examples

Mechanisms

Sensory receptors

Mechanoreceptors Chemical receptors TRP family of ion channels Cough receptor

Temperature sensitivity pH sensitivity Overexpression of TRPV1 Overexpression of others

Neuropeptides

Tachykinins (i.e. substance P)

Mediates afferent neural response

Afferent nerves

Small-diameter myelinated fiber Bronchial C-fibers

Axonal hyperexcitability Decreased inhibitory tone

Brainstem reflexes

Overlap of cough and respiratory nuclei

Brainstem trauma Neural adaptation

Cortex influence Altered perception Behavioral maladaptation Efferent neuromuscular spasm

Neurosis, psychosis Tic, habit, secondary gain

Efferent nerve overstimulation Muscular spasm

(TRP: Transient receptor potential; TRPV1: Vanilloid capsaicin receptor).

Respiratory retraining is a speech therapy approach that guides the breathing pattern to reduce stimulation of the cough reflex and PVFM behaviors. Similarly, laryngeal desensitization exercises can be performed to reduce laryngeal irritability.68 Pharmacologic suppression with medications used for neurogenic cough is also used. The use of laryngeal botulinum toxin injection into the thyroarytenoid muscles has been anecdotally observed to be effective in severe cases of cough, PVFM, and respira­ tory dystonia.69

CONCLUSION Treating patients with cough can be challenging due to the frequent multifactorial nature. The key to diagnosis remains a thorough, contemporaneous history, and the first objective should be to exclude serious underlying medical conditions. A protocolized approach to obtain chest radiography and eliminate ACE inhibitor as a first step is essential for setting the stage for more complicated patients. Stratification of cough based on duration will then allow for a more manageable differential diagnosis,

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and objective testing for chronic cough leads to better long-term management. More recent advances in the understanding of cough pathophysiology have recognized the concept of the unified airway, highlighting the role of a multidiscipline team to include the otolaryngologist, pulmonologist, gastroenterologist, speech pathologist, and others. This complex understanding of pathological cough also has relevance to treating patients with the irritable larynx and PVFM.

REFERENCES 1. Altman KW, Irwin RS. Cough: a new frontier in oto­laryn­ gology. Otolaryngol Head Neck Surg. 2011;144(3):348-52. 2. Madison JM, Irwin RS. Cough: a worldwide problem. Otolaryngol Clin North Am. 2010;43(1):1-13, vii. 3. Krouse JH, Altman KW. Rhinogenic laryngitis, cough, and the unified airway. Otolaryngol Clin North Am. 2010; 43(1):111-21. 4. Krouse JH. The unified airway—conceptual framework. Otolaryngol Clin North Am. 2008;41(2):257-66, v. 5. Altman KW, Irwin RS. Cough specialists collaborate for an interdisciplinary problem, Otolaryngol Clin N Am. 2010; 43:xv-xix. 6. Canning BJ. Afferent nerves regulating the cough reflex: mechanisms and mediators of cough in disease. Otolaryngol Clin N Am. 2010;43:15-25. 7. Barnes PJ. Neurogenic inflammation in the airways. Respir Physiol. 2001;125:145-54. 8. Kuzniar TJ, Morgenthaler TI, Afessa B, et al. Chronic cough from the patient's perspective. Mayo Clin. Proc. 2007; 82(1):56-60. 9. Irwin RS, Baumann MH, Bolser DC, et al. Diagnosis and management of cough executive summary: ACCP evidencebased clinical practice guidelines. Chest. 2006;129(1 Suppl):1S-23S. 10. Morice AH, McGarvey L, Pavord I, British Thoracic Society Cough Guideline Group. Recommendations for the man­ agement of cough in adults. Thorax. 2006;61(Suppl 1): i1–24. 11. Cerveri I, Accordini S, Corsico A, et al. Chronic cough and phlegm in young adults. Eur Respir J. 2003;22(3):413-7. 12. Irwin RS, Madison JM. The persistently troublesome cough. Am J Respir Crit Care Med. 2002;165(11):1469-74. 13. Irwin RS, Curley FJ, French CL. Chronic cough. The spectrum and frequency of causes, key components of the diagnostic evaluation, and outcome of specific therapy. Am Rev Respir Dis. 1990;141(3):640-7. 14. Irwin RS, Boulet LP, Cloutier MM, et al. Managing cough as a defense mechanism and as a symptom. A consensus panel report of the American College of Chest Physicians. Chest. 1998;114:133S-81S. 15. Rubin BK. Mucus and mucins. Otolaryngol Clin North Am. 2010;43(1):27-34, vii–viii. 16. Morice AH. Epidemiology of cough. Pulm Pharmacol Ther. 2002;15(3):253-9.

17. 2010_Top_Therapeutic_Classes_by_RX.pdf.imshealth.com. http://www.imshealth.com/deployedfiles/ims/Global/ Content/Corporate/Press%20Room/Top-line%20Market% 20Data/2010%20Top-line%20Market%20Data/2010_Top_ Therapeutic_Classes_by_RX.pdf. [Last accessed 4 Jan 2012. 18. Lacourcière Y, Brunner H, Irwin R, et al. Effects of modulators of the renin-angiotensin-aldosterone system on cough. Losartan Cough Study Group. J Hypertens. 1994; 12(12):1387-93. 19 US Department of Labor. The OSHA Hazard Comm­unica­ tion Standard (HCS) Regulations (Standards-29 CFR). USA, Occupational Safety and Health Administration (OSHA). Appendix A to the Hazard Communication Standard, 1994. 20. Pavord ID, Wardlaw AJ. The A to E of airway disease. Clin Exp Allergy. 2010;40(1):62-7. 21. Jansen DF, Schouten JP, Vonk JM, et al. Smoking and airway hyperresponsiveness especially in the presence of blood eosinophilia increase the risk to develop respiratory symptoms: a 25-year follow-up study in the general adult population. Am J Respir Crit Care Med. 1999;160(1):259-64. 22. Janson C, Chinn S, Jarvis D, et al. Effect of passive smoking on respiratory symptoms, bronchial responsiveness, lung function, and total serum IgE in the European Community Respiratory Health Survey: a cross-sectional study. Lancet. 2001;358(9299):2103-9. 23. Larsson ML, Loit HM, Meren M, et al. Passive smoking and respiratory symptoms in the FinEsS Study. Eur Respir J. 2003;21(4):672-6. 24. Brooks SM. Occupational, environment, and irritantinduced cough. Otolaryngol Clin N Am. 2010;43:85-96. 25. Curley FJ, Irwin RS, Pratter MR, et al. Cough and the common cold. Am Rev Respir Dis. 1988;138(2):305-11. 26. Diehr P, Wood RW, Bushyhead J, et al. Prediction of pneu­monia in outpatients with acute cough – a statistical approach. J Chronic Dis. 1984;37(3):215-25. 27. Bolser DC. Pharmacologic management of cough. Oto­ laryngol Clin North Am. 2010;43(1):147-55, xi. 28. Pavord ID, Chung KF. Management of chronic cough. Lancet. 2008;371(9621):1375-84. 29. Braman SS. Postinfectious cough: ACCP evidence-based clinical practice guidelines. Chest. 2006;129(1 Suppl):138S-46S. 30. Rohani P, Drake JM. The decline and resurgence of pertussis in the US. Epidemics. 2011;3(3-4):183-8. 31. Hoppe JE. Comparison of erythromycin estolate and erythromycin ethylsuccinate for treatment of pertussis. The Erythromycin Study Group. Pediatr Infect Dis J. 1992; 11(3):189-93. 32. Murry T, Sapienza C. The role of voice therapy in the management of paradoxical vocal fold motion, chronic cough, and laryngospasm. Otolaryngol Clin North Am. 2010;43(1):43-66. 33. Irwin RS. Unexplained cough in the adult. Otolaryngol Clin North Am. 2010;43(1):167-80, xi–xii. 34. Smyrnios NA, Irwin RS, Curley FJ, et al. From a prospective study of chronic cough: diagnostic and therapeutic aspects in older adults. Arch Int Med. 1998;158(11):1222.

Chapter 46: Cough 35. Pratter MR. Chronic upper airway cough syndrome secondary to rhinosinus diseases (previously referred to as postnasal drip syndrome): ACCP evidence-based clinical practice guidelines. Chest. 2006;129(1 Suppl):63S-71S. 36. Naclerio RM. Allergic rhinitis. N Engl J Med. 1991;325 (12):860-9. 37. Koufman JA. Laryngopharyngeal reflux is different from classic gastroesophageal reflux disease. Ear Nose Throat J. 2002;81(9 Suppl 2):7-9. 38. Merati AL. Reflux and cough. Otolaryngol Clin North Am. 2010;43(1):97-110, ix. 39. Adhami T, Goldblum JR, Richter JE, et al. The role of gastric and duodenal agents in laryngeal injury: an experimental canine model. Am J Gastroenterol. 2004;99(11):2098-106. 40. Johnston N, Dettmar PW, Bishwokarma B, et al. Activity/ stability of human pepsin: implications for reflux attributed laryngeal disease. Laryngoscope. 2007;117(6):1036-9. 41. Irwin RS, French CL, Curley FJ, et al. Chronic cough due to gastroesophageal reflux. Clinical, diagnostic, and pathogenetic aspects. Chest. 1993;104(5):1511-7. 42. Irwin RS. Chronic cough due to gastroesophageal reflux disease: ACCP evidence-based clinical practice guidelines. Chest. 2006;129(1 Suppl):80S-94S. 43. Hanson DG, Jiang J, Chi W. Quantitative color analysis of laryngeal erythema in chronic posterior laryngitis. J Voice. 1998;12(1):78-83. 44. Park W, Hicks DM, Khandwala F, et al. Laryngopharyngeal reflux: prospective cohort study evaluating optimal dose of proton-pump inhibitor therapy and pretherapy predictors of response. Laryngoscope. 2005;115(7):1230-8. 45. Richter JE, Castell DO. Gastroesophageal reflux. Pathogenesis, diagnosis, and therapy. Ann Intern Med. 1982;97(1):93-103. 46. Sifrim D, Dupont L, Blondeau K, et al. Weakly acidic reflux in patients with chronic unexplained cough during 24 hour pressure, pH, and impedance monitoring. Gut. 2005;54(4):449-54. 47. Agrawal A, Roberts J, Sharma N, et al. Symptoms with acid and nonacid reflux may be produced by different mechanisms. Dis Esophagus. 2009;22(5):467-70. 48. Corrao WM, Braman SS, Irwin RS. Chronic cough as the sole presenting manifestation of bronchial asthma. N Engl J Med. 1979;300(12):633-7. 49. Brightling CE, Ward R, Goh KL, Wardlaw AJ, et al. Eosinophilic bronchitis is an important cause of chronic cough. Am J Respir Criti Care Med. 1999;160(2):406-10. 50. Berry MA, Hargadon B, McKenna S, et al. Observational study of the natural history of eosinophilic bronchitis. Clin Exp Allergy. 2005;35(5):598-601. 51. Crapo RO, Casaburi R, Coates AL, et al. Guidelines for methacholine and exercise challenge testing-1999. This official statement of the American Thoracic Society was adopted by the ATS Board of Directors, July 1999. Am J Respir Crit Care Med. 2000;161(1):309-29.

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52. Dicpinigaitis PV. Chronic cough due to asthma: ACCP evi­ dence-based clinical practice guidelines. Chest. 2006;129(1 Suppl):75S-9S. 53. Cheriyan S, Greenberger PA, Patterson R. Outcome of cough variant asthma treated with inhaled steroids. Ann Allergy. 1994;73(6):478-80. 54. Irwin RS, French CT, Smyrnios NA, et al. Interpretation of positive results of a methacholine inhalation challenge and 1 week of inhaled bronchodilator use in diagnosing and treating cough-variant asthma. Arch Intern Med. 1997; 157(17):1981-7. 55. Brightling CE. Chronic cough due to nonasthmatic eosinophilic bronchitis: ACCP evidence-based clinical practice guidelines. Chest. 2006;129(1 Suppl):116S–21S. 56. Morrison M, Rammage L, Emami AJ. The irritable larynx syndrome. J Voice 1999;13:447-55. 57. Lee H, Woo P. Chronic cough as a sign of laryngeal sensory neuropathy: diagnosis and treatment. Ann Otol Rhinol Laryngol. 2005;114:253-7. 58. Bryson A. Neurological complications of influenza A2-Hong Kong-68 virus. 1970;2(14):654. 59. Nagel MA, Traktinskiy I, Stenmark KR, et al. Varicellazoster virus vasculopathy: immune characteristics of virusinfected arteries. Neurology. 2013; 80(1):62-8. 60. Mehndiratta M, Pandey S, Nayak R, et al. Acute onset distal symmetrical vasculitic polyneuropathy associated with acute hepatitis B. J Clin Neurosci. 2013;20(2):331-2. 61. Cao L, Butler MB, Tan L, et al. Murine immunodeficiency virus-induced peripheral neuropathy and the associated cytokine responses. J Immunol. 2012;189(7):3724-33. 62. Robinson-Papp J. Infectious neuropathies. Continuum. 2012;18(1):126-38. 63. Irwin RS. Unexplained cough in the adult. Otolaryngol Clin N Am. 2010;43:167-80. 64. Canning BJ, Chou YL. Cough sensors. I. Physiological and pharmacological properties of the afferent nerves regulating cough. Handb Exp Pharmacol. 2009;187: 23-47. 65. Mazzone SB, McGovern AE. Na+-K+-2Cl- cotransporters and Cl- channels regulate citric acid cough in guinea pigs. J Appl Physiol. 2006;101(2):635-43. 66. Paton JF. Pattern of cardiorespiratory afferent convergence to solitary tract neurons driven by pulmonary vagal C-fiber stimulation in the mouse. J Neurophysiol. 1998;79(5):2365-73. 67. Christopher KL, Morris MJ. Vocal cord dysfunction, para­ doxic vocal fold motion, or laryngomalacia? Our under­ standing requires an interdisciplinary approach. Otolaryngolog Clin North Am. 2010;43(1):43-66. 68. McCabe D, Altman KW. Laryngeal hypersensitivity in the World Trade Center-exposed population: the role for respiratory retraining. Am J Respir Crit Care Med. 2012; 186(5):402-3 69. Altman KW, Mirza N, Ruiz C, et al. Paradoxical vocal fold motion: presentation and treatment options. J Voice. 2000;14(1):99-103.

Chapter 47: Pulmonary Disorders and Voice

613

CHAPTER

47

Pulmonary Disorders and Voice Amanda I Gillespie, Seema Jeswani, Ryan C Branski

INTRODUCTION This chapter outlines the role of the larynx as part of the respiratory system and reviews the effects of common respiratory and respiratory-related disorders on laryngeal function, as well as voice disorders with strong respiratory components. The impact of treatments for respiratory disease on voice is also discussed.

BASIC LARYNGEAL–RESPIRATORY PHYSIOLOGY During normal tidal breathing, the upper airway provides 25–60% of overall respiratory resistance.1-3 The larynx is an important factor in the determination of respiratory resistance, airflow volume, and rate of breathing. Laryngeal resistance during breathing changes to meet ventilatory needs. During inspiration for tidal (normal) breathing, the glottal opening is wide, providing low resistance. For tidal expiration, the vocal folds move slightly toward midline, and resistance increases marginally compared with inspiration.1,4,5 Inspiratory resistance is typically lower than expiratory resistance.3,4 Air pressure and airflow interact with the vocal folds for finely tuned adjustments necessary to create alterations in voicing (onsets and offsets), intensity, and frequency.6 Lung volumes change with varying intensity and length demands of upcoming utterances, implying a preplanning of the respiratory–laryngeal system to meet communicative needs.7 In addition, the major inspiratory muscle, the diaphragm, is active throughout phonated phrases to make fine pressure and airflow adjustments

necessary in connected speech.8,9 Abdominal and thoracic respiratory musculature coactivate during speech for optimal control of respiration during phonation.9 Normal respiration can be functionally over-ridden by higher level cognitive communicative demands.8

VOICE PROBLEMS IN RESPIRATORY DISEASE Obstructive Disorders Asthma Asthma is a chronic inflammatory disorder associated with increased airway hyper-responsiveness. It is cur­rently estimated that 300 million people suffer from the condi­ tion worldwide, and its prevalence increases by 50% every decade.10 Individuals with asthma or other lung disease have a greater likelihood of experiencing dysphonia than individuals without lung disease.11 Asthma co-occurs in up to 38% of adult patients with muscle tension dysphonia (MTD), a voice problem in the absence of structural or neurologic pathology.12 Comorbid asthma and voice prob­ lems affect children as well, with some estimates revealing 7% of children with asthma are dysphonic.13 Patients with asthma present with reduced maximum phonation times, increased noise to harmonic ratio, and perceptually dysphonic voices when compared with nonasthmatic speakers.14 When bronchoconstricted during acute asthma attack, laryngeal resistance during expiration is increased from baseline.15,16 This increased resistance is thought to aid

614

Section 4: Voice Disorders

Fig. 47.1: Laryngeal presentation of a 39-year-old male with asthma requiring inhaled corticosteroids treatment. He presented with a two-week history of progressively worsening dysphonia.

in hyperinflation of the lower airways, preventing further alveolar collapse.15 Glottal narrowing may also represent an efferent response to the attack, which stimulates laryn­ geal afferents.15 Inhaled corticosteroids (ICS) represent the pharma­ cologic standard of care for patients with asthma. Dyspho­ nia associated with ICS occurs in between 8% and 58% of patients.17 Although asthmatics may have a predilection for reduced lung function for phonatory support, inhaled steroid treatment is also likely contributory to dysphonia. The most common cause of ICS-associated dysphonia is candidiasis (fungal laryngitis) associated with ICS use. Candida can present in the pharynx, supraglottis, and glottis.18 It is typically treated with oral antifungal medications. Typical laryngoscopic findings of dysphonic asthmatic patients on steroid treatment include mucosal changes (often fungal in nature), vocal fold bowing, and supraglottic hyperfunction.19 Whether these changes are due to the steroid itself or the delivery media has not been established. Use of a spacer, gargling after treatment, and either cessation or alteration of steroid use until improve­ ment of symptoms has been suggested (Fig. 47.1).20

Chronic Obstructive Pulmonary Disease Chronic obstructive pulmonary disease (COPD) is a respiratory disease encompassing chronic bronchitis and emphysema. COPD is the fourth leading cause of death in the United States and affects approximately 14% of adults worldwide.21 Cigarette smoking is the primary risk factor for developing COPD.21 Airflow obstruction in

COPD is characterized by a rapid decline in forced expi­ ratory volume in one second caused by decreased lung elastic recoil associated with airway inflammation, fibrosis, increased mucous production, and smooth muscle hyper­ trophy.21 Lung hyperinflation and thoracic volume increase as the condition progresses21 and contribute to the heigh­ tened physical work of breathing in people with COPD, as well as increased perception of dyspnea. Relevant to the present chapter, dyspnea during speech is common in people with COPD.22 Specifically, individuals with COPD complain of dyspnea with loud voice use, singing, and phonating in background noise.23 Lung hyperinflation and related high lung volumes in COPD may make it more difficult for the larynx to control resistance appropriate for phonation. In addition, recent data suggest individuals with COPD may have reduced laryngeal sensitivity, which may contribute to voice and swallowing dysfunction.24 Relatedly, a disco-ordination between breathing and swallowing has been implicated as a cause of oropharyngeal dysphagia in people with COPD.25 Pharmacologically, bronchodilators and ICS are often used in conjunction to treat COPD.26 Behaviorally, respiratory muscle strength training has been found to improve quality of life and decrease dyspneic symptoms in people with COPD.23,27 As with asthma, ICS therapy may have deleterious effects on laryngeal mucosa and further contribute to voice problems in this population.

RESTRICTIVE DISORDERS Idiopathic Pulmonary Fibrosis Idiopathic pulmonary fibrosis (IPF) is a chronic, progres­ sive, fibrotic disease of the lung interstitium occurring in approximately 4 per 100,000 persons aged 18–34 years, and in up to approximately 227 per 100,000 among those ≥   7 5 years.28 The literature is sparse with regard to the impact of this process on phonation, but one might presume that the vocal symptoms likely do not differ significantly from those in patients with obstructive pulmonary disease. However, recent reports indicated that laryngeal resis­tance was, in fact, reduced in patients with IPF when compared with control subjects and patients with COPD. Furthermore, greater variability in laryngeal resistance was observed in patients with IPF compared with patients with COPD or controls. These data support the active role of the larynx in respiration, particularly in individuals with compromised pulmonary function.29

Chapter 47: Pulmonary Disorders and Voice

Fig. 47.2: Intraoperative photo of a 69-year-old woman who presen­ ted with one year of progressive dysphonia. Pathology report from biopsy of true vocal fold lesions revealed laryngeal tuberculosis. Source: Libby Smith, DO.

Sarcoidosis Sarcoidosis is a systemic inflammatory process that can affect any organ, but pulmonary localization is the most common manifestation. The larynx is rarely affected, but it may occur in isolation or as a component of systemic disease. Symptoms for laryngeal involvement include hoarseness, dysphagia, dyspnea, and life-threatening airway obstruction.30 Respiration may be compromised due impaired pulmonary function or direct impact of disease on the larynx itself. Furthermore, treatments for sarcoidosis involving the larynx include tracheotomy, low-dose radiation, surgical excision, systemic steroids, and intralesional steroids,31 all of which are likely to have a deleterious effect on voice.

TUBERCULOSIS Tuberculosis (TB) is a multisystem disease caused by the pathogen Mycobacterium tuberculosis, with myriad presentations and manifestations. An estimated 8.7 million new cases of TB were diagnosed in 2011, with the majority of disease burden in Asia and South Africa.32 Laryngeal TB is one of the most common extrapulmonary disease manifestations with a reported incidence varying from  5 mm in length. The elevation of the inner perichondrium is only posterior, and the gortex is carefully packed posteriorly, taking time after each small amount is packed to make sure that the gortex is not too high or over packed (Fig 64.7). Unlike silastic, where modifications can be easily made, a high gortex implant or one that is overcorrected makes it very difficult to correct. Once placed, the gortex can be held in place with a stitch through the cartilage at the level of the window. An arytenoid adduction or an arytenoidopexy13 can be performed at the same time as silastic medialization. Although many surgeons perform these relatively routi­ nely,12 they are procedures that require more experience, particularly the arytenoidopexy. I have also found that there are very few cases where this is needed. A well carved and placed silastic implant will serve to correct almost all glottal gaps. In addition, there are no reported series of arytenoid adduction either with or without silastic that are better than those described by my procedure above. Nonetheless, in the rare cases that this is needed, the silastic is carved and placed as noted above, and then removed. A posterior window is made in the thyroid carti­lage (Fig. 64.8) exposing the arytenoid and a stitch is placed an pulled forward and tied in a location that will allow rotation of the vocal process to rotate medially and at a vertical plane that is at the same level of the other side (Figs. 64.9 and 64.10). An AA can be done

indepen­dently, where the suture would be tied into posi­ tion after confirming the amount of tension on the suture by both visualization and listening to the patient voice and MPT. In most cases, silastic is used with the AA and in such cases the silastic is then replaced and vocal fold posi­tion is verified, at which time the suture can be tied through the thyroid cartilage. The patients do not go to the recovery room and return directly to the in and out center. We re-evaluate the larynx 2–3 h after the surgery. If there is no swelling or significant bruising they are discharged to home. If they come from a long distance (many of our patients do), they are dis­ charged to a local hotel. Only patients who have bila­teral medializations or those who have an arytenoid add­uc­ tion are admitted to hospital for 24 h. They are seen back the next day for dressing and drain removal, steri-strips are applied and a light pressure dressing is placed for an additional 24 h. They can get the incision wet and if there is any drainage from the drain site, a small dressing or bandage can be applied. They are asked to use their voices carefully and with no heavy lifting or straining for 10 days. They are seen back for follow-up in six weeks if there are no problems. The patient is cautioned that intubation in the future should be done carefully and with a small endotracheal tube, while nonintubation anesth­esia either by mask or a laryngeal-mask airway is preferred in patients who have had a prior ML.

Chapter 64: Medialization Laryngoplasty (Thyroplasty) and Arytenoid Rotation/Adduction

Fig. 64.9: A stitch is placed in the posterior arytenoid to allow for rotation of the vocal process to the midline, further medializing the vocal fold. Courtesy: Cleveland Clinic Foundation.

CONCLUSION Medialization laryngoplasty with or without an aryte­ noid procedure has become one of the most utilized and predictably successful procedures for the treatment of UVFP. The results support consideration for ML as the primary surgical procedure for patients requiring a per­ manent procedure for UVFP. Outcomes are predictable and immediate, complications are rare, and revisions are very uncommon.

REFERENCES 1. Rosenthal-Swibel L, Benninger MS, Deeb RH. Vocal fold immobility: A longitudinal analysis of etiology over 30 years. Laryngoscope. 2007;117:1864-70. 2. Friedman AD, Burns JA, Heaton JT, et al. Early versus late injection medicalization for unilateral vocal fold paralysis. Laryngoscope. 2010;120:2042-46. 3. Arviso LC, Johns MM, Mathison CC, et al. Long-term outcomes of injection laryngoplasty in patients with potentially recoverable vocal fold paralysis. Laryngoscope. 2010;120:2237-40. 4. Smith LJ, Rosen CA, Niyonkuru C, et al. Quantitative elec­ tromyography improves prediction in vocal fold paralysis. Laryngoscope. 2012;122:855-59.

811

Fig. 64.10: With the stitch in placed in the posterior arytenoid it can be pulled anteriorly until the medial position of the vocal fold is confirmed with visualization and listening to the voice. After the silastic is placed, the suture can be tied to hold in position. Courtesy: Cleveland Clinic Foundation.

5. Jacobson BH, Johnson A, Grywalski C, et al. The voice handicap index (VHI): development and validation. J Speech-Lang Path. 1997;6:66-70. 6. Lundy DS, Casiano RR, Xue JW. Can maximum phona­ tion time predict voice outcome after thyroplasty Type I? Laryngoscope. 2004;114:1447-54. 7. Isshiki N, Morita H, Okamura H, et al. Thyroplasty as a new phonosurgical technique. Acta Otolaryngol. 1974;78:451-17. 8. Friedrich G. Titanium vocal fold medializing implant: introducing a novel implant system for external vocal fold medialization. Ann Otol Rhinol Laryngol. 1999;108:79-86. 9. Schneider B, Denk DM, Bigenzahn W. Acoustic assessment of the voice quality before and after medialization thyro­ plasty using the titanium vocal fold medialization implant (TVFMI). Otolaryngol Head Neck Surg. 20031;128:815-22. 10. Montgomery WW, Montgomery SK. Montgomery thyro­ plasty implant system. Ann Otol Rhinol Laryngol. 1997; 106:1-16. 11. Cummings CW, Purcell LL, Flint PW. Hydroxylapatite laryngeal implant for medialization. Preliminary report. Ann Otol Rhinol Laryngol. 1993;102:843-51. 12. Netterville JL, Stone RE, Civantos FJ, et al. Silastic medi­ alization and arytenoid adduction: the Vanderbilt experi­ ence: a review of 116 phonosurgical procedures. Ann Otol Rhinol Laryngol. 1993;102:413-24. 13. Zeitels SM, Hochman I, Hillman RE. Adduction aryte­ nopexy: a new procedure for paralytic dysphonia with implications for implant medialization. Ann Otol Rhinol Laryngol. 1998;173:2-24.

Chapter 65: Reinnervation

813

CHAPTER Reinnervation

65

Robert R Lorenz, Roger L Crumley

HISTORY OF LARYNGEAL REINNERVATION Laryngeal reinnervation has fascinated surgeons for many decades. Surgeons in the early 1900s attempted various means to rehabilitate vocal folds paralyzed by recurrent laryngeal nerve (RLN) injuries. The first known successful case of laryngeal reinnervation for unilateral vocal fold paralysis (VFP) was reported by Frazier in 1924.1 In this paper, Frazier described a single case report of successful restoration of voice with an ansa hypoglossi–RLN anas­ tomosis. However, this did little to influence the accep­tance of reinnervation as an option, and many other proce­dures were subsequently described. Many of these experimen­ tal procedures were attempts to restore inspiratory abduc­ tion to a paralyzed vocal fold and were designed for potential use in patients with bilateral VFP. It was not until the 1960s when laryngeal transplanta­ tion prompted further utilization of reinnervation techni­ ques. Takenouchi and Ogura described usage of an ansa hypoglossi neuromuscular pedicle in 1967.2,3 Tucker, how­ ever, refined and popularized the technique in a series of publications.4-6 Although these techniques were origi­ nally designed to restore abductive movement in bilateral VFP with airway impairment, they avowed that it was possible to restore meaningful innervation to laryngeal muscle, whether it be abductive [posterior cricoarytenoid (PCA)] or adductive means. The era of laryngeal reinner­ vation investigation was thereby launched by the Tucker, Ogura, and Takenouchi group of scientists. Tucker’s concept of laryngeal reinnervation, with a nerve–muscle pedicle incorporating a portion of anterior

belly of the omohyoid muscle inserted into the PCA muscle for abduction in patients with bilateral VFP. Tucker subsequently modified this approach for manage­ ment of unilateral VFP and implanted the pedicle into the TA muscle. However, the subsequent lack of reproducibi­ lity of his results by the larger laryngology community may have resulted from the fact that most patients with laryngeal paralysis have some amount of intact dysfunc­ tional or limited innervation to the TA muscle, and it is not physiologically possible to reinnervate an already innervated muscle, even if the existing innervation is suboptimal. The senior author’s Triological thesis was in part designed to further research the mechanisms inherent in the neuromuscular pedicle technique, while trying an alternative type of reinnervation utilizing nerve transfer as opposed to the nerve–muscle pedicle technique.

MODERN-DAY REINNERVATION: NERVE TRANSFER In 1982, the senior author published his Triologic Society thesis on selective laryngeal reinnervation for bilateral VFP utilizing phrenic nerve transfer to the PCA muscle7 (Fig. 65.1). He subsequently (1984) described several selective rein­nervation techniques using the aforemen­ tioned phrenic transfer to PCA, and combining it with attem­pted selective reinnervated VF adduction using other nerves, including the ansa-hypoglossi/cervicalis to the adductor division of RLN.8 Since the RLN is transected, this would avoid the problem of existing innervation preventing reinnervation. Subsequently, many scientists

814

Section 6. Vocal Fold Paralysis/Paresis

Fig. 65.1: Modern-day reinnervation technique: nerve transfer with direct anastomosis from the ansa to the RLN.

and surgeons have focused on reinnervation for unila­ teral/VF paralysis using branches from the ansa cervi­ calis/ansa hypoglossi nerve loop that supplies branches to the strap muscles anastomosed to the RLN (Fig. 65.2).8,9 By providing a new nerve supply, the para­lyzed vocal fold often achieves a median position, with muscular ten­sion and bulk similar to the nonimpaired vocal fold. The abductor and adductor fibers within the RLN are distributed randomly, and when regenerated axons extend within the endoneurial tubules, they reinner­ vate both abductor and adductor muscles.10 Since the adductor mus­cles as a group are stronger than abductors, the rein­ nervated vocal fold repositions itself at or near the midline, resulting in complete glottic closure during phonation.11 In addition, the ansa cervicalis provides a resting tone to the reinnervated muscles, providing low-amplitude, weak neural excitation that restores vocal fold bulk, tone, and tension to the reinnervated cord, rather than functional motion (Type I synkinesis).11a This combination of features allows the vocal folds to meet during phonation and to have sufficient symmetry to prevent irregular oscillation during most phonatory tasks. Swallowing function and the efficiency of cough are also usually improved. It is important to counsel patients preoperatively that return of motion of the affected vocal fold in abduction and adduction is neither intended nor achieved. Then, the goal of this procedure is to restore quiet resting muscle tone to the four intrinsic muscles and, importantly, to restore relatively normal anatomic positioning of the arytenoid cartilage, its vocal process, and accordingly the posterior vocal fold.

Fig. 65.2: Schematic diagram for left VFP, directly anastomosing the transected strap muscle nerve stump off of the ansa hypoglossi ansa cervicalis loop to the RLN.

Indications/Contraindications (Table 65.1) • Unilateral vocal fold motion impairment resulting from RLN injury • This operation generally can be done at any time following unilateral RLN injury, but it is generally preferred to wait 9 months or longer, so as not to preclude recovery via spontaneous RLN regeneration (except in cases of obvious and known complete RLN transection). • Laryngeal electromyography (LEMG) is commonly utilized to confirm that denervation (fibrillation poten­tials) is present in one or more of the intrinsic mus­ cles, most commonly the TA muscle. This is especially helpful in paralysis of more than 2 years duration to rule out electrical silence that suggests either nonfunctional motor endplates, muscular dener­vation atrophy or scar, any of which will lead to unsuccessful reinnervation results. In addition to fibrillation potentials, excellent results may be obtained if either polyphasic or normal motor action poten­ tials are seen. Therefore, in patients with poor vocal quality in association with laryngeal synkinesis, this operation can restore excellent vocal/phonatory results

Chapter 65: Reinnervation

815

Table 65.1: Candidacy for favorable reinnervation results

Favorable

Unfavorable

Age

Less than 70 years

Greater than 70

Co-morbidities

None, good nutritional status

Diabetic, steroid use, cancer

Timing

Within 2 years of onset

Paralysis for greater than 2 years

Results expectations

Can tolerate 3–4 months wait

Need immediate improvement

Paralysis cause

Idiopathic, vagal or distal RLN

Injury at RLN insertion site

Ansa status

Intact with stimulation of muscle

Known injury to ansa system, ipsilateral or bilateral

EMG findings (first 18 months)

No need for EMG

(No need)

EMG findings (after 18 months)

Action or fibrillation potentials

Electrical silence

•

•

•

•

•

by restoring quiet resting tone to all four intrin­sic muscles [TA, lateral cricoarytenoid, interaryte­noid (IA), and PCA]. Adductor spasmodic dysphonia in select cases (most commonly when patients do not tolerate Botox injec­ tions or wish a more permanent resolution of symp­ toms after having attempted repeat Botox therapy). Prior irradiation and other comorbidities, such as dia­ betes, are not absolute contraindications, but patients should be advised that results may be affec­ ted by suboptimal nerve regeneration and perhaps should consider a different technique, such as media­ lization thyroplasty. Older patients regenerate nerves at a slower rate and will take longer for the reinnervation to occur. Young patients are good candidates for laryngeal reinner­va­ tion, assuming that a functional TA muscle has suc­ cessfully developed and has been verified with LEMG. When deciding between medialization with an implant versus reinnervation, neither procedure precludes the other. While implantation is theoretically reversible, one might suspect that the resulting paraglottic space scar may affect future reinnervation results, while reinnervation avoids damage to laryngeal structure, and therefore might be preferred initially in a possible sequential situation. The time from operation to the usual synkinetic result and subsequent voice restoration is dependent on the length of the RLN stump to which the donor nerve is anastomosed. Previous injury at the cricoarytenoid joint during thyroidectomy or invasion from thyroid cancer does not preclude reinnervation, since the nerve can be dissected through the cricopharyngeus muscle and even intralaryngeal via a thyroid cartilage window creation (Figs. 65.3 and 65.4). There are two

loops of the ansa cervicalis nerve root system: the anterior (also referred to as the ansa hypoglossi) and the posterior (which arises from the cervical nerve rootlets). If either of these branches of the loop has been sacrificed, the resulting branch can be stimulated intraoperatively to determine if it has significant innervation to the resultant strap muscles and can still be used as a donor nerve successfully. If not, the contralateral ansa cervicalis is preferred.

REINNERVATION SURGICAL PROCEDURE Reinnervation for unilateral vocal cord paralysis is most commonly performed under general anesthesia due to the intraoperative manipulation of the laryngeal structure and the possible need for extensive dissection if the RLN stump is encased in scar. Often, patients with the need for immediate voice improvement cannot tolerate the 2–4 months of waiting for axonal regrowth and wish to undergo temporary injection medialization concurrently. The sequence of procedures must be decided upon, since patients with injection medialization performed first may have the injectate compressed or misaligned by the subse­ quent endotracheal tube, while patients who undergo inje­ ction second have increased laryngeal swelling to content with when judging the correct amount of medialization material to inject. A horizontal incision is created in a position similar to a thyroidectomy and often biased to the side of the reinnervation. The approach is most commonly lateral to the strap muscles, since the area dissected must be con­ nected between donor and recipient nerves. The loop of the ansa is encountered immediately after dissecting beneath the omohyoid muscle that is transected and immediately superficial to the internal jugular vein. While the nerve branches of the ansa that supply the sterno­

816

Section 6. Vocal Fold Paralysis/Paresis

Fig. 65.3: In cases of traumatized RLN from previous surgery, the cricopharyngeus is divided off the lateral border of the thyroid cartilage to allow for dissection of the RLN (seen here parallel to the trachea) into the laryngeal musculature.

Fig. 65.4: By rotating the thyroid cartilage medially, locating the RLN is facilitated by using the handle of the hook as a guide, which points directly at the RLN, 3–4 mm off the rotated cartilage.

hyoid muscle provide the maximum length for a donor nerve, the authors commonly utilize the common stump of nerve that branches to supply the strap muscles off of the ansa loop to provide an excellent size match to the RLN. If this proves to be insufficient in length to react with the laryngeal area, either the two arms of the loop can be mobilized superiorly or the RLN can be divided more distally to increase the recipient length contribution. If the RLN injury is from a vagal or chest injury, there should not be a significant scar in the cricothyroid joint region to interfere with dissection or mobilization of the recipient nerve, and the RLN nerve stump should be cut as short as possible to allow for a tension-free nerve anastomosis, while minimizing the length of regrowth required from the anastomosis to the motor endplates (1–3 cm from the insertion at the cricopharyngeus). If there has been an injury to the RLN creating the paralysis, dissection of the remaining stump should be performed such that a nontraumatized recipient nerve is all that exists between the anastomosis and the motor endplates. This may require division of the inferior constrictor and subsequently the cricopharyngeus muscle fibers to follow the RLN intralaryngeally (Fig. 65.1). Rotation of the thyroid cartilage structures contralaterally via a retractor hooked around the cartilage border will often suffice for adequate, improved access. When it is positioned correctly, the handle of the hook will point to the RLN, which will be just beneath the cricopharyngeus muscle and only 3-4 mm off the end of the hook. Rarely, the posterior border of the thyroidal cartilage will need to be resected to

facilitate additional exposure. While intraoperative nerve stimulation can give the surgeon excellent information as to the presence of ansa innervation of the strap muscles in cases of previous neck surgery, stimulation of the RLN trunk does not always correlate to cricoarytenoid joint motion due to synkinesis presence. Some surgeons prefer to use the nerve integrity monitor endotracheal tube, which sometimes aids in identification of the RLN and also confirms continuity of the distal RLN from the site of stimulation. The microsurgery required for the anastomosis is commonly performed with either a microscope or loupes. Besides rendering the anastomosis tension free, the tech­ nique should include a minimum number of interrupted sutures (usually only three) with 9-0 monofilament nylon or similar thickness. A postoperative drain is often optional and patients are often discharge within 24 hours. If a high vagal nerve lesion exists, it can be helpful to reinnervate the ipsilateral cricothyroid muscle with a cricothyroid to cricothyroid “jump” graft to increase postreinnervation pitch control.12 The donor nerve can often be the extra RLN that would otherwise be discarded or the greater auricular, superficial cervical, or other sensory nerves, but these donor nerves should most often be split lengthwise, since the significant thickness is problema­ tic to insert into the CT muscles. In addition, the CT muscle requires some amount of injury to initiate the reinnervation process at the insertion site. Lastly, a greater auricular nerve to superior laryngeal nerve anastomosis can improve the amount of sensory innervation of the

Chapter 65: Reinnervation larynx if swallowing function has been significantly compromised in the patient. After successfully regaining swallowing function, if the patient subsequently finds that the resultant sensations localizing to the pinna during swallowing are problematic, the sensory anastomosis can be transected in the office under local anesthesia without difficulty, and improved swallowing is usually not compromised since compensatory measures have been developed. Patients without concurrent vocal fold injection media­ lization will experience no immediate postoperative chan­ges in their voice or laryngeal function. The timing of the subsequent voice improvement will be dependent upon the length of RLN stump, but usually begins at the 3 month mark. This interval may be somewhat shorter for younger patients in their 20s and longer for more elderly patients. The patients without improvement in their voice 9 months postoperatively will likely have no future voice improvement from this procedure. In patients without functioning ipsilateral ansa cer­ vicalis nerves, contralateral donor nerves can be utilized.13 In such cases, the RLN length needs to be maximized to be able to reach the opposite ansa system and is usually positioned anterior to the trachea (Figs. 65.5A to C). Voice imp­rovement can take up to 6 months in such patients due to the significantly longer distance within the recipient RLN for axonal regrowth to occur.

PUBLISHED FUNCTIONAL RESULTS In 2011, the results of a multicenter, randomized clinical trial were published, comparing vocal fold medialization laryngoplasty with laryngeal reinnervation.14 The authors of both chapters contributed patients to the study, and although the study protocol was suspended prematurely, sufficient patients had been recruited, enabling evaluation of 12 patients from each of the two cohorts that were evaluated 6 and 12 months post-treatment. This is the only study to date to compare medialization laryngoplasty and reinnervation with a randomized, controlled metho­ dology. After 12 months, both study groups showed signi­ ficant improvement in ratings by untrained listeners, blinded speech pathologist grade, roughness, breathiness, asthenia, strain (GRBAS) scores, and voice-related quality of life scores, without significant differences between the two groups. But, in patients under the age of 52, the reinnervation patients had significantly better improve­ ment than older patients in the same treatment group, and had significantly better RUL and GRBAS scores than

817

A

B

C Figs. 65.5A to C: Schematic diagram for reinnervation in cases of a high right, multiple cranial nerve injury: (A) the contralateral ansa is utilized when ipsilateral hypoglossi has been injured, (B) a great auricular supply is anastomosed to the superior laryngeal nerve for added sensation, (C) jump graft is placed from CT to CT for improved tone and pitch control.

patients less than 52 in the medialization laryngoplasty cohort. Older patients did better with the medialization laryngoplasty than their corresponding older reinnerva­ tion counterparts. Despite the premature suspension of patient enrollment, these results suggest that laryngeal reinnervation should be considered in patients with VFP on an equal par as medialization laryngoplasty, especially in younger patients. By far the largest series of results from reinnervation was published from China.15 The results of reinnervation following unilateral VFP caused by thyroid surgery in 237 patients were compared to non-affects age- and gendermatched controls. In addition to a significant preoperative to postoperative improvement in glottic closure, vocal fold edge, vocal fold position, phase symmetry, and regu­ larity in the paralysis cohort, there were no statistical differences compared to the control group with a mean follow-up of 5.2 years. In addition, postoperative EMG demonstrated that the affected laryngeal muscles were reinnervated successfully. All, but four, patients were able to have satisfactory restoration of vocal function. While two patients had perioperative issues, the poor results in the remaining two patients were attributed to preexisting paralysis of greater than 3 years duration.

818

Section 6. Vocal Fold Paralysis/Paresis

In a single-institution study of 48 patients undergoing laryngeal reinnervation surgery, Lorenz et al. found that, of the 36 patients with sufficient data and follow-up to be reviewed, all, but one, had improvement in postoperative objective voice metrics.16 The one failure occurred in a patient with an 18-year history of previous laryngeal paralysis following a motor vehicle accident, suggesting that in patients with extended histories of paralysis, scarring, maladaptive voice behavior, or muscle atrophy are the possible causes for failure, and these patients may be better served by mechanical repositioning techni­ ques. The authors found that in patients who undergo concurrent injection medialization with reinnervation, an initial improvement in voice quality was reported, and then around 8–12 weeks after the surgery, a decrement in voice function occurred. Subsequently, 3–4 months post­operatively, a lasting improvement occurred in the voice, suggesting an absorption of the injectate, followed by a durable repositioning of the vocal fold by the reinnervation.

FUTURE INVESTIGATION More recent work has concentrated on the possibility of producing volitional abduction and adduction of the reinnervated vocal fold. While most of the published work is in bilateral VFP, where the aim is to create some amount of abduction for maintenance of a viable airway, with unilateral VFP, the more important function would be adduction for improved voice and swallowing. This “selective reinnervation” anatomy has been reviewed by authors such as Marie, Damrose, and Kwak.17-19 In the proposed schema by Kwak, the branches of the RLN were traced distally into the laryngeal musculature. If the nerve branch to the TA and IA muscles was transected 2 mm after the take-off of the branch to the PCA, sufficient length would be allowed to the TA/IA adductor group to be anastomosed to the ansa cervicalis. Meanwhile, the 2 mm stump that had branched to this adductor group is inserted into the PCA compartment, which still had its original PCA branch intact. In essence, the surgeon was doubly innervating the PCA, while removing the possibility of synkinesis to the adductor group by supplying a new donor nerve from the ansa. The RLN, now doubly innervating the abductor muscle, is anastomosed to a jump graft from the phrenic, which would cycle the PCA with respiratory stimulation.

SUMMARY In most patients with unilateral VFP, normal or nearnormal voice can be achieved through reinnervation. Even when trauma has been caused to the distal RLN through previous surgery, postoperative reinnervation results have been documented through controlled studies to have excellent outcomes. The future of selective reinnervation to produce volitional motion of the reinnervated vocal fold is promising, as scientists understand more about the intralaryngeal nerve anatomy. Along with medialization laryngoplasty, reinnervation is a tool the laryngologist will want at his/her disposal to give patients all the options for restoration of vocal function.

REFERENCES 1. Frazier CH. Anastomosis of the recurrent laryngeal nerve with the descendens noni. JAMA. 1924;83:1637. 2. Takenouchi S, Ogura JH, Kawasaki M, et al. Autogenous transplantation of the canine larynx. Laryngoscope. 1967; 77(9):1644-67. 3. Takenouchi S, Koyama T, Kawasaki M, Ogura JH. Movements of the vocal cords. Acta OtoLaryngol. 1968;65(1):33-50. 4. Lyons RH, Tucker HM. Delayed restoration of abduction in the paralyzed canine larynx. Arch Otolaryngol. 1974; 100:176-9. 5. Tucker HM. Human laryngeal reinnervation: long-term experience with the nerve–muscle pedicle technique. Laryn­go­scope. 1978;88:598-604. 6. Rusnov M, Tucker HM. Laryngeal reinnervation for uni­ lateral vocal cord paralysis: long-term results. Ann Otol Rhinol Laryngol. 1981;90(1): 457-9. 7. Crumley RL. Experiments in laryngeal reinnervation. Laryngoscope. 1982;Supplement No. 30 (92;9):1-27. 8. Crumley RL. Selective reinnervation of vocal cord adduc­ tors in unilateral vocal cord paralysis. Ann Otol Rhinol Laryngol. 1984;93:351-6. 9. Crumley RL, Izdebski K. Voice quality following laryngeal reinnervation by ansa hypoglossi transfer. Laryngoscope. 1986;96:611-6. 10. Dedo HH. Electromyographic and visual evaluation of recurrent laryngeal nerve anastomosis in dogs. Ann Otol Rhinol Laryngol. 1971;80:664-8. 11. Miyauchi A, Inoue H, Tomoda C, et al. Improvement in phonation after reconstruction of the recurrent laryngeal nerve in patients with thyroid cancer invading the nerve. Surgery. 2009;146:1056-62. 11a. Crumley RL. Laryngeal synkinesis revisted. Ann Otol Rhinol Laryngol. 2000;109(4):365-71. 12. Lamarre ED, Lorenz RR, Milstein C, et al. Laryngeal rein­ nervation after vagal paraganglioma resection: a case report. Am J Otolaryngol. 2011;32(2):171-3.

Chapter 65: Reinnervation 13. Wang W, Chen S, Chen D, et al. Contralateral ansa cervica­ lis-to-recurrent laryngeal nerve anastomosis for unilateral vocal fold paralysis: a long-term outcome analysis of 56 cases. Laryngoscope. 2011;121(5):1027-34. 14. Paniello RC, Edgar JD, Kallogjeri D, el al. Mediali­zation versus reinnervation for unilateral vocal fold paralysis: a multicenter randomized clinical trial. Laryngo­ scope. 2011;121:2172-9. 15. Wang W, Chen D, Chen S, et al. Laryngeal reinnervation using ansa cervicalis for thyroid surgery-related unilateral vocal fold paralysis: a long-term outcome analysis of 237 cases. PLoS ONE. 2011;6(4): e19128. doi:10.1371/journal. pone.0019128.

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16. Lorenz RR, Esclamado RM, Teker AM, et al. Ansa cervicalisto-recurrent laryngeal nerve anastomosis for unilateral vocal fold paralysis: experience of a single institution. Ann Otol Rhinol Laryngol. 2008;117(1): 40-45. 17. Marie JP, Lacoume Y, Laquerriere A, et al. Diaphragmatic effects of selective resection of the upper phrenic nerve root in dogs. Respir Physiol Neurobiol. 2006;154:419-30. 18. Damrose EJ, Huang RY, Burke GS, et al. Surgical anatomy of the recurrent laryngeal nerve: implications for laryngeal reinnervation. Ann Otol Rhinol Laryn. 2003;112(5):434-8. 19. Kwak PE, Friedman AD, Lamarre ED, et al. Selective rein­nervation of the posterior cricoarytenoid and inter­ arytenoid muscles: an anatomical study. Laryngoscope. 2010;120(3):463-7.

Chapter 66: Surgery for Bilateral Vocal Fold Immobility

821

CHAPTER

Surgery for Bilateral Vocal Fold Immobility

66

Mona Abaza

INTRODUCTION Bilateral vocal fold immobility (BVFI) represents a com­ plex and potentially fatal problem that stems from many etiologies. From bilateral vocal fold paralysis (BVFP) to fixation of the cricoarytenoid joints (CJF), with or without posterior glottis stenosis (PGS), bilateral vocal fold immobility (BVFI) can require differing treatments based on the etiology, the age of the patient, and the degree of symptoms. From mild chronic respiratory distress misdiagnosed as asthma, to moderate respiratory distress exacerbated by other comorbidities, such as weight gain and cardiac issue, to biphasic stridor as an acute airway emergency BVFI can present in many ways. Although many options exist to enlarge the glottic airway, maintaining the complicated balance between respiration, voice, and swallow functions often requires the sacrifice of one for another. From the long-term issues of tracheostomy dependence to chronic aspiration to the possibility of acute issues such as dyspnea, stridor, pulmo­ nary edema,1 and vocal dysfunction, BVFI requires a careful consideration of the etiology, treatment, and out­ come for each individual patient. Understanding the often necessary tradeoff between voice and airway is of critical importance for both the surgeon and patient.

ETIOLOGY The complicated integration of respiration, swallowing, and phonation requires functioning cricoarytenoid joints with independent abduction of each arytenoid and coordinated neurological input. The presence of all of

these components allows multiple glottic functions to occur. Interference with any of these aspects can lead to bilateral immobility. Initially, immobility most commonly leads to respiratory compromise, but voice abnormalities can be the presenting sign. BVFI can be caused by neurologic compromise of bilateral recurrent laryngeal nerves (RLNs) or mecha­ nical obstruction of arytenoid movement, either at the cricoarytenoid joint or at the posterior glottis. Differen­ tiating mechanical fixation, CJF, and PGS from neuro­ logic impairment (BVFP) is critical for determining both etiology and appropriate treatment. Numerous dis­orders have been attributed to both types of dysfunction. One study found anterior neck surgery, and cricotracheal separation can be predictive of BVFP, while intubation history was associated with CJF.2 Mechanical etiologies are many and often elucida­ ted from the history. Traumatic or prolonged intubation (Fig. 66.1), endolaryngeal CO2 resection of papillomas, external beam radiation to the larynx, external trauma, cricoarytenoid joint arthritis, condromas and chondro­ sarcomas, and other laryngeal tumors have been reported to cause CJF or PGS.3 High suspicion for mecha­ nical problems should exist in the initial presentation of post­ surgical patients whose RLNs were not at risk during the procedure or in those with slowly progressive onset. Figure 66.1 demonstrates a posterior glottis band deve­lo­ ped after prolonged intubation. In adults, RLN paralysis, unilateral and bilateral, was found most commonly to be iatrogenic in nature (79%), with 19.8% being caused by tumors or trauma, and only a small percentage being idiopathic.4 One of the more

822

Section 6. Vocal Fold Paralysis/Paresis

Fig. 66.1: Postoperative view of right lateralization and partial arytenoidectomy.

common cervical procedures causing injury remains a thyroidectomy. Incidence of BVFP in total thyroidectomy is very rare. In a Quebec study,5 only one of a hundred completion thyroidectomies resulted in bilateral paralysis. ­Another large-scale study of 932 patients had a perma­ nent bilateral paralysis rate of 0%,6 although several temporary cases were noted, at least one nerve recove­ red in all patients. Zakaria et al. found the incidence of BVFI 0.58%, with none permanents, in 340 thyroidectomy cases.7 The use of RLN monitoring in preventing bilateral RLN injury has been somewhat variable in its outcome. Dralle et al., in Germany, noted 89.1% of departments used a monitor and that 90% of surgeons changed their second half plan in a thyroidectomy with demonstrate contralateral injury.8 Alesina et al. did not find it helpful in reducing the incidence of RLN injury to the contra­ lateral side of a known paralysis, with a 6.2% injury rate in the monitoring group versus 2.5% in the nerve visualization group on thyroid re-dos.9 A decrease in even transient nerve palsy was found with the use of nerve monitoring verses simple visualization in another cohort.10 Sitges-Serr et al. reported when they lost a unilateral signal in the first side of a total thyroidectomy (5.5% of their cases), only one did not recover and in no case was a signal lost on the second side.11 Another group did find a statistically significant decrease in contrala­ teral nerve injury and resulting bilateral injury, when a monitor indicated an issue.12 They attributed this to the surgeon changing the second-side surgical plan to pre­ vent a second injury. It has been theorized that the

variable course and branching of the RLN may play a role in the varied results of monitoring studies. In a cohort of 1638 RLNs identified in thyroid surgery, 64.5% had an extralaryngeal branch, and in the 447 who had monitor­ing during the procedure, the anterior branches exhibited increased electrical activity compared with the others.13 Other neurologic etiologies described have included infectious processes such as clinically silent subdural hematoma,14 staphylococcal cervical spondylodiscitis,15 tuberculosis,16,17 brachial plexus neuropathy,18 and pri­ mary herpes simplex.19,20 Neurological injury has been descri­bed in the use of single-lumen21 and double-lumen tube endotracheal intubation22 and with cervical burn contrac­ture release,23 adductor Botox injections,24 vin­ cristine-induced,25,26 systemic lupus erythematosus,27 B-12 deficiency,28 Kaposi sarcoma,29 hyponatremia,30 as well as several neurological conditions, such as GuillainBarré,31 Mobius syndrome,32 Parkinson’s disease,33 central pontine myelinolysis,34 amyotrophic lateral sclerosis,35 congenital myasthenic syndrome.36 Pediatric etiologies differ as do treatments. While BLVI is the second most common cause of neonatal stridor, over half resolve spontaneously. The etiologies vary in this population from neurologic disorders, malformations, traumatic, iatrogenic, and idiopathic.37 Iatrogenic causes, such as postoperatively, after esophageal atresia and tracheoesophageal fistula repair have been reported.38 Cotts et al. showed an incidence of 10% bilateral immobi­ lity and an additional 2% of bilateral diaphragm paralysis after pediatric cardiac surgery,39 but neurological disor­ ders still dominate as the etiology.40

EVALUATION The differentiation of BVFI into mechanical versus neu­ rological is critical to determine which treatment options are viable and how invasive the treatment needs to be. PGS often requires more aggressive treatment choices, so it is very important to identify. The examination of the patient begins with the history component. History of prolonged intubation, anterior neck surgery, and cervical trauma all reveal obvious critical information, but more subtle clues exist as well. Progressive stridor over time, attributed to asthma can indicate the slow progressive worsening of PGS. An acute poor voice and aspiration with slight improvement of the voice along with worsening of the airway over time can indicate the slow medicalization of the vocal fold in bilateral paralysis. The degree of

Chapter 66: Surgery for Bilateral Vocal Fold Immobility stridor, duration of difficulties, precipitating or preceding factors all play a role in pointing to a specific etiology. As mentioned voice abnormalities are usually not the presenting factor but can be a useful component. Rigid or flexible visualization of the vocal fold motion and the maximum airway aperture during a sniff provide clues to etiology and severity. Recording of the video images allows slow motion playback for detection of subtle movements or change in airway size over time. If no frank glottis motion abnormality is noted or the patient’s symptoms seem more significant than the pathology, evaluation of subglottic and tracheal airway should be done. This should also be considered in all patients when the etiology is unknown or can predispose to multilevel issues, such as trauma or iatrogenic causes. The ability to differentiate vocal fold palsy from fixation is critical,41 often affecting the interventions that best suit the patient. While slight motion of the arytenoids or synkinetic motion can help indicate that the joint is not fixed, the ultimate evaluation is palpation of the joint under anesthesia. Simpson et al. found that vibratory asymmetry in mobile vocal folds was a reliable predictor of vocal fold paresis in laryngeal electromyography (LEMG) testing, but that it was a poor predictor of side or bilaterality.42 Pulmonary function tests can provide useful info­r­ mation, particularly the flow volume loops. Truncated loops indicating a fixed upper airway obstruction can prompt a pulmonary refer for evaluation of the glottis and subglottis. Although pulmonary bronchoscopies can visualize the vocal folds, they are less useful in dynamic evaluations of motion than flexible laryngoscopic studies, so while the pulmonologist may have hints that this is the issue, they usually refer to otolaryngology for confirmation and treatment. Swallow studies are not a diagnostic tool in this setting but can provide useful information in considering treat­ ment options. A study of unilateral and BVFI found that 50% (8/16) patients aspirated, as compared with 42% and 37%, for left and right immobility, respectively.43 This is an important component of the workup as several of the interventions can have profound effect on swallowing function. Understanding their preoperative swallowing function can offer insight into potential postoperative impairment. The LEMG is often discussed as an evaluation modal­ ity. It may not be available at every location, and a certi­fied neurologist is important. In many centers, a combine neurology–laryngology team can provide accurate place­ ment and diagnostic evaluation in these complicated

823

patients. Berkowitz et al. demonstrated that LEMG com­ bined with intercostal EMG could help diffe­ rentiate be­tween adherent recurrent regeneration from RLN injury from abnormal medullary respiratory input.44 Understanding reinnervation pathways and timetables, the implication of synkinetic pathways and aberrant inner­ vation is important in understanding the results in LEMG and their prognostic capabilities. While often not the definitive answer in these situations, the study can provide useful information in planning the management of these patients. It is generally a method more frequently used in an adult than in the pediatric population, but it is gaining traction there. It was found to be 86.36% accurate when compared with endoscopy in children. While there were no definitive predictors of tracheostomy, LEMG grad­ ing was accurate and did correlate with need for tra­ cheostomy.45 Operative evaluation provides the ability to differ­ entiate between mechanical fixation and neurologic impairment in the most definitive way, palpation of the cricoarytenoid joint, and posterior glottis. This will indicate the degree of fixation: bilateral complete versus a unilateral fixation with a posterior scar band. The thick­ ness and location of scar will indicate the individual patient’s amendable to different surgical interventions. It is important to have multiple options for anesthesia in these patients. Patients with small fixed glottis apertures will not be intubatable endotracheal, unlike those with mobile but neurologically impaired arytenoids. Jet venti­ lation ability, with anesthesiologists trained in this method and with appropriate equipment is an option. Tracheo­ stomy remains an important consideration in many of these patients, either temporary or permanent. Some of the procedures to statically improve the airway can cause temporary glottis edema, requiring an alternate airway. In addition, a tracheostomy with a speaking valve improves the airway, preserves voice and limits the swallowing dysfunction in many patients, so it is a reasonable option to consider.

TREATMENT Original approaches to enlarging the airway opening began as early as the 1900s with external arytenoid pro­ cedures.46 Eventually, endoscopic approaches evolved in this area. It is important to understand that the vast majority of the original techniques to address BVFI are static procedures. These are still often used today and

824

Section 6. Vocal Fold Paralysis/Paresis

Fig. 66.2: Asymmetrical transverse cordotomy.

provide an increase in the glottis opening but do not affect the functional motion of the vocal folds. Because of this, they can have profound effects on the ability to perform other functions, such as swallowing or speaking. Newer information on reinnervation and pacing may resolve some of these issues in the future.

TRACHEOSTOMY Although numerous other options exist, one of the most common treatments remains tracheostomy. It alleviates airway restriction while minimally effecting voice and swallowing function. Patients often do not favor this option due to quality of life and adjustment issues,47,48 which this leads to the development of alternate proce­ dures to widen the posterior glottis.

ARYTENOID AND POSTERIOR GLOTTIS PROCEDURES These ablative procedures are some of the first static procedures to be used. Ossoff et al. described a total ary­ tenoidectomy in 1984. With Crumley49 this further evolved into a medial arytenoidectomy technique, leaving the vocal process intact, in 1993.50 Tranverse cordectomy, described in 1991,51 is now called cordotomy to more aptly describe the transverse incision or release of the vocal fold near the vocal process, rather than a true resection of the vocal fold. These procedures can be completed unilaterally or bilaterally, and debate over this is significant (Fig. 66.2).

While transverse cordotomy is often completed bila­te­ rally,52 a study of unilateral procedures indicated im­pro­ved dyspnea with fewer vocal changes and no need for tra­ cheostomy.53 While their mean follow-up was 22 months, two patients died of malignancy early in the study, indi­ cating a patient selection bias. Demir et al. found that smaller amounts of tissue ablation were needed to maintain a satisfactory airway without reducing voice but self-admitted to an arbitrary classification system.54 Bilateral proponents state the advantages of a single-stage procedure and more likely decannulation,55 but clear data remain elusive. It is important to adequately counsel the patient about postoperative considerations of voice and swallowing function deterioration. The need for temporary trach­ eostomy often depends on the procedures chosen, the degree of tissue destruction, unilateral versus bilateral procedures, and the patient comorbidities. The use of ste­ roids intraoperatively and postoperatively remains contro­ versial, as is the routine use of antireflux medications in these patients. No definitive data exist for either. Because these are destructive procedures and not reversible, it is important to not perform them until the chance for spontaneous recovery has completely passed. Postoperative revision surgery have been reported anywhere from 0%56 to 28.6%.55 Granulation tissue is rarely seen but can be a cause of postoperative airway distress. One of the most significant issues with studies about treatments for BVFI is the subjective nature of the out­ come measures. A study by Gorphe et al. demonstrated successful decannulation of five patients after endoscopic laser arytenoidectomy, with expected worsening acou­ stic measurements, but no improvement in spirometric measures.57 Yilmaz58 did demonstrate improved respira­ tory ability in 90% patients with expected vocal changes from a total endoscopic arytenoidectomy. Interestingly, no significant change in the functional outcomes swallow­ ing scales was noted postoperatively. Ablative procedure results are often highly successful for decannulation and improved airway success but less is known about vocal quality, swallowing, and pulmonary outcomes.59 The variability of outcomes in these studies can be found in the theoretical models of mechanical fixation versus neurologic paralysis. In many paralysis patients, residual adductor function and anatomical forces of an arytenoidectomy should not preclude adduction during phonation and swallowing but would indicate less success in static fixation or patients with inspiratory adductor function.60

Chapter 66: Surgery for Bilateral Vocal Fold Immobility

A

825

B

Figs. 66.3A and B: Suture lateralization.

The variability of the results may be explained by the inherent differences in individual patient airflow pat­ terns. Gokan et al. showed a lack of correlation between pulmonary patterns and dyspnea levels and glottis size using computed tomography. They concluded overall loss of muscle tone might be a contributing factor in some patients. Laser treatment results are different based on the etiology. Endoscopic laser procedures have a signi­ ficantly higher revision rate for PGS, 23% versus 5% for bilateral immobility.61 One additional static option used in the pediatric population, but not in adults, is the posterior cricoid split with rib graft62 after the age of one year. Usually, these patients have accompanying laryngeal or subglottic issues but can be an adjunct to widen the glottis aperture. Ablative procedures used in children have also demonstrated improved airways with “satisfactory” voices and occasional aspiration issues.63 There is little data on long-term outcomes in patients with these techniques.

ARYTENOID LATERAL FIXATION Another option for treatment is suture laterofixation, a potentially reversible, nonablative procedure (Figs. 66.3A and B). Initially done as an adjunct to an attempt at dynamic attachment of the omohyoid to the arytenoid, the proce­dure’s success was credited to the arytenoidopexy not muscle movement.64 The first endoscopic approaches to this required tracheostomy,65 but eventual modification simplified the technique with the use of a speciali­zed needle carrier.66 Arytenoidectomy can be performed in isolation or in combination with lateralization techniques (Fig. 66.4).

The arytenoidectomy or submucosal cordectomy is com­ pleted first. If performed unilaterally, the more medial vocal fold is usually selected. A suture is passed below the posterior one third of the vocal fold and through the thyroid ala and then the skin. The other end of the suture is passed superior, looping the vocal process to prevent remedialization. If a specialized needle driver is not avail­ able, 18-G needles and a smaller suture loop can also be used. Yilmaz used a combination of total arytenoidec­ tomy, medial mucosal advancement, and endoscopic microsuture lateralization.67 He demonstrated improved airway without significant swallowing difficulties but a worsened voice. Damrose’s review, which cited date to support modi­ fications of the technique by increasing suture size or utilizing two sutures, increased the technique’s use and made it an important part of the surgical armamenta­rium.68 Adjusting the lateral fixation sutures final tension on post­ operative day one has been suggested as a method to allow balance of airway patency and voice quality.69 It can be used as an early technique to prevent need for tracheo­ stomy,70 as reports of fibrosis resulting in fixation can occur as early as seven months.71 Oysu et al. used the technique in 13 patients in acute emergent situation with only one patient requiring a tracheostomy.72 It has been reported as a safe and effective method in children as well,73 pre­venting lifelong affects of ablative procedures. Woodson reported on 11 patients with arytenoid abduc­ tion and indicated it was the most effective in patients with 1 year follow-up.

838

Section 6: Vocal Fold Paralysis/Paresis

Voice was improved or preserved in almost all cases. About 35/40 patients were decannulated, 3 after comple­ mentary treatment. Ventilation parameters were improved in three-quarters of the cases. Arytenoid abduction was observed during inspiration at least on one side in 27/40 patients, even on both sides in 16/40 patients (14/30 if no previous endolaryngeal scar) (Figs. 67.10 and 67.11). In one case with unsuccessful previous endoscopic enlarge­ ment and scar, breathing was improved enough to permit a secon­dary medialization. Phrenic nerve function recovery was observed in most of the cases. New indications are currently in progress: rare cases of bilateral vocal fold paralysis in aperture (generally the consequence of a strongly denervated larynx) and secon­ dary reinnervation after endoscopic procedure when the arytenoids remain passively mobile. This last indication has received ethical approval to conduct a new prospec­ tive trial.

REINNERVATION OF BILATERAL VOCAL CORD PARALYSIS IN CHILDREN Tucker has reported reinnervation by ansa cervicalis nerve muscle pedicle transfer to the PCA (abovementioned procedure in adults) with some success: 50% decan­ nulation rate in children following this procedure in 9 of 18 tracheotomized children under 5 years of age.44 Some other teams reported similar success with the technique in a limited number of children.45,46 Failures were attributed to alteration of the passive arytenoid mobility. We have performed bilateral selective reinnervation of abductor and adductor muscles with upper phrenic nerve roots (as described above in adults) in 5 young patients (3 under 3 years old). Two of them were of conge­ nital origin, with remaining PCA trophicity and passive arytenoid mobility. One was secondary to cervicotho­ racic removal of lymphangioma, with remaining bilateral RLN and left phrenic nerve paralysis.47 The first operated patient (17 years old) recovered bila­ teral active inspiratory abduction of the arytenoids with preservation of a normal voice. The patient was decannu­ lated.48 Three years later, he was able to play rugby (3 days a week).49 One of the younger boys greatly improved with slight residual stridor during intensive efforts. The first 3 patients were decannulated. We are currently waiting for the evaluation of the fourth and fifth patients. In conclusion, laryngeal reinnervation can be con­ sidered as an optimal treatment for bilateral laryngeal

paralysis in some selected cases. It can be proposed in young patients as a first intention treatment, before some irreversible endoscopic or external treatments with unpre­ dictable results. A few phrenic nerve root resections do not significantly preclude the diaphragmatic function.

REFERENCES 1. Nguyen M, Junien-Lavillauroy C, Faure C. Anatomical intralaryngeal anterior branch study of the recurrent (inferior) laryngeal nerve. Surg Radiol Anat. 1989;11(2):123-7. 2. Damrose EJ, Huang RY, Ye M, et al. Surgical anatomy of the recurrent laryngeal nerve: implications for laryngeal reinnervation. Ann Otol Rhinol Laryngol. 2003;112(5): 434-8. 3. Maranillo E, Leon X, Ibanez M, et al. Variability of the nerve supply patterns of the human posterior cricoarytenoid muscle. Laryngoscope. 2003;113(4):602-6. 4. Prades JM, Faye MB, Timoshenko AP, et al. Microsurgical anatomy of intralaryngeal distribution of the inferior laryngeal nerve. Surg Radiol Anat. 2006;28(3):271-6. 5. Sunderland S, Swaney WE. The intraneural topography of the recurrent laryngeal nerve in man. Anat Rec. 1952; 114:411-26. 6. Crumley RL, McCabe B. Regeneration of the recurrent laryngeal nerve. Laryngoscope. 1982;90:442-7. 7. Marie JP. (Contribution à l’étude de la réinnervation laryngée expérimentale; intérêt du nerf phrénique). Laryngeal rein­ nervation: special interest with the phrenic nerve. [PhD Dissertation. Medical Sciences.]. Rouen: Rouen; 1999. 8. Obongo R, Duclos C, Guerout N, et al. Unmuscle peut il recevoir une double innervation? Mise au point d’un modèle sur un muscle sous hyoïdien chez le rat. In: Congrès National de la Société Française d’ORL. Paris, France; 2012. 9. Marie JP, Tardif C, Lerosey Y, et al. Selective resection of the phrenic nerve roots in rabbits. Part II: Respiratory effects. Respir Physiol. 1997;109(2):139-48. 10. Marie JP, Laquerriere A, Lerosey Y, et al. Selective resection of the phrenic nerve roots in rabbits. Part I: cartography of the residual innervation. Respir Physiol. 1997;109(2):127-38. 11. Marie JP, Lacoume Y, Laquerriere A, et al. Diaphragmatic effects of selective resection of the upper phrenic nerve root in dogs. Respir Physiol Neurobiol. 2006;154(3):419-30. 12. Verin E, Marie JP, Tardif C, Denis P. Spontaneous recovery of diaphragmatic strength in unilateral diaphragmatic paralysis. Respir Med. 2006;100(11):1944-51. 13. Verin E, Marie JP, Similowski T. Cartography of human diaphragmatic innervation: preliminary data. Respir Physiol Neurobiol. 2011;176(1-2):68-71. 14. Marie J-P, Bon Mardion N, Paviot A, et al. Bilateral functional reinnervation in bilateral vocal fold paralysis: new indications. In: IFOS Congress. Seoul, South Korea; 2013. 15. Marie J-P. Human bilateral laryngeal réinnervation: impli­ cations for transplantation. In: American Laryngological Association (ALA) Combined Otolaryngology Spring Meet­ ings. Phoenix, Arizona, USA; 2009.

Chapter 67: Reinnervation for Bilateral Vocal Fold Paralysis 16. Marina MB, Marie JP, Birchall MA. Laryngeal reinnervation for bilateral vocal fold paralysis. Curr Opin Otolaryngol Head Neck Surg. 2011;19(6):434-8. 17. Tucker HM, Harvey J, Ogura JH. Vocal cord remobilization in the canine larynx. Arch Otolaryngol. 1970;92(6):530-3. 18. Tucker HM. Laryngeal transplantation: current status 1974. Laryngoscope. 1975;85(5):787-96. 19. Tucker HM. Human laryngeal reinnervation: long-term experience with the nerve-muscle pedicle technique. Lary­ ngoscope. 1978;88(4):598-604. 20. Tucker HM. Nerve-muscle pedicle reinnervation of the larynx: avoiding pitfalls and complications. Ann Otol Rhinol Laryngol. 1982;91(4 Pt 1):440-4. 21. Tucker HM. Long-term results of nerve-muscle pedicle reinnervation for laryngeal paralysis. Ann Otol Rhinol Laryngol. 1989;98(9):674-6. 22. Levine H, Tucker HM. Surgical management of the paralyzed larynx. In: Bailey BJ, Biller HF (Eds). Surgery of the larynx. Philadelphia, PA: Saunders, WB;1985:117-34. 23. Crumley RL. Update of laryngeal reinnervation concepts and options. In: Bailey BJ, Biller HF (Eds). Surgery of the larynx. Philadelphia, PA: Saunders, WB;1985:135-47. 24. Marie JP, Lerosey Y, Dehesdin D, et al. Experimental reinnervation of a strap muscle with a few roots of the phrenic nerve in rabbits. Ann Otol Rhinol Laryngol. 1999; 108(10):1004-11. 25. Crumley RL, Horn K, Clendenning D. Laryngeal reinner­ vation using the split-phrenic nerve-graft procedure. Otolaryngol Head Neck Surg. 1980;88(2):159-64. 26. Crumley RL. Experiments in laryngeal reinnervation. Laryngoscope. 1982;92(9 Pt 2 Suppl 30):1-27. 27. Crumley RL. Phrenic nerve graft for bilateral vocal cord paralysis. Laryngoscope. 1983;93(4):425-8. 28. Rice DH. Laryngeal reinnervation. Laryngoscope. 1982;92 (9 Pt 1):1049-59. 29. Mahieu HF, van Lith-Bijl JT, Groenhout C, Tonnaer JA, de Wilde P. Selective laryngeal abductor reinnervation in cats using a phrenic nerve transfer and ORG 2766. Arch Otolaryngol Head Neck Surg. 1993;119(7):772-6. 30. van Lith-Bijl JT, Mahieu HF, Stolk RJ, et al. Laryngeal abductor function after recurrent laryngeal nerve injury in cats. Arch Otolaryngol Head Neck Surg. 1996;122(4):393-6. 31. van Lith-Bijl JT, Stolk RJ, Tonnaer JA, et al. Laryngeal abductor reinnervation with a phrenic nerve transfer after a 9-month delay. Arch Otolaryngol Head Neck Surg. 1998;124(4):393-8. 32. Crumley RL. Selective reinnervation of vocal cord adductors in unilateral vocal cord paralysis. Ann Otol Rhinol Laryngol 1984;93(4 Pt 1):351-6. 33. van Lith-Bijl JT, Stolk RJ, Tonnaer JA, et al. Selective laryngeal reinnervation with separate phrenic and ansa cervicalis nerve transfers. Arch Otolaryngol Head Neck Surg. 1997;123(4):406-11. 34. Marie JP, Dehesdin D, Ducastelle T, et al. Selective reinnervation of the abductor and adductor muscles of the canine larynx after recurrent nerve paralysis. Ann Otol Rhinol Laryngol. 1989;98(7 Pt 1):530-6.

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35. Zheng H, Zhou S, Li Z, et al. [Reinnervation of the posterior cricoarytenoid muscle by the phrenic nerve for bilateral vocal cord paralysis in humans]. Zhonghua Er Bi Yan Hou Ke Za Zhi. 2002;37(3):210-4. 36. Li M, Zheng H. Reinnervation of the bilateral posterior cricoarytenoid muscle using left phrenic nerve in patients with bilateral vocal cord paralysis. In: IFOS Congress. Seoul, South Korea, 2013. 37. Li M, Chen S, Zheng H, et al. Reinnervation of bilateral posterior cricoarytenoid muscles using the left phrenic nerve in patients with bilateral vocal fold paralysis. PLoS One. 2013;8(10):e77233. 38. Marie JP, Lacoume Y, Magnier P, et al. Selective bilateral motor reinnervation of the canine larynx. Laryngo-RhinoOtologie. 2000; S188-9. 39. Marie JP, Laquerriere A, Choussy O, et al. Thyrohyoid branch of the hypoglossal nerve in the canine; perspectives for larynx reinnervation. Eur Arch Oto Rhino Laryngol. 2000:S1,S11. 40. Marie J-P, Laquerriere A, Choussy O, et al. Thyrohyoid branch of the hypoglossal nerve in the canine; perspectives for larynx reinnervation. Eur Arch Oto Rhino Laryngol. 2000:S1,S11,257. 41. Marie JP, Choussy O, Lacoume Y, et al. Delayed total motor reinnervation of the canine larynx. In: Where upper airway and digestive tract meet. Amsterdam; 2001. 42. Marie J-P. Nerve reconstruction. In: Remacle M, Eckel HE (eds), Surgery of larynx and trachea. Berlin: SpringerVerlag;2009. 43. Marie J-P. Ten years’experience in selective bilateral reinnervation of the larynx in humans. In: American Laryn­ gological Association. Neurolaryngology Study Group. May 14-15, 2014; Las Vegas, Nevada, USA; 2014. 44. Tucker HM. Vocal cord paralysis in small children: prin­ ciples in management. Ann Otol Rhinol Laryngol. 1986;95 (6 Pt 1):618-21. 45. Nunez DA, Hanson DR. Laryngeal reinnervation in children: the Leeds experience. Ear Nose Throat J. 1993;72(8):542-3. 46. Fayoux P, Delattre A, Delforge A. Réhabilitation laryngée par transfert neuro-musculaire d’omo-hyoïdien (intervention de Tucker)chez l’enfant. In: Société de Laryngologie des Hôpitaux de Paris. Nov 24, 2007, Paris; 2007. 47. Marie J-P. Laryngeal reinnervation in bilateral vocal fold paralysis in children. In: American Association of Pediatric Otorhinolaryngology, COSM. May 16-18, 2014; Las Vegas, Nevada, USA; 2014. 48. Marie JP, Vérin E, Woisard V, et al. Successful reinnervation of congenital bilateral vocal cord paralysis. In: IX Congress of European Society of Pediatric Otorhinolaryngology; 2006 18-21/06/2006; Paris; 2006. 49. Marie JP, Vérin E, Woisard V, et al. Réinnervation sélective des paralysies laryngées bilatérales en fermeture. Premiers résultats. In: Société de Laryngologie des Hôpitaux de Paris; 2007 24/11/2007; Paris; 2007. 50. Tucker HM. Selective reinnervation of paralyzed mus­ culature in the head and neck: functioning autotrans­ plantation of the canine larynx. Laryngoscope. 1978;88 (1 Pt 1):162-71.

SECTION Airway Obstruction and Stenosis

7

Chapter 68: Laryngotracheal Stenosis—Definitions and Pathogenesis

843

CHAPTER

Laryngotracheal Stenosis— Definitions and Pathogenesis

68

Alessandro de Alarcón, Aliza P Cohen, Michael J Rutter

OVERVIEW Stenoses of the larynx and trachea can be divided into two broad categories—conditions that are congenital and those that are acquired. Congenital stenoses include any abnormalities of the laryngotracheal complex that are evident at birth or shortly thereafter. Acquired stenoses can be attributed to a broad spectrum of etiologies, including trauma, systemic disease, granulomatous disease, and infectious processes; they may also be idiopathic. This chapter describes a number of congenital and acquired stenoses likely to be encountered in an airway practice, providing a brief description of their pathogenesis. Our aim is to lay the foundation for a more in-depth discussion of the diagnosis and management of these disease processes.

include dyspnea and voice change, correlates with the size and position of the web. Thin webs may escape detection because neonatal intubation for airway distress may lyse the web. Thick webs require open reconstruction, with either reconstruction of the anterior commissure or place­ ment of a laryngeal keel. Approximately 40% of patients with thick membranous webs require tracheotomy place­ ment. There is a strong association between anterior glottic webs and velocardiofacial syndrome.1 Supraglottic webs represent fewer than 2% of conge­ nital laryngeal webs. These webs are diaphragmatic out­ growths that usually arise anteriorly. If partial, they provide air passage posteriorly. The web is typically thickened ante­ riorly and thins out toward the posterior edge. Symptoms, including dyspnea and voice change, depend on the size

CONGENITAL STENOSES Laryngeal Laryngeal Webs Laryngeal webs may be either glottic or supraglottic; how­ ever, more than 90% are glottic. These webs arise during the early weeks of embryogenesis, resulting from failure of the glottic airway to recanalize (Fig. 68.1). As recanalization commences posteriorly and progresses anteriorly, in severe cases complete laryngeal atresia may occur. In less severe cases, a thin anterior glottic web may be the only remnant of the recanalization process. Although some webs are gossamer thin, most anterior glottic webs are thick and usually associated with a subglottic “sail” compromising the subglottic lumen. The severity of symptoms, which

Fig. 68.1: Endoscopic view of a congenital glottic web.

844

Section 7. Airway Obstruction and Stenosis

and position of the web. Ten percent of children with supraglottic webs have associated congenital anomalies.

Subglottic Stenosis As with laryngeal webs, the cause of congenital subglot­ tic stenosis (SGS) is thought to be a failure of the laryngeal lumen to recanalize. Congenital SGS is comparatively rare. It is defined as a lumen 4.0 mm in diameter or less at the level of the cricoid. This condition is one of a con­ ti­ nuum of embryologic failures that include laryngeal atresia, stenosis, and webs. In the absence of trauma, an abnormality of the cartilage or subglottic tissues is also considered to be congenital. In its mildest form (0–50% obstruction), congenital SGS manifests with a normalappearing cricoid with a smaller than average diameter, usually with an elliptical shape. Mild SGS may manifest in recurrent upper respiratory infections in which mini­ mal subglottic swelling precipitates airway obstruction. More severe cases (Fig. 68.2) may present with acute airway compromise at delivery. If endotracheal intuba­tion is successful, the patient may require intervention before extubation. When intubation cannot be achieved, tracheo­ tomy placement at the time of delivery may be lifesaving. Important to note, infants may have surprisingly few symptoms, and even those with grade 3 SGS (71–99% obstruction) (Fig. 68.3) may not be symptomatic for weeks or months. Levels of stenotic severity are graded according to the Myer-Cotton grading system (Fig. 68.4).2 Congenital stenosis is often associated with other congenital head and neck lesions and syndromes (e.g. a small larynx in Down syndrome). After the initial

Fig. 68.2: Endoscopic view of a grade II subglottic stenosis.

management of congenital SGS, the larynx grows with the patient and may not require surgical intervention. However, if initial management requires intubation, there is considerable risk of developing an acquired SGS in addition to the underlying congenital SGS.

Tracheal Complete Tracheal Rings As with laryngeal stenosis, tracheal stenosis can be either congenital or acquired. Although rare, the most common congenital condition causing tracheal stenosis is complete tracheal rings (Fig. 68.5). In a normal trachea, luminal support is provided by incomplete rings of cartilage, with a posterior sheet of muscle (the trachealis) completing the circumference of the trachea. In patients with complete tracheal rings, the cartilaginous rings are circular and may affect varying lengths of the trachea. In addition, the trachealis muscle is absent. This anomaly is often life threatening. It presents with progressive worsening of res­ piratory function over the first few months of life, stridor, retractions, and marked exacerbation of symptoms during intercurrent upper respiratory tract infections. Children with tracheal stenosis generally exhibit a biphasic wetsounding breathing pattern referred to as “washing machine breathing,” which transiently clears with cough­ ing. The risk of respiratory failure increases with age, as the infant typically grows faster than the stenosis. Decom­ pensation may occur around 4 months of age and often occurs in association with an upper respiratory tract infection.

Fig. 68.3: Endoscopic view of a grade III subglottic stenosis.

Chapter 68: Laryngotracheal Stenosis—Definitions and Pathogenesis

845

Fig. 68.5: Endoscopic view of complete tracheal rings.

Fig. 68.4: Levels of airway obstruction in the Myer-Cotton grading scale with endoscopic views of each level.

ACQUIRED STENOSES Injury and Trauma Postintubation In 1965, McDonald and Stocks3 advocated long-term naso­ tracheal intubation in the management of the unstable neonatal airway. Although this revolutionized neonatal care, particularly for premature infants, there was a cor­ responding increase in the incidence of acquired SGS in neonates with prolonged stays in neonatal intensive care units. The incidence of combined congenital and acqui­ red SGS also rose as infants with congenital SGS were intubated for airway compromise—often with inappro­­ priately large endotracheal tubes. Acquired SGS resulting from prolonged neonatal intubation is now more com­ mon than congenital SGS in the pediatric age group. Posterior glottic stenosis (Fig. 68.6) also is a common sequela of prolonged intubation and is often misdiagno­ sed as bilateral vocal fold paralysis; associated fibrosis or ankylosis of the cricoarytenoid joints may occur. In adults, postintubation stenosis is often associated with prolonged intubation and ventilation. The pathogenesis of laryngotracheal stenosis related to postintubation injury is not yet clear. Autopsy studies

demonstrate that there is a period of ulceration and nec­ rosis of cricoid mucosa in the first hours and days of intubation.3 In some cases, however, healing and reepithe­ lialization in the cricoid region have been reported to occur while the endotracheal tube remained in place.4 Overall, 1–8% of neonates develop stenosis after prolonged intubation.5 The incidence has steadily dropped over the last three decades despite the longer periods of intubation that have become commonplace in increasingly smaller infants. This drop can be attributed to the use of appro­ priately sized endotracheal tubes. Ideally, an endotracheal tube should leak air around it with subglottic pressures below 20–25 cm of water.

Thermal Injuries Thermal injuries of the glottis and subglottis may occur without thermal injury to the trachea and lung due to the cooling of air by the upper airway and reflex closure of the vocal folds. Thermal injuries from steam, posses­ sing 4,000 times the heat-carrying capacity of heated air or gas, may cause significant laryngeal burns. Laser airway fires may be particularly damaging. The pathophysio­ logy of stenosis in laryngeal thermal injuries is thought to be governed by three factors: direct thermal injury, toxic effects of combustion products, and prolonged intubation. Once the scar tissue has matured, airway recon­struc­ tion may be successfully undertaken.6

Blunt Trauma If trauma is mismanaged or unrecognized, it may lead to laryngeal stenosis. Sources of internal trauma include

846

Section 7. Airway Obstruction and Stenosis life-saving intervention, it may result in a complica­tion rate as high as 32%.7

Systemic Gastric Acid Reflux Disease

Fig. 68.6: Endoscopic view of posterior glottic stenosis.

foreign bodies and instrumentation during endoscopic pro­cedures. These forms of trauma usually lead to glottic and subglottic scarring and resultant stenosis. External forms of laryngeal trauma, such as motor vehicle acci­dents, sports-related injuries, and assaults, including blunt and penetrating trauma, can also produce laryn­ gotra­ cheal stenosis. Anterior blunt trauma, as sustained in motor vehicle accidents or sports-related injuries, usually leads to pos­ terior supraglottic and glottic stenosis. An external force at the hypopharyngeal level may cause scar formation between the epiglottis and posterior pharyngeal wall. Fracture of the hyoid bone displaces soft tissues poste­ riorly, narrowing the laryngeal inlet. These injuries may also cause web formation on the posterior hypopharyn­ geal wall and stenosis in the postcricoid area. Blunt and penetrating trauma may lead to laceration or hematoma formation in the glottis, which will produce laryngeal stenosis if not treated appropriately.

Post-tracheotomy Stenosis During a tracheotomy, additional injury may result in laryngotracheal stenosis or suprastomal collapse. Secon­ dary infection, chondritis, or pressure exerted by the cur­vature of the tracheotomy may result in stenosis or suprastomal collapse above the tracheotomy site. Steno­ sis may occur because of a high tracheotomy, which is per­formed through the thyroid, cricoid, or first tracheal car­ tilage; a high tracheotomy also includes cricothy­ roi­ dotomy. Although this procedure is well known to oto­laryn­gologists and emergency room physicians as a

Gastroesophageal reflux disease (GERD) is defined as a chronic condition in which the lower esophageal sphinc­ ter allows gastric acids to reflux into the esophagus, causing heartburn, acid indigestion, and possible injury to the esophageal lining. It is common in children and disproportionately prevalent in children with SGS. Laryn­ geal endoscopy findings have historically been poor in establishing this diagnosis. In fact, gross reflux may occur with no obvious clinical signs on endoscopy. The current gold standard for diagnosis is impedance probe testing. Further assessment of GERD is carried out based on the clinician’s assessment of the relevant symptoms of each individual patient. Patients are managed with H2 blockers and proton pump inhibitors or fundoplication prior to reconstructive surgery. Several studies8-11 have investigated the association of GERD and airway stenosis in adults. Koufman8 reported that in a group of 32 patients with laryngotracheal steno­ sis, 78% had laryngopharyngeal reflux identified by pH probe testing. Although this association has also been shown in children, a direct correlation between reflux and stenosis causation has not been demonstrated.

Eosinophilic Esophagitis Eosinophilic esophagitis (EE) is an uncommon disorder that represents a chronic immune/antigen-mediated eso­ phageal disease characterized clinically by symptoms related to esophageal dysfunction and histologically by eosinophil-predominant inflammation. It is often asso­ ciated with a food allergy, resulting in eosinophilic inflam­ mation of the esophagus. Many children with EE also have esophageal, laryngotracheal, and sinonasal complaints, although many are asymptomatic.12 If untreated, EE may have a significant effect on the aerodigestive tract. In patients with active EE, the laryngotracheal complex is often inflamed. In this setting, surgery frequently elicits a brisk inflammatory response that can lead to graft failure or restenosis. If EE is present, our experience indicates that medical management followed by repeat endoscopy with biopsies is prudent. Once biopsies reveal that there is no active EE, surgery can be performed.

Chapter 68: Laryngotracheal Stenosis—Definitions and Pathogenesis

Polychondritis, Amyloidosis, and Wegener’s Granulomatosis Relapsing polychondritis is characterized by progressive inflammation of cartilaginous structures such as the septum, the dorsum of the nose, and the ear cartilages in the lower endotracheal bronchial tree. Approximately 20% of patients have airway manifestations, which may include SGS or focal stenosis of the lower endotracheal bronchial tree.13 Amyloidosis is an extremely uncommon group of disorders that results from abnormal deposits of amyloid in various tissues of the body. Depending on the structure of the particular amyloid, the protein can accumulate in an isolated tissue or be widespread, affecting numerous organs and tissues. Typically, however, amyloidosis invol­ ves only one site, with the most common airway site being the larynx. In this setting, disease management commonly consists of surgical resection. When there are multiple sites of involvement within the airway, a workup should be performed to assess the possible presence of systemic amyloidosis. In rare cases, amyloid deposits may cause subglottic or tracheal stenosis. Wegener’s granulomatosis (currently referred to as gra­ nulomatosis with polyangiitis) is an uncommon disorder with an unknown etiology. This disorder causes inflam­ mation of the blood vessels, restricting blood flow to various organ systems, including the kidney, lungs, and upper respiratory tract. Reports of SGS in patients with this condition vary from 8.5% to 50%.14-16 Biopsies may reveal a vasculitis or diffused inflammation. Often biop­ sies of the subglottis are nondiagnostic. In the setting of active inflammation, an antineutrophil cytoplasmic anti­ body (C-ANCA) test will establish the diag­nosis. A septal perforation is an early sign of the dis­order. Treatment for the disease is typically led by a rheumatologist. Once the disorder is quiescent, open surgical treatment may be considered.

Infectious Infectious etiologies of laryngotracheal stenosis are rare in the United States. Typically, they involve an inflam­ matory reaction due to an airway infection or are secondary to cicatrix formation in the airway. In our expe­ rience, pseudomonal infection has been associated with significant destruction of laryngotracheal structures. This is often due to pseudomonas infection of the cartilages during intubation. Affected patients often require multiple

847

surgeries and prophylactic treatment for pseudomonal colonization prior to surgery. As a historical note, prior to the era of vaccination, diphtheria resulted in laryn­ gotracheal stenosis; this is now extremely rare in the US.

Granulomatous Tuberculosis of the larynx is the most common granu­ lomatous disease of the larynx, and it is usually associated with pulmonary disease. The most common sites for laryn­ geal tuberculosis are the interarytenoid space, arytenoid cartilages, posterior surface of the true vocal folds, and laryngeal surface of the epiglottis. Patients may present in the early stages of disease with diffuse edema and ery­ thema of the vocal folds, which may mimic an early-stage glottic carcinoma. However, disease progression manifests with nodular lesions and ulceration of the epithelium, which can lead to perichondritis and chondritis. Due to interarytenoid muscular involvement or cricoarytenoid joint fixation, patients may also present with symptoms that mimic vocal fold paralysis. Diagnosis is made by demonstration of Mycobacterium tuberculosis. Successful treatment usually leads to complete healing of the larynx. If the disease is not treated, chondritis and necrosis will result in extensive laryngeal scarring and stenosis.

Idiopathic When there is no identifiable cause of stenosis, it is con­ sidered idiopathic. This occurs more frequently in women and in association with reflux. The overall assessment of these patients typically results in low yield. Treatment varies, depending on the degree of stenosis and associated symptoms.

REFERENCES 1. Miyamoto RC, Cotton RT, Rope AF, et al. Association of anterior glottic webs with velocardiofacial syndrome (chro­ mosome 22q11.2 deletion). Otolaryngol Head Neck Surg. 2004;130:415-7. 2. Myer CM 3rd, O’Connor DM, Cotton RT. Proposed grading system for subglottic stenosis based on endotracheal tube sizes. Ann Otol Rhinol Laryngol. 1994;103:319-23. 3. McDonald IH, Stocks JG. Prolonged nasotracheal intuba­ tion. Br J Anaesth. 1965;37:161-73. 4. Quiney RE, Gould SJ. Subglottic stenosis: a clinicopatho­ logical study. Clin Otolaryngol Allied Sci. 1985;10:315-27. 5. Ratner I, Whitfield J. Acquired subglottic stenosis in the very low-birth-weight infant. Am J Dis Child. 1983;137:40-43. 6. White DR, Preciado DA, Stamper B, et al. Airway reconstruc­ tion in pediatric burn patients. Otolaryngol Head Neck Surg. 2005;133:362-5.

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Section 7. Airway Obstruction and Stenosis

7. McGill J, Clinton JE, Ruiz E. Cricothyrotomy in the emer­ gency department. Ann Emerg Med. 1982;11:361-4. 8. Koufman JA. The otolaryngologic manifestations of gastro­ esophageal reflux disease (GERD); a clinical investigation of 225 patients using ambulatory 24-hour pH monitoring and an experimental investigation of the role of and pep­ sin in the development of laryngeal injury. Laryngoscope. 1991;101(Suppl 53):1-78. 9. Toohill RJ, Ulualp SO, Shaker R. Evaluation of gastroesoph­ ageal reflux in patients with laryngotracheal stenosis. Ann Otol Rhinol Laryngol. 1998;107:1010-4. 10. Walner DL, Stern Y, Gerber ME, et al. Gastroesophageal reflux in patients with subglottic stenosis. Arch Otolaryngol Head Neck Surg. 1998;124:551-5. 11. Maronian NC, Azadeh H, WaughP, et al. Association of laryngopharyngeal reflux disease and subglottic stenosis. Ann Otol Rhinol Laryngol. 2001;110:606-12.

12. Dauer EH, Ponikau JU, Smyrk TC, et al. Airway manifesta­ tions of pediatric eosinophilic esophagitis: a clinical and histopathologic report of an emerging association. Ann Otol Rhinol Laryngol. 2006;115:507-17. 13. Ernst A, Boiselle P, Sung A, et al. Relapsing polychondritis and airway involvement. Chest. 2009;135:1024-30. 14. Langford CA, Sneller MC, Hallahan CW, et al. Clinical features and therapeutic management of subglottic ste­ nosis in patients with Wegener’s granulomatosis. Arthritis Rheum. 1996;39:1754-60. 15. Gluth MB, Shinners PA, Kasperbauer JL. Subglottic stenosis associated with Wegener’s granulomatosis. Laryngoscope. 2003;113:1304-7. 16. Screaton NJ, Sivasothy P, Flower CD, et al. Tracheal involve­ ment in Wegener’s granulomatosis: evaluation using spiral CT. Clin Radiol. 1998;53:809-15.

Chapter 69: Tracheostomy

849

CHAPTER

69

Tracheostomy John Heaphy, Rod Rezaee, Pierre Lavertu

HISTORY Tracheotomy was depicted on Egyptian tablets as early as 3600 bce. The Hindu Rigvedain 2000 bce makes reference to the procedure, and Hippocrates (460–380 bce) described intubation of the trachea for ventilation support, but the first tracheostomy is generally credited to Asclepiades of Persia in 124 bce. Similar procedures were also described by Greek physicians Aesculapius and Aretaeus and the Roman Gallenus. Alexander the Great (356–323 bce) reportedly used his sword to open the airway of a soldier choking on a bone.1-4 In the late 1700s, in Paris, Chaussier (1746–1828) established translaryngeal intubation in neonates with obstructed airways and first administered oxygen to newborns. The next major advancement was the first cuffed tracheostomy tube by the German Trendelenburg in 1869. Chevalier Jackson standardized the procedure in 1932 by outlining the necessary steps and warning about possible complications from high tracheostomy or cricothyroidotomy.5-7 Recently, more minimally invasive procedures have been explored. In 1985, Ciaglia et al. introduced the percutaneous dilatational tracheotomy (PDT), which has gained widespread acceptance in intensive care units (ICUs) and trauma centers as a viable alternative to the traditional open tracheotomy.8

INDICATIONS Reasons to perform a tracheotomy are numerous and include the following: 1. Bypass an airway obstruction due to congenital ano­ maly, vocal cord paralysis, inflammatory disease, or oncological or benign pathology 2. Prolonged intubation*/reduce the probability of sub­ glottic stenosis 3. Assist respiration over prolonged periods 4. Extensive structural trauma to the face and/or neck 5. Concurrent ablative head and neck procedures and/or extensive reconstruction to the mandible or maxilla 6. Obstructive sleep apnea 7. Inability to intubate 8. Aspiration reduction and pulmonary toilet 9. More secure airway for home ventilation in patients with neuromuscular or other chronic diseases. The complications associated with the procedure and the risks of prolonged translaryngeal intubation should be considered in light of the patient’s respiratory, anatomy, and physiological characteristics; the presenting patho­ logy and prognosis; the institutional facilities, and the skill of personnel.10-15

CONTRAINDICATIONS Almost all patients can be considered for the standard, open surgical tracheotomy, but not all will meet the

*There is no statistically significant improvement with performance of an early (within four days of intuba­tion) versus late (>10  days intubation) tracheotomy in mortality or other important secondary outcomes.9

850

Section 7: Airway Obstruction and Stenosis

Fig. 69.1: Landmarks are marked on the patient, including the thyroid notch, the inferior border of the cricoid, the sternal notch, and the intended location of the incision.

criteria for a percutaneous tracheotomy. Significant burn injury and infection of the trachea have been reported as relative contraindications to the open procedure, but there are no absolute contraindications.15 Percutaneous tracheotomy is best performed on patients who have already been intubated and are to be avoided in situations requiring emergency airway access.12 Other contraindications include cervical spine injury, aged  50%. Therefore, most patients present with a severity of disease that necessitates treatment. The most common practice for patients with idiopathic SGS is to manage patients endoscopically initially, which tends to offer symptomatic relief for an average of 12 months.3 Subsequent endoscopic treatments are needed often, but most patients can experience long-term relief after an average of 2.5–3 treatments. Once patients require signifi­ cant numbers of treatment (> 10), consideration should be given to open surgical resection to prevent adverse sequelae of treatment, such as glottic stenosis.

878

Section 7: Airway Obstruction and Stenosis

Fig. 71.1: The healed scar of a mature subglottic stenosis. Courtesy: Dr C Milstein.

AUTOIMMUNE SGS MANAGEMENT Autoimmune diseases most commonly affecting the sub­ glottis include GPA, previously known as Wegner’s granulo­ matosis, relapsing polychondritis, and rarely, sarcoidosis. Similar to idiopathic SGS, GPA involvement of the sub­ glottis involves a circumferential inflammatory response of the epithelium, followed by maturation of scar. The difference is that the GPA patient will sometimes present for care during the initial inflammatory event due to the presence of other organ system involvement such as pulmo­ nary or renal disease. In addition, previously diagnosed GPA patients may subsequently flare after the disease has been identified as an inflammatory exacerbation in the larynx. The difference in appearance between these two stages (acute inflammation and mature scar) is relatively easy to discern by the experienced laryngologist, as the inflammatory stage is marked by erythema, edema of the epithelium, and possibly visible granulation tissue. Mature scar, in contrast, is often white, rigid, with visible cicatricial bands of fibrosis (Fig. 71.1). Is it worthwhile determining if the patient is in an inflam­ matory stage or has matured to scar formation bec­ause the former is responsive to systemic steroids, whereas the latter is unresponsive and requires surgical interven­ tion when symptoms are sufficient to warrant treatment? Unfortunately, successful treatment of the inflammatory stage does not preclude the disease to maturing to later scar formation and stenosis. Similar to idiopathic causes, treatment of GPA SGS is most commonly endoscopic

Fig. 71.2: Lateral subglottic swelling of relapsing polychondritis.

initially, reserving open surgery for recalcitrant cases or disease that involves the glottis. Relapsing polychondritis SGS rarely demonstrates maturation of scar, but rather appears as lateral ledges of inflammation beneath the true vocal folds while preser­ ving the anteroposterior airway (Fig. 71.2). It is frequently systemic steroid responsive, but due to the softening of the tracheal cartilage, often a T-tube is required for main­ tenance of the tracheal lumen, and the upper limb of the tube can be used to maintain the opening of the subglottis simultaneously. Dilation of SGS due to relapsing polychon­ dritis is usually not effective.

TRAUMATIC SGS MANAGEMENT Traumatic SGS caused by endolumenal trauma (endo­ tracheal tubes) is often successfully treated by endoscopic therapies to both widen the lumen and prevent subse­ quent fibrosis to form. Subglottic damage is often due to tracheostomy tube injuries. Reasons including inappropri­ ately high tube placement, migration of the tube superiorly, and suprastomal granulation tissue are all common causes of failure to decannulate patients after tracheotomy. The cause of the superior migration is unknown but may be due to movement from swallowing or external neckties that pull the tube superiorly. Such cases often lack healthy cricoid cartilage framework to support the subglottic lumen, and an open surgical procedure is commonly required to re-establish a long-term open airway.

879

Chapter 71: Subglottic Stenosis

EVALUATION The goals of careful history taking in the patient with SGS are first to establish the etiology of the stenosis and then detail the relationship between previous treatment and improvement of symptoms. The lack of autoimmune sero­ logic markers and nonlaryngeal disease manifestations is used to rule out autoimmune etiologies, but this deter­ mination can be changing and rheumatologic consulta­ tion is commonly helpful. Patient histories often describe

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Infection of the subglottis can occur as with common laryngotracheobronchitis (croup), or even bacterial etio­ logies such as Haemophilus influenza, which respond to antibiotics and supportive therapies. More commonly, pre existing stenoses from other etiologies can become superinfected, such as GPA SGS becoming infected by Staphylococcus aureus (Fig. 71.3). These situations are challenging, since Staphylococcus commonly colonizes the airway of GPA patients, and systemic antibiotics are difficult to deliver in sufficient concentration to the endo­ lumenal airway epithelium. When such patients fail oral antibiotics and are significantly symptomatic from the crusting obstructing their subglottis, IV antibiotics and even direct application of mupirocin to the subglottis topically may be needed to resolve the infection.

symptoms, which are misattributed to reactive pulmonary disease, and the earliest signs of airway noise or dyspnea are often the initiation of significant stenosis. Pulmonary function tests demonstrate restriction of both inspira­ tory and expiratory flow, but their value over patients’ subjective complaints of dyspnea is questionable. Office assessment of the patient includes flexible nasal fiberoptic endoscopy to exclude glottic involvement, vocal fold fixa­ tion and posterior commissural interarytenoid stenosis, and impending airway compromise. Computed tomo­ graphic (CT) scan of the larynx can be helpful to rule out cartilaginous involvement, but it is not required for isolated, nontraumatic SGS. Three dimensional CT scans have advanced to be able to highlight cartilaginous defects, which are helpful when planning subsequent surgical intervention (Fig. 71.4). Operative biopsy of the subglottis is used to rule out granulomatosis disease, amyloidosis, and infection, but care should be given to prevent further trauma through aggressive biopsies, which may exacer­ bate future scarring. Classification of the laryngotracheal stenosis is commonly performed through the use of the Myer Cotton system, which is based on circumferential stenosis with four staging degrees depending on the percent­ age of reduction in cross sectional area, using values of 50% and 70% narrowing to define stenosis grades.5 While the length and location are recorded, they do not affect the 1–4 grading system. ­

INFECTIOUS SGS MANAGEMENT

Fig. 71.4: Three-dimensional computed tomographic scan demon strating cartilaginous defect secondary to an extended tracheotomy. Courtesy: Dr M Benninger.

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Fig. 71.3: Subglottic stenosis complicated by concurrent Staphylococcus aureus infection. Courtesy: Dr C Milstein.

880

Section 7: Airway Obstruction and Stenosis

COMPLEX STENOSIS While isolated SGS has a straightforward treatment algo­ rithm, including intervention when symptomatic, and pro­ gression from endoscopic to open surgical treatment in a small fraction of refractory patients, some patients will present with multilevel disease involving the glottis or trachea, or disease previously instrumented to an extent, which has caused fixation of the vocal cords or scarring to an extent that prevents endoscopic improvement. Many of these patients will present with a pre-existing tracheotomy and need to have an individual treatment algorithms developed. It is often useful to focus the counseling on function, including transoral breathing, voice, swallowing, and tubeless airway maintenance. Patients and family members need to understand that functions need to be balanced, and improving one commonly comes at the cost of another. While every patient desires normal voice, transoral breathing, normal swallowing, and the lack of a tube, complex patients’ expectations need to be set appro­ priately or else future treatment decisions will be governed by inappropriate anticipations.

TRACHEOTOMY AND LARYNGOPHARYNGEAL REFLUX In patients with uncomplicated SGS, a tracheotomy to either temporize the airway, or to facilitate endoscopic surgery, is most commonly not required. Isolated SGS is usually slowly progressive, and with proper communica­ tion between the patient and their provider team, can be addressed without tracheotomy. But in cases in which close coordination of care is not feasible, or in multilevel stenosis cases, or in patients with other comorbidities, tracheotomy should not be avoided. Several authors have postulated that extraesophageal reflux may be causative of idiopathic SGS, or may play a role in worsening autoimmune-associated SGS.6,7 In our own series of patients with SGS, we did not find a known diagnosis of reflux changed likelihood of needing multiple surgeries.3 In addition, there is a question of cause and effect, since patients with SGS generate more negative intrathoracic pressure due to their increased inspiratory effort, potentiating reflux after the development of SGS. Regardless, like most providers, our group tends to treat patients prophylactically with antireflux medication, espe­ cially postoperatively, and in patients with sympto­matic reflux disease.

TREATMENT: ENDOSCOPIC SURGERY The guiding principle of endoscopic surgery is to cause as little disruption to the epithelium of the subglottis as possible to avoid subsequent restenosis due to circum­ ferential trauma of the airway lining. Perhaps the most important part of endoscopic therapy in preventing sub­ sequent restenosis is the direct injection of steroid into the stenotic lining. In the 1990s, GPA investigators at the National Institutes of Health demonstrated that the addition of steroid injection into their treatment algorithm reduced their rate of tracheotomy from 50% of SGS patients to 0%.8,9 If one thinks of the SGS as a hypertrophic scar, similar to a cutaneous keloid, it is understandable that direct steroid therapy can have a significant impact on reducing fibroblast function and subsequent cicatricial scar formation. Under general anesthesia, the patient’s larynx is ex­posed using a rigid laryngoscope with ports for jet ventilation. If jet ventilation was not successful in maintaining adeq­uate oxygenation, intermittent intubation and apnea was occasionally required. Endoscopy is undertaken to examine the airway and to assess for areas of additional stenosis, other synchronous lesions, and biopsy when required. Photo documentation of the stenotic segment is obtained with a 0° Hopkins rod telescope, which is passed through the stenosis to ensure adequate identification of the pre­sence of multilevel disease. A submucosal injection at the level of the stenosis is performed with a long-acting corticosteroid, most often 1–2 cm3 of Depo-Medrol, 40  mg/cm3, with attempts to inject in four quadrants of the stenosis. Next, under microscopic magnification, up to four radial incisions are made into the area of stenosis. This is completed with a CO2 laser or “cold” (with a sickle knife or scissors), taking care to preserve intervening mucosa between the incisions and not to violate the carti­ lage deep to the scar tissue. The CO2 laser is typically set at 4 W in a continuous mode. Next, balloon dilation with a radial controlled expansion balloon has replaced more traumatic methods such as bougie, due to the ability to place the balloon directly at the area of narrowing and spare the critical posterior commissure from trauma. The balloon is inflated up to 6 atm for one minute to adequately dilate the subglottis, and it is limited by the apnea required during the process, causing some desaturation to occur. It needs to be remembered that the subglottis is bounded by the cricoid, a circumferential cartilage. Aggressive dilation of stenosis, which involves the trachea, can have disastrous effects of rupturing the posterior trachealis muscle, and

Chapter 71: Subglottic Stenosis

Microflaps

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Several authors have reported the use of microflaps to endoscopically resect the underlying scar tissue of SGS while preserving the overlying epithelium. Dedo and Catten developed a CO2 laser submucosal resection with local mucosal rotation flap technique that required half of the stenosis to be addressed endoscopically every 2 months until the process abates.14 More recently, European authors describe a similar approach while concurrently applying mitomycin C to the operative site.15 Although resection of the stenosis to the level of the perichondrium is a logical goal of endoscopic treatment, outcomes have yet to be demonstrated that are superior to standard endo­ scopic steroid injection and dilation.

TREATMENT: OPEN SURGERY When recalcitrant SGS does not respond to serial endo­ scopic therapies, open laryngeal architecture surgery is contemplated. In most series, this progression along the treatment algorithm occurs in only 5–10% of patients with isolated SGS.3 This rate is significantly higher in patients with multilevel disease, which includes the glottis, and in disease of higher Myer–Cotton grading. As outlined above,

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patients with post traumatic SGS, especially tracheotomy caused cartilaginous destruction, also have a higher rate of progression to open surgery. Post open surgical techniques included cricoid augmen­ tation procedures, usually with cartilage grafts, either in an anterior cricoid split, a posterior cricoid split, or a com­ bination of the two. While posterior cricoid augmentation remains an excellent technique for glottic stenosis, most modern day open surgeons have progressed to cricotra­ cheal resection with anastomosis of thyroid cartilage to trachea for isolated SGS. Relative contraindications in our own practice for cricotracheal resection include poorly controlled diabetes, systemic steroid therapy, likely need for intubation in the near future, obstructive sleep apnea, and concomitant pulmonary disease. Active autoimmune inflammation should be controlled with systemic medica­ tions rather than open surgical resection, and it may lead to delayed healing and poor results. Patients should be warned preoperatively that their voice will be hoarse for some period postoperatively and that the quality of their voice may differ permanently with a decrease of fundamental frequency of approximately 10 Hz. This effect can be even more pronounced in women as shown by Smith et al. with a mean decrease in funda­ mental frequency of 21 Hz in the 14 women they evaluated having undergone cricotracheal resection.16 The reason for this decrease in fundamental frequency is that the cricothyroid muscle is resected at its attachment to the anterior cricoid ring, resulting in an inability to tense the vocal fold, which is the normal physiologic function of the cricothyroid muscle.

Cricotracheal Resection Technique Figures 71.5A to C demonstrate a common lesion of the subglottis and upper trachea, a frequent indication for cricotracheal resection for circumferential SGS. Not only is the anterior subglottis narrowed, but also the posterior thickening impedes airway patency. Resection of such lesions is begun with induction of anesthesia by transoral intubation with a small caliber endotracheal tube, often of an extended length to permit later entrance into the trachea without violating the balloon cuff. If the stenosis is of such caliber that dilation must take place before intubation, jet ventilation is used temporarily during the dilation, which is minimal, to avoid causing much edema. A previously existing tracheostomy tube can be used for induction but is changed immediately to translaryngeal intubation such that the tracheostomy tube does not -

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one needs to proceed with caution with more inferior stenoses.10 Mitomycin C may be applied topically to the area of dilation with a cottonoid pledget at a concentration of 0.4  mg/cm3 for one minute and repeated two to three times. This antimetabolite produced by Streptomyces caespitosus has been shown to have antineoplastic pro­ perties and inhibits fibroblast proliferation both in vivo and in vitro.11 The literature surrounding its efficacy to successfully treat and prevent recurrence of SGS has been mixed.12,13 Photodocumentation is again obtained and intubation is avoided to prevent further trauma to the epithelium, and the patient is either mask ventilated until breathing spontaneously, or a laryngeal mask away is used for airway protection. Chest radiographs can be used postprocedure to rule out a pneumothorax caused by the jet ventilation and are especially useful in patients who have a secondary, more distal airway stenosis in which jet ventilation can cause air entrapment in a lung segment and lead to overinflation. Endoscopic surgery is commonly done on an outpatient basis with postoperative humidification and antireflux medication used as protective measures against restenosis.

881

882

Section 7: Airway Obstruction and Stenosis

A

B

C

Figs. 71.5A to C: The anterior and lateral views (A, B) of a combined subglottic and upper tracheal stenosis. The dashed lines are the planned cuts for resection of the external cartilage framework, including the anterior arch of the cricoid. The lateral, internal view (C), with dashed incision locations, and the dotted lines indicating the submucosal resection of the diseased epithelium overlying the posterior cricoid cartilage plate. Source: Reprinted with permission, Cleveland Clinic Center for Medical Art & Photography (c) 2004-2013. All rights reserved.

obstruct the operative field. After intubation, the head is extended with a shoulder roll, and a transverse incision is made from sternocleidomastoid to sternocleidomastoid superior to the manubrium. The skin flaps are raised subplatysmally superiorly to the hyoid bone and inferiorly to the clavicles. The strap muscles are separated, and the thyroid gland is divided at the isthmus. Neither suprahyoid nor infrahyoid release maneuvers are routinely used. The trachea is dissected in a pretracheal plane, very close to the cartilaginous rings to avoid damaging the recurrent laryngeal nerves, which are not identified routinely. The trachea is dissected down to the carina to produce the mobility for future anastomosis, and care is taken to avoid dividing its lateral blood supply. The cricothyroid muscle is elevated laterally to permit lateral division of the cricoid laminae. The proximal line of resection transects the cricothyroid membrane just inferior to thyroid cartilage and bevels laterally through the lateral laminae of the cricoid cartilage, usually more than halfway to a midlateral line. A posterior cut at the inferior level of the cricoid cartilage is made, which may not resect the full extent of the posterior stenosis within the cricoid lamina. The stenosis within the cricoid is then resected off the posterior lamina once it is fully visualized with direct vision through the transected airway. A transverse cut against the posterior plate of the cricoid cartilage inferior

to the vocal cords and arytenoid cartilages is made, leaving the denuded posterior plate of the cartilage intact. The distal level of resection should be determined earlier by endoscopic visualization. If the inferior border of the stenosis is in question, the initial transection always should be made slightly more superiorly because repeat resection more inferiorly is always possible. The first preserved ring is beveled backward from a high point in the anterior midline to the lower margin of that ring, creating an inverted U, and care is taken not to fracture this ring (Fig. 71.6). At this point, a posterior membranous wall flap is formed to fit over the exposed posterior plate of the cricoid cartilage. The length of flap is determined by the amount of exposed posterior lamina. If needed, an addi­ tional anterior tracheal ring may be sacrificed to lengthen this posterior flap. The shoulder roll is then removed and the field made orderly to prepare for closure. Endotracheal intubation is temporarily switched to cross-table ventilation to permit optimal access to the posterior wall closure. Vicryl sutures are placed between the inferior margins of the posterior plate of cricoid cartilage to the base of the distal poste­ rior tracheal flap (Figs. 71.7A and B). These sutures are clamped to the drapes such that they can be tied later in the order of the most anteromedial suture first, lateral suture second, and posteromedial suture last. Next, Vicryl

Chapter 71: Subglottic Stenosis

883

Fig. 71.6: Excess posterior trachealis is preserved as an advancement “flap” to cover over the exposed posterior cricoid plate cartilage. Note that the superior-most preserved tracheal cartilage is shaved laterally to create the “prow” of the ship to be available to anastomose. Source: Reprinted with permission, Cleveland Clinic Center for Medical Art & Photography (c) 2004-2013. All rights reserved.

A

B

Figs. 71.7A and B: The anterior view (A) that would occur in the instance of a laryngofissure to demonstrate the posterior trachealis flap being approximated to the preserved laryngeal epithelium. The lateral view (B) demonstrates the flap in correct position against the cricoid plate, with the trachea anastomosed directly to the thyroid cartilage anteriorly. Source: Reprinted with permission, Cleveland Clinic Center for Medical Art & Photography (c) 2004-2013. All rights reserved.

rings, followed by the thyroid cartilage to the first tracheal inverted U ring. Tying of sutures begins after the patient is reintubated transorally and starts with the endolaryn­ geal sutures, continues with the anteromedial sutures, and progresses laterally and posteriorly to the posterior mid­ line (Fig. 71.8). Strap muscles can be approximated over the anastomotic suture line, adding an additional layer of closure. Nonsuction drains are placed, the head is kept in a flexed position, and the patient is extubated immediately. -

sutures approximate the tip of the posterior membranous wall flap of the trachea to the distal laryngeal mucosal line of resection within the cricoid cartilage. These sutures are placed from within the larynx, but the knots are arranged to lie outside the lumen and are clamped over the patient’s head temporarily so as to avoid confusion with the exter­ nal anastomotic sutures. Lastly, Vicryl is used to complete the anastomotic closure, starting through the remnant of lateral cricoid cartilage to the second and third tracheal

884

Section 7: Airway Obstruction and Stenosis

Fig. 71.8: After tying all sutures, the final appearance after cricotracheal resection. Source: Reprinted with permission, Cleveland Clinic Center for Medical Art & Photography (c) 2004-2013. All rights reserved.

Post Open Repair Care and Complications In cases of cricotracheal resection without T-tube place­ ment, patients are extubated immediately postoperatively. For patients with edema, one to two doses of steroid are used to decrease swelling without significantly impair­ ing anastomotic healing. Vocal cord function is assessed, and the neck is kept in a flexed position (pillows and strict nursing precautions usually suffice rather than a “Grillo stitch” from the chin to the chest) for two weeks postopera­ tively. Patients are fed via nasogastric tube for 1–2 weeks, after which a swallow study is performed before starting an oral diet. Humidified air is used to decrease the risk of mucus plugs forming at the anastomotic suture line. If superior access is required during the surgery, or if sufficient postoperative swelling occurs to limit breathing, a laryngofissure and T-tube are used (Figs. 71.9A and B) with the superior end of the T-tube placed just supe­rior to the glottis. This T-tube is subsequently removed under general anesthesia 3–4 weeks postoperatively, during which time the airway is assessed endoscopically for pate­ncy and vocal cord motion, and any granulation tis­sue is removed. Complications generally involve issues of either reste­ nosis, failure of the anastomosis to heal, or vocal fold dysfunction. When restenosis at the anastomosis occurs,

A

B

Figs. 71.9A and B: In the instance of a laryngofissure and T-tube placement, the thyroid cartilage is divided in the midline. The T-tube is often inverted, with an extended limb rising above the level of the glottis, and a shorter limb extending inferiorly into the tracheal lumen. The horizontal T-tube limb should be positioned inferior to the new anastomotic level. Source: Reprinted with permission, Cleveland Clinic Center for Medical Art & Photography (c) 2004-2013. All rights reserved.

conservative treatment with dilation often can correct a limited obstruction. Repeat resection and anastomosis may be required if one suspects that a technical error occurred during the initial operation. Posterior glottic stenosis, either from scarring, from a high resection, or from vocal fold immobility is a difficult problem to over­ come. A laser cordotomy of the less mobile vocal fold may augment the airway sufficiently to permit unlabored breath­ing, albeit at the cost of glottic competence, result­ ing in decreased voice quality. The most emergent and concerning complication is that of a nonhealing anasto­ mosis. Patients with diabetes and those on steroids are the most susceptible to this comp­lication, which, owing to the proximity of the great vessels, can be life threatening. Often the most prudent course of action is to retreat, placing a T-tube and giving antibiotics while the wound progresses and matures, after which the airway is reassessed to determine if a tracheotomy-free airway is possible once the healing process is finished.

STENTS Similar to tracheal stenosis, metallic stents for SGS should not be used in patients who are candidates for future

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Chapter 71: Subglottic Stenosis

REFERENCES

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Subglottic stenosis is a difficult problem for laryngologists, complicated by the fact that there is no standard algorithm for the treatment. The etiology of the stenosis needs to be kept in mind when determining timing and type of treatment, with a strong bias against treatment in the patient who is not symptomatic. In our own review of 10 years at a single academic institution, we found that when managed endoscopically, patients are sympto­ matically improved but recurrence rates remain high. Multiple endoscopic options exist including CO2 laser versus cold knife, balloon dilation, and the use of mito­ mycin C, but direct injection of steroid remains the mainstay of successful treatment. Only a small percent­ age of patients go on to require an open procedure, and most commonly in patients with complex, multilevel stenosis, and in patients with previous tracheotomies. Open surgery most commonly deployed is cricotracheal resection, and although invasive with permanent effects on the voice quality, the results specific to control of stenosis are excellent.



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resection and anastomosis. As subglottic endothelial healing and granulation tissue incorporates itself into the metal, hemoptosis and restenosis often occurs. Removal of the stent endoscopically is not possible, and even open removal demonstrates a nearly nonsalvageable cartila­ ginous airway framework. In addition, metal stents pre­ clude the ability to perform emergent tracheotomies in situations of acute airway obstruction. Silicone stents have been increasingly used in tracheal airway pathology due to their soft and nonreactive nature. Migration of the stent and obstruction are commonly quoted potential compli­ cations, so most often a silicone stent for SGS is performed in the form of a T tube, which allows for anchoring of the stent by the horizontal limb, which also serves as a safety valve in case the vertical limb becomes obstructed acutely. All patients with T tubes should be instructed on how to remove them in case of any emergency, and should car­ ry spare tracheostomy tubes to re establish a temporary airway if such instances arise.

CHAPTER

72

Tracheal Stenosis Sonali Sethi, Thomas R Gildea

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Advanced knowledge of the tracheal anatomy, configura tion, size, and proportions is important in order to correctly manage tracheal stenosis and provide good treatment outcomes. The trachea is defined as the inferior aspect of the cricoid cartilage, at the level of the sixth or seventh cervical vertebra, down to the main carina. The trachea is divided into the extrathoracic and intrathoracic trachea. The extrathoracic trachea lies above the suprasternal notch and is approximately one-third of the tracheal length. The

Because of the nature of airflow dynamics, small changes in the diameter of the trachea and length of the narrowed section create significant changes in airflow that result in rapidly progressive dyspnea requiring urgent intervention. An airway change of 30% creates symptoms, and a change of 80% produces dire distress. The work of breathing depends on the degree of pressure drop along a stenosis.2 This pressure drop depends not only on the degree of stenosis but also on the flow of velocity through the stenotic lesion: (∆P = kV2((R/r)2−1)2) where ∆P = pressure drop k = constant R = radius of the normal lumen

TRACHEAL ANATOMY

SEVERITY OF AIRWAY NARROWING



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Tracheal stenosis is an entity whose etiologic factors have changed drastically in the past century and is a challenging management problem that may cause severe morbidity and life-threatening airway compromise. Benign disease is an increasingly recognized problem in cases of tracheal stenosis and can be either congenital or acquired. A combination of endoscopic tools and techniques can be applied to successfully manage tracheal stenosis. When endoscopic therapy is used to treat tracheal steno sis, it should be without significant sequelae and not interfere with the future potential for surgery. Therefore, the therapeutic process involves a selection between conservative, endoscopic, and surgical procedures, but the results are not always satisfactory. A multidisciplinary approach is usually recommended, as the decision for a specific intervention is dictated by the needs of each patient and demands a high degree of expertise and collaboration between otolaryngologists, interventional pulmonologists, and thoracic surgeons.

intrathoracic trachea falls below the suprasternal notch and makes up two-third of the remaining tracheal length. The length of the normal adult trachea is 10–14 cm. The trachea maintains its structural support with 18–24 C-shaped cartilaginous anterior rings. The posterior wall of the trachea is a membranous band which contains glands, small arteries, nerves, lymph vessels, and elastic fibers making it vulnerable to injury. The diameter of the trachea in adult men ranges from 1.3 cm to 2.5 cm and in women from 1.0 cm to 2.1 cm1 (Fig. 72.1). The blood supply to the cervical trachea is supplied by the superior and inferior thyroid arteries. The mediastinal trachea is sup plied by the bronchial arteries. Extensive dissection around the trachea causes ischemia.



INTRODUCTION

888

Section 7: Airway Obstruction and Stenosis

Fig. 72.1: Anatomy of the proximal tracheobronchial tree. Source: Redrawn with permission from Simhoff et al.1

r = radius of the stenosis V = flow velocity. The pressure drop across the stricture doubles when a 70% stenosis is observed. Patients are usually sympto­ matic with exertion at 50% obstruction and symptomatic at rest with 70% obstruction.

MORPHOLOGY AND CLASSIFICATION Tracheal stenosis may be classified according to the morphological aspects of simple or complex stenosis. Simple stenoses comprise short segments ( 1 cm), circumferential contraction scarring and/or associated with malacia or loss of cartilaginous support. In order to predict interventional success, several laryn­ gotracheal stenosis classifications have been proposed. However, these classification systems have limitations and rely on the physician’s skills and judgment for classification.

Laryngotracheal stenosis was first classified by Cotton based on the degree of airway narrowing.3 Myer et al. revised the original Cotton grading system by determin­ ing the degree of tracheal stenosis using standard endo­ tracheal tubes as guides and observing how they pass through the narrowest point.4 Together, the Myer–Cotton system is based on circumferential stenosis with four staging degrees based on the percentage of reduction in the cross-sectional area, using cutoff values of 50% and 70% narrowing to define grades. Location and length are noted, but do not affect the grade of stenosis. This was later followed by Grundfast et al., who looked at factors predictive of outcome in patients treated for stenosis and opted for a more descriptive form of classification.5 They addressed airway opening by measuring its diameter at the narrowest point. The measurement of length and four types of consistency (soft, hard, cartilaginous, and mixed) was added. Contrary to these classifications, McCaffrey suggested that treatment success depends on the subsites involved and the length of the stenosis, but does not take into account the degree of luminal reduction (Table 72.1).6 Locations were confined to the glottis, subglottic area, and upper trachea. Another step toward creating a multidimensional system was attemp­ ted by Anand et al. who reviewed the treatment of tracheal stenosis, mostly postintubation cases, and charac­ terized stenoses based on severity, location, length, and number of stenoses.7 Most recently, Freitag et al. attemp­ ted to propose a standardized classification scheme with descriptive images and diagrams for rapid and uniform classification of central airway stenosis (Fig. 72.2). It allows for accommodation for a single area of simple stenosis to those with multiple complex stenoses. This system divides stenosis into structural and dynamic types and further classifies the disease by degree of steno­sis, location, and the transition zone or abruptness of stenosis.8 In general, stage I lesions have the highest success rate while stage IV lesions have the lowest. In addition, complex stenoses have a lower endoscopic treatment success rate compared to simple stenoses. Tracheal stenosis includes various morphologic de­ scrip­tions such as A-shaped, circumferential, weblike, com­ plex, eccentric, pseudostenosis, and mixed with certain morphologies being characteristic of etiology (Figs. 72.3A to C). For example, post-tracheostomy stenosis is typically A-shaped or triangular; idiopathic subglottic stenosis is typically a circumferential (concentric) simple lesion; and postintubation tracheal stenosis (PITS) can be hour­ glass or complex. Morphology can affect flow dynamics,

Chapter 72: Tracheal Stenosis Table 72.1: Tracheal stenosis classification systems.

Grade

Myer–Cotton system

McCaffrey system

Grade/stage I

3,600 deaths.2 It is most common among males, and is especially common among those with a history of smoking,3 with some suggesting that the larynx is the organ most susceptible to the deleterious effects of chronic carcinogen inhalation.4 The incidence in males declined between 1980 and 2005 and increased in females during the same time, most likely due to the changing patterns of tobacco use.3 Squamous cell car­ cinoma (SCCa) is the most common type of cancer involving the larynx, comprising >95% of these cancers.3,5 Premalignant and early malignant changes can challenge the multifunctional larynx. While symptoms can lead to diagnosis at an earlier stage than similar cancers in other sites of the head and neck, the resultant morbidity from the disease and its treatment can be significant. Moreover, the optimal diagnosis and treatment of these lesions can be confounded by other benign conditions. These benign conditions, including traumatic, infectious, and congeni­ tal abnormalities, can contribute to laryngeal dysfunction and mimic premalignant and early malignant lesions. A detailed history and careful examination are imperative in the diagnosis and management of laryngeal diseases. The contemporary management of early laryngeal premalignant and malignant lesions must establish equi­ poise between oncologic success and minimal treatment morbidity. Although the survival rates for laryngeal can­ cer have remained stable for the last several decades,

advances in both surgical and nonoperative therapies offer patients multiple treatment options to achieve this desired balance between excellent rates of cure with ever decreasing morbidity.4 The contemporary treatment conversation for early laryngeal cancer and premali­ gnancy has therefore shifted from survival outcomes and organ preservation to include measures of voice outcome, quality of life, and even cost.1 ­

INTRODUCTION

MIMICRY It is crucial to establish the correct diagnosis. Numerous conditions can appear to imitate the early changes of cancer. Figures 74.1A to D demonstrate several examples of benign conditions that could be confused with malig­ nancy. A thorough history is required; a long history of smoking and alcohol abuse would raise concern for even an apparently benign lesion. An absence of this history does not exclude malignancy; however, even patients with no history of alcohol or tobacco use may present with malignancy. Any lesion or change of the larynx should be carefully examined with a mirror, utilizing the enhanced visualization of flexible laryngoscopy and videostrobo­ scopy without reservation to complement the exam. In one series of 25 cases of early glottic carcinoma reviewing the benefits of videostroboscopy, the authors noted abnormal vocal fold stiffness and absent mucosal waves in each patient that was not apparent on routine, flexible laryngoscopy.6 When distinguishing between malignant disease and a host of other pathologies, an understanding of potential alternative diagnoses and their presentations

916

Section 8: Premalignant and Early Laryngeal Cancers

A

B

C

D

Figs. 74.1A to D: Common mimickers of early laryngeal cancer. (A) Vocal fold nodule; (B) Hemorrhagic polyp; (C) Recurrent respiratory papillomatosis; (D) Laryngeal candidiasis. Source: Dr Paul Bryson, The Cleveland Clinic Foundation.

is crucial. Knowledge of the clinical features of laryngeal pathology can also contribute to an accurate diagnosis.7

DYSPLASIA The differentiation between benign and malignant lesions can be difficult, as aforementioned. Spanning between benign and malignant lesions, there exists a subset of clini­ cally apparent lesions that are neither benign nor con­sistent with invasive carcinoma (Figs. 74.2A and B). Leukoplakia, erythroplakia, and mixed leukoerythroplakia are clinical descriptors, while the term dysplasia is used to describe microscopic cellular atypia. Each has been noted to harbor an increased risk of transformation to SCCa when com­ pared to normal epithelium,8 with the clinical description

of leukoplakia indicating the presence of keratin on the surface of the normally nonkeratinizing mucosa.9 In the setting of atypia without frank invasion, clinically appa­ rent areas are known as dysplastic lesions, squamous intraepithelial lesions (SILs), or squamous intraepithe­ lial neoplasia.10 The last term is discouraged, as a high percentage of these lesions will never progress to become neoplasms. In the absence of histologic dysplasia, the clinical changes of leukoplakia have been noted to progress to SCCa in 4–11% of cases.8,9 Although any leukoplakia can progress to become cancer, it is clear that the presence of histopathologic dysplasia is a marker for an increased risk of malignant degeneration. Rates of progression to malignancy in the setting of histologic atypia increase to

Chapter 74: Premalignant and Early Malignant Lesions of the Larynx

A

917

B

Figs. 74.2A and B: Dysplasia. (A) Clinical changes secondary to dysplasia of the right true vocal fold. (B) Leukoplakia from dysplasia of the bilateral true vocal folds. Source: Dr Paul Bryson, The Cleveland Clinic Foundation.

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Pathology

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Confusion may arise from the multiple terms and grad­ ing systems that are used to describe histopathologically the clinical entity of leukoplakia. Each system relies on the assumption that more atypical lesions will have a greater rate of progression to malignancy, with each

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attempting to provide superior prognostic information.8 The World Health Organization (WHO) and Ljubljana Grading systems are frequently used, and atypia is divided into three stages of progressive dysplasia, with the WHO classification adding benign keratosis and carcinoma in situ (CIS) as bookends to the Ljubljana system8 (Figs. 74.3A to E). The multiple grading systems in use underscore the fact that there is no perfect system. Numerous studies have noted that each of the systems suffers from flaws in reliability.8,11,15 Binary systems of grading dysplasia are more reproducible, but may offer less prognostic value than the graded systems discussed above. Clinically, this confusion is most relevant in acknowledgement of the limitations of intervention based on the classification of dysplasia. Within that paradigm, it is noteworthy that improvements in reliability and reproducibility have been found following group training of pathologists.8,15 This highlights the need for a close working relationship between the surgeon and pathologist, as well as the need for pathologists well versed in the field of laryngeal dysplasia. ­

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>30% in some series, with other studies citing rates as high as 50%.11,12 The microscopic findings that histologically differentiate dysplastic lesions are thought to correlate with genetic changes in the stratified squamous epi­ thelium.8 It is likely that these genetic changes underlie the current understanding that the more microscopically atypical a lesion, the greater the likelihood of malignant transformation.9 Although severely atypical lesions are more likely to become cancer, the majority of dysplastic lesions do not progress in this fashion.8 It is difficult to know the role of invasive therapies directed at controlling atypical cells that are not malignant when most patients, even patients with microscopic findings of severe dysplasia, will not progress to invasive carcinoma.10,13,14 The prolonged interval between the diagnosis of dysplasia and the ultimate development of laryngeal carcinoma, estimated to have a mean time of six years, necessitates long standing follow up and further complicates the treatment paradigm.13 An example of this clinical dilemma is illustrated by the patient with early dysplasia who is lost to follow up and presents years later with an advanced stage laryngeal cancer.

Genetics The current prognostic limitations have spurred the search for additional methods to predict the course of dysplastic lesions. The presence of both inciting oncogenes and defe­ ctive tumor suppression is often necessary for a laryngeal lesion to progress to cancer, with generally 4–10 mutations necessary for abnormal cells to become malignant.4,16

918

Section 8: Premalignant and Early Laryngeal Cancers

A

B

C

D

E

Figs. 74.3A to E: Examples of pathologic lesions staged using the WHO system of grading squamous dysplasia of the upper aerodigestive tract. (A) Benign hyperplasia with hyperkeratosis shows a thickening of the epithelium without atypia or architectural distortion. (B) Mild dysplasia is subtle, but shows mild cytologic atypia that involves only the lower third of the epithelium. (C) Moderate dysplasia displays increased nuclear atypia, along with architectural disarray, involving the lower two-thirds of the epithelium. (D) Severe dysplasia displays prominent nuclear atypia and architectural distortion, extending into the upper one-third of the epithelium. (E) CIS is characterized by full-thickness involvement of the epithelium by abnormal cells. An invasive squamous cell carcinoma was directly adjacent to this photo. Source: Dr Deborah Chute, The Cleveland Clinic Foundation.

His­tologic changes have been noted to correlate with these progressive genetic events.4 Immunohistochemistry uti­ lizes genetic markers to add to traditional histopathology.

In general, proteins related to cell proliferation and cell-cycle regulation have been used (p53, p16, and cyclin D1) as markers of potential genetic insults, similar to other lesions

Chapter 74: Premalignant and Early Malignant Lesions of the Larynx

Diagnosis

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Dysplasia of the larynx can lead to symptoms such as dysphonia, dyspnea, dysphagia, and otalgia, with the symptoms varying significantly based on the specific loca­ tion of the lesion. Supraglottic lesions, especially, can lead to otalgia due to proximity to the vagus nerve, which innervates both the larynx and the ear. This relation­ ship underscores the need for laryngeal examination if otalgia symptoms are not explained by appropriate aural pathology.5 Dysphonia is often the earliest sign of glottic patho logy.While there is a wide variation between recommen dations from different authors regarding appropriate diagnostic intervention for dysphonia, a 2009 consensus statement from the American Academy of Otolaryngo­ logy—Head and Neck Surgery Foundation does offer some guidelines.19 Dysphonia is to be evaluated with laryngeal visualization if it persists for > 3 months or sooner if a malignant pathology is suspected. Antibiotics, corticosteroids, and antireflux medications are not to be routinely utilized in the absence of suggestive symp­ tomatology. Furthermore, imaging such as computed tomography is not to be obtained prior to visualization of the larynx. Surgical intervention, as discussed below, serves a vital role in both the diagnosis and management of this disease. When concerning laryngeal lesions are identified and more information is necessary, biopsy may be justified. Historically, some lesions have been followed until concern was high enough to justify the risk of general anesthesia.20 In these cases, office based biopsy may be appropriate, with some authors suggesting that staging and biopsies may be as accurate as when completed in the operative suite.21 Patient selection is critical in this situation.20 ­

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of the upper aerodigestive tract. Markers of proliferation (Ki67, PCNA), angiogenesis (vascular endothelial growth factor or VEGF), apoptosis dysregulation (Bcl 2), trans­ membrane receptor dysfunction (epidermal growth factor receptor, EGFR), and cell adhesion (osteopontin, cortac­ tin, and CD44) have also been studied and utilized with varying results. The finding of clinicopathologic similarities within tumor groups containing common genetic events suggests that, in the future, dysplasia and tumor classi­ fication may rely to some degree on genotyping.15,17 Although genetic analysis continues to offer the promise of improving personalized prognostication and treatment, clinicopathologic stage and histologic details remain the major determinants of tumor classification and treatment at this time.11,17

919

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Management The management of laryngeal dysplasia is a contentious subject.10,14,22 24 Historically, vocal fold stripping, the prac­ tice of removing the affected mucosa to the anterior commissure, had been used for suspicious lesions. Due to suboptimal voice outcomes with aggressive removal of the mucosa, this practice has widely been supplanted by laryngeal microsurgery to excise the lesions with microflap techniques.7,22 Suspicious laryngeal lesions have been managed with direct microlaryngoscopy followed by excision with phonomicrosurgical instrumentation or varied lasers. The use of intraoperative frozen section -



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Risk factors in the development of laryngeal dysplasia and malignancy are important for patient education and treat­ ment. A preponderance of evidence indicates tobacco smoke to be the most prominent risk factor. Risk of dys­ plastic changes has been found to be related to age at initiation as well as duration of smoking. Alcohol acts synergistically with tobacco exposure. Increased risk of laryngeal cancer has been found to persist > 40 years after smoking cessation.10 Additionally, environmental expos­ ures to products such as heavy metals, paint, and asbestos, among others, can lead to an increased incidence. Gastroesophageal reflux disease has been suggested as a potential risk factor in the development of dysplasia and laryngeal cancer for decades. Studies comparing the incidence of gastric resection18 noted a much higher rate of gastric resection among patients with a history of laryngopharyngeal cancer, possibly suggesting a role of reflux. The same group also directly demonstrated a much higher rate of asymptomatic reflux in a group of patients with laryngeal cancer. While many studies have demonstrated potential links, small sample sizes and the retrospective nature of the series make it difficult to definitively associate the two and define the level of risk.10 Similarly, the relationship between human papillomavirus (HPV) infection and laryngeal dysplasia or malignancy remains incompletely understood. With the virus vari­ ably identified in laryngeal samples, reported odds ratios of progression to malignancy among HPV infected indi­ viduals remain more modest than those noted in other sites such as the tonsil. This suggests that a direct infectious link is less likely to occur.10

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Development/Inciting Factors

920

Section 8: Premalignant and Early Laryngeal Cancers

analysis offers the advantage of single-stage intervention with pathologic guidance of resection margins. The use of a CO2 laser has been found to be beneficial to some practitioners, who cite the precision and hemostatic pro­ perties of the laser as being advantageous. There are concerns, however, for heat spread causing injury to the deeper lamina propria layer of the vocal fold. Other lasers, such as the pulsed dye laser (PDL) and the pulsed potassium titanyl phosphate (KTP) laser, described below, offer significant advantages in treating broad, superficial lesions such as premalignant dysplasias in both the operating suite and the outpatient clinic.25-27 In most cases, an initial visit to the operating room or an office-based biopsy to map dysplasia and identify possible subclinical tumors is prudent before initiating PDL or pulsed KTP laser therapy, which has the disadvantage of not resulting in a pathologic specimen for tissue analysis.5 It can be difficult to differentiate regions of dysplasia from the surrounding, less-affected tissues, as clinical findings, such as leukoplakia, are not always present with underlying microscopic pathology. Various techniques including autofluorescence and 5-aminolevulinic acid (5-ALA) capitalize on the variability between dysplastic cells and the surrounding, less-affected mucosa.22 Despite early promise, these techniques have not been widely adopted in the routine clinical setting. Narrow band imaging (NBI) is being utilized in the outpatient clinic and may add benefit in that setting, where video documentation allows for subtle changes to be chronicled. Direct excision of laryngeal dysplasia is often proble­ matic due to the wide areas of affected tissue. Chronic exposure to carcinogens over a broad area is common, which can result in field cancerization. Patient education is a key component to management discussions. Continued smoking, severe dysplasia, poor patient follow-up, and other factors may tip the scales in favor of more aggres­ sive and earlier management. Radiation therapy may offer some benefit when resection of broad areas would be necessary and would result in great morbidity or when recurrence has occurred despite multiple resections and there is concern for organ preservation. Sengupta et al. noted CIS control rates >90% with radiation therapy, with failures occurring as late as 13 years after treatment.28 Sadri et al., in 2006, reviewed the available literature regard­ ing rates of dysplasia control and progression, concluding that radiation therapy is most effective at controlling dys­ plasia, although this benefit must be weighed against

the morbidity of laryngeal radiation.14 Local control rates without progression to malignancy > 93% were found with radiation, as opposed to about 80% for lesions managed surgically. Some more recent data suggest that these lesions may be well managed with the KTP laser, poten­ tially decreasing morbidity and preserving the option of radiation for refractory lesions.25,26 These modalities lend themselves well to in-office therapy and are becoming more wide spread in that setting. Chemoprevention and phototherapy are other, less proven, techniques for manag­ ing laryngeal dysplasia.14

EARLY GLOTTIC CANCER Definition If dysplasia is the presence of cellular atypia extending to the basement membrane, SCCa is the invasion of this atypia through the basement membrane. Violation of this barrier signifies the ability of the lesion to not only be invasive at the local site but also have potential for regio­ nal and distant metastasis. A tumor progression model has been proposed for SCCa that suggests a natural prog­ res­sion along the path from atypical cells through the various stages of dysplasia up to CIS. From this point, breach of the basement membrane becomes a micro­ invasive carci­noma that can then become widely invasive carcinoma.5

Genetics and Pathologic Variants Any of the previously mentioned genetic variations or insults can be involved in progression of cells from dys­ plasia to malignancy. Cancer is due to accumulated genetic insults that have enabled the affected cells to avoid normal immune surveillance, demonstrate a survival advantage relative to other cells, and progress due to dysregulated cell cycles that increase the risk of local or metastatic harm. The aforementioned genes in the discussion of dys­ plasia remain relevant to the discussion of malignancy. Matrix metalloproteins and prostaglandins such as COX2, encoded by PTSG2, have also been found to play roles in the progression to more aggressive tumor phenotypes.17 For those lesions that have progressed beyond dys­ plasia, there are morphologic variants of SCCa that may arise and identification of these may offer prognostic implications. Table 74.1 reviews some of the more common SCCa subtypes.

Chapter 74: Premalignant and Early Malignant Lesions of the Larynx

921

Table 74.1: Histomorphologic variants of squamous cell carcinoma.67,68

Pathological

Clinical

Verrucous

Broad, pushing borders and well differentiated

Locally aggressive, limited metastatic potential

Papillary

Frond like exophytic architecture

Frequent recurrences, good prognosis. Perhaps associated with HPV

Basaloid

Similar to basal membrane of typical stratified squa­ mous epithelium, but admixed with conventional SCCa

Similar to poorly differentiated SCCa: aggressive with early metastases

Spindle cell69

Mesenchymal phenotype with definitive squamous differentiation

Polypoid and exophytic, laryngeal predilection. Often excised completely at initial biopsy.

Adenosquamous

Distinct squamous component with less obvious and Aggressive: Early local metastases and frequent local atypical glandular components; abnormal surface recurrence epithelium

68

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Subtype

(HPV: Human papilloma virus; SCCa: Squamous cell carcinoma).

Anatomic Considerations of Disease Management Anatomy

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The larynx comprises three distinct subsites: the supra­ glottis, the glottis proper, and the subglottis (Fig. 74.4). Knowledge of both macroscopic anatomy and microscop­ ic features of the larynx provides invaluable diagnostic, prognostic, and treatment information to the surgeon. The supraglottis extends from the tip of the epiglottis to the superior aspect of the true vocal folds. Embryologi­ cally, it is derived from the midline buccopharyngeal pri­ mordium and the third and fourth branchial arches. This derivation explains the rich lymphovasculature present, which in turn explains the relatively high rate of regional metastasis, which is often bilateral.5 Most malignancies of the supraglottis are present at the epiglottis and can readily transverse the foramina of the epiglottic cartilage, resulting in progression of tumor staging from T1 to T3 due to involvement of multiple subsites. Other subsites of the supraglottis include the false vocal folds, the aryepiglottic fold, and the arytenoids. Lesions of the aryepiglottic folds may behave in a manner similar to hypopharyngeal tumors of the pyriform sinus.29 The glottis comprises the inferior and posterior sur­ faces of the true vocal folds, being measured as the 1 cm region immediately distal to the supraglottis. Whereas the supraglottis demonstrates rich lymphatics, the glottis proper does not, with T1–T2 lesions having rates of regional metastasis 90% for T1 lesions. Trends in current management include a reduction in open surgical procedures, given the excellent survival data with less morbid interventions through a transoral or endoscopic approach.36 Given the success in treating early stage laryngeal cancer with most patients, the conversation has now turned to patient reported voice outcomes, long term larynx preservation, and other measures of quality of life.37 40 One study noted a five year larynx preservation rate that was higher for early glottic cancer patients treated initially with transoral surgery (93 versus 83%), but at the cost of increased voice deficiency for T2 lesions.38 Another study comparing transoral laser versus radiation therapy for stage I and stage II carcinomas found improved laryngeal preser­ vation, with only 1 of 143 patients ultimately requiring laryngectomy. Consistent with other studies, Voice Handi­ cap Index scores were significantly lower at all time points for those managed with radiation therapy.41 In determining the optimal therapy for individual patients, education and patient preference are imperative. Frank discussion of anticipated voice demands, a patient’s ability to follow up, and long term goals are expectations in the modern care of laryngeal lesions.



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Management

924

Section 8: Premalignant and Early Laryngeal Cancers

Fig. 74.6: Cordectomy.46-48

Lasers While the full description of laryngeal laser surgery is reviewed in other chapters, laser resection either in the operating room or in the outpatient clinic may be an ideal approach. Of the multiple lasers in use for superficial lesions, the 585 nm PDL and the 532 nm pulsed KTP laser are the most popular and work by heat transfer from the laser to the oxyhemoglobin of the treated tissues. This is effective in debulking broad areas of affected tissue with minimal deeper spread of tissue damage, with the obvious advantage for premalignant lesions.25-27,50 Some authors

are extending these results to early malignancies with close follow-up.50 A primary disadvantage when performed in the office setting is the number of treatments needed for disease resolution and also the lack of tissue available for pathologic review. Either could result in delayed diagnosis of deeper lesions that would necessitate more aggressive therapies, although one study found 100% organ preser­ vation in a small group with a mean of 27 months of follow-up.50 These authors reported an average of 2–3 trips to the operating suite, with an additional 1–2 outpatient treatments with the laser over the course of the series.

Chapter 74: Premalignant and Early Malignant Lesions of the Larynx

Vertical and Extended Hemilaryngectomy The vertical hemilaryngectomy is a versatile, transcervical, organ sparing procedure that offers en bloc resection for T1–2 lesions, as well as potential therapy for selected T3 or rare T4 tumors. Absolute contraindications include subglottic extension >1 cm, a nonmobile cricoarytenoid joint, cartilage invasion, and extralaryngeal soft tissue involvement. Skin flaps are raised, the strap musculature is lateralized, perichondrium is preserved, and a midline thyrotomy, as well as a cricothyroidotomy and a superior petiole incision to expose the tumor, is performed. The strap musculature or perichondrium is then utilized for recon­ struction of the neoglottis. For lesions with involvement of either the anterior commissure (with up to one third of the contralateral true vocal fold) or a single cricoarytenoid joint without fixation, the vertical hemilaryngectomy may be extended via either a frontolateral or posterolateral hemilaryngectomy, respectively.5

Laryngofissure and Cordectomy ­

This procedure provides control to only T1 tumors of a single vocal fold. It is performed via a midline thyrotomy and exposure of both vocal folds, followed by resection of the tumor confirmed by frozen pathology.5 Voice out­ comes have been found to be superior to those obtained via partial laryngectomies.52

Supraglottic Laryngectomy

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For supraglottic lesions, a horizontal or supraglottic laryn­ gectomy offers another organ sparing option with out­ comes better than radiation therapy. The larynx is removed above the glottis to the hyoid bone via a transverse incision between the junction of the superior one third and the inferior two third of the thyroid cartilage, and the elevated perichondrium is sutured to the base of the tongue. All patients require tracheostomy and will require extended rehabilitation before swallowing is possible. For those patients who have adequate pulmonary reserve and nonsevere general health comorbidities allowing them to undergo this procedure, long term speech is generally quite good. T1–3 lesions are amenable to this approach, with absolute contraindications dictated by the extent of the surgery and postoperative recovery. These include vocal fold fixation, cartilage involvement, significant base of tongue extension, and involvement of the apex of the pyriform sinus.5 -

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Partial open laryngectomy provides a surgical alternative to patients with early laryngeal tumors. In some cases, these procedures are being offered to patients with more advanced or recurrent tumors or in circumstances when adequate transoral exposure cannot be achieved. In other cases, robotics and newer transoral instrumentation have extended the reach of partial laryngectomies beyond the traditional open techniques (discussed below). Diligence and discipline in patient selection and procedure recom­ mendation are necessary for optimal outcomes. Relative contraindications, such as overall health status, pulmo­ nary reserve, and patient cooperation with postoperative rehabilitation, must be considered, as well as the specific anatomic contraindications to each approach. With all open procedures, voice outcomes are generally considered to be inferior, making these procedures often considered as salvage following failed transoral surgery or radiation therapy. Consideration of the three valves that protect the airway, the true vocal folds, the false vocal folds, and the epiglottis/aryepiglottic folds, will ensure that the surgical approach to the involved larynx preserves at least a single measure of prevention of aspiration. Failure to do so may result in chronic aspiration and the subsequent sequelae of recurrent pneumonia.

Supracricoid Partial Laryngectomy With success rates near those demonstrated by total lary­ ngectomy, the supracricoid partial laryngectomy offers a salvage or primary treatment option for patients who have cartilage or glottic involvement that would preclude supraglottic laryngectomy. All laryngeal structures supe­ rior to the cricoid may be removed, with the notable exclusion of a single arytenoid. The cricohyoidopexy or ­

Partial Laryngectomies

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With deeper or larger lesions where pathology is necessary, the carbon dioxide laser is a modality with extended range and excellent hemostasis.51 Adaptations to this laser allow utilization through a handheld fiberoptic device (OmniGuide, Cambridge, MA, USA), and this is one system that is utilized in a transoral laser approach. Extensive literature suggests similarities in survival, voice outcomes, and cost between radiation and surgical thera­ pies. An advantage of transoral resection, both laser and nonlaser treatments, includes the preservation of further treatment options, should tumor recurrence occur.41 Con­ sideration for further transoral resection, partial laryn­ gectomy, radiation, chemotherapy, and total laryngectomy all remain as viable options, should they be needed.

925

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Section 8: Premalignant and Early Laryngeal Cancers

cricohyoidoe­piglottopexy serves to reconstruct the laryn­ geal valve neces­sary to prevent aspiration, and aryepiglo­t­tic or ary­te­noid to the tongue base provides coarse speech. Sperry et al. pre­sented five years’ overall survival of 100% in their series of appropriately selected T2 patients, with a 91% larynx pres­ervation rate among those previously irradiated.53

Near-total Laryngectomy For those patients with subglottic or tracheal tumor involve­ ment, the near-total laryngectomy can provide unilate­ral resection of an entire hemilarynx including tracheal resection. The anterior aspect of the contralateral true vocal fold may also be sacrificed. Tracheostomy is neces­ sary for respiration, but speech is enabled via a dynamic tracheoesophageal shunt, utilizing the residual arytenoid as a valve for speech.5 In many instances, tracheoesopha­ geal punc­ture with prosthesis has replaced this procedure.

Radiation Therapy As has been described previously, single-modality radia­ tion therapy offers the potential of preserving laryngeal function for early-stage laryngeal cancer and, where appro­priate, dysplasia. Disease-free survival rates >90% are con­sistently found in multiple series for early T1 lesions, with a corresponding drop as the lesions advance in stage.54,55 As with surgery, the anterior commissure histo­ ri­cally has presented a challenge to single-modality radi­­ ation therapy. Recent adjustments in dosing may offer some promise at overcoming the unfortunate decrea­ sed histori­cal success of treating these lesions. Intensitymodulated radiation therapy (IMRT) uses computed tomography to identify and treat specific tumor areas rather than broad fields. This allows for both the boost­ ing of treatment at sites of concern and decreasing doses near critical struc­tures. The neck may be simulta­ neously treated if there is suspicion or probability of involvement. Salvage options include partial laryngec­ tomy options as above, but often result in total laryn­ gec­tomy.56 Salvage rates exceeded 70% following failed radiotherapy and were not dependent on tumor staging in one series.57 The majority of patients will have improve­ ment in voice outcomes following radia­tion therapy.55

Chemotherapy and Biological Therapy Currently there is no well-described role for chemotherapy. There has been a complete response to some patients

following induction chemotherapy. This group remains the minority, and response is poorly understood.58 More recent results suggest that primary treatment of glottic cancers with chemotherapy is not an effective treatment strategy, with 0 of 32 patients demonstrating persis­tent locoregional response in one series.59 Platinum-based agents predominate when utilized for head and neck cancers, and have demonstrated greatest efficacy when used concurrently with radiation therapy. While not gener­ ally appropriate for early-stage laryngeal tumors outside of the rigors of approved clinical trials, cetuximab is an EGFR inhibitor that is a targeted genetic therapy and has received approval for use in head and neck cancers. Other therapeutics, gefitinib, erlotinib, have been developed to inhibit the same EGFR pathway further downstream from the initial target of cetuximab.

DEVELOPMENT OF CENTERS OF EXCELLENCE Given the diversity of patient populations and the increas­ ing speed of developing technologies, there has been a recent trend toward the development of centers of excel­ lence for the treatment of laryngeal cancer. Such speciali­ zation offers the promise of consolidating resour­ces and training to allow all patients the opportunity to receive per­ sonalized care. Specific examples include the use of IMRT, which may not be available at all centers, and organ-sparing salvage surgeries, which necessitate both appropriate sur­ geon training and considerable volume for best results.

FUTURE DIRECTIONS The future of diagnosing and managing squamous dys­ plasia and early glottic cancers will utilize genetic markers to predict which lesions will progress to frank malignancy. Understanding of the biologic mechanism will allow for personalized treatment strategies based on each tumor’s unique profile. The use of these markers to identify which lesions will need intensification beyond single-modality therapy will prove vital to improving outcomes. Narrow band imaging, or NBI, which has been utilized in Barret’s esophagus and other mucosal lesions, is now being applied to the larynx. Using specific wavelengths of light that are preferentially absorbed by hemoglobin, the blue and green light utilized in NBI can bypass the most superficial layers of mucosa to highlight vascular changes in the mucosal capillaries.60-62 By analyzing the patterns

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Chapter 74: Premalignant and Early Malignant Lesions of the Larynx

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1. Waghmare CM, Agarwal J, Bachher GK. Quality of voice after radiotherapy in early vocal cord cancer. Expert Rev Anticancer Ther. 2010;10(9):1381 8. 2. Howlader N, Noone AM, Krapcho M, et al. (2012). SEER cancer statistics review, 1975–2010. [Online]. Available from http://seer.cancer.gov/statfacts/html/laryn.html [Accessed May 2013]. 3. Schultz P. Vocal fold cancer. Eur Ann Otorhinolaryngol Head Neck Dis. 2011;128(6):301 8. 4. Loyo M, Pai SI. The molecular genetics of laryngeal cancer. Otolaryngol Clin North Am. 2008;41(4):657 72. 5. Merati AL, Bielamowicz SA (Eds). Textbook of Laryngology. San Diego, CA: Plural Publishing, Inc; 2007. p. 502. 6. Crumley RL. Videostroboscopy in the assessment of early glottic carcinoma. Arch Otolaryngol Head Neck Surg. 1989; 115(12):1415. 7. Zeitels SM. Premalignant epithelium and microinvasive cancer of the vocal fold: the evolution of phonomicrosurgi­ cal management. Laryngoscope. 1995;105(3):1 51. 8. Eversole LR. Dysplasia of the upper aerodigestive tract squamous epithelium. Head Neck Pathol. 2009;3(1):63 68.



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9. Isenberg JS, Crozier DL, Dailey SH. Institutional and com­ prehensive review of laryngeal leukoplakia. Ann Otol Rhinol Laryngol. 2008;117(1):74 79. 10. Gale N, Michaels L, Luzar B, et al. Current review on squa­ mous intraepithelial lesions of the larynx. Histopathology. 2009;54(6):639 56. 11. Rodrigo JP, Garcia Pedrero JM, Suarez C, et al. Biomarkers predicting malignant progression of laryngeal epithelial precursor lesions: a systematic review. Eur Arch Otorhino­ laryngol. 2012;269(4):1073 83. 12. Spielmann PM, Palmer T, McClymont L. 15 year review of laryngeal and oral dysplasias and progression to invasive carcinoma. Eur Arch Otorhinolaryngol. 2010;267(3):423 7. 13. Weller MD, Nankivell PC, McConkey C, et al. The risk and interval to malignancy of patients with laryngeal dysplasia; a systematic review of case series and meta analysis. Clin Otolaryngol. 2010;35(5):364 72. 14. Sadri M, McMahon J, Parker A. Management of laryn­ geal dysplasia: a review. Eur Arch Otorhinolaryngol. 2006; 263(9):843 52. 15. Nankivell P, Weller M, McConkey C, et al. Biomarkers in laryngeal dysplasia: a systematic review. Head Neck. 2011;33(8):1170 6. 16. Almadori G, Bussu F, Cadoni G, et al. Multistep laryngeal carcinogenesis helps our understanding of the field cancerization phenomenon: a review. Eur J Cancer. 2004; 40(16):2383 8. 17. Makitie AA, Monni O. Molecular profiling of laryngeal cancer. Expert Rev Anticancer Ther. 2009;9(9):1251 60. 18. Galli J, Cammarota G, Volante M, et al. Laryngeal carcinoma and laryngo pharyngeal reflux disease. Acta Otorhino­ laryngol Ital. 2006;26(5):260 3. 19. Schwartz SR, Cohen SM, Dailey SH, et al. Clinical practice guideline: hoarseness (dysphonia). Otolaryngol Head Neck Surg. 2009;141(3):S1 S31. 20. Shah MD, Johns MM III. Office based laryngeal procedures. Otolaryngol Clin North Am. 2013;46(1):75 84. 21. Postma GN, Bach KK, Belafsky PC, et al. The role of trans­ nasal esophagoscopy in head and neck oncology. Laryn­ goscope. 2002;112(12):2242 3. 22. Johnson FL. Management of advanced premalignant laryngeal lesions. Curr Opin Otolaryngol Head Neck Surg. 2003;11(6):462 6. 23. Dispenza F, De Stefano A, Marchese D, et al. Management of laryngeal precancerous lesions. Auris Nasus Larynx. 2012;39(3):280 3. 24. Mehanna H, Paleri V, Robson A, et al. Consensus state­ ment by otorhinolaryngologists and pathologists on the diagnosis and management of laryngeal dysplasia. Clin Otolaryngol. 2010;35(3):170 6. 25. Sheu M, Sridharan S, Kuhn M, et al. Multi institutional experience with the in office potassium titanyl phosphate laser for laryngeal lesions. J Voice. 2012;26(6):806 10. 26. Zeitels SM, Franco RA Jr, Dailey SH, et al. Office based treatment of glottal dysplasia and papillomatosis with the 585 nm pulsed dye laser and local anesthesia. Ann Otol Rhinol Laryngol. 2004;113(4):265 76.

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of these vascular changes, it has been reported that the positive and negative predictive values of endoscopy can be improved over traditional white light endoscopy.62 Optical coherence tomography (OCT) is another imaging modality that provides details to the depth of a lesion. Using the reflective properties of light, OCT can provide improved details of tissue immediately below the mucosa in a manner similar to a vertical histologic section.63 Laryngeal use has been described to a limited degree, with ongoing research.64 The use of fluorescent labels tagged to antibodies that localize to head and neck tumors also offers some promise in improving tumor localization.65 Robotic technology has become increasingly prevalent in head and neck surgeries. As comfort with the appli­ cation increases, relatively small series are becoming available that demonstrate success rates with robotic resections similar to that obtained via conventional trans­ oral approaches or radiation therapy. Mendelsohn et al. reported on one series of 18 supraglottic lesions addres­ sed with robotic assisted supraglottic laryngectomy that demonstrated 100% disease specific survival at two years.66 Advantages over traditional transoral approaches include improved visualization in appropriately selected cases and advanced range of motion, among others. Further applications and refinements to the current use of lasers, including expansion in the office setting, are also likely to continue.

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Section 8: Premalignant and Early Laryngeal Cancers

27. Zeitels SM, Akst LM, Burns JA, et al. Office-based 532-nm pulsed KTP laser treatment of glottal papillomatosis and dysplasia. Ann Otol Rhinol Laryngol. 2006;115(9): 679-85. 28. Sengupta N, Morris CG, Kirwan J, et al. Definitive radio­ therapy for carcinoma in situ of the true vocal cords. Am J Clin Oncol. 2010;33(1):94-95. 29. Spector JG, Sessions DG, Emami B, et al. Squamous cell carcinomas of the aryepiglottic fold: therapeutic results and long-term follow-up. Laryngoscope. 1995;105(7):734-46. 30. Mendenhall W, Sulica L, Sessions RB. Early stage cancer of the larynx. In: Harrison LB, Sessions R, Hong W (Eds). Head and Neck Cancer: A Multidisciplinary Approach, 2nd edition. Philadelphia, PA: Lippincott Williams & Wilkins; 2004. 31. Armstrong W, Vokes D, Maisel R, et al. (Eds). Malignant tumors of the larynx. Cummings Otolaryngology—Head and Neck Surgery, 5th edition. Philadelphia, PA: Mosby/ Elsevier; 2010. 32. Zeitels SM, Kirchner JA. Hyoepiglottic ligament in sup­ raglottic cancer. Ann Otol Rhinol Laryngol. 1995;104(10): 770-5. 33. Edge S, Byrd D, Compton CC, et al. (Eds). Larynx. AJCC Cancer Staging Manual, 7th edition. New York, NY: Springer; 2010. 34. Harwood AR, DeBoer G. Prognostic factors in T2 glottic cancer. Cancer. 1980;45(5):991-5. 35. McCoul ED, Har-El G. Meta-analysis of impaired vocal cord mobility as a prognostic factor in T2 glottic carcinoma. Arch Otolaryngol Head Neck Surg. 2009;135(5):479-86. 36. Silver CE, Beitler JJ, Shaha AR, et al. Current trends in initial management of laryngeal cancer: the declining use of open surgery. Eur Arch Otorhinolaryngol. 2009; 266(9):1333-52. 37. Misono S, Merati AL. Are patient-reported voice outcomes better after surgery or after radiation for treatment of T1 glottic carcinoma? Laryngoscope. 2011;121(3):461-2. 38. Remmelts AJ, Hoebers FJ, Klop WM, et al. Evaluation of laser surgery and radiotherapy as treatment modalities in early stage laryngeal carcinoma: tumour outcome and quality of voice. Eur Arch Otorhinolaryngol. 2013;270(7):2079-87. 39. Hartl DM, Ferlito A, Brasnu DF, et al. Evidence-based review of treatment options for patients with glottic cancer. Head Neck. 2011;33(11):1638-48. 40. Yoo J, Lacchetti C, Hammond JA, et al. (Head and Neck Cancer Disease Site Group). Role of endolaryngeal surgery (with or without laser) compared with radiotherapy in the management of early (T1) glottic cancer: a clinical practice guideline. Curr Oncol. 2013;20(2):132-5. 41. Kerr P, Mark Taylor S, Rigby M, et al. Oncologic and voice outcomes after treatment of early glottic cancer: transoral laser microsurgery versus radiotherapy. J Otolaryngol Head Neck Surg. 2012;41(6):381-8. 42. Back G, Sood S. The management of early laryngeal cancer: options for patients and therapists. Curr Opin Otolaryngol Head Neck Surg. 2005;13(2):85-91.

43. van Gogh CD, Verdonck-de Leeuw IM, Wedler-Peeters J, et al. Prospective evaluation of voice outcome during the first two years in male patients treated by radiotherapy or laser surgery for T1a glottic carcinoma. Eur Arch Otorhino­ laryngol. 2012;269(6):1647-52. 44. Hirano M, Hirade Y, Kawasaki H. Vocal function following carbon dioxide laser surgery for glottic carcinoma. Ann Otol Rhinol Laryngol. 1985;94(3):232-5. 45. Minni A, Barbaro M, Rispoli G, et al. Treatment with laser CO2 cordectomy and clinical implications in management of mild and moderate laryngeal precancerosis. Eur Arch Otorhinolaryngol. 2008;265(2):189-93. 46. Remacle M, Eckel HE, Antonelli A, et al. Endoscopic cordectomy. A proposal for a classification by the working committee, European Laryngological Society. Eur Arch Otorhinolaryngol. 2000;257(4):227-31. 47. Remacle M, Hantzakos A, Eckel H, et al. Endoscopic supraglottic laryngectomy: a proposal for a classification by the working committee on nomenclature, European Laryngological Society. Eur Arch Otorhinolaryngol. 2009; 266(7):993-8. 48. Remacle M, Van Haverbeke C, Eckel H, et al. Proposal for revision of the European Laryngological Society classi­ fication of endoscopic cordectomies. Eur Arch Otorhino­ laryngol. 2007;264(5):499-504. 49. Canis M, Martin A, Ihler F, et al. Transoral laser micro­ surgery in treatment of pT2 and pT3 glottic laryngeal squamous cell carcinoma—results of 391 patients. Head Neck. 2014;36(6):859-66. 50. Zeitels SM, Burns JA, Lopez-Guerra G, et al. Photoangiolytic laser treatment of early glottic cancer: a new management strategy. Ann Otol Rhinol Laryngol Suppl. 2008;199:3-24. 51. Beitler JJ, Johnson JT. Transoral laser excision for early glottic cancer. Int J Radiat Oncol Biol Phys. 2003;56(4): 1063-6. 52. Kandogan T, Sanal A. Quality of life, functional outcome, and voice handicap index in partial laryngectomy patients for early glottic cancer. BMC Ear Nose Throat Disord. 2005;5(1):3. 53. Sperry S, Rassekh CH, Laccourreye O, et al. Supracricoid partial laryngectomy for primary and recurrent laryngeal cancer. JAMA Otolaryngol Head Neck Surg. 2013;139: 1226-35. 54. Chera BS, Amdur RJ, Morris CG, et al. T1N0 to T2N0 squa­ mous cell carcinoma of the glottic larynx treated with definitive radiotherapy. Int J Radiat Oncol Biol Phys. 2010; 78(2):461-6. 55. Khan MK, Koyfman SA, Hunter GK, et al. Definitive radio­ therapy for early (T1-T2) glottic squamous cell carcinoma: a 20 year Cleveland clinic experience. Radiat Oncol. 2012; 7:193. 56. Barthel SW, Esclamado RM. Primary radiation therapy for early glottic cancer. Otolaryngol Head Neck Surg. 2001;124(1):35-39. 57. Li M, Lorenz RR, Khan MJ, et al. Salvage laryngectomy in patients with recurrent laryngeal cancer in the setting of nonoperative treatment failure. Otolaryngol Head Neck Surg. 2013;149(2):245-51.

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Chapter 74: Premalignant and Early Malignant Lesions of the Larynx

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malignant laryngeal lesions: an in vivo study. Otolaryngol Head Neck Surg. 2011;145(1):91 99. Day KE, Sweeny L, Kulbersh B, et al. Preclinical comparison of near infrared labeled cetuximab and panitumumab for optical imaging of head and neck squamous cell carcinoma. Mol Imaging Biol. 2013;15(6):722 9. Mendelsohn AH, Remacle M, Van Der Vorst S, et al. Out­ comes following transoral robotic surgery: supraglottic laryngectomy. Laryngoscope. 2013;123(1):208 14. Stelow EB, Mills SE. Squamous cell carcinoma variants of the upper aerodigestive tract. Am J Clin Pathol. 2005; 124:S96 109. Russell JO, Hoschar AP, Scharpf J. Papillary squamous cell carcinoma of the head and neck: a clinicopathologic series. Am J Otolaryngol. 2011;32(6):557 63. Thompson LD, Wieneke JA, Miettinen M, et al. Spindle cell (sarcomatoid) carcinomas of the larynx: a clinicopathologic study of 187 cases. Am J Surg Pathol. 2002;26(2):153 70. Edge S, Byrd D, Compton C, et al. (Eds.) AJCC Laryngeal. AJCC Cancer Staging Manual, 7th edition. New York, NY: Springer; 2010. -

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58. Laccourreye O, Brasnu D, Bassot V, et al. Cisplatin fluo­ rouracil exclusive chemotherapy for T1 T3N0 glottic squamous cell carcinoma complete clinical responders: five year results. J Clin Oncol. 1996;14(8):2331 6. 59. Divi V, Worden FP, Prince ME, et al. Chemotherapy alone for organ preservation in advanced laryngeal cancer. Head Neck. 2010;32(8):1040 7. 60. Piazza C, Del Bon F, Peretti G, et al. Narrow band imaging in endoscopic evaluation of the larynx. Curr Opin Otolaryngol Head Neck Surg. 2012;20(6):472 6. 61. Lin YC, Wang WH, Lee KF, et al. Value of narrow band imaging endoscopy in early mucosal head and neck cancer. Head Neck. 2012;34(11):1574 9. 62. Ni XG, He S, Xu ZG, et al. Endoscopic diagnosis of laryngeal cancer and precancerous lesions by narrow band imaging. J Laryngol Otol. 2011;125(3):288 96. 63. Burns JA. Optical coherence tomography: imaging the larynx. Curr Opin Otolaryngol Head Neck Surg. 2012; 20(6):477 81. 64. Burns JA, Kim KH, deBoer JF, et al. Polarization sensitive optical coherence tomography imaging of benign and

Chapter 75: Classification of Transoral Laser Microsurgery

931

CHAPTER

Classification of Transoral Laser Microsurgery

75

Scott Troob, Gady Har-El

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In the decade that followed Steiner’s first large-scale series, several similar studies were published out of insti tutions around Europe.4-14 These series grouped patients by T-stage and reported the endpoints of local recurrence, locoregional control, recurrence free survival, overall survival, margin status, and need for adjuvant radiotherapy.

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EARLY CLASSIFICATION SCHEMES OF TRANSORAL LASER MICROSURGERY

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The first written description of endoscopic cordectomy as a method to treat glottic carcinoma was published in 1920 by Lynch.1 Since that time, this minimally invasive technique has been developed by surgeons at select institutions and championed as an alternative to open procedures. Transoral laser microsurgery assumed its modern form when Strong first described the use of the CO2 laser as an alternative to cold steel in his 1975 report.2 Wolfgang Steiner of the University of Göttingen, Germany, later contributed the technique of deliberate, sequential resection of glottic carcinoma. For lesions not amenable to en bloc resection, he advocated defining the interface between cancer and normal tissue by bisecting the lesion under endoscopic view, followed by the step-wise removal in two or more fragments. This method afforded a clean resection with a smaller margin of healthy tissue removed at the time of operation, thus better preserving function of the larynx. His 1993 publication was the first large series of patients treated by this method, and served as the benchmark for future comparative outcome analysis.3

Functional outcomes were also reported, including voice quality and the long-term need for either tracheostomy or feeding tubes. Despite the overall rigor of these reports, the general applicability of the results was compromised by the significant variation in reporting the extent of resection. Most series used the general term “cordectomy” and when the extent was reported, it was in relation to the layers of the glottis. Conventions for naming the cordectomies were needed, and it became generally agreed to term resections of the epithelium “superficial cordectomy,” those extending to the vocalis muscle “partial cordectomy,” and those includ ing a complete resection of the vocal fold (down to and including the thyroid perichondrium) “total cordectomy.” Any resection that was more extensive, such as those including the arytenoid cartilages, was termed “extended cordectomy.” In 1990, Thumfart proposed a classification scheme of endolaryngeal laser resection in a series of T1 and T2 lesions.15 In this classification, type I described a laserdecortication of one or both vocal folds, leaving the vocal muscle intact. Type II described a cordectomy, leaving the anterior commissure behind. Type III described the extended cordectomy, indicated for lesions involving the bilateral vocal folds or the anterior commissure. For lesions involving the anterior commissure, resection extended down to the thyroid cartilage and into the sub glottic region along the cricothyroid membrane to the upper margin of the cricoid cartilage. Type III often inc luded resection of one of the arytenoid cartilages. Type IV, or endolaryngeal exenteration, entailed a complete resec tion of one or both vocal and false folds in possible combination with an arytenoidectomy if the lesion

INTRODUCTION

932

Section 8: Premalignant and Early Laryngeal Cancers

Table 75.1: ELS classification of endoscopic cordectomy

Type

Name

Intent

Indicated lesions

I

Subepithelial

Diagnostic therapeutic

Hyperplasia, dysphasia, carcinoma in situ (CIS) without microinvasion

II

Subligamental

Diagnostic therapeutic

Severe leukoplakia CIS with possible microinvasion

III

Transmuscular

Therapeutic

Small superficial cancers with mobile vocal folds

IV

Total or complete cordectomy

Therapeutic

T1a, can include false vocal fold, cancer infiltrates the vocal fold and is diagnosed prior to surgery

Va

Extended cordectomy encompassing contralateral vocal fold

Therapeutic

T1b cancers superficially reaching the commissure without infiltrating it

Vb

Extended cordectomy encompassing ipsilateral arytenoid

Therapeutic

Vocal fold carcinoma involving posteriorly the vocal process but sparing the arytenoid

Vc

Extended cordectomy encompassing ventricular fold

Therapeutic

Ventricular cancers or for transglottic cancers that spread from the vocal fold to the ventricle

Vd

Extended cordectomy encompassing subglottis

Therapeutic

VI

Extended cordectomy encompassing the anterior commissure and the anterior part of both vocal folds

Therapeutic

extended to the arytenoid. The resection included the inner perichondrium of the thyroid and cricoid cartilages as well as the cricothyroid membrane. Remacle proposed another classification system in 1997.16 In his report, type I described resection of the entire epithelium, leaving the vocal ligament intact. Type II described removal of the vocal fold from the vocal process to the anterior commissure, passing through the inferior thyroarytenoid muscle. Type IIIa removed the vocal fold along the internal side of the thyroid ala. Type IIIb described any cordectomy where the anterior commissure was removed. While the aforementioned classification systems served descriptive purposes in their individual series, the variation in the systems confounded comparison of the results between institutions.

ELS CLASSIFICATION OF ENDOSCOPIC CORDECTOMY In 2000, the Working Committee on Nomenclature of the European Laryngological Society (ELS) introduced a consensus classification system with several aims in mind.17 The first goal was to standardize the description of the vari­ous cordectomies. Second, the committee sought to provide a classification system that would allow for the interpretation and comparison of postoperative results

between institutions. The committee acknowledged that the technique of endolaryngeal resection was not standar­ dized, and that it takes years of training to both master the procedure and understand its limitations in treating glottic carcinomas. Thus, their third aim was to provide a common nomenclature in hopes of improving the training of laryngologists learning such procedures. The proposed system is based on describing the sur­ gical margins of the various cordectomies and is inde­ pendent both of technique and of the instrumentation used, whether laser or cold steel. Each type of cordectomy is given a common name and a numeric designation. In creating this classification, the authors hoped to introduce a system that was practical for everyday use. Toward a similar end, they avoided subdivision of categories when­ ever possible (Table 75.1). The ELS later updated the classification system to address the issue of lesions arising at the anterior com­ missure.18 According to the initial classification sys­tem, lesions arising in the anterior commissure were grouped with unilateral lesions extending to the anterior commissure and also with lesions extending to the contralateral vocal fold. Such lesions range from T1a to T2. Many authors suggested that the original classification introduced bias in the reporting of oncologic and functional outcomes. To address this confusion, the type VI cordectomy was introduced:

Chapter 75: Classification of Transoral Laser Microsurgery

933

Fig. 75.1: ELS type I cordectomy—subepithelial.

Fig. 75.2: ELS type II cordectomy—subligamental.

Fig. 75.3: ELS type III cordectomy—transmuscular.

Fig. 75.4: ELS type IV cordectomy—total or complete.

• Type I: A subepithelial cordectomy is limited to removal of the epithelium, often in its entirety, moving through the superficial lamina propria. Because this superficial layer of the lamina propria is not a barrier to invasion, this procedure is viewed as diagnostic only (Fig. 75.1). • Type II: A subligamental cordectomy removes both the epithelium and Reinke’s space along with the vocal ligament. The plane of dissection is between the vocalis muscle and the vocal ligament, and can extend from vocal process to anterior commissure. In the view of the committee, this cordectomy is therapeutic only for cases of microinvasive carcinoma or severe CIS with the possibility of microinvasion (Fig. 75.2). • Type III: The transmuscular cordectomy proceeds through the vocalis muscle, and may extend from vocal process to anterior commissure. Resection of a portion of the ventricular fold is often performed at the time of a type III cordectomy for the purposes of exposing the entire vocal fold. Type III is therapeutic for small superficial cancers with mobile vocal folds (Fig. 75.3). • Type IV: A total or complete cordectomy is performed if deep infiltration of the vocalis muscle is suspected.

Resection extends from vocal process to anterior commissure, and the depth extends to the internal perichondrium of the thyroid ala. A type IV cordectomy may also include a partial or total removal of the ventricular fold to facilitate complete resection of the vocal fold (Fig. 75.4). • Type Va: In the extended cordectomy encompassing the contralateral vocal fold, resection extends across the anterior commissure to treat bilateral lesions. This resection involves removal of Broyle’s ligament, and may include removal of a portion of the petiole. This approach is recommended for lesions superficially reaching the anterior commissure without invasion. For lesions staged at T1b involving the anterior commissure, it is necessary to extend the resection to include the subglottic mucosa and cricothryoid membrane, given their propensity to spread to this region (Fig. 75.5). • Type Vb: Extended cordectomy encompassing the arytenoid is performed for lesions of the vocal fold involving the vocal process with a mobile vocal fold (Fig. 75.6).

934

Section 8: Premalignant and Early Laryngeal Cancers

Fig. 75.5: ELS type Va cordectomy—extended cordectomy encompassing contra lateral vocal fold.

Fig. 75.6: ELS type Vb cordectomy—extended cordectomy encompassing ipsilateral arytenoid.

Fig. 75.7: ELS type Vc cordectomy—extended cordectomy encompassing ventricular fold.

Fig. 75.8: ELS type Vd cordectomy—extended cordectomy encompassing subglottis.

•

Type Vc: Extended cordectomy encompassing the ven­ tricular fold is selected for transglottic lesions or for glottic lesions with significant spread into the ventricle (Fig. 75.7). • Type Vd: An extended cordectomy encompassing the subglottis is selected if significant subglottic extension is evident. The resection proceeds up to 1 cm beneath the glottis to the level of the cricoid cartilage (Fig. 75.8). • Type VI: An extended cordectomy encompassing the anterior commissure and the anterior part of both vocal folds is selected for lesions originating at the anterior commissure without infiltration of the thyroid cartilage. The resection may include the anterior angle

of the thyroid cartilage. The petiole of the epiglottis may be excised and dissection carried inferior to remove Broyle’s ligament. Inferiorly, the resection may proceed to include the subglottic mucosa and the cricothryoid membrane. Resection of the ventricular folds may be necessary for exposure (Figs. 75.9A and B).

ELS CLASSIFICATION FOR ENDOSCOPIC SUPRAGLOTTIC LARYNGECTOMY The evolution of treatment of supraglottic lesions via endoscopic resection followed a parallel course to glottic

Chapter 75: Classification of Transoral Laser Microsurgery

A

935

B

Figs. 75.9A and B: ELS type VI cordectomy—extended cordectomy encompassing the anterior commissure and the anterior part of both vocal folds.

IV

Tumors of the threefolds’ region Ventricular fold Arytenoid

lesions. Vaughn first described the technique utilizing the laser in 1978.19 The first series of patients were published by Zeitels in 1990 20 and Davis in 1991.21 In similar fashion to the system described for glottic lesions, the ELS proposed another classification system

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­

T1–T2 tumors of the infra hyoid endolaryngeal epiglottis. If tumor extends to petiole, resection must inc lude the pre-epiglottic space

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III

­

Medial supraglottic laryngectomy without resection of the pre-epiglottic space IIa suprahyoid IIb infrahyoid Medial supraglottic laryngectomy with resection of the pre-epiglottic space IIIa without extension to ventricular fold IIIb with extension to the ventricular fold Lateral supraglottic laryngectomy IVa IVb

­

II

Small size superficial lesions of the free edge of the epiglottis, the aryepiglottic fold, the arytenoid, or the ventricular fold or any other part of the supraglottis T1 lesions of the of supra/ infrahyoid laryngeal surface of epiglottis

­

Limited excision

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in 2009 for the various endoscopic supraglottic laryngec tomies used to treat early stage supraglottic carcinoma (Table 75.2):22 • Type I: Describes a limited endoscopic supraglottic laryngectomy excision of superficial lesions on the free border of the epiglottis the aryepiglottic fold, aryte noid, or the ventricular fold (Fig. 75.10). • Type II: This type is broken down into two procedures, selected to treat small and superficial T1 tumors. For those lesions of the suprahyoid epiglottis, the upper half of the epiglottis is resected with the plane of dissection proceeding through the pre-epiglottic space but does not entail its removal (type IIa). For infrahyoid lesions (type IIb), the entire epiglottis is removed. Dissection proceeds in the pre-epiglottic space with out its complete excision. The pharyngoepiglottic, aryepiglottic, and ventricular folds are preserved. • Type III: A medial supraglottic laryngectomy with resection of the pre-epiglottic is employed if a supra glottic lesion extends to the petiole. Incision proceeds from vallecula to hyoid bone, and inferiorly along the thyrohyoid membrane to the inner surface of the thyroid cartilage. The contents of the pre-epiglottic space are then removed down to the level of the ante rior commissure. The resection is deemed a type IIIa if there is no extension to ventricular fold. If the lesion extends to the ventricular folds, they can be removed as well (type IIIb). • Type IV: A lateral supraglottic laryngectomy is em ployed for lesions of the threefolds’ region includes ­

Table 75.2: ELS classification of endoscopic supraglottic laryngectomy

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Section 8: Premalignant and Early Laryngeal Cancers

Figs. 75.10: ELS – endoscopic supraglottic laryngectomy.

the free edge of the epiglottis, the pharyngoepiglottic fold, and the aryepiglottic fold. Resection includes the free edge of the epiglottis, the threefolds’ region, and the ventricular fold (type IVa). If there is extension to a mobile arytenoid, it may be included in the resection (type IVb).

REFERENCES 1. Lynch R. Intrinsic carcinoma of the larynx, with a second report of cases operated on by suspension and dissection. Trans Am Laryngol Assoc. 1920(42):119-24. 2. Strong MS. Laser excision of carcinoma of the larynx. Laryngoscope. 1975;85(8):1286-9.

3. Steiner W. Results of curative laser microsurgery of laryngeal carcinomas. Am J Otolaryngol. 1993;14(2):116-21. 4. Casiano RR, Cooper JD, Lundy DS, et al. Laser cordectomy for T1 glottic carcinoma: a 10-year experience and video­ stroboscopic findings. Otolaryngol Head Neck Surg. 1991; 104(6):831-7. 5. Motta G, Villari G, Motta S, et al. Use of CO2 laser in con­ servative surgery of glottic tumors. Acta Otorhinolaryngol Ital. 1991;11(1):25-34. 6. Eckel HE, Thumfart WF. Laser surgery for the treatment of larynx carcinomas: indications, techniques, and preli­ minary results. Ann Otol Rhinol Laryngol. 1992;101(2 Pt 1): 113-18. 7. Piquet JJ, Chevalier D. Laser and glottis excision. Ann Otolaryngol Chir Cervicofac. 1993;110(4):227-29.

Chapter 75: Classification of Transoral Laser Microsurgery

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16. Remacle M, Lawson G, Jamart J, et al. CO2 laser in the diagnosis and treatment of early cancer of the vocal fold. Eur Arch Otorhinolaryngol. 1997;254(4):169-76. 17. Remacle M, Eckel HE, Antonelli A, et al. Endoscopic cordectomy: a proposal for a classification by the working committee, European laryngological society. Eur Arch Otorhinolaryngol. 2000;257(4):227-31. 18. Remacle M, Van Haverbeke C, Eckel H, et al. Proposal for revision of the European laryngological society classification of endoscopic cordectomies. Eur Arch Otorhinolaryngol. 2007;264(5):499-504. 19. Vaughan CW. Transoral laryngeal surgery using the CO2 laser: laboratory experiments and clinical experience. Laryngoscope. 1978;88(9 Pt 1):1399-1420. 20. Zeitels SM, Vaughan CW, Domanowski GF. Endoscopic management of early supraglottic cancer. Ann Otol Rhinol Laryngol. 1990;99(12):951-56. 21. Davis RK, Kelly SM, Hayes J. Endoscopic CO2 laser exci sional biopsy of early supraglottic cancer. Laryngoscope. 1991;101(6 Pt 1):680-83. 22. Remacle M, Hantzakos A, Eckel H, et al. Endoscopic supraglottic laryngectomy: a proposal for a classification by the working committee on nomenclature, European laryngological society. Eur Arch Otorhinolaryngol. 2009; 266(7):993-8.











8. Czigner J, Savay L. Primary CO2 laser chordectomy in vocal cord carcinoma. Laryngorhinootologie. 1994;73(8):432-6. 9. Thumfart WF, Eckel HE, Sprinzl GM. Classification of endolaryngeal laser partial laryngectomies. Adv Otorhino laryngol. 1995;49:212-4. 10. Motta G, Esposito E, Cassiano B, et al. T1-T2-T3 glottic tumors: Fifteen years experience with CO2 laser. Acta Otolaryngol Suppl. 1997;527:155-9. 11. Damm M, Sittel C, Streppel M, et al. Transoral CO2 laser for surgical management of glottic carcinoma in situ. Laryngoscope. 2000;110(7):1215-21. 12. Desloge RB, Zeitels SM. Endolaryngeal microsurgery at the anterior glottal commissure: controversies and obser vations. Ann Otol Rhinol Laryngol. 2000;109(4):385-92. 13. Ogoltsova E, Paches A, Matyakin E. Comparative evaluation of the efficacy of radiotherapy, surgery and combined treatment of stage I-II laryngeal cancer (T1-2N0M0) on the basis of co-operative studies. J Otorhinolaryngol. 1990 (3):3-7. 14. Spector JG, Sessions DG, Chao KS, et al. Stage I (T1 N0 M0) squamous cell carcinoma of the laryngeal glottis: therapeutic results and voice preservation. Head Neck. 1999;21(8):707-17. 15. Thumfart WF, Eckel HE. Endolaryngeal laser surgery in the treatment of laryngeal cancers: the current cologne con cept. HNO. 1990;38(5):174-8.

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SECTION Office Laryngeal Surgery

9

Chapter 76: Setup and Safety in Office Procedures

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CHAPTER

76

Setup and Safety in Office Procedures Steven A Bielamowicz

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The major advances in laryngology in the past two decades have been related to enhanced office diagnostics and office treatments. Although other chapters in this textbook will cover operating room setup and safety, this chapter covers these facets in the office setting. Our ability to diagnose illness in laryngology rests on a thorough physical examination. The modern physical examination utilizes high-quality video recordings of specific laryngeal motion. Advances in video and scope technology allows for very high quality examination of the human larynx in motion. To be able to examine the larynx, the laryngologist is required to work with awake patients as they engage in voice tasks. In addition, the setup of the room is critical for optimal viewing of the laryngeal examination. The setup for the laryngology examination room ideally allows the laryngologist, patient, assistant, and observers to view laryngeal motion in real time and in slow motion after the examination has been completed. Archiving of the video data is essential for long-term management of these patients. Over the past 20 years, I have used numerous setups in different clinical environments and believe that I have learned the optimal setup. Regarding the chair in which the patient sits, the modern hydraulic otolaryngology chair is the most versatile. This type of chair can allow for a thorough head and neck examination as well as a thorough laryngeal examination. This type of chair allows the examiner to stand or sit while performing the examination and allows for the chair to recline if a patient develops a vagal response. Alternatively, one can use a stan dard nonwheeled office guest chair for the examination.

This type of chair requires the examiner to remain seated during the examination. This is not an ideal chair for the standard head and neck examination as the laryngologist must bend over or stoop to perform a thorough oral, nasal, and otologic examination. However, this type of chair is quite comfortable for the patient and is advantageous for shorter adults and adolescents, as their feet are better supported in the office chair as compared with the standard otolaryngology chair. For a laryngologist, the laryngeal examination is the most important diagnostic test. A good laryngeal examination requires an excellent view of the larynx during a large group of voiced and voiceless tasks. During both the transoral and transnasal laryngeal examination, the best view of the larynx is obtained in the sniffing position. Every patient should be asked to lean forward at their waist while seated, put their elbows on their knees, and extend their neck (Fig. 76.1). This will put the patient in the sniffing position. However, not all patients can tolerate this position, e.g. those with hip arthritis and extensive cervical fusion. The sniffing position moves the tongue and epiglottis into an anterior position, allowing a good view of the larynx and supraglottic structures without obstruction by the supraglottis or tongue base. For the right-handed laryngologist, the physician usually stands on the right side of the patient and will sit or stand in front of the patient for a rigid laryngeal examination, whereas the physician stands slightly to the right of the patient during a flexible examination. The greatest flexibility in room design is to place the ENT cabinet to the right of the patient behind the patient chair, and the video tower to the left of the patient behind the

OFFICE SETUP

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Section 9: Office Laryngeal Surgery

Fig. 76.2: This drawing details the optimal placement of equipment in the laryngologist’s examination room. Detailed are the hydraulic examination chair, the SMR unit, video tower, physician desk, and video screens.

Fig. 76.1: As seen in this photograph, the patient is seated in a hydraulic otolaryngology chair with her waist bent forward and her elbows on her knees. Her neck is slightly extended and the occiput is forward of her shoulders. This is the office sniffing position.

patient chair (Fig. 76.2). This type of setup allows for an assistant to interact with the video tower during and after the examination, allowing the physician free mobility to interact with the patient after the examination. The assistant can save the video data, tag the data, save speci­ fic images, and create a report while the physician is discussing the findings and treatment options with the patient. The screen on the video tower is principally used by the assistant. Due to the angle viewing issues with flat screen technology, this screen is not optimally positioned for the laryngologist. Another larger monitor (42–50 inch) clone of the tower monitor is ideally angled toward the examining laryngologist. This is the principal monitor that the physician uses during the examination. A third monitor should be placed on the wall opposite the patient. The height of this monitor should be at a the eye level of the patient. The exact height of this patient clone monitor should be set depending upon the preferred sitting or standing examination height of the physician (Fig. 76.3). The optimal examination heights will be covered in the ergonomics section below.

OFFICE ERGONOMICS

Fig. 76.3: An optimal laryngeal examination and treatment room.

Ergonomics are essential to the long-term musculoskeletal health of the surgeon. Early in a physician’s career, one must maintain excellent posture and ergonomics when working with patients in the office. Ergonomics in the office will limit the development of musculoskeletal disease, including cervical and lumbar osteoarthritis and

Chapter 76: Setup and Safety in Office Procedures

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OFFICE TREATMENT PREPARATION Treatment in the office has become a mainstay in modern laryngology practice. Prior to considering performing a therapeutic procedure, it is important to select patients carefully, especially early in one’s career. Most importantly, it is necessary to have a compliant patient. Adult patients

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disk disease. The chair should be at an optimal height to prevent the examiner from stooping. As one gets older, correction of aging vision change is also essential to maintain optimal focus when viewing monitors as well as examining the oral cavity. For those younger readers, one day you will find yourself moving your optimal reading distance and patient examination distance further away from your previous focal distance. At this time, you should seek the advice of an eye care specialist and obtain correction. Adequate vision correction will allow for good body pos ture. In addition, ergonomics involves arm posture. When performing flexible laryngoscopy, it is important to learn to hold your arms with your elbows into your side, thus reducing neck, arm and shoulder tension (Fig. 76.4). This can be done by either examining patients with your hands up or hands down. Either technique can be per formed in an ergonomic fashion. Ideally, one will be comfortable with both techniques, as patient factors may require a transition from one technique to the other. This is especially true when examining patients who cannot transfer and must be examined in a motorized chair.

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Fig. 76.4: The left screen is a demonstration of poor ergonomics. Notice that the physician is leaning forward with his elbows away from his body and wrist in a flexed position. In the right screen, the physician’s positioning has improved. The elbows are at his side, the wrists are in a neutral position, and the physician is standing upright.



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with developmental delay or traumatic brain injury who have difficulty with compliance are poor candidates for an office therapeutic intervention. Many patients will be quite afraid of an office intervention and may express or demons trate anxiety. These patients can usually be treated in the office as long as the physician and staff are comforting, reassuring, and encouraging. I have found that some of the most anxious patients can be the best subjects, as their motivation to comply appears to relieve their anxiety. One should plan extra time when treating anxious patients, because this group of patients appreciates thorough explanation of the treatment process. From a planning standpoint, the tolerance of the office examination often predicts the tolerance of an office treatment. In addition to the patient’s mindset, the patient’s anatomy will influence the physician’s selection of sub jects for office treatment. A transoral injection can be very difficult in a patient with a strong gag reflex, a large tongue, and a small jaw. Likewise, a transnasal treatment with a flexible channeled laryngoscope [e.g. potassium titanyl phosphate (KTP) laser treatment] can be difficult in patients with a narrow or obstructed nasal cavity. The channeled video laryngoscope often measure ≥ 4.0  mm and thus bilateral bony septal spurs and heavy turbinate bone can make the instrumentation of the nasal cavity problematic. Also, a patient who cannot tolerate an upright position or who has a severe resting tremor, a short neck, or is so obese that the cervical landmarks cannot be palpated will be challenging. The position of the patient during treatment is often modified compared with the sniffing position used for the examination. Laryngeal Botox via a transcervical app roach is often performed with the patient sitting upright with the neck in an extended position. Alternatively, this procedure is also commonly performed with the patient reclining in cervical extension. During transnasal guidance for a transcervical injection augmentation, the patient is positioned in an upright position as opposed to the sniffing position. This change in positioning is necessary to provide working room for the surgeon to access the neck while performing the injection. However, the upright position limits the view of the larynx during a transnasal or transoral examination. The positioning during the sniffing position is optimal for transnasal instrumentation of the larynx as when performing laryngeal biopsies, laser treatment, and bronchoscopies. For an office esophagoscopy, placing the patient in an upright seated position with the neck in a neutral position is ideal.

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Section 9: Office Laryngeal Surgery

Fig. 76.5: The flexible catheter for drip anesthesia is positioned in the laryngeal inlet during the laryngeal gargle procedure.

TOPICAL MEDICATION In addition to proper patient positioning, the use of topical medication can be helpful for the management of the laryngology patient in the office setting. For transnasal instrumentation, oxymetazoline or cocaine is very effective to decongest the nasal mucosa. Oxymetazoline is the preferred choice as this medication is inexpensive, well tolerated, and has minimal addictive potential during single-dose use. This is an easily aerosolized medication that can be spayed into the nasal cavity. This alpha adre­ nergic agent provides nasal mucosal constriction, maxi­ mizing the space for nasal instrumentation. In subjects undergoing nasal instrumentation with a large flexible scope, as seen in transnasal esophagoscopy, application of oxymetazoline on a cottonoid pledget provides a better treatment response than topical spray. In addition to oxymetazoline, topical lidocaine provides mucosal pain relief. The topical formulation is usually a 4% lidocaine solution that can be used as a singular pro­ duct or is often mixed with oxymetazoline. The com­pound is easy to administer via atomization. Thus, this provides adequate anesthesia and topical decongestion for the nasal mucosa during a transnasal examination. In addi­ tion, 10% lidocaine is available as an oral spray and is often used for transoral examinations in patients who cannot tolerate a transoral examination due to a strong gag reflex. For subjects who are embarking upon a laryn­ geal treatment, adequate anesthesia of the true vocal folds is necessary. The sensory fibers of the vocal fold are derived from the recurrent laryngeal nerve. As this

is a mixed motor and sensory nerve, the only method to control sensation without impairing vocal fold motion is via a topical, mucosal anesthetic approach. For office bronchoscopy, laryngeal biopsy, or vocal fold treatment with a laser, vocal fold anesthesia is imperative. While inhalation of 4% nebulized lidocaine is helpful, many patients are not adequately anesthetized. As described to me by Blake Simpson, MD, I routinely use a small catheter that fits into the working channel of the flexible channeled laryngoscope (Blake Simpson, personal communication, 2008). The flexible catheter is fitted with a 3-cc syringe half filled with 4% lidocaine. After nebulization, the channeled laryngoscope is brought into place and the catheter is positioned into the laryngeal inlet, without touching the vocal folds (Fig. 76.5). The patient is asked to say a prolonged /i/ while lidocaine is slowly dripped onto the vocal folds. At first, the patient may not be able to hold out a prolonged /i/ as the inhalation of lidocaine is often inadequate to provide dense anesthesia of the vocal folds allowing for tolerance of the drip anesthesia. As the vocal folds become anesthetized, the patient will develop a tolerance of the fluid on the vocal folds and perform a laryngeal gargle. After this, a few drops of lidocaine into the tracheal during an abducted gesture will assure infraglottic anesthesia. This anesthetic technique is somewhat time consuming but markedly enhances patient compliance. This approach has become routine for patients undergoing laryngeal biopsies, office bronchoscopy or laser treatment and is very effective. For patients undergoing office laryngeal Botox or diagnostic laryngeal electromyography, laryngeal anesthesia is not necessary if one is approaching the thyro­ arytenoid, cricothyroid, or posterior cricoarytenoid muscle. However, the injection technique requires that the needle remains submucosal. For patients receiving an injection augmentation, dense anesthesia of the vocal fold is unneces­sary. If one remains submocosal via a transcar­ tilaginous approach, no vocal fold anesthesia is necessary. However, a transcricothyroid membrane or thyrohyoid membrane approach requires a mild topical anesthesia to prevent coughing. A transtracheal block with 4% lido­ caine is quite helpful for injection augmentation via a transhyoid or transcricoid membrane approach. For office esophagoscopy, no anesthesia in the hypopharynx or larynx is required. Any anesthesia in the pharynx will interfere with the patient’s ability to swallow and interfere with the esophagoscopy. However, excellent anesthesia and topical decongestants within the nasal cavity is the key to a successful esophagoscopy.

Chapter 76: Setup and Safety in Office Procedures

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OFFICE AIRWAY RESTRICTION

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The evaluation of the adult patient with a restricted airway deserves special consideration. The laryngologist sees patients in the office with bilateral vocal cord paralysis, severe Reinke’s edema, Wegener’s granulomatosis, sar coidosis, rhinoscleroma, idiopathic subglottic stenosis, laryngeal stenosis, and tracheal stenosis. All of these patients can have a compromised airway, and it is impor tant to perform a thorough examination of the affected area in a safe manner. Any adult patients with these illnesses that arrives ambulatory to the office can be examined in the office through a routine transnasal or transoral examination. However, to examine these patients up to or past the critical stenosis must be done very carefully.

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Office procedures in laryngology are quite safe. However, some basic safety equipment is necessary. For laser procedures, wavelength-specific eye protection is required for all staff members in the room as well as the patient. These glasses should have side guards to prevent stray laser light from entering the eye, which can lead to retinal damage. The most common office lasers are the KTP and pulsed dye lasers, and less commonly the CO2 lasers. Using bare fibers pose added risk to the people in the room, as a long surface area is exposed to the environment and any break that might inadvertently occur in a bare fiber can lead to significant laser light exposure, especially in close proximity of the break. Unlike the operating room, issues of light reflection are minimal in the awake patient, as no additional metal instrumentation is introduced into the patient during the procedure. Furthermore, posting signs on all entrance doors to the treatment room is required to alert any outside personal of the dangers inherent to laser use. For increased patient tolerance and safety, simultan eous suction should be used when performing office laser treatment. Smoke generated from the use of the laser is noxious to the patient. The smell generated during a laser treatment can be nauseating to the patient and the odor can be limited by simultaneous suction during laser treat ment. Smoke and odor evacuation while using a channe led flexible laryngoscope using the port of the scope with the laser fiber in place provides excellent control of any laser smoke or odor seen in the office setting. The use of KTP and pulse dye laser generates a limited amount of smoke as compared with the use of a CO2 laser.

After adequate topical anesthesia via nebulization, drip anesthesia, or transtracheal block, these patients can be examined as long as they have an adequate airway to maintain ventilation. For example, in the case of the patient with a 5-mm tracheal airway secondary to intu bation-induced stenosis, the awake patient will not tolerate passing a 4-mm-outer-diameter scope through the area of stenosis to examine the distal airway. Heightened anxiety or possible trauma to the area of the stenosis could result in airway obstruction. It is important to avoid these situations. However, the laryngologist can still examine the degree of narrowing in this patient example as long as one limits the scope to the area above the stenosis. Likewise, a patient with a 2-mm glottic airway with combined inspiratory and expiratory stridor will tolerate an office examination above the glottis but will likely not tolerate an examination through the glottis and may push the patient toward a critical airway. Any scope position that does not easily allow for the patient to ventilate without worsening of breathing is safe. If one will be seeing patients with significant airway impairment in the office, it is important to be able to administer oxygen and perform an expedient surgical airway.

OFFICE COMPLICATION MANAGEMENT The most common complication in the evaluation and treatment of the laryngology patient in the office is epistaxis and a vagal response. Epistaxis may occur in patients who are undergoing transnasal examinations, especially if they have a prior history of epistaxis, septal spurs, and bony inferior turbinate hypertrophy. In these patients, it is important to use a small scope to limit trauma. If you feel resistance when passing the scope, then the patient usually experiences discomfort and this procedure should be terminated. In these situations, the scope is seen push ing into the tissues. Pushing into the distensible mucosa of the inferior turbinate is safe and does not result in trauma, whereas pushing the scope into the tightly attached septal mucosa or floor of nose will often result in trauma or bleeding. In some adults and younger children, they may not be able to tolerate the smallest scope in your office. Depending upon the illness that one is examining, a transoral examination may be adequate. However, if the laryngologist is trying to pass a channeled laryngoscope in a patient undergoing office treatment and the patient has a tight nasal airway, they may be unsuccessful without ­

OFFICE SAFETY

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Section 9: Office Laryngeal Surgery

severely traumatizing the nasal tissues. This can lead to significant epistaxis, synechia, or septal perforation. One may be forced to treat these patients in the operating room under general anesthesia through a transoral route. If significant bleeding is encountered, management by the otolaryngologist must be performed with possible nasal packing, as covered elsewhere in this book. The most common complication is a vagal response. This is a response due to significant tenth cranial nerve stimulation in the nasal cavity when passing a flexible scope. As a result of this instrumentation, afferent stimulation of the vagus nerve in the nose can induce parasympathetic auto­ nomic responses of the vagus nerve, leading to bradycardia. In addition, hypotension results from sudden reduction or cessation of sympathetic activity and relaxation of arterial resistance vessels.1 Thus, these patients have both heart

slowing and an inappropriate relaxation of the arterial system; they lose central nervous system blood flow and will develop a brief loss of consciousness. The patient will report that they are light headed and begin to look pale and diaphoretic. When these symptoms are seen, it is necessary to terminate the procedure and lay the patient down, ideally in reverse Trendelenburg. This position enhances central nervous system blood flow. The principal adverse event associated with a vasovagal response is a fall. By early procedure termination and placing the patient safely in the Trendelenburg position, injuries can be avoided.

REFERENCE 1. Van Lieshout JJ, Wieling W, Karemaker JM, et al. The vasovagal response. ClinSci (Lond). 1991;81(5):575-86.

Chapter 77: Anesthesia for Office-Based Laryngology

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CHAPTER

Anesthesia for Office-Based Laryngology

77

Catherine Rees Lintzenich

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lidocaine may also be used as a lubricant for the endo scope to provide further anesthesia during the procedure. Oral or pharyngeal anesthesia is rarely needed during transnasal laryngoscopy, transoral laryngoscopy, or trans nasal esophagoscopy. When necessary, topical cetacaine spray or benzocaine spray may be applied to the oropha rynx. Viscous lidocaine may also be gargled and swallowed by the patient for pharyngeal anesthesia. Tracheobronchoscopy in the awake patient requires further topical anesthesia of the larynx. This procedure can usually be accomplished with ≤3 mL of additional topical anesthesia. This is administered directly onto the vocal folds and into the trachea in a slow drip. It is helpful to have the patient gently phonate during administra tion to essentially “gargle” the medication in the larynx.2 The patient should be asked to breathe in deeply after the laryngeal gargle to allow some of the medication to enter the trachea before the patient swallows. 4% lidocaine is the most commonly used medication for topically anes thetizing the larynx. The medication can be administered via the working channel of the endoscope (or a sheath) or via a separate catheter. A small rubber catheter can be passed through the opposite nasal passage to deliver the lidocaine while watching with the endoscope. Alterna tively, a transoral laryngeal cannula or atomizer may be used through the mouth to deliver the lidocaine while watching with the transnasal endoscope. Laryngeal or tracheal procedures may require further anesthetic maneuvers. Topical lidocaine can be delivered via a nebulizer to topicalize the laryngotracheal mucosa.3 The author uses 4 mL of 4% plain lidocaine in a nebulizer

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Advances in endoscope technology have allowed for greater precision and visualization during office-based laryngology procedures. Patients are pursuing more mini mally invasive procedures, leading to greater adoption of office procedures by otolaryngologists. In addition to the transoral approach, transnasal and transcutaneous proce dures, such as injections, biopsies, and laser treatments, can be readily performed in the nonsedated patient. Appropriate anesthesia is the most important primary step in ensuring the success of such procedures in the awake patient. This chapter will present the appropriate use of local and topical anesthesia for these procedures, the pharmacologic considerations of the most commonly used topical medication (lidocaine), and hemodynamic concerns surrounding office-based procedures. Transnasal laryngoscopy is performed with minimal amounts of topical nasal anesthesia. Indeed, some practi tioners avoid topical nasal anesthetics altogether for trans nasal laryngoscopy, citing cost and unpleasant taste.1 Because of the larger caliber of most transnasal esophago scopes, additional nasal anesthesia may be necessary. A local anesthetic, such as 2 or 4% lidocaine or 2% tetracaine, is combined with oxymetazoline or neosynephrine, which vasoconstricts the nasal passages. Approximately 0.5 mL of this solution is administered by spray via a powered atomizer or commercially available disposable atomizer syringe. Alternatively, cotton pledgets or swabs can be soaked in the anesthetic solution and packed in the nasal cavity for several minutes. Some practitioners find it useful to apply 2% viscous lidocaine on long cotton swabs to anesthetize the middle turbinate and septum. 2% viscous

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Section 9: Office Laryngeal Surgery

PHARMACOLOGIC CONSIDERATIONS FOR TOPICAL LIDOCAINE

Fig. 77.1: Superior laryngeal nerve block.

over approximately 10 minutes. A small amount of topical anesthesia may still need to be dripped on to the vocal folds. Rarely, superior laryngeal nerve block is indica­ ted.4 This block should be performed bilaterally and will thoroughly anesthetize the supraglottis and much of the glottis. Again, a small amount of topical lidocaine on the glottis may be necessary. The superior laryngeal nerve block is performed with plain lidocaine in a volume of 1 to 2 mL per side. The goal of the injection is to block the internal branch of the superior laryngeal nerve where it pierces the thyrohyoid membrane. The hyoid bone and the superior border of the thyroid cartilage are palpated and the midpoint is estimated. The midpoint between the neck midline and the superior cornu of the hyoid bone is also estimated, and the injection is performed at the intersection of these two locations (Fig. 77.1). The endpoint of anesthesia to the larynx is assessed on an individual patient and procedure basis. When the patient is no longer gagging, does not cough during lidocaine administration, and does not react to endosco­ pic palpation of the supraglottic and glottic structures, the endpoint has been reached.5 There is no advantage to over-anesthetizing the larynx, and in fact, aggressive anesthesia to the laryngopharynx can make the procedure more difficult due to aspiration of saliva. The topical anesthesia techniques described above provide about 20 to 25 minutes of working time in the larynx. However, because of residual anesthesia effects, the patient should be cautioned not to eat or drink for 60 minutes after anesthesia to limit aspiration risk. The most common complaints of topical laryngotracheal anesthesia include bitter taste of the medication and globus sensation. Some patients describe a sensation of not being able to swallow or breathe. This is due to loss of sensory feedback, and the concern is typically assuaged with reassurance.

The topical anesthetics used in laryngology office proce­ dures include esters (e.g. tetracaine and benzocaine) and amides (e.g. lidocaine and bupivacaine). These drugs reversibly block sodium channels in nerve fiber lipid membranes.6 When applied topically, they are effective at blocking pain and temperature signals. Maximum dose references are known for these anesthetics. However, the absorption of these medications across mucous membranes after topical administration is not known and is probably higher than with subcutaneous administration. Lidocaine is an amide local anesthetic with 45 to 60 minutes' duration of action and 90-second topical onset. Maximum dose of plain lidocaine is 3–5 mg/kg. Because the topical absorption is not known, it is best to stay on the lower side of that range for laryngotracheal procedures in the office. The patient’s weight should be obtained before the procedure and the maximum dose calculated. When using 4% lidocaine, the dose accumulates quickly (4 mL of 4% lidocaine delivers 160 mg), so caution is advised. Lidocaine toxicity has not been reported in the otola­ ryngology literature for office-based laryngotracheal pro­ cedures; nonetheless, it is important to identify the signs of toxicity when using this medication. Lidocaine toxicity may involve the central nervous system (CNS) and the cardiovascular system. CNS symptoms typically occur prior to cardiovascular symptoms, including dizziness and a feeling of being lightheaded, followed by visual dis­ turbances and tinnitus. Progressive CNS symptoms include tremors and twitching, followed by seizures if untreated. Coma and respiratory depression may ensue, along with cardiac collapse from depressed cardiac motility.7 Treatment of lidocaine toxicity should occur with the earliest symptoms. Minor symptoms such as tinnitus are treated by cessation of lidocaine administration. More advanced symptoms such as seizures are treated with sed­ atives and preparation for ventilatory support and cardiac resuscitation, if necessary. Transport to an intensive care facility is indicated for severe symptoms. Cardiovascu­ lar toxicity may be treated with lipid emulsion therapy in extreme cases. Published guidelines regarding manage­ ment of local anesthetic systemic toxicity are available from the American Society of Regional Anesthesia.7 Lidocaine allergy, both cutaneous and anaphylactic, is rarely reported with local administration. Lidocaine and other amide local anesthetics should be avoided when the patient reports a previous reaction to lidocaine.

Chapter 77: Anesthesia for Office-Based Laryngology

substantial changes in blood pressure and heart rate during office-based laryngeal surgery and transnasal esophagoscopy.

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Most in-office laryngotracheal procedures are performed without hemodynamic monitoring, but changes in hemodynamic status can occur during these procedures. High levels of comfort and low levels of complications have been reported in large series of transnasal esophagoscopy, laryngeal biopsy, and laryngotracheal laser procedures.10-12 Situational vasovagal syncope may occur during these procedures. This is typically associated with a prodrome of nausea, diaphoresis, lightheadedness, and tingling.13 Loss of consciousness may ensue. Treatment is termination of the procedure, initiation of hemodynamic monitoring, and prompt positioning of the patient in the reclined position with legs above the heart. A conscious patient with vasovagal prodromal symptoms may be positioned with the head between the legs instead of supine. The necessity of routine hemodynamic monitoring during office-based laryngology procedures is not clear but is likely advisable in those patients with cardiovascular risk factors. Ongkasuwan et al. demonstrated significant changes in systolic blood pressure and heart rate during transnasal laryngoscopy that were not associated with topical anesthesia administration.14 It is unclear if these changes are clinically significant. In two separate studies, Yung and Courey15 and Morrison et al.16 reported more



HEMODYNAMIC CONCERNS DURING OFFICE-BASED LARYNGOTRACHEAL PROCEDURES





1. Sunkaraneni VS, Jones SE. Topical anaesthetic or vasocon strictor preparations for flexible fibre-optic nasal pharyngo scopy and laryngoscopy. Cochrane Database Syst Rev. 2011; 16(3):CD005606. 2. Hogikyan ND. Transnasal endoscopic examination of the subglottis and trachea using topical anesthesia in the otolaryngology clinic. Laryngoscope. 1999;109(7Pt1):1170-3. 3. Rosen CA, Simpson CB. Peroralvocal fold augmentation in the clinic setting. Operative techniques in laryngology. Leipzig, Germany: Springer;2008. 4. Sulica L, Blitzer A. Anesthesia for laryngeal surgery in the office. Laryngoscope. 2000;100(10 pt 1):1777-9. 5. Wang SX, Simpson CB. Anesthesia for office procedures. Otolaryngol Clin N Am. 2013;(46):13-9. 6. Wolfe JW, Butterworth JF. Local anesthetic systemic toxicity: update on mechanisms and treatment. Curr Opin Anaesthesiol. 2011;24(5):561-6. 7. Neal JM, Bernards CM, Butterworth JF, et al. ASRA practice advisory on local anesthetic systemic toxicity. RegAnesth Pain Med. 2010;35(2):152-61. 8. Brown C, Bowling M. Methemoglobinemia in broncho scopy: a case series and a review of the literature. J Bronchol Interv Pulmonol. 2013;20(3):241-6. 9. Chowdhary S, Bukoye B, Bhansali AM, et al. Risk of topical anesthetic-induced methemoglobinemia: a 10-year retro spective case-control study. JAMA Intern Med. 2013;13: 173(9):771-6. 10. Postma GN, Cohen JT, Belafsky PC, et al. Transnasal esophagoscopy revisited (over 700 consecutive cases). Laryngoscope. 2005;115:321-3. 11. Koufman JA, Rees CJ, Frazier WD, et al. Office-based laryn geal laser surgery: a review of 443 cases using three wave lengths. Otolaryngol Head Neck Surg. 2007;137:146-51. 12. Rees CJ, Halum SL, Wijewickrama RC, et al. Patient tolerance of in-office pulsed dye laser treatments to the upper aerodigestive tract. Otolaryngol Head Neck Surg. 2006;134:1023-7. 13. Jardine DL. Vasovagal syncope. Cardiol Clin. 2013;31(1): 75-87. 14. Ongkasuwan J, Yung KC, Courey MS. The physiologic impact of transnasal flexible endoscopy. Laryngoscope. 2012;122(6):1331-4. 15. Yung KC, Courey MS. The effect of office-based flexible endoscopic surgery on hemodynamic stability. Laryngo scope. 2010;120(11):2231-6. 16. Morrison MP, O’Rourke A, Dion GR, et al. Hemodynamic changes during otolaryngological office-based flexible endoscopic procedures. Ann Otol Rhinol Laryngol. 2012; 121(11):714-8.

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Methemoglobinemia is a rare and potentially fatal com plication of topical anesthetics. Methemoglobin is formed when ferrous iron is oxidized to ferric iron in the hemo globin molecule. Methemoglobin does not bind oxygen and causes intact hemoglobin to have increased oxygen affinity. This decreases the oxygen available for peripheral tissues and causes oxygen desaturations. When methemo globin is > 20%, cyanosis and respiratory distress may occur. Importantly, pulse oximetry is unreliable in the setting of methemoglobinemia. Mild cases (methemoglobin < 30%) are treated with supplemental oxygen administration and cessation of topical anesthetic, with resolution over the following 24 hours. In severe cases, intravenous methylene blue, transfusion, or hemodialysis may be used.8 Methemo globinemia occurs in  2 mm. Thus, excisions are not really possible, but biopsies can be taken with this techni­que. Alternatively, with two flexible endoscopes, two instru­ ments can be utilized, extending the interventional options. In theory, any combination of transoral/transnasal visualization and instrument routing can be used. When combined, predominantly transnasal fiberscopic visuali­ zation is selected for monitoring the endolarynx, while the surgical instrument is routed transorally. Thus, more degrees of freedom for lateral instrument movements are provided. Furthermore, this allows for usage of larger and thicker instruments in the larynx.

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Fig. 78.2: Instrument table: one-handed laryngeal spray device (upper right corner), different kinds of anesthetics (upper left), two cups for lidocaine and hot water (lower left), cotton swab and surgical instrument with cupped forceps (center).

Fig. 78.3: Detachable tip for indirect transoral laryngeal surgery: rounded cupped forceps.

Fig. 78.4: Detachable tip for indirect transoral laryngeal surgery: straight cupped forceps.

Fig. 78.5: Various detachable tips for indirect transoral laryngeal surgery.

MEDICATION AND ANESTHESIA The topic is covered elsewhere in this textbook. Thus, only specific aspects will be briefly discussed here.

Medication

 

In terms of food and beverage intake prior to surgery, we recommend 2 hours of fasting (“non per oral—NPO”). We saw that the patients who were fasting for > 2 hours seem to have a higher level of nervousness, which is disadvantageous for indirect surgery. Sedation is only needed in very rare cases. If so, sedation can be achieved by 3.5–7 mg midazolam per oral, two hours prior to the

operation. For suppressing a cough response, we routinely administer antitussive medication per oral (e.g. 30 mg of codeine). Steroids are given to patients undergoing augmentation or major manipulation within the larynx (e.g. 100 mg prednisolone per oral after surgery and the same dosage the day after surgery), but not for excisions. Antibiotics are very rarely used, but indications might be for other reasons, e.g. endocarditis prophylaxis.

Monitoring -

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We recommend that vital signs should be checked pre and post operatively in all cases: blood pressure,

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Section 9: Office Laryngeal Surgery

pulse rate, and oxygen saturation. It is advisable to moni­ tor pulse rate and oxygen saturation with a pulse oximeter throughout the entire surgery. Usually, 1–2 hours of postoperative monitoring of vital signs is sufficient. A postoperative laryngoscopic check is advisable to rule out complications like bleeding and swelling. When patients are sedated, and definitely when midazolam is administered, the monitoring period may have to be extended from one to eight hours (especially in elderly patients). National medical and legal aspects apply and may differ widely from country to country.

“Verbal” Anesthesia We consider sufficient “verbal anesthesia” of utmost importance for successful office-based larynx surgery, with verbal reassurance to the patient during the entire procedure—it is a crucial prerequisite for the success of the intervention. Keep in mind that patients appointed for office-based surgery will be anxious and will be extremely aware of all of the circumstances related to “their” surgery. Besides circumstances supporting confidence, trust, and reassurance, it cannot be stressed enough how critical the “verbal anesthesia” (especially the doctor’s voice) com­ forts patients, reduces gag response, and helps to calm the patients down—making interventions of all kinds easier for the surgeon.

Intranasal Anesthesia

cocaine for topical anesthesia, which is one of the most potent substances. However, we feel that such drugs have too many drawbacks and can be avoided. After spraying, we use a swab to apply the anesthetic onto the mucosa. It also has the advantage of testing “touch sensitivity”, acquainting the patient to the new touch sensations and also predicting tolerance of further instrumental inter­ vention.

Anesthetizing the Upper Airway When starting the operation and as soon as topical anes­ thesia is applied onto the surfaces of the oral cavity and mesopharynx, the surgeon should—without losing time— move on with the procedure without further delay and spray lidocaine into the hypopharynx and larynx. After spraying the entire upper airway, including the endola­ rynx, then the aryepiglottic folds (Fig. 78.6), the ventricular folds, and the vocal folds should additionally be anes­the­ tized with a lidocaine-soaked cotton swab. It is helpful to check sufficient numbing by touching surfaces with the cotton swab. After thousands of procedures, we can state—as a rule of thumb—that the more posterior one gets (toward the arytenoids), the more likely a gag response is elicited. NB: fixation of the cotton wadding covering the tip of the curved cotton holder instrument (the “swab”) must be checked by the surgeon before intracorporeal use, since slipping off of the cotton due to inappropriate winding of the cotton would risk potential aspiration.

Use of 4% lidocaine, topically sprayed on the inferior and/ or middle turbinates, is very effective. In some cases, nasal decongestants combined with topical anesthesia are help­ful.

Intraoral Anesthesia When approaching the larynx transorally, topical anesthe­ sia is usually sprayed on selected areas: under the tongue, faucial arches, base of the tongue, posterior wall of the mesopharynx, lateral side of the epiglottis. Lidocaine (2%, 4%, or even 10%) is administered via spray and/or applied with a soaked, blunt cotton swab. When lidocaine or tetracaine is dissolved in an alcoholic solution, the patients might feel a sudden “burn” after the first spray (this often is the case, e.g. with Xylonest and Gingicain). In our hands, tetracaine is also a very useful anesthetic, because the anesthetic effect is even more pronounced than with lidocaine. We know that some authors use

Fig. 78.6: Swabbing of aryepiglottic fold. Lateral access into the endolaryngeal lumen. With this approach the gag response is mostly not elicited.

Chapter 78: Excisions of Laryngeal Masses

 

Palpation–Biopsy–Excision When instrument movements are tolerated within the larynx, the surgical instrument is advanced in the same manner and position as the swab. Cupped forceps should be introduced in a closed position, thus avoiding scratching of the mucosa in cases of sudden, unexpected laryngeal

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When we look at the past 25 years of performing office based procedures, we find that we were lucky that we have not encountered any serious complications. For instance, in the very rare cases of laryngospasm that may occur, e.g. when too much lidocaine is suddenly sprayed in large amounts into the larynx, we had to interrupt the procedure and ask the patient to undertake an effortful cough, to swallow all secretions, and afterward to breathe through the nose while closing the mouth. Transnasal breathing is a very good trigger for vocal fold abduction and results in widening of the glottis. Other causes for gag response or laryngospasm can be seen, e.g. when the mucosa has not been anesthetized sufficiently or an instrument touches the mucosa too forcefully. This can happen in the posterior part of the larynx and anywhere at the arytenoid hump—a typical gag triggering response area with high touch sensitivity. Nevertheless, good topical anesthesia of the endola­ rynx with spraying and swabbing should lead to sufficient, long term numbing in > 80% of the cases. An anesthe­ tized condition for excisions can be achieved in some patients within 2–3 minutes, and in others it takes 10 or more minutes. We realize that in approximately 5–10% of patients, the situation will not allow at all—or sufficient time—for accessing the endolarynx for surgery due to early re onset of gagging, repetitive swallowing, or coughing. Luckily, there is a habituation effect and a “learning curve” for most patients. We then offer that the same procedure might work at a second trial on another day. Approximately 5% of patients are not able to undergo indirect surgery with the above mentioned anesthesia measures. We then can try to additionally infiltrate lidocaine next to the superior laryngeal nerve via a transcutaneous nerve block (lidocaine with epinephrine 1%) in the region of the posterior part of the thyrohyoid membrane. Such an injec­ tion is not in all cases as easily performed as it sounds, because precise positioning of the needle and injection in the desired region may be difficult in patients with thicker necks.

that will follow during the surgical intervention. This imitation of the movements gives helpful feedback to the patient (immediate learning curve!), reassures that there is no pain, and also feeds back to the surgeon as to how the procedure might be tolerated. It is a kind of instant mapping of individual upper airway trigger zones for gag response. We prefer endolaryngeal instrument passage through a lateral approach, i.e. advancing the instrument over the aryepiglottic fold and avoiding touching the tip of the epiglottis as well as the arytenoid hump (Fig. 78.7). This pathway is favorable because it mostly avoids eliciting the gag response. In some rare cases, midline passage touching the median part of the tongue base and sliding over the tip of the epiglottis is easier than the lateral laryngeal approach (Fig. 78.8). However, in the authors’ opinion, the lateral pathway should be the first choice. Fortunately, in many patients pathologic lesions are located at the midmembranous part of the vocal folds, which are—luckily!—not very sensitive to manipulation, making interventions easy when the most sensitive gag response triggering zones of the supralarynx are (by ) passed (Fig. 78.9). -

Anesthesia-related Risks, Failures, and Complications

955

TRANSORAL SURGERY Whatever you plan to do, you should perform it in a speedy, but not rushed manner. The operation starts with the cotton swab, which anticipates all movements

Fig. 78.7: Transoral operation: curved instrument with cupped forceps follows the same route into the endolarynx. Easiest way to perform rigid transoral surgery.

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Section 9: Office Laryngeal Surgery

Fig. 78.8: Transoral operation: medial access into the endolaryngeal lumen. Rarely this route is easier. Also, the tip of the instrument cannot be overseen freely when compared to lateral access of the instrument.

Fig. 78.9: Transoral operation: cupped forceps in a closed position. The tip of the instrument is used to palpate the right vocal fold. Because of lateral access to the endolarynx, the movements of the instrument can be seen clearly. Here, sulcus vocalis was ruled out.

movements. Before grasping the targeted tissue, a brief palpation of the vocal folds with closed cupped forceps will give an impression of how much the following instru­ ment movements will be tolerated (Fig. 78.9). We advise to check superficial lesions of the vocal folds for pliability in a superior–inferior (up and down) and posterior–anterior (back and forth) palpatory movement. In cases of soft vocal fold polyps, we recommend to pro­ ceed in the following sequence: make two pre­determined epithelial discontinuities (notches) at the anterior and posterior margins of the lesion with the tip of the forceps by pinching and tearing the marginal epithelium. This will help you to avoid inadvertent de-epithelialization of the adjacent mucosa by undesired stripping during instrumental pull on the body of the lesion. Now, grasp the polyp with a delicate squeeze, let loose, and check the (iatrogenic) tissue indentation marks for how much tissue you would have excised if you had punched it out. If your grasp was placed correctly, continue and grasp again the entire polyp and remove it with the identical tissue grip. Avoid trying to punch the lesion out, since it will not work reliably. Keep in mind that the pulling direction of the instrument is preferably from anterior to posterior, and the vector is almost in parallel with the longitudinal axis of the vocal fold. Avoid medial pull, because with medial pull unpredictable tear and stripping of adjacent, normal epithelium will likely happen. With the anteriorto-posterior pull vector, the epithelium will tear at the anterior notch and will stop at the posterior notch. After excision of the polyp body, you might want to straighten

out the margins for epithelial “corners” at the notches (socalled dog’s ears). You can also use the tip of the cupped forceps for this action. Sometimes a small hemorrhage by capillary bleeding might follow—it should not frighten the surgeon when some drops of blood spread endolaryngeally. Be aware that after swallowing or throat clearing, even a few drops of blood will color the entire endolarynx, since blood is very effective in coloring secretions. To avoid unneces­ sary patient’s concerns when seeing “red”, we do not let the patient view the procedure online on a second monitor. After a short and soft (!) throat clear or “airbrush” by hissing—or wiping of the vocal fold with the closed forceps (still containing the tissue specimen), the surgeon will have the occasion to visualize the vocal fold and decide whether its contour is straight or if additional trimming is needed. When videolaryngostroboscopy is available for assessment of phonatory function and while the endoscope and cupped forceps are still in place, it is advisable to immediately switch over to the strobe function and to assess mucosal movements during phona­ tion before lamina propria swelling begins. Because the swelling of healthy, surrounding tissues will almost always begin after a couple of minutes, be aware that you do not excise too much (healthy!) tissue when keeping on excising all “swollen” tissues.

TRANSNASAL SURGERY Precise tissue excisions from the endolarynx can hardly be performed transnasally. However, biopsies can be

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Chapter 78: Excisions of Laryngeal Masses

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done and then “blindly” excise too much tissue. To avoid this complication, it is advised to excise only those tissues where margins can be overseen. Thus, first “bite” into the lesion, see how the tissue indentation marks would have done, and if in doubt, leave tissue the way it is, i.e. unexcised, and take a wait and see attitude. See your patient on one of the following days and give the procedure a second chance. There is almost always a habituation for the patients with easier access to the larynx at a second trial. Another complication may occur when patients are on anticoagulation medication. We try to avoid surgery when patients are on coumarin, but we do surgery when patients are on clopidogrel or acetylsalicylic acid medication. We have never seen severe bleeding forcing us to move the patient to an emergency operation in general anesthesia or having the patient to be hospitalized. Furthermore, no cases were encountered where airway compromising swelling of the larynx was seen after biopsy or excision. (NB: injection laryngoplasty may be a different case). Also, in > 25 years of performing office based proce­ dures, neither severe cardiovascular reactions nor signi­ ficant bradycardia has been encountered. Some few cases of vasovagal reactions have been handled by supine positioning—legs up and monitoring of patient! We do not routinely administer atropine anymore and have not done so for approximately10 years. Sedation is only used in our practice in < 5% of interventions. We have also noted only very few cases of short lasting episodes of laryngospasm in the spraying part of topical anesthesia. These self limiting events can be treated rapidly and effectively with reassur­ ance and breathing techniques.



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taken quite easily. While transoral techniques separate visualization and surgical instrument movements, this is not the case in transnasal (single) endoscope techniques. When using a flexible endoscope with an instrument channel, it must be kept in mind that endoscopic move­ ments (for better visualization of the endolarynx) inevitably result in movements of the instrument that is routed through the instrument channel. A channeled single use endoscope sheath can be used to cover the endoscope and deliver an instrument through the paralleled channel adjacent to the endoscope, when a flexible endoscope with instrument channel is not available. Biopsies can be taken with a flexible small forceps routed through the instrument channel of the flexible endoscope. This procedure can hardly be handled by one person. It is advisable that the surgeon holds and directs the endoscope, and may even advance the forceps onto the tissue. But a second person is needed to open and close the forceps. When successful, the forceps may be withdrawn alone or together with the endoscope. When two surgeons work together, coordinated and concerted actions have to be trained before a harmonized intervention can be performed. Ricci Maccarini, de Rossi, and Borragan proved that a team approach for transnasal office based intervention is an alternative to surgery in general anesthesia, and they developed their transnasal interventional techniques with specially designed instruments to a very high level of expertise (even when not all interventions are true in office procedures because some of them require intravenous analgesia with sedation and monitoring, which is provided by an anesthesiologist in an operating room). Removal of tissues can also be performed with a tissue destruction technique: laser coagulation, carbonization, or evaporation/ablation with different laser types. The easiest way is transnasal laser surgery with a flexible glass fiber passed through the instrument channel. Laser pulses can be applied in a noncontact or in contact mode. Laser procedures can be handled by one surgeon. Mostly, it is easier to do it with two surgeons, who have to collaborate with high coordination to perform successfully in their concerted action.



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In general, after many thousands of interventions in the office, including all kinds of biopsies and excisions, we have not encountered any severe complications. Some­ times it could be that a surgeon cannot visualize the region of interest and thus, may feel urged to get the procedure



POSSIBLE COMPLICATIONS

1. Try to anesthetize your patient quickly. We recommend using 10% lidocaine or tetracaine spray. Remember that gagging triggers more gagging. Your learning curve will enable you to avoid initiation of gag response attacks while you anesthetize, probe, and monitor your patient while swabbing. 2. Take the lateral approach into the superior endolarynx via the aryepiglottic folds. The tip of the epiglottis is a very sensitive trigger area for gag response, so try to avoid touching this part. 3. Impeded view of the larynx during surgery due to fogged lenses is an annoying disturbance or even disruption. Glide your rigid endoscope over the base of the tongue in a quick in and out movement (in the direction of



HELPFUL ADVICE IN SPECIAL SITUATIONS

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Section 9: Office Laryngeal Surgery

the endoscope) to wipe the lens. Warming of the rigid endo­scope tip in hot water (in a cup standing on a tray) immediately before endoscopy is a helpful anti-fog measure. 4. “Foamy” secretions pooling in the piriform sinuses and spilling over into the endolarynx after topical anesthesia can be defoamed with a teaspoon of Dimeticonum (Sime­thicone) (e.g. Sab simplex). Let the patient swallow once, and the foam will disappear immediately. 5. To avoid scratching of the mucosa with your instru­ ment during a sudden cough or gag response, be sure that the instrument is kept closed until immediately before grasping the tissue. 6. Instrumental palpation of the lesion gives additio­ nal information about the tissue properties and tells you how to possibly best approach the lesion for excision. 7. In transnasal biopsy cases, you may want to access the lesion by using the contralateral nasal side for the endonasal endoscope passage. This enables a better angu­ lation of the tip of the flexible endoscope to visualize the targeted area, e.g. the vocal fold.

ACKNOWLEDGMENTS Special thanks go to Jürgen Wendler, John Rubin, and Mike Benninger for assistance in improving this chapter.

REFERENCES 1. Wendler J. Personal communication. Oral presentation at World Voice Conference (Luxor, Egypt). 2012. 2. Von Bruns V. Die erste Ausrottung eines Polypen in der Kehlkopfshöhle durch Zerschneiden ohne blutige Eröffnung der Luftwege nebst einer kurzen Anleitung zur Laryngo­ skopie. The first eradication of a polyp in the laryngeal cavity via dissection without sanguinary opening of the airways along with a brief instruction on laryngoscopy. Tübingen: Laupp & Siebeck;1862. 3. Von Bruns V. Die Laryngoskopie und die laryngoskopi­ sche Chirurgie. Laryngoscopy and laryngoscopic surgery 2. Ausgabe. Tübingen: Verlag der H. Laupp'schen Buch­ handling;1873. 4. Friedrich G, Remacle M, Birchall M, et al. Defining phono­ surgery: a proposal for classification and nomenclature by the Phonosurgery Committee of the European Laryngo­ logical Society (ELS). Eur Arch Otorhino­ laryngol. 2007; 264(10):1191-200. 5. Rosen CA, Amin MR, Sulica L, et al. Advances in officebased diagnosis and treatment in laryngology. Laryngo­ scope. 2009;119:S185-212.

Chapter 79: Office-Based Laryngeal Laser Surgery

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CHAPTER

79

Office-Based Laryngeal Laser Surgery Christopher M Bingcang, Seth H Dailey

A laser is light energy harnessed to effect changes to targeted tissues. In contrast to visible light, which scatters

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LASER BACKGROUND

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Office-based laryngeal laser surgery (OBLLS) has been practiced for nearly a decade with safety and efficacy while decreasing costs of healthcare.1 Used to treat benign laryngeal pathology, this treatment modality has develo ped within the latter half of the 20th century from the merging of technological advancements in optics and lasers. In 1968, Sawashima and Hirose described the first use of fiberoptic endoscopes in the larynx, but their poor image resolution prevented substitution for direct laryngoscopy.2 Within the last decade, advances with digi tal imaging using flexible distal-chip endoscopes have provided unparalleled high definition approximating the resolution achieved in operative direct laryngoscopy. The first use of laser in laryngology was described in 1972 by Jako and Strong who used a carbon dioxide (CO2) laser to treat benign and premalignant laryngeal lesions.3 Other lasers were designed over the following decades, and in 1998, the first use of the pulsed-dye laser (PDL) was documented for treatment of laryngeal papillomatosis under direct laryngoscopy.4,5 Subsequently this techno logy was merged with the flexible endoscope and treat glottal dysplasia or recurrent respiratory papillomatosis (RRP) in the unsedated patient. Thus, the first OBLLS was described in 2004 by Zeitels et al.6

energy in random vectors, laser beams are focused into a single vector, referred to as collimated light. The collimated light is created by passing light energy through a lasing medium of gas, liquid, or solid phase, which selectively amplifies specific wavelengths of light, which is, in turn, preferentially absorbed by different tissues. Consequently, a laser may be selected for its wavelength to selectively treat tissues that preferentially absorb that wavelength while reducing collateral damage to other tissues. The targeted tissue is referred to as the chromophore for its respective laser.7 In addition to selecting lasers based on its chromo phore, the surgeon may modulate the delivery of energy by modifying various parameters, referred to as laser settings: (1) power (energy per time), (2) energy, and (3) duration of exposure. Once these settings have been selected, the surgeon may further modulate energy delivery by altering the distance from the laser tip to the target tissue. While collimated light from lasers such as CO2 have negligible divergence, lasers that are delivered via a glass fiber have a 15°–20° divergence from the initial beam’s vector, such that the energy diffuses with increas ing distance.7 Altering the distance from the fiber tip to the target tissue results in change to energy delivery per area, referred to as irradiance. High irradiance vaporizes tissue, whereas low irradiance coagulates tissue. Vaporization refers to the heating of intracellular water to steam, causing subsequent cell destruction. Coagulation refers to the effect of denaturing of proteins, which causes disorganization rather than destruction of the target tissue. The balance between vaporization and coagulation has permitted sur geons to vary treatment effects to specific pathology. In

HISTORY OF OFFICE-BASED LARYNGEAL LASER SURGERY

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Section 9: Office Laryngeal Surgery

summary, the energy delivered to tissues in OBLLS may be modulated by the surgeon by the following: (1) selec­ tion of a laser with the desired chromophore, (2) selection of the laser energy settings, and (3) alteration of the irra­ diance by changing distance of the fiber tip to the target tissue.7

Photoangiolytic Lasers Four lasers are currently in use for OBLLS: (1) potassium titanyl phosphate (KTP), (2) PDL, (3) CO2, and (4) thulium: yttrium-aluminum-garnet. KTP and PDL are considered photoangiolytic lasers that target oxyhemoglobin, whereas CO2 and thulium are considered ablative lasers that target water. Both KTP and PDL deliver energy through a glass fiber and are easily passed through the working channel of a flexible endoscope. Selective absorption of energy by oxyhemoglobin results in improved hemostasis over CO2 laser. This effect is believed to be caused by the des­ truction of the supporting microvasculature. As a result, collateral thermal injury is reduced, which reduces damage to the epithelium and superficial lamina propria (SLP), consequently diminishing the risk of vocal fold scarring. Subsequently vocal fold pliability is preserved.6,8,9 The KTP (Aura XP; American Medical Systems, Minne­ tonka, MN) was initially described for use in unsedated patients for office-based laryngeal surgery in 2006 by Zeitels et al.10 and uses a 532-nm wavelength.7 Its advan­ tages over PDL are believed to be a more effective intra­ vascular coagulative effect, leading to decrease in vessel rupture noted in PDL use.11 Another advantage is the decreased cost of KTP, which requires less maintenance than PDL.12 Table 79.1 summarizes key KTP laser charac­ teristics compared with other office-based lasers.

The PDL (Photogenica SV; Cynosure, Westford, MA), in contrast to KTP, uses a liquid laser medium to create a 585-nm wavelength beam. PDL was first described for use in the office setting in 2004 by Zeitels et al., who successfully treated glottal dysplasia and RRP.6 PDL has the advantage of creating a “cleavage plane” between the basement membrane and SLP, allowing for improved epithelial and SLP preservation while obliterating the vascular supply to vocal fold lesions.8,13 Consequently, PDL has been felt to be superior to KTP for treating glottal dysplasia.8,13

Ablative Lasers Unlike the photoangiolytic lasers, CO2 and thulium utilize wavelengths that are strongly absorbed by water. Although the 10,600-nm CO2 laser has had a long-track history of use in direct laryngoscopy, it has only been used in officebased procedures for less than a decade. Recent deve­ lopment of the Photonic Band-Gap Fiber (OmniGuide Communications, Inc, Cambridge, MA), a flexible fiber con­sisting of a hollow-core tube surrounded by a dielectric mirror, has allowed the use of CO2 within a flexible endo­ scope. Its successful use in a large series of patients was first described by Koufman et al. in 2007.14 Compared to KTP and PDL, the CO2 with OmniGuide fiber permits a deeper, more efficient treatment of bulky disease.15 In contrast, its disadvantages include its proclivity to cause vocal fold scarring, its poorer hemostatic properties, and the Photonic Band-Gap Fiber’s increased expense over standard glass fiber. These characteristics have led to its use to treat bulky disease in regions other than the vocal folds.

Table 79.1: Summary of office-based laryngeal laser surgery lasers

Laser

Chromophore

Delivery

Potassium-titanyl- 532 phosphate

Wavelength, nm

Oxyhemoglobin

0.4 and 0.6 mm fiberoptic -Lower risk of vocal fold scarring -Increased hemostasis over ablative lasers -Less bleeding than pulsed-dye laser (PDL)

Advantages

Pulsed dye laser (PDL)

585

Oxyhemoglobin

0.4 and 0.6 mm fiberoptic -Lower risk of vocal fold scarring -Increased hemostasis over ablative lasers

Carbon dioxide (CO2)

10,600

Water

1.2-mm hollow core with dielectric mirror (photonic bandgap fiber)

-Increased depth of penetration allowing treatment of bulky disease

Thulium

2013

Water

0.6 mm fiberoptic

-Increased depth of penetration allowing treatment of bulky disease -“Contact” mode capable -Improved hemostasis over CO2

Chapter 79: Office-Based Laryngeal Laser Surgery



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SPECIFIC APPLICATIONS One of the values of OBLLS is the ability to surgically treat recurrent benign laryngeal disease that in the past would have required the repeated use of general anesthetics. Traditionally, the surgeon would need to weigh the benefits of treating leukoplakia or papillomatosis against the risks of repeated exposure to general anesthetics. Consequently, the surgeon would often wait until the patient experienced significant functional decline to initiate surgical intervention. Fortunately, OBLLS has reduced the threshold to treat laryngeal disease, resulting in the ability of a surgeon to take action earlier than before. Therefore, OBLLS has demonstrated its utility in treating recurrent laryngeal disease such as leukoplakia with dysplasia6,8,10 and RRP.6,10,13 In addition, because of its photoangiolytic properties, KTP and PDL have been used extensively in the office for

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The advantages of OBLLS over direct laryngoscopy include its increased safety and decreased costs. OBLLS is performed as an outpatient procedure without sedation. Therefore, the patient avoids risks associated with undergoing general anesthesia and requires no cardiopulmonary monitoring,17 although monitoring may be warranted in patients with poorer cardiopulmonary status.18 In addition to its safety, OBLLS is well tolerated by patients. A survey conducted by Rees et al. found that 87% of patients undergoing OBLLS preferred treatment unsedated in the office setting over the operating room under general anesthesia.19 Another advantage of OBLLS is its reduced costs to the patient and third party payers. Certainly, the patient experiences decreased time off work, has reduced outof-pocket costs, may drive to and from the appointment, and no additional person must accompany the patient. Likewise, OBLLS is less costly to third party payers, as there are no operating room or anesthesia fees, thereby saving an estimated $5000 per case.1



ADVANTAGES OF OBLLS

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vocal fold ectasias and varices,9,20 along with hemorrhagic polyps,9,21 and by extension for nonhemorrhagic polyps as well.22,23 Indeed, the indications for using the photoangiolytic lasers have expanded yet further to nonhemorrhagic lesions. Altogether OBLLS has been used with varying degrees of success to treat Reinke’s edema,24 cysts,14 vocal fold granuloma,25 amyloidosis,14 and vocal fold scar.26 It has been hypothesized that the photoangiolytic lasers create a nonspecific thermal injury surround ing target chromophores, which initiates a wound repair process ultimately leading to lesion regression.27 Table 79.2 summarizes the laryngeal pathology currently being treated with office-based lasers. It should be noted that before any laser treatment begins, histopathologic diagnosis may need to be obtai ned for many laryngeal disease processes if possibility of malignancy is a concern. Specifically, leukoplakia and laryngeal papillomatosis should be biopsied either in the operating room with direct laryngoscopy under general anesthesia or in the office with flexible laryngoscopy under local anesthesia.6,13 ­

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Like CO2, the 2013-nm thulium:YAG laser (Revolix Jr; LISA Laser, Pleasanton, CA) targets water. Unlike CO2, thulium uses a glass fiber similar to the photoangiolytic lasers. Advantages of thulium over CO2 include better hemostatic effect, and the ability to use contact and non contact modes similar to that found with photoangiolytic lasers.14,16 Like CO2, thulium may also be used for its tissue cutting and ablative effect.

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PATIENT SELECTION AND PREPARATION Although OBLLS has allowed treatment of multiple laryngeal pathologies, it is essential for the surgeon to use good judgment in selecting appropriate patients for unsedated procedures. Such procedures are still not risk free, and patients should be appropriately counseled. Table 79.2: Laryngeal pathology treated with office-based laryngeal laser surgery

Pathology

KTP

PDL

CO2

Thulium

Amyloidosis

+

Cysts

+

Leukoplakia/dysplasia

+

+

+

Ectasias/varices

+

+

+

Granuloma

+

+

+

+

Polyp, hemorrhagic and nonhemorrhagic

+

+

Reinke’s edema/polypoid corditis

+

+

Laryngeal papilloma

+

+

+

+

Scar

+

+

+

The pathology above has been documented in the literature to have treated with laser in the office-based setting. (KTP: Potassium-titanyl-phosphate; PDP: Pulsed-dye laser).

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Section 9: Office Laryngeal Surgery

Further­more, a clear explanation of the procedure as well as the preparation process to the patient should decrease patient anxiety, increase compliance, and increase the likeli­hood of success.

Contraindications to OBLLS While there are no absolute medical contraindications to OBLLS, some patients may be more appropriately treated under general anesthesia; contraindications relate to a patient’s inability to comply with or fully tolerate the procedure. First, a patient who is unable to communicate and follow instructions may be unable to comply. Second, patients with severe anxiety or heightened gag reflexes may have a tendency to move and may be better managed under general anesthesia. Finally, patients with tight nasal vaults due to septal deviation or turbinate hypertrophy may not be able to tolerate the flexible endoscope and may need to be managed under general anesthesia or via a transoral route.28

Instrumentation and Equipment Office-based laryngology may be performed with stan­dard equipment and instruments commonly found in many academic otolaryngology clinic suites without need for cardiopulmonary monitoring. Such common equipment includes high-flow suction and a powered otolaryngology examination chair. High-definition video towers, distalchip endoscopes with working channels, and laser towers, however, are more expensive and less commonly found in general otolaryngology practices. Nonetheless, highdefinition video towers with distal-chip endoscopes allow more optimal exposure of pathology and are prefer­ red over standard fiberoptic endoscopes. Figure 79.1 depicts an example of the layout of the examination chair, the video tower, and KTP laser tower. Although most OBLLS is performed via transnasal route using flexible endoscopes, laser work may optionally be performed transorally with visualization through a rigid 70° telescope and delivering the laser fiber through an Abraham curved catheter. Verma and Dailey descri­ bed the successful use of this approach on patients who experienced high nasal discomfort from transnasal endo­ scopes.28 Because of the longer track record and more widely used approach of transnasal endoscopy, the remainder of this chapter will focus on performing OBLLS using the transnasal approach with a flexible endoscope.

Fig. 79.1: Typical equipment layouts for office-based laser laryngeal surgery. The tower is a distal-chip high-definition-capable video tower, attached to a unit that allows video and photodocumentation. To the right is the laser tower, which is relatively small and easy to transport. Also notable is the flexible endoscope, which is connected to room suction. No cardiopulmonary monitors are needed.

Laser Precautions The potential for inadvertent harm to patient and operat­ ing personnel from stray laser fire has been discussed. Consequently, all persons in the procedure room should comply with all laser precautions. First, the door to the room is closed and signage to alert potential in-comers of laser use is placed on the door. Personnel and the patient in the room are distributed appropriate laser safe eyewear. Each laser has specific laser eyewear that filters the corresponding wavelength of light, and therefore eyewear for different lasers should not be used. Suction is used during the procedure to evacuate plume, which allows improved visualization and decreases the patient’s discomfort with the noxious odor of laser-treated tissue. To prevent transmission of biologically active particles from potentially infective lesions such as papilloma, safety masks are donned by all personnel in the room.

Patient Preparation— Positioning and Relaxation Not unlike operative direct laryngoscopy, successful awake flexible laryngoscopy requires appropriate patient positioning to optimize access and exposure of the target tissue. Moreover, appropriate patient positioning decrea­ ses surgeon fatigue and increases the patient’s comfort

Chapter 79: Office-Based Laryngeal Laser Surgery

­

Most patients require three aliquots, but care should be taken to avoid overanesthetizing the patient lest secre tions overaccumulate. On the other hand, a patient with a history of hypersensitive gag reflex may require more than three aliquots. Figure 79.2 depicts a patient undergoing transnasal flexible laryngoscopy just prior to delivery of anesthetic. Should the patient undergo a transoral approach, oropharyngeal anesthetic may be substituted. In this case, three atomized sprays of 4% lidocaine are applied trans orally to the tonsillar fossa, soft palate, posterior pharyn geal wall, and base of tongue. The “laryngeal gargle” anesthetic may then be accomplished transorally with an Abraham cannula.28

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­

­

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Patient comfort is optimized with topical anesthetic. The surgeon administers topical anesthetic in two parts: (1) nasal and (2) endolaryngeal. Nasal anesthetic is adminis tered prior to patient positioning to allow 5 minutes to elapse for full efficacy. First, the nasal cavity is anesthetized and decongested with an aerosolized mixture of 50/50 oxymetazoline/4% lidocaine. If additional anesthe tic is desired, intranasal placement of cottonoid pledgets soaked with 4% lidocaine may be placed. In addition, the surgeon may also elect to administer 5 mL of nebulized lidocaine if the patient has exhibited extreme hypersensitivity to prior laryngoscopic interventions; however, most patients will not require this. After nasal anesthetic has been applied, direct laryn geal anesthetic, also known as the “laryngeal gargle”,30 is performed. Topical lidocaine 4% is administered through the working channel of a flexible endoscope suspended just superior to the larynx. The first milliliter is dropped onto the epiglottis. A second milliliter is dripped onto the glottis while the patient is instructed to phonate. As the patient phonates the lidocaine distributes along the false vocal folds, epiglottis, arytenoids, and pyriform sinus.

­



Anesthesia

Fig. 79.2: A patient is undergoing flexible laryngoscopy and is about to undergo laryngeal anesthetic with the “laryngeal gargle”. Immediately before lasering, the surgeon, the patient, and all room personnel will don laser-safe glasses.

­



and ability to tolerate the procedure, thereby increasing potential length of the procedure. The patient is seated with hips back in the chair and torso bent forward at the waist, such that the chin is extended in a “sniffing position”. The patient’s arms are held loosely between the knees. The height of the patient’s chair is placed so that the surgeon may stabilize the arms to the torso and decrease arm fatigue. As OBLLS is performed without any intravenous seda tion, the patient’s comfort and anxiety must be managed through relaxation techniques. The goal of relaxation techniques is to maximize treatment time by decreasing anxiety and increasing compliance. The authors have found the following approach to allow all but very few patients to successfully undergo OBLLS.29 First, the patient is encouraged to relax the more powerful muscles of the head and neck: the muscles of mastication, the forehead musculature, the trapezius, and the tongue muscles. Second, the patient is asked to breathe slowly and fully, which serves to decrease the patient’s heart rate, and also to provide a slower and more predictable target when lasering. Finally, the patient is encouraged to keep the eyes open and to fixate on a single point to prevent buildup of excess facial muscle tension.

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SURGICAL TECHNIQUE Before beginning laser treatment, the laser settings as well as laser safety precautions are verified. All personnel, including the patient, should wear laser-safe protective goggles and filtered respirator masks if lasering potentially infective material such as papillomas. Suction should be activated to remove plume, which serves both to improve visualization and to decrease noxious fumes to the patient. The laser fiber with a protective sheath is inserted into the working channel of the endoscope until the sheath is seen on the monitor. It is imperative to use the protective sheath to avoid causing an exposed laser fiber tip to damage the lining of the working channel. A water-based surgical lubricant is used to facilitate advancement of the sheath.

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Section 9: Office Laryngeal Surgery

Once 1 to 2 mm of sheath is visible on screen, the laser fiber is advanced beyond the sheath an additional 5 mm. These distances from the tip of the fiber to the tip of the endoscope have been described as varying from as small as 1 mm to 2 cm.13,31 A shorter working distance between the endoscope tip and fiber tip allows increased control over the endoscope and a more magnified view of the target lesion, but it may increase the chance of contact with the endoscope and the endolarynx, thereby activat­ ing gag or cough reflexes in some patients despite the use of local anesthetic. Thus, the surgeon’s experience and the patient’s reactivity may determine the optimal distance between the tip of the endoscope and the tip of the fiber. In contrast, the distance from the fiber tip to the target lesion determines the treatment effect desired between ablation and coagulation as previously discussed. Either the entire endoscope or laser fiber alone may be advanced or withdrawn to titrate such a treatment effect. It is advis­ able to begin laser treatment from a larger distance initially to avoid excessive energy transfer to the target tissue. This working distance will either be 0 mm—i.e. contacting the lesion—or approximately 2 mm. Contact with the lesion favors ablative effect, whereas a ≥ 2 mm distance favors photocoagulation, which preserves epithelium.6 Distance has been described also to vary up to 7 mm away from the target lesion.32 The surgeon becomes adept at

judging this distance with experience as well as by visual feedback of the changes of the target tissue. In many cases, lesions such as papillomatosis may be so bulky as to prevent sufficient removal with blanching effects alone. Often, bulky papillomatosis may be treated efficiently by “contacting“ the laser fiber tip against the lesion. This allows a higher amount of energy delivery with less beam divergence to affect the target tissue. This causes deeper penetration of coagulation down to the base of the lesion while not significantly damaging deeper layers such as the lamina propria. The bulky lesion becomes friable and may effectively be peeled off cleanly without significantly disturbing the vocal fold lamina propria, thereby preventing unwanted scar formation. It is important to note that the endpoint for treatment is not determined by absolute energy delivered, but rather by such visual feedback. The visual endpoint for treat­ ment for ablation is vaporization of the target lesion, accompanied by the surrounding brownish coloration caused by coagu­lation of blood vessels. Endpoint for treat­ ment with photo­coagulation is the blanching of the target tissue, separation of epithelium from underlying subepi­ thelial tissue, and mucosal ecchymosis.6 Figures 79.3A to C through 79.5 illustrate the blanching of tissue and dar­ kening of blood vessels, which indicate the desired photocoagulative effect, while preserving the epithelial layer. Figure 79.6A to C demonstrates KTP laser treat­ment of bulky papilloma.

A

B

Figs. 79.3A and B: Leukoplakia of the left vocal fold. Example of leukoplakia (A) before and (B) during potassium-titanyl-phosphate laser treatment. Notable is the blanching of the lesion as well as area immediately surrounding, thus indicating coagulation of the lesion’s feeding vessels.

Chapter 79: Office-Based Laryngeal Laser Surgery

A

965

B

Figs. 79.4A and B: Hemorrhagic polyp of the right vocal fold. Example of a hemorrhagic polyp (A) before and (B) during potassiumtitanyl-phosphate laser treatment. Again notable is the blanching, but also darkening of the lesion, indicating coagulation of blood.

A

B ­

Figs. 79.5A and B: Laryngeal papillomatosis. Example of a laryngeal papilloma (A) before and (B) after potassium-titanyl-phosphate laser treatment. Again notable is the blanching of the lesion.

POSTOPERATIVE CARE AND OUTCOMES Postoperative Care and Follow-up After laser treatment is completed, the patient is asked to avoid food or liquid for 30 minutes to 1 hour after the

termination of the procedure, to allow the effects of the local anesthetic to wear off, thereby reducing the risk for possible aspiration. The patient is then placed on a period of strict voice rest of at least 3 days. Voice rest has been described as few as 3 days and as long as 7 days.12,13,27,32 Patients should be counseled that treatment effects will not be immediate, but rather will occur over 1 month

966

Section 9: Office Laryngeal Surgery

A

B

C

Figs. 79.6A to C: Sequential videos of potassium-titanyl-phosphate treatment of papilloma. Sequential videos of treatment of papilloma (A) narrow band imaging (NBI) enhances visualization of vascularization; blanching of the right vocal fold papilloma may be contrasted with the left fold papilloma. (B) Continued energy delivery creates an ablative effect, which more rapidly reduces bulkiness of lesion; NBI is switched off midway to reveal appearance under standard light. (C) Further reduction of the papilloma bulk is performed.

and certainly by 3 months.21,33 Therefore, follow-up with videostroboscopic evaluation should occur within that period of time, although specific follow-up has been highly variable between practices and also depends on the type of lesion. Nevertheless, average follow-up was approxi­ mately 3 to 5 weeks13,27,32,34 and in some 4 to 8 weeks.10,25 Because follow-up is so varied, it is useful to understand the history of vocal folds after laser treatment. Kim and Auo used PDL to treat 270 patients with vocal fold polyps and found that at 1 week, the patients had a rough voice quality and the vocal folds were found to have petechiae, whitish colored debris, and edematous swelling of the

vocal folds.22 These significantly improved by 3 weeks, and subsequently the vocal fold mucosal wave returned at 2 months. In addition, subjective and perceptual measures improved significantly.22 Being familiar with this healing pattern, surgeons may then elect to have their patients’ follow-up either after the disappearance of the posttreatment inflammatory changes after 3 weeks, or after the vocal fold mucosal wave is expected to return at 2 months. At the follow-up visit, assessment of the patient’s overall perception of their voice, as well as examination with videostroboscopy, allow the surgeon and patient to determine if appropriate regression of disease has

Chapter 79: Office-Based Laryngeal Laser Surgery

epithelium and SLP. Ayala et al. demonstrated that the vocal fold structure of PDL-treated dysplasia returned to a normal appearance within 3–4 weeks post-treatment.8 Hirano et al. studied both vocal fold stiffness and voice function in patients undergoing KTP for Reinke’s edema, dysplasia, and polyps; mean phonatory time, voice grading with GRBAS (Grade, Roughness, Breathiness, Asthenia, Strain), and vocal fold stiffness all improved significantly.9 Pitman et al. confirmed similar findings for KTP laser treatment for Reinke’s edema but also confir med histologically that epithelium was well preserved.24 These studies have thus demonstrated the ability of OBLLS to preserve the vibratory function of the vocal folds, thereby establishing its efficacy. ­

­

­

occurred, or if retreatment is required either with repeat OBLLS versus formal operative direct laryngoscopy. The general practice of the authors is to have the patient return in 3 months to allow full, optimal healing. Within this interval, the patient undergoes voice therapy. The purpose of voice therapy after OBLLS is to treat secon dary functional voicing disorders that may have developed from compensation from diseased anatomy as well as to reinforce optimal vocal behavior.31

967

Outcomes of OBLLS on Vocal Fold Anatomy Several large series have established the efficacy of OBLLS to induce disease regression while preserving laryngeal

LARYNGOTRACHEAL STENOSIS



­

­

­

OBLLS has found expanded use in the treatment for laryngotracheal stenosis (LTS). Patients with LTS may have medical comorbidities such as obesity and difficulty with intubation; such patients may benefit from interventions under local rather than general. Indeed, several groups have begun treating such patients with supraglottic, sub glottic, and tracheal stenosis in the operating room with mild sedation. These groups have used flexible broncho scopes with fiber-based lasers like CO2-Omni Guide and Nd:YAG. These treatment modalities are performed under mild or no sedation to allow patients to ventilate spon taneously and cooperate with instructions. Two to three wedge excisions in the stenotic area are performed with the laser; circumferential treatment is avoided to prevent de-epithelialization that predisposes to recurrence. One or more laser treatments are usually needed and have demonstrated some success. Leventhal et al.37 treated 16 patients with acquired subglottic stenosis with Nd:YAG laser in the operating room under mild sedation. Of these patients, four of seven tracheostomy-dependent patients were successfully decannulated with six laser treatments. Patients without tracheostomies required two to three laser treatments to resolve their symptoms of airway obstruction. Koufman et al.14 and Zozzaro et al.38 have described use of the OmniGuide CO2 laser in patients with LTS in the office and operating room setting, respectively. Balloon dilation may also be combined with laser treatment on awake patients. Andrews et al.39 describe the use of a combination of Nd:YAG laser followed by balloon tracheoplasty under mild sedation in the operat ing room. Balloons were inflated to 2–6 atm and held for ­

­

While studies have established both the safety and tolerability of the OBLLS, patients should nonetheless be informed on potential, albeit low-frequency, complications. Local discomfort is frequently experienced but usually adequately tolerated; these sensations may include local discomfort in the nasal cavity, hyperactive gag reflex, the unsettling sensation of heat in the laryngopharynx, and discomfort from buildup of secretions. Minor epistaxis may occur in a few patients,6 but no large studies have reported any significant epistaxis requiring nasal packing, even in patients who are either on anticoagulation or on antiplatelet medications. A feared, known complication from CO2 laser treatment is vocal fold scarring and formation of anterior glottic web35 and theoretically may occur with photoangiolytic lasers. However, many large series using the photoangiolytic lasers for vocal fold lesions have reported no formation of vocal fold scars, which is believed to be due to preservation of destruction of epithelial layers.14,32,36 Other reported complications by Koufman et al. include a report of a fiber tip breaking within the patient, but fortunately this was retrieved after quick recognition.14 Likewise, only one patient in a series of 406 patients studied by Koufman et al. suffered a vasovagal episode with no other untoward complications. Local hemorrhage at the treatment site was noted, especially with PDL.10 One patient in a series of 47 patients studied by Mouadeb and Belafsky required hospitalization for an obstructing airway from acute inflammation from laser treatment of Reinke’s edema; the patient improved after observation and treatment with intravenous corti costeroids.32



Complications

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Section 9: Office Laryngeal Surgery

30 seconds per dilation. Sixteen of 18 patients with tracheal stenosis required three procedures or fewer to achieve stable symptoms with a mean 8.6 months between each procedure. Many other groups continue to use the laser in the office settings for treating LTS and it is now even being used to treat supraglottic stenosis; Stevens et al. have recently described use of the KTP laser in the clinic setting to successfully treat supraglottic stenosis in five patients.40 It is expected that management of LTS using the laser in the office setting will continue to increase in the near future.

CONCLUSION The OBLLS is a safe and effective, well-tolerated proce­ dure, with the potential to significantly reduce health-care costs. In addition, OBLLS allows a paradigm shift toward a more proactive approach to treating recurrent laryngeal disease such as papillomatosis and leukoplakia. The role for OBLLS has expanded to include other benign laryngeal pathology and LTS, and therefore it has potential to increase patient satisfaction and decrease morbidity.

REFERENCES 1. Rees CJ, Postma GN, Koufman JA. Cost savings of unsedated office-based laser surgery for laryngeal papillomas. Ann Otol Rhinol Laryngol. 2007;116(1):45-8. 2. Sawashima M, Hirose H. New laryngoscopic technique by use of fiber optics. J Acoust Soc Am. 1968;43(1):168-9. 3. Strong MS, Jako GJ. Laser surgery in the larynx. Early clinical experience with continuous CO2 laser. Ann Otol Rhinol Laryngol. 1972;81(6):791-8. 4. McMillan K, Shapshay SM, McGilligan JA, et al. A 585-nanometer pulsed dye laser treatment of laryn­geal papillomas: preliminary report. Laryngoscope. 1998; 108(7):968-72. 5. Bower CM, Waner M, Flock S, et al. Flash pump dye laser treatment of laryngeal papillomas. Ann Otol Rhinol Laryngol. 1998;107(12):1001-5. 6. Zeitels SM, Franco RA, Dailey SH, et al. Office-based treatment of glottal dysplasia and papillomatosis with the 585-nm pulsed dye laser and local anesthesia. Ann Otol Rhinol Laryngol. 2004;113(4):265-76. 7. Moseley H, Oswal V. Laser biophysics. In: Oswal V, Remacle M (eds). Principles and Practice of Lasers in Otorhino­ laryn­gology and Head and Neck Surgery. The Hague, Netherlands: Kugler Publications; 2002:5-30. 8. Ayala C, Selig M, Faquin W, et al. Ultrastructural evaluation of 585-nm pulsed-dye laser-treated glottal dysplasia. J Voice. 2007;21(1):119-26. 9. Hirano S, Yamashita M, Kitamura M, et al. Photo­coagu­ lation of microvascular and hemorrhagic lesions of the vocal fold with the KTP laser. Ann Otol Rhinol Laryngol. 2006;115(4):253-9.

10. Zeitels SM, Akst LM, Burns JA, et al. Office-based 532-nm pulsed KTP laser treatment of glottal papillomatosis and dysplasia. Ann Otol Rhinol Laryngol. 2006;115(9): 679-85. 11. Broadhurst MS, Akst LM, Burns JA, et al. Effects of 532 nm pulsed-KTP laser parameters on vessel ablation in the avian chorioallantoic membrane: implications for vocal fold mucosa. Laryngoscope. 2007;117(2):220–5. 12. Zeitels SM, Burns JA. Office-based laryngeal laser surgery with local anesthesia. Curr Opin Otolaryngol Head Neck Surg. 2007;15(3):141-7. 13. Franco RA. In-office laryngeal surgery with the 585-nm pulsed dye laser. Curr Opin Otolaryngol Head Neck Surg. 2007;15(6):387-93. 14. Koufman JA, Rees CJ, Frazier WD, et al. Office-based laryngeal laser surgery: a review of 443 cases using three wave­ lengths. Otolaryngol Head Neck Surg. 2007;137(1): 146-51. 15. Halum SL, Moberly AC. Patient tolerance of the flexible CO2 laser for office-based laryngeal surgery. J Voice. 2010;24(6):750-4. 16. Zeitels SM, Burns JA, Akst LM, et al. Office-based and microlaryngeal applications of a fiber-based thulium laser. Ann Otol Rhinol Laryngol. 2006;115(12):891-6. 17. Young VN, Smith LJ, Sulica L, et al. Patient tolerance of awake, in-office laryngeal procedures: a multi-institutional perspective. Laryngoscope. 2012;122(2):315-21. 18. Morrison MP, Rourke AO, Dion GR, et al. Hemodynamic changes during otolaryngological office-based flexible endoscopic procedures. Ann Otol Rhinol Laryngol. 2012; 121(11):714-8. 19. Rees CJ, Halum SL, Wijewickrama RC, Koufman JA, Postma GN. Patient tolerance of in-office pulsed dye laser treatments to the upper aerodigestive tract. Otolaryngol Head Neck Surg. 2006;134(6):1023-7. 20. Zeitels SM, Akst LM, Burns JA, et al. Pulsed angiolytic laser treatment of ectasias and varices in singers. Ann Otol Rhinol Laryngol. 2006;115(8):571-80. 21. Mallur PS, Tajudeen BA, Aaronson N, et al. Quantification of benign lesion regression as a function of 532-nm pulsed potassium titanyl phosphate laser parameter selection. Laryngoscope. 2011;121(3):590-5. 22. Kim HT, Auo HJ. Office-based 585 nm pulsed dye laser treatment for vocal polyps. Acta Oto-laryngologica. 2008; 128(9):1043-7. 23. Ivey CM, Woo P, Altman KW, Shapshay SM. Office pulsed dye laser treatment for benign laryngeal vascular polyps: a preliminary study. Ann Otol Rhinol Laryngol. 2008;117(5):353-8. 24. Pitman MJ, Lebowitz-Cooper A, Iacob C, et al. Effect of the 532nm pulsed KTP laser in the treatment of Reinke’s edema. Laryngoscope. 2012;122(12):2786-92. 25. Clyne SB, Halum SL, Koufman JA, et al. Pulsed dye laser treatment of laryngeal granulomas. Ann Otol Rhinol Laryngol. 2005;114(3):198-201. 26. Mortensen MM, Woo P, Ivey C, et al. The use of the pulse dye laser in the treatment of vocal fold scar: a preliminary study. Laryngoscope. 2008;118(10):1884-8.

Chapter 79: Office-Based Laryngeal Laser Surgery

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34. Kuet ML, Pitman MJ. Photoangiolytic laser treatment of recurrent respiratory papillomatosis: a scaled assessment. J Voice. 2013;27(1):124-8. 35. Ossoff RH, Werkhaven JA, Dere H. Soft-tissue complications of laser surgery for recurrent respiratory papillomatosis. Laryngoscope. 1991;101(11):1162-6. 36. Zeitels SM, Burns JA. Office-based laryngeal laser surgery with the 532-nm pulsed-potassium-titanyl-phosphate laser. Curr Opin Otolaryngol Head Neck Surg. 2007;15(6): 394-400. 37. Leventhal DD, Krebs E, Rosen MR. Flexible laser broncho scopy for subglottic stenosis in the awake patient. Arch Otolaryngol Head Neck Surg. 2009;135(5):467-71. 38. Zozzaro M, Harirchian S, Cohen EG. Flexible fiber CO2 laser ablation of subglottic and tracheal stenosis. Laryngoscope. 2012;122(1):128-30. 39. Andrews BT, Graham SM, Ross AF, et al. Technique, utility, and safety of awake tracheoplasty using combined laser and balloon dilation. Laryngoscope. 2007;117(12): 2159-62. 40. Stevens MS, Chang A, Simpson CB. Supraglottic stenosis: etiology and treatment of a rare condition. Ann Otol Rhinol Laryngol. 2013;122(3):205-9.













27. Sheu M, Sridharan S, Kuhn M, et al. Multi-institutional experience with the in-office potassium titanyl phosphate laser for laryngeal lesions. J Voice. 2012;26(6):806-10. 28. Verma SP, Dailey SH. Overcoming nasal discomfort—a novel method for office-based laser surgery. Laryngoscope. 2011;121(11):2396-8. 29. Verma SP, Smith ME, Dailey SH. Transnasal tracheoscopy. Laryngoscope. 2012;122(6):1326-30. 30. Hogikyan ND. Transnasal endoscopic examination of the subglottis and trachea using topical anesthesia in the oto laryngology clinic. Laryngoscope. 1999;109(7 Pt 1): 1170-3. 31. Shah MD, Johns MM. Office-based laryngeal procedures. Otolaryngol Clin North Am. 2013;46(1):75-84. 32. Mouadeb DA, Belafsky PC. In-office laryngeal surgery with the 585nm pulsed dye laser (PDL). Otolaryngol Head Neck Surg. 2007;137(3):477-81. 33. Burns JA, Zeitels SM, Akst LM, et al. 532 nm pulsed potassium-titanyl-phosphate laser treatment of laryngeal papillomatosis under general anesthesia. Laryngoscope. 2007;117(8):1500-4.

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Chapter 80: Office-Based Esophagology

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CHAPTER

Office-Based Esophagology

80

Maggie A Kuhn, Peter C Belafsky

BACKGROUND



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Swallowing disorders are common. Frequently encoun tered among residents of skilled nursing facilities (>50%), the prevalence of reported dysphagia among adults in an ambulatory setting is quite appreciable, approaching 22%.1-3 Dysphagia is a symptom not a disease, and the symptom of dysphagia can vary considerably from an isolated sensation of a lump in the throat to profound swallowing dysfunction and complete dependence on nonoral tube feedings. Because of this variability, the diagnostic workup and development of a management strategy for dysphagia are often complicated. A significant percentage of patients reporting dysphagia has no objective evidence of swallowing dysfunction. Furthermore, some patients with profound swallowing dysfunction will report only mild symptoms. Because dysphagia is frequently a symptom driven disease, and these symptoms differ in their impact to an individual’s quality of life, it is impor tant to be able to accurately quantify the severity of the patient’s complaints. The ten-item Eating Assessment Tool (EAT-10) is a validated self-administered disease-specific symptom inventory for dysphagia.4 It has proven useful in assessing initial symptom severity and in monitoring treatment efficacy. It has recently been translated into Spanish, Chinese, Japanese, and Portuguese. A recent review of patients presenting to our Swallowing Center demonstrated reflux as the most common etiology for the chief complaint of dysphagia (27%) followed by late effect of radiation (14%), and 13% of individuals had no identifiable cause for to account for their symptoms.5 Patients with a dysphagia complaint localizing to the chest

predictably have an esophageal cause for their symptoms. And, approximately one-third of patients who localize swallowing dysfunction to their cervical region will also have an esophageal etiology for their symptom (Fig. 80.1). Thus, in the absence of an identifiable oropharyngeal cause for the symptom of dysphagia, patients with solid food dysphagia should have an esophageal evaluation regardless of where they localize the symptom. Technologic advances during the past two decades have facilitated the transition of the comprehensive esophageal evaluation as well as many therapeutic interventions to the office setting. Many contemporary swallowing centers have the diagnostic tools of endoscopy, fluoroscopy, esophageal

Fig. 80.1: Fluoroscopic videoesophagram displaying a 13-mm barium tablet stuck in the midportion of the esophagus (white arrow). The patient is localizing the location of dysphagia to the cervical region with her right hand (black arrow).

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Section 9: Office Laryngeal Surgery

manometry, and impedance pH testing readily available. Transnasal flexible esophagoscopy (TNE) has enabled the otolaryngologist to perform a variety of office-based interventions, including biopsy, stricture and web dila­ tion, botulinum toxin injection, foreign body retrieval, tra­cheoesophageal puncture, and feeding tube insertion.

ANATOMY AND PHYSIOLOGY The esophagus is a muscular conduit extending from the upper esophageal sphincter (UES) to the lower esophageal sphincter (LES) at the gastroesophageal (GE) junction, approximately 40 cm from the incisors. The UES is a 3to 4-cm-long high-pressure zone composed of fibers from the inferior pharyngeal constrictor muscle, the cricopharyngeus muscle (CPM) and the proximal circumferential muscle of the cervical esophagus. The rigid cricoid cartilage forms the anterior portion of the UES. The CPM is a striated muscle that attaches bilaterally to the posterolateral cricoid cartilage. Unique from other muscles, the CPM is highly elastic, allowing distension driven by a passing bolus or active distraction.6 The esophageal wall is formed by mucosa, submucosa, muscle, and fibrous adventitia. The mucosa is stratified squamous epithelium through the length of the esophagus and transitions to gastric columnar epithelium at the Z-line, which normally corresponds to the GE junction. The muscles of the esophagus are layered with internal fibers running circumferentially and external fibers oriented longitudinally. The superior one-third of the esophagus contains skeletal muscle, the inferior one-third is smooth muscle, and the middle one-third is mixed. The esophagus has no serosa and is instead surrounded by tunica adventitia. In the distal esophagus, the LES is a 2- to 4-cm-long high-pressure zone generated by intrinsic esophageal muscle fibers, the esophageal hiatus of the diaphragm, and positive intra-abdominal pressure. Combined with the esophagus’ angle of entry into the stomach (angle of His) the LES helps prevent against reflux of gastric contents into the esophagus. Blood is supplied from the inferior thyroid artery superiorly, and more distally, branches of the thoracic aorta and intercostal vessels provide segmental blood supply. Inferiorly, the esophagus receives blood supply from the left gastric artery. Cranial nerves IX and X as well as sympathetic nerve fibers from cranial cervical ganglia innervate the esophagus. The myenteric plexus of Auerbach lies between the longitudinal and circular layers of muscle.

The primary function of the esophagus is to transmit food and liquid boluses from the pharynx to the stomach. At rest, the esophagus is collapsed and closed off at both ends by high-pressure sphincters.7 The esophageal phase of swallowing begins when the bolus tail passes through the UES. The UES is tonically contracted, preventing air from entering the esophagus and protecting the airway from reflux of esophageal and gastric contents. Normal resting pressure of the UES ranges from 30 to 110 mmHg. This baseline pressure is generated from the passive elastic properties of the surrounding tissues as well as continuous electrical spike activity. With swallowing or regurgitation, the CPM relaxes to allow passage of a liquid or food bolus into the esophagus or egress of air or vomit from the esophagus. During deglutition, UES opening relies on CPM relaxation as well as laryngeal elevation and effective pharyngeal bolus propulsion. The sphincter subsequently undergoes distension followed by collapse and contraction.8 Movement along the length of the esophagus is aided by gravity but ultimately depends on the coordinated series of circular muscle contraction and relaxation, or peristalsis. Peristalsis has an initial rapid inhibitory phase that is followed by a longer wave of contraction. This propulsive process is hardwired with contraction of more distal segments occurring at longer latencies after the swallow. In normal individuals, primary peristalsis continues through the length of the esophagus regardless of bolus speed or even stoppage; this peristaltic wave is completed within 10 seconds. A subsequent swallow before primary peristalsis is complete results in cessation of the wave, or deglutitive inhibition. Following primary peristalsis, mural stretch receptors respond to any retained bolus and stimulate secondary peristalsis. Tertiary contractions are transient, nonpropulsive contractions often seen in individuals with esophageal dysmotility. At rest, the LES is tonically contracted at pressures ranging from 10 to 45 mmHg. The LES relaxes with every swallow and remains open for 6–8 seconds.

CLINICAL PRESENTATION Dysphagia to solid foods or pills is the hallmark symptom of those with esophageal swallowing disorders. Careful questioning will help further localize the site of an individual’s swallowing complaint. Other common manifestations of esophageal phase dysfunction include pyrosis, chest pain, cough, weight loss, regurgitation, and hematemesis. Eliciting a thorough medical history is important for generating a differential diagnosis. Important to

Chapter 80: Office-Based Esophagology

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TRANSNASAL ESOPHAGOSCOPY

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Advances in flexible endoscopic technology have led to the evolution of ultrathin endoscopes that are easily and safely passed transnasally for evaluation of the upper aero digestive tract in the unsedated patient.9 Since 2000, TNE has been popularized by otolaryngologists, and its applications continue to expand.10-12 Although initially thought to be inferior to conventional peroral esophagoscopy in image quality and diagnostic ability,13,14 TNE using ultrathin distal chip videoendoscopes has been shown to offer equivalent image quality and diagnostic accuracy as standard methods of sedated, peroral esophagoscopy.15-17 Furthermore, TNE affords both direct and indirect cost savings, improved safety profile and better patient tolerance when compared with conventional esophagogastroduodenoscopy (EGD).18,19 Comparison studies have found patient tolerance of unsedated TNE to be equivalent or superior to sedated EGD.20,21 Over 70% of patients prefer to have unsedated TNE.22 Indications for TNE may be esophageal, extraesopha geal, and interventional.23 The most common indication for TNE is as a screening evaluation for patients with reflux, dysphagia, and globus, accounting for 80% of examinations.24 Although the need to screen the esophagus in patients with symptoms of laryngopharyngeal reflux

is uncertain, there is evidence that extraesophageal reflux symptoms, especially chronic cough, better predict the presence of esophageal adenocarcinoma than the typical reflux symptoms of heartburn and regurgitation.25 Other less common indications for TNE include unexplained weight loss, hemoptysis, chest pain, odynophagia, and evaluation of suspected esophageal foreign body. Esophageal pathology is extremely common in patients after definitive treatment for head and neck cancer. Among head and neck cancer survivors evaluated with TNE 3 months after treatment, 63% had esophagitis, 23% had esophageal stricture, 9% had candidiasis, 8% had Barrett metaplasia, and 4% had a second primary malignancy.26 Thus, we routinely perform TNE in all individuals who present to our center after definitive treatment for head and neck cancer. Figure 80.2 displays the most common findings identified during TNE. To perform transnasal esophagoscopy, an unsedated patient is seated upright in a standard ENT examination chair (Fig. 80.3). Cardiac monitoring is not necessary and ideally the patient is kept nil per os for 3 hours prior to the procedure. Although a full stomach may enhance nausea, it is not a contraindication to the procedure. The patient’s nasal cavity is sprayed with 1:1 oxymetazoline 0.05% and lidocaine 4%. If the patient has a hypersensitive gag reflex, the patient may be given two teaspoons of 2% viscous lidocaine to gargle and swallow. Distal chip esophagoscopes are capable of air insufflation, water instillation, and suction and have a working port allowing for biopsy, injection, and guide wire placement. The endoscope is lubricated with 2% viscous lidocaine and passed through the more patent nasal cavity.



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consider are comorbid conditions such as autoimmune disease, diabetes, GE reflux, and neurodegenerative dis orders. A history of radiation therapy or exposure, cervical spine surgery, treatment for tuberculosis, fundoplication, and esophagectomy should be considered. A complete review of medication, tobacco, alcohol, and drug use is also relevant. The spectrum of esophageal disease comprises benign and malignant processes. Most esophageal etiologies of dysphagia are commonly related to esophageal dysmotility or esophagitis. Other pathologies include benign webs, rings and strictures, diverticula, and neoplasms. The initial physical examination should include a comprehensive examination of the head and neck evaluation including transnasal flexible laryngoscopy with flexible endoscopic evaluation of swallowing (FEES). Although FEES is superior for characterizing oropharyngeal phase disorders, as a preliminary tool, it is useful for ruling out pharyngeal causes of dysphagia complaints and for evaluating secretion tolerance. When an esophageal etiology is suspected, further workup is warranted, and when pro perly equipped, this workup can be completed entirely in the office.

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Fig. 80.2: The most common reported findings on unsedated transnasal esophagoscopy.

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Section 9: Office Laryngeal Surgery

Fig. 80.3: Positioning for office-based unsedated transnasal eso­ phagoscopy.

Supraesophageal structures including the nasopha­ rynx, velum, oropharynx, larynx, and hypopharynx are first examined. After the laryngeal examination, the endoscope is placed just above the tip of the epiglottis in the home position. A hand is placed on the patient’s shoulder and the patient is asked if she/he is comfortable enough to continue. Eye contact is made with the patient and she/he is then instructed that she/he will be asked to swallow the endoscope. The eye contact and human touch are essential to keep the patient at ease and reduce anxiety. The esophagus is entered by placing the tip of the endoscope into a pyriform sinus and asking the patient to lean forward, flex the chin toward the neck and swallow. Instructing the patient to “close your lips and pretend you are swallowing a big piece of spaghetti”, often provides reassurance as to the benign nature of the procedure. While the patient swallows, the scope is advanced through the UES into the cervical esophagus.27 If there is difficulty passing the scope into the esophagus, a teaspoon of 2% viscous lidocaine may be placed into the patient’s oral cavity. The patient is instructed to hold the lidocaine in the mouth and, as the endoscope is positioned in the pyriform sinus near the esophageal inlet, the patient is asked to flex their chin toward the chest and swallow. The lidocaine bolus will open the UES during deglutition and will lubricate the endoscope as it passes into the esophagus. If this is not successful in allowing entrance into the esophagus, the examination should be terminated and a fluoroscopic swallow study obtained to rule out the presence of CPM dysfunction or a Zenker’s diverticulum. If known CPM dysfunction or Zenker’s diverticulum exists,

Fig. 80.4: Placement of a guidewire through the transnasal endoscope and into the esophagus in a patient with a Zenker’s diverticulum. The endoscope can be advanced over the guidewire once it has been safely passed 30 to 40 cm into the esophagus.

intubating the esophagus can be performed with the assistance of a guide wire (Hydra Jagwire Guidewire, Boston Scientific, Natick, MA, USA). The guide wire is placed through the esophagoscope and advanced under direct vision into the esophagus as the patient is instructed to swallow (Fig. 80.4). If the guide wire enters a diverticulum or cannot traverse an obstructing cricopharyngeus or cervical stenosis, it will curl and be seen re-entering the pharynx. If the guide wire can be passed 30 to 40  cm without curling back into the pharynx, the clinician can be assured that it has safely traversed the diverticulum and UES. The esophagoscope can then be passed safely over the guide wire into the esophagus without the risk of perforation. Once the endoscope is safely passed into the midesophagus, the wire can be removed. Once the esophagus is entered, the endoscope is immediately advanced to the midportion of the esopha­ gus. Keeping the tip of the endoscope in the region of the UES is uncomfortable and will promote gagging. This region will be thoroughly examined at the end of the procedure as the endoscope is withdrawn. The eso­ phagus is immediately suctioned of air and fluid and the examiner’s free hand is again placed on the patients shoulder and eye contact is made. The patient is reassured that “this is as bad as the procedure is going to get” and asked “are you comfortable enough to proceed with the examination?” If there is noticeable discomfort or gagging, the procedure is terminated and an examination under intravenous sedation is scheduled. The midportion

Chapter 80: Office-Based Esophagology



phase dysphagia. The examination was initially described by Belafsky and Rees in 2009 and is entitled “Guided Observation of Swallowing in the Esophagus (GOOSE)”.28 At the end of a standard FEES, the esophagoscope is passed through the UES into the cervical esophagus. Normal esophageal emptying time is approximately 13 seconds. Any residue present in the esophagus after this time indicates an esophageal abnormality.28 GOOSE may be performed by offering the patient boluses of puree, liquid, cracker, and pills with the scope held in a series of three positions: above the aortic compression, above the LES, and retroflexed within the stomach (Fig. 80.7).28 During this procedure, organic esophageal pathology, abnormal esophageal motility, and bolus transit time may be evaluated. In a study comparing the utility of GOOSE to fluoroscopy and manometry, GOOSE had a 71% con cordance with fluoroscopy and an 83% concordance with ­

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of the esophagus is then insufflated with air and the esophagoscope is advanced to the GE junction. The posi tion of the squamocolumnar junction (Z-line), normally situated at the GE junction, is noted from above and below the LES during a retroflexed view from within the stomach. The stomach is suctioned free of air at the end of the procedure and the esophagoscope is carefully withdrawn. Withdrawing the endoscope will center the tip and provide an optimal view during removal. The presence of structural abnormalities including dilation, hernias, or diverticula (Figs. 80.5A to C) is noted as are other find ings such as esophagitis (Figs. 80.6A to C), neoplasms, strictures, webs, rings, or foreign bodies. Normal findings during endoscope withdrawal include an impression of the left main stem bronchus and more proximally, an ante rior impression of the aortic arch at 25 cm from the naris. A functional esophagoscopy, or FEES of the esophagus, may be performed in patients with suspected esophageal

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A

B

C

Figs. 80.5A to C: Abnormal findings during transnasal esophagoscopy. (A) A large hiatal hernia (asterisk) visualized during a retroflexed view (white arrow). Gastric rugae are seen traversing the hiatus of the diaphragm (black arrow). (B) An epiphrenic diverticulum (white arrow) is identified just proximal to the lower esophageal sphincter (black arrow). (C) The postoperative remnant of a Zenker’s diverticulum is visible (asterisk) posterior to the proximal esophagus (black arrow) containing a guidewire.

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Section 9: Office Laryngeal Surgery

A

B

C

Figs. 80.6A to C: Endoscopic findings of peptic esophageal disease. (A) Erosive (LA Class A) esophagitis is seen as is a peptic stricture proximal to the gastroesophageal junction; (B) The distal esophagus shows a long segment suggestive of Barrett’s esophagus; (C) An advanced adenocarcinoma of the distal esophagus with food debris is identified.

Fig. 80.7: Guided observation of swallowing in a patient with the complaint of pills getting stuck in the cervical region displays a pill and liquid esophageal stasis above the distal peptic stricture.

manometry.28 GOOSE identified pathology not recognized on fluoroscopy and manometry in 62% of patients. The TNE has enabled the otolaryngologist to perform a variety of office-based interventions. The expanding list of unsedated office procedures performed via TNE includes biopsy, stricture and web dilation, botulinum toxin injection (Figs. 80.8A to C), foreign body retrieval, tracheoesophageal puncture (Figs. 80.9A to D), and feeding tube insertion.29,30 Complications from TNE are rare. In 3% of patients, the 5.1-mm endoscope cannot be passed through a tight nasal vault.12 Epistaxis and vasovagal reaction, the most commonly reported complications, occur in fewer than 3% of patients.31 Because TNE is performed on unseda­ ted patients, cardiopulmonary complications associated with traditional peroral esophagoscopy under sedation are reduced.32

Chapter 80: Office-Based Esophagology

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B

C

Figs. 80.8A to C: Interventions performed during transnasal eso phagoscopy. (A) A Biopsy is taken of irregular squamocolumnar junction suspicious for intestinal metaplasia; (B) Upper esophageal sphincter dilation is performed in a patient with cricopharyngeus muscle dysfunction; (C) A retroflexed endoscopic view (white arrow) allows for botulinum toxin injection into the lower esophageal sphincter (LES) (black arrow) in a patient with hypertensive LES. ­

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Radiographic evaluation of the esophagus is performed as a screen during a videofluoroscopic swallow study (VFSS) or as a dedicated examination of the esophageal phase of deglutition, termed an esophagram. Recent evidence suggests that an esophageal screen as part of a VFSS predicts esophageal abnormalities and is useful for guiding further evaluation of the esophagus.33 However, with a sensitivity of only 63%, the esophageal screen should not replace an esophagram when an esophageal swallowing disorder is suspected. The esophagram is a more complete examination and includes evaluation of the stomach and the duodenum. In our center, esophagrams are performed using video fluoroscopy and digital recording while following a standard protocol. The protocol precludes certain individuals from completing an esophagram, including those who are

unable to swallow a large bolus, have severe pharyngeal obstruction, have a high likelihood of aspiration, or are unable to achieve proper positioning. Our protocol begins with swallowing a single 20cc barium bolus while stand ing, which is recorded in an anteroposterior (AP) orienta tion. Next, ingestion of a 13-mm barium tab is recorded in AP; obstruction to passage by a tab of this size sug gests clinically important narrowing. The patient is then positioned in a right anterior oblique position on a table to eliminate the contribution of gravity to the bolus as it traverses the esophagus. In this position, a single 20cc bolus is swallowed followed by sequential swallows to distend the esophagus and GE junction. Lastly, after the patient has swallowed nearly 400cc of barium, the water siphon test is performed. The patient is asked to drink water while bringing the knees to the chest and bearing down; this evaluates for the presence of GE reflux. ­

ESOPHAGRAM

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Section 9: Office Laryngeal Surgery

A

B

C

D

Figs. 80.9A to D: Tracheoesophageal puncture performed in office with transnasal esophagoscopy. (A) The desired position is identified (asterisk) by palpation through the stoma; (B) An 18-gauge needle is inserted under direct visualization; (C) A guidewire is placed through the needle before it is removed; (D) The puncture is dilated and a catheter is secured in place while awaiting fitting of a prosthesis.

A normal esophagram will show an indentation from the arch of the aorta on the left side of the midesophagus. Just distal to this, an indentation from the left mainstem bronchus is sometimes visible. In the area where the esophagus transitions from skeletal to smooth muscle, or the junction of the upper one-third and lower twothirds, slowed transit of the tab may be observed. This is considered normal for what is known as the esophageal “dead zone”. Commonly identified during an esophagram are motility disorders with findings of decreased primary stripping waves, esophageal stasis, intraesophageal reflux, and tertiary contractions. Abnormalities of the GE junction including paraesophageal hernia, rings, achalasia, and stricture are readily seen during esophagram. Fluoroscopy is the best way to evaluate UES pathology such as Zenker’s

diverticulum, CPM dysfunction, cricopharyngeal web, and pharyngoesophageal stenosis (Fig. 80.10). Findings on esophagram should be correlated to the patient’s complaints and endoscopic results to determine if they are clinically significant.

ESOPHAGEAL MANOMETRY Although endoscopy provides a direct view of the aero­ digestive tract from the nasal vestibule to gastric body, it is limited in its ability to objectively quantify pharyngeal and UES pressure as well as esophageal motility. The introduction of high-resolution manometry (HRM) into the functional assessment of swallowing significantly increases the clinician’s ability to diagnose and classify disordered deglutition. Solid-state HRM typically has 36

Chapter 80: Office-Based Esophagology

A

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D

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Figs. 80.10A to D: Abnormalities identified during fluoroscopic video esophagram. (A) A moderately obstructing cricopharyngeal bar (black arrow); (B) A cricopharyngeal web (black arrow); (C) The gastroesophageal junction shows a sliding hiatal hernia (black arrow) and Schatzke’s B ring (arrow heads); (D) Esophagram demonstrates the classic “bird beak” appearance of achalasia.

circumferential sensors spaced 1-cm apart. Pharyngeal and esophageal motility are characterized by using pressure topography plots (Fig. 80.11). HRM has proven beneficial in distinguishing between pharyngeal weakness, poor pharyngeal and UES relaxation, incomplete upper esophageal relaxation, esophageal body motility, and LES function. Our HRM protocol involves a 5-minute assessment of UES and LES baseline function followed by the evaluation of 12 5-mL water swallows. Pharyngeal peak pressures are evaluated from the soft palate to the UES.

Then UES baseline, UES relaxation, and pharyngeal-UES coordination are evaluated. These pressure relationships are essential in evaluating a patient for surgery on the UES. The best candidates for CPM myotomy have elevated UES residual pressure, elevated hypopharyngeal intrabolus pressure, and normal pharyngeal and hypopharyngeal peak pressures. Furthermore, HRM is the best way to evaluate for esophageal motility disorders (Figs. 80.12A to C). Table 80.1 depicts the Chicago classification of esophageal motility disorders on HRM.34

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Section 9: Office Laryngeal Surgery

Fig. 80.11: Normal high-resolution manometry (HRM) pressure topography plot with complete upper esophageal relaxation (UES) (asterisk). LES = lower esophageal sphincter.

A

B

C

Figs. 80.12A to C: Abnormal findings on high-resolution esophageal manometry (HRM). (A) Elevated upper esophageal residual pressure (asterisk) suggestive of cricopharyngeus muscle dysfunction with intact pharyngeal pressures (black arrow); (B) Hypertensive lower esophageal sphincter (LES) with elevated residual LES pressure (asterisk) and resultant elevated intrabolus pressure (black arrow); (C) Incomplete LES relaxation (asterisk) with esophageal pressurization consistent with esophageal achalasia, type 2.

Table 80.1: The Chicago classification of esophageal motility disorders on high-resolution manometry

Classification

Description

Esophageal aperistalsis without impaired lower esophageal sphincter (LES) relaxation

Failed peristalsis in all tests swallows with or without a hypotensive LES. If asso­ ciated with a hypotensive LES is considered consistent with scleroderma

Achalasia

Esophageal aperistalsis with impaired LES relaxation

Hypertensive esophageal peristalsis

Further classified as distal esophageal spasm, compartmentalized esophageal pressurization, and nutcracker esophagus

Functional esophageal obstruction

Incomplete deglutitive LES relaxation in the setting of preserved esophageal peristalsis

CONCLUSION Comprehensive in-office evaluation of the esophagus is feasible with today’s advanced and evolving technology.

Identifying individuals who should undergo diagnostic esophageal procedures requires a thorough understanding of the spectrum of esophageal disorders and their common presentations. A detailed history with head and

Chapter 80: Office-Based Esophagology neck examination should guide further evaluation. Nearly, one-third of individuals who identify dysphagia arising from above the clavicles will have an esophageal etiology for swallowing dysfunction. Therefore, it is prudent to have a low threshold to screen the esophagus. Contemporary instruments for such evaluation include TNE, GOOSE, video fluoroscopy, and HRM. With appropriate patient selection and topical anesthesia, TNE-based interventions are performed in the office with ease and acceptable patient tolerance. The capability to offer these procedures to unsedated patients confers benefits of lower cost and lost wages, shorter recovery time, no risk of anesthesia, and convenience.

REFERENCES 1. Mold JW, Reed LE, Davis AB, et al. Prevalence of gastroesophageal reflux in elderly patients in a primary care setting. Am J Gastroenterol. 1991;86:965-70. 2. Wilkins T, Gillies RA, Thomas AM, et al. The prevalence of dysphagia in primary care patients: a HamesNet Research Network study. J Am Board Fam Med. 2007;20:144-50. 3. Smithard DG, O’Neill PA, Parks C, et al. Complications and outcome after acute stroke. Does dysphagia matter? Stroke. 1996;27:1200-04. 4. Belafsky PC, Mouadeb DA, Rees CJ, et al. Validity and reliability of the Eating Assessment Tool (EAT-10). Ann Otol Rhinol Laryngol. 2008;117:919-24. 5. Hoy M, Domer A, Plowman EK, et al. Causes of dysphagia in a tertiary-care swallowing center. Ann Otol Rhinol Laryngol. 2013;122:335-8. 6. Sivarao DV, Goyal RK. Functional anatomy and physiology of the upper esophageal sphincter. Am J Med. 2000;108 (Suppl 4a):27S-37S. 7. Frenz D SR. Surgical anatomy of the pharynx and esophagus: basic science and clinical review. New York: Thieme, Stuttgart; 2006. 8. Schroeder PL, Richter JE. Swallowing disorders in the elderly. Semin Gastrointest Dis. 1994;5:154-65. 9. Shaker R. Unsedated trans-nasal pharyngoesophagogastroduodenoscopy (T-EGD): technique. Gastrointest Endosc. 1994;40:346-8. 10. Aviv JE, Takoudes TG, Ma G, et al. Office-based esophago­ scopy: a preliminary report. Otolaryngol Head Neck Surg. 2001;125:170-5. 11. Amin MR, Postma GN, Setzen M, et al. Transnasal eso­ phagoscopy: a position statement from the American Bronchoesophagological Association (ABEA). Otolaryngol Head Neck Surg. 2008;138:411-4. 12. Belafsky PC, Postma GN, Daniel E, et al. Transnasal eso­­ phagoscopy. Otolaryngol Head Neck Surg. 2001;125:588-9. 13. Dean R, Dua K, Massey B, et al. A comparative study of unsedated transnasal esophagogastroduodenoscopy and conventional EGD. Gastrointest Endosc. 1996;44:422-4.

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14. Birkner B, Fritz N, Schatke W, et al. A prospective randomized comparison of unsedated ultrathin versus standard esophagogastroduodenoscopy in routine outpatient gastroenterology practice: does it work better through the nose? Endoscopy. 2003;35:647-51. 15. Sorbi D, Gostout CJ, Henry J, et al. Unsedated smallcaliber esophagogastroduodenoscopy (EGD) versus conventional EGD: a comparative study. Gastroenterology. 1999;117:1301-7. 16. Thota PN, Zuccaro G Jr, Vargo JJ 2nd, et al. A randomized prospective trial comparing unsedated esophagoscopy via transnasal and transoral routes using a 4-mm video endoscope with conventional endoscopy with sedation. Endoscopy. 2005;37:559-65. 17. Saeian K, Staff DM, Vasilopoulos S, et al. Unsedated transnasal endoscopy accurately detects Barrett’s metaplasia and dysplasia. Gastrointest Endosc. 2002;56:472-8. 18. Saeian K. Unsedated transnasal endoscopy: a safe and less costly alternative. Curr Gastroenterol Rep. 2002;4:213-7. 19. Yagi J, Adachi K, Arima N, et al. A prospective randomized comparative study on the safety and tolerability of transnasal esophagogastroduodenoscopy. Endoscopy. 2005;37: 1226-31. 20. Garcia RT, Cello JP, Nguyen MH, et al. Unsedated ultrathin EGD is well accepted when compared with conventional sedated EGD: a multicenter randomized trial. Gastroenterology. 2003;125:1606-12. 21. Mulcahy HE, Kelly P, Banks MR, et al. Factors associated with tolerance to, and discomfort with, unsedated diagnostic gastroscopy. Scand J Gastroenterol. 2001;36:1352-7. 22. Jobe BA, Hunter JG, Chang EY, et al. Office-based unsedated small-caliber endoscopy is equivalent to conventional sedated endoscopy in screening and surveillance for Barrett’s esophagus: a randomized and blinded comparison. Am J Gastroenterol. 2006;101:2693-703. 23. Postma GN. Transnasal esophagoscopy. Curr Opin Oto­ laryngol Head Neck Surg. 2006;14:156-8. 24. Postma GN, Cohen JT, Belafsky PC, et al. Transnasal esophagoscopy: revisited (over 700 consecutive cases). Laryngoscope. 2005;115:321-3. 25. Reavis KM, Morris CD, Gopal DV, et al. Laryngopharyngeal reflux symptoms better predict the presence of esophageal adenocarcinoma than typical gastroesophageal reflux symptoms. Ann Surg. 2004;239:849-56; discussion 856-848. 26. Farwell DG, Rees CJ, Mouadeb DA, et al. Esophageal pathology in patients after treatment for head and neck cancer. Otolaryngol Head Neck Surg. 2010;143:375-8. 27. Postma GN, Belafsky PC, Aviv JE. Atlas of transnasal esophagoscopy. Philadelphia, PA: Lippincott Williams & Wilkins; 2007. 28. Belafsky PC, Rees CJ. Functional oesophagoscopy: endoscopic evaluation of the oesophageal phase of deglutition. J Laryngol Otol. 2009;123:1031-4. 29. Belafsky PC, Allen K, Castro-Del Rosario L, et al. Wireless pH testing as an adjunct to unsedated transnasal esophagoscopy: the safety and efficacy of transnasal telemetry capsule placement. Otolaryngol Head Neck Surg. 2004;131:26-8.

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30. Allen J, Belafsky PC. Seldinger technique for in-office tracheoesophageal puncture. Ear Nose Throat J. 2010;89:355-6. 31. Dumortier J, Napoleon B, Hedelius F, et al. Unsedated transnasal EGD in daily practice: results with 1100 consecutive patients. Gastrointest Endosc. 2003;57:198-204. 32. Arrowsmith JB, Gerstman BB, Fleischer DE, et al. Results from the American Society for Gastrointestinal Endoscopy/U.S. Food and Drug Administration collaborative

study on complication rates and drug use during gastroi­ ntestinal endoscopy. Gastrointest Endosc. 1991;37:421-7. 33. Allen JE, White C, Leonard R, et al. Comparison of esophageal screen findings on videofluoroscopy with full esophagram results. Head Neck. 2012;34:264-9. 34. Kahrilas PJ, Ghosh SK, Pandolfino JE. Esophageal motility disorders in terms of pressure topography: the Chicago Classification. J Clin Gastroenterol. 2008;42:627-35.

SECTION Voice Practice and New Innovations

10

Chapter 81: New and Emerging Technology

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CHAPTER

New and Emerging Technology

81

Diane M Bless, Charles N Ford

INTRODUCTION New and emerging technology drives advances in all aspects of medical care. Emerging technologies are com­ing from many diverse fields—biotechnology, physics, biochemis­­­ try, computer science, and mathematics. Tech­no­logical advances are providing insight into laryngeal disorders and enhancing our ability to make accurate diagnoses, select optimal treatment, and better predict treatment outcomes. Representative of the most promising emer­ging technolo­ gies affecting laryngology, we have selected bioinformatics (including robotics and ambulatory moni­toring), optics, regenerative medicine, and high-throughput gene-based technologies as the focus of this chapter.

BIOINFORMATICS Technological advances in bioinformatics and robotics are especially relevant to the future practice of laryngo­ logy. Bioinformatics represents a synergistic interactive rela­tionship between computers and biological systems. Harvey Fineberg, President of the Institute of Medicine, cited emergence of information technology as the essen­ tial driving force for improving health care efficacy.1 The capacity of computer systems to rapidly process large volumes of data is providing medical caregivers with effec­ tive tools to improve critical cognitive components of diagnosis, including efficient gathering and synthesis of data. These systems provide an opportunity to amass and process huge amounts of data from multiple tests and institutions to derive patterns specific to different populations and disorders. Current versions of computerbased differential diagnosis generators are proving useful

and have demonstrated excellent sensitivity in generating comprehensive differential diagnosis lists. New and emer­ ging systems provide improved specificity, rank diagnoses, and indicate critical diagnoses that must be ruled out.2 Such systems can lead to improved management of laryngeal conditions, such as laryngopharyngeal reflux by limiting costly, unnecessary tests and empirical “shotgun” clinical trials. In providing efficient high-speed interconnectivity, computers enhance communication and coordination of care, limit many system-related errors, and improve dia­g­ nostic accuracy and clinical management. The increased capacity of computer systems, plus recent advances in artificial intelligence and robotics, provides a synergistic framework that is transforming medical practice. “The Robot Will See You Now” is the pro­ vo­cative title of Jonathan Cohn’s 2013 Atlantic article3 presenting a plausible case for robots outperforming physi­ cians in providing accurate diagnoses and treatment recom­ mendations. This is based on the fundamental ability of computers to rapidly acquire large volumes of data, as well as evolving artificial intelligence technology that improves the computer’s ability to process, interpret, and apply rele­ vant information. Additionally, computers are not prone to “anchoring bias”: a human tendency to rely too heavily on simple algorithms and single pieces of information, which may account for a third of misdiagnoses. Watson, the arti­ ficial intelligence IBM computer famous for winning the quiz show Jeopardy, has been increasingly dedicated to medical applications. In a trial run, a simulated patient with metastatic lung cancer was presented to the computer; the computer not only recognized known biomarkers that predict tumor behavior but also demonstrated its capacity

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Section 10: Voice Practice and New Innovations

Fig. 81.1: Three network components of robotic surgery system: (1) ergonomic surgeon’s console, (2) interactive robotic arms and telescopes, and (3) high-definition three-dimensional display monitors.

to assimilate critical up-to-date information by searching for a recently reported mutation that drives metastatic lung cancer. Recognizing this mutation was the key for recommending a less morbid and more effective (targeted) treatment that would provide a significant chance of cure. This is not surprising, considering Watson can process 200 million pages of content in  $500,000, depending on what existing equipment can be incorporated and the breadth of the new practice. This substantial capital outlay is a key consideration in setting up a voice practice. While the short-term expenditure can be a deterrent, the effort

A cornerstone of setting up a new voice practice is the development of a collaborative relationship between the laryngologist and a voice therapist (also called a voice pathologist), who is an SLP with expertise in voice disor­ ders. This element of a new voice practice can be the most difficult to build, yet integral to its success. The importance of a skilled voice therapist cannot be overemphasized. While the laryngologist is responsible for the medical and surgical aspects of the voice disorder, the voice therapist is tasked with assessment and optimization of vocal hy­ giene, coordination of the subsystems of voice production (respiration, vibration, resonance), and behavioral aspects of the voice disorder. The voice therapist also contributes to the diagnostic process when the diagnosis is unclear, by providing diagnostic therapy to help the physician dif­ ferentiate subtypes of hyperfunctional disorders (e.g. muscle tension dysphonia vs spasmodic dysphonia) or clarify whether a presentation is purely functional or with a possible neurologic component. In many types of voice disorders, it is the voice therapist, not the laryngologist, who carries the therapeutic load and on whom the hope for improvement rests. The value of teaming up with a voice therapist to provide interdisciplinary care was

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recognized early in the emergence of voice care as a sub­ speci­alty, as evidenced by the von Leden-Moore col­la­ boration in the 1950s. For the laryngologist considering a potential colla­ borator, some familiarity with the qualifications of voice therapists is helpful. The treatment of voice disorders is a small part of the SLP curriculum in an 18- to 24-month masters program, similar to how otolaryngology is a very small part of the medical school curriculum and laryn­ go­logy has historically been a small part of a typical oto­ laryngo­ logy residency. After the masters SLP degree, there is a 9-month clinical fellowship in which the SLP practices in a clinical setting under supervision. This could take place in a school system, skilled nursing facility, an acute or rehabilitative hospital, and/or a general SLP pri­ vate practice. Rarely do clinical fellows work in a voice clinic, although this is an accepted venue for American Speech-Language-Hearing Association-recognized fellow­ ship training. Completion of the clinical fellowship leads to the CCC-SLP certification (Certificate of Clinical Com­ petence in Speech–Language Pathology). An SLP can gain subspecialty training in the treatment of voice disorders in many ways, both formal and informal. One of the most well-recognized voice programs is the Summer Vocology Institute (SVI) organized by the National Center for Voice and Speech. This is an intensive eight-week program that combines speech science, vocal pedagogy, medicine, and theater training. Graduates of the SVI become certified vocologists. Other formal training can be obtained through continuing education at courses and conferences focused on voice, particularly those hosted by major voice centers. Internships at voice clinics provide informal educational opportunities. The best qualification, however, is actual clinical experience working at a voice center. An extensive musical background, especially one in vocal performance, choral conducting, or vocal pedagogy, is an added benefit. These credentials aside, the ultimate gauge of whether a voice therapist (or any physician for that matter) will become an indispensible member of the voice team rests on therapeutic outcome and patient satisfaction. Perhaps even more important than for laryngologists, a success­ ful voice therapist should also have excellent auditory dis­criminatory skills and be an expert at the perceptual analysis of all types of voice disorders. The voice team may include additional expertise in the singing voice. A singing voice specialist is a singing teacher with special training in the anatomy and physio­ logy of voice production, who can work in concert with

the clinicians to help rehabilitate a singer with an injured or suboptimal voice.6 Most are members of the National Association of Teachers of Singing (NATS). Some singing voice specialists are SLPs with classical vocal training. A voice teacher or singing teacher is a musical instructor focusing on singing technique and production of the sing­ ing voice. Voice teachers generally do not have a clinical background. A vocal pedagogue is a voice teacher who specializes in classical singing technique, understands the anatomy and physiology of singing voice production, and works with the singer to optimize the singing voice. A vocal coach works with the singer on repertoire, style, stage presentation, and other aspects of performance. These definitions are not strict, and there can be crossover between the roles. Although a singing voice specialist is often an integral part of a voice team, patients may have their own voice teachers or vocal coaches, who become an ad hoc part of the voice team. For optimal outcome, the voice therapist and voice teacher or vocal coach should work together with open lines of communication regarding the singer’s course of vocal rehabilitation. The structure of the new voice team can take many forms, ranging from each member of the team seeing patients in their own respective practices connected only through mutual referrals, to members working within the same practice in an integrated fashion. The latter would be considered a voice center. A laryngologist setting up a new voice practice may need to actively seek out voice therapists and singing voice specialists in the area to promote interest in establishing a therapeutic collabo­ ration. If they do not exist, they may be recruited from elsewhere. Alternatively, interested SLPs and voice tea­ chers may be encouraged to acquire additional training to gain the necessary expertise to function as members of the voice team.

THE EXTENDED VOICE CARE TEAM In addition to the core voice team members who have a direct connection to the voice problem, other types of health-care providers are sometimes recruited to assist in the management of the voice problem. Since excessive muscle tension and tightness of the neck, shoulder, and general upper body often contribute to or at least coexist with hyperfunctional voice disorders in a subset of patients, working with a physical therapist or massage therapist to address the upper body can be helpful and sometimes instrumental. It is well known to voice coaches how posture can affect the singing voice. Approaches such as

Chapter 82: Developing a Voice Practice the Alexander Technique have been employed as a way to alleviate generalized muscle tension and stress in general. These same types of approaches have shown promise for the speaking voice as well. Hands-on techniques such as myofascial release are generally preferred over approaches that focus on strengthening such as those using electrical stimulation. Additional benefit from a physical thera­ pist is exploration of ergonomic issues in the workplace. Office-based employees are frequently multi-tasking with computer use and phone use simultaneously. A physical therapist can offer suggestions for posture management and hands-free phone communication. Although there is no consensus on which of the formal and informal approaches are preferable, the common theme is that there should be some consideration to incor­ porating some type of muscle tension reduction program in a comprehensive voice disorders clinic. This approach should be considered with or without the presence of vocal fold pathology, just as voice therapy is part of beha­­ vioral modification. The ultimate goal should be avoid­ance of surgery or optimization of postoperative rehabi­ lita­ tion and reducing recurrence of the underlying problem. For a first-time referral, it is often helpful for the physi­ cian to speak directly to the therapist to communi­cate the reason for the referral and to explain the connection between the benefits from their therapy and improved voice production. Some patients with hyperfunctional or functional voice disorders may also benefit from counseling or formal psychotherapy for anxiety, depression, or stress manage­ ment. The scenario can vary from one extreme, where the psychological symptoms are entirely due to the presence of the voice problem, to the other extreme, where an underlying psychological condition plays a major role in the pathogenesis of the voice problem. Since very few psychiatrists and psychologists have specific familiarity with psychological conditions that either trigger or are worsened by voice problems, it can be difficult to identify an appropriate referral destination for the voice patient. If the patient is referred to a psychiatrist, it is important for the psychiatrist to go beyond pharmaceutical therapy as single-modality treatment. An underlying condition that drives a voice problem can require dedicated, extensive counseling. In addition to the treatment of any generalized anxiety disorder, the specific anxiety associated with the voice problem should also be addressed. While it is always helpful for the otolaryngologist to speak with any new provider a patient is referred to, it may be particularly important for this communication to take place with a

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psychiatrist or psychologist new to the referral network of the voice practice. It is critical to explain the voicerelated nature of the referral so that the therapy may be tailored. The best way to identify an appropriate provider is to call potential providers, explain the voice problem and suspicion for a psychological component, and gauge the fit of that provider’s practice to the patient’s needs.

THE EXTENDED HEALTH CARE TEAM It is important for a new voice practice to identify physicians in other specialties who can assist with the care of the voice patient. The three key specialties are gastroen­ terology, neurology, and pulmonology. A high-quality net­work of colleagues in these specialties forms an exten­ ded health-care team for the voice patient. A gastroenterologist can assist in the evaluation and management of complex reflux disorders, esophageal dysmotility, Barrett’s esophagus, esophagitis, and other disorders that can manifest with symptoms initially locali­ zed or referred to the larynx. A gastroenterologist with subspecialty training in esophageal disorders is prefer­able, but very few gastroenterologists have such qualifica­tions. One with expertise and, more importantly, a willingness to collaborate will make a valuable colleague. Neurologists are important to a voice practice in many ways. Neuromuscular specialists are called upon to rule out systemic neurologic conditions (e.g. amyotrophic lateral sclerosis) when the presenting laryngeal symptoms and findings raise such suspicion. Movement disorder specialists are often involved in the optimization of medi­ cal management for vocal tremors and regional dystonias affecting the larynx. For a voice practice that desires to incorporate diagnostic laryngeal electromyo­ graphy, colla­boration with an electromyographer is highly recom­men­ded. Establishing a good relationship with pulmonologists and allergists will not only secure expertise for the voice patient’s underlying pulmonary disease but also foster referrals for patients with airway stenosis or paradoxical vocal fold motion disorders who first present to these physicians. Table 82.2 lists the individuals who may be involved in the care of a voice patient.

MARKETING AND OUTREACH The basic principles of building a referral base and growing a voice practice are the same as those for any medical

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Section 10: Voice Practice and New Innovations

Table 82.2: Voice team members and other collaborators

The voice team

The “extended” voice team

Medical consultants

Laryngologist

Physical therapist

Gastroenterologist

Voice therapist

Massage therapist

Neurologist

Singing voice specialist

Psychologist/psychiatrist

Pulmonologist

Voice coach/acting-voice specialist

practice. Direct and indirect marketing efforts are needed to make the community aware of the new service. There is, however, an important distinction between a voice prac­tice and a neurotology, skull base, or head and neck oncologic practice, and this distinction calls for a diffe­ rent approach or mindset to the marketing effort. Many patients are not referred for surgical expertise but are referred for problems that fall well within the scope of general otolaryngology, e.g. hoarseness, cough, or throat discomfort. These refer­rals are made solely at the disc­ retion of the referring physi­cian. The new voice practice must bear this in mind in the outreach efforts. Potential referring physicians will only send referrals if they gain an appreciation of how a referral to the voice practice can help them take better care of their patients. The voice practice must add to, not take away from, the care they already provide. A good place to begin the marketing effort is the home institution of the new laryngologist or the affiliated hosp­ ital. The laryngologist should first make the acquaintance of other otolaryngologists, then approach the pulmonolo­ gists, internists, thyroid surgeons, spine surgeons, and car­ diotho­ racic surgeons to make himself or herself available for consultations. In the outpatient setting, it is worth­while to visit other otolaryngology practices who may seek laryngo­logy referral. In addition to one-on-one visits, the grand rounds format in the hospital setting is particularly effective in reaching a large number of poten­ tial referring providers. Next, it is critically important to reach out to SLPs in the community. If a voice practice does not already exist in the area, the new voice practice will likely fill a niche that particularly appeals to SLPs who have been asked to address voice problems by other physicians. Making the connection with the SLP community presents a great opportunity for mutual education. In the authors’ expe­ rience, SLPs without a voice background are generally eager to learn something about the medical aspect of voice care and laryngology in general. Conversely, there is always something a laryngologist can learn from SLPs.

Beyond the health-care providers, the next level of outreach should target those individuals and institutions whose primary mission involves the vocal performance arts. This group includes choir directors, voice teachers, music schools and voice departments, and performance arts venues. The laryngologist should find out if a local chapter of the NATS exists. If a local chapter of the Voice Foundation has yet to be established, it would be reasonable for the new laryngologist to play an active role in organizing one in conjunction with other interested voice professionals in the area. As pointed out earlier in this chapter, teachers have a high incidence of dysphonia. Outreach to local school systems will definitely identify the new voice practice as a valued resource for the teaching profession. Education regarding vocal hygiene, the impor­ tance of voice amplification systems, and so on can be done at the schools or provided as seminars offered by the voice center team.

CONTINUING EDUCATION The establishment of a voice practice does not end with completion of the ensemble of personnel and equip­ment. Like the rest of medicine, voice care and laryngology evolve as new science, technology, and clinical insight imp­rove and change clinical care. The laryngologist must stay abreast of the latest developments through continu­ ing education. This could take the form of meeting atten­dance and journal reading. In addition to the annual meetings of the professional organizations with a sub­ stantial voice and laryngology focus such as the ALA, the American Broncho-Esophagological Association, and the Voice Foundation, there are also a growing number of national and regional conferences and symposiums orga­ ni­zed around the topic of voice and phonosurgery. These provide great opportunities to not only acquire new medi­ cal know­ledge but also exchange ideas with physicians from other voice clinics on setting up and running a voice practice.

Chapter 82: Developing a Voice Practice

REFERENCES 1. Roy N, Merrill RM, Gray SD, et al. Voice disorders in the general population: prevalence, risk factors, and occu­ pational impact. Laryngoscope. 2005;115:1988-95. 2. Roy N, Merrill RM, Thibeault S, et al. Prevalence of voice disorders in teachers and the general population. J Speech Lang Hear Res. 2004;47:281-93. 3. VerdoliniK, Ramig LO. Review: occupational risks for voice problems. Logoped Phoniatr Vocol. 2001;26:37-46.

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4. Sataloff RT. Introduction. In: Sataloff RT (ed.), Professional voice: the science and art of clinical care, 3rd edn. San Diego: Plural Publishing; 2005. 5. American Laryngological Association. Laryngology Fellow­ ship Guidelines. http://www.alahns.org/i4a/pages/index. cfm?pageid=3337. (Retrieved 25 August 2013). 6. Sataloff RT, Heman-Ackah YD, Hawkshaw MJ. Voice care professionals: a guide to voice care providers. In: Sataloff RT (ed), Professional voice: the science and art of clinical care, 3rd edn. San Diego: Plural Publishing; 2005.

Chapter 83: Laryngeal Transplantation

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CHAPTER

Laryngeal Transplantation

83

David G Lott, Marshall Strome

INTRODUCTION The larynx is a unique organ in that it governs phonation, swallowing, and breathing; doing so in part through the opposing motion of the vocal folds. If that action is altered, then any of these vital functions may be disrupted. Segmental damage to the airway can potentially lead to a permanent tracheostomy tube. Similarly, loss of laryngeal function can be associated with severe aspiration requir­ ing permanent parenteral alimentation. Socially, most detrimental to patient quality of life may be the loss of phonatory ability. Many patients have confided that they felt as if they lost their identity when they lost their voice. In the case of permanent laryngeal incompetence secondary to cancer or severe trauma, frequently there is not a good traditional therapeutic option that can restore all three functions. Laryngeal transplantation has the potential to restore swallowing, respiration without a tracheos­ tomy or tracheostoma, and speak with a human voice. Human laryngeal transplantation was first studied in the 1960s in animal models by Boles,1 Ogura et al.,2 and Silver et al.3 Kluyskens and Ringoir4 first performed a subtotal laryngeal transplant in 1969. There were no neuronal or microvascular anastamoses performed. The transplant preserved the recipient perichondrium as the blood supply. Unfortunately, the tumor quickly recurred while on immunosuppression and interest in laryngeal transplantation waned for the next two decades. There are barriers to overcome for laryngeal trans­ plantation to become a viable option for a large patient cohort. First, the larynx is considered a nonvital organ since it is possible to survive after a resection. The ethics

of subjecting patients to the potential complications of transplantation for a nonvital organ is a primary concern. This topic is discussed thoroughly in a publication by Genden and Urken.5 Second, transplantation requires life­ long immunosuppression, which is accompanied by many known adverse effects. Most notably, the relative risk of developing a malignancy while on immunosuppression has been estimated to be up to 400 times that of the general population.6 This increase in risk currently prohibits trans­ plantation in cancer patients. Despite this risk, 75% of surveyed laryngectomy patients said they would accept a larynx transplant if offered.7 The patient’s desire for larynx functionality questions the nonvital classification. Lastly, restoring vocal fold motion is in its infancy with some successes reported to date. In 1987, the senior author began to investigate the potential of laryngeal transplantation. He focused on rein­ nervation, revascularization, immunosuppression, and the ethics of laryngeal transplantation. A rat laryngeal trans­ plantation model was developed to investigate the maxi­ mum tolerated total ischemia time,8 preservative solu­tions, stages of histologic rejection,9 and immunosup­ pres­sive regimens.10 Once the research supported the feasi­bility, the first human total laryngeal transplantation was performed on January 4, 1998 by a team of surgeons led by the senior author.11

THE FIRST TOTAL HUMAN COMPOSITE LARYNGEAL TRANSPLANT After extensive interviews, counseling, and testing, a 40-year-old man with a dysfunctional larynx secondary to

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Section 10: Voice Practice and New Innovations

Fig. 83.1: Surgical technique of the first successful composite total laryngeal transplant. Vascular anastomoses included the donor right internal jugular vein to the recipient right facial vein, donor left middle thyroid vein to recipient left internal jugular vein, donor superior thyroid arteries to the recipient superior thyroid arteries. Nerve anastomoses included both superior laryngeal nerves and only the right recurrent laryngeal nerve.

trauma was chosen. He had suffered a crush injury to his larynx and pharynx during a motorcycle accident 20 years earlier. Despite multiple attempts at another institution to reconstruct his larynx, he remained aphonic and tra­ cheotomy dependent. The donor was a 40-year-old brain-dead man from a ruptured cerebral aneurysm. He met all the predetermi­ ned criteria for acceptance in regard to human leukocyte antigen matching (4 of 5) and serum virology. The donor organ harvest included the entire pharyngolaryngeal complex, including six tracheal rings and the thyroid and parathyroid (PTH) glands (Fig. 83.1). The organ complex was stored in the University of Wisconsin solution during transport until revascularization 10 hours later. The recipient received cyclosporine, azathioprine, and methylprednisolone prior to surgery. Perfusion was re-es­­tablished to the donor organ as the first step of the transplant. The donor’s right superior thyroid artery was anastomosed to that of the patient. The proximal end of the donor’s right internal jugular vein was anastomosed to the patient’s right common facial vein. Blood flow through the transplanted thyroid gland, six tracheal rings, larynx, and pharynx was observed within 30 minutes of clamp release. Once perfusion was established, a narrow field laryn­ gectomy was performed. The recipient’s thyroid lobes remained and the hyoid bone was left in place. A majority

of the donor’s pharynx was utilized to widen the patient’s stenotic pharyngoesophageal complex. The donor laryn­ geal cartilage was sutured to the hyoid bone to allow for laryngeal elevation. Five of the donor’s tracheal rings were sutured to the recipient’s tracheostoma. The stoma was left open as a safety mechanism. The left-sided vascular anastomoses were then comp­ leted. This included the donor superior thyroid artery to the recipient superior thyroid artery and the donor middle thyroid vein to the recipient internal jugular vein. Both superior laryngeal nerves were located and reanasto­ mosed. Only the recipient’s right recurrent laryngeal nerve could be located for reinnervation. Postoperatively, the patient was maintained on muro­ monab-CD3, cyclosporine, methylprednisolone, and myco­ phenolate mofetil. Initial aspiration was controlled with glycopyrrolate and atropine, which were later dis­conti­ nued. After observation in the hospital for one month, the patient’s transplanted trachea was noted to be slightly edematous on endoscopy and showed no signs of rejection on biopsy. Three months post-transplant, the supraglottis and vocal folds were sensitive to touch. Purposeful swal­ lowing, taste, and smell returned. Subsequent barium swal­ lows revealed no aspiration. To evaluate thyroid func­tion, a four-hour uptake of iodine-123 demonstrated 83% activity in the transplanted thyroid lobes, as well as 17% in the patient’s native thyroid. Thyroid function tests and serum calcium and phosphate all remained within normal ranges.

Chapter 83: Laryngeal Transplantation

1007

pneumonia, which cleared rapidly with intravenous anti­ biotics. Fifteen months post-transplant, the patient presen­ ted with a decrease in voice quality. He was noted to have an episode of acute rejection. After three daily doses of 1 gm/ day of methylprednisolone, his larynx and voice returned to normal. A second episode of rejection occurred about 5 years later due to laboratory error in measuring tacroli­ mus levels falsely high. As a result, the patient’s medica­tion fell below therapeutic levels. Laryngeal edema was observed during the acute rejection episode, but quickly returned to normal once medication levels returned to the therapeutic range.

IMMUNOSUPPRESSION REDUCTION

Fig. 83.2: Mouse and rat laryngeal transplantation diagram. Arterial inflow is through the donor common carotid artery anastomosed to recipient common carotid artery. Vascular supply is based on superior thyroid artery pedicled via the external carotid artery. Venous outflow is through the donor contralateral common carotid artery anastomosed to recipient internal jugular vein.

The first post-transplant voicing occurred on the 3rd postoperative day. After one month, both true vocal folds were in a lateral position, creating a breathy voice. The right fold (the side of the recurrent nerve anastomosis) was midline by four months. At six months, the left had media­ lized. Electromyographic (EMG) measurements confirmed rein­nervation of both folds and bilateral volitional cri­ cothy­roid function.12 We postulated that the surprising finding of innervation on the left is likely due to “fieldrein­nervation”, in which the left thyroarytenoid muscle is supplied by surrounding motor nerves. Subjective and objective measures of phonation including pitch, jitter, intensity, and maximal phonation time were within the normal range at 36 months post-transplant. Interestingly, the patient became a motivational speaker. He stated his quality of life improved “immeasurably” subsequent to the transplantation. Postoperative complications were few and far between. The patient did experience three early episodes of trache­ obronchitis, which were successfully treated with oral amoxicillin clavulanate. At 16 weeks post-transplant, the patient inadvertently stopped his trimethoprim and sulfa­ methoxazole and developed Pneumocystis carinii

As previously discussed, the primary limitation to laryn­ geal transplantation, and transplantation in general, is immunosuppression. Our lab and others have investigated possible ways to reduce the amount of immunosuppres­ sion given to a patient while still preventing rejection. A variety of animal models have been developed to study laryngeal transplantation including dog,1-3 mouse,13,14 and pig.15 These models all offer complementary infor­ mation forming the basis on which to build further understanding into laryngeal transplantation. Our lab has focused on the rat and mouse models since they are wellestablished transplant models, significant information is known about their immune systems, and are relatively inexpensive. Our models place the transplanted organ in tandem with the native larynx (Fig. 83.2). We utilize an arteriovenous shunt with arterial inflow through one superior thyroid artery and venous outflow through the con­tralateral superior thyroid artery. In 2002, the rat model’s revisions were published, as well as a revised grading scale of rejection.16 The mouse model14 and a mouse rejection grading scale17 were published later. Over time and > 3000 transplants, these models have shown overall nearly 100% survivability, and a > 90% graft evaluability. Furthermore, we have demonstrated that performing a total parathy­ roidectomy on the recipient during transplantation can utilize the production of parathormone from the rat trans­ planted larynx as a marker of graft viability rather than having to sacrifice the animal for histologic evaluation.18 This has allowed for a new generation of studies examin­ing the ability to ‘pulse’ immunosuppressives and ‘salvage’ the organ if parathormone levels drop. In early studies on immunosuppression for laryngeal transplantation, Haug et al.19 have correlated the laryngeal rejection grade, cyclosporine A (CSA) concentration, and

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Section 10: Voice Practice and New Innovations

CSA intramuscular dosing. They performed a blinded study looking at different dosages for CSA monotherapy. CSA was dosed at either 1.0, 2.5, 5.0, 7.5, or 10 mg/kg/ day. Significantly, different average CSA concentrations were achieved among each group of five transplanted rats. Rejection gradings within the top 3 doses of CSA were not significantly different. However, significant pathologic allograft rejection correlated with CSA concentrations below 250 ng/cc. This study helped develop the minimum level of CSA required to obtain optimum graft survival when used as the sole agent for immunosuppression. Lorenz et al.20 studied the ability to decrease the amount of CSA by adding prednisone to cyclosporine. In a multiarm study containing 220 transplantations, multiple doses of both cyclosporine and prednisone were admi­ nistered. The transplanted organs were evaluated at both 15 and 30 days post-transplantation. They found that the addition of 1.0 mg/kg/day of prednisone allowed CSA doses to be reduced to 2.0 mg/kg and still demonstrate no significant rejection at 30 days post-transplantation. Although the combination of low-dose CSA and predni­ sone significantly improved graft survival when compared with CSA alone at the equivalent dose, prednisone mono­ therapy demonstrated rates of rejection similar to no immunosuppression at all. Nelson et al.21 further demonstrated that combination therapy of other immunosuppressives would also allow for decreased levels while maintaining graft viability. In that study, experiments were conducted between tacroli­ mus (FK506) alone at varying levels, and tacrolimus combi­ ned with mycophenolate mofetil at varying levels. Groups were examined at either 15 or 30 days post-transplantation. As expected, increasing levels of tacrolimus demon­ strated increasing efficacy of immunosuppression. However, low-dose tacrolimus in combination with mycophenolate mofetil achieved comparable results. Continued investigations into combined therapy elicited the exciting finding that tolerance of the trans­ planted organ can be induced with a very low dose of combined immunosuppressants. Akst et al.22 treated trans­ planted rats with tacrolimus and mouse anti-rat alpha beta T-cell receptor monoclonal antibodies (ab-TCR) for only seven days after the transplant. All grafts demonstrated viability at 100 days. Skin grafting, mixed lymphocyte reaction, and flow cytometry revealed that tolerance was neither donor specific nor related to prolonged depletion of T-cell populations.

IMMUNOSUPPRESSION IN THE CANCER PATIENT The ability to induce tolerance with very low doses of immunosuppression and subsequent reduction of the undesirable side effects facilitates the ability to transplant more patients. However, that degree of immunosuppres­ sion is still prohibitive in cancer patients, which represent the vast majority of laryngeal transplantation candidates. It may be allowable to transplant patients with large benign or low-grade malignant laryngeal tumors or those with laryngeal cancer who are already on a post-transplant immunosuppression regimen. These patients are relatively rare. The recipient pool may be further expanded by trans­ planting patients who have already undergone laryngec­ tomy for cancer, and there is no sign of recurrent cancer after five years. Ultimately, the largest group of patients who stand to benefit are those presenting with locally advanced laryngeal cancer. There are approximately 7000 new cases of advanced laryngeal cancer per year in the United States.23 To date, two transplants have been performed for locally advanced head and neck cancer reconstruction— the nonrevascularized partial laryngeal transplant in 19694 and a tongue transplant in 2003. Unfortunately, both patients rapidly succumbed to recurrent disease. There are at least three areas of investigation that are promising for possible transplantation in malignancy. The first is to add an antineoplastic agent to the immunosuppression regimen. The second is to directly modify immune cells to maintain immunocompetence while accepting the transplant. Lastly, bioengineering of an organ with the patients’ own cells should bypass the need for immuno­ suppression altogether. The second and third areas will be discussed later in the chapter. Everolimus (SDZ-RAD) is an intriguing immunosup­ pressive option for transplantation in cancer patients.24 It is a derivative of rapamycin and belongs to the mTOR (mammalian target of rapamycin) class of immunosup­ pressants. It blocks the translation of mRNA in critical cell cycle regulatory proteins, thereby inhibiting proli­ feration of intimal cells, lymphocytes, and tumor cells. Everolimus has shown both immunosuppressive and antitumor properties. The antitumor properties have been demonstrated in several animal and human tumor cell lines, including squamous cell carcinoma.25-27 In addition, it has been shown to inhibit the development of posttransplant lymphoproliferative disorders.28 Data from our laryngeal transplant models have provided support for the use of everolimus as an effective immunosuppres­ sive in laryngeal transplantation.29,30

Chapter 83: Laryngeal Transplantation

A

B

D A mouse squamous cell carcinoma cell line was used to determine the effect of everolimus on the growth of both intradermal tumors and pulmonary metastases.31 Mice received either everolimus 1 mg/kg/bid, everolimus 0.5 mg/kg/bid, cyclosporine 7.5 mg/kg/day, or no treat­ ment. Everolimus showed statistically significant tumor inhibition at 1.0 mg/kg/bid and 0.5 mg/kg/day when compared with mice treated with cyclosporine and to untreated animals (p  6 years. During that time, there was a slight shift of the electrode position

and anode corrosion. The patient did need periodic injec­ tions of botulinum toxin to antagonize the adductors.51 Although the results were promising, the authors stated that there were difficulties in the translation of the techno­ logy to humans and problems with electrode corrosion. Further animal studies are underway to improve these issues. Ultimately, what is requisite for laryngeal innervation in the context of transplantation is to consistently achieve a glottic aperture on abduction of 14–16 mm. The two episodes of rejection experienced by our patient were associated with a sudden alteration in voice quality followed shortly thereafter by the onset of significant edema. Without attaining the aforementioned aperture, the airway could be seriously compromised during an episode of acute rejection. Sensory function of the transplanted larynx is also important to the success of the transplant. Blumin et al.52 studied reinnervation of the transplanted dog larynx. In a randomized, controlled study, 10 dogs had their superior laryngeal nerves transected. Five of the dogs had the nerves reanastomosed. All dogs were tested for laryngospasm in response to hydrochloric acid stimula­ tion both preoperatively and six months postoperatively. None of the dogs regained normal laryngospastic respon­ ses, but the reanastomosed dogs exhibited protective EMG activity and coughing. The control group exhibited no response. In our human laryngeal transplant patient, the supraglottis and vocal folds were sensitive to touch at three months postoperatively, initiating a severe cough. Stimulation through the stoma on the right side of the upper trachea elicited a sensation of touch without cough. Stimulation of the left side was not sensed.

EXPLANT At 14.5 years after the first composite head and neck transplant, which included the larynx, explantation was necessary. Over the prior five years, a subtle but progressive contracture of the larynx could be noted in retrospect on sequential videos. This almost certainly was the result of chronic rejection. Our animal studies of chronic rejection provide a histologic understanding of this process. Clini­ cally, in the last year, our patient experienced increased aspiration with fluids, a decrease in voice quality, and persistent pain. Sensory testing revealed a dramatic reduc­ tion in sensation compared to prior testing. The thyroid function, which for three years post-transplant was found to be 80% donor derivation and 20% recipient, reverted to 100% recipient just prior to explant. Fibrosis seen

Chapter 83: Laryngeal Transplantation histologically in our chronic rejection animal model was undoubtedly the reason for this. The patient, on his own, decreased his steroid dose to help with the aspiration. The subsequent increased laryngeal swelling initially helped decrease the aspiration but was insufficient in the long term. Attempted vocal fold augmentation by injection was unsuccessful as anticipated. The decision was made to explant the larynx. Following extirpation, the pharyngeal remnant was augmented with a free flap. The histology of the excised larynx showed ulceration, acute and chronic inflammation, and dense fibrosis. These were all seen previously in our rejection animal models. On postexplant follow-up, a small 3-4 mm HPV-asso­ ciated oropharyngeal malignancy was identified. The rela­ tionship of HPV and immunosuppression in the context of the etiology of his cancer remains an open question. Our patient considers his experience worthwhile for multiple reasons, some of which include the ability to have a human voice with pitch control, sense of smell, and an overall feeling of well-being. Today, he communicates via transesophageal puncture speech. He has recently stated that, if given the opportunity, he would opt for another transplant. Unfortunately, this is no longer possible given his recent history of malignancy.

CONCLUSION Total laryngeal transplantation is now a reality. With it comes the potential of restored laryngeal function for many patients who have had to suffer the hardships and embarrassment of life without human voicing capability. There is still much to be learned and improved upon from the first transplant and the few that have followed. The most recent larynx transplant in the United States was performed in 2010.53 With all of the research currently underway in trans­ plantation medicine, the day is likely not too far away when many of the questions highlighted in this chapter will be answered. The immune system will be modified to allow for donor-specific tolerance while keeping immu­ nosurveillance intact, or immunosuppression may be completely bypassed through regenerative techniques. Glottic function might be restored through selective rein­ nervation or laryngeal pacing. Once these are a reality, laryngeal transplantation will be able to benefit many people who have undergone a laryngectomy for malignancy. At that time, thousands of people will regain their voices and their identities.

1013

REFERENCES 1. Boles R. Surgical replantation of the larynx in dogs: a progress report. Laryngoscope. 1966;76:1057-67. 2. Ogura JH, Kawasald M, Takenouchi S, et al. Replantation and transplantation of the canine larynx. Ann Otol. 1966;75:295-312. 3. Silver CE, Liebert PS, Som ML. Autologous transplantation of the canine larynx. Arch Otolaryngol. 1967;86:95-102. 4. Kluyskens P, Ringoir S. Follow-up of a human larynx transplantation. Laryngoscope. 1970;80:1244-50. 5. Genden EM, Urken ML. Laryngeal and tracheal transplan­ tation: ethical limitations. Mt Sinai J Med. 2003;70:163–5. 6. Brenner MJ, Tung TH, Jensen JN, et al. The spectrum of com­ plications of immunosuppression: is the time right for hand transplantation? J Bone Joint Surg Am. 2002;84:1861-70. 7. Potter CP, Birchall MA. Laryngectomees’ views of laryngeal transplantation. Transpl Int. 1998;11:433-8. 8. Strome M, Wu J, Strome S, et al. A comparison of preserva­ tion techniques in a vascularized rat laryngeal transplant model. Laryngoscope. 1994;104:666-8. 9. Strome S, Brodsky G, Darrell J, et al. Histopathologic cor­ relates of acute laryngeal allograft rejection in a rat model. Ann Otol Rhino/Laryngol. 1992;101:156-60. 10. Strome M, Strome S, Darrell J, et al. The effects of cyclo­ sporin A on transplanted rat allografts. Laryn­ goscope. 1993;103:394-8. 11. Strome M, SteinJ, Esclamado R, et al. Laryngeal trans­ plantation: a case report and 40-month follow-up. N Engl J Med. 2001;344:1676-9. 12. Lorenz RR, Hicks DM, Shields RW Jr, et al. Laryngeal nerve function after total laryngeal transplantation. Otolaryngol Head Neck Surg. 2004;131:1016-8. 13. Genden EM, Iskander A, Bromberg JS, et al. The kinetics and pattern of tracheal allograft reepithelialization. Am J Respir Cell Mol Bioi. 2003;28:673-83. 14. Shipchandler TZ, Lott DG, Lorenz RR, et al. New mouse model for studying laryngeal transplantation. Ann Otol Rhinol Laryngol. 2009;118:465-8. 15. Birchall MA, Bailey M, Barker EY, et al. Model for experimental revascularized laryngeal allotransplantation. Br j Surg. 2002;89:1470-5. 16. Lorenz RR, Dan O, Fritz MA, Strome M. Rat laryngeal transplant model: technical advancements and a redefined rejection grading system. Ann Otol Rhinol Laryngol. 2002;111:1120-7. 17. Lott DG, Shipchandler TZ, Dan O, et al. A new mouse laryn­geal transplantation rejection grading system. Laryn­ goscope. 2010;120(1):39-43. 18. Nelson M, Dan O, Strome M. Evaluation of parathyroid hormone as a functional biological marker of rat laryngeal transplant rejection. Laryngoscope. 2003;113:1483-6. 19. Haug M 3rd, Dan O, Wimberley S, et al. Cyclosporine dose, serum trough levels, and allograft preservation in a rat model of laryngeal transplantation. Ann Otol Rhinol Laryngol. 2003;112:506-10.

1014

Section 10: Voice Practice and New Innovations

20. Lorenz RR, Dan O, Fritz MA, et al. Immunosuppressive effect of irradiation in the murine laryngeal transplanta­ tion model: a controlled trial. Ann Otol Rhinol Laryngol. 2003;112:712-5. 21. Nelson M, Fritz M, Dan O, et al. Tacrolimus and mycophe­ nolate mofetil provide effective immunosuppression in rat laryngeal transplantation. Laryngoscope. 2003;113:1308-13. 22. Akst LM, Siemionow M, Dan O, et al. Induction of toler­ ance in a rat model of laryngeal transplantation. Trans­ plantation. 2003;76:1763-70. 23. Birchall MA, Lorenz RR, Berke GS, et al. Laryngeal trans­ plantation in 2005: a review. Am J Transplant. 2006;6:20-6. 24. Sedrani R, Cottens S, Kallen J, et al. Chemical modification of rapamycin: the discovery of SDZ RAD. Transplant Proc. 1998;30:2192-4. 25. Mabuchi S, Altomare DA, Cheung M, et al. RAD001 inhibits human ovarian cancer cell proliferation, enhances cisplatin-induced apoptosis, and prolongs survival in an ovarian cancer model. Clin Cancer Res. 2007;13:4261-70. 26. Fernandez A, Marcen R, Pascual J, et al. Conversion from calcineurin inhibitors to everolimus in kidney transplant recipients with malignant neoplasia. Transpl Proc. 2006;38:2453-5. 27. Khariwala SS, Kjaergaard J, Lorenz R, et al. Everolimus (RAD) inhibits in vivo growth of murine squamous cell carcinoma (SCC VII). Laryngoscope. 2006;116:814-20. 28. Boulay A, Zumstein-Meeker S, Stephan C, et al. Antitumor efficacy of intermittent treatment schedules with the rapamycin derivative RADOO 1 correlates with prolonged inactivation of ribosomal protein S6 kinase 1 in peripheral blood mononuclear cells. Cancer Res. 2004;64:252-61. 29. Khariwala SS, Knott PD, Dan O, et al. Pulsed immuno­ suppression with everolimus and anti-ab TCR: laryngeal allograft preservation at six months. Ann Otol Rhinol Laryngol. 2006;115:74-80. 30. Lott DG, Dan O, Lu L, et al. Long-term laryngeal allograft survival using low-dose everolimus. Oto-HNS. 2010;142:72-8. 31. Khariwala SS, Kjaergaard J, Lorenz R, et al. Everolimus (RAD) inhibits in vivo growth of murine squamous cell carcinoma (SCC VII). Laryngoscope. 2006;116:814-20. 32. Lott DG, Khariwala S, Dan O, et al. Ten-month laryngeal allograft survival using pulsed everolimus and anti-ab TCR antibody immunosuppression. Ann Otol Rhinol Laryngol. 2011;120:131-6. 33. Genden EM, Mackinnon SE, Yu S, et al. Portal venous ultraviolet B-irradiated donor alloantigen prevents rejection in circumferential rat tracheal allografts. Otolaryngol Head Neck Surg. 2001;124:481-8. 34. Gorti GK, Birchall MA, Haverson K, et al. A preclinical model for laryngeal transplantation: anatomy and muco­ sal immunology of the porcine larynx. Transplantation. 1999;68:1638-42. 35. Rees LE, Ayoub O, Haverson K, et al. Differential major histocompatibility complex class II locus expression on human laryngeal epithelium. Clin Exp Immunol. 2003; 134:497-502. 36. Friedman AD, Dan O, Drazba JA, et al. Quantitative analysis of OX62-positive dendritic cell distribution in the rat laryngeal complex. Ann Otol Rhinol Laryngol. 2007;116(6):449-56.

37. Govindaraj S, Gordon R, Genden EM. Effect of fibrin matrix and vascular endothelial growth factor on reepithelialization of orthotopic murine tracheal transplants. Ann Otol Rhinal Laryngol. 2004;113:797-804. 38. Lott DG, Dan O, Lu L, et al. Decoy NF-kB fortified immature dendritic cells maintain laryngeal allograft integrity and provide enhancement of regulatory T-cells. Laryngoscope. 2010;120(1):44-52. 39. Xu MQ, Suo YP, Gong JP, et al. Prolongation of liver allograft survival by dendritic cells modified with NF-kB decoy oligo­ deoxynucleotides. World J Gastroenterol. 2004;10:2361-8. 40. Tiao MM, Lu L, Tao R, et al.. Prolongation of cardiac allograft survival by systemic administration of immature recipient dendritic cells deficient in NFkB activity. Ann Surg. 2005;241:497-505. 41. Macchiarini P, Jungebluth P, Go T, et al. Clinical trans­ plantation of a tissue-engineered airway. Lancet. 2008;372 (9655):2023-30. 42. Huber JE, Spievack A, Simmons-Byrd A, et al. Extracellular matrix as a scaffold for laryngeal reconstruction. Ann Otol Rhinol Laryngol. 2003;112(5):428-33. 43. Baiguera S, Gonfiotti A, Jaus M, et al. Development of bioengineered human larynx. Biomaterials. 2011;32(19): 4433-42. 44. Stavroulaki P, Birchall M. Comparative study of the laryn­ geal innervation in humans and animal employed in laryn­ geal transplantation research. J Laryngol Otol. 2001;115: 257-66. 45. Baldissera F, Cantarella G, Marini G, et al. Recovery of inspi­ ratory abduction of the paralyzed vocal cords after bilat­ eral reinnervation of the cricoarytenoid muscles by one single branch of the phrenic nerve. Laryngoscope. 1989; 99:1286-92. 46. Marie JP, Tardif C, Lerosey Y, et al. Selective resection of the phrenic nerve roots in rabbits: part II: respiratory effects. Respir Physiol. 1997;109:139-48. 47. Marie J-P, Lacoume Y, Laquerrie`re A, et al. Diaphragmatic effects of selective resection of the upper phrenic nerve root in dogs. Respir Physiol Neurobiol. 2006; 154:419-30. 48. Marie J, Lacoume Y, Magnier P, et al. Selective bilateral motor reinnervation of the canine larynx. Laryngo-RhinoOtologie. 2000;79:S188-9. 49. Marie JP. Nerve reconstruction. In: Remacle M, Eckel HE (eds), Surgery of larynx and trachea. Heidelberg: Springer; 2010:279-94. 50. Zealear DL, Billante CR, Courey MS, et al. Reanimation of the paralyzed human larynx with an implantable electrical stimulation device. Laryngoscope. 2003;113:1149-56. 51. Mueller AH. Laryngeal pacing for bilateral vocal fold immo­ bility. Curr Opin Otolaryngol Head Neck Surg. 2011;19: 439-43. 52. Blumin JH, Ye M, Berke GS, et al. Recovery of laryngeal sensation after superior laryngeal nerve anastomosis. Laryn­goscope. 1999;109:1637-41. 53. http://www.ucdmc.ucdavis.edu/welcome/features/20102011/01/20110126_larynx_transplant_qa.html

Index Note: Page numbers followed by f and t indicate figures and tables, respectively.

A 5-aminolevulinic acid (5-ALA) 920 Abdominal pressure 23 Abductor dilatory functions 92 Abductor laryngospasm 92 Abductor spasmodic dysphonia 94, 524 techniques of botulinum toxin injections 524 Abraham-type catheter 793 Abrikosoff tumor 761 Absent neural input 58 Abundant minor salivary gland 760 Abundant myxoid stroma 765 Academic voice clinics 998 Academic voice practice 997 Accent method 315 Accuracy of acoustic analysis 157 Accurate technical specifications 292 Acellular grafts 1011 Acetylcholine release 514 Achlorhydria 573 Acid-fast bacilli 594 Acid and nonacid reflux 589 Acid reflux 651 Acid reflux irritation 617 Acoustic-perceptual measures 372 Acoustic analysis 155, 161 Acoustic and aerodynamic instrumentation 311 Acoustic and aerodynamic vocal-function tests 698 Acoustic energy of voice 51 Acoustic filter 76 Acoustic pressure waveform 63 Acoustic pressure waves 64 Acquired immune deficiency syndrome (AIDS) 548 Acquired stenoses 845 injury and trauma 845 blunt trauma 845 post-tracheotomy stenosis 846 postintubation 845 thermal injuries 845 systemic 846 eosinophilic esophagitis 846

granulomatous 847 idiopathic 847 infectious 847 polychondritis, amyloidosis, and Wegener’s granulomatosis 847 Acupuncture therapy for vocal pathology 356 Acute inflammation 878 Acute inflammatory polyneuropathy 512 Acute laryngeal trauma 665 Acute laryngitis 543 acute bacterial laryngitis 545 supraglottitis 546 epidemiology 544 infectious laryngitis 545 acute viral laryngitis 545 croup 545 other acute bacterial laryngitis 547 acute fungal laryngitis 547 allergic laryngitis 550 angioedema 550 immunocompromised patient 548 noninfectious acute laryngitis 548 phonotrauma 548 smoke, fumes, and occupational exposures 550 thermal laryngitis 549 pathophysiology 543 Acute laryngotracheal bronchitis 545 Acute phonotrauma 543 Acute vocal fold 438 Adam’s apple 26, 645 Adam’s apple resection 253f Adaptive respiratory reflex 599 Addison’s disease 343 Adduction arytenopexy 781 Adductor spasmodic dysphonia 510, 778, 782 Adenoid cystic carcinoma 760 Adrenal dysfunction 647 Adrenal glands 654 Adrenal medulla 766 Adrenergic decongestants 510 Adrenergic receptor antagonists 340 Adrenocorticotrophic hormone 355, 643 Adult derived stem cells 108

Advanced techniques of laryngopharyngeal endoscopy 20 Aeroacoustics of whisper 86 Aerodigestive region 5 Aerodigestive tract (ADT) 4 Aerodigestive tract among mammals 5 Aerodynamic analysis 155, 161 Aerodynamic energy 51 Aerodynamic myoelastic theory 195 Aerodynamic parameters 56, 171 airflow 56 current clinical assessment 56 subglottal pressure 56 vocal efficiency 56 Aerodynamic turbulence 158 Aerodynamic voice parameters 365 Age-related dysphonia 635 Aggressive malignant lesions 766 Aging of the vocal fold mucosa 50 Aging voice 635 central nervous system pathology 636 geriatric dysphonia 635 presbyphonia 635 history and examination 637 professional vocalist 638 future directions 639 rejuvenation of the aging voice 637 Air pollutants 534t Airway fire 394 Airway management technique 399 Airway passage 23 Alcohol abuse 449 Alcoholism 593 Alexander technique 501, 1001 Allergic angioedema 551 Allergic etiology 601 Allergic inflammatory response 593 Allergic rhinitis 467 Altered vocal parameters 655 Alzheimer’s disease 644 American Academy of Otolaryngology 493 American College of Chest Physicians (ACCP) 604 American College of Radiology (ACR) 298 American Journal of Medical Sciences 235 American Laryngological Association (ALA) 998

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Laryngology

American Speech Language and Hearing Association (ASHA) 155 American Thyroid Association 141 America’s weight gain 131 Amplitude of oscillation 161 Amplitude of vibration 210t Amplitude perturbation quotient 158 Amplitude quotient 165 Amygdala 90 Amyloidosis 566, 593, 892 Amyotrophic lateral sclerosis (ALS) 270, 506, 636, 822 Anabolic steroids 644, 655 Analog waveform 291 Analysis of vocal folds 193 Anatomical identification of the nerve 280 Anatomical structure of the human larynx 23 Anatomic analysis of the paraglottic space 237 Anatomic asymmetry for larynx 54 Anatomic axes 188 Anatomy 119 Anatomy of human vocal folds 5 Anatomy of the glottis 45 Anatomy of the pediatric airway 25 Anatomy of voice and speech production 4 Ancestral branchial arches 24 Androgen receptors 644 Anesthesia for office-based laryngology 947 hemodynamic concerns during office based laryngotracheal procedures 949 pharmacologic considerations for topical lidocaine 948 Anesthesiology and clinical airway management 385 airway emergency cart 389 airway pathology issues 390 acute epiglottitis 391 airway tumors, polyps, and papillomas 393 angioedema 391 Ludwig’s angina 393 retropharyngeal abscess 393 anesthesia for cricothyrotomy and tracheostomy 399 anesthesia for laryngologic procedures 394 anesthesia for neck dissection and laryngectomy 399 anesthesia for panendoscopy 397

anesthesia in cases of airway trauma 398 awake intubation 388 head and neck flap reconstructive surgery 400 perioperative fluid administration 400 phonosurgery and other microlaryngeal procedures 399 preoperative evaluation 385 prevention and management of airway fires 394 rapid sequence induction 397 supraglottic airways 390 Anesthetic technique 394 Anesthetic technique for panendoscopy 397 Angiotensin-converting enzyme (ACE) 140, 464 Angiotensin-converting enzyme inhibitors 339t, 601t Angiotensin II receptor antagonists 339t, 340 Annotation 301 Annular fibers 499 Ansa cervicalis nerves 528 Ansa hypoglossi nerve supply 832 Ansa hypoglossi–RLN anastomosis 813 Anterior arch 238 Anterior commissure retrusion technique 787 Anterior face of the thyrohyoid muscle 836 Anterior glottic stenosis 860 management 860 presentation 860 surgical technique 861 endoscopic approach 861 open approach 864 Anterior glottis 45 Anterior glottis stenosis 873 Anterior membranous vocal fold 214 Anterolateral arytenoid surface 35 Anteroposterior compression 488 Antiacetylcholine receptor (ACHR) 513 Anticholinergic effects 346 Anticholinergic medication 511 Anticholinesterases 514 Anticoagulants 341t Antihistamines 337t First-generation antihistamines 337t Second-generation antihistamines 337t Third-generation antihistamines 337t Antimuscarinic agents 336 Antiplatelet agents 341t

Antirheumatic medications 559 Antitussives 338 Aortic compression 975 Aperiodic oscillatory 204 Aperiodic phonation 55f Aperiodic vibration 56 Appendix 729 Apple quicktime (MOV) 297 Arbitrary classification system 824 Architecture of the vocal fold mucosa 45 Archival components 288 Arcus cartilaginis cricoideae 32f Arnold Chiari malformations 631 Arteriovenous malformations 759 Aryepigiottic fold 26, 32, 36, 93, 244f Aryepiglottic muscles 32 Aryepiglottic structures 72 Arytenoid adduction 779, 781 Arytenoid adduction techniques 30 Arytenoid cartilage 32, 33, 37, 38f, 45, 238 Arytenoid during phonation and inspiration 247f Arytenoid humps 25 Arytenoid injury 265 Arytenoid perichondrium 712 Arytenoid phonation 247f Arytenoid reduction 781 Arytenoid subluxation 860 Arytenoids’ cartilages 35 Asbestos 906 Assessing outcomes of voice treatment 363 baseline effect 372 comparison between subjective and objective outcomes 370 objective outcomes 363 acoustic assessment 363 aerodynamic assessment 365 perceptual outcomes 366 consensus auditory-perceptual evaluation of voice 366 development of the patient questionnaire of vocal performance 368 development of the Singing Voice Handicap Index 368 development of the voice-related quality of life 368 development of the Voice Handicap Index-10 367 development of the Voice Outcome Survey 368 development of the Voice Symptom Scale 368 GRBAS scale 366

Index subjective outcomes 367 video laryngostroboscopy 366 surgical outcomes assessment 371 benign soft tissue lesions 371 glottic insufficiency 371 laryngeal dystonia 371 suspected malignancy 371 utilization of objective outcomes 365 acoustic assessment 365 aerodynamic assessment 365 utilization of perceptual outcomes 366 CAPE-V as an outcome measure 366 GRBAS as an outcome measure 366 video laryngostroboscopy 367 utilization of subjective outcomes 369 Singing Voice Handicap 369 V-RQOL 369 Voice Handicap Index-10 369 VOISS 370 VOS 369 VPQ 370 Assessment of the subglottis 140 Asthma attack 613 Asthma cough variant asthma (CVA) 607 Asymmetric amplitude 208 Asymmetric tension 58 Asymmetric vocal fold tension 206 Asymmetry quotient 165 Atherosclerosis 130 Atrophic epithelium 687 Atrophic mucosa 653 Attractor’s lure 480 Atypical asthma 461 Atypical cells 142 Auditory feedback 474 Auditory perception 161 Auerbach’s plexus 587 Auscultation of the lungs 603 Autoimmune-related dysphonia 124 Autoimmune disease 461 464, 877 Autoimmune disorders of the larynx 565 amyloidosis 566 methods 565 relapsing polychondritis 567 rheumatoid arthritis 569 sarcoidosis 568 scleroderma 570 symptoms 565 systemic lupus erythematosus 569 treatments 565 Autolaryngoscopy 16 Automatic breathing 89

Autonomic system 336 Avoiding the pitfalls of stroboscopy 221

B b-adrenergic agonists 338 Babington’s glottiscope 16f Bacterial laryngitis 557 Barbed suture 668 Barium esophagography 588 Barium esophagram 606 Barrett’s esophagus 555, 588, 595 Barrett’s nondysplastic metaplasia 595 Basal ganglia disorders 280 dystonia 280 myopathic disorders 281 neuromuscular junction disorders 281 upper motor neuron disorders 282 Basement membrane 687 Basement membrane zone (BMZ) 46, 416 Basic clinical protocols 161 Basic flexible fiberoptic laryngoscopy 182 Basic laryngeal-respiratory physiology 613 Basic minimum assessment protocol 164 Basic properties of oscillating systems 64 Basin of attraction 480 phonatory basin of attraction 481 Basophile cells 644 Bay areas running club studies 133 Behavior modification therapies 416 Benign hyperplasia 918 Benign mixed tumor 760 Benign tumors of the larynx 757 cartilaginous neoplasms 759 chondromas 759 glandular neoplasms 760 oncocytoma 760 pleomorphic adenoma 760 muscle neoplasms 763 leiomyoma 763 rhabdomyoma 765 neoplasms of adipose origin 765 lipoma 765 neoplasms of neural origin 761 granular cell tumors 761 neurofibroma 762 neurolemmoma/schwannoma 762 neuroendocrine neoplasms 765 paraganglioma 765 other rare neoplasms 767 desmoid 767 fibrous histiocytoma 768 myxoma 768

1017

vascular neoplasms 757 hemangiomas 758 vascular malformations 759 Benign vocal fold abnormalities 415 Bernoulli forces 871 Bernoulli’s principle 53 Best-of-breed solutions 308 Bethesda grading system 141 Big 4 plus 2 129 Bilateral auricular chondritis 567t Bilateral carotid endarterectomy 460 Bilateral diffuse vocal fold 723 Bilateral laryngeal motor neuron control 90 Bilateral subepithelial fibrous masses 681f Bilateral thyroarytenoid muscles 529 Bilateral vocal cord paralysis 835 Bilateral vocal fold atrophy 638 Bilateral vocal fold immobility (BVFI) 821 Bilateral vocal fold paralysis 460, 512, 629 Bimodal jitter 271 Binary systems of grading dysplasia 917 Binocular vision 418 Biological dynamics of vocal fold injury 108 Biologic marker 506 Biologic scaffolds 108 Biomarker validation 993 Biomechanical effects of interventions 58 ideal larynx 59 Biomechanics and vocal fold structure 51 basic concepts 51 characteristics of different vocal fold layers 52 mass 51 stiffness 51 viscoelasticity 52 viscosity 52 Biomechanics of common disorders 56 benign mass lesion 57 Biomechanics of laryngeal injury 660 developmental influences 660 Biomechanics of vocal fold vibration 53 supraglottal restoring force 53 theories of vocal fold vibration 53 myoelastic–aerodynamic theory 53 Biopsy-proven benign thyroid nodules 142 Biopsy specimens 594 Bizarre configuration 268 Blast injuries 666 Blastomycosis 558 Blood-brain barrier 507 Blood-stream 544 Blood cells 236 Blood vessels 337

1018

Laryngology

Blunt injury 661 arytenoid injuries 661 clothesline, strangulation, and hyoid injuries 661 cricoid injuries 661 endolaryngeal and nerve injuries 662 thyroid cartilage injuries 661 Body-mass index 188 Body fatty mass 644 Body of the vocal fold 195 Bony skeletal parameters 25 Bordetella pertussis 603 Botulinum toxin 509, 514, 782 Botulinum toxin treatment 510 Botulinum toxin type A 710 Bovine collagen 371 Boxer’s training program 132 Bozzini’s lichtleiter 16f Brachial plexus neuropathy 822 Bradykinesia 507 Brainstem 643 Brainstem and midbrain systems 89 Brainstem nuclei 609 Brainstem reflex 609 Brain stimulation 615 Branchial arches 237 Branch manifestation 350 Breath control techniques 604 Breathy phonation 58 Breathy voice 519 Breathy voice quality 216 Broadcast video environment 292 Broadway singers 443 Bronchial anomalies 465 Bronchial arteries 587 Bronchial spurs 740 Bronchiectasis 604 Bronchogenic carcinoma 604 Bronchogenic tumors 604 Broyles’ tendon 30, 32 Broyles’ ligament 808, 933 Brünings needle 719 Brünings syringe 718f Buccopharyngeal fascia 592 Buckling of the lamina 26 Bulbar motor neurons 511

C C-fiber receptors 600f Cafe coronary 11 Calcic imaging 237 Calcium channel blockers 339t Calcium hydroxylapatite (CAHA) 797 Camera control unit (CCU) 291

Cantorial soloist 321 Cappella singer 321 Capsule of the cricothyroid joint 32 Carbon dioxide detection system 388t Carbon dioxide laser 417, 419, 710 Carcinoma in situ 911 Cardiac anomalies 631 Cardiac electrical instability 473 Cardiac rhythm 69 Cardiovascular activity 132 Cardiovascular apparatus 645 Care of the professional voice 443 additional examinations 451 patient history 443 commitments 445 environmental irritants 447 hormonal changes 448 importance 445 jaw joint 448 long-term goals 445 menopause 448 menstrual irregularity 448 particular stress 448 physical condition 446 trouble with bowels or belly 448 upcoming 445 vocal career 445 voice commitments 444 voice problem 444 voice quality 445 physical examination 449 general ear, nose, and throat examination 449 laryngeal examination 450 objective tests 450 Cartilage of the larynx 247f Cartilage thyroide 246f Cartilage window 779 Cartilage’s lamina 34 Cartilaginous adduction 74 Cartilaginous anterior rings 887 Cartilaginous defects 879 Cartilaginous rings 892 Cartilaginous structures 892 Cartilago arytenoidea 32f Cartilago corniculata 32f Castrato 655 Catastrophic failure 475 Cathode ray tube (CRT) 288 Caudal border of the basiocciput 6 Caudal oblique part 35 Causes of pediatric dysphonia 628t Caustic ingestion 590, 594 Cavernous hemangiomas 758 Cavitation 663

Cell membrane 263, 641 Cell surface receptors 641 Cement dust 906 Central dogma of molecular biology 100 Central nervous system control 89 cortical voice control 89 periaqueductal gray 90 Central nervous system neoplasm 446 Central nervous system pathology 461 Cepstral peak prominence (CPP) 159, 365 Cerebral electrophysiology 473 Cerebral palsy 123 Cerebral tissue 644 Cerebrospinal fluid (CSF) 507 Cerebrovascular event 636 Certified good manufacturing processes (CGMP) 350 Cervical and throat cancer 134 Cervical cytology 653 Cervical esophagus 587 Cervical lymphadenopathy 140 Cervical spine 236, 498 Cervical spine injuries 665 Cervical spine shadow 236 Cervical vertebrae 6, 24 Cervical vertebral body 25 Chaga’s disease 592 Channel of an endoscope 20 Chaos analyses 159 Chaos theory 473 Chaotic and near-chaotic phenomena 70 Chaotic oscillations 228 Chaotic systems 159 Characteristics of sounds 146 Charcot-Marie-Tooth disease 279, 512 Charge coupled device (CCD) 182 Chemical analogue of progesterone 342 Chemical keel 671 Chemoreception in the larynx 91 Chest voice 199 Chest X-ray 608 Chinese herbal therapy 115, 350, 501 Chloride ion 91 Chondroid tumor 860 Chondrosarcoma 462 Choral singer 321 Chromium ion 430 Chronic bronchitis 602, 608 Chronic cough 140, 461, 599 Chronic dysphonia 487 Chronic granulomatous disease 568 Chronic inflammation 461 Chronic inflammatory disease 58 Chronic laryngitis 341, 460, 466, 553 autoimmune laryngitis 558

Index rheumatoid arthritis 559 sarcoidosis 558 systemic lupus erythematosus 559 Wegener’s granulomatosis 558 direct irritation 553 allergy 556 inhalants 556 laryngopharyngeal reflux 554 vocal trauma 553 idiopathic 559 prolonged ulcerative laryngitis 559 infectious laryngitis 557 bacterial laryngitis 557 blastomyces dermatitidis 558 Candida albicans 557 Mycobacterium tuberculosis 558 Chronic laryngitis 589 Chronic obstructive pulmonary disease (COPD) 385, 614 Chronic refractory cough 617 Chronic rhinogenic laryngitis 604 Chronic vocal strain 449 Churg-Strauss syndrome 462 Cicatricial pemphigoid 462 Ciliated columnar epithelium 45 Cinefluoroscopy 596 Cineradiography of the vocal tract 235 Circumferential cartilage 880 Circumlaryngeal massage 357 Classic central fibrinoid necrosis 462 Classic parasympathetic paraganglion 766 Classification of laryngoplasty 777 classification 777 nomenclature 777 principles of different types of LPL 778 approximation LPL 778 expansion LPL 782 lateralization TPL 782 relaxation LPL 787 tensioning LPL 784 vocal fold myectomy 784 Classification of transoral laser microsurgery 931 early classification schemes 931 ELS classification for endoscopic supraglottic laryngectomy 934 ELS classification of endoscopic cordectomy 932 Clathrin-dependent endocytic mechanism 739 Cleveland Clinic data 133 Cleveland Clinic voice studio 116 Cleveland Clinic’s Arts and Medicine Institute 115

Clinical effects of stimulation of the parasympathetic system 336 Clinical effects of stimulation of the sympathetic system 336t Clinical effects of xerostomia 336t Clinical examination of vibration 209 interpretation of videostroboscopy 209 normal variations 209 Clinical myotonia 269 Clinical practice of laryngology 287 Clinical value of laryngeal electromyography 279 Closed phase 74 Closed quotient (CQ) 72 Clothesline injuries 661 CO2 laser 419 Cochlear function 473 Cocktail party effect 147 Cold intolerance 139 Cold knife excision 727 Cold turkey 130 Collagen fibers 636 Collagen fibrillogenesis 48 Collagen injection 372 Collagenous fibers 46, 50 Collagen vascular disorders 593 Collimation beam thickness 243 Common business internet connections 304 Common carotid artery 1007 Common mode rejection ratio (CMRR) 264 Communication disorders 161 Comorbid asthma 613 Compensatory dysphonia 320 Compensatory hypertrophy 636 Complementary and alternative medicines and voice 349 acupuncture 356 herbal therapy 350 allergies 354 inflammation 354 upper respiratory tract infection 354 hypnotherapy/ neuroimmunopsychology 357 neuromuscular therapy/massage 357 vitamins/minerals 356 Complementary and integrative medicine (CIM) 349 Complementary professional filters 113 Complex repetitive discharges 268 Computer-aided diagnosis (CADX) systems 306 Computer aided detection (CADE) 306

1019

Concentric needle electrode 266 Concurrent tracheitis 558 Conduit for breathing 773 Configuration of glottis closure 213 Confocal microscopy 1010 Congenital laryngeal cysts 629 Congenital myasthenic syndrome 822 Congenital stenoses 843 laryngeal 843 laryngeal webs 843 subglottic stenosis 844 tracheal 844 complete tracheal rings 844 Congenital structural anomalies of the vocal fold 468 Consensus Auditory-Perceptual Evaluation of Voice (CAPE-V) 155, 366, 625 Constrictor muscles 507 Contiguous musculature 9 Continuous wave 432 Contour of the skull base 24 Contralateral vocal cord 902 Contralateral vocal fold 774 Control of sound source quality 73 Control of vocal fold vibration 53 fundamental frequency 53 hydration 54 symmetry 54 vocal fold adduction 53 vocal fold contour 54 Conus elasticus 39 Conventional CT 241 Conventional CT scanners 242 Conventional esophagoscopy (CE) 588 Conventional light bulb 430 Cookie cutter 695 Corniculate tubercle 244f Coronavirus 545 COR pulmonale 385 Cortical bone marrow cavity 237 Cortical learned voluntary laryngeal control system 89 Corticobulbar pathway 89f, 90 Cortisol secretions 134 Cough-vomit syndrome 604 Cough 599 acute cough 603 causes 603 upper respiratory tract infections 603 chronic cough 604 upper airway cough syndrome 604 classification 599 differential diagnoses 602

1020

Laryngology

exclusionary diagnoses 602 angiotensin-converting enzyme (ACE) inhibitors 602 chronic bronchitis 602 history and physical examination 601 history taking 601 physical examination 601 pathophysiology 599 subacute cough 603 Cough reflex 599 Cover body theory 46 Cranial muscle 514 Cranial nerve nuclei 506 Craniofacial syndrome 465 Craniofacial trauma 665 Cricoarytenoid ankylosis 835 Cricoarytenoid joint (CAJ) 33, 569 Cricoarytenoid joint abnormalities 322t Cricoarytenoid joint arthritis 683 Cricoarytenoid joint axis 238 Cricoarytenoid muscle 59 Cricoid and arytenoid cartilages 32f Cricoid and thyroid cartilage 1011 Cricoid cartilages 26 Cricoid lamina 30, 35 Cricoids arch 30 Cricoid´s lamina 33 Cricopharyngeal bar 460 Cricopharyngeal myotomy 591 Cricopharyngeal sphincter 11 Cricopharyngeal web 978 Cricopharyngeus 590 Cricopharyngeus muscle 591 Cricopharyngeus muscle dysfunction 980f Cricothyroid (CT) muscle 35, 199, 272, 326, 784 Cricothyroid contraction 54, 205 Cricothyroid joint rotation 33 Cricothyroid joints 32, 33, 662 Cricothyroid membrane 238, 241, 522, 83, 25 Cricothyroid space 33 Cricothyroid subluxation 780, 785 Cricotracheal separation 821 Crista arcuata 32f Crohn’s disease 867 Crookes tube 235 Crucial peripheral components 4 CT scan for voice disorders 235 anatomy related to radiography 237 cartilages of the larynx 237 phylogenetically 237 soft tissues of the larynx 238 conventional and numerized radiology 236

computerized tomography scanning volumic (CT) scan 236 fluoroscopy—laryngography 237 magnetic resonance imaging (MRI) 236 positron emission tomography (PET) scan 237 xeroradiography 237 CT scan 239 acquisition 239 applications for acquisition 241 applications for reconstruction 241 basics of helical CT scan 239 contrast 241 pitch matrix field of view power supply 241 principles of the CT scan 241 reconstruction 240 slice thickness/collimation 241 dynamic aspects of the larynx 238 clinical and multimedia assessment of laryngeal diseases 239 history 235 kymography 235 tomography 235 X-ray 235 vocal scan 243 advantages of helical CT scan 243 limits of helical CT scan 244 reconstruction 243 Cuneiform tubercle 244f Current reflux treatment 124 Curved alligators 691 Cushing’s syndrome 343 Cutaneous hemangiomas 466 Cycle attractor 480 Cyclic adenosine monophosphate 654 Cyclosporine A (CSA) 1007 Cystic hygromas 466 Cyst removal 698

D Decannulation 824 Decreased amplitude 208 Dedo microlaryngoscope 417 Deep brain stimulation (DBS) Deep flexors 497 Deep lamina propria (DLP) 4 Deep layers of the lamina proria 415 Definitive management of laryngeal injuries 667 endoscopic interventions 667 endoscopic suturing 667 laser welding 668

tissue glues 668 transcutaneous laryngeal suture placement 668 external interventions 668 access 668 framework stabilization 670 hyoid fractures 670 tissue loss 670 keels and stents 671 keels 671 stents 671 medical interventions 672 antibiotics 672 antireflux medications 672 corticosteroids 672 rigid endoscopy 667 Degree of vocal fold adduction 53 Dehydroepiandrosterone (DHEA) 643 Delphian node 41 Denervation atrophy 832 Dental caries 336 Deoxyribonucleic acid (DNA) 100 Dermal fibroblasts 108 Developing a voice practice 997 extended health care team 1001 extended voice care team 1000 history 997 marketing and outreach 1001 practice environment 998 resources 998 training 997 voice team 999 Development of the human aerodigestive tract 7 Development of vocal fold mucosa 49 Development of vocal fold pathology 105 Diabetes mellitus 593 Diadochokinesis 183 Diagnosing acute laryngeal trauma 664 classification of fractures 665 concomitant/distracting injuries and timing of repair 665 pharyngoesophageal injury 666 imaging 664 management strategies 666 acute airway obstruction present 666 acute obstruction 667 signs and symptoms 664 visualizing the larynx 665 Diagnosis of dystonia 280 Diagnosis of reflux-induced cough 606 Dicom integration 302 Dietary reference intakes (DRI) 356 Diet therapy 655

Index Differences with loudness 201 Difficult intubation 387f Difficult supraglottic airway placement 387f Difficulty swallowing 463 Diffuse laryngeal edema 574f DiGeorge syndrome 468 Digestive tract 23 Digital imaging and communications in medicine (DICOM) standards board 292 Digital kymograph (DKG) 164 Dilated saccule 729 Dimensional analysis 480 Diphtheria 15, 134 Diplophonia 229 Diplopia 507 Directed energy voice treatment (DEVT) 324 Direct endoscopy 17 Direct laryngoscopy 187, 522 Direct measurements of voice assessment 163 high-speed imaging 164 videokymography 165 Disorders of muscle 514 inclusion body myositis 514 oculopharyngeal muscular dystrophy 514 Disorders of the neuromuscular junction 513 botulism 514 myasthenia gravis 513 organophosphate toxicity 514 Disorders related to aging 635 Dissection of polypoid 692f Distal-chip endoscopy 19 Distal-chip laryngoscope 183, 184 Distal end of the laryngoscope 182 Distal stump 528 Distant metastases 142 Domain of otolaryngology 507 Dopamine antagonists 511 Dorsal motor nucleus of the vagus (DMV) 93f Dorsal swallowing group (DSG) 93f Dynamical disorders of voice 472 Dynamical trajectory 479 Dysphagia 514, 566 Dysphagia in esophageal disorders 587 complications 596 esophageal disorders 590 acquired esophageal disorders 590 caustic ingestion 594 congenital esophageal disorders 590

eosinophilic esophagitis 593 esophageal diverticula 590 esophageal foreign body hernia 590 infectious esophagitis 594 inflammatory/infectious esophagitis 593 physiologic or motility disorders 592 esophageal neoplasm 594 Barrett’s esophagus and adenocarcinoma 594 benign esophageal neoplasm 595 surveillance in HNCA 595 evaluation 587 direct observation 588 indirect observation 588 physiologic studies 589 Dysphonia 119, 139, 319 Dysphonic voices 147, 148 Dysplastic keratotic epithelium 105 Dysplastic lesions 916 Dystonic tremor 508

E Edema of the vocal mucosa 650 Edge detection 164f EGG waveform 163 Eight endocrine glands 642 Elastic fibers 887 Elastic fibrocartilage 26 Elastin fibers 52 Electroglottography (EGG) 70 Electrokymography for heart 235 Electrolyte hydration viscocity 600f Electromyographic recordings 91 Electronic medical record (EMR) 134 Electronic stroboscope 194 Electrophoresis 507 Elevated residual les pressure 980f Elicitation of vocalization 90 Elite singers 329 Elongated larynx 7 Embryonic development 7 Emergency airway management protocols 673 Emotional vocalization 89 Endocrine disorders 124 Endocrine organs 643 Endolaryngeal mucous 163 Endolarynx 668 Endoluminal occlusion 888 Endoplasmic reticulum (RER) 48 Endorphin impairment 647

1021

Endoscopic camera 290 Endoscopic knot tying technique 669 Endoscopic laryngoscopy 650 Endoscopic laser supraglottic laryngectomy 908 Endoscopic postcricoid advancement flap 871 Endothelial glycocalyx 400 Endotracheal tube (ETT) 272, 394, 417, 810 Energy dissipation 436 Environmental hazards 123 Environment and allergies 533 Eosinophilic bronchitis 464 Eosinophilic cytoplasm 765 Eosinophilic esophagitis 467, 593 Epigastric pain 594 Epiglottic inversion 94 Epiglottic primordium 8 Epiglottic tip 8 Epiglottis 8 Epineurial anastomosis 528 Epithelial cordotomy 691 Epithelial lesion 322t Epithelial precursor lesions 906 Epstein-Barr virus 512, 608, 631 Esophageal-bronchial reflex 575, 606 Esophageal adenocarcinoma (EAC) 592 Esophageal atresia (EA) 590 Esophageal dead zone 978 Esophageal dilation 594, 588 Esophageal diverticula 590 Esophageal lumen 590 Esophageal motility disorder 592 Esophageal rings 590 Esophageal stricture 594 Esophageal swallowing disorder 977 Esophageal webs 590 Esophagopharyngeal reflux (EPR) 573 Esophagoscopy 588 Esophagram 977 Esoteric physics concept 429 Essential tremor 509 Estrogen 644 Etiologies of chronic laryngitis 553 Etiologies of dysphonia 463 Etiology of laryngeal stenosis 877 Evaluating the dynamics of a system 475 attractors 475 dimension 478 trajectories in state space 475 Evaluation of a vocalist 139 Evaluation of the stomach and the duodenum 977 Evaluation of voice disorders 624

1022

Laryngology

Examination of the thyroid gland 140 Excessive thyroid hormone replacement 342 Excisions of laryngeal masses 951 excisions in office-based surgery 951 biopsy/excision 951 medication and anesthesia 953 anesthesia-related risks, failures, and complications 955 anesthetizing the upper airway 954 intranasal anesthesia 954 intraoral anesthesia 954 medication 953 monitoring 953 verbal anesthesia 954 possible complications 957 setting 952 instrumentation 952 positioning 952 transnasal surgery 956 transoral surgery 955 palpation–biopsy–excision 955 Exophytic 687 Explant 1012 Export in an image archive 302 Extended hemilaryngectomy 925 Extensors of the neck 497 External beam radiation therapy 866 External laryngeal musculature 497 External media storage 294 External rectus 263 Extra-adrenal paraganglia 766 Extracapsular ligamental structures 32 Extracardiac rhabdomyomas 765 Extracellular matrix (ECM) 45, 99, 436 Extracellular matrix gene 436 Extracellular matrix in superficial layer of lamina propria 47 Extracellular space 567, 648 Extraesophageal reflux (EER) 573 Extralaryngeal malignancies 460, 616 Extrapyramidal disease 636 Extrathoracic trachea 887 Extrinsic compression 460 Extrinsic laryngeal muscles 509 Extrinsic laryngeal musculature 448 Extrinsic muscles 33 Eyelid ptosis 514

F Facial affect 507 Facies articularis thyroidea 32f Failure of mucosal wave propagation 208 Falsetto phonation 51

Falsetto voice 199 False vocal cord 710 False vocal fold 37, 200, 238, 417 Fast-spin echo techniques 237 Fatigue of the voice 444 Fatty tissue 237 Female hormonal effect of estrogens 649f Female hormonal effect of the EP 649f Female vocal folds 201 Female voice 645 Feminine voice 655 Fetal larynx 9 Fetal life 9 Fiber-based lasers 20 Fiber density 271 Fiberoptic scope 184 Fibrillar proteins 892 Fibroblasts in the lamina propria 48 Fibroelastic cartilage 30 Fibroepithelial polyp 16 Fibrotic lamina propria 593 Fibrous proteins 435 Fibrovascular deposit lesion 208 File transfer protocol (FTP) 295 Fine-needle aspiration 108 Fine-tuning a video image 298 First total human composite laryngeal transplant 1005 Fixation of the anterior commissure tendon (AC) 29f Fixed anterior commissure 35 Fixed glottis apertures 823 Flaccid fold 206 Flaccid vocal fold 51, 778 Flattened inspiratory 616 Flexible esophagoscopy 588 Flexible fiberoptic laryngoscope 509 Flexible fiberoptic nasopharyngolaryngoscopy (FFNPL) 859 Flexible fiber optic scope 290 Flexible laryngoscope 140, 182, 287 Flexible laryngoscopic guidance 522 Flexible laryngoscopy 140, 182, 183, 665, 911 advantages 184 disadvantages 184 equipment 182 technique 183 Flexible laryngoscopy technology 184 Flexible nasal fiberoptic endoscopy 879 Flexible rhinolaryngoscopy 709 Flexible tracheoscopy 140 Flexible vocal folds 81 Floppy vocal folds 204

Flow loop 616 Fluoroscopy 237 Follicle stimulating hormone (FSH) 641 Follicular neoplasm 142 Food and Drug Administration (FDA) 350 Food felons 133 Forehead musculature 963 Foreign body retrieval, tracheoesophageal puncture 976 Fourier transform 66, 365 Fourth of the big 4 plus 2 134 Fovea oblonga 32f Frame grabbers 298 Frank aspiration 514 Freon gas 123 Frequencies of the vocal fold vibrations 159 Frequency analysis 66 Frequency and amplitude modulation 203 Frequency quadruplets 472f Frontal operculum (FO) 89f Frontal view 236 Fuhrman’s modification of the Schaefer classification 665 Fulminant disease 548 Functional and perceptual voice 638 Functional dysphonia 487 Functional esophagoscopy 975 Functional voice disorders 632 Function of the laryngeal skeleton 759 Fundamental frequency 157 Fungal infection 322t

G G-amino-butyric acid 510 Gag reflex 182 Gait abnormalities 507 Galen’s anastomosis 40 Gallows system 417 Gantry angles 241 Garcia’s method of clinical laryngoscopy 16 Gardasil vaccine 739 Gastric acid 573, 649 Gastric acid reflux irritation 444 Gastric neoplasia 594 Gastric refluxate 575 Gastric stromal tumors 604 Gastroesophageal irritation 354 Gastroesophageal reflux disease (GERD) 320, 346, 463, 554, 590, 601, 601t, 606, 892 Gastrointestinal tract 599

Index Gastropharyngeal reflux (GPR) 573 Gender-related dimorphism 646 Gender differences 201 Gene-environment interaction 101 Gene expression 100, 104 Gene expression and abnormal vocal folds 104 Gene expression in animal models of vocal fold injury 105 Gene expression in vocal fold pathology 104 Generation of voice 773 Genes, proteins, and future therapy 107 Genes encoding cell 103 Genetic disorders 99, 459, 512 Genetic markers 142 Genetic mutation 142 Genetics and voice 99 Genome 641 Geriatric voice dysfunction 635 Gilles de la Tourette’s syndrome 511 Glandular cells 646, 653 Glandular epithelium 9, 644 Glandular secretions 644 Glee choir singer 321 Glidescope 400 Global impact of a voice disorder 174 Globus pharyngeus 554, 588 Globus sensation 723 Glomerulonephritis 558 Glomus tumors 766 Glossoepiglottic folds 30 Glossopiglottic valleculae 32 Glottal aerodynamics 472 Glottal airflow 72 Glottal area waveform (GAW) 164, 200 Glottal axis 165 Glottal closure 74, 366, 444 Glottal closure pattern 163 Glottal configuration 81, 203 Glottal cycle 72, 163, 165, 196, 203, 472f Glottal cycle periodicity 165 Glottal flow pulse 74 Glottal fry 200 Glottal gap 58, 778 Glottal incompetence 617 Glottal phonatory status 365 Glottal waveform 163 Glottic airway 773 Glottic closure 631 Glottic configuration 51, 774 Glottic function 1013 Glottic hyperfunction 488, 490 Glottic injury 734 Glottic insufficiency 57, 509

dehydration and edema 58 presbylaryngis 58 recurrent laryngeal nerve paralysis 57 vocal fold scar 58 Glottic involvement 879 Glottic space 236 Glottic webs 623 Glottis length 25 Glottographic waveform analysis 480 Goldenhar syndrome 391 Gold laser 20 Golgi apparatus (GA) 48 Golgi tendon organs 91 Gore-tex bolster 785 Gore-tex keel 671 Gospel singers 321 Granular cell layer 906 Granular cell myoblastoma 761 Granular cells 762 Granular cell tumor 762f Granulation tissue 824, 864 Granulomas of the larynx 682 Granulomata 573 Granulomatosis disease 879 Granulomatosis with polyangiitis (GPA) 877 Graphics interchange format (GIF) 298 Gray scale 159 Greater amplitude 202t Greater mucosal wave 202t Green’s description of direct laryngeal visualization 187 Green’s method 17 Grey-coded histograms of spectra 68f Grey-coded spectrum 69 Grillo stitch 884 Gross abnormal closure 206 Gross anatomy of the larynx 23 adult larynx 26 joints of the larynx 32 membranous structures and ligaments 30 skeletal framework 26 blood supply and venous drainage 40 developmental aspects 24 embryology 24 gender-related differences 26 infant larynx 25 laryngeal musculature 33 extrinsic muscles 34 intrinsic muscles 35 laryngeal spaces and areas 36 lymphatic drainage 40 motor and sensory innervation 39 phylogenetic aspects 23 Gross glottis closure 206

1023

Growth hormone 643 Guillain-Barré syndrome 512 Gynecologic cervical smears 644

H Haeckel’s biogenetic law 25 Half-moon-shaped resection 780 Hammer toe 512 Hard glottal attacks (HGA) 323 Harmonic-to-noise ratio (HNR) 159 Harmonic series 67 Harmonic structure 365 Havas rotatable malleable instruments 712f Head and neck paraganglioma 766 Head and neck squamous cell carcinoma (HNSCC) 462 Head register 199 Hearing loss 449 Heisenberg’s principle 69 Helical computer-assisted tomography 243 Helical CT scan of the larynx 241 Heller myotomy 592 Hemoptysis 466 Hemorrhagic mass 243 Hemorrhagic polyp 680 Hepatic growth factor 639 Hereditary motor and sensory neuropathy (HMSN) 512 High-quality periodic signal 159 High-resolution esophageal manometry (HRM) 980f High-resolution manometry 596 High-speed cinematography 193 High-speed video imaging 225 High-speed videolaryngoscopy 239 High-speed video use in functional and neurogenic dysphonia 231 High phonation 209 Hip joints 497 Histology of the larynx 4 History of condylomata 466 History of laryngology 15 Hl7 transport communication 302 Hoarse voice 775 Holinger’s classic studies 757 Holistic psychotherapy 115 Hollinger-type anterior commissure laryngoscope 417 Hollinger laryngoscope 407 Home grown solutions 299 Homo ancestors 13 Homogeneous leukoplakic lesions 906 Hong Kong flu 512

1024

Laryngology

Hooked wire electrodes 267, 278 Hooke’s law 52 Hopkins rod telescope 880 Hormone-gene journey 642 Hormone replacement therapy 655 Hormones and female voice 641 Hormone therapy 124 Horner syndrome 506 Hounsfield units 242f Household smoke 130 Human cancer pathway finder 105 Human cortical vocalization region 90 Human genome 107 Human immunodeficiency virus (HIV) 608 Human laryngeal transplantation 1005 Human larynx 7, 24, 773 Human larynx matrix 1011 Human papilloma virus (HPV) 462, 993 Human speech 24 Human thyroarytenoid muscle 5 Human vocal communication 24 Human vocal folds 436 HU scale 242 Hyaline cartilage 26, 1011 Hyaluronic acid gel 105, 371, 796 Hydroxylapatite (HA) 796 Hyoepiglottic ligament 37, 665 Hyoid bone 25, 34, 662 Hyperadducted group 488 Hyperextended neck 249 Hyperfunctional behavior 448 Hyperfunctional dysphonia 280 Hypertrophic scars 48 Hypertrophy of striated muscles 644 Hypochlorhydria 573 Hypodimensional dysfunction 480 Hypofunctional disorders 323 Hypoglossal nerve 836 Hypopharyngeal pouch 590 Hypopharyngeal tumors of the pyriform sinus 921 Hypothalamic-pituitary axis 649 Hypothalamo-hypophyseal axis 645 Hypothalamo-hypophyseal pituitary axis 644 Hypothalamus-pituitary axis 644

I Iatrogenic trauma 58 Iatrogenic vocal fold disorders 461 Iatrogenic vocal fold scar 800 Idiopathic demyelinating disorder 512 Idiopathic pulmonary fibrosis (IPF) 614 Idiopathic vocal fold paralysis 512

Image storage and retrieval 287 archival process 293 acquisition 294 network archive systems 294 components of image archiving 288 digital image display 292 digital imagery 289 medical cameras 290 medical digital video 293 medical image 289 video basics 291 compression 296 still image compression 297 video compression 296 frame grabbing technology 298 advanced archive features 301 archive access and review 299 archive management 299 archive recording features 299 digital imaging and communications in medicine 298 distributing the archive 300 integration 302 viewing imagery in the archive 300 future image archival technologies 303 advanced cloud archive systems 305 live telemedicine 304 pattern recognition 306 store and forward 304 telemedicine 303 three-dimensional recording and archive 306 video magnification 307 historical perspective 288 integration case study 307 Immature dendritic cells (IDC) 1011 Immobile left vocal fold 782 Immobile vocal fold 514 Immune-mediated destruction 506 Immune deficiencies 467 Immune function 99 Immune system components 565 Immune system disease 464 Immunomodulation 1010 Immunosuppression 1013 Immunosuppression in the cancer patient 1008 Immunosuppression reduction 1007 Impaired glottic function 426 Import imagery 301 Inclusion body myositis (IBM) 514 Incomplete glottic closure 698 Increased amplitude 202t

Indirect laryngoscopy 15 early development 15 Indirect laryngoscopy 181 Indirect measurements of voice assessment 156 acoustic analysis 156 basic recording requirements 157 fundamental frequency 157 intensity 158 nonlinear measures 159 perturbation measures 158 spectral-based measures 159 voice range profile 159 aerodynamic analysis 161 additionally derived measures 163 airflow 161 subglottal pressure 162 electroglottography 163 Infantile hemangiomas 466 Infant larynx 25 Infectious esophagitis 594 Inferior border of the cricoid 8 Inferior cerebellar artery 506 Inferior cornua 32 Inferior horns 29 Inferior thyroid arteries 887 Inferior tuberculum 274f Inflammatory exacerbation 878 Influence of nonlinearity 475 Infrahyoid strap muscles 34 Inhalation allergy 556 Inhaled corticosteroids (ICS) 614 Inner perichondrium 782 Insomnia scales 135 Intensity range of phonation 158 Interarytenoid mucosa 606 Interarytenoid muscle 91, 94, 274f Interarytenoid scar band 869 Interarytenoid synechia 835 Intercellular adhesion molecule 1 (ICAM-1) 354 Interference pattern 270 Intermediate lamina propria (ILP) 4 Internal blunt laryngeal trauma 549 Internal branch of the superior laryngeal nerve 93 Internal jugular vein 528, 1006 Internal laryngeal trauma 465 Internal larynx 862f Internal plica 4 International Association of Phonosurgery 777

Index Interpretation and synthesis of the voice disorder based on videostroboscopy 219 Interstitial fluids 263 Interstitial proteins 47 Interstitial tissues 651 Intra-articular steroids 570 Intra-arytenoid bar 709, 712 Intracellular compartment 263 Intracellular receptors 642 Intraoperative nerve monitoring (IONM) 280 Intraoral air pressures 365 Intrathoracic trachea 887 Intrathyroid cartilage 29 Intravenous contrast 243 Intrinsic and extrinsic muscle of the larynx 196 Intrinsic laryngeal muscle 272 Intrinsic laryngeal muscle fiber type 13 Intrinsic laryngeal muscles 35, 39, 320, 356, 831 Intrinsic larynx 33 Intrinsic muscles 4, 34 Invasive carcinoma 105, 907 Involuntary sounds 3 Ionized zinc 354 Irritable larynx 608 Isolated vibratory amplitude 219 Isopotential lines 270 Isshiki technique 253f

J Japanese Society of Logopedics and Phoniatrics 450 GRBAS scale 146 Jerusalem longevity studies 133 Jugular ganglia 94 Junction of the cerebrum 643

K Kaplan-Meier curves 130 Karaoke singer 321 Keratin cyst 701f Kerrison rongeur 808 Killian’s triangle 591 Kirstein’s laryngoscopy position 19f Kittner sponges 735 Klebsiella rhinoscleromatis 893 Kolmogorov entropy measures 159 Korsakoff–Wernicke’s syndrome 346 Kulchitsky cells 766 Kymography 235

L Lamina of the cricoid 30 Lamina propria 5, 46, 46f, 104, 122, 639 Lamina propria layer 681 Largest-caliber laryngoscope 417 Laryngeal-respiratory disorders 617 Laryngeal abnormalities 902 Laryngeal adductor reflex 93 Laryngeal adductor response 92 Laryngeal aditus 25 Laryngeal airway 23 Laryngeal allograft rejection 1010 Laryngeal amyloidosis 566 Laryngeal angioedema 125 Laryngeal biomechanics 777 Laryngeal burns 673 Laryngeal cancer 17, 20, 184, 915 Laryngeal cartilages 26, 625 Laryngeal cleft 464t, 623 Laryngeal closure 23 Laryngeal control 89 Laryngeal cortex 90 Laryngeal corticobulbar pathways 91 Laryngeal cysts 697 assessment of vocal function 698 classification and histology 697 diagnosis 698 incidence 697 pathogenesis 697 postoperative considerations 702 surgical management 698 preoperative considerations 698 surgical technique 699 Laryngeal descent 11 Laryngeal discomfort 367 Laryngeal disease 108, 239, 466 Laryngeal disorders 459 chief and/or secondary complaints 459 difficulty breathing 460 difficulty swallowing 460 etiologies of hoarseness difficulty swallowing, and difficulty breathing 460 hoarseness 459 cough 463 etiologies of chronic cough 463 etiology 459 incidence 459 prevalence 459 Laryngeal dystonia 280 Laryngeal electromyography (LEMG) 263, 450, 626, 773 basic components 267

1025

common abnormal EMG findings 268 insertional activity 267 recruitment 268 spontaneous activity 267 waveform morphology 267 basic neurophysiology 263 clinical applications 278 electrodiagnostic apparatus 264 interpretation 276 safety considerations 267 single-fiber EMG 270 Laryngeal electromyography (LEMG) testing 823 Laryngeal epithelium 555 Laryngeal framework 238 Laryngeal framework fractures 665 Laryngeal framework surgery (LFS) 59, 777 Laryngeal gargle 793, 963 Laryngeal granulomas 705 management 706 Laryngeal imaging 155 Laryngeal injury 461 Laryngeal innervation 39 Laryngeal leukoplakia 901 Laryngeal lumen 729 Laryngeal manual therapy (LMT) 501 Laryngeal mask ariway (LMA) 549 Laryngeal mass 239 Laryngeal masses and neoplasms 462 Laryngeal mechanoreceptors 91, 93f Laryngeal milieu 774 Laryngeal motion 505 Laryngeal motor neurons 93 Laryngeal mucosa 30, 93, 94, 437 Laryngeal mucus 645 Laryngeal muscles 90, 91, 263, 270 Laryngeal musculature 23, 24, 615 Laryngeal nerve 773 Laryngeal nerve reinnervation 631 Laryngeal papilloma 739 epidemiology 739 histopathology 740 presentation 742 transmission 740 treatment 743 adjuvant 746 follow-up 751 surgical 744 virology 739 Laryngeal papillomatosis 631, 766 Laryngeal pathology 113, 241, 961 Laryngeal posturing group 488 Laryngeal proprioception 89, 91

1026

Laryngology

Laryngeal reflexes 92 abductory laryngeal reflexes 92 combined abductory and adductory reflexes 94 Laryngeal reflexes 92t Laryngeal reinnervation 813 history 813 nerve transfer 813 indications/contraindications 814 published functional results 817 surgical procedure 815 Laryngeal rejection grade 1007 Laryngeal resistance 162, 613 Laryngeal schwannomas 762 Laryngeal sensation of airflow 94 Laryngeal sensory receptors 95 Laryngeal spasm 460, 604 Laryngeal squamous cell cancers 993 Laryngeal squamous cell carcinoma 101 Laryngeal stroboscopy 699 Laryngeal structures 25 Laryngeal surface 236 Laryngeal tissue 26, 72 Laryngeal transplantation 1005 Laryngeal transplant models 1008 Laryngeal trauma 659, 665, 778 epidemiology 659 historical considerations 659 blunt injuries 659 penetrating injury 660 war-related laryngeal injury 660 Laryngeal tremor 637 Laryngeal tuberculosis 558 Laryngeal valve system 509 Laryngeal ventricle 36 Laryngeal videostroboscopy 193 Laryngeal vocal folds 3 Laryngocele 236, 729 Laryngomalacia 25 Laryngopathia gravidarum 655 Laryngopharyngeal biopsies 19 Laryngopharyngeal diseases 19 Laryngopharyngeal reflux (LPR) 123, 184, 320, 336, 463, 464, 550, 554f, 554, 573, 617 airway manifestations of extraesophageal reflux 577 laryngotracheal stenosis 577 components of gastric 573 conservative therapy 582 H2 receptor antagonists 582 lifestyle modifications 582 medical treatment 582 proton pump inhibitors 582

surgical management of reflux 583 differences between LPR and GERD 575 pathophysiology 575 prevalence and role of laryngopharyngeal reflux in laryngeal cancer 577 diagnosis 578 quality of life instrument 579 esophagoscopy 579 laryngopharyngoscopy 579 radiologic imaging 581 reflux detection 579 reflux 573 pathological manifestations of refluxate 573 role of nonacid and weakly acid reflux in laryngeal inflammation and disease 575 tissue and fluids assay 581 treatment 581 modifiable risk factors 582 Laryngopharyngeal reflux disease (LPRD) 95, 120, 139, 141, 683, 726, 902 Laryngopharynx 555 Laryngoplasty (LPL) 777 Laryngopyoceles 730 Laryngoscope removal 188 Laryngotracheal airway 188 Laryngotracheal groove 24 Laryngotracheal injury 664 Laryngotracheal mucosa 947 Laryngotracheal reconstruction 670, 1011 Laryngotracheal stenosis 888 Laryngotracheitis 466 Laryngovideostroboscopy 193 Larynx 4 Larynx of air-breathing 23 Larynx of human infants 10 Larynx’s behavior 479 Laser fiber 964 Laser physics and principles 429 laser properties 430 modes of operation 432 principles of operation 430 Lateral border of the saccule 37 Lateral cricoarytenoid muscle (LCA) 521, 528, 826 Lateral cricoarytenoid muscle, closure of the posterior part of the glottis 779 Lateral cricoarytenoid muscle 30, 274f, 710, 780 Lateral food channels 5 Lateral glossoepiglottic folds 32 Lateral pharyngeal wall 32

Lateral pharyngotomy 762 Lateral plane 236 Lateral vibratory amplitude 196 Laver’s voice profile analysis 146 Lee Silverman voice treatment (LSVT) 507 Left subclavian artery 590 Legato phrase 325 Leukoplakia, erythroplakia 916 Leukoplakia 109 epidemiology 905 etiology 905 evaluation 109 biopsy technique 904 leukoplakia reclassified without biopsy 902 leukoplakia warranting biopsy 902 presenting symptoms 109 management 908 pathologic classification 906 gross morphology (appearance) 906 histopathology 906 prognosis 908 Levator scapulae 499 Level of the basioccipital bone 8 Lichtenberger needle driver 862 Lidocaine 20 Limb muscles 91 Limb muscle weakness 514 Linear system 474f Lip flutter with voicing co-ordination 325 Lipoprotein envelope 739 Liquid chromatography-mass spectrometry 102f Liquid crystal display (LCD) 289f, 292 Ljubljana classification 907 Loft register 199 Lombard effect 122 Longer closed phase 202t Longitudinal esophageal fibers 30 Longitudinal joint axis 33 Long papillae 593 Longus colli 499 Loud phonation 202, 209 Low-density lipoprotein (LDL) cholesterol 133 Low-grade dysplasia 595 Low-grade perichondritis 710 Lower esophageal sphincter (LES) 606, 980f Lower fibers of the trapezius 503 Lower lip of the vocal fold 199 Lower mean phonatory airflow 162 Lower motor neuron and laryngeal nerve disorders 278 Lower motor neuron disease 636

Index Lower motor neurons (LMNs) 263 Lower respiratory tracts 9 Low phonation 209 Ludwig’s angina 393 Lugol’s solution 902 Lumbar vertebrae 499 Luminal stenting 670 Lung hyperinflation 614 Lung pressure 474f Lung volume 474f Lupus erythematosus 608 Luteinizing hormone (LH) 641 Lyme disease 631 Lymphatic drainage 24 Lymphoid hyperplasia 602 Lymph vessels 887 Lynch suspension laryngoscope 18 Lynch’s work 665

M Macintosh and Miller laryngoscopes 388 Macula flava 49 Magnifying rigid telescopes 195 Mainstem bronchus 978 Male larynx 201 Male voice 655 Malignant transformation 762 Mallampati index 188 Mammalian larynx 26 Management of laryngopyoceles 735 Management protocols for voice rehabilitation 315 Managing glottic stenosis 859 history and physical examination 859 imaging studies 860 laryngeal electromyography 860 pulmonary function tests 860 Managing stress 134 Manofluorography 591 Manometric data 592 Manubrium sterni 34 Manuel Garcia’s description of the awake larynx 181 Massachusetts Institute of Technology 988 Massage therapy 115 Mass excision 59 injection laryngoplasty 60 medialization thyroplasty and arytenoid adduction 59 photoangiolytic laser ablation of Reinke’s edema 59 polyp removal 59 voice rest and therapy 60 Mass lesions 195, 230

Mast cells 537 Material of the vocal fold 204 Mathematical algorithms 292 Matrix metalloproteinases (MMPs) 105, 639 Mature scar 878 Maxillofacial trauma 391 Maximal expiratory pressure 615 Maximal inspiratory pressure 615 Maximal voluntary ventilation 615 Maximum flow declination rate (MFDR) 72, 163 Maximum phonation time (MPT) 162, 174, 365, 625 McAdams criteria 567 McCaffrey system 889 Mean phonatory airflow (MPA) 162 Mean sagittal diameter of the cricoids arch 30 Measurement of the strength of sound 64 Measurements of voice quality 169 Measuring quality of life 170 Mechanical laryngitis 543 Mechanical oscillator 63 Mechanical stimuli 600f Mechanical stroboscopy units 193 Mechanical ventilation 569 Mechanical voice disorder 490 Mechanoreceptor sensitivity 617 Media annotation 301f Medial head of the gastrocnemius 263 Medialization laryngoplasty 805 etiology 805 surgical technique 806 anesthesia 807 setup 807 special equipment 807 treatment 805 Medialization of the ventricular fold 779 Medialization of the vocal fold 779 Medialization thyroplasty 59 Medialization TPL 778 Medial microflap technique 420 Median glossoepiglottic fold 244f Median sagittal diameter 27f Median sagittal line 27f Mediastinal trachea 887 Medical applications of X-rays 235 Medical expenditure panel survey 349 Medical therapy, medication and the voice 335 anticoagulants and antiplatelet medications 340 corticosteroids 343

1027

inhaled steroids 343 general observations 335 hormone replacement therapy 342 androgen therapy 343 oral contraceptives 343 peri/postmenopausal hormone replacement therapy 342 thyroid replacement hormone 342 psychoactive drugs 344 proton pump inhibitors 346 receptor antagonists 346 specific drug groupings 336 antihistamines 336 antihypertensives 339 antitussives 338 sympathomimetics 337 Meissner’s plexus 587 Membrane receptors 641 Membranous vocal fold 82, 195, 631 Menopausal voice syndrome 652 clinical signs 653 sex hormone medication and voice disorders 655 treatment 655 Menstrual cycle 124 Menstrual-like cycle 644 Mesenchymal components 760 Metallic stents 895 Meteorological factors 533 Methylenedioxypyrovalerone 338 Methylprednisolone 800 Methylprednisolone acetate 895 Microalligator forceps 862 Microanatomy of the vocal folds 45 Microcurved scissors 690 Microflap techniques 726 Microlaryngeal tubes (MLTS) 386 Micromanipulator 18 Microsoft Windows media format (WMV) 296 Microsurgical scissors 691 Midmembranous vocal fold area 59, 198, 687 Miemembranous vocal fold lesions 680 Mild dysplasia 907 Mild squamous dysplasia 909 Millar pressure transducer 83 Minilarynx 26 Minimal edema 439 Minimal subglottic pressure 203 Minor vocal fold injury 663 Mirror exam 140 Mirror image 212 Mirror laryngoscopy 16, 181 advantages 182

1028

Laryngology

disadvantages 182 equipment 181 technique 181 Mitomycin-C 881 MIT Technology Review 987 Mixed leukoerythroplakia 916 Mobile cricoarytenoid joint 780 Mobile vocal folds 664 Mobius syndrome 822 Modal phonation 209 Modal register 198 Modal voice 199 Model of phonation 474f Moderate dysplasia 907 Moderate squamous dysplasia 909 Modern-day reinnervation technique 814f Modern Singing Handicap Index (MSHI) 314 Molecular biology techniques 100 Mongolian gazelle 7 Monopolar electrodes 272 Monozygotic twins 103 Montgomery prosthesis 806 Montgomery T-tube 895 Motivating and sustaining behavior change 135 Motivational speakers 139 Motor axons 263 Motor cortex 90 Motor neuron disease 636 Motor neuron disorders 511 amyotrophic lateral sclerosis 511 poliomyelitis and postpolio syndrome 511 Motor unit contract 270 Mouse transplantation model 1010 MRNA via the transcription factor 642 Mucopurulent secretions 605 Mucosa dryness 536 Mucosal hygiene 221t Mucosal injury 877 Mucosal irritants 447 Mucosal tear 438 Mucosal wave 198, 202 Mucosal wave propagation 201 Mucus plugs 546 Mucus viscosity 320 Multidisciplinary evaluation and voice lab 113 beyond traditional clinic boundaries 114 beyond traditional lab boundaries 116 evaluation format 114 model of care 113

Multiple neurologic abnormalities 519 Multiple sclerosis (MS) 123, 461, 446, 636 Multiple system atrophy (MSA) 508 Muscle crico-thyroid 246f Muscle disorders 459 Muscle fibers 266 Muscle issues 319 Muscle motor unit 270 Muscle spindles 91 Muscle tension dysphonia (MTD) 163, 320, 488, 499, 519, 613, 616, 632 Muscle thyrohyoid 246f Muscular process (MP) 29f Muscular tension dysphonia 174 Musculature 131 Musculoskeletal tension dysphonia 490 Mushroom portion 355 Musical notes 147 Myasthenia gravis 123, 270, 444 Mycobacterium avium intracellulare (MAI) 594 Myelin 506 Myer-Cotton system 879 Myoelastic–aerodynamic theory 53, 72 Myofascial structures 499 Myofibrillar adenosine triphosphatase 264 Myopathic disorders 281 Myotonic dystrophy 269 Myotonic potentials 269 Myxedema 593

N Narrow band imaging (NBI) 184, 902 Nasal anesthetic 963 Nasal cavity 125 Nascent units 268 Nasogastric tube 92 Nasopharyngeal 398 National Association of Teachers of Singing (NATS) 1000 National Center for Voice and Speech (NCVS) 157 National Electrical Manufacturers Association (NEMA) 298 National Health and Nutrition Examination Survey Studies 131 National Trauma Data Bank (NTDB) 659 Navigator software package 248 Near-total laryngectomy 926 Neck and cervical spine 499 Neck and jaw injuries 124

Neck dissection 142 Nerve anastomoses 1006 Nerve fibers 761 Nerve healing 773 Nerve impulse 270 Nerve muscle pedicle 832, 833 Nerve–muscle pedicle technique of tucker 833 Neurogenic cough 601t, 608 Neurogenic dysfunction of the larynx 487 Neurolaryngological pathology 450 Neurolaryngologic diseases 20 Neurolaryngology diseases 636 Neuroleptic malignant syndrome 345 Neurolinguistic programming (NLP) 358 Neurological disease 123, 161, 506 Neurologic disorders of the voice 505 movement disorders 507 multiple system atrophy 508 parkinsonism 507 multiple sclerosis 506 neurolaryngologic evaluation 505 stroke 506 Neuromuscular degeneration 615 Neuromuscular disorders 615 Neuromuscular therapy (NMT) 357 Neuropsychiatric disease 609 New and emerging technology 985 ambulatory monitoring 987 bioinformatics 985 genetics-based technology 992 optical coherence tomography 989 optics 988 regenerative medicine 991 robotics 986 tissue engineering 991 Nitrous oxide (N2o) 386 Nodose ganglia project 94 Nodose ganglion (NG) 93f Nodular diathesis 221t Nodular diathesis configuration 215 Nodular lesions 906 Nodules, polyps 320 Noise-to-harmonic ratio (NHR) 364 Noise energy 159 Nomenclature of laryngeal lesions 679 miscellaneous lesions 682 laryngeal granulomas 682 rheumatologic disease-related lesions 683 vocal fold lesions 679 epithelial lesions 679 lesions of the lamina propria 680 Reinke’s edema 682

Index vascular lesions 682 Non-alergic rhinitis 600f Non-Hodgkin’s lymphoma 594 Non-neoplastic vocal fold lesions 370 Non-postinfectious cough 601t Nonacidic reflux 555 Nonasthmatic eosinophilic bronchitis (NAEB) 463, 601t, 604 Nonasthmatic inflammatory airway disease in adults 608 Nondysplastic keratotic epithelium 105 Nonerosive inflammatory polyarthritis 567t Nonhomogeneous leukoplakic lesions 906 Nonkeratinized stratified squamous 30 Nonlinear dynamics theory 473 Nonlinear system 474f Nonneoplastic lesions 757 Nonrheumatologic disorders 593 Nonselective reinnervation 832 Nonvibrating segment of the vocal fold 219 Nonvibration portion 210t Noon unit 537 Normal aging 635 Normal biologic function 104 Normal chest radiograph 601 Normal human voice 195 Normal larynx 921f Normal phonation 84 Normal vocal fold 104, 195, 219 Normal voice 312 Nose and laser energy 20 Nose disorders 535t Nuclear magnetic resonance (NMR) 993 Nuclear pyknosis 644 Nuclear receptors 641 Nucleus ambiguous 90, 520 Nucleus retroambiguus (NRA) 89f Nucleus tractus solitarius (NTS) 93f Number 2 of the big 4 plus 2 131 Nutrition 133 Nutritional deficiencies 906 Nyquist frequency 64

O Obese man 653 Obese menopausal woman 654 Oblique belly of the cricothyroid muscles 785 Oblique line 29f Oblong fovea 30 Obstructive sleep apnea (OSA) 16, 385 Ocular inflammation 567t Oculopharyngeal dystrophy 514

Odynophagia 544 Oertel’s laryngostroboscope 17f Office-based endoscopic procedures 998 Office-based esophagology 971 anatomy and physiology 972 clinical presentation 972 esophageal manometry 978 esophagram 977 transnasal esophagoscopy 973 Office-based interventions 976 Office-based laryngeal laser surgery 959 advantages 961 history 959 laryngotracheal stenosis 967 laser background 959 ablative lasers 960 photoangiolytic lasers 960 patient selection and preparation 961 anesthesia 963 contraindications 962 instrumentation and equipment 962 laser precautions 962 patient preparation 962 postoperative care and outcomes 965 complications 967 outcomes 967 postoperative care and follow-up 965 specific applications 961 surgical technique 963 Office-based laryngeal surgery 19 Office-based laryngology 19 Office-based laser laryngeal surgery 20 Office-based vocal cord injections 19 Olfactory stimulation 92 Omohyoid muscle 528 Oncocytic adenomatous hyperplasia 760 Oncocytic cysts 760 Oncocytic cysts of the larynx 760 Opaque spheroid 697 Open quotient (OQ) 72, 164 Operative equipment 998 Optical coherence tomography (OCT) 988 Optical illusion 196 Oral axis 188 Oral cavity 125 Oral infections 336 Oral mucositis 336 Organic dysfunction of the vocal folds 219 Organ of voice 15 Oropharyngeal squamous cell carcinoma 462 Oropharynx 125 Oscillating frequency 196 Oscillating source 196

1029

Oscillating vocal folds 81 Oscillatory motion of the palate 509 Oscillatory path 436 Ossified cartilage 237 Ossoff-Pilling scope 417 Ossoff-Pilling laryngoscope 407 Otolaryngic evaluation of a vocalist 139 Otolaryngologic pharmacopeia 510 Ovarian hormone 649 Ovoid stent 861 Oxyhemoglobin molecules 419 Oxymetazoline 337 Oxyphilic adenoma 760 Ozone depletion 533

P Palatopharyngeal sphincter muscle 7 Panels of molecular 142 Papilloma parallel 423 Paradoxical vocal fold motion (PVFM) 465, 604, 632 Paradoxical vocal fold movement disorder 616 Paraglottic space 39, 238 Parallel beam of radiation 429 Paralyzed vocal fold 813 Paraneoplastic syndrome 592 Parathyroid glands 643 Paresthesias 507 Parkinson hypophonia 507 Parkinsonian tremor 507 Parkinson’s disease (PD) 123, 446, 461, 506, 615, 636, 822 Partial cordectomy 874, 931 Parts of the glottis 38f Patent ductus arteriosus (PDA) 631 Pathological changes in vocal fold vibration 203 mass effect 203 problems of glottal closure and competence 206 tension 204 Pathological phonation 465 Patient-Reported Outcomes Measures (PROMS) 169 Patient self-evaluation measures 155 Pediatric acoustic values 624 Pediatric endoscopic arytenoidectomy 874 Pediatric laryngeal trauma 672 Pediatric laryngology 464 chronic cough and reflux 467 congenital and genetic anomalies 468 difficulty breathing and stridor 465

1030

Laryngology

overview and impact 465 difficulty swallowing 468 overview and impact 468 dysphonia 465 overview and impact 465 specific etiologies of difficulty breathing or dysphonia 465 benign lesions and tumors of the larynx 466 infection 466 other causes of acute and chronic laryngitis 467 recurrent respiratory papillomatosis 466 vocal fold dysfunction 465 specific extralaryngeal etiologies of chronic cough and reflux 467 eosinophilic esophagitis 467 systemic disease 467 Pediatric larynx 26 Pediatric tracheotomies 465 Pediatric vocal cord paralysis 625 Pediatric vocal fold paralysis 629 Pediatric Voice-Related Quality of Life (PVRQOL) 172t Pediatric voice disorders 623 differential diagnoses 626 evaluation of children with dysphonia 624 acoustic and aerodynamic analysis 625 adjuvant testing 626 laryngeal visualization and imaging 625 perceptual analysis 624 quality-of-life measures 626 management and treatment 626 treatment algorithms 628 congenital and acquired cysts 629 functional voice disorders 632 laryngeal papillomatosis 631 postlaryngotracheal reconstruction 632 reflux laryngitis 629 vascular anomalies 629 vocal fold paralysis 629 vocal nodules and masses 628 voice disorders on children 623 normal pediatric speech and voice 624 Pediatric Voice Handicap Index (pVHI) 172t, 314 Pediatric Voice Outcomes Survey (PVOS) 175, 172t, 626

Pedunculated morphology 687 Pedunculated polyps 423 Penetrating trauma 662 iatrogenic laryngeal trauma 663 Pepsin 573 Pepsin assay 709 Perception of voice 145 dimensions 146 loudness 148 pitch 147 quality 149 future directions 151 historical perspective 145 Perceptual analysis 624 Perceptual assessment of voice quality 155 Perceptual voice evaluation 114 Periaqueductal gray 90, 520 Periodicity 69 Periodic oscillation 70, 164f Periodic phonation 55f Peripheral nerve disorders 511 Guillain-Barré syndrome 512 hereditary motor and sensory neuropathy 512 idiopathic vagal or recurrent laryngeal nerve neuropathy 511 Peripheral nervous systems 4 Peripheral neuromotor control of the larynx 10 Peripheral neuropathy 459 Peroneal muscular atrophy 512 Perturbation measures 158 Pertussis 134 Pes cavus 512 Petiole of the epiglottis 774 Pharyngeal airways 188 Pharyngeal axis 188 Pharyngeal mucosal perfusion pressure 549 Pharyngeal pouch 460 Pharyngeal stenosis 460 Pharyngeal web 460 Pharyngocutaneous fistula 588 Pharyngoesophageal segment (PES) 587 Pharyngolaryngography 237 Phase of vibration 210t Phenylpropanolamine 338 Phonation range 54 Phonation resistance training exercise 638 Phonation threshold pressure (PTP) 162 Phonation threshold pressure and phonation instability pressure 55 aerodynamic assessment 56

effect of pathology on phonation range 55 Phonatory apparatus 509 Phonatory organ 505 Phonatory vibration 94 Phonetogram 55 Phoniatrical voice group 538 Phonomicrosurgery 375 perioperative management 379 adjunct medications 380 airway management 379 anesthetic considerations 379 antibiotics 380 antivirals 381 coordination with operating room staff 380 gentle emergence 380 laryngotracheal anesthesia 381 paralysis 380 reflux management 381 steroids 380 tube selection 379 postoperative management 381 follow-up 382 immediate postoperative period 381 return to clinic 382 voice rest 381 preoperative management 375 medical management 375 voice therapy 377 risks of surgery 378 counseling 378 exams/recordings 379 medicolegal considerations 379 minimizing risks 378 Phonomicrosurgery setup and instrumentation 403 anesthesia 404 difficult laryngeal exposure 407 operating chair and operating room setup 409 optics and visualization 410 microscope 410 optical telescope 410 patient history and examination 403 patient positioning and laryngeal exposure 405 safety 408 tissue dissection 410 instrumentation 412 laser versus cold instruments 410 Phonosurgical Committee of the European Laryngological Society 777 Phonosurgical instrumentation 187 Phonotrauma 320

Index Phonotraumatic behavior 158 Phonovibrogram (PVG) 164 Photoangiolytic ablation 59 Photoangiolytic lasers 727 Photodynamic therapy (PDT) 431 Photonic emission 235 Phrenic nerve 832, 1012 Phrenic nerve graft 834 Physical activity 131 Physiological role of spindles 91 Physiological test 91 Physiological voice treatment approach 315 Physiology of normal vocal fold vibration 195 Physiology of phonation 435, 777 Physiology of the vocal folds 17 Pierre-Robin sequence 391 Pineal gland 643 Pinna and ear canal 146 Piriform sinus 29f, 30, 417 Pitch chroma 147 Pitch distortion 449 Pitch perturbation quotient 158 Pixel ratios for video 296 Plane of dissection 420 Plaque cricoid 246f Plaque rupture 130 Plastic grocery bag 132 Platysma muscles 263 Pleomorphic adenoma 760 Plethora of algorithms 158 Pneumonia 134 Poincaré section 70 Polycyclic aromatic hydrocarbons 906 Polypoid 726 Polypoid corditis 723 Polypoid degeneration 723 Polyvinyl chloride (PVC) 386 Pons and brainstem regions 90 Poor volume 775 Portable archive solutions 294 Portion size and food choices 133 Post-tracheostomy tracheal stenosis (PTTS) 891 Post-tracheotomy 251f Posterior commissural interarytenoid stenosis 879 Posterior commissure hypertrophy 575f Posterior cricoarytenoid (PCA) muscle 273, 274f, 524, 813, 826, 834f, 1012 Posterior end of the thyroid cartilage 27f Posterior glottal chink 201, 209 Posterior glottic stenosis 865 classification 867

etiology 866 arthritis of cricoarytenoid joint 867 endolaryngeal surgery 866 ET intubation 866 external laryngeal trauma 866 gastropharyngeal reflux disease 867 neoplasms 867 radiation therapy 866 operative evaluation 867 presentation 865 treatment 868 alternative approaches 873 choice of surgical approach for PGS 874 endoscopic surgery 869 history 869 indications for surgical intervention 869 medical treatment 868 open surgery 873 other sites of stenosis 874 special considerations 874 treatment of pediatric PGS 873 Posterior glottic stenosis 821, 884 Posterior glottis 37, 45 Posterior lamina 882 Posterior membranous 882 Posterior superior temporal gyrus (PSTG) 89f Posterior trachealis muscle 880 Posterior wall of the glottis 30 Posterior wall of the trachea 887 Postinfectious cough 601t Postintubation dysphonia 549 Postlaryngeal mucosal surgery 439f Postnonlaryngeal surgery 439f Postnasal drip (PND) 463 Postoperative vocal therapy 143 Postphonation whispers 83 Postpolio syndrome 511 Postsynaptic acetylcholine receptors 636 Posttransplant lymphoproliferative disorders 1008 Postural reflexes 507 Posture and muscle tension 497 assessment by the clinician 501 laryngeal manual therapy 503 phonation and pain 501 physiotherapeutic intervention, acute 502 posture-related voice disorders 500 treatment 501 vocal efficiency 497 Potassium-titanylphosphate 960t

1031

Potassium-titanylphosphate (KTP) laser 59, 591 Potent proton pump inhibitors (PPIS) 346 Pousielle’s law 869 Pre-epiglottic adipose tissue 30 Pre-epiglottic space 39, 922 Pre-menstrual voice syndrome (PMVS) 646 Pre-appointment questionnaires 119 Prefabricated titanium plates 782 Premalignant (dysplasia) 906 Premalignant and early malignant lesions of the larynx 915 development of centers of excellence 926 dysplasia 916 development/inciting factors 919 diagnosis 919 genetics 917 management 919 pathology 917 early glottic cancer 920 anatomic considerations of disease management 921 genetics and pathologic variants 920 management 923 staging 922 mimicry 915 surgery 923 chemotherapy and biological therapy 926 lasers 924 partial laryngectomies 925 radiation therapy 926 transoral 923 Premenopausal female 652 Premenopausal symptoms 652 Premenstrual dysphonia 650 Premenstrual voice syndrome 646 physiological and anatomical signs 650 timing of phonosurgery in women 652 treatment 651 Premenstrual voice syndrome 648 Prephonatory glottis 74 Presbylaryngis 58, 635 Presumed psychogenic aphonia 618 Prevention and management of laser airway fires 396t Primary motor strip 90 Primary muscular imbalances 500 Principle of stroboscopy 164 Principles of phonomicrosurgery 415 exposure and endoscopes 417 instrumentation 418

1032

Laryngology

lateral microflap technique 422 postoperative management 424 preoperative management 416 techniques of microdissection with laser intsrumentation 423 ablation 423 dissection 423 truncation 423 techniques of microdissection with nonlaser intsrumentation 420 medial microflap 420 Principles of voice therapy 311 goal setting 316 normal and abnormal voice 312 pretreatment 313 principles of treatment 314 Professional singer 321 Professional voice 372 Progesterone 644 Prolonged ulcerative laryngitis (PUL) 559 Protein expression data 108 Proteomics 101 Protocol of acquisition 241 Protonic imaging 236 Proton pump inhibitors (PPIS) 545, 593, 672 Proximal cut adductor branch 834 Pseudobulbar palsy 123 Pseudoephedrine 337 Pseudoephedrine amphetamine 338 Pseudoepitheliomatous hyperplasia 762 Pseudoepitheliomatous hyperplasia of the mucosa 762 Pseudosulcus 554 Pseudosulcus vocalis 573, 574f, 720 Psychoacoustic perspective 145 Psychoacoustic sensation 66 Psychogenic dysphonia 122 Psychogenic voice disorders 357 Psychosocial traits 709 Psychotropic medications 449 Puberty 644 Pulmonary disease 459, 467, 879 Pulmonary embolism 342 Pulmonary function tests 823 Pulmonology medicine 599 Pulsed-potassium-titanyl phosphate 568 Pulsed dye laser (PDL) 419, 920, 960t Pulsed laser 433 Pyogenic granulomas 705 Pyriform sinus 732

Q Quadrangular membrane 32, 35, 37 Quadrilateral hyaline alae 29 Quality of computer monitors 292 Quality of fiberoptic imaging 792 Quality of life and patient-reported outcomes 169 Quality of life measurement instruments 170 Quality of tobacco 905 Quantifying voice impairment 451 Quantitative acoustic analysis 998 Quantitative analysis of laryngeal imaging techniques 156 Quantitative assessment of laryngeal function 279 Quasiperiodic portion of the voice 196 Quasiperiodic vibration 197 Quasiperiodic vocal fold 196 Quiet whisper 437

R Rabbit vocal fold fibroblasts 425 Radiation therapy 161 Radiesse voice gel 797 Radioactive gold grain implants 758 Radioactive iodine (RAI) 142 Radiofluorography 591 Radiographic appearance of lung disease 601t Rainbow passage 158 Rate quotient 165 Rat thyroarytenoid muscle 101 Real vocal tract 474f Recommended dietary allowances (RDA) 356 Rectangular zone 482 Recurrent inflammatory episodes 567 Recurrent laryngeal nerve (RLN) 93f, 143, 519, 636, 774, 766 Recurrent respiratory papillomatosis (RRP) 462, 623, 631, 739, 757, 800, 866 Reduction of abductor spasm 524 Reflexive cough 89 Reflux-induced pharyngolaryngitis 709 Reflux disease 901 Reflux episodes 606 Reflux esophagitis 593 Reflux finding score (RFS) 554 Reflux laryngitis 122 Reflux of bile 574 Reflux severity index 120

Reflux symptom index 554 Reflux testing 124 Register of phonation 199 Regular vocal fold oscillation 210 Reiki therapy 115 Reinke’s edema (RE) 47, 59, 157, 203, 377, 462, 682, 723, 727, clinical presentation 723 pathophysiology 723 treatment 725 Reinke’s polyposis 556 Reinke’s potential space 723 Reinke’s space 45, 125, 651, 933 Reinnervation for bilateral vocal fold paralysis 831 in children 838 nerve–muscle pedicle with the ansa hypoglossi 832 results 833 technique 832 selective reinnervation using the phrenic nerve 834 indication 835 results 837 technique 835 Reinnervation research in laryngeal transplantation 1011 Reiter’s syndrome 867 Relapsing polychondritis (RP) 460, 567, 892 Relaxation of smooth muscle 592 Renal disease 878 Reports in an image archive 301 Resonance/articulatory subsystem 319 Resonant voice therapy 315 Respiratory-laryngeal system 613 Respiratory apnea 93 Respiratory distress 629 Respiratory dystonia 609 Respiratory problems 447 Respiratory syncytial virus 603 Retinoblastoma tumor suppressors 740 Retrocricoid tunnel 836 Rheological properties 472 Rhesus monkey 90 Rheumatoid arthritis (RA) 124, 568, 464, 608 Rheumatoid nodules 462 Rhinosinusitis 599 Rib cage 324 Rigid bronchoscope 894 Rigid laryngeal endoscopy 182 Rigid laryngoscopy 184 advantages 186 disadvantages 186

Index equipment 184 technique 184 Rigid tracheobronchoscopy 188 Ringer’s solution 400 Risk factors for GERD 606 Risk factors for heart disease 130 Rock singer 321, 443 Roentgen cinema 235 Roentgen rays 235 Role of stroboscopy 488 Root of tongue (lingual tonsil) 244f Rostral trachea 94 RSI questionnaire 120 Rudimentary vocal ligament 439

S Saccular cyst 729 Saccular disorders 729 anatomy 729 classification 729 diagnosis 730 clinical presentation 730 evaluation 732 etiology 730 management 732 endoscopic approach 733 external approach 735 Sagittal diameters 26 Salbutamol 338 Salivary gland secretion 336 Sampling 64 Samter’s triad 393 Santorini’s cartilage 26, 30 Scanning speech 507 Scarlet fever 893 Scar tissue mass 715 Schaefer-Fuhrman classification 665 Schatzki’s ring 590 Schwann cells 762 Secondary sexual characteristics 644 Sedated esophagoscopy 588 Sella turcica 642 Sensorimotor cortex 520 Sensorimotor reflexes 89 Sequential resection of glottic carcinoma 931 Serial digital interface (SDI) 293 Serotonin-uptake inhibitors 336 Setup and safety in office procedures 941 office airway restriction 945 office complication management 945 office ergonomics 942 office safety 945 office setup 941

office treatment preparation 943 topical medication 944 Severe dysplasia 907 Severe hoarseness 159 Sex hormone on voice 645 Sex hormones and the larynx 643 Sexually transmitted diseases 134 Shimmer measurement 159 Shock waves 663 Shorter open phase 202t Shorter vocal fold length 202t Short thyromental distance 188 Shoulder girdle 499 Shy-Drager syndrome 508 Sickle knife 420 Signal-to-noise ratio 159, 174 Signet ring-shaped cricoid cartilage 661 Silastic medialization 810 Silver staining 90 Simple posterior glottic webs 869 Sine waves 66 Singing voice 319 Singing voice disorders 535t Singing Voice Handicap Index (S-VHI) 172t Singing voice specialist (SVS) 115 Single-fiber EMG 271 Single-fiber muscle action potentials 268 Sinus of Morgagni 35 Sinusoidal model 66 Sinusoidal vibratory pattern 203t Sixth cervical vertebra 243 Six tracheal rings 1006 Skeletal framework 23, 26 Skeletomembranous framework 23 Skin endpoint titration test 537 Skull base 23 Sleep apnea 131 Small access tunnel 718 Smaller vocal folds 157 Small laryngeal cancer 171 Small larynx 545 Small vessel vasculitis 558 Smear test 646f Smooth muscle constriction 600f Sniffing position 183, 417 Solid stainless steel needle 266 Somatic motor system 498 Sophisticated image archive system 293 Sound and acoustic recordings 63 Sound spectrum 66 Source-filter theory 76 Spasmodic dysphonia 20, 163, 165, 508 essential tremor 509 essential voice tremor 509

1033

treatment 510 Spasmodic dysphonia 509, 519 diagnosis 519 etiology 520 injections through the thyrohyoid space 523 injection through the cricothyroid membrane 522 techniques of botulinum toxin injections 522 treatment 520 botulinum toxin 521 electrical stimulation 521 surgery 521 Spasmodic dysphonia 999 Specific parameters of voice 174 Spectral analysis of the waveform 67 Spectrogram 69 Spectrogram graph 69 Speech-Language-Hearing Association 114 Speech-language pathologist (SLP) 322, 312 Speech materials 366 Speech of prehumans 4 Speech therapy 416 Speed index 165 Speed quotient (SQ) 164 Sphenoid bone 642 Sphincteric closure 23 Spinal cord injuries 616 Spindle-shaped glottic insufficiency 507 Spine injuries 666 Spirometry monitors 608 Split phrenic nerve 834 Squamocolumnar junction 975 Squamous cell carcinomas 467 Squamous cells 99 Squamous dysplasia 905 Squamous epithelium 4, 45 Squamous intraepithelial lesions (SILS) 916 Squamous intraepithelial neoplasia 906 Squamous mucosa 645 Squamous precursor lesions 905 Staging of laryngopharyngeal reflux 708t Stand-alone archives 294 Standard DTAP vaccine 604 Standard fiberoptic endoscopes 195 Staphylococcal cervical spondylodiscitis 822 Static glottal opening 81 Steady phonation 162 Sternoclavicular ligament 34 Sternocleidomastoid 500

1034

Laryngology

Sternocleidomastoid muscle 34, 503 Sternohyoid muscle 34 Steroid-induced psychosis 343 Steroid inhalers 556 Stiffness due to scarring 230 Stiff vocal folds 778 Stochastic noise behavior 72 Stockholm voice evaluation approach 146 Strap muscles 91 Stray laser beams 394 Streaming media 304f Stream of food 23 Strength of sound 76t Stress-strain curves 52 Stroboscopic examination 194, 450, 695 Stroboscopic light 239 Stroboscopic mucosal wave analysis 680 Stroboscopic parameters 422 Stroboscopy 113 Stroboscopy effect 196 Stroboscopy features 207 Stroboscopy image 208 Stroboscopy principle 194 Strobovideolaryngoscopy 113, 119, 280, 715 Stroke 506 Structural glycoproteins 435 Stylohyoid ligament 29, 32 Stylopharyngeal muscles 35 Subcortical brain mechanisms 90 Subcutaneous emphysema 664 Subepithelial cordectomy 924f Subglottal pressure 56 Subglottic cancer 252f Subglottic cysts 629 Subglottic edema 461, 554, 574f Subglottic pressure 162, 195 Subglottic stenosis 464t, 877 autoimmune SGS management 878 complex stenosis 880 etiology influences management 877 evaluation 879 idiopathic SGS management 877 infectious SGS management 879 stents 884 tracheotomy and laryngopharyngeal reflux 880 traumatic SGS management 878 treatment: endoscopic surgery 880 microflaps 881 treatment: open surgery 881 post open repair care and complications 884 Subharmonic oscillation 472f Subjective outcome measures 372

Subligamental cordectomy 924f Submucosal violet red plaques 594 Subtle motion impairment 186 Sulcus vergeture 720 Sulcus vocalis 322t, 681, 715, 720 Sulphuric acid 123 Summer Vocology Institute (SVI) 1000 Superficial cordectomy 931 Superficial lamina propria (SLP) 4, 697, 960, 687 Superficial layer 52 Superficial layer of the lamina propria (SLP) 46, 435 Superior laryngeal nerve (ISLN) 39, 93, 93f, 94, 142, 143, 278, 1006, 1012 Superior laryngeal nerve block 948f Superior laryngeal nerve paralysis 52, 444 Superior thyroid arteries 1006, 1007f Supracricoid partial laryngectomy 925 Supragiottic 761f Supraglottic airway device 390 Supraglottic configuration of the larynx 200 Supraglottic hyperfunction 186, 437 Supraglottic laryngectomy 925 Supraglottic larynx 40 Supraglottic mass 732 Supraglottic space 32 Suprahyoid muscles 34 Suprahyoid musculature 587 Suprasternal notch 887 Surgery for bilateral vocal fold immobility 821 arytenoid and posterior glottis procedures 824 arytenoid lateral fixation 825 botulinum toxin use 826 etiology 821 evaluation 822 laryngeal pacing 826 laryngeal reinnervation 826 tracheostomy 824 treatment 823 treatment choice 827 Surgical anatomy of the thyroid gland 143 Surgical management of spasmodic dysphonia 527 abductor spasmodic dysphonia 530 bilateral type I thyroplasty for abductor spasmodic dysphonia 530 PCA section for abductor spasmodic dysphonia 530 adductor spasmodic dysphonia 527

denervation-reinnervation 527 recurrent nerve section 529 selective laryngeal adductor 527 thyroarytenoid myomectomy and transoral procedures 529 type II thyroplasty 529 Surgical reinnervation of the larynx 832 Sustentacular cells 766 Suture lateralization 825f, 826 Swallowing disorders 588 Swallow studies 823 Syllable strings 365 Sympathomimetic amines 337 Sympathomimetic medications 338 Symptomatic relief 510 Symptomatic vocal fold scarring 715 Symptomatic voice therapy 315 Symptoms of dysphonia 123 Symptoms of hypothyroidism 139 Synchronized electronic flash stroboscopy 193 Synchronous motion 235 Synthetic extracellular matrix 801 Syphilis 15 Systemic immunosuppressive therapy 558 Systemic lupus erythematosus (SLE) 462, 559, 569 Systemic neurologic disorder 506 Systemic steroids 869 Systemic toxicity 514 Systolic pressure 158

T T-cell costimulatory molecule 1010 Talbot’s law 196 Talipes equina 512 Tall columnar nonciliated cells 760 Tardive dyskinesia 345 Teflon granulomas 719 Teflon injection 255f Temporal bone 32 Temporomandibular joint (TMJ) dysfunction 124, 448 Temporomandibular joint 416 Tension asymmetry 54 Tensor tympani 263 Testicles 643 Tetanus immunization status 134 Theatre singer 321 Theca interna 646 Theory of nonlinear dynamics 473 Thermal injury 125 Thermal relaxation time 433

Index Thiazide diuretics 339 Thick epithelium 593 Thicker lamina propria 201, 439 Thick mucosa 26 Thinner vocal fold 203t Thoracic esophagus 587 Thoracic muscle 121, 616 Thoracic spine 498 Thoracic vascular 631 Throat disorders 535t Thulium laser 20 Thyroarytenoid contraction 53 Thyroarytenoid denervation 521 Thyroarytenoid muscles 52, 93, 195, 202, 241, 270f, 326, 415, 521, 522, 636, 784, 800 Thyroarytenoid muscle mechanism 203 Thyroarytenoidmyectomy 521, 372 Thyroepiglottic ligament 30, 32 Thyroepiglottic muscle 35, 37 Thyroglossal duct cyst 251f Thyrohyoid ligament 26 Thyrohyoid membrane 29, 39, 765, 922 Thyrohyoid muscle 34, 29 Thyroid ALA 779 Thyroid and sex hormone abnormalities 124 Thyroid angles 27f Thyroid asymmetry 28f Thyroid cartilage 25, 26, 27f, 32, 237, 274f, 646, 662f Thyroid cartilage fracture 239 Thyroid cartilage growth 631 Thyroid disease 141 Thyroid dysfunction 157 Thyroidectomy 142 Thyroid hormones 643 Thyroid lamina 528 Thyroid lobectomy 142 Thyroid mass 140 Thyroid nodule 140, 141 Thyroid perichondrium 931 Thyroid stimulating hormone 641 Thyroid surgery 143 Thyroid´s lamina 29 Thyroplasty (TPL) 777 Tibetan plateau 355 Tiny fissure of squamous epithelium 697 Tissue momentum 51 Tissue morphology 436 Tissue trauma from vibrational strain 436 Tobacco 130 Tobacco use 901 Toluidine blue 902 Tongue protrusion 688

Tooth fracture 416 Topical anesthesia 20 Total laryngeal transplant 1006 Total laryngectomy 759 Total or complete cordectomy 924f Tracheal anomalies 465 Tracheal esophageal speech 195 Tracheal length 887 Tracheal stenosis, metallic stents for SGS 884 Tracheal stenosis 887, 891, 895 etiology 890 congenital tracheal stenosis 890 idiopathic tracheal stenosis (ITS) 891 infection 893 inflammatory conditions 892 postintubation/post-tracheostomy management 893 balloon dilation 893 contact cryotherapy 895 electrocautery knife 894 instrumentation 893 intraluminal steroids 895 laser 894 Mitomycin-C 895 Montgomery T-tube 895 stents 895 morphology and classification 888 severity of airway narrowing 887 tracheal anatomy 887 Tracheal surgery 895 Tracheal washings 709 Tracheobronchial bud 24 Tracheobronchial rupture 662 Tracheobronchoscopy 709 Tracheoesophageal fistula (TEF) 590 Tracheoesophageal fistula repair 466, 822 Tracheoesophageal puncture 978f Tracheostomy 590, 849 complications 854 early 854 immediate 854 late 855 contraindications 849 history 849 indications 849 percutaneous dilatational tracheotomy 856 techniques 850 emergency tracheotomy and cricothyroidotomy 852 mediastinal tracheostomy 853 open tracheotomy 850 percutaneous tracheotomy 851 postoperative care 853

1035

tracheotomy in children 853 Traditional Chinese medicine (TCM) 350, 501 Trager approach 501 Trajectory of the vocal folds 199 Trans-sexual surgery 239 Transcranial magnetic stimulation 90 Transglottal pressure 85, 86 Transglottic cancer 37 Transition zone 415 Translaryngeal intubation 667 Transmuscular cordectomy 924f Transnasal esophagoscope (TNE) 19, 588, 596 Transoral laser thyroarytenoid myoneurectomy 529 Transoral robotic surgery (TORS) 986 Transplanted larynx 1010f Transplanted thyroid gland 1006 Transportation-related laryngeal trauma 659 Transversal diameter 30 Transverse belly of the cricothyroid muscles 784 Transverse cordotomy 874 Trauma theory 697 Traumatic intubation 877 Treating the singing voice 319 assessment and goal setting for the singing voice 323 laryngeal function 324 posture and breath management 323 establishing career longevity 329 history of dysphonia in the singer 319 medical problems 320 mental problems 320 mucosal issues 320 mucous problems 320 muscle issues 319 overall health 329 register integration 328 treatment program for the dysphonic singer 322 understanding the singer with dysphonia 320 understanding voice use demands for the singer 321 Treatment for reflux 555 Treatment of chronic cough 606 Treatment of leukoplakia 904 Treatment of vocal fold paralysis 775 Tremor symptoms 510 Tricyclic antidepressants 346 Tricyclic depressants 336 Trigger laryngeal closure 505

1036

Laryngology

Trigger point myotherapy 501 True vocal folds 553 True glomera 766 Truncation of the vocal fold polyp 692 Truncation vocal fold nodules 423 Tube exchange catheters 388t Tube phonation 327 Tuberculosis 15 Tucker’s concept 813 Tumor mass 236 Tumor necrosis factor (TNF) 568 Turbulent airflow 69, 81 Turbulent noise source 85 Types of tobacco 130 Typhoid fever 893 Typical asthma 607

U Ulcerative laryngitis 560 Ultrahigh speed photography 113 Uncontrolled epilepsy 90 Unencapsulated semisolid fluid 681 Unidirectional microphone 157 Unilateral vocal fold paralysis (UVFP) 206, 460, 616, 631, 638, 773, 813 Unilateral vocal paralysis 370 United States Department of Agriculture (USDA) 356 Unmanaged stress 134 Unsedated endoscopic techniques 19 Unsedated vocal cord 20 Unusual tumor 461 Upper aerodigestive tract 140, 183 Upper airway cough syndrome (UACS) 463, 604 Upper esophageal sphincter (UES) 511, 587 Upper fibers of the trapezius 499 Upper respiratory infections (URI) 459, 760 Upper respiratory region 9 Upper respiratory tract 9 Upper torso 497 Using dicom and HL7 for image archive integration 302 Uterine cervix 18

V Vagus nerve 39 Valsalva maneuver 23, 732 Valuable tool 140 Value of consecutive differences 271

Variable focal length lens 418 Varicella 134 Vascular anastomoses 1006 Vascular anomalies 464t Vascular dilation 600f Vascularized mucosal flap 871 Vascular leiomyoma 765 Vascular lesion 322t Vehicular laryngeal trauma cases 660 Velocardiofacial syndrome 468 Venom hypersensitivity 551 Ventral cervical 528 Ventral cervical rami 528 Ventral respiratory group (VRG) 93f Ventral swallowing group (VSG) 93f Ventricle of Morgagni 336 Ventricles 238 Ventricular fold (false) 244f Ventricular fold 26 Ventricular fold hyperplasia 26 Verbal–vocal communication system 4 Vertebral column 25 Vertical axis 475 Vertical hemilaryngectomy 925 Vertical midline 661 Vertical plane 810 Vertigo 507 Vestibular ligament 32 Vibration therapy 325 Vibratory amplitudes 165 Vibratory asymmetry 193 Vibratory cycle 197 Vibratory mode 328 Vibratory symmetry 206 Vicryl sutures 882 Video compression comparison 297f Video documentation 140 Video laryngoscopy 239 Video laryngostroboscopy (VLS) 239, 366, 625 Videostroboscopic examination 796 Videostroboscopy 140, 143, 194, 566f Videostroboscopy image 195 Videostroboscopy setup 999 Videostroboscopy video 197 Viral upper respiratory tract infection 601t Virtual arthroscopy 238 Virtual dissection 238, 239 Virtual endoscopy 241 Virtual endoscopy and virtual dissection 245 Viscoelasticity 52 Viscous saliva 336 Visual-perceptual outcome measures 370

Visual analogue scale 150 Visual examination 140 Visualization of the vallecula 183 Vocal abuse 444 Vocal behaviors 311 Vocal cord palsy 460 Vocal cord paralysis 229 Vocal cord surgery 902 Vocal disorders 113 Vocal disruption 519 Vocal distress 635 Vocal dysfunction 120, 565 Vocal efficiency 56, 497 Vocal endurance 329 Vocal fatigue 367, 566 Vocal fatigue and dysphonia 122 Vocal fold (VF) 29f, 45, 140, 237 Vocal fold abductors 36f Vocal fold adduction 74 Vocal fold atrophy 778 Vocal fold augmentation 507 Vocal fold bradykinesia 507 Vocal fold cells 103 Vocal fold collision force 60 Vocal fold cover 202 Vocal fold cyst 416, 629, 681f Vocal fold cytology 653 Vocal fold dysfunction 460 Vocal fold edema 573 Vocal fold edge 698 Vocal fold elongation 33, 51 Vocal fold epithelium 104, 644, 902 Vocal fold fibroblasts 108 Vocal fold fixation 879 Vocal fold gene expression 103 Vocal fold granuloma 20, 466, 575f Vocal fold health 104 Vocal fold histology 5 Vocal fold immobility 464t, 662 Vocal fold injection 20, 791 anesthesia 793 transcricothyroid 794 transoral 793 transthyrohyoid 794 transthyroid 795 history 791 injection materials 795 autologous fat injection 796 calcium hydroxylapatite 797 collagen 795 fibroblasts 801 gelfoam 795 hyaluronic acid 796 radiesse voice gel 797 superficial vocal fold injection 799

Index operating room versus in office 792 Vocal fold injury 105, 544 Vocal fold length 158 Vocal fold lesions 618 Vocal fold ligament 422 Vocal fold lubrication 336, 449 Vocal fold mass 195, 141 Vocal fold medicalization 29 Vocal fold motion 194 Vocal fold mucosa 46f, 99, 101, 524, 553 Vocal fold nodules 322t, 415, 687, 690 assessment 688 features 688 presentation 687 treatment 689 nonsurgical 689 surgical 690 Vocal fold oscillation 194 Vocal fold palsy 778 Vocal fold paralysis 174, 206, 210, 265, 399, 506 Vocal fold paresis 511, 514 Vocal fold pathology 104, 460, 490, 618 Vocal fold polyp 327, 415, 479, 680, 691 KTP laser excision 694 surgical excision 691 Vocal fold polyps and nodules 57 Vocal fold pseudobowing 488 Vocal fold pseudoflaccidity 488 Vocal fold scar basic concepts, research 716 current therapy 716 potential prevention 716 surgery 716 treatment 716 Vocal fold scar formation 105 Vocal fold scarring 161 Vocal folds smear test 646f Vocal fold stiffness 163 Vocal fold tissue 695 Vocal fold vibration 54, 74, 103, 171, 193, 195, Vocal fold vibration image 194 Vocal fold vibratory cycles 364 Vocal fold vibratory function 194 Vocal fold viscosity 162 Vocal fold volume 784 Vocal function exercises (VFES) 638 Vocal hygiene 528 Vocal hygiene measures 416 Vocal intensity 158 Vocalis ligament 195 Vocalis muscle 4, 35, 195 Vocalizations 3 Vocal ligament 32, 46, 243, 415, 681

Vocal mechanism 158, 443 Vocal nodules 628 Vocal pathologies 82, 201 Vocal Performance Questionnaire (VPQ) 172t Vocal physiology 113 Vocal pitch 145 Vocal polyps 59 Vocal process (VP) 29f, 30 Vocal process granulomas 705, 712 Vocal process of the arytenoid cartilage 37 Vocal production 319 Vocal quality-of-life studies 635 Vocal rehabilitation 472 Vocal rest 438 Vocal scan 238, 243 Vocal sounds 3 Vocal system 157 Vocal technique 320 Vocal tract 4, 158, 204 Vocal tract acoustics 472 Vocal tract anatomy 76t Vocal tract articulators 24 Vocal tract geometry 76 Vocal tract protocol 249 Vocal training history 123 Vocal trauma 556 Vocal trauma and reflux 553 Vocal vibratory function 193 Vocational singer 321 Voice Activity and Participation Profile (VAPP) 172t, 314 Voice as a dynamical system 69 Voice biology 101, 108 Voice breaks 229, 519 Voice clinicians 147 Voice coach 1002t Voice Disability Coping Questionnaire (VDCQ) 172t Voice disorders 99, 169, 311, 565 Voice fatigue 237, 239 Voice Handicap Index (VHI) 120, 172, 172t, 313, 367, 626, 635, 698, 783f Voice Handicap Index-10 (VHI-10) 120, 172t, 175 Voice Handicap Index-Partner (VHI-P) 172t Voice history 119 chief complaint 120 family history 126 history of present illness 121 medications and allergies 124 occupational history 122

1037

past medical history 123 past surgical history 125 preappointment evaluation 119 social history 125 Voice impairment and disability 451 Voice laboratory measurements (VLMS) 368 Voice measurements 156t direct measurements 156t high-speed laryngeal imaging 156t stroboscopy 156t video kymography 156t indirect measurements 156t acoustic analysis 156t aerodynamic analysis 156t electroglottography 156t Voice mutation 643 Voice offset 228 Voice onset and offset 227 Voice Outcome Survey (VOS) 172t, 368, 626 Voice performers 239 Voice problems 613 Voice problems in respiratory disease 613 cancer 616 chronic obstructive pulmonary disease 614 glottal incompetence 617 lesions 618 psychological disorders 618 neurologic disorders 615 amyotrophic lateral sclerosis 615 Parkinson’s disease 615 spinal cord injuries 616 obstructive disorders 613 asthma 613 respiratory characteristics 616 muscle tension dysphonia 616 paradoxical vocal fold movement disorder (PVFMD) 616 PVFMD and chronic cough 617 restrictive disorders 614 idiopathic pulmonary fibrosis 614 sarcoidosis 615 tuberculosis 615 Voice production 119, 169, 242f, 63, 643 Voice professionals 139 Voice quality 145, 443 Voice quality perception 152 Voice range profile (VRP) 159 Voice-related dysfunction 121 Voice-related patient-reported outcomes measures 172 Voice-related quality-of-life (VRQOL) 626, 638

1038

Laryngology

Voice-related quality-of-life score 175, 368, 698 Voice-related symptoms 77 Voice-sound modification 74 Voice rest 60, 435 combination with medical management to manage dysphonia 438 history and rationale 435 importance 435 isolation to manage dysphonia 438 postoperative for nonlaryngeal surgery 439 postoperative voice rest for phonosurgery 438 practical considerations 439 Voice source 72 Voice symptom scale (VoiSS) 172t Voice therapist 1002t, 311 Voice therapy 280, 784 Voice training 416 Voicing techniques 494 Volumetric acquisition 241 Voluntary movement 507 Von-Recklinghausen’s disease 762 Vowel production 158 Vowel quadrilateral 327 Vowel sounds 12

W Waist circumference 133 Wallenberg syndrome 90, 506 Wallerian degeneration 773 Water siphon test 977 Waveform morphology of the motor unit 267 Weak cough 773 Weak swallow 773 Weak voice 773 Wegener’s granulomatosis 462, 558, 683, 892, 895 West Nile virus and cytomegalovirus 512 Whisper 82 acoustics 85 aerodynamics 84 generalized aerodynamics 85 glottal configuration 82 Whisper and phonation 81 Whisper control 85 Whispered vowels 86 Whisper glottal area 85 Whispering dysphonia 520 White plaques 557 Williams syndrome 100 Wilson’s Buffalo Voice Profile System 146

Woodwind and brass instruments 438 World Health Organization 367 World Trade Center 603 World Voice Day events 116

X Xeroradiography 237 Xerostomia 140, 450 Xylometazoline 338

Y Yamaha Music and Wellness Institute 116 Yoga and meditation 501 Young’s modulus 52

Z Z-line 975 Zeiss microscope 18 Zeitel’s glottiscope 861 Zenker’s diverticulum 590, 591, 974, 978 Zero amplitude of movement 217 Zone of detection 266